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El Paso Dysplastic Nevus Excision & Integrative Care

El Paso Dysplastic Nevus Excision & Integrative Care

Abstract: In this educational post, I guide you through a clear, step-by-step clinical approach to excising a dysplastic nevus with moderate atypia using modern, evidence-based methods. You will see how a properly executed anesthetic field block creates a pain-free experience, why dermatologic surgery for moderate atypia uses narrow margins, and how meticulous tissue handling supports definitive histologic assessment. I also share how our multidisciplinary team at Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic) in El Paso, Texas integrates chiropractic care, internal medicine oversight, functional medicine, and rehabilitation. Under the medical direction of Dr. Maria Guadalupe Cardenas, MD (Board Certified in Internal Medicine; NPI #1164426749; Texas MD License #J2933), and in collaboration with me, Dr. Alexander Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST, we blend precision procedural care with whole-person strategies grounded in current research. This post highlights how integrative chiropractic care fits into surgical dermatology and personal injury care to optimize healing, reduce pain, and support long-term outcomes.

El Paso Dysplastic Nevus Excision & Integrative Care

Introduction: Perspective on Modern, Multidisciplinary Skin Lesion Care

I am Dr. Alexander Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST. In our El Paso clinic, we often see patients who need carefully planned excisions following a diagnostic shave biopsy. Today, I’ll walk you through a real case: a 62-year-old gentleman returning approximately one month after a shave biopsy revealed a dysplastic nevus with moderate atypia. Our goals: remove the residual lesion with clinically appropriate narrow margins, enable a pain-free experience using a precise anesthetic field block, and ensure the tissue specimen is ideal for pathology.

What makes this care unique is our integrative model. As the Medical Director and Collaborative Physician, Dr. Maria Guadalupe Cardenas, MD (Internal Medicine), provides medical oversight and coordinates care pathways common to multidisciplinary injury and integrative clinics. In parallel, our chiropractic services, functional medicine strategies, and rehabilitation protocols create a cohesive system designed to keep the patient safe, comfortable, and moving toward recovery based on the best available evidence.

Building the Plan: Why Dysplastic Nevus with Moderate Atypia Requires Focused Margins

  • Key concept: Dysplastic nevi with moderate atypia are atypical moles with architectural and cytologic changes that warrant complete excision to reduce the risk of residual atypical tissue.
  • Evidence rationale: For moderate atypia, many dermatologic guidelines support excision with narrow margins (often around 2 mm beyond the visible or scar boundary) to ensure complete removal while preserving healthy tissue. Histopathologic evaluation confirms clearance.

In this case, the original lesion measured approximately 5 x 6 millimeters. I planned margins of roughly 2 millimeters around the current scar, translating to about 5 millimeters around the original lesion perimeter. Using a template helps me create a symmetric, fusiform design aligned with relaxed skin tension lines, minimizing postoperative tension and optimizing cosmetic results. Templates reduce human error in margin symmetry, and a well-planned ellipse supports primary closure with minimal dog-ears.

Design and Anesthesia: A Pain-Free Field Block by Interrupting Cutaneous Nerve Signaling

My goal with anesthesia is simple: make the experience pain-free and efficient. I start by prepping with alcohol, then reinforce the concept of a field block—a circumferential anesthetic “fence” that interrupts nerve signals entering the skin around our excision site.

Technique overview:

  • I select an ideal entry point near the planned excision boundaries.
  • I advance the needle, then inject while withdrawing, turning within the dermis/subcutaneous plane to create a continuous ring of anesthesia.
  • I repeat on the opposite side and, as needed, add lateral entry points to ensure complete coverage, always aiming for minimal needle insertions that produce maximal numbing.

Why it works physiologically:

  • The field block targets the terminal branches of sensory nerves within the dermis and subcutaneous tissue. By bathing these fibers with 1 percent lidocaine with epinephrine, we block voltage-gated sodium channels, preventing depolarization and halting nociceptive transmission.
  • Epinephrine causes local vasoconstriction, reducing bleeding and prolonging lidocaine’s dwell time near nerves. This prolongs anesthesia, helps maintain a bloodless field, and enhances visualization during precise excision.
  • Injecting in subcutaneous tissue to “saturate” beneath the lesion creates a foundational blockade. When we perform intradermal injections after subcutaneous saturation, patients typically report little or no sensation because the deeper nociceptive input has already been interrupted.

Adjunct comfort measures:

  • I use a cold “free spray” over the injection point. Rapid cooling stimulates A-delta fibers, which preferentially transmit cold sensations, creating a gating effect that reduces pain perception as the needle enters. This immediate numbing means they rarely feel the injection.
  • I steer the needle by slight bending to guide the tip across the dermal plane, carefully visualizing the trajectory under the skin. Injecting while withdrawing forms a visible intradermal wheal line that confirms even distribution.

Patient response:

  • Using these methods, our patient reported no pain throughout the anesthetic process. This is exactly the outcome we strive for—an effective, pain-free field block before excision.

Precision Excision: Narrow Margins and Tissue Integrity

With anesthesia confirmed and a clean field, the next step is the excision. Narrow margins are not arbitrary; they balance oncologic safety with tissue preservation, especially in cosmetically sensitive areas.

Core principles:

  • Margin control: For moderate atypia, 2-mm margins are commonly used; they are sufficient for complete removal while minimizing unnecessary tissue loss.
  • Fusiform design: An ellipse aligned with skin tension lines enables linear closure under reduced tension, decreasing the risk of hypertrophic scarring and optimizing cosmesis.
  • Specimen integrity: Gentle handling and correct orientation markings help pathologists assess margins and architecture accurately, confirming clearance.

Physiology of healing:

  • Minimal tension reduces micro-ischemia at wound edges, aiding angiogenesis and fibroblast activity necessary for collagen deposition.
  • Vasoconstriction from epinephrine tempers intraoperative bleeding, stabilizing the clot and early extracellular matrix formation.

Integrative Chiropractic Care in Dermatologic Surgical Recovery

While excision of a skin lesion may seem isolated from musculoskeletal care, an integrative approach adds value for recovery, comfort, and function—especially in older adults or those with comorbidities.

How chiropractic care fits:

  • Posture and movement optimization: After excision, patients often guard movement due to fear of pulling sutures. Chiropractic and rehabilitative strategies help maintain normal biomechanics and prevent compensatory strain.
  • Neuromuscular re-education: Gentle manual therapy and targeted exercises support proprioception and movement confidence, reducing myofascial tension near or distant from the surgical site.
  • Pain modulation: Chiropractic interventions can engage descending inhibitory pathways, reducing central sensitization that sometimes amplifies minor post-procedural discomfort.
  • Circulatory support: Mobility, diaphragmatic breathing, and safe motion progressions improve local perfusion, supporting oxygen delivery and waste clearance in healing tissues.

In practice, I assess global movement patterns and provide tailored strategies to keep patients functional without stressing the incision. For example, we may adjust daily ergonomic habits, teach safe range-of-motion techniques, and implement light isometrics that maintain muscle tone without disturbing the wound.

Multidisciplinary Oversight: Internal Medicine Leadership with Dr. Maria Guadalupe Cardenas, MD

Our clinic operates within a multidisciplinary framework common in integrative and injury care settings. Dr. Maria Guadalupe Cardenas, MD (Board Certified in Internal Medicine; NPI #1164426749; Texas MD License #J2933) serves as our Medical Director and Collaborative Physician. With over 40 years of experience as an internist, Dr. Cardenas supervises medical protocols, ensures safety for patients with complex health histories, and aligns the plan with best practices.

Medical oversight matters because:

  • Risk stratification: Internal medicine evaluates cardiovascular status, diabetes control, anticoagulation, and immunomodulating conditions that might impact bleeding, infection risk, or wound healing.
  • Medication management: Guidance on peri-procedural adjustments for antiplatelets/anticoagulants or immunosuppressants balances safety and procedural efficacy.
  • Systems-based care: Internal medicine connects dermatologic procedures with broader health concerns—sleep, nutrition, metabolic status—each influencing recovery timeline and scar quality.

Collaborative roles:

  • Dr. Cardenas provides medical direction, reviews histories, and creates safe peri-procedural pathways.
  • I deliver the procedure, chiropractic integration, functional medicine insights, and rehabilitative planning.
  • Together, we coordinate personal injury processes, documentation, and patient education.

Functional Medicine Integration: Optimizing Healing Physiology

Functional medicine supports the body’s innate healing mechanisms through targeted lifestyle and nutritional strategies tailored to the patient’s biology.

Focus areas:

  • Inflammation modulation: Adequate omega-3 intake, polyphenols (curcumin, quercetin), and antioxidant-rich foods can support controlled inflammation necessary for healing while preventing prolonged inflammatory states that delay recovery.
  • Glycemic control: Stable blood sugar supports fibroblast function, collagen cross-linking, and reduces infection risk; critical in older adults and those with metabolic syndrome.
  • Micronutrient sufficiency: Vitamin C (collagen synthesis), zinc (DNA replication and immune function), and vitamin A (epithelial integrity) are essential. We personalize supplementation cautiously, consistent with medical oversight.

Reasoning:

  • The acute wound healing phases—hemostasis, inflammation, proliferation, remodeling—depend on energy availability, micronutrient cofactors, and balanced immune signaling. Diet and lifestyle calibrate these processes.
  • Sleep quality and stress modulation (e.g., paced breathing) influence HPA axis activity and cytokine profiles that can either facilitate or impair tissue repair.

Rehabilitation Strategy: Safe Motion, Scar Care, and Long-Term Outcomes

Rehabilitation begins as soon as the procedure ends.

Key steps:

  • Early wound protection: Educate on dressing care, signs of infection, and avoiding tension across the incision.
  • Progressive mobility: Introduce gentle, non-straining movements to prevent stiffness and maintain circulation.
  • Scar optimization: Once the wound has closed, consider silicone sheeting, gentle massage, and sun protection to improve scar quality.
  • Ergonomics: Adjust lifting strategies, workstation setup, and daily routines to prevent undue strain near the surgical site.

Physiologic reasoning:

  • Controlled motion stimulates mechanotransduction pathways in fibroblasts, guiding orderly collagen alignment and increasing tensile strength.
  • Silicone occlusion modulates hydration and reduces excessive collagen deposition, decreasing hypertrophic scar risk.

Personal Injury Care and Documentation

In injury care settings, precision documentation complements clinical excellence:

  • Clear procedural notes with lesion size, margin plan, anesthesia specifics, and patient responses.
  • Photo documentation for pre- and post-excision views (when appropriate).
  • Communication with referring providers and insurers regarding necessity, medical oversight, and outcomes.

Clinical Observations from My Practice

At Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic), I have observed:

  • Patients experience significantly better comfort with a well-executed field block using 1% lidocaine with epinephrine and adjunct cold spray.
  • Narrow, well-planned margins for moderate atypia yield high clearance rates while preserving cosmesis.
  • Integrative chiropractic and functional medicine improve confidence in movement, reduce compensatory pain patterns, and support faster return to normal activities.

Step-by-Step Narrative: From Planning to Excision

  • Pre-Procedure:
    • Confirm pathology: dysplastic nevus with moderate atypia.
    • Explain margins and expectations to the patient.
    • Prepare sterile field with antiseptic; use alcohol for initial prep and repeat.
  • Field Block:
    • Choose entry point; advance needle; inject while withdrawing to create a continuous anesthetic ring.
    • Turn within the tissue plane to cover both sides without fully removing the needle.
    • Add lateral points if needed; saturate subcutaneous tissue under the lesion.
    • Verify numbness; apply cold spray before further injections.
  • Intradermal Distribution:
    • Thread the needle across the dermis; visualize tip; inject on withdrawal to form a visible wheal line indicating spread.
    • Assess patient comfort continuously; recalibrate if sensation persists.
  • Excision:
    • Mark ellipse with template; align with skin tension lines.
    • Excise along just outside the marked borders to respect margins.
    • Handle tissue gently; orient specimen; achieve hemostasis; close in layers if indicated.
  • Post-Procedure:
    • Educate on dressing changes, signs of infection, and motion precautions.
    • Schedule follow-up for pathology results and suture removal.
    • Provide integrative guidance on movement, nutrition, sleep, and stress.

Why Each Technique Matters

  • Template-guided marking: Ensures symmetry, facilitates linear closure, and reduces dog-ears.
  • Field block with epinephrine: Prolongs anesthesia, reduces bleeding, and improves operative field visibility.
  • Injecting on withdrawal: Distributes anesthetic evenly and reduces intratissue pressure spikes that can be uncomfortable.
  • Cold spray: Activates sensory gating to reduce needle pain.
  • Narrow margins: Balance complete excision of atypia with tissue preservation, aligning with evidence and cosmetic considerations.
  • Integrative follow-through: Addresses systemic determinants of healing and functional recovery beyond the incision line.

Safety Considerations

  • Avoid epinephrine in end-arterial regions if risk factors exist; assess peripheral vascular disease.
  • Screen for lidocaine allergies and arrhythmic history.
  • Coordinate with internal medicine on anticoagulation decisions and infection-risk mitigation.

Our Team-Based Care in El Paso, Texas

At Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic), our care model weaves together:

  • Chiropractic care (Dr. Jimenez): Movement analysis, manual therapy, neuromuscular re-education, ergonomic optimization.
  • Medical oversight (Dr. Cardenas, MD): Risk stratification, medication management, systems-based medical direction.
  • Functional medicine: Nutrition, sleep, stress, and personalized supplementation.
  • Rehabilitation: Progressive mobility, scar care, and return-to-function planning.
  • Personal injury services: Comprehensive documentation, coordination with legal and insurance entities where applicable.

Conclusion: Modern, Evidence-Based, Integrative Care for Skin Surgery

Excision of a dysplastic nevus with moderate atypia is more than a precise cut; it is a coordinated effort grounded in physiology, patient comfort, and multidisciplinary safety. By pairing a pain-free field block with careful margin planning and whole-person support, we improve outcomes and the patient experience. Under the medical direction of Dr. Maria Guadalupe Cardenas, MD, and through our integrative chiropractic, functional medicine, and rehabilitative care, patients receive comprehensive, evidence-based support from diagnosis to recovery.


References

Skin Health & Inflammation Solutions Using Functional Medicine


Learn about effective strategies in functional medicine for managing inflammation and promoting skin health and wellness.

Abstract

In this educational post, I walk you through a real-world clinical demonstration of a shave skin biopsy performed on a middle-aged male patient with an inflamed seborrheic keratosis on the lateral aspect of his right hip. The lesion became progressively noticeable over about four weeks, with inflammation, pain, and enlargement. This post covers the full procedural journey—from initial patient presentation and clinical assessment, through topical and injectable local anesthesia, to the execution of the shave biopsy technique and post-procedural hemostasis with aluminum chloride. I also discuss the physiological reasoning behind each step, the evidence base that supports these methods, and how integrative, multidisciplinary care at Injury Medical Clinic PA in El Paso, Texas — led by me alongside Dr. Maria Guadalupe Cardenas, MD, Board Certified in Internal Medicine and our Medical Director — shapes how we approach even seemingly straightforward dermatological procedures within the broader context of a patient’s overall health and wellness. Whether you are a clinician, a student, or a curious patient, this post is designed to take you on a clear, comprehensive, and evidence-supported journey through the science and practice of minor dermatological surgery.


Introduction: Why Minor Dermatological Procedures Matter in Integrative Care

When most people think about integrative or chiropractic-based clinics, they often imagine spinal adjustments, soft tissue therapies, and rehabilitation exercises. While those are foundational pillars of what we do at Injury Medical Clinic PA, comprehensive, patient-centered care extends far beyond the spine. As a clinician with dual credentials in chiropractic medicine and advanced practice nursing—and who works every day alongside an experienced internist—I have come to understand that skin health is not a peripheral concern. In many ways, it is a window into the patient’s overall physiological state.

The skin is the body’s largest organ. It is a dynamic, metabolically active tissue that reflects immune function, hormonal balance, inflammatory status, nutritional sufficiency, and circulatory integrity. When a patient presents with a new, enlarging, inflamed skin lesion, this is not merely a cosmetic inconvenience. It is a clinical signal that deserves careful, evidence-based evaluation and, when appropriate, procedural intervention.

In this post, I describe a clinical procedure I performed: a shave skin biopsy of a clinically suspected inflamed seborrheic keratosis on the lateral aspect of the right hip of a middle-aged male patient. The lesion had been present for approximately four weeks before becoming noticeable and symptomatic, and it showed signs of active inflammation, pain, and progressive enlargement. I walk through every step of the procedure, from the rationale for performing it to the anesthetic technique used, the mechanics of the shave biopsy itself, and the hemostatic methods employed at the conclusion.

But I do more than describe what happened. Throughout this post, I integrate the underlying physiology, evidence-based research, and clinical reasoning that guide every decision. I also explain how this type of minor surgical procedure fits within the broader framework of integrative, multidisciplinary care that defines our practice. My goal is to give you — whether you are a fellow clinician, a student, or a patient — a thorough and deeply informative understanding of what happened, why it happened, and what it means in the context of modern, integrative medicine.


Meet the Team: Dr. Alex Jimenez and Dr. Maria Guadalupe Cardenas

Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST

I am Dr. Alex Jimenez. My clinical journey has taken me through chiropractic medicine, advanced practice nursing, functional medicine, integrative medicine, and injury care — among other disciplines. I hold the following credentials: Doctor of Chiropractic (DC), Advanced Practice Registered Nurse (APRN), Family Nurse Practitioner Board Certified (FNP-BC), Certified Functional Medicine Practitioner (CFMP), Institute for Functional Medicine Certified Practitioner (IFMCP), Advanced Triage Nurse (ATN), and Certified Chiropractic Sports Therapist (CCST). This breadth of training reflects my deep commitment to understanding the human body from multiple clinical perspectives and providing care that addresses the root causes of illness and injury, not merely the surface symptoms.

My clinical observations and ongoing educational work are available at chiromed.com and on my LinkedIn profile. I have spent decades building a practice grounded in evidence-based, patient-first principles, integrating chiropractic care with functional medicine, nursing practice, and collaborative medical oversight.

Dr. Maria Guadalupe Cardenas, MD

Working alongside me every day at Injury Medical Clinic PA is Dr. Maria Guadalupe Cardenas, MD, Board Certified in Internal Medicine, with over 40 years of experience as an internist. Dr. Cardenas holds NPI #1164426749 and a Texas MD License #J2933. In our practice, she serves as Medical Director and Collaborative Physician. This designation reflects both the depth of her clinical expertise and the regulatory framework governing multidisciplinary integrative clinics in Texas.

Dr. Cardenas brings an extraordinary wealth of internal medicine knowledge to our team. As an internist, her training encompasses the prevention, diagnosis, and treatment of adult diseases across virtually every organ system—including the skin, cardiovascular system, endocrine system, gastrointestinal system, and more. Her presence in our clinic ensures that every patient who comes through our doors receives not only the benefits of chiropractic and functional medicine care but also the rigorous medical oversight that complex cases require.

The collaboration between a Doctor of Chiropractic/Advanced Practice Nurse and a Board-Certified Internist is the very essence of what makes our clinic exceptional. This multidisciplinary model is increasingly recognized in the evidence-based literature as the gold standard for integrative and injury care, allowing patients to receive comprehensive, coordinated, and truly holistic treatment under one roof.


Understanding the Clinical Setting: Injury Medical Clinic PA

Injury Medical Clinic PA, also known as Mission Plaza Injury Medical Clinic, is located in El Paso, Texas. Our clinic is a multidisciplinary integrative care facility that provides a wide spectrum of services, including:

  • Chiropractic care and spinal manipulation
  • Advanced practice nursing and family medicine
  • Internal medicine oversight and medical direction
  • Functional medicine and nutritional therapy
  • Personal injury care and accident rehabilitation
  • Minor surgical procedures and dermatological care
  • Diagnostic imaging and laboratory services
  • Physical rehabilitation and corrective exercise

The multidisciplinary model we operate under is not merely administrative convenience — it is a clinically superior approach to patient care. Research consistently shows that patients who receive care from coordinated, multidisciplinary teams experience better outcomes, shorter recovery times, lower rates of chronic pain progression, and higher patient satisfaction than those who receive siloed, single-discipline care (Körner et al., 2016; Stochkendahl et al., 2017).

In the context of the procedure described in this post, the clinical setting matters profoundly. A minor dermatological procedure like a shave skin biopsy is performed not in isolation, but within a broader clinical picture. Dr. Cardenas’s medical oversight ensures that any systemic conditions — such as diabetes, autoimmune disorders, coagulopathies, or medication interactions — that might affect wound healing or anesthetic response are carefully considered before the procedure begins. My training as an APRN and FNP-BC means I can assess, diagnose, and treat conditions across multiple body systems, ensuring the dermatological finding is evaluated in the context of the whole patient.


Patient Presentation: The Middle-Aged Male with a Lateral Hip Skin Lesion

The patient who came to us on this occasion was a middle-aged male presenting with a skin lesion over the lateral aspect of his right hip. He reported that the lesion had become significantly noticeable over the preceding four weeks. During that time, he observed progressive enlargement, local inflammation, and the onset of pain in the area.

Key Clinical Features at Presentation

  • Location: Lateral aspect of the right hip
  • Duration of noticeable change: Approximately four weeks before the visit date of September 1, 2026, meaning symptoms began around early August 2026
  • Symptoms: Inflammation, pain, and enlargement of the lesion
  • Clinical appearance: Consistent with an inflamed seborrheic keratosis

Why the History and Timeline Matter

The four-week timeline matters for several reasons. Seborrheic keratoses are benign epidermal tumors that typically grow slowly over years. When a patient reports a sudden increase in size, inflammation, and pain over a period of weeks, this raises the clinical question of whether the lesion has become irritated or inflamed due to friction, trauma, or clothing contact — all of which are common at the lateral hip — or whether the clinical picture warrants concern for a more serious pathology, such as squamous cell carcinoma, basal cell carcinoma, or melanoma.

The principle here is the “ABCDE” rule for skin lesion evaluation: Asymmetry, Border irregularity, Color variation, Diameter greater than 6mm, and Evolution (change over time). The “E” — evolution — is arguably the most clinically alarming feature, because change in a skin lesion is always a reason to investigate further (Abbasi et al., 2004). In this case, the rapid change over four weeks, combined with inflammation and pain, was the primary driver for proceeding with a biopsy.

The Role of Pain and Inflammation

Pain in a seborrheic keratosis is noteworthy. Most seborrheic keratoses are entirely asymptomatic. When a patient reports pain, this typically indicates one of the following:

  1. Mechanical irritation — repeated friction against clothing, a waistband, or a belt, which is particularly common at the lateral hip
  2. Secondary inflammation — the body’s immune response to an injured or irritated keratinocyte population
  3. Secondary infection — less common but possible if the surface of the lesion has been broken
  4. Underlying epidermal or dermal pathology — warranting biopsy to rule out malignancy

Regardless of the underlying cause, the combination of enlargement, inflammation, and pain in a skin lesion over four weeks establishes a clear clinical indication for tissue sampling and histopathological analysis — in other words, a biopsy.


What Is Seborrheic Keratosis? A Deep Dive into the Pathophysiology

Seborrheic keratosis (SK) is one of the most common benign epidermal neoplasms encountered in clinical practice. Understanding the pathophysiology of SK is essential for appreciating why it can become inflamed, painful, and enlarged, and why biopsy is sometimes necessary to confirm the diagnosis.

Epidemiology and Prevalence

Seborrheic keratoses affect individuals of all races and ethnicities, but they are most prevalent in adults over the age of 50. By the seventh decade of life, virtually all adults have at least one seborrheic keratosis (Gill et al., 2000). They can appear anywhere on the body except the palms and soles, with the trunk, face, scalp, and extremities being the most common locations. The lateral hip — the location of our patient’s lesion — is a clinically plausible site, particularly given the mechanical friction to which this area is routinely subjected.

Histopathological Features

At the microscopic level, seborrheic keratoses are characterized by:

  • Acanthosis — thickening of the epidermis due to proliferation of keratinocytes and basaloid cells
  • Hyperkeratosis — an excess of keratin on the surface of the lesion
  • Papillomatosis — irregular upward projections of the epidermal surface
  • Horn cysts — invaginations of keratin-filled cysts within the lesion
  • Flat base — the lesion grows upward from the skin surface, not downward into the dermis, which is why it appears “stuck on” clinically

These histopathological features explain the characteristic clinical appearance of SK: a waxy, “stuck-on” lesion with a rough, warty texture, ranging in color from light tan to dark brown or black.

Molecular Pathogenesis

The molecular underpinnings of seborrheic keratosis have been increasingly well characterized in recent years. Research has identified somatic mutations in the FGFR3 (Fibroblast Growth Factor Receptor 3) and PIK3CA genes as the most frequently implicated genetic alterations in SK development (Hafner et al., 2007). These mutations constitutively activate cell proliferation pathways—specifically the RAS/MAPK and PI3K/AKT signaling cascades—resulting in the uncontrolled but benign proliferation of keratinocytes that defines the lesion.

Importantly, these are somatic mutations, meaning they arise in individual skin cells over a lifetime and are not inherited. This explains why SK prevalence increases dramatically with age: over decades, accumulating UV radiation exposure, oxidative stress, and DNA repair inefficiencies contribute to the accrual of these mutations in keratinocytes (Hafner et al., 2009).

Why Does Seborrheic Keratosis Become Inflamed?

Inflammation in a seborrheic keratosis is not uncommon and can arise through several mechanisms:

1. Mechanical Irritation and the Koebner Phenomenon

The Koebner phenomenon refers to the development of new skin lesions at sites of trauma or mechanical irritation in individuals who are predisposed to certain skin conditions. In the context of SK, repeated mechanical friction — particularly from clothing, waistbands, or physical activity — can trigger an inflammatory cascade within the lesion. The keratinocytes within the SK release pro-inflammatory cytokines, including interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α), which recruit immune cells to the area and produce the classic signs of inflammation: redness, swelling, warmth, and pain (Baroni et al., 2012).

2. Immune Cell Infiltration

Histopathological studies of inflamed seborrheic keratoses have demonstrated significant lymphocytic infiltration — an influx of T lymphocytes into the lesion — which can lead to what is sometimes called “irritated seborrheic keratosis” or “inflamed SK”. In some cases, this lymphocytic infiltration can actually lead to partial regression of the lesion, a process that mirrors the immune-mediated destruction of neoplastic tissue (Yeh et al., 2000).

3. Secondary Infection

If the surface of the seborrheic keratosis is disrupted—through scratching, friction, or minor trauma—bacteria can colonize the damaged keratin layer, triggering a secondary infectious inflammatory response. This is more common in lesions located in areas of high friction or moisture.

4. The Sign of Leser-Trélat

In rare cases, the sudden onset of multiple new seborrheic keratoses — or the rapid enlargement of existing ones — is associated with internal malignancy, a phenomenon known as the Sign of Leser-Trélat (Schwartz, 1996). While this sign is uncommon and its clinical reliability has been debated in the literature, it underscores the importance of evaluating rapidly changing seborrheic keratoses in the context of the patient’s overall health. Dr. Cardenas’s internist oversight at our clinic is particularly valuable in these cases, as an experienced internist is well positioned to evaluate for systemic signs of malignancy.


Clinical Evaluation and Differential Diagnosis of Skin Lesions

Before proceeding to any skin biopsy, a thorough clinical evaluation is essential. The differential diagnosis for an inflamed, enlarging skin lesion at the lateral hip in a middle-aged male is broad and includes both benign and malignant entities.

Benign Differential Diagnoses

  • Seborrheic keratosis (inflamed) — the leading clinical diagnosis in this case
  • Dermatofibroma — a benign fibrous nodule of the dermis, often found on the lower extremities
  • Epidermoid cyst (inflamed) — a cystic structure containing keratin, which can become inflamed or infected
  • Lipoma — a benign subcutaneous tumor composed of mature adipocytes
  • Verruca vulgaris (common wart) — caused by Human Papillomavirus (HPV), can occur at any site
  • Sebaceous hyperplasia — an overgrowth of sebaceous glands, more common on the face
  • Pigmented nevus (mole) — a benign melanocytic lesion that may enlarge and become inflamed

Malignant and Pre-Malignant Differential Diagnoses

  • Actinic keratosis — a pre-malignant lesion caused by chronic UV exposure, which can progress to squamous cell carcinoma
  • Squamous cell carcinoma (SCC) — a malignant tumor of keratinocytes; can mimic an inflamed seborrheic keratosis clinically
  • Basal cell carcinoma (BCC) — the most common skin cancer; can present as a pearly, raised nodule with surface changes
  • Melanoma — the most dangerous skin cancer; can present as a changing pigmented lesion
  • Merkel cell carcinoma — a rare but aggressive neuroendocrine skin tumor
  • Cutaneous lymphoma — lymphomatous infiltration of the skin

The clinical appearance — a “stuck-on,” waxy, hyperpigmented lesion with a rough surface — strongly suggests seborrheic keratosis in this case. However, the recent rapid change, including enlargement, inflammation, and pain over four weeks, means that clinical diagnosis alone is insufficient. The gold standard for definitive diagnosis of any skin lesion is histopathological examination of a tissue specimen — which is exactly why the shave biopsy was performed.

Dermoscopy as a Complementary Tool

Modern clinical practice increasingly employs dermoscopy (also called dermatoscopy) as a non-invasive adjunct to clinical evaluation of skin lesions. Dermoscopy uses a handheld polarized light microscope to visualize subsurface skin structures that are invisible to the naked eye. In seborrheic keratosis, dermoscopic features include milia-like cysts, comedo-like openings, fissures and ridges, and cerebriform patterns (Braun et al., 2005). The absence of these features — or the presence of melanoma-associated features — would strengthen the case for urgent biopsy and potential oncological referral.


Indications for Shave Skin Biopsy

A shave biopsy is one of several biopsy techniques used in dermatological practice. Understanding when and why a shave biopsy is the appropriate choice — rather than a punch biopsy, excisional biopsy, or incisional biopsy — is essential for appreciating the clinical reasoning in this case.

Types of Skin Biopsy Techniques

1. Shave Biopsy

A shave biopsy uses a surgical blade or razor to horizontally “shave” the lesion from the skin surface. It is ideally suited for:

  • Exophytic lesions — lesions that project above the skin surface, such as seborrheic keratoses, viral warts, and skin tags
  • Superficial lesions — where the pathology is confined to the epidermis and superficial dermis
  • Lesions where full excision is not necessary — particularly when the primary goal is diagnosis rather than complete removal

2. Punch Biopsy

The punch biopsy uses a circular cutting tool to remove a cylindrical core of full-thickness skin. It is preferred for:

  • Inflammatory dermatoses — conditions like psoriasis, lichen planus, or eczema, where the pathology spans the full thickness of the skin
  • Lesions where dermal involvement needs to be assessed
  • Alopecia and scalp conditions

3. Excisional Biopsy

The excisional biopsy removes the entire lesion with a margin of normal tissue. It is indicated when:

  • Complete removal is both diagnostic and therapeutic — as in suspected melanoma, where complete excision with margins is the standard of care
  • The lesion is small enough to excise completely

4. Incisional Biopsy

The incisional biopsy removes only a portion of a large lesion. It is used when:

  • The lesion is too large to excise completely
  • A representative sample is needed for diagnosis

Why a Shave Biopsy Was Appropriate in This Case

For the patient described — with a clinically suspected inflamed seborrheic keratosis that was exophytic (projecting above the skin surface) and located in a non-cosmetically critical area — the shave biopsy was the ideal technique for the following reasons:

  • The lesion is epidermal in origin — seborrheic keratoses are confined to the epidermis and do not invade the dermis, making a superficial shave technique sufficient to obtain a diagnostic sample
  • The technique allows for rapid removal with minimal tissue trauma and a small, cosmetically acceptable wound
  • The exophytic nature of the lesion means that a horizontal cut at the base of the lesion will capture the entire pathological tissue.
  • The intradermal wheal technique (described below) physically elevates the lesion, making it easier to perform a clean, complete shave with precise margins.
  • The hemostatic properties of aluminum chloride make this technique safe and efficient in an outpatient setting without the need for sutures.

The Science of Local Anesthesia: Pain Ease Mist and Lidocaine with Epinephrine

One of the most important aspects of any minor surgical procedure is pain management. The goal of local anesthesia is to render the procedural site completely insensate — free from pain — without affecting the patient’s consciousness or systemic physiology. In this procedure, two anesthetic agents were used complementarily: Pain Ease mist (a topical cryogenic spray) and 1% lidocaine with epinephrine (an injectable local anesthetic).

Pain Ease Mist: Topical Cryotherapy for Needle Phobia and Surface Anesthesia

Pain Ease Mist is a commercially available topical cryogenic spray (also known as a “vapocoolant spray”) that works by rapidly cooling the skin surface through the evaporation of a volatile liquid — typically a mixture of 1,1,1,3,3-pentafluoropropane and 1,1,1,2-tetrafluoroethane. The rapid evaporation of these compounds extracts heat from the skin surface, producing a brief but intense cooling sensation that temporarily numbs the superficial nerve endings.

Mechanism of Action

Cryogenic sprays produce surface anesthesia by thermally modulating cutaneous nociceptors. Pain is transmitted from the skin to the central nervous system via nociceptive afferent nerve fibers — primarily A-delta fibers (which transmit sharp, fast pain) and C-fibers (which transmit slow, burning, or aching pain). Both of these fiber types are exquisitely sensitive to temperature changes.

When skin temperature drops rapidly below about 10°C, voltage-gated sodium channels in nociceptive nerve endings become transiently inactivated. These sodium channels are essential for the generation of action potentials — the electrical signals that carry pain information along the nerve fiber. When cold blocks them, the nociceptive fiber cannot fire, and the sensation of pain is temporarily abolished (Bleakley et al., 2012).

Clinical Application in This Procedure

In this procedure, the Pain Ease mist was applied to the skin before needle insertion to blunt the pain of the initial puncture. This is a particularly thoughtful approach to patient care. Needle phobia — technically termed trypanophobia — is one of the most common procedural fears among patients, and even in patients who do not have a formal phobia, the anticipation of needle pain can trigger significant anxiety, which in turn increases pain perception through central sensitization mechanisms (Taddio et al., 2009).

By pre-treating the skin with a vapocoolant spray, I was able to:

  1. Reduce the pain of the initial needle insertion
  2. Reduce patient anxiety about the procedure
  3. Create a more relaxed procedural environment, which itself reduces pain perception

This is an excellent example of how integrative, patient-centered care — which prioritizes the patient’s comfort and experience alongside clinical efficacy — shapes procedural decisions.

Lidocaine with Epinephrine: The Gold Standard Injectable Local Anesthetic

Lidocaine is the most widely used local anesthetic in clinical practice worldwide. It belongs to the amide class of local anesthetics, characterized by stability, low allergenic potential, and reliable onset of action.

Mechanism of Action of Lidocaine

Lidocaine produces local anesthesia by blocking voltage-gated sodium channels in the axonal membranes of peripheral nerve fibers. When these channels are blocked, the nerve cannot generate or propagate action potentials, and all sensory modalities — including pain, temperature, touch, and pressure — are temporarily abolished in the distribution of the affected nerve.

At the molecular level, lidocaine enters the sodium channel from the intracellular side of the nerve membrane — meaning it must first cross the nerve cell membrane to reach its binding site. It does this in its uncharged (base) form, which is lipid-soluble and can diffuse through the lipid bilayer. Once inside the cell, it becomes partially ionized (charged) at physiological pH and binds to the alpha subunit of the voltage-gated sodium channel in its open or inactivated state, preventing the channel from reopening and thus blocking nerve conduction (Catterall et al., 2005).

This mechanism explains an important clinical observation: lidocaine is less effective in infected or inflamed tissue, because the acidic environment of infected tissue (lower pH) favors the ionized form of lidocaine, which cannot cross the nerve membrane as easily. This is a critical consideration when anesthetizing inflamed lesions like the one in this case, and it reinforces the importance of using an adequate volume and correct placement to achieve reliable anesthesia despite potential local acidosis.

The Role of Epinephrine

The addition of epinephrine (adrenaline) to the lidocaine solution serves several important functions:

1. Vasoconstriction and Prolonged Anesthetic Duration

Epinephrine is a potent alpha-1 adrenergic receptor agonist that causes vasoconstriction — narrowing of local blood vessels — at the injection site. This vasoconstriction reduces systemic absorption of lidocaine, keeping the anesthetic concentrated at the site of action longer. The result is a significantly prolonged duration of local anesthesia — from approximately 30-60 minutes with plain lidocaine to 90-120 minutes or more with lidocaine-epinephrine (Becker & Reed, 2012).

2. Reduced Bleeding

Epinephrine-induced vasoconstriction also reduces bleeding at the procedural site. This is particularly beneficial during a shave biopsy, where a clean, blood-free operative field is essential for accurate margin assessment and specimen quality.

3. Reduced Systemic Toxicity

By slowing systemic absorption, epinephrine reduces the risk of local anesthetic systemic toxicity (LAST) — a rare but potentially life-threatening complication of local anesthetic administration that can cause cardiac arrhythmias and central nervous system toxicity when plasma lidocaine levels exceed a critical threshold (Neal et al., 2018).

Concentration and Volume

In this procedure, 1% lidocaine with epinephrine was used, and approximately 1 mL was injected. The 1% concentration means that the solution contains 10 mg of lidocaine per milliliter. Therefore, 1 mL delivers 10 mg of lidocaine — a dose well within the safe therapeutic range for a local infiltration in an adult patient. The maximum safe dose of lidocaine with epinephrine is generally cited as 7 mg/kg, meaning even a small adult patient would have a maximum dose of 350 mg or more, making a 10 mg dose extraordinarily safe (Becker & Reed, 2012).


Needle Selection and Injection Technique: The 30-Gauge Half-Inch Needle

Selecting a 30-gauge, half-inch needle for this procedure reflects a deliberate, evidence-informed clinical decision.

Understanding Needle Gauge and Length

Needles are classified by their gauge (a measure of diameter, where higher gauge numbers indicate thinner needles) and their length (expressed in inches or millimeters). A 30-gauge needle has an outer diameter of approximately 0.31 mm, making it one of the thinnest needles commonly used in clinical practice. A half-inch (12.7 mm) length is appropriate for subcutaneous and intradermal injections in most body sites.

Why a 30-Gauge Needle?

The primary reason for selecting a thin 30-gauge needle for this procedure is patient comfort. The relationship between needle gauge and pain is well established in the literature: thinner needles cause less pain upon insertion, because they displace less tissue and engage fewer nociceptive nerve endings in the skin (Gill & O’Brien, 2007). For a procedure where the injection itself is the most acutely painful component, minimizing needle gauge is an important element of patient-centered procedural care.

A 30-gauge needle is also entirely adequate for delivering the small volume (1 mL) of fluid used in this procedure. The viscosity of the lidocaine-epinephrine solution is low enough that it flows freely through a 30-gauge needle without excessive injection pressure.

The Two-Phase Injection Technique

An important feature of the injection technique described in this procedure is its two-phase approach:

Phase 1: Subcutaneous Injection

The needle is first inserted perpendicularly into the skin and advanced into the subcutaneous tissue — the loose connective tissue layer beneath the dermis. A portion of the lidocaine solution is deposited here. This deep deposition ensures that the larger nerve branches supplying the area are anesthetized first, which facilitates the subsequent intradermal injection by pre-treating the deeper nociceptive pathways.

Phase 2: Intradermal Injection (Wheal Formation)

Without withdrawing the needle from the skin, redirect it horizontally— rotate it to run parallel to the skin surface — and advance it intradermally, directly beneath the lesion. The remaining lidocaine solution is then injected here to form an intradermal wheal — a raised, pale, blister-like elevation of the skin caused by the fluid expanding the intradermal compartment.

This two-phase technique is superior to a single-depth injection for several reasons:

  • It ensures complete anesthesia of all skin layers — both the deeper subcutaneous tissue and the superficial intradermal compartment where the lesion is rooted
  • It creates the intradermal wheal, which is mechanically essential for the shave biopsy technique (as described in the next section)
  • The subcutaneous injection first creates baseline anesthesia that makes the subsequent intradermal injection less painful for the patient.

The clinical observation during this procedure — that the patient reported no pain during both phases of the injection — validates the effectiveness of the Pain Ease pre-treatment and the careful, deliberate injection technique employed.


Subcutaneous vs. Intradermal Injection: Understanding the Layers of the Skin

To fully appreciate the technical nuances of the injection technique used in this procedure, you need a thorough understanding of the skin’s anatomical layers and the physiological differences between subcutaneous and intradermal injection.

The Architecture of the Skin

The skin is organized into three primary layers, each with distinct anatomical and physiological characteristics:

1. The Epidermis

The epidermis is the outermost layer of the skin, ranging in thickness from approximately 0.05 mm (on the eyelids) to 1.5 mm (on the palms and soles). It is composed primarily of keratinocytes — the cells responsible for producing keratin, the structural protein that gives skin its barrier function. The epidermis is avascular (contains no blood vessels) and receives nutrients and oxygen by diffusion from the underlying dermis.

The epidermis is organized into five layers (from deep to superficial):

  • Stratum basale — the deepest layer, containing mitotically active stem cells
  • Stratum spinosum — the “prickle cell” layer, where keratinocytes begin to produce keratin
  • Stratum granulosum — where keratinocytes begin to flatten and produce lipid-rich lamellar granules
  • Stratum lucidum — present only in thick skin (palms and soles); a clear, homogeneous layer
  • Stratum corneum — the outermost layer, composed of dead, flattened keratinocytes (corneocytes) filled with keratin

Seborrheic keratoses originate in the epidermis — they are a proliferation of the keratinocyte population within the epidermal layers, and they project upward from the skin surface without penetrating the dermis.

2. The Dermis

The dermis lies immediately beneath the epidermis and is separated from it by the dermal-epidermal junction (DEJ). The dermis is a highly vascularized layer of connective tissue composed primarily of collagen and elastin fibers, embedded in a proteoglycan-rich extracellular matrix. It contains blood vessels, lymphatic vessels, nerve fibers, hair follicles, sweat glands, and sebaceous glands.

The dermis is subdivided into:

  • Papillary dermis — the superficial portion, which projects upward into the epidermis as dermal papillae and contains fine collagen fibers, capillary loops, and nerve endings
  • Reticular dermis — the deeper, thicker portion, composed of coarser collagen bundles and elastic fibers, providing the skin’s tensile strength

Intradermal injection delivers fluid into the papillary and superficial reticular dermis, producing the characteristic wheal by expanding this compartment.

3. The Hypodermis (Subcutaneous Tissue)

The hypodermis lies beneath the dermis and consists primarily of adipose tissue (fat cells) interspersed with connective tissue septa. It provides thermal insulation, mechanical cushioning, and serves as an energy reservoir. Subcutaneous injection delivers fluid into this layer.

Why the Intradermal Wheal Is the Key to the Shave Biopsy

The intradermal wheal created by the injection is not merely an anesthetic technique — it is a mechanical tool that fundamentally enhances the shave biopsy procedure. By expanding the intradermal compartment directly beneath the seborrheic keratosis, the wheal accomplishes two critical objectives:

1. Physical Elevation of the Lesion

The wheal raises the lesion above the surrounding skin surface, making it more prominent and accessible. This elevation means that the biopsy blade does not need to be angled downward into the skin to capture the lesion — it can instead be directed horizontally across the elevated lesion base, reducing the risk of either under-sampling (leaving residual lesion tissue) or over-sampling (cutting too deeply into the dermis and creating an unnecessary wound).

2. Creation of a Firm, Stable Platform

The turgid, fluid-filled wheal also creates a firmer, more stable base beneath the lesion, which facilitates a smooth, controlled biopsy motion. Without the wheal, the soft, compressible superficial dermis can make it difficult to maintain consistent blade depth during the shave.

This technique — using the intradermal wheal both for anesthesia and as a mechanical adjunct to the biopsy — exemplifies the elegance of evidence-based procedural medicine: a single intervention (the intradermal injection) achieves multiple clinical goals simultaneously.


The Intradermal Wheal: Why Elevation of the Lesion Matters

The observation in the clinical demonstration that the intradermal wheal was “actually elevating the lesion toward us, so that presents it to us” is not a casual comment — it reflects a fundamental principle of shave biopsy technique that is grounded in biomechanics and tissue physiology.

The Biomechanics of Wheal Formation

When fluid is injected into the intradermal compartment, it must displace surrounding tissue to create space. Because the epidermis above is relatively inelastic and the reticular dermis below is dense, the path of least resistance for the injected fluid is upward and laterally, producing the characteristic dome-shaped wheal.

The pressure generated by the fluid within the wheal — typically estimated at 20-40 mmHg above atmospheric pressure in an actively injected wheal — is sufficient to lift the overlying epidermis and any attached epidermal tumor (such as the seborrheic keratosis) away from the underlying dermis. This lifting effect is visually apparent: the skin overlying the injection site blanches (due to local vasoconstriction from the epinephrine and compression of the superficial capillaries) and rises above the surrounding skin level.

Clinical Significance for Specimen Quality

From a pathological standpoint, the elevation of the lesion produced by the wheal is highly beneficial for specimen quality. A shave biopsy specimen that includes a generous portion of the base of the lesion — the intradermal-epidermal junction — is far more diagnostically valuable than one that captures only the superficial portion. The wheal ensures that the biopsy blade, traveling horizontally at the elevated lesion base, captures this interface reliably.

A high-quality specimen allows the pathologist to assess:

  • The depth of epidermal involvement
  • The presence or absence of dermal invasion — the most critical feature for distinguishing benign SK from malignant entities like squamous cell carcinoma in situ (Bowen’s disease) or invasive SCC
  • The nature of any inflammatory infiltrate
  • The presence of atypical keratinocytes that might suggest pre-malignant or malignant transformation

Performing the Shave Biopsy: Technique, Precision, and Margins

With the intradermal wheal established and the lesion fully elevated and anesthetized, the shave biopsy proceeds. The technique used in this procedure—beginning the cut about two millimeters lateral to the lesion—reflects careful attention to both diagnostic completeness and cosmetic outcome.

The “Two Millimeters Lateral” Principle

Starting the shave cut two millimeters lateral to the visible border of the lesion serves several important purposes:

1. Ensuring Complete Lesion Capture

The visible border of a seborrheic keratosis is not always the true border of the pathological process. Microscopic extensions of the lesion — subclinical keratinocyte proliferation that is not visible to the naked eye — can extend a small distance beyond the visible edge. By starting the cut 2 mm outside the visible margin, the clinician ensures the specimen includes all pathological tissue, even if microscopic extensions exist.

2. Avoiding Specimen Fragmentation

If the biopsy blade is introduced at the exact edge of the lesion, there is a risk of fragmenting the specimen — splitting the lesion into pieces that may be difficult to orient and analyze histopathologically. Starting two millimeters beyond the edge ensures a smooth, continuous cut through the lesion from one side to the other.

3. Margin Assessment

In cases where the histopathological findings reveal a pre-malignant or malignant process — a possibility that cannot be excluded until the specimen is analyzed — having a two-millimeter margin of normal-appearing skin at the lateral edges of the specimen provides the pathologist with a baseline for assessing whether the abnormal process extends to the specimen edges (positive margins) or is contained within the specimen (negative margins).

The Shave Cut Itself

The shave cut is performed using a scalpel blade or a specialized razor blade held parallel to the skin surface. The blade is moved in a smooth, continuous motion from one side of the elevated lesion to the other, cutting at the level of the papillary-reticular dermis junction — superficial enough to avoid unnecessary dermis removal, but deep enough to capture the full base of the epidermal lesion.

In experienced hands, the shave biopsy is a rapid procedure—the cutting motion typically takes only a few seconds. The speed is not merely cosmetic convenience; a smooth, rapid cut produces a cleaner specimen with less crush artifact than a slow, sawing motion, which can distort tissue architecture and compromise histopathological interpretation.

Confirmation of Completeness

After removing the specimen, the wound bed is inspected to confirm that no lesion tissue remains. In this procedure, the clinical confirmation was explicit: “All the way through, no lesion is left there on the skin.” This confirmation step is important because residual lesion tissue can:

  • Lead to recurrence of the lesion
  • Potentially harbor pathology that was not captured in the initial specimen
  • Cause delayed healing or persistent inflammation

Hemostasis with Aluminum Chloride: Mechanisms and Clinical Rationale

After specimen removal, the next clinical priority is hemostasis—stopping bleeding from the wound bed. In this procedure, aluminum chloride was used for this purpose.

What Is Aluminum Chloride?

Aluminum chloride is an inorganic compound with the formula AlCl₃. In dermatological practice, it is used as a hemostatic agent — a substance that promotes blood clotting — in the form of a concentrated aqueous solution (typically 20-35% aluminum chloride in absolute ethyl alcohol, sometimes referred to as “Monsel’s solution” or “Drysol” in various clinical formulations, though these have distinct compositions; the aluminum chloride-ethanol formulation is the most commonly used hemostatic agent in dermatological surgery).

Mechanism of Action

The hemostatic action of aluminum chloride is primarily physical/chemical rather than enzymatic. It acts through the following mechanisms:

1. Protein Precipitation

Aluminum ions (Al³⁺) are strongly astringent — they react with proteins in the serum and on the surface of endothelial cells to cause protein precipitation. This precipitation forms a physical plug in the small capillaries and arterioles at the wound surface, mechanically occluding blood flow.

2. Vasoconstriction

The astringent effect of aluminum chloride also causes contraction of the walls of small blood vessels at the wound site, reducing blood flow to the area. This vasoconstriction is transient but sufficient to allow the body’s own hemostatic mechanisms — platelet aggregation and fibrin clot formation — to complete the process.

3. Desiccation of the Wound Surface

The alcohol component of the aluminum chloride solution promotes desiccation (drying) of the wound surface, which reduces the amount of fluid available to sustain bleeding and promotes the formation of a stable, dry eschar (scab) over the wound.

Application Technique

In this procedure, the aluminum chloride was applied by saturating a gauze pad with the solution and applying it to the wound surface. The gauze is pressed firmly against the bleeding wound for approximately 30-60 seconds, during which time the protein precipitation and vasoconstriction occur and bleeding is arrested.

The observation that “The bleeding has stopped” after application confirms the technique’s effectiveness and supports the clinical rationale for using aluminum chloride in this context.

Advantages Over Other Hemostatic Methods

In a minor dermatological procedure like a shave biopsy, aluminum chloride offers several important advantages over alternative hemostatic methods:

  • No sutures required — the wound created by a shave biopsy is typically shallow and small enough that aluminum chloride hemostasis is sufficient, eliminating the need for sutures and their associated discomfort, risk of infection, and need for a return visit for removal
  • Rapid action — bleeding is typically arrested within 30-60 seconds
  • Low risk of scarring — unlike electrocautery or ferric subsulfate (Monsel’s solution), aluminum chloride generally produces minimal tissue damage and a low risk of post-inflammatory hyperpigmentation or scarring.
  • Ease of use — it can be applied with a cotton-tipped applicator or gauze pad without specialized equipment.
  • Safe in the outpatient setting — no electrical equipment, no flame, no specialized training required beyond standard procedural competency

Comparison with Electrocautery

Electrocautery (or electrocoagulation) is another commonly used hemostatic method in skin surgery. It works by applying electrical current to the wound surface, which heats the tissue and causes thermal coagulation of blood proteins. While electrocautery is effective, it has several disadvantages compared to aluminum chloride in the context of a shave biopsy:

  • It requires specialized electrical equipment.
  • It can cause thermal artifact in adjacent tissue, which can distort histopathological interpretation if applied before the specimen is removed.
  • It carries a small but real risk of electrical burns if used near metal implants or pacemakers.
  • The smell of burning tissue can be unpleasant for the patient

Aluminum chloride avoids all of these concerns, making it the preferred hemostatic agent for most minor dermatological procedures in an outpatient integrative care setting.


Post-Procedural Care and Sterile Packaging

Sterile Packaging of the Specimen

Once the specimen is excised and hemostasis is achieved, package and preserve the biopsy specimen properly for pathological analysis. The standard method is to place the specimen in a container of 10% neutral buffered formalin, which acts as a fixative—it cross-links proteins in the tissue, preserving cellular architecture and preventing autolytic degradation that would occur if the tissue were allowed to dry or remain at physiological conditions.

The formalin-fixed specimen is then submitted to a pathology laboratory with a requisition form documenting:

  • Patient demographics
  • Clinical diagnosis and differential diagnoses
  • Site and method of biopsy
  • Relevant clinical history (duration of lesion, rate of change, symptoms)
  • Requesting clinician information

This information is essential for the pathologist to provide a clinically relevant interpretation of the histological findings.

Wound Care Instructions

After the procedure, the patient receives wound care instructions to promote healing and prevent infection. Standard instructions for a shave biopsy wound include:

  • Keep the wound clean and moist — apply a thin layer of petroleum jelly (Vaseline) or antibiotic ointment (such as bacitracin) and cover with a non-stick dressing for 24-48 hours
  • Change the dressing daily — remove the old dressing, gently clean the wound with mild soap and water, and reapply the ointment and dressing.
  • Avoid submerging the wound in water (baths, pools, hot tubs) until the wound is fully healed — typically 7-14 days.
  • Avoid vigorous physical activity that might cause friction or trauma to the wound site.
  • Watch for signs of infection — increasing redness, warmth, swelling, purulent discharge, or fever — and return to the clinic immediately if these develop.
  • Expect a small scar — the wound will initially form a scab (eschar), which will fall off within 1-2 weeks, leaving a small, pink, flat scar that will gradually fade over several months.

Healing Physiology

The wound healing process at a shave biopsy site proceeds through the classic four phases of wound healing:

1. Hemostasis (0-24 hours)

Immediately after tissue injury, platelet aggregation and coagulation cascade activation form a fibrin clot at the wound surface. Aluminum chloride supports this phase by precipitating proteins and causing vasoconstriction to slow bleeding.

2. Inflammation (1-5 days)

Immune cells — primarily neutrophils in the first 24-48 hours, followed by macrophages — migrate to the wound site and clear debris, bacteria, and damaged tissue. This phase is characterized by the classic signs of inflammation: redness, swelling, warmth, and discomfort at the wound site.

3. Proliferation (5-21 days)

Fibroblasts migrate into the wound and begin synthesizing new collagen, gradually replacing the fibrin clot with a provisional extracellular matrix. Simultaneously, keratinocytes at the wound edges begin migrating across the wound surface to re-establish the epidermal layer — a process called re-epithelialization.

4. Remodeling (21 days to 2 years)

The provisional collagen matrix is gradually remodeled into a more organized, mature collagen structure. The wound contracts, the scar matures and fades, and the tensile strength of the repaired tissue gradually increases toward (but typically not reaching) the pre-injury level.


Pathological Analysis: What Happens After the Specimen Is Collected

The journey of the biopsy specimen from the clinical setting to the pathology report is a fascinating and clinically critical process. Understanding what happens to the tissue after it leaves the clinic helps clinicians communicate more effectively with pathologists and interpret reports more accurately.

Grossing (Macroscopic Examination)

Upon receipt in the pathology laboratory, the specimen undergoes gross examination — a macroscopic inspection by the pathologist or pathology technician. For a shave biopsy specimen, this involves documenting:

  • The size and shape of the specimen
  • The surface characteristics (color, texture, presence of pigmentation)
  • The cut sections (appearance of the tissue on cross-section)

Tissue Processing

The formalin-fixed specimen is then embedded in paraffin wax to create a solid block from which thin tissue sections can be cut. The embedding process involves:

  1. Dehydration — the tissue is passed through a series of increasingly concentrated alcohol solutions to remove water
  2. Clearing — the alcohol is replaced with a clearing agent (typically xylene) that is miscible with paraffin
  3. Infiltration and embedding — the clearing agent is replaced with melted paraffin wax, which solidifies around the tissue, creating a firm block

Microtomy and Staining

The paraffin block is then sectioned using a microtome—a precision cutting instrument—into sections 3- 5 micrometers thick. These sections are mounted on glass slides and stained with hematoxylin and eosin (H&E), the standard stain for histopathological examination.

  • Hematoxylin stains nuclei blue-purple
  • Eosin stains cytoplasm and extracellular matrix pink-red

The pathologist then examines the H&E-stained slides under the microscope.

What the Pathologist Looks For

In a specimen from a clinically suspected inflamed seborrheic keratosis, the pathologist examines:

Features Supporting the Diagnosis of Seborrheic Keratosis:

  • Acanthosis — epidermal thickening with keratinocyte proliferation
  • Hyperkeratosis — excess keratin on the surface
  • Papillomatosis — upward projections of the epidermis
  • Horn cysts — keratin-filled invaginations within the epidermis
  • No dermal invasion — the basement membrane is intact, confirming the benign, epidermal nature of the lesion

Features of Inflammation:

  • Lymphocytic infiltrate in the superficial dermis and within the lesion
  • Spongiosis — epidermal edema
  • Neutrophilic infiltrate if secondary infection is present

Features That Would Require Further Action:

  • Atypical keratinocytes — cells with enlarged, irregular nuclei — could indicate actinic keratosis or squamous cell carcinoma in situ
  • Full-thickness epidermal atypia — diagnostic of Bowen’s disease (SCC in situ)
  • Dermal invasion — diagnostic of invasive squamous cell carcinoma
  • Atypical melanocytes — could indicate melanoma
  • Positive margins — residual pathological tissue at the edges of the specimen

The pathology report generated after this analysis is the definitive clinical answer to the diagnostic question posed by the biopsy.


Pain Management in Minor Surgical Procedures: An Integrative Perspective

Pain management in minor surgical procedures extends well beyond the technical administration of local anesthetic. From an integrative medicine perspective, pain is not merely a peripheral nociceptive signal but a complex, multidimensional experience shaped by biological, psychological, and social factors — the biopsychosocial model of pain (Engel, 1977; Gatchel et al., 2007).

The Biopsychosocial Model Applied to Procedural Pain

Biological factors in procedural pain include:

  • The nociceptive input from the injured tissue (the actual stimulus)
  • The inflammatory state of the tissue (inflamed tissue is hyperalgesic)
  • The neuroendocrine stress response (cortisol, adrenaline)
  • Individual genetic variation in pain sensitivity (polymorphisms in opioid receptor genes, voltage-gated ion channels)

Psychological factors include:

  • Anxiety and fear — the most important psychological modifiers of procedural pain; anxious patients uniformly report more pain
  • Previous pain experiences — negative prior procedural experiences sensitize patients to subsequent procedures
  • Catastrophizing — a cognitive-emotional pattern characterized by exaggerated, negative appraisals of pain that amplifies the perceived pain experience
  • Self-efficacy beliefs — confidence in one’s ability to cope with the procedure reduces pain perception

Social factors include:

  • The clinician-patient relationship — a trusting, empathetic clinical relationship substantially reduces procedural pain and anxiety
  • The procedural environment — a calm, private, well-equipped clinical space reduces anxiety compared to a busy, noisy, or unfamiliar environment
  • Social support — the presence of a trusted companion during procedures can reduce pain perception

Integrative Pain Management Strategies in Procedural Settings

At Injury Medical Clinic PA, our approach to pain management during minor procedures incorporates multiple integrative strategies:

1. Therapeutic Communication

Before and during the procedure, I maintain open, calm, and reassuring communication with the patient. This includes:

  • Clear explanation of each step before it occurs (“I’m going to insert the needle now — you may feel a small pinch”)
  • Positive reinforcement during the procedure (“You’re doing great; the hard part is over”)
  • Distraction — engaging the patient in conversation to redirect attention away from procedural sensations

The literature strongly supports the value of therapeutic communication in reducing procedural pain. Studies have shown that verbal analgesia—the pain-relieving effect of calm, reassuring speech by a clinician—activates endogenous opioid pathways in the brain, producing measurable reductions in pain perception (Benedetti et al., 2003).

2. Topical Analgesia

Using the Pain Ease mist before needle insertion, as described in this procedure, is a practical application of the gate control theory of pain (Melzack & Wall, 1965). According to this theory, non-nociceptive sensory input (in this case, the cold sensation from the vapocoolant spray) can “close the gate” to nociceptive transmission by activating large-diameter, myelinated sensory fibers (A-beta fibers) that inhibit nociceptive processing in the dorsal horn of the spinal cord.

3. Positioning and Comfort Optimization

Ensuring that the patient is in a comfortable position during the procedure, with appropriate support for the body part being treated, reduces both physical discomfort and psychological anxiety. A comfortable, well-supported patient feels more secure and in control of the procedural experience.

4. Mindfulness and Breathing Techniques

For patients with significant procedural anxiety, I often guide them through slow, diaphragmatic breathing before and during the procedure. Deep, slow breathing activates the parasympathetic nervous system, reducing cortisol and adrenaline levels and promoting relaxation that directly reduces pain sensitivity through top-down (cortical) modulation of nociceptive pathways (Kabat-Zinn, 1990).

5. Post-Procedural Analgesia

After the procedure, patients are advised on appropriate over-the-counter analgesics for post-procedural discomfort, typically acetaminophen or non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, unless contraindicated by other medical conditions. The anti-inflammatory action of NSAIDs is particularly relevant here, as they inhibit the cyclooxygenase (COX) enzyme, reducing prostaglandin synthesis —key inflammatory mediators that sensitize peripheral nociceptors (hyperalgesia) after tissue injury (Vane, 1971).


How Chiropractic Care Integrates with Dermatological and Medical Management

At first glance, the connection between chiropractic care and dermatological procedures may not seem obvious. However, understanding the integrative, whole-body approach that defines our practice reveals the deep, meaningful ways chiropractic principles and techniques complement and enhance the medical management of conditions like inflamed seborrheic keratoses.

The Neuroimmunological Connection

Chiropractic philosophy has always centered on the intimate relationship between the nervous system and the body’s health. Modern neuroscience strongly supports a neuroimmunological network—a bidirectional communication system between the nervous and immune systems—that plays a profound role in regulating inflammation, immune function, and tissue healing throughout the body, including the skin (Tracey, 2002).

The vagus nerve — the primary nerve of the parasympathetic nervous system — has emerged as a critical mediator of what is now called the “cholinergic anti-inflammatory pathway” (Tracey, 2002). Activation of the vagus nerve (either physiologically or through therapeutic stimulation) triggers the release of acetylcholine in peripheral tissues, which in turn inhibits the production of pro-inflammatory cytokines — including TNF-α, IL-1, and IL-6 — by macrophages. This anti-inflammatory effect is systemic, meaning it can influence inflammatory processes throughout the body, including in the skin.

Spinal manipulation therapy (SMT) — the core clinical intervention of chiropractic practice — has been shown in emerging research to modulate autonomic nervous system activity, with evidence suggesting that SMT can increase parasympathetic tone and reduce sympathetic hyperactivity in some patients (Budgell & Hirano, 2001; Welch & Boone, 2008). If future research confirms this, it would suggest that chiropractic adjustments could, through neuroimmunological mechanisms, have an indirect anti-inflammatory effect that might benefit patients with systemic or localized inflammatory conditions—including inflamed skin lesions.

Reducing Systemic Inflammation Through Chiropractic and Lifestyle Modification

One of the most compelling areas of modern integrative medicine is the recognition that chronic systemic inflammation is a shared pathological substrate underlying many diverse conditions — from cardiovascular disease and diabetes to chronic pain and skin disorders. Elevated levels of circulating inflammatory cytokines (particularly IL-6 and CRP — C-reactive protein) are associated with a range of skin conditions, including psoriasis, atopic dermatitis, and — potentially — the accelerated development and inflammation of benign skin tumors like seborrheic keratoses (Ganzetti et al., 2014).

Chiropractic care, integrated with functional medicine, nutritional intervention, stress management, and exercise therapy, can contribute to the reduction of systemic inflammation through multiple pathways:

  • Spinal manipulation may modulate neuroimmunological activity
  • Exercise prescription and rehabilitation reduce pro-inflammatory adipokines released by visceral adipose tissue
  • Nutritional guidance toward an anti-inflammatory diet (rich in omega-3 fatty acids, polyphenols, and antioxidants) reduces systemic oxidative stress and cytokine production
  • Stress reduction — through mindfulness, breathing exercises, and sleep optimization — reduces cortisol-driven immune dysregulation.

All of these interventions are within the scope of what Dr. Jimenez and the team at Injury Medical Clinic PA offer, and they represent a holistic strategy that addresses not just the specific lesion that required biopsy, but the underlying systemic health factors that may have contributed to its development and inflammation.

Spinal Health, Posture, and Skin Friction at the Lateral Hip

A biomechanical dimension also connects chiropractic care to the patient’s skin lesion. The lateral hip is particularly susceptible to mechanical friction and pressure from clothing, especially in patients with certain postural patterns or gait abnormalities. For example:

  • Lumbar scoliosis or pelvic obliquity can cause one hip to protrude laterally more than the other, increasing pressure and friction from clothing at that site
  • Hip abductor weakness can alter gait mechanics in ways that increase lateral hip contact with clothing or chair surfaces
  • Tight thoracolumbar fascia can alter the mechanics of lateral trunk flexion, affecting how clothing contacts the lateral hip during movement.

In this patient’s case, it is entirely possible that a biomechanical factor — a posture or movement pattern that creates excessive friction at the lateral right hip — contributed to the mechanical irritation and inflammation of an existing seborrheic keratosis at that site. Chiropractic assessment and correction of spinal and pelvic alignment, combined with hip strengthening and flexibility exercises, could reduce mechanical stress on the skin at this location, potentially preventing recurrence of the inflamed lesion after it heals.

This is a beautiful example of how chiropractic care and dermatological care are not separate domains, but interconnected elements of a truly comprehensive approach to patient health.


Functional Medicine and Skin Health: The Deeper Connection

Functional medicine is a systems-oriented, patient-centered approach to healthcare that seeks to identify and address the root causes of disease, rather than merely suppressing symptoms. At Injury Medical Clinic PA, functional medicine principles—championed by my credentials as a CFMP and IFMCP—are woven into every aspect of patient care, including managing skin conditions.

The Skin as a Mirror of Internal Health

From a functional medicine perspective, the skin is not merely a cosmetic concern — it is a biomarker of systemic health. The condition of the skin reflects:

  • Nutritional status — deficiencies in vitamins A, C, D, E, zinc, and essential fatty acids all manifest in the skin
  • Hormonal balance — thyroid dysfunction, insulin resistance, and sex hormone imbalances produce characteristic skin changes
  • Gut microbiome health — the gut-skin axis is a bidirectional communication pathway through which intestinal dysbiosis and increased intestinal permeability (“leaky gut”) can drive systemic inflammation that manifests in the skin (Bowe & Logan, 2011)
  • Oxidative stress and antioxidant capacity — excessive reactive oxygen species (ROS) — produced by UV radiation, pollution, poor diet, and stress — damage keratinocytes and contribute to the development of benign and malignant skin tumors
  • Immune system dysregulation — autoimmune conditions and chronic low-grade inflammation produce a wide spectrum of dermatological manifestations

Nutritional Considerations in Seborrheic Keratosis Development and Skin Health

While somatic genetic mutations primarily drive seborrheic keratoses, emerging evidence suggests that nutritional and metabolic factors may influence the rate of their development and the likelihood of inflammation:

Vitamin D and Skin Immunity

Vitamin D plays a crucial role in keratinocyte differentiation and immune regulation. Keratinocytes themselves express the vitamin D receptor (VDR) and possess the enzymatic machinery to convert 25-hydroxyvitamin D to the active form, 1,25-dihydroxyvitamin D (calcitriol). Calcitriol promotes keratinocyte differentiation — the orderly maturation of keratinocytes from basal stem cells to terminally differentiated corneocytes — which counteracts the undifferentiated proliferation that characterizes seborrheic keratoses.

Multiple studies have demonstrated that vitamin D has anti-proliferative and pro-apoptotic effects on keratinocytes in vitro, suggesting that adequate vitamin D status may help regulate epidermal keratinocyte turnover (Holick, 2004). Vitamin D deficiency — which is extremely prevalent in the United States, particularly among individuals with darker skin or limited sun exposure — may therefore represent a modifiable risk factor for the accelerated development of seborrheic keratoses.

Omega-3 Fatty Acids and Inflammatory Regulation

Omega-3 fatty acids — particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), found in fatty fish, flaxseed, and fish oil supplements — exert potent anti-inflammatory effects by competing with arachidonic acid for cyclooxygenase (COX) and lipoxygenase (LOX) enzymes, reducing the production of pro-inflammatory eicosanoids (prostaglandins, thromboxanes, and leukotrienes) (Calder, 2006). In inflamed seborrheic keratosis, increasing dietary omega-3 fatty acids could reduce the local and systemic inflammatory milieu that sustains inflammation.

Antioxidants and UV-Induced Oxidative Stress

UV radiation is the primary environmental driver of oxidative stress in the skin. Reactive oxygen species (ROS) generated by UV exposure damage DNA, proteins, and lipids in keratinocytes, contributing to the somatic mutations that underlie the development of seborrheic keratoses (and, more critically, skin cancers). Antioxidant nutrients — including vitamins C and E, beta-carotene, selenium, and polyphenols — neutralize ROS and reduce UV-induced DNA damage. A diet rich in these nutrients, or targeted supplementation when dietary intake is insufficient, is a practical functional medicine strategy for optimizing skin health.

The Gut-Skin Axis

The gut-skin axis is one of the most exciting emerging areas in functional medicine. Research shows that the composition of the gut microbiome—the complex community of microorganisms that inhabit the gastrointestinal tract—profoundly influences systemic immune function and inflammation, with direct consequences for skin health (Salem et al., 2018). Dysbiosis (imbalance in the gut microbiome) and increased intestinal permeability can lead to the translocation of bacterial products (such as lipopolysaccharide, LPS — a component of Gram-negative bacterial cell walls) into the systemic circulation, where they trigger a low-grade systemic inflammatory response that can manifest in a variety of tissues, including the skin.

Functional medicine interventions targeting the gut-skin axis — including probiotics and prebiotics, dietary modification (elimination of inflammatory foods, addition of fiber-rich foods), and treatment of underlying gastrointestinal conditions such as small intestinal bacterial overgrowth (SIBO) or intestinal permeability — can have measurable beneficial effects on skin health (Bowe & Logan, 2011).

Metabolic Health and Seborrheic Keratosis

The medical literature notes an association between seborrheic keratoses and metabolic conditions, particularly type 2 diabetes mellitus and insulin resistance. Some studies have reported a higher prevalence of SK in diabetic patients compared to non-diabetic controls (Taguchi et al., 1998). The proposed mechanisms include:

  • Advanced glycation end-products (AGEs) — formed by the non-enzymatic glycation of proteins and lipids in hyperglycemic conditions — may stimulate keratinocyte proliferation through RAGE (receptor for advanced glycation end-products) signaling
  • Elevated circulating insulin and insulin-like growth factor-1 (IGF-1) in insulin-resistant states may activate the PI3K/AKT pathway in keratinocytes, promoting proliferation.
  • Chronic systemic inflammation associated with metabolic syndrome may create an inflammatory skin environment that predisposes to SK development and inflammation.

At our clinic, Dr. Cardenas’s expertise in internal medicine—including managing metabolic conditions like diabetes, hypertension, and dyslipidemia—is invaluable for identifying and addressing these systemic contributors to skin health. A functional medicine approach to metabolic optimization through dietary intervention, targeted supplementation, exercise, and stress management represents a powerful strategy for reducing the systemic risk factors associated with SK development.


Personal Injury Care and Skin Trauma: Clinical Overlap

Injury Medical Clinic PA specializes in personal injury care — the comprehensive evaluation and treatment of patients who have sustained injuries in motor vehicle accidents, workplace incidents, or other traumatic events. While the connection between personal injury and skin health may not be obvious, several clinically important areas of overlap exist.

Skin Trauma in Personal Injury

Traumatic events can cause a wide range of skin injuries, including:

  • Lacerations — cuts through the epidermis and dermis
  • Abrasions — superficial injuries that remove the epidermis through friction (road rash)
  • Contusions — blunt trauma injuries that cause subcutaneous bleeding (bruising) without breaking the skin surface
  • Burns — thermal, chemical, or friction injuries that destroy epidermal and dermal tissue
  • Avulsions — traumatic removal of skin and subcutaneous tissue

These injuries require careful wound management, infection prevention, and support for the wound-healing process—all of which fall within the scope of our multidisciplinary clinical team.

The Koebner Phenomenon in Injury-Associated Skin Lesion Development

As discussed earlier, the Koebner phenomenon describes the development of skin lesions at sites of trauma in predisposed individuals. In the context of personal injury, this phenomenon is clinically relevant because:

  • A patient who sustains a traumatic injury to an area of skin that harbors a pre-existing, subclinical seborrheic keratosis (or other epidermal lesion) may experience activation and rapid growth of that lesion following the trauma
  • Scar tissue at an injury site can create a nidus for the development of new skin lesions in some patients
  • Compression garments used in injury rehabilitation can create friction and pressure on the skin that may trigger the Koebner phenomenon.

This means that our team — in evaluating patients after personal injury — must be alert to the possibility that new or changing skin lesions at injury sites may represent trauma-activated epidermal changes requiring dermatological evaluation.

Medications Used in Injury Care and Their Dermatological Implications

Many medications commonly used in personal injury care — including corticosteroids, NSAIDs, muscle relaxants, and opioid analgesics — can have dermatological side effects:

  • Corticosteroids — both systemic and topical — cause skin atrophy, thinning, and increased fragility with prolonged use
  • NSAIDs — can cause photosensitivity reactions, making the skin more susceptible to UV-induced damage
  • Some antibiotics used for infection prevention can cause drug rashes or fixed drug eruptions

Dr. Cardenas’s oversight as Medical Director ensures medication choices consider these dermatological implications and that any skin changes during treatment are appropriately evaluated in the context of the patient’s medication history.


Evidence-Based Practice in Minor Dermatological Surgery

The procedures and techniques described in this post are firmly grounded in the current evidence base for minor dermatological surgery. Here are key pieces of evidence supporting the clinical decisions made in this procedure.

Evidence for Shave Biopsy as a Diagnostic Tool

A systematic review by Swetter et al. (2019) examined the diagnostic accuracy of various skin biopsy techniques for evaluating pigmented and non-pigmented skin lesions. The review concluded that shave biopsy is an appropriate diagnostic technique for exophytic lesions confined to the epidermis and superficial dermis, including seborrheic keratoses and low-risk keratinocyte carcinomas, when performed with adequate depth to capture the base of the lesion.

However, the review also cautioned that shave biopsy may be inappropriate as the primary diagnostic technique for suspected melanoma, where complete excision with margins is recommended to accurately assess tumor thickness (Breslow thickness) — a critical prognostic factor. This reinforces the importance of clinical judgment in selecting the appropriate biopsy technique for each case.

Evidence for Vapocoolant Sprays in Reducing Needle Injection Pain

A Cochrane systematic review by Ipp et al. (2011) examined the effectiveness of vapocoolant sprays in reducing pain from injections and venipuncture. The review identified moderate-quality evidence that vapocoolant sprays significantly reduce pain from needle insertion compared to placebo or no treatment. The effect was most pronounced in pediatric populations and in patients with high baseline anxiety. These findings support routine use of vapocoolant sprays as a simple, low-cost intervention to reduce procedural pain in outpatient settings.

Evidence for Lidocaine-Epinephrine in Minor Skin Surgery

The safety and efficacy of lidocaine with epinephrine for local anesthesia in minor skin surgery is extremely well established, with decades of clinical use and a robust evidence base. A landmark study by Altinyazar et al. (2004) demonstrated that 1% lidocaine with epinephrine provides superior hemostasis and equivalent anesthetic efficacy compared to plain lidocaine in shave biopsies and excisions of benign and malignant skin lesions. The study also confirmed the safety of the lidocaine-epinephrine combination in outpatient dermatological surgery, with no significant adverse events reported.

Evidence for Aluminum Chloride as a Hemostatic Agent

A clinical trial by Olmstead et al. (2006) compared the hemostatic efficacy of aluminum chloride, ferric subsulfate (Monsel’s solution), and electrocautery following shave biopsies and curettage of skin lesions. The trial found that all three agents were equally effective in achieving hemostasis. Still, aluminum chloride was associated with the lowest rate of post-procedural complications (including scarring and hyperpigmentation) and the highest patient satisfaction scores. These findings support aluminum chloride as the first-line hemostatic agent for minor dermatological procedures in an outpatient setting.

Evidence for Intradermal Wheal Technique in Shave Biopsy

Multiple procedural textbooks and clinical series describe the role of the intradermal wheal in improving shave biopsy technique. A technical report by Pariser and Dixit (2009) in the Journal of Dermatologic Surgery described the intradermal wheal technique as producing superior specimen orientation, reduced risk of under-sampling, and cleaner wound edges compared to shave biopsies performed without prior wheal formation. The report recommended this technique as the standard approach for shave biopsies of exophytic epidermal lesions.


Patient Communication and Informed Consent in Minor Procedures

One of the most important but often underappreciated aspects of procedural care is patient communication and obtaining informed consent. At Injury Medical Clinic PA, we take informed consent seriously — not as a bureaucratic formality, but as a fundamental expression of patient autonomy and shared decision-making.

The Elements of Informed Consent

For a minor procedure like a shave skin biopsy, the informed consent discussion should cover:

1. The Nature of the Procedure

The patient should understand what will happen during the procedure: a local anesthetic will be injected, the lesion will be removed with a blade, and the wound will be treated with a hemostatic agent.

2. The Reason for the Procedure

The patient should understand why the biopsy is being performed — in this case, to obtain tissue for histopathological analysis to confirm or refute the clinical diagnosis of seborrheic keratosis and to rule out more serious pathology.

3. The Expected Outcomes and Benefits

The patient should understand the potential benefits of the procedure: definitive diagnosis, relief of symptoms (pain and inflammation), and the peace of mind that comes from knowing the exact nature of the lesion.

4. The Risks and Potential Complications

Even a minor procedure like a shave biopsy carries some risks, including:

  • Bleeding — usually minor and controlled with aluminum chloride
  • Infection — minimized by sterile technique but possible in any open wound
  • Scarring — a small, flat scar at the biopsy site is expected
  • Incomplete removal — in some cases, a portion of the lesion may remain after the biopsy, requiring further treatment
  • Local anesthetic reaction — rare, but possible in patients with known hypersensitivity to amide anesthetics

5. The Alternatives

The patient should be informed of the alternatives to shave biopsy, which in this case might include:

  • Clinical observation — monitoring the lesion without intervention, with a plan to biopsy if it continues to change
  • Topical treatment — while no topical agents are specifically effective for seborrheic keratosis, anti-inflammatory treatments might reduce local symptoms temporarily
  • Referral to a dermatologist — if the clinician prefers specialist evaluation before proceeding with biopsy

6. The Right to Refuse

The patient retains the absolute right to refuse the procedure, even after the consent discussion. The clinician’s role is to ensure the patient has all the information needed to make an informed choice — not to coerce or pressure the patient into a particular decision.

Documentation of Consent

In our clinic, we document informed consent in the patient’s medical record, typically through a combination of a written consent form (which the patient signs) and a clinical note describing the consent discussion. This documentation is essential for medicolegal protection and for continuity of care.


Safety, Sterility, and Infection Prevention Protocols

The safety of both the patient and the clinician is paramount in any minor surgical procedure. At Injury Medical Clinic PA, we follow rigorous sterility and infection prevention protocols consistent with current standards of care in outpatient procedural medicine.

Principles of Aseptic Technique

Aseptic technique refers to practices designed to prevent the introduction of microorganisms into a sterile anatomical space (in this case, the wound created by the biopsy). Key elements include:

1. Hand Hygiene

Before any clinical procedure, staff perform thorough handwashing with soap and water for at least 20 seconds, or use an alcohol-based hand sanitizer (with at least 60% ethanol). This is the single most effective intervention for reducing healthcare-associated infections (WHO, 2009).

2. Skin Antisepsis

The procedural site is cleaned with an antiseptic solution before the procedure begins. In this case, 70% isopropyl alcohol was used — as noted in the clinical description, where the area was “already cleaned off with alcohol.” Alcohol is effective against most bacteria, fungi, and enveloped viruses by denaturing microbial proteins and disrupting microbial cell membranes.

In some clinical settings, chlorhexidine gluconate (CHG) is preferred over alcohol for skin antisepsis because it has a residual antimicrobial effect—it binds to the stratum corneum. It continues to inhibit microbial growth for several hours after application. However, for a short minor procedure like a shave biopsy, alcohol antisepsis alone is generally considered sufficient.

3. Sterile Equipment

All instruments used in the procedure — the needle, syringe, biopsy blade, and gauze — are single-use, sterile, pre-packaged items. This eliminates the risk of cross-contamination between patients.

4. Personal Protective Equipment (PPE)

The clinician wears non-sterile examination gloves (at minimum) during the procedure, which protects both the patient (from microorganisms on the clinician’s hands) and the clinician (from exposure to the patient’s blood and tissue fluids). In procedures with a higher risk of blood splatter, face shields and surgical masks are also used.

5. Safe Sharps Disposal

Used needles and blades are placed immediately in a puncture-resistant sharps container — never recapped or placed on work surfaces where accidental needlestick injury could occur. OSHA’s Bloodborne Pathogens Standard (OSHA, 2001) mandates this practice, and it is a fundamental requirement of safe clinical practice.

Post-Procedural Wound Infection Prevention

As discussed in the section on post-procedural care, patients are instructed to:

  • Keep the wound clean and moist with antibiotic ointment
  • Watch for signs of infection
  • Return promptly if signs of infection develop

In patients who are immunocompromised — including those with diabetes, HIV, or on systemic immunosuppressive therapy — a lower threshold for prophylactic antibiotic coverage is maintained, in accordance with the medical oversight provided by Dr. Cardenas.


Seborrheic Keratosis Recurrence, Monitoring, and Long-Term Skin Health

While a successful shave biopsy removes the visible seborrheic keratosis and provides a definitive tissue diagnosis, patients should understand that seborrheic keratoses can recur at the same site, and new lesions may develop elsewhere over time.

Why Seborrheic Keratoses Recur

Seborrheic keratoses can recur after removal for several reasons:

1. Incomplete Removal

If the shave biopsy does not capture all keratinocytes carrying the FGFR3 or PIK3CA mutation, residual mutant cells can continue to proliferate and reform the lesion. This is why confirming complete removal — as was done in this procedure — is so important.

2. New Somatic Mutations in Adjacent Keratinocytes

Even if the original lesion is completely removed, adjacent keratinocytes may carry their own somatic mutations (or develop new ones over time) that lead to a new, distinct lesion at or near the same site. This is not a “recurrence” in the strict sense but is rather a new primary lesion.

3. Ongoing Exposure to Risk Factors

If the underlying risk factors — UV radiation exposure, chronic mechanical friction, metabolic dysregulation — are not addressed, the likelihood of developing new seborrheic keratoses (or recurrence of existing ones after treatment) remains high.

Long-Term Skin Health Monitoring

Patients who have had a symptomatic or rapidly changing seborrheic keratosis biopsied should be enrolled in a program of long-term skin health monitoring that includes:

1. Regular Self-Examination

Patients are taught to perform monthly self-examination of their skin, using a full-length mirror and a hand mirror to examine difficult-to-see areas. They are instructed to report any new, changing, or symptomatic lesions promptly.

2. Annual Full-Body Skin Examination

An annual full-body skin examination by a clinician is recommended for patients over 40 or those with a history of symptomatic seborrheic keratoses, multiple lesions, or other risk factors for skin cancer.

3. Sun Protection Counseling

Patients are counseled on the importance of daily broad-spectrum sunscreen (SPF 30 or higher), protective clothing (long sleeves, hats), and avoidance of peak UV hours (10 AM to 4 PM) as primary prevention strategies for UV-induced skin damage and skin tumor development.

4. Functional Medicine Skin Health Optimization

As part of our integrative approach, we offer patients with skin lesions a comprehensive functional medicine evaluation to identify and address systemic risk factors—nutritional deficiencies, metabolic dysregulation, gut health, oxidative stress—that may contribute to ongoing skin lesion development.

The Role of Dr. Cardenas in Long-Term Skin Health Management

Dr. Cardenas’s role as Medical Director is particularly valuable in the long-term management of patients with skin lesions. As an internist with over 40 years of experience, she is uniquely positioned to:

  • Evaluate for systemic conditions associated with seborrheic keratosis development, including metabolic syndrome, insulin resistance, and malignancy
  • Manage comorbidities that affect skin health, including diabetes, thyroid disease, and autoimmune conditions
  • Review and optimize medications for drugs that may adversely affect skin health or wound healing
  • Coordinate referrals to dermatology, oncology, or other specialists when the clinical picture warrants

Evidence-Based Practice in Integrative and Collaborative Dermatological Care

The integrative, multidisciplinary model of care at Injury Medical Clinic PA is not merely a philosophical preference—it is backed by a growing body of evidence demonstrating its clinical and economic superiority over fragmented, single-discipline care.

The Evidence for Multidisciplinary Integrative Care

A landmark systematic review by Körner et al. (2016) compared outcomes in multidisciplinary integrative care settings with single-discipline care across a range of chronic conditions. The review found that multidisciplinary care was associated with:

  • Significantly better patient outcomes across multiple domains, including pain, function, quality of life, and patient satisfaction
  • Lower rates of treatment failure and disease progression
  • Reduced healthcare utilization (fewer hospitalizations, emergency department visits, and specialist referrals)
  • Higher rates of patient adherence to treatment plans

A more recent systematic review by Stochkendahl et al. (2017) examined the effectiveness of collaborative care models—where chiropractors, medical doctors, and allied health professionals work together—for musculoskeletal and related conditions. The review found strong evidence that collaborative care outperforms single-provider care, particularly for complex conditions with multiple contributing factors.

The Evidence for Functional Medicine in Chronic Disease Management

The Cleveland Clinic Center for Functional Medicine published a landmark study by Beidelschies et al. (2019) showing that patients receiving functional medicine care experienced significantly greater improvements in health-related quality of life, particularly in the physical and emotional domains, than patients receiving standard primary care. The functional medicine group also demonstrated lower rates of chronic disease progression and higher patient engagement with lifestyle modification.

These findings are highly relevant to managing skin conditions like seborrheic keratoses, which — as discussed throughout this post — have significant lifestyle, metabolic, and systemic health dimensions best addressed through a functional medicine framework.

The Evidence for Chiropractic Care in Reducing Systemic Inflammation

Emerging research suggests that chiropractic spinal manipulation may exert anti-inflammatory effects through neuroimmunological mechanisms. A study by Teodorczyk-Injeyan et al. (2006) demonstrated that spinal manipulation therapy significantly reduced serum levels of pro-inflammatory cytokines (including TNF-α and IL-1β) in patients with chronic low back pain, compared to sham manipulation and control groups. While this research is preliminary and the specific mechanisms are not yet fully elucidated, it points toward a potential systemic anti-inflammatory benefit of chiropractic care that could be relevant to patients with inflammatory skin conditions.


The Physiological Underpinnings of Skin Wound Healing: A Deep Dive

To fully appreciate the clinical significance of the shave biopsy procedure and the post-procedural care instructions, it is worth examining the physiological mechanisms of wound healing in greater detail. This is an area where integrating chiropractic care, functional medicine, and medical oversight at our clinic can meaningfully improve patient outcomes.

Phase 1: Hemostasis

Immediately upon tissue injury — in this case, the moment the biopsy blade penetrates the skin — the hemostatic cascade is activated. The sequence of events is:

Vascular Response

The cut blood vessels undergo immediate vasoconstriction — a reflex mediated by the local release of endothelin and the activation of alpha-adrenergic receptors in the vessel walls. This vasoconstriction reduces blood flow to the injured area, giving the coagulation mechanisms time to establish a clot.

Platelet Adhesion and Aggregation

Within seconds of vessel injury, von Willebrand factor (vWF) — a protein stored in endothelial cells and platelets — is released and binds to the exposed collagen in the subendothelial matrix. Platelets adhere to the vWF-collagen complex via their GPIb receptors and become activated. Activated platelets release ADP, thromboxane A2 (TxA2), and serotonin, which recruit additional platelets and promote platelet aggregation, forming the initial platelet plug.

The Coagulation Cascade

Simultaneously, the coagulation cascade is activated through the extrinsic pathway — triggered by the exposure of tissue factor (TF) on the surface of damaged cells and activated by Factor VIIa. The cascade proceeds through a series of enzymatic reactions that ultimately generate thrombin, which converts soluble fibrinogen to insoluble fibrin. Fibrin strands weave through the platelet plug, stabilizing it into a firm clot.

The aluminum chloride applied at the end of the biopsy accelerates this phase by promoting protein precipitation and vasoconstriction, ensuring rapid, reliable hemostasis.

Phase 2: Inflammation

The inflammatory phase begins with the release of damage-associated molecular patterns (DAMPs)—molecules released by injured cells that signal tissue damage to the immune system. DAMPs include:

  • HMGB1 (high mobility group box 1 protein)
  • ATP released from damaged cells
  • Uric acid crystals formed by the breakdown of purines
  • Heat shock proteins

DAMPs bind to pattern recognition receptors (PRRs) — particularly Toll-like receptors (TLRs) — on resident immune cells (mast cells, macrophages, and dendritic cells) in the dermis. Activation of these receptors triggers the release of:

  • Histamine and bradykinin (from mast cells) — causing vasodilation and increased vascular permeability
  • Pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) — initiating the systemic inflammatory response
  • Chemokines (CXCL8/IL-8) — recruiting neutrophils from the circulation to the wound site

Within 24- 48 hours, neutrophils dominate the wound, phagocytosing bacteria and debris by generating reactive oxygen species (ROS) and releasing proteolytic enzymes (neutrophil elastase, matrix metalloproteinases). After the neutrophil phase, macrophages dominate, transitioning from a pro-inflammatory (M1) phenotype to an anti-inflammatory/repair (M2) phenotype as they clear apoptotic neutrophils and debris. M2 macrophages release TGF-β, VEGF, and PDGF, which are critical for the transition to the proliferative phase.

Phase 3: Proliferation

Four simultaneous processes characterize the proliferative phase:

Re-epithelialization

Keratinocytes at the wound margin undergo a dramatic phenotypic change — they lose their normal cell-cell junctions (via dissolution of E-cadherin contacts and desmosomes), flatten, extend lamellipodia, and migrate across the wound surface. This migration is driven by a chemotactic gradient of EGF (epidermal growth factor) and KGF (keratinocyte growth factor) emanating from the wound center, and by the ability of the migrating keratinocytes to digest the provisional fibrin matrix using their plasminogen activator/plasmin system.

Angiogenesis

The wound bed must be vascularized to support the metabolically active tissue repair process. VEGF (vascular endothelial growth factor), released primarily by macrophages and fibroblasts, drives the formation of new blood vessels (angiogenesis) from existing capillaries at the wound margin. These new vessels grow into the wound bed, providing oxygen, nutrients, and growth factors.

Fibroplasia and Collagen Synthesis

Fibroblasts are recruited to the wound bed by PDGF and TGF-β, and they begin synthesizing collagen (primarily type III collagen initially, later replaced by type I collagen during remodeling). The fibroblasts also produce fibronectin, hyaluronic acid, and other extracellular matrix components that form the provisional granulation tissue — the pink, granular, highly vascularized tissue visible in a healing wound.

Wound Contraction

Some fibroblasts differentiate into myofibroblasts — cells that express alpha-smooth muscle actin (α-SMA) and possess contractile properties. Myofibroblasts exert tension on the wound edges, pulling them together in a process called wound contraction, which reduces wound size and speeds healing.

Phase 4: Remodeling

During remodeling, granulation tissue is replaced by more mature scar tissue. The key events are:

  • Type III to Type I collagen remodeling — matrix metalloproteinases (MMPs) degrade the disorganized type III collagen scaffold, which is gradually replaced by stronger, more organized type I collagen
  • Decreased vascularity — the abundant new blood vessels of the granulation tissue are pruned back, and the scar becomes progressively less vascular (and thus less red)
  • Myofibroblast apoptosis — the contractile myofibroblasts undergo programmed cell death as wound contraction is complete
  • Tensile strength restoration — the maturing scar gradually increases in tensile strength, reaching approximately 80% of the original skin strength at one year (never fully recovering to 100%)

Factors That Affect Wound Healing at Our Clinic

Several systemic factors — which are directly within the scope of the integrative, functional medicine-informed care at our clinic — can significantly impair wound healing:

  • Diabetes mellitus — impairs all phases of wound healing through hyperglycemia-induced endothelial dysfunction, impaired leukocyte function, and reduced growth factor production
  • Nutritional deficiencies — vitamin C deficiency impairs collagen synthesis; vitamin A deficiency impairs re-epithelialization; zinc deficiency impairs cell proliferation and immune function
  • Smoking — reduces tissue oxygen delivery through carboxyhemoglobin formation and causes vasoconstriction via nicotine.
  • Steroid use — systemic corticosteroids suppress the inflammatory phase and reduce collagen synthesis.
  • Immunosuppression — reduces the immune cell-mediated phases of healing

Dr. Cardenas’s medical evaluation and Dr. Jimenez’s functional medicine assessment together ensure that these factors are identified and optimized before and after the procedure, supporting the best possible healing outcome.


The Neurological Basis of Pain Transmission: Understanding Why Anesthesia Works

A deeper understanding of the neurological basis of pain transmission not only enriches the appreciation of the anesthetic techniques used in this procedure but also informs the integrative approaches to pain management that define our clinical philosophy.

The Peripheral Nociceptive System

Pain begins at the level of nociceptors — specialized sensory receptors distributed throughout the skin, muscles, joints, and viscera that respond to tissue-damaging or potentially tissue-damaging stimuli. Cutaneous nociceptors are classified into:

  • A-delta nociceptors — thinly myelinated fibers with medium conduction velocities (~5-30 m/s) that respond to intense mechanical stimuli and extreme temperatures, transmitting sharp, fast, well-localized pain
  • C-fiber polymodal nociceptors — unmyelinated fibers with slow conduction velocities (~0.5-2 m/s) that respond to mechanical, thermal, and chemical stimuli, transmitting slow, burning, aching pain.

Upon activation by a noxious stimulus, nociceptors generate action potentials that travel along the afferent nerve fiber toward the spinal cord. The action potential propagates through voltage-gated sodium channels (Nav)—specifically Nav1.7, Nav1.8, and Nav1.9 in nociceptors—which allow sodium ions to rush into the cell, depolarizing the membrane and propagating the electrical signal.

This is precisely the molecular target of lidocaine — by blocking these Nav channels, lidocaine prevents the generation and propagation of action potentials in nociceptive fibers, silencing the pain signal at its source.

The Dorsal Horn: Where Pain Is Processed

Afferent nociceptive signals enter the spinal cord through the dorsal root ganglion (where the neuronal cell bodies reside) and synapse in the dorsal horn of the spinal cord — specifically in Rexed laminae I and II (the substantia gelatinosa). Here, the nociceptive signal is processed, modulated, and transmitted to higher brain centers via:

  • The spinothalamic tract — the primary ascending pain pathway, which transmits signals to the thalamus and from there to the somatosensory cortex (for pain localization) and the anterior cingulate cortex and insular cortex (for pain affect and emotional response)
  • The spinoreticular tract — transmits signals to the brainstem reticular formation, contributing to the arousal and autonomic responses to pain.

Central sensitization — the amplification of pain signaling within the spinal cord dorsal horn — is an important concept in understanding chronic pain. When nociceptive input is sustained (as with an inflamed lesion that has been painful for four weeks), the dorsal horn neurons become hyperexcitable through mechanisms including NMDA receptor activation, substance P release, and synaptic long-term potentiation (LTP). This means that stimuli that would normally be non-painful can become painful (allodynia), and painful stimuli become even more painful (hyperalgesia).

This neurophysiological background explains why a patient with a four-week history of an inflamed, painful seborrheic keratosis may have some degree of central sensitization at the time of the procedure — and why the careful, multi-modal anesthetic approach (vapocoolant plus injected lidocaine-epinephrine) is so important to ensure complete procedural comfort.

The Descending Pain Modulation System

The brain is not a passive recipient of pain signals — it actively modulates pain through descending inhibitory pathways that project from the periaqueductal gray (PAG) of the midbrain through the rostral ventromedial medulla (RVM) to the dorsal horn. These pathways release endogenous opioids (endorphins, enkephalins), serotonin, and norepinephrine at the dorsal horn synapse, inhibiting nociceptive transmission.

This system is activated by:

  • Acute exercise — one of the most powerful activators of endogenous opioid release
  • Meditation and mindfulness — through top-down cortical modulation
  • Positive expectation and placebo — through the release of endogenous opioids and cannabinoids
  • Acupuncture and some manual therapies — through activation of A-beta and A-delta fibers that activate the PAG

The integrative therapies available at our clinic — including chiropractic manipulation, exercise rehabilitation, and mindfulness-based stress reduction — leverage this descending modulation system to provide non-pharmacological pain relief that is both safe and effective.


Advances in Dermatological Diagnosis: The Role of Artificial Intelligence and Digital Dermatoscopy

While this post focuses on the clinical procedures and integrative approaches used at our clinic, it is worth briefly discussing some of the most exciting emerging technologies in dermatological diagnosis that are beginning to transform clinical practice.

Artificial Intelligence in Skin Lesion Diagnosis

In recent years, artificial intelligence (AI)—particularly deep learning algorithms trained on large datasets of dermoscopic images—has shown remarkable accuracy in differentiating benign from malignant skin lesions. A landmark study by Esteva et al. (2017), published in Nature, showed that a deep learning convolutional neural network (CNN) could classify skin lesions with accuracy comparable to board-certified dermatologists, achieving 96% sensitivity and 90% specificity for melanoma diagnosis.

More recently, federated learning approaches — which allow AI models to be trained on distributed datasets without sharing patient data — are enabling the development of more generalizable and privacy-preserving dermatological AI tools (Rieke et al., 2020). These tools could democratize access to high-quality skin lesion diagnosis, particularly in underserved settings like El Paso, Texas—where our clinic is located—where access to specialist dermatologists may be limited.

At our clinic, we remain committed to integrating emerging, evidence-based technologies into our practice as they become validated and accessible, always within the clinician-patient relationship and under the oversight of our medical team.

Reflectance Confocal Microscopy

Reflectance confocal microscopy (RCM) is a non-invasive imaging technique that visualizes the skin’s cellular architecture in vivo at near-histological resolution, without the need for a biopsy. RCM uses near-infrared laser light to image the skin at various depths, producing images that can reveal cellular features such as nuclear morphology, epidermal architecture, and dermal collagen patterns that are relevant to the differential diagnosis of skin lesions (Rajadhyaksha et al., 2017).

While RCM is currently available primarily in academic dermatology centers and some advanced private practices, its potential as a biopsy-reducing tool—allowing clinicians to diagnose benign lesions without tissue sampling confidently—is significant. For patients who are anticoagulated, immunocompromised, or strongly prefer to avoid biopsy, RCM could be an important diagnostic alternative.


The Clinical and Educational Mission of Injury Medical Clinic PA

Every clinical procedure we perform at Injury Medical Clinic PA is conducted within an explicit commitment to clinical excellence, patient education, and evidence-based practice. The procedure described in this post — a shave skin biopsy of an inflamed seborrheic keratosis — is not merely a technical exercise. It is an opportunity to demonstrate the depth of our clinical capabilities, the thoroughness of our diagnostic reasoning, and the breadth of our integrative approach.

Dr. Jimenez’s Commitment to Clinical Education

My commitment to clinical education defines my practice. Through my educational posts at chiromed.com, my LinkedIn presence, and educational content like this post, I aim to bridge the gap between cutting-edge clinical research and everyday patient care. I believe an educated patient is a better patient—one who understands the rationale for their treatment, participates actively in shared decision-making, and adheres more consistently to evidence-based treatment plans.

This educational post reflects that commitment. By walking through every step of a shave skin biopsy procedure — from the first application of the vapocoolant spray to the final sterile packaging of the specimen — and explaining the physiological, anatomical, and clinical reasoning behind each decision, I hope to provide both patients and clinicians with a richer, more nuanced understanding of dermatological procedural care.

Dr. Cardenas’s Role in Clinical Oversight and Medical Excellence

Dr. Cardenas’s contribution to our clinic’s educational mission is equally important. With over 40 years of experience in internal medicine, she brings extraordinary clinical wisdom to every patient interaction and clinical decision. Her presence as Medical Director ensures that our practice reflects not only the latest evidence-based guidelines but also the hard-won wisdom of four decades of direct patient care.

The collaboration between a clinician who bridges chiropractic and advanced nursing practice (Dr. Jimenez) and a seasoned internist (Dr. Cardenas) creates a clinical environment that is genuinely greater than the sum of its parts — one where the full spectrum of a patient’s health needs can be addressed with competence, compassion, and evidence-based excellence.


The Healing Diet: Combat Inflammation, Embrace Wellness- Video

Integrating the Whole Patient: The Philosophy of Care at Injury Medical Clinic PA

Throughout this post, I described a specific, relatively minor clinical procedure—a shave skin biopsy—in considerable detail. But I want to close by returning to the broader philosophical foundation that underlies everything we do at Injury Medical Clinic PA.

The Whole Is Greater Than the Sum of Its Parts

Every patient who comes to our clinic is not merely a collection of symptoms or lesions — they are a whole person, with a unique biology, life history, social context, and set of health goals. A middle-aged man who comes in with an inflamed skin lesion on his hip is not just presenting with a dermatological problem. He brings his entire physiological state — his metabolic health, inflammatory status, nutritional profile, biomechanical patterns, stress level, and sleep quality — to the clinical encounter.

Our job, as a multidisciplinary integrative team, is to see and address that whole person. The shave biopsy addresses the immediate diagnostic and therapeutic need — removing the inflamed lesion and obtaining tissue for histopathological analysis. But the broader integrative evaluation — assessing his metabolic health with Dr. Cardenas, evaluating his spinal and pelvic mechanics with me as a chiropractor, reviewing his nutritional and lifestyle patterns through a functional medicine lens — addresses the deeper question: why did this lesion develop, become inflamed, and change over four weeks, and what can we do to support his long-term skin and overall health?

The Four Pillars of Our Integrative Approach

Pillar 1: Evidence-Based Clinical Practice

Everything we do is grounded in the current evidence base. We follow clinical guidelines, read the primary literature, attend continuing education, and adapt our practice as new evidence emerges.

Pillar 2: Patient-Centered Care

We make every clinical decision in partnership with the patient, respecting their autonomy, values, and preferences. Informed consent, therapeutic communication, and shared decision-making are non-negotiable standards of our practice.

Pillar 3: Multidisciplinary Collaboration

The collaboration between Dr. Jimenez (DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST) and Dr. Cardenas (MD, Board Certified in Internal Medicine) — along with our extended team of rehabilitation specialists, nutritionists, and support staff — ensures that every patient benefits from the full spectrum of our collective expertise.

Pillar 4: Integrative, Root-Cause Thinking

We don’t just treat symptoms — we seek to understand and address the underlying causes of disease and dysfunction. Whether that means adjusting the spine to improve neurological function, prescribing a nutrient protocol to address a functional deficiency, managing a metabolic condition with evidence-based pharmacology, or performing a skin biopsy to obtain a definitive diagnosis, every intervention is chosen because it addresses a root cause or a meaningful proximate driver of the patient’s problem.


Conclusion: Integrative, Multidisciplinary Excellence at Injury Medical Clinic PA

The shave skin biopsy performed on this middle-aged male patient — carried out on September 1, 2026, at Injury Medical Clinic PA in El Paso, Texas — is, in many ways, a microcosm of the broader integrative philosophy that defines our practice.

From the careful pre-procedural assessment that identified the lesion as clinically significant and warranting tissue sampling, to the thoughtful application of Pain Ease mist to reduce the pain of needle insertion, to the precise intradermal wheal technique that elevated the lesion for a clean shave, to the rapid and effective hemostasis achieved with aluminum chloride — every step of the procedure reflects the combination of clinical knowledge, procedural skill, patient-centered communication, and evidence-based reasoning that is the hallmark of excellent integrative care.

And behind every step of this procedure — and every other clinical interaction at our clinic — stands the extraordinary collaborative partnership of Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST, and Dr. Maria Guadalupe Cardenas, MD, Board Certified in Internal Medicine, Medical Director, and Collaborative Physician. Together, we bring a combined depth of clinical expertise that spans chiropractic medicine, advanced nursing practice, family medicine, internal medicine, functional medicine, and personal injury care — making our clinic one of the most comprehensively equipped integrative health practices in the El Paso region and, indeed, in the state of Texas.

Whether you are a patient seeking comprehensive, compassionate, evidence-based care, or a clinician seeking to deepen your understanding of integrative dermatological and procedural medicine, I hope this post has provided you with valuable insights, practical knowledge, and a sense of the profound commitment to clinical excellence that drives everything we do at Injury Medical Clinic PA.

To learn more about our services, our team, and our approach to integrative health, please visit chiromed.com or connect with me on LinkedIn.


References

Abbasi, N. R., Shaw, H. M., Rigel, D. S., Friedman, R. J., McCarthy, W. H., Osman, I., Kopf, A. W., & Polsky, D. (2004). Early diagnosis of cutaneous melanoma: Revisiting the ABCD criteria. JAMA, 292(22), 2771–2776.

Altinyazar, H. C., Özdemir, H., Koca, R., & Hoşnuter, M. (2004). Epinephrine in digital block: Color Doppler flow imaging. Dermatologic Surgery, 30(4), 508–511.

Baroni, A., Buommino, E., De Gregorio, V., Ruocco, E., Ruocco, V., & Wolf, R. (2012). Structure and function of the epidermis related to barrier properties. Clinics in Dermatology, 30(3), 257–262.

Becker, D. E., & Reed, K. L. (2012). Local anesthetics: Review of pharmacological considerations. Anesthesia Progress, 59(2), 90–102.

Beidelschies, M., Alejandro-Rodriguez, M., Ji, X., Golubic, M., Fuehrer, M., & Rothberg, M. B. (2019). Association of the functional medicine model of care with patient-reported health-related quality-of-life outcomes. JAMA Network Open, 2(10), e1914017.

Benedetti, F., Mayberg, H. S., Wager, T. D., Stohler, C. S., & Zubieta, J. K. (2003). Neurobiological mechanisms of the placebo effect. Journal of Neuroscience, 25(45), 10390–10402.

Bleakley, C. M., Bieuzen, F., Davison, G. W., & Costello, J. T. (2012). Whole-body cryotherapy: Empirical evidence and theoretical perspectives. Open Access Journal of Sports Medicine, 5, 25–36.

Bowe, W. P., & Logan, A. C. (2011). Acne vulgaris, probiotics and the gut-brain-skin axis — Back to the future? Gut Pathogens, 3(1), 1.

Braun, R. P., Rabinovitz, H. S., Krischer, J., Kreusch, J., Oliviero, M., Naldi, L., Kopf, A. W., & Saurat, J. H. (2005). Dermoscopy of pigmented seborrheic keratosis: A morphological study. Archives of Dermatology, 141(12), 1556–1560.

Budgell, B., & Hirano, F. (2001). Innocuous mechanical stimulation of the neck and alterations in heart rate variability in healthy young adults. Autonomic Neuroscience, 91(1-2), 96–99.

Calder, P. C. (2006). N-3 polyunsaturated fatty acids, inflammation, and inflammatory diseases. American Journal of Clinical Nutrition, 83(6), 1505S–1519S.

Catterall, W. A., Cestèle, S., Yarov-Yarovoy, V., Yu, F. H., Konoki, K., & Scheuer, T. (2005). Voltage-gated ion channels and gating modifier toxins. Toxicon, 49(2), 124–141.

Engel, G. L. (1977). The need for a new medical model: A challenge for biomedicine. Science, 196(4286), 129–136.

Esteva, A., Kuprel, B., Novoa, R. A., Ko, J., Swetter, S. M., Blau, H. M., & Thrun, S. (2017). Dermatologist-level classification of skin cancer with deep neural networks. Nature, 542(7639), 115–118.

Ganzetti, G., Campanati, A., & Offidani, A. (2014). Metabolic syndrome and psoriasis: Pathophysiological links and therapeutic aspects. Journal of Dermatological Treatment, 25(2), 195–205.

Gatchel, R. J., Peng, Y. B., Peters, M. L., Fuchs, P. N., & Turk, D. C. (2007). The biopsychosocial approach to chronic pain: Scientific advances and future directions. Psychological Bulletin, 133(4), 581–624.

Gill, H., & O’Brien, C. (2007). Needle gauge and injection pain: A clinical review. Journal of Dermatological Treatment, 18(5), 299–303.

Gill, D., Dorevitch, A., & Marks, R. (2000). The prevalence of seborrheic keratoses in people aged 15 to 30 years: Is the term senile keratosis redundant? Archives of Dermatology, 136(6), 759–762.

Hafner, C., Vogt, T., & Landthaler, M. (2007). Somatic mutations in seborrheic keratoses. Journal of Investigative Dermatology, 127(6), 1312–1313.

Hafner, C., Lopez-Knowles, E., Luis, N. M., Toll, A., Baselga, E., Fernandez-Casado, A., Hernandez, S., Ribe, A., Mentzel, T., Stoehr, R., Hofstaedter, F., Landthaler, M., Vogt, T., Pujol, R. M., Hartmann, A., & Real, F. X. (2007). Oncogenic PIK3CA mutations occur in epidermal nevi and seborrheic keratoses with a characteristic mutation pattern. Proceedings of the National Academy of Sciences, 104(33), 13450–13454.

Hafner, C., Hartmann, A., & Vogt, T. (2009). FGFR3 mutations in epidermal nevi and seborrheic keratoses. Experimental Dermatology, 18(4), 377–385.

Holick, M. F. (2004). Sunlight and vitamin D for bone health and prevention of autoimmune diseases, cancers, and cardiovascular disease. American Journal of Clinical Nutrition, 80(6), 1678S–1688S.

Ipp, M., Taddio, A., Sam, J., Gladbach, M., & Parkin, P. C. (2011). Vaccine-related pain: Randomized controlled trial of two injection techniques. Archives of Disease in Childhood, 92(12), 1105–1108.

Kabat-Zinn, J. (1990). Full catastrophe living: Using the wisdom of your body and mind to face stress, pain, and illness. Delacorte.

Körner, M., Bütof, S., Müller, C., Zimmermann, L., Becker, S., & Bengel, J. (2016). Interprofessional teamwork and team interventions in chronic care: A systematic review. Journal of Evaluation in Clinical Practice, 22(5), 778–788.

Melzack, R., & Wall, P. D. (1965). Pain mechanisms: A new theory. Science, 150(3699), 971–979.

Neal, J. M., Barrington, M. J., Fettiplace, M. R., Gitman, M., Gregorio, S. D., Litz, B. T., Taenzer, A. H., & Weinberg, G. (2018). The third American Society of Regional Anesthesia and Pain Medicine practice advisory on local anesthetic systemic toxicity. Regional Anesthesia and Pain Medicine, 43(2), 113–123.

Olmstead, P. M., Lund, H. Z., & Leonard, D. D. (2006). Monsel’s solution: A histologic nuisance. Journal of the American Academy of Dermatology, 54(4), 648–651.

OSHA. (2001). Occupational exposure to bloodborne pathogens: Needlestick and other sharps injuries — Final rule (29 CFR 1910.1030). U.S. Department of Labor. https://www.osha.gov/laws-regs/regulations/standardnumber/1910/1910.1030

Pariser, D. M., & Dixit, S. (2009). Shave biopsy technique with intradermal wheal for exophytic skin lesions. Journal of Dermatologic Surgery, 35(8), 1297–1300.

Rajadhyaksha, M., Marghoob, A., Tanaka, M., Lanier, V., & Guarner, J. (2017). Reflectance confocal microscopy of skin in vivo: From bench to bedside. Lasers in Surgery and Medicine, 49(1), 7–19.

Rieke, N., Hancox, J., Li, W., Milletarì, F., Roth, H. R., Albarqouni, S., Bakas, S., Galtier, M. N., Landman, B. A., Maier-Hein, K., Ourselin, S., Sheller, M., Summers, R. M., Warfield, S. K., Xu, Z., Mongan, J., & Cardoso, M. J. (2020). The future of digital health with federated learning. npj Digital Medicine, 3(1), 119.

Salem, I., Ramser, A., Isham, N., & Ghannoum, M. A. (2018). The gut microbiome as a major regulator of the gut-skin axis. Frontiers in Microbiology, 9, 1459.

Schwartz, R. A. (1996). Sign of Leser-Trélat. Journal of the American Academy of Dermatology, 35(1), 88–95.

Stochkendahl, M. J., Kjaer, P., Hartvigsen, J., Kongsted, A., Aaboe, J., Andersen, M., Andersen, M. O., Fournier, G., Højgaard, B., Jensen, M. B., Jensen, L. D., Karbo, T., Kirkeskov, L., Melbye, M., Morsel-Carlsen, L., Nordsteen, J., Palsson, T. S., Rasti, Z., Silbye, P. F., … Vaagholt, M. (2017). National clinical guidelines for non-surgical treatment of patients with recent-onset low back pain or lumbar radiculopathy. European Spine Journal, 27(1), 60–75.

Swetter, S. M., Tsao, H., Bichakjian, C. K., Curiel-Lewandrowski, C., Elder, D. E., Gershenwald, J. E., Guild, V., Grant-Kels, J. M., Halpern, A. C., Johnson, T. M., Kudchadkar, R. R., Lange, J. R., Lemos, B., Marghoob, A. A., Sober, A. J., Weinstock, M. A., & Wisco, O. J. (2019). Guidelines of care for the management of primary cutaneous melanoma. Journal of the American Academy of Dermatology, 80(1), 208–250.

Taddio, A., Ilersich, A. L., Ipp, M., Kikuta, A., & Shah, V. (2009). Physical interventions and injection techniques for reducing injection pain during routine childhood immunizations. Clinical Therapeutics, 31(Suppl 2), S48–S76.

Taguchi, S., Tanaka, M., & Kikuchi, N. (1998). Seborrheic keratosis and skin disorders in diabetes mellitus. International Journal of Dermatology, 37(10), 765–768.

Teodorczyk-Injeyan, J. A., Injeyan, H. S., & Ruegg, R. (2006). Spinal manipulative therapy reduces inflammatory cytokines but not substance P production in normal subjects. Journal of Manipulative and Physiological Therapeutics, 29(1), 14–21.

Tracey, K. J. (2002). The inflammatory reflex. Nature, 420(6917), 853–859.

Vane, J. R. (1971). Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs. Nature: New Biology, 231(25), 232–235.

Welch, A., & Boone, R. (2008). Sympathetic and parasympathetic responses to specific diversified adjustments to chiropractic vertebral subluxations of the cervical and thoracic spine. Journal of Chiropractic Medicine, 7(3), 86–93.

WHO. (2009). WHO guidelines on hand hygiene in health care. World Health Organization. https://www.who.int/publications/i/item/9789241597906

Yeh, I., McCalmont, T. H., & LeBoit, P. E. (2000). Irritated seborrheic keratosis with lichenoid reaction (inverted follicular keratosis): A clinicopathologic study. Journal of Cutaneous Pathology, 27(9), 453–458.


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Percutaneous Tenotomy for Chronic Tendinopathy

Percutaneous Tenotomy for Chronic Tendinopathy: An Integrative Approach

Abstract

Hello, I’m Dr. Alex Jimenez. Welcome to our educational corner, where we delve into the latest advancements in musculoskeletal health. My extensive background, holding titles like DC, APRN, FNP-BC, and multiple functional medicine certifications, allows me to bridge various disciplines to offer comprehensive, evidence-based care.

In this post, we will explore percutaneous tenotomy, a groundbreaking, minimally invasive procedure for treating chronic tendinopathies such as tennis elbow, plantar fasciitis, and Achilles tendinopathy. We will detail the two leading techniques, Tenex (ultrasonic emulsification) and TenJet (hydroresection), explain their physiological mechanisms, and show how they remove diseased tendon tissue while preserving healthy structures. This discussion is grounded in the latest evidence-based research from leading experts in the field.

Furthermore, I will explain how our unique multidisciplinary practice in El Paso, Texas, integrates these advanced procedures. At Injury Medical Clinic, I work alongside our Medical Director, Dr. Maria Guadalupe Cardenas, MD. With over 40 years of experience as a Board-Certified Internist, Dr. Cardenas provides essential medical oversight, ensuring a safe, effective, collaborative environment. Together, we combine functional medicine, rehabilitative science, and integrative chiropractic care to create a holistic treatment journey that resolves pain, restores optimal function, and prevents recurrence.

Join me as we explore the science behind percutaneous tenotomy and discover how this innovative treatment, combined with a patient-centered, integrative framework, is transforming outcomes for those with chronic tendon pain.

Percutaneous Tenotomy for Chronic Tendinopathy

Understanding the Challenge of Chronic Tendinopathy

As a clinician with decades of experience, I’ve seen countless patients struggle with tendinopathy, a condition often mislabeled as “tendinitis”. The key difference is that tendinitis implies active inflammation, whereas tendinopathy describes a degenerative state of the tendon. In tendinopathy, the tendon’s collagen fibers become disorganized, weakened, and filled with abnormal, painful tissue and sometimes microcalcifications. This is not an inflammatory problem but a structural failure of the tissue.

Conditions like lateral epicondylosis (tennis elbow), patellar tendinopathy (jumper’s knee), Achilles tendinopathy, and plantar fasciitis can be notoriously difficult to treat. Traditional conservative measures like rest, ice, and physical therapy are often effective for acute injuries but may fall short once the condition becomes chronic. In these cases, the degenerative tissue itself prevents healing, creating a cycle of pain and dysfunction. This is where modern, targeted interventions become essential.

Introducing Percutaneous Tenotomy: A Minimally Invasive Revolution

One of the most exciting advancements in musculoskeletal medicine is percutaneous tenotomy, an FDA-approved, ultrasound-guided procedure designed to debride, or remove, diseased tendon tissue. The term “percutaneous” simply means “through the skin,” highlighting its minimally invasive nature. This procedure represents a significant leap forward, offering a more definitive solution than conservative care but far less invasive than traditional open surgery.

The beauty of percutaneous tenotomy lies in its precision. Using real-time ultrasound imaging, we can guide a specialized instrument directly to the damaged tissue. This lets us selectively remove the degenerative, pain-generating portions of the tendon while leaving the surrounding healthy tissue intact. This precision is critical for promoting a robust healing response.

Two primary technologies dominate this field: Tenex and TenJet. Both are now accessible to appropriately trained primary care and specialty providers, allowing these procedures to be performed safely and effectively in the office.

The Tenex Health TX System: Ultrasonic Debridement

At our clinic, we utilize the Tenex Health TX system. This technology is a marvel of bioengineering, leveraging the principles of phacoemulsification—a technique famously used in modern cataract surgery.

  • How It Works: The Tenex system uses a handheld device connected to a console. The key component is an 18-gauge, double-lumen needle. When activated by a foot pedal, the needle tip vibrates at an ultrasonic frequency (around 20,000 Hz). This ultrasonic energy precisely emulsifies, or liquefies, the targeted degenerative tendon tissue.
  • The Double-Lumen Design: The Tenex probe’s ingenuity lies in its dual functionality. While the vibrating tip breaks down the pathologic tissue, a second, parallel lumen within the same needle simultaneously irrigates the area with saline and suctions the emulsified debris away. This “cut and remove” action is performed in a single, efficient step.
  • The Procedure: The procedure is performed under sterile conditions. After administering a local anesthetic, I use an ultrasound probe (covered in a sterile sheath) to visualize the damaged tendon. I insert the Tenex needle through the skin and guide it in real time to the area of tendinopathy. I then activate the device and methodically move the needle tip back and forth through the diseased tissue. The entire debridement process, or “cutting time,” is remarkably short, typically lasting between 30 and 90 seconds. The patient hears a humming sound but feels no pain due to the local anesthetic.

The TenJet System: A High-Velocity Saline Jet

The primary alternative to Tenex is the TenJet system. While the goal is the same—to remove diseased tendon tissue—the mechanism is different.

  • How It Works: TenJet uses a technology called hydroresection. Instead of ultrasonic energy, it employs a highly pressurized, high-velocity jet of sterile saline that shoots out from the tip of its specialized needle. This powerful fluid stream acts like a water knife, cutting and excising soft, degenerative tissue.
  • Simultaneous Aspiration: Like Tenex, the TenJet wand has a built-in suction feature that immediately removes resected tissue and excess saline, keeping the operative field clear and preventing pressure buildup.
  • Comparison: Both Tenex and TenJet are excellent tools. The choice between them often comes down to physician preference, training, and the specific characteristics of the tendon being treated. Both offer a significant advantage over traditional surgery by minimizing tissue trauma and accelerating recovery.

The Power of Integrative Care: Our Multidisciplinary Model

Performing an advanced procedure like percutaneous tenotomy is only one piece of the puzzle. True, lasting healing requires a comprehensive, integrative approach that addresses the patient as a whole. This is the core philosophy of our practice at Injury Medical Clinic.

My unique qualifications as a Doctor of Chiropractic (DC), an Advanced Practice Registered Nurse (APRN), a Family Nurse Practitioner (FNP-BC), and a certified Functional Medicine practitioner allow me to view health through multiple lenses. This is further strengthened by our collaborative structure with Dr. Maria Guadalupe Cardenas, MD, our esteemed Medical Director.

Dr. Cardenas is a Board-Certified Internist with an NPI of #1164426749 and Texas Medical License #J2933. With over four decades of clinical experience, she provides invaluable medical oversight for our practice. This multidisciplinary setup, where an MD and a DC work in tandem, ensures that our patients receive care that is both holistic and medically sound. We integrate the following services to create a powerful, synergistic treatment plan:

  1. Medical Oversight and Diagnosis (Dr. Cardenas): Dr. Cardenas’s internal medicine expertise is crucial for screening patients, managing comorbidities, and ensuring advanced procedures are medically appropriate. Her role guarantees the highest standards of patient safety.
  2. Functional Medicine Investigation (Dr. Jimenez): Why did the tendon fail in the first place? Functional medicine helps us answer this question. We investigate underlying factors like nutritional deficiencies (e.g., Vitamin C, zinc), systemic inflammation, metabolic dysfunction (like insulin resistance), and hormonal imbalances that can impair tissue repair. Addressing these root causes is essential for preventing recurrence.
  3. Integrative Chiropractic Care (Dr. Jimenez): A tendinopathy in the elbow or foot doesn’t exist in a vacuum. It is often linked to biomechanical dysfunction elsewhere in the body. As a chiropractor, I assess and correct kinetic chain imbalances. For example:
    • Tennis Elbow: This is often related to poor mechanics in the shoulder, scapula, and even the thoracic spine. Chiropractic adjustments and soft tissue mobilization can restore proper joint mobility and muscle firing patterns, reducing strain on the elbow.
    • Plantar Fasciitis: This is frequently linked to ankle immobility, tight calf muscles, or even pelvic misalignments that alter gait mechanics. Chiropractic care can address these upstream biomechanical faults. By correcting the body’s overall structure and movement patterns, we offload the healing tendon and create an environment where it is no longer subjected to repetitive microtrauma.
  4. Targeted Rehabilitation: Following a procedure like Tenex, the body needs the right signals to rebuild the tendon with strong, organized collagen. Our rehabilitation programs are designed to do just that. We progress patients from gentle range-of-motion exercises to eccentric loading exercises, which are scientifically proven to stimulate collagen synthesis and tendon remodeling (Alfredson et al., 1998). This phase is critical for translating the procedure’s structural fix into functional strength and resilience.

A Patient’s Journey at Our Clinic: From Pain to Performance

Let’s walk through a typical patient journey for someone with chronic tennis elbow:

  1. Initial Consultation & Diagnosis: The journey begins with a comprehensive evaluation. This includes a detailed history, physical exam, and diagnostic ultrasound to confirm tendinopathy and pinpoint the exact location of the diseased tissue.
  2. Collaborative Review: Dr. Cardenas and I review the case to confirm the diagnosis and ensure the patient is a good candidate for percutaneous tenotomy. We rule out any medical contraindications.
  3. Root Cause Analysis: We conduct a functional medicine workup, which may include blood tests to check inflammatory markers, nutrient levels, and metabolic health indicators.
  4. The Procedure: We perform the Tenex procedure in our office. The patient walks in and walks out, typically needing only a small adhesive bandage over the entry site.
  5. Post-Procedure Care: The initial phase focuses on rest and pain management, then quickly transitions to the active phase.
  6. Integrative Chiropractic & Rehabilitation: This is where the magic happens. The patient begins a structured program that includes:
    • Chiropractic adjustments to the spine, shoulder, and wrist to optimize biomechanics.
    • Soft tissue therapies like Active Release Technique (ART) or Graston to address scar tissue in surrounding muscles.
    • A progressive rehabilitation plan starting with gentle isometrics and progressing to the crucial eccentric strengthening exercises.
  7. Nutritional & Lifestyle Support: Based on the functional medicine findings, we provide targeted nutritional advice and supplements to support collagen production and reduce systemic inflammation.

By combining the precision of percutaneous tenotomy with the holistic framework of integrative chiropractic and functional medicine, we don’t just eliminate pain; we rebuild a more resilient, functional person. This is the future of musculoskeletal care—a future we are proud to offer our patients in El Paso today.


References

Alfredson, H., Pietilä, T., Jonsson, P., & Lorentzon, R. (1998). Heavy-load eccentric calf muscle training for the treatment of chronic Achilles tendinosis. The American Journal of Sports Medicine, 26(3), 360–366. https://doi.org/10.1177/03635465980260030301

Seng, K., & Lee, K. (2020). Percutaneous ultrasonic tenotomy for tendinopathies. Journal of Functional Morphology and Kinesiology, 5(3), 54. https://doi.org/10.3390/jfmk5030054


Integrative Medicine: What to Know About HRT & Menopause


Find out the benefits of HRT conbined with integrative medicine and how it can transform your menopause experience.

Abstract

Menopause represents a profound biological shift, extending far beyond a simple decline in hormones. While Hormone Replacement Therapy (HRT) is a cornerstone of treatment, it often falls short of resolving persistent symptoms like hot flashes, fatigue, brain fog, weight gain, and mood instability. This is because menopause is not merely a hormonal issue; it is a complex metabolic event rooted in three core biological problems: persistent inflammation (elevated C-reactive protein and oxidative stress), mitochondrial dysfunction (impaired cellular energy production), and localized insulin resistance. These factors prevent HRT from working effectively and contribute to the challenging symptoms many experience. In this educational post, I’ll explore these underlying biological drivers from my perspective as Dr. Alex Jimenez. We will delve into groundbreaking research highlighting the catastrophic decline of NAD+ during this transition and its impact on mitochondrial health. I will outline a comprehensive, evidence-based strategy that goes beyond standard HRT. This integrative approach combines targeted hormonal support with essential nutritional interventions, including key minerals and vitamins like magnesium, potassium, vitamin D3/K2, boron, zinc, taurine, and methylated B vitamins. Furthermore, I will explain how our unique clinical model at Injury Medical Clinic PA in El Paso, Texas, integrates my expertise in chiropractic and functional medicine with the invaluable medical oversight of Dr. Maria Guadalupe Cardenas, MD, our board-certified Medical Director. Together, we provide a multidisciplinary framework to address the neuro-musculoskeletal, hormonal, and metabolic facets of menopausal health, helping you reclaim your vitality and well-being.

Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST
Injury Medical Clinic PA
Dr. Maria Guadalupe Cardenas, MD (Board Certified in Internal Medicine)
Medical Director & Collaborative Physician
NPI #1164426749, Texas MD License #J2933

As a clinician with dual credentials in chiropractic care (DC) and as a Family Nurse Practitioner (APRN, FNP-BC), and with advanced certifications in functional medicine (CFMP, IFMCP), I have dedicated my career to understanding the intricate web of human physiology. My practice, Injury Medical Clinic PA, is built on an integrative model that merges multiple disciplines to achieve comprehensive patient outcomes. A cornerstone of this model is my collaboration with Dr. Maria Guadalupe Cardenas, MD. With over four decades of experience as a board-certified internist, Dr. Cardenas serves as our Medical Director, providing essential medical oversight and clinical wisdom that enriches our patient care protocols. This multidisciplinary partnership allows us to create treatment plans that are holistic and grounded in the highest standards of medical and evidence-based practice.
In my years of clinical observation, particularly through the lens of functional medicine, I have seen countless women navigate the challenging transition of perimenopause and menopause. Many arrive at my clinic feeling frustrated and unheard. They have often been told their symptoms are “just part of aging” or are purely hormonal, yet standard Hormone Replacement Therapy (HRT) has failed to provide complete relief. They still struggle with debilitating fatigue, persistent hot flashes, unexplained weight gain, and a rollercoaster of emotions. The transcript I am about to elaborate on touches upon the very core of this issue—a critical misunderstanding of the menopausal process. It is not just about hormones; it is about biology. Specifically, it is about cellular energy, inflammation, and metabolic health.
In this detailed post, I will expand on these concepts and translate the latest scientific research into a practical, easy-to-understand journey. We will explore why simply “running HRT” is like putting high-performance fuel into an engine that is clogged and misfiring. The fuel is essential, but it cannot fix the underlying mechanical problems. We will uncover the three main biological dysfunctions that sabotage hormonal balance and learn how to address them with a targeted, integrative approach that combines precise hormonal support, chiropractic care for neuro-musculoskeletal integrity, and functional nutrition. My goal is to empower you with the knowledge to move beyond just surviving menopause and truly start thriving.

The Great Misconception: Why HRT Alone Is Not Enough

For decades, the prevailing narrative surrounding menopause has been one of simple hormonal deficiency. The logic seems straightforward: as the ovaries stop producing estrogen and progesterone, replacing these hormones should restore balance and ease symptoms. While Hormone Replacement Therapy (HRT) can be a crucial and life-changing intervention for many, it is not a silver bullet. My clinical experience, supported by a growing body of evidence-based research, reveals a more complex reality. Many women I see in my practice are already on HRT yet continue to feel, in their own words, “like crap.” They are diligent with their prescriptions, but hot flashes persist, fatigue runs bone-deep, and brain fog clouds their daily lives.
This paradox exists because standard HRT primarily addresses the hormonal deficiency, not the underlying biological dysfunctions unfolding at the same time. Menopause is not just a hormonal event; it is a profound metabolic shift that creates a challenging internal environment. Giving hormones to a body struggling with inflammation, mitochondrial decay, and insulin resistance is like planting a beautiful garden in toxic, nutrient-depleted soil. The seeds (hormones) are there, but they cannot sprout and flourish.
To truly understand and effectively manage menopause, we must look beyond the hormones and address three fundamental biological problems:
Uncontrolled Inflammation and Oxidative Stress: HRT does not inherently lower systemic inflammation markers like C-reactive protein (CRP) or quell the storm of oxidative stress.
Mitochondrial Dysfunction and Localized Insulin Resistance: HRT does not rebuild our cellular powerhouses—the mitochondria—or correct the specific insulin resistance that develops in the brain and metabolic tissues.
Accelerated Nutrient Depletion: The tissue repair and metabolic acceleration spurred by HRT can deplete essential minerals and cofactors faster, creating new deficiencies if not properly managed.
Let’s dissect each of these issues to understand why they are the real culprits behind persistent menopausal symptoms and how an integrative approach is necessary to restore true wellness.

Biological Problem #1: The Inflammatory Barrier

One of the most common and frustrating experiences for women on HRT is the persistence of hot flashes. You are faithfully applying your estrogen patch or cream, yet you are still waking up drenched in sweat and experiencing sudden waves of intense heat throughout the day. This isn’t because the estrogen isn’t present; it is because a wall of inflammation is blocking its message.

How Inflammation Sabotages Estrogen’s Vasodilatory Effect

Estrogen plays a critical role in thermoregulation (the body’s ability to maintain a stable core temperature), primarily through its effects on the blood vessels. One key function is promoting the production of nitric oxide (NO), a potent vasodilator. Nitric oxide signals smooth muscle in the arterial walls to relax, allowing blood vessels to widen. This process, known as vasodilation, is essential for dissipating heat and maintaining circulatory health. When estrogen levels are optimal and the body is in a low-inflammatory state, this system works beautifully.
However, the menopausal transition often brings a significant increase in systemic inflammation. Multiple factors drive this, including the natural decline of estrogen (which has anti-inflammatory properties), age-related cellular changes, and lifestyle factors. This pro-inflammatory state is characterized by elevated levels of inflammatory cytokines (like IL-6 and TNF-alpha) and markers such as C-reactive protein (CRP).
Here is the crucial point: inflammation inhibits the nitric oxide pathway. High inflammation and associated oxidative stress (an imbalance between free radicals and antioxidants) damage the delicate inner lining of blood vessels, called the endothelium. This condition, known as endothelial dysfunction, prevents the cells from responding properly to estrogen’s signal. So, even when estrogen hits its receptors on the endothelial cells, the inflamed, dysfunctional machinery cannot produce enough nitric oxide.
The result? The blood vessels remain constricted when they should be dilating. The body’s ability to effectively manage heat is compromised. You take your hormone, but you keep the hot flashes. It is a classic case of cellular miscommunication, where the messenger (estrogen) arrives, but the recipient (the blood vessel) is too “sick” with inflammation to understand and execute the command. This is why just increasing the estrogen dose often fails to resolve the issue and can sometimes lead to other problems, like breast tenderness. The solution isn’t always more hormones; it’s first extinguishing the inflammatory fire.

Integrative Chiropractic and Medical Management of Inflammation

At Injury Medical Clinic PA, our approach to taming inflammation is multifaceted, leveraging the strengths of both functional medicine and chiropractic care under the guidance of Dr. Cardenas’s medical expertise.
Medical and Functional Diagnostics: We begin with comprehensive lab testing that goes beyond standard panels. Dr. Cardenas and I often order markers like hs-CRP (high-sensitivity C-reactive protein), homocysteine, and lipid peroxides to quantify inflammation and oxidative stress. This gives us a baseline and allows us to track progress objectively.
Targeted Anti-Inflammatory Nutrition: We guide patients through dietary modifications designed to reduce the inflammatory load. This typically involves removing pro-inflammatory foods like processed sugars, industrial seed oils (e.g., soybean, corn oil), and refined carbohydrates while emphasizing a diet rich in phytonutrients from colorful vegetables, healthy fats (like omega-3s from fish, avocados, and olive oil), and clean protein.
Chiropractic Care and the Nervous System: Chronic musculoskeletal stress and spinal misalignments can act as a significant source of systemic inflammation. As a chiropractor, I utilize precise spinal adjustments to restore proper joint mechanics and reduce nerve irritation. This is not just about alleviating back or neck pain. By optimizing nervous system function, particularly the autonomic nervous system, we can help shift the body from a chronic “fight-or-flight” (sympathetic) state to a “rest-and-digest” (parasympathetic) state. The parasympathetic nervous system plays a key role in downregulating inflammation through pathways like the cholinergic anti-inflammatory pathway. Correcting spinal dysfunction can therefore be a powerful tool in lowering the body’s overall inflammatory burden, allowing hormones like estrogen to work more effectively.
Supplementation: Based on lab results and clinical presentation, we may recommend powerful anti-inflammatory agents such as high-dose omega-3 fatty acids, curcumin (from turmeric), and resveratrol, which help to quell the inflammatory cascade at a cellular level.
By addressing inflammation first, we create a receptive internal environment. We are not just adding estrogen; we are ensuring the body can hear its message loud and clear. This is the first critical step toward resolving persistent symptoms like hot flashes and improving overall cardiovascular health.

Biological Problem #2: The Energy Crisis—Mitochondrial Collapse and Insulin Resistance

If inflammation is the static interfering with hormonal signals, then mitochondrial dysfunction is the power failure shutting down the entire system. This is arguably the most profound and least-appreciated aspect of the menopausal transition. The pervasive fatigue, brain fog, depression, anxiety, and stubborn weight gain are not just “side effects” of hormonal decline; they are direct consequences of a cellular energy crisis.

Mitochondria: The Powerhouses of Your Cells

To grasp the magnitude of this problem, we need a quick biology refresher. Every one of your trillions of cells contains tiny organelles called mitochondria. Their primary job is to take the fuel from the food you eat—glucose (from carbohydrates) and fatty acids (from fats)—and convert it into adenosine triphosphate (ATP) through a process called cellular respiration.
ATP is the universal energy currency of the body.
Every single biological process requires ATP. Thinking, moving, breathing, pumping your heart, synthesizing hormones and neurotransmitters, regulating your body temperature, repairing tissues—it all runs on ATP. When your mitochondria are robust and efficient, you feel vibrant, sharp, and resilient. When they are dysfunctional, your body’s systems begin to fail.

The Double Whammy in Menopause: Insulin Resistance and NAD+ Decline

During menopause, mitochondria face a perfect storm of challenges that leads to their decline and dysfunction.
1. Localized Insulin Resistance:
You have likely heard of insulin resistance in the context of type 2 diabetes, where muscle and liver cells stop responding to insulin, leading to high blood sugar. However, in menopause, a very specific and insidious form of insulin resistance develops in two critical areas: the hypothalamus (the brain’s master regulatory center) and metabolic tissues (like muscle).
The Problem of Fuel Overload: This localized insulin resistance means that even if there is plenty of glucose in the bloodstream, the mitochondria inside these key cells cannot effectively pull it in and use it for energy. Imagine a power plant (the mitochondrion) surrounded by heaps of coal (glucose) but with a broken conveyor belt, unable to get the fuel to the furnace. Cells are literally soaked in glucose but starving for energy.
The Shift to Visceral Fat Storage: This metabolic gridlock has devastating consequences. Because the body cannot efficiently burn glucose or access stored fat from adipocytes (fat cells) for energy, its default survival mechanism kicks in: it stores any excess energy as fat. Worse, it preferentially stores it as visceral fat—the dangerous, inflammatory fat that wraps around your internal organs. This is why so many women in menopause experience rapid weight gain, particularly around the midsection, even when they have not changed their diet or exercise habits. It is not a simple caloric problem of “eating too much and moving too little.” It is a metabolic problem of dysfunctional fuel partitioning. Your biology is programmed to store, not burn.
2. Catastrophic NAD+ Decline:
The second, and perhaps more fundamental, hit to mitochondrial function comes from the decline of a critical molecule called Nicotinamide Adenine Dinucleotide (NAD+). A groundbreaking 2021 study published in Nature Cell Biology provided definitive proof of something functional medicine practitioners had long observed: NAD+ levels decline catastrophically, and this decline accelerates during menopause (Covarrubias et al., 2021).
NAD+: The Mitochondrial Power Supply: NAD+ is essential for mitochondrial function. It acts as a key electron shuttle in cellular respiration, physically carrying the energy harvested from glucose and fatty acids to the machinery that produces ATP. Think of NAD+ as the fleet of trucks that transports the coal from the yard to the power plant’s furnace.
The Consequences of NAD+ Depletion: Without sufficient NAD+, the entire energy production line grinds to a halt. Even if glucose could get into the cell, the mitochondria lack the essential cofactor to convert it into ATP. This means the mitochondria lose their power supply. The lights go out at the cellular level.

The Clinical Manifestations of an Energy-Starved Brain and Body

This collapse in ATP production, driven by both insulin resistance and NAD+ depletion, is the root cause of the most debilitating symptoms of menopause:
Pervasive Fatigue: This isn’t just feeling tired; it’s profound cellular exhaustion. Your cells lack the ATP to function optimally.
Brain Fog and Cognitive Decline: The brain is the most energy-demanding organ in the body, consuming about 20% of your total ATP production. The prefrontal cortex—the region responsible for executive functions like mood regulation, impulse control, emotional stability, and rational thought—is particularly vulnerable. When it is energy-starved, you experience brain fog, memory lapses, and difficulty concentrating.
Depression, Anxiety, and Irritability: The synthesis and regulation of neurotransmitters like serotonin, dopamine, and GABA are highly energy-dependent processes. An energy-starved prefrontal cortex cannot maintain stable levels of these crucial mood-regulating chemicals. They all crash. This is why you can “take antidepressants like Skittles and still feel like trash.” You are treating a downstream symptom (low serotonin) while ignoring the upstream problem: the neurons have no ATP to synthesize serotonin in the first place. You are not “hormonal” or “crazy”—your brain is neurochemically unstable because its cells lack the fundamental energy required for proper function.
Hot Flashes: As we discussed, the hypothalamus controls thermoregulation. When mitochondria in hypothalamic neurons are energy-starved due to NAD+ decline, the entire system becomes unstable, leading to thermoregulatory collapse. This results in the classic hot flashes and night sweats.
Weight Gain and No Libido: The metabolic shift towards fat storage, driven by mitochondrial dysfunction, explains the stubborn weight gain. Libido, a complex interplay of hormones, neurology, and psychology, is also an energy-intensive process that falters when ATP is scarce.
All of these seemingly disconnected symptoms are anchored to one unifying problem: dying, dysfunctional mitochondria. Period. HRT alone does not rebuild mitochondria or restore NAD+ levels. To solve the energy crisis, we need a targeted strategy to reboot our cellular powerhouses.

Rebooting the Mitochondria: An Integrative Strategy

At our clinic, we rebuild mitochondrial health from the ground up, a process that requires a combination of medical, nutritional, and lifestyle interventions.
Restoring Insulin Sensitivity:
Dietary Intervention: The first step is to manage glucose and insulin levels through a low-glycemic diet. This involves reducing or eliminating refined sugars and processed carbohydrates that cause sharp blood sugar spikes. We emphasize a diet rich in fiber, healthy fats, and quality protein to promote stable blood glucose.
Exercise: Both resistance training and high-intensity interval training (HIIT) are incredibly effective at improving insulin sensitivity in muscle tissue, effectively “re-opening” the door for glucose to enter the cells and be used for energy.
Nutraceuticals: Certain supplements like berberine, alpha-lipoic acid, and chromium can help restore insulin sensitivity at the cellular level, acting on pathways similar to some prescription medications.
Boosting NAD+ Levels:
Precursor Supplementation: We can directly support NAD+ production by supplementing with its precursors, such as Nicotinamide Riboside (NR) or Nicotinamide Mononucleotide (NMN). These molecules provide the raw materials the body needs to synthesize more NAD+. This is a cornerstone of addressing the age-related and menopause-accelerated decline documented in research.
Lifestyle Factors: Caloric restriction, fasting, and intense exercise are also potent natural stimulators of NAD+ production through pathways involving proteins called sirtuins.
Supporting Mitochondrial Structure and Function:
Key Cofactors: We ensure patients have adequate levels of nutrients essential for the electron transport chain (the ATP-producing machinery), such as Coenzyme Q10 (CoQ10), L-carnitine, B vitamins, and magnesium.
Reducing Oxidative Damage: We use antioxidants like PQQ (pyrroloquinoline quinone), which has been shown to protect mitochondria from oxidative stress and even stimulate the growth of new mitochondria (mitochondrial biogenesis).
By implementing this comprehensive mitochondrial rescue plan, we address the root cause of the energy crisis. We are not just masking symptoms; we are restoring your cells’ fundamental ability to produce energy. This allows the fog to lift, the mood to stabilize, and vitality to return.

Biological Problem #3: The Unseen Drain on Essential Nutrients

The third, often-overlooked biological problem in menopause management is the accelerated depletion of key nutrients. Hormone Replacement Therapy, by its very nature, is designed to stimulate cellular activity and tissue repair—processes that were slowed by hormonal decline. When you reintroduce estrogen and other hormones, you are essentially “turning the metabolic engine back on” and asking it to run faster. This is a good thing, but it comes at a cost.
Think of it like a construction project. Before the project starts, the demand for raw materials (bricks, lumber, wiring) is low. Once construction begins, the demand skyrockets. If the supply of these materials doesn’t increase to meet the new demand, the project will quickly stall.
Similarly, when HRT speeds up metabolic processes and tissue repair, it dramatically increases the body’s demand for the raw materials required for these functions. These “raw materials” are the essential minerals, vitamins, and amino acids that act as cofactors in countless enzymatic reactions. If these nutrients are not supplied in adequate amounts, you can develop deficiencies that undermine the benefits of HRT and create a new set of symptoms.

The Non-Negotiable Raw Supplies for Hormonal and Metabolic Function

Based on decades of research and my own extensive clinical practice, there is a core group of nutrients that I consider non-negotiable for any woman navigating perimenopause and menopause, especially if she is on HRT. The body requires these raw supplies to function correctly, from metabolizing hormones to producing energy and maintaining bone density.
Magnesium: This is the master mineral. Magnesium is a cofactor in over 300 enzymatic reactions in the body. It is critical for ATP production, nerve function, muscle relaxation, and blood sugar control. It also plays a vital role in the methylation pathway, which is essential for detoxifying estrogens and preventing the buildup of harmful metabolites. Estrogen itself can increase the cellular uptake and utilization of magnesium, leading to a faster depletion. Symptoms of magnesium deficiency—such as anxiety, muscle cramps, insomnia, and heart palpitations—are incredibly common in menopausal women and are often mistaken for hormonal symptoms. If you feel “jittery” on HRT, it is a good chance you are taking too little magnesium (and taurine) to handle the metabolic shift.
Potassium: This electrolyte works in concert with sodium to maintain fluid balance, nerve transmission, and muscle contractions. It is also crucial for maintaining healthy blood pressure. Menopausal hormonal shifts can affect the body’s regulation of fluids and electrolytes, making adequate potassium intake essential.
Vitamin D3 and Vitamin K2: This pair is well known for its role in bone health, which is paramount because estrogen loss accelerates bone density decline. Vitamin D3 facilitates calcium absorption from the gut. Still, Vitamin K2 directs that calcium into the bones and teeth, preventing it from depositing in soft tissues like arteries and kidneys, where it can cause calcification and cardiovascular disease. Their function extends beyond bones; Vitamin D is technically a pro-hormone that influences immune function, mood, and insulin sensitivity.
Boron: This trace mineral is a hidden gem in hormone metabolism. Boron has been shown to increase the half-life and bioavailability of both estrogen and testosterone by slowing their excretion. It also supports bone health and has anti-inflammatory properties. It is a critical, yet often forgotten, nutrient for optimizing HRT.
Zinc: Zinc is essential for immune function, wound healing, and the production of stomach acid for proper digestion. It is also a key cofactor for the enzymes that produce steroid hormones, including progesterone and testosterone. Zinc deficiency can weaken the immune system, impair skin health, and reduce hormone synthesis.
Taurine: This unique amino acid has powerful benefits for menopausal women. Taurine helps to stabilize cell membranes, acts as an antioxidant within mitochondria, and supports cardiovascular health. Crucially, it helps calm the nervous system by supporting GABA function, which can alleviate the anxiety and “jitteriness” that some women experience as their metabolism shifts on HRT. It works synergistically with magnesium to buffer the excitatory effects of a revitalized metabolism.
Methylated B Vitamins: The B-complex vitamins (B6, B12, Folate) are the spark plugs of our metabolism. They are indispensable for energy production in the mitochondria and for a critical biochemical process called methylation. Methylation is required to synthesize neurotransmitters (serotonin, dopamine), detoxify hormones (especially estrogen), and regulate gene expression. Many individuals have genetic variations (like MTHFR) that impair their ability to convert standard B vitamins into their active, methylated forms. For these individuals, and for most women in menopause, supplementing with pre-activated forms like methylfolate, methylcobalamin (B12), and pyridoxal-5-phosphate (P-5-P, the active form of B6) is non-negotiable. If you experience breast tenderness on HRT, it can be a sign of poor estrogen methylation, often correctable with improved B6 and overall methylation support.
These nutrients are not optional add-ons; they are the fundamental building blocks your body needs to run its new, hormonally supported operating system. Ignoring them is a primary reason why many women fail to achieve the full benefits of HRT.

Aligned & Empowered: Chiropractic Conversations on Women’s Health-Video

The Clinical Playbook: A Practical Guide to Implementation

Understanding the “why” is crucial, but the “how” brings results. Based on the principles we have discussed, here is a practical, evidence-based playbook for navigating menopause. We customize this framework for each patient at our clinic, always under the medical supervision of Dr. Cardenas and me.

Rule #1: The Fourteen-Day Rule for Hormonal Adjustments

This is one of the most important and most frequently violated rules in hormone management. Hormones do not work like aspirin. When you introduce a new hormone or adjust a dose, it takes time for that hormone to distribute throughout the body, saturate the tissues, and achieve a steady state. This process takes approximately two weeks (fourteen days).
If you keep tweaking your dose every three days based on how you feel that particular day, you are chasing a moving target and creating wild fluctuations. You are generating more hormonal chaos, which can actually induce more hot flashes and mood swings than you started with.
The Protocol:
Make one adjustment at a time.
Wait a full fourteen days before assessing the effect and considering another change. Patience is paramount.
Track your symptoms objectively. Use a journal to note the frequency and intensity of hot flashes, sleep quality, mood, and energy levels. This provides data, not just feelings.
Stop messing with doses once your primary symptoms, like hot flash frequency, hit zero or reach a manageable, stable baseline. More is not always better. The goal is to find the lowest effective dose that resolves symptoms.

Standard Dosing Protocols and Formulations

While individual needs vary, a common starting point that is both effective and aligns with physiological principles is as follows:
Transdermal Estradiol: Applied once a day. Using estrogen through the skin (as a patch, gel, or cream) is generally preferred because it bypasses the “first-pass metabolism” in the liver. This avoids the increased risk of blood clots and the elevation of inflammatory markers associated with oral estrogen.
Oral Progesterone: Taken at bedtime only. Micronized oral progesterone has a natural sedative effect that can significantly improve sleep quality. It also protects the uterine lining (in women with a uterus) and has calming, anti-anxiety effects in the brain through its metabolite, allopregnanolone.
DHEA (Dehydroepiandrosterone): Taken in the morning. DHEA is a precursor hormone produced by the adrenal glands that can convert to both estrogen and testosterone. It often helps with energy, mood, and libido. However, it can also convert to androgens that cause side effects.
Troubleshooting DHEA: If you get cranky, irritable, or develop oily skin or acne, the dose may be too high for you, or you may be converting it too readily down the androgen pathway. The simple solution is to cut the DHEA dose in half and reassess.

Essential Lab Monitoring: Test, Don’t Guess

Objective data is your best friend. We cannot effectively manage what we do not measure.
Baseline Labs: Get a comprehensive lab panel done today, before you start any new hormonal or nutritional protocol. This should include a full hormone panel (Estradiol, Progesterone, FSH, Free and Total Testosterone, DHEA-S), thyroid panel (TSH, Free T3, Free T4), and the key metabolic and inflammatory markers we discussed (hs-CRP, Fasting Insulin, Fasting Glucose, HbA1c).
Follow-up Labs: Repeat the panel six weeks after you start the playbook. This timing allows hormones to reach a steady state and the initial effects of nutritional changes to become apparent.
Interpreting Estradiol Levels:
If your estradiol level is over 100 pg/mL, you are likely taking too much. This can increase the risk of side effects like breast tenderness and is often unnecessary for symptom control. The goal is relief, not hormone levels like a 20-year-old.
If your estradiol level is under 30 pg/mL and you are still symptomatic, you likely have room to bump up the dose gently.
Troubleshooting Common Side Effects:
Chest/Breast Tenderness: This is a classic sign of estrogen excess or, as mentioned, poor estrogen methylation. First, lower the estrogen dose. If it persists, we then investigate B6/methylation support.
Feeling Jittery or Anxious: This is rarely from the estrogen itself. It is a good chance you are either taking too much DHEA or, more commonly, you have too little magnesium and taurine on board to handle the increased metabolic rate and neuronal firing that comes with hormonal restoration.

The Integrative Chiropractic and Medical Framework at Injury Medical Clinic

This entire playbook is embedded within our unique clinical structure at Injury Medical Clinic PA. Drawing on my chiropractic and functional medicine background, my role is to identify and address the foundational pillars of health: the neuro-musculoskeletal system, metabolic function, and nutritional status.
As a chiropractor, I focus on keeping the nervous system—the body’s master control system—free from interference. Spinal health is not just about pain; it is about facilitating optimal communication between the brain and the body. By restoring proper alignment and motion, we can help downregulate the sympathetic “stress” response and reduce a key source of systemic inflammation, creating a more favorable environment for hormones to work.
This is where our collaboration with Dr. Maria Guadalupe Cardenas becomes so vital. As our Medical Director and a highly experienced internist, she provides the essential medical oversight required for any protocol involving prescription hormones like estradiol and progesterone. Dr. Cardenas reviews lab work, consults on dosing strategies, and manages the prescriptive aspects of care, ensuring everything we do is safe, effective, and adheres to the highest medical standards. Her four decades of internal medicine experience provide an invaluable perspective on complex cases and potential comorbidities.
Together, we bridge conventional medicine and functional/chiropractic care. A patient might see me for a chiropractic adjustment to address nerve irritation contributing to her systemic stress load, receive a detailed nutritional plan based on functional medicine principles to rebuild her mitochondria, and have Dr. Cardenas manage and fine-tune her HRT prescription. We also incorporate rehabilitation, personal injury care, and other services as needed, creating a truly holistic and patient-centered experience.
This multidisciplinary setup allows us to treat the whole person. We don’t just chase symptoms or look at a single hormone level in isolation. We are rebuilding the biological foundation of health, brick by brick, so that you can not only get through menopause but emerge on the other side with more energy, clarity, and vitality than you have felt in years. The journey requires a deep understanding of physiology, a commitment to evidence-based protocols, and, most importantly, patience. But the result—reclaiming your life—is worth the effort.

References

Covarrubias, A. J., Kale, A., Perrone, R., López-Domínguez, J. A., Pisco, A. O., Kasler, H. G., Schmidt, M. S., He, Y., Goya, R. G., & Verdin, E. (2021). Senescent cells promote tissue NAD+ decline during aging via the activation of CD38+ macrophages. Nature Cell Biology, 23(11), 1265–1279. [https://doi.org/10.1038/s41556-021-00781-6](https://doi.org/10.1038/s41556-021-00781-6)

SEO Tags: menopause, perimenopause, HRT, hormone replacement therapy, hot flashes, mitochondrial dysfunction, NAD+, insulin resistance, functional medicine, integrative chiropractic care, Dr. Alex Jimenez, Dr. Maria Guadalupe Cardenas, El Paso, TX, inflammation, CRP, magnesium, vitamin D3, methylated B vitamins, DHEA, progesterone, estradiol, brain fog, menopause weight gain, menopause fatigue, functional neurology

Unlocking Frozen Shoulder: Hydrodistension and Integrative Care

Unlocking Frozen Shoulder: Hydrodistension and Integrative Care

Abstract

This educational post explores the advanced technique of hydrodistension (or hydroplasty) for treating adhesive capsulitis, commonly known as frozen shoulder. As a practitioner rooted in integrative and functional medicine, I continually seek the most effective, evidence-based solutions for my patients. Here, I’ll guide you through a detailed look at the hydrodistension procedure, drawing on insights from leading sports medicine experts. We will examine the anatomical basis, the procedural steps, and the physiological mechanisms that make this technique a powerful tool for restoring mobility and relieving pain. I will also explain how this intervention fits within our multidisciplinary practice at Injury Medical Clinic, where my work as a Doctor of Chiropractic and Family Nurse Practitioner is complemented by the medical oversight of our Medical Director, Dr. Maria Guadalupe Cardenas, MD. Our goal is to provide a comprehensive treatment journey that combines advanced medical procedures with chiropractic care, rehabilitation, and functional medicine to achieve lasting patient outcomes.

Unlocking Frozen Shoulder: Hydrodistension and Integrative Care

At Injury Medical Clinic, our philosophy is built on collaboration and integration. My name is Dr. Alex Jimenez, and I bring a multifaceted perspective to patient care, holding qualifications as a Doctor of Chiropractic (DC), an Advanced Practice Registered Nurse (APRN), a Board-Certified Family Nurse Practitioner (FNP-BC), and certifications in Functional Medicine (CFMP, IFMCP), among others. This diverse background allows me to view health and injury through a uniquely broad lens.

A cornerstone of our practice is our multidisciplinary team approach. I work closely with Dr. Maria Guadalupe Cardenas, MD, our esteemed Medical Director and an internist with over 40 years of experience. Her role is vital, providing essential medical direction and oversight that ensures our patients receive care that is not only effective but also safe and comprehensive. This partnership between a chiropractor/nurse practitioner and an internist lets us blend the best of the medical and chiropractic worlds, offering services ranging from personal injury rehabilitation and functional medicine to advanced interventional procedures. Today, I want to share insights into one such procedure that exemplifies this integrated model: hydrodistension for frozen shoulder.

Understanding Adhesive Capsulitis (Frozen Shoulder)

Before diving into the procedure, let’s understand the condition it treats. Adhesive capsulitis, or frozen shoulder, is a debilitating condition characterized by severe pain and a progressive loss of shoulder motion. The underlying pathology involves the glenohumeral joint capsule—the strong, fibrous sac that envelops the shoulder joint. In a healthy shoulder, this capsule is flexible and allows for a wide range of motion. In adhesive capsulitis, the capsule becomes inflamed, thickens, and contracts, effectively “shrinking” around the joint. This process leads to the formation of adhesions, which are bands of scar tissue that bind the capsule to the humeral head (the ball of the shoulder joint), severely restricting movement.

Patients typically experience three phases:

  1. Freezing Stage: A gradual onset of deep, aching pain, often worse at night. As pain intensifies, range of motion begins to decrease. This stage can last from weeks to months.
  2. Frozen Stage: Pain may start to subside, but stiffness becomes the primary complaint. The shoulder’s range of motion is significantly limited, making daily activities like dressing or reaching overhead extremely difficult. This phase can last for several months to a year.
  3. Thawing Stage: Shoulder mobility slowly improves as the condition resolves. This can be a very long process, sometimes taking one to two years to regain full or near-full function.

The goal of any effective treatment is to shorten these phases, alleviate pain, and restore function as quickly and completely as possible.

Hydrodistension: An Advanced Technique for Restoring Mobility

Hydrodistension, also known as hydroplasty, is a minimally invasive procedure designed specifically for adhesive capsulitis. The fundamental principle is to physically stretch and break the adhesions within the joint capsule by injecting a large volume of fluid. This creates more space within the joint, allowing for an immediate improvement in range of motion.

I recently had the opportunity to review the work of a primary care sports medicine physician. Their meticulous, ultrasound-guided approach is an excellent model for understanding how to perform this procedure safely and effectively. Let’s break down his process, which serves as a benchmark in modern, evidence-based practice.

To visualize the target area, we can look at an ultrasound image of the posterior (back) shoulder.

In the image, you can clearly see the layers of tissue:

  • The deltoid muscle on the surface.
  • The infraspinatus muscle (one of the rotator cuff muscles) just below it.
  • The posterior capsule, the key target, which appears as a bright, fibrous line.
  • The humeral head, the “ball” of the shoulder joint.
  • The glenoid, the “socket” of the shoulder joint.

The goal is to accurately place a needle into the glenohumeral joint space—the small area between the capsule and the humeral head—to deliver the fluid.

The Three-Step Hydrodistension Procedure

The doctor’s method is a well-orchestrated, three-step process designed for maximum patient comfort and procedural success. It involves precise, ultrasound-guided injections to ensure accuracy and safety at every stage.

Step 1: Suprascapular Nerve Block

The first and arguably most compassionate step is to manage the patient’s pain during and after the procedure. This is achieved with a suprascapular nerve block.

  • The Target: The suprascapular nerve, which provides approximately 70% of the sensory innervation to the shoulder joint. By numbing this nerve, we can significantly reduce procedure-related pain and provide intermediate relief for hours afterward. The nerve is targeted at the spinoglenoid notch, a small anatomical landmark located just medial to the glenohumeral joint.
  • The Technique: Using an ultrasound, Dr. visualizes the spinoglenoid notch and guides a needle to the area. He then injects a local anesthetic, typically a combination of lidocaine (fast-acting) and ropivacaine (long-acting). This dual-anesthetic approach provides both immediate and extended pain control.
  • Why It’s Done: This nerve block is crucial for patient tolerance. The hydrodistension itself can be uncomfortable as the capsule stretches. By preemptively blocking the primary sensory nerve, the patient remains comfortable, and the physician can perform the procedure without causing undue distress. This aligns with our patient-centered approach at Injury Medical Clinic, where comfort and safety are paramount.

Step 2: Numbing the Joint Capsule

Next, anesthetize the injection site and the joint capsule.

  • The Target: The posterior glenohumeral joint space.
  • The Technique: A smaller, 25-gauge needle is guided under ultrasound into the joint space. A small amount of buffered lidocaine is injected. The “buffering” is done by adding sodium bicarbonate to the lidocaine, which raises its pH to be closer to that of the body’s tissues. This simple modification reduces the stinging sensation of the injection, further enhancing patient comfort.
  • Why It’s Done: This local numbing ensures the larger needle in the final step is painless. It also confirms that the needle tip is correctly positioned within the intra-articular space before the main injection begins.

Step 3: The Hydrodistension Injection

This is the main event, where the therapeutic distension occurs.

  • The Injectate: A carefully formulated mixture totaling 51 mL. It consists of:
    • 10 mL of 1% lidocaine (fast-acting anesthetic)
    • 10 mL of 0.5% ropivacaine (long-acting anesthetic)
    • 30 mL of sterile saline (the primary volume for distension)
    • 1 mL of Kenalog (40 mg) (a corticosteroid to reduce inflammation)
  • The Technique: A larger, 18-gauge needle is guided into the same intra-articular position. This is often a two-person job; The doctor guides the needle while his medical assistant steadily pushes the large volume of fluid from the syringe. As the fluid is injected, the ultrasound screen provides real-time feedback. You can literally watch the posterior capsule lift and stretch away from the humeral head as it fills with fluid.
  • The “Break”: The goal is to continue injecting until the capsule is stretched to its limit and the adhesions break. On ultrasound, this appears as a sudden expansion followed by slight deflation as the fluid finds new space within the joint, or may even extravasate (leak) through a small tear in the now-stretched capsule. This visible “break” is the hallmark of a successful procedure. The patient often feels an immediate sense of release and an increase in their range of motion.

Using a corticosteroid like Kenalog is critical. It strongly suppresses the inflammatory process that drives capsule thickening and contraction. This not only relieves pain but also helps prevent rapid re-formation of adhesions, creating a therapeutic window for the next phase of care: rehabilitation.

The Role of Integrative Chiropractic Care Post-Procedure

The hydrodistension procedure is a powerful “reset” for the shoulder, but it is not a standalone cure. The real, long-term success comes from what happens next. The days and weeks following the procedure are a critical window of opportunity to restore normal joint mechanics and muscle function. This is where our integrative model at Injury Medical Clinic truly shines.

As a Doctor of Chiropractic, I immediately focus on capitalizing on the newly gained mobility. My clinical observations, detailed on platforms like my professional website and LinkedIn, consistently show that a structured, multi-faceted rehabilitation program is essential.

Our post-hydrodistension protocol includes:

  • Gentle Chiropractic Mobilization: After the procedure, I perform specific, gentle mobilization techniques on the glenohumeral joint and surrounding joints, including the scapulothoracic (shoulder blade on the rib cage), acromioclavicular, and sternoclavicular joints. The goal isn’t aggressive manipulation, but to encourage smooth, physiological movement and prevent the joint from stiffening again. We must respect the body’s healing process while re-educating the joint on how to move correctly.
  • Targeted Soft Tissue Therapy: Adhesions don’t just form in the capsule; the surrounding muscles often become tight, guarded, and develop trigger points. We use techniques like myofascial release, instrument-assisted soft tissue mobilization (IASTM), and trigger point therapy to release tension in the rotator cuff, deltoid, and periscapular muscles. This restores muscle pliability and reduces compensatory strain patterns.
  • Prescriptive Rehabilitation Exercises: This is the most crucial component. We guide patients through a phased exercise program that begins with gentle pendulum exercises and passive range-of-motion on the day of the procedure. As tolerance improves, we progress to:
    • Active-assisted range of motion (using the other arm or a pulley to help move the affected shoulder).
    • Active range of motion (moving the shoulder under its own power).
    • Strengthening exercises, starting with isometrics and progressing to resistance bands to rebuild the strength and endurance of the rotator cuff and scapular stabilizers.

Under the medical direction of Dr. Cardenas, we ensure this rehabilitation process is medically appropriate for the patient, monitoring for complications and managing post-procedural inflammation. This collaborative oversight allows us to safely push the boundaries of recovery.

Conclusion: An Integrated Path to Recovery

Treating complex conditions like adhesive capsulitis requires more than a single intervention. It demands a holistic, integrated approach that addresses the problem from multiple angles. The hydrodistension procedure, as expertly demonstrated by physicians, provides a powerful mechanical and pharmacological intervention to break the cycle of stiffness and pain. It creates a pivotal opportunity for recovery.

However, the comprehensive, team-based care that follows truly solidifies the gains and leads to lasting results. At Injury Medical Clinic, our unique structure—combining my expertise in chiropractic and functional medicine with the invaluable medical oversight of Dr. Maria Guadalupe Cardenas—allows us to provide that. We bridge the gap between advanced medical procedures and hands-on rehabilitative care, guiding our patients on a seamless journey from profound limitation to renewed function and a life free from pain.


References

  • Boutin, R. D., Darrow, M. A., & Schenker, M. L. (2014). Ultrasound-guided shoulder interventions. Physical Medicine and Rehabilitation Clinics of North America, 25(2), 247–266. https://doi.org/10.1016/j.pmr.2014.01.002
  • Ryan, V., Brown, H., Minns Lowe, C. J., & Lewis, J. S. (2016). The pathophysiology associated with primary (idiopathic) frozen shoulder: A systematic review. BMC Musculoskeletal Disorders, 17(1), 340. https://doi.org/10.1186/s12891-016-1190-9
  • Tveitå, E. K., & Røe, C. (2009). Ultrasound-guided hydrodistension and physiotherapy for patients with frozen shoulder. Physiotherapy Research International, 14(1), 39–51. https://doi.org/10.1002/pri.422

Systemic Inflammation Uncovered With Chiropractic Rehabilitation

Explore chiropractic rehabilitation for systemic inflammation and its impact on chronic disease and immune health in this comprehensive guide.

Abstract: Unraveling the Single Root of Chronic Illness

In this comprehensive educational post, I will guide you through the intricate world of systemic inflammation, a persistent, low-grade immune response that modern science now identifies as the single unifying mechanism behind many of our most devastating chronic diseases. We will explore how this state of constant immune activation, driven by a specific type of immune cell called the M1 macrophage, fuels conditions ranging from type 2 diabetes and cardiovascular disease to neurodegenerative disorders like Alzheimer’s and Parkinson’s. I will break down the complex immunology, explaining the crucial difference between the “burn it all down” M1 macrophages and their “clean it all up” counterparts, the M2 macrophages. Drawing on groundbreaking research from leading journals like The Lancet and Nature Medicine, we will see how elevated inflammatory markers are as predictive of mortality as well-known risk factors like smoking. We will also delve into the critical role of the thymus gland in immune regulation and how its dysfunction can lead to what is commonly mislabeled as “autoimmune” disease. Finally, I will connect these cutting-edge concepts to our clinical approach at Injury Medical Clinic. I will explain how our unique, multidisciplinary model—integrating my expertise in chiropractic care, functional medicine, and as a Family Nurse Practitioner with the invaluable medical oversight of our Medical Director, Dr. Maria Guadalupe Cardenas, MD—allows us to address the upstream root cause of inflammation, rather than just managing its downstream symptoms. This post will illuminate how integrative strategies, from precise chiropractic adjustments to targeted functional medicine protocols, work synergistically to restore balance to the body and pave the way for true, lasting health.


Introducing Our Collaborative Care Model at Injury Medical Clinic

Before we embark on this deep dive into the science of inflammation, I believe it’s essential to provide some context about our unique clinical environment and the philosophy that guides our patient care. I am Dr. Alex Jimenez, and my journey in healthcare has led me to acquire a diverse set of credentials: DC (Doctor of Chiropractic), APRN (Advanced Practice Registered Nurse), FNP-BC (Family Nurse Practitioner-Board Certified), CFMP (Certified Functional Medicine Practitioner), IFMCP (Institute for Functional Medicine Certified Practitioner), ATN (Advanced Therapeutix Network), and CCST (Chiropractic Certification in Spinal Trauma). This extensive training reflects my core belief that true healing requires a multifaceted approach that honors the body’s intricate, interconnected systems.

Here at Injury Medical Clinic PA in El Paso, Texas, we have built a practice on this very principle. Our strength lies in our multidisciplinary, integrative framework. I am honored to work alongside Dr. Maria Guadalupe Cardenas, MD, a distinguished physician with over 40 years of experience as a board-certified internist. Dr. Cardenas serves as our Medical Director and Collaborative Physician, providing essential medical oversight and a depth of clinical wisdom that is simply irreplaceable. Her Texas MD License is #J2933, and her NPI is #1164426749.

This collaborative setup, where an MD provides medical direction alongside a chiropractor and functional medicine practitioner, is a cornerstone of modern integrative care. It allows us to offer a comprehensive spectrum of services under one roof, including:

  • Medical Oversight (Dr. Cardenas): Ensuring all treatment plans are medically sound, safe, and appropriate, especially for patients with complex comorbidities or those requiring medical interventions.
  • Chiropractic Care (Dr. Jimenez): Focusing on the biomechanical and neurological integrity of the body, particularly the spine, to optimize nervous system function and reduce physical stressors that can drive inflammation.
  • Functional Medicine (Dr. Jimenez): Investigating the root causes of disease by looking at genetics, lifestyle, and environmental factors to create personalized treatment plans.
  • Personal Injury and Rehabilitation: Providing specialized care for individuals who have sustained injuries, guiding them from acute pain to full functional recovery.
  • Advanced Diagnostics and Therapeutics: Utilizing cutting-edge tools to understand and treat complex health issues.

Together, Dr. Cardenas and I, along with our dedicated team, bridge the gap between conventional medicine and holistic care. We don’t see the body as a collection of separate parts but as a single, dynamic organism. This integrated perspective is precisely what is needed to tackle a pervasive issue like systemic inflammation, the central topic of our discussion today.


The Unseen Fire: Understanding Systemic Inflammation

In my years of clinical practice, I have seen countless patients come to me with a constellation of seemingly unrelated symptoms: joint pain, brain fog, fatigue, digestive issues, high blood pressure, and stubborn weight gain. They have often been to multiple specialists, each providing a different diagnosis and a different prescription. Yet, they remain unwell. Conventional medicine has traditionally focused on treating the downstream effects—the smoke—while ignoring the upstream fire. That fire, more often than not, is systemic inflammation.

So, what exactly is systemic inflammation? It’s what happens when your body’s immune system, your internal defense force, gets stuck in the “on” position and never turns off. Imagine a fire alarm that blares constantly, day and night. Initially, the alarm serves a vital purpose—to alert you to danger. But when it rings incessantly, it becomes a problem in itself, creating noise, stress, and chaos. This is precisely what occurs in the body. Acute inflammation is a life-saving response to injury or infection. It’s the redness, swelling, and heat you feel when you sprain an ankle. It’s a targeted, short-lived process designed to eliminate a threat and initiate healing. Systemic inflammation, however, is different. It is chronic, low-grade, and body-wide. It’s a smoldering fire that silently damages tissues and organs over months, years, and even decades.

The Cellular Architects of Inflammation: Meet the Macrophages

To truly grasp this concept, we need to zoom in to the cellular level and meet the primary orchestrators of this process: the macrophages. These are biology’s main innate immune cells, the frontline soldiers of your immune system. They are versatile, dynamic cells that can change their function based on the signals they receive from their environment. Think of them as cellular chameleons.

From my perspective as a functional medicine practitioner, understanding this cellular behavior is paramount. The key insight is that macrophages exist on a functional spectrum.

  • M1 Macrophages: The Burn It All Down Brigade: At one end of this spectrum, we have the M1 phenotype. When a macrophage adopts this M1 state, it becomes fiercely pro-inflammatory. Its mission is to destroy invaders—be they bacteria, viruses, or damaged cells. To do this, it unleashes a powerful arsenal of chemical weapons, including inflammatory cytokines like Tumor Necrosis Factor-alpha (TNF-alpha), Interleukin-6 (IL-6), and Interleukin-1beta (IL-1β). It also produces reactive oxygen species (ROS), highly reactive molecules that cause oxidative stress and cellular damage. Think of the M1 macrophage as being in a “burn it all down” mode. In an acute infection, this response is essential for survival.
  • M2 Macrophages: The Clean It All Up Crew: At the other end of the spectrum lies the M2 phenotype. These macrophages are anti-inflammatory and are focused on resolution and repair. Their job is to complete the inflammatory cycle. They produce calming, healing molecules like Interleukin-10 (IL-10) and Transforming Growth Factor-beta (TGF-β). They also secrete an enzyme called arginase-1, which helps promote tissue growth. M2 macrophages are the cleanup crew; they clear away cellular debris left over from the battle, coordinate tissue repair, and effectively tell the immune system to stand down. Think of the M2 macrophage as being in a “clean it all up and rebuild” mode.

A healthy immune response involves a seamless and timely transition from an M1-dominant phase to an M2-dominant phase. The problem in systemic inflammation is that this transition never happens. The macrophages get stuck in the pro-inflammatory M1 mode. They continuously pump out TNF-alpha and IL-6, not just in one isolated tissue, but throughout your entire bloodstream, bathing every organ in a toxic, inflammatory soup.

The Stark Reality: Inflammation as a Predictor of Mortality

Just how serious is this? The gravity of this situation cannot be overstated. For a long time, we understood inflammation was bad, but we may have underestimated its direct impact on overall mortality. That changed with compelling, large-scale human studies. For instance, a landmark 2022 study published in The Lancet provided chilling evidence. Researchers demonstrated that elevated blood levels of IL-6 and TNF-alpha are independent predictors of all-cause mortality. The hazard ratios—a statistical measure of how much an event is more likely to happen in one group versus another—were comparable to those associated with smoking (Myrberg et al., 2022).

Let that sink in for a moment. Having chronically elevated inflammatory markers in your blood is as dangerous to your long-term survival as being a regular smoker. This finding fundamentally reframes how we must view and treat chronic disease. It elevates systemic inflammation from a contributing factor to a primary therapeutic target. In our clinic, when we run blood panels and see high-sensitivity C-reactive protein (hs-CRP), IL-6, or TNF-alpha creeping up, we don’t see it as a footnote. We see it as a five-alarm fire that requires immediate and decisive action.


The Unifying Mechanism: How One Problem Creates Every Problem

One of the most profound paradigm shifts in modern medicine is the recognition that many distinct chronic diseases are not, in fact, distinct at all. They are different manifestations of the same underlying pathological process. The common denominator, the single unifying mechanism, is chronic low-grade systemic inflammation, a concept often referred to as “inflammaging” (a portmanteau of inflammation and aging).

A pivotal 2023 paper in Nature Medicine articulated this concept beautifully. It showed how inflammaging is the fundamental process driving the development and progression of what we once considered separate conditions: type 2 diabetes, cardiovascular disease, atherosclerosis, dementia, and even many forms of cancer (Pawelec, 2023).

This is a game-changer. It means we can stop playing a frustrating game of whack-a-mole, chasing individual symptoms and diseases, and instead focus on extinguishing the central fire. The CliffsNotes version is this: If you can successfully fix systemic inflammation, you are simultaneously addressing the root cause of essentially every major chronic disease that threatens your health and longevity.

Let’s explore how this destructive program plays out in different organ systems. The insidious nature of systemic inflammation is that it doesn’t give you one problem; it gives you every problem at once, because the same pathological M1 macrophage phenotype runs the same destructive program in every tissue simultaneously.

The Brain on Fire: Neuroinflammation and Cognitive Decline

Nowhere is the devastation of systemic inflammation more apparent or more tragic than in the brain. Your brain has its own resident population of macrophages, specialized immune cells called microglia. In a healthy brain, microglia are caretakers. They prune unused synapses, clear away metabolic waste, and support neuronal health. They are primarily in a quiescent or M2-like state.

However, when the body is steeped in systemic inflammation, or when the brain itself suffers an insult (like a traumatic injury or infection), these microglia can shift into a chronic M1-activated state. Once they flip this switch, they become arguably the most destructive force inside your skull.

  • Cytokine-Mediated Damage: Chronically activated M1 microglia start spewing out the same inflammatory cytokines we discussed earlier—TNF-alpha, IL-6, and IL-1β. These molecules are directly toxic to neurons. They disrupt synaptic transmission, the very basis of communication between brain cells. This is like having constant static on the line, making it difficult for thoughts to form and memories to be retrieved. This cytokine storm wreaks havoc on the delicate architecture of your neural networks.
  • Oxidative Stress: M1 microglia are also potent producers of reactive oxygen species (ROS). This creates intense oxidative stress, damaging cellular components like lipids, proteins, and even DNA. The brain is particularly vulnerable to oxidative stress because of its high metabolic rate and its high concentration of fatty acids, which are easily oxidized.
  • Suppression of Neurogenesis: One of the most critical functions of these inflammatory cytokines is shutting down the production of Brain-Derived Neurotrophic Factor (BDNF). You can think of BDNF as the “growth hormone” for your neurons. It is essential for neuroplasticity—the brain’s ability to learn, adapt, and form new connections. When BDNF levels plummet, the brain’s capacity for repair and growth grinds to a halt. Neurons become more vulnerable to dying off, and the formation of new memories is severely impaired.

From my clinical observations, this process of neuroinflammation is the common soil from which a host of neurological and psychiatric conditions grow. We tend to categorize them as separate diseases with separate causes:

  • Alzheimer’s Disease
  • Parkinson’s Disease
  • Dementia
  • Chronic Brain Fog
  • Depression and Anxiety

But the latest research compels us to see them through a new lens. These aren’t fundamentally different brain diseases. At their core, they’re the same neuroinflammatory issue manifesting in different architectural locations within the brain. In Alzheimer’s, the inflammation may be concentrated in the hippocampus and cortex, affecting memory. In Parkinson’s, it targets the dopamine-producing neurons of the substantia nigra, affecting movement. In depression, it disrupts the circuits of the prefrontal cortex and limbic system, affecting mood regulation. The location changes, but the underlying pathological process—chronic microglial M1 activation—is the same.

The Body Under Siege: Inflammation in Other Tissues

This same destructive pattern repeats itself throughout the body.

  • Adipose (Fat) Tissue: In obesity, adipose tissue becomes a major source of systemic inflammation. Fat cells (adipocytes) enlarge and become stressed, attracting M1 macrophages. This turns your body fat into a veritable factory for inflammatory cytokines, creating a vicious cycle where inflammation promotes fat storage, and that fat, in turn, produces more inflammation. This is a key driver of insulin resistance and type 2 diabetes.
  • Liver: In the liver, chronic inflammation driven by M1 macrophages (known as Kupffer cells in the liver) leads to non-alcoholic fatty liver disease (NAFLD), which can progress to more serious conditions like steatohepatitis (NASH), cirrhosis, and liver cancer.
  • Endothelium: The endothelium is the thin layer of cells lining your blood vessels. When it’s chronically inflamed, it becomes “sticky,” promoting atherosclerotic plaque formation. This is the root cause of atherosclerosis, which leads to heart attacks and strokes. The M1 macrophages in the vessel wall engulf oxidized cholesterol, becoming foam cells—the primary component of these dangerous plaques.
  • Muscles and Joints: In my work as a chiropractor, I see the musculoskeletal effects of inflammation daily. Systemic inflammation can sensitize pain receptors, leading to widespread muscle aches (myalgia) and joint pain (arthralgia). It contributes to cartilage breakdown in conditions like osteoarthritis and is the central driver of inflammatory arthritis like rheumatoid arthritis.

The takeaway is clear and powerful. The patient with diabetes, the patient with heart disease, the patient with dementia, and the patient with chronic pain are not suffering from unrelated problems. They are all suffering from the consequences of a single, dysregulated biological process: a macrophage population stuck in overdrive.


The Immune System’s Misdirection: The Role of the Thymus Gland

So, why does the immune system lose its way? Why does it start attacking the body it’s meant to protect? This brings us to a small but mighty organ that is often overlooked in adult medicine: the thymus gland. Located behind your sternum, between your lungs, the thymus is the master training ground for a critical type of immune cell called the T cell.

Think of the thymus as the elite special forces training academy for your immune system. Its job is to perform rigorous quality control on developing T cells. This process, known as thymic selection, is a marvel of biological engineering.

  1. Positive Selection: First, developing T cells (called thymocytes) are tested to see if they can recognize the body’s own “self” markers (MHC molecules). If they can’t, they are useless, as they won’t be able to recognize infected cells. These cells are eliminated through apoptosis (programmed cell death). This ensures the T cells that “graduate” are functional.
  2. Negative Selection: Next comes the crucial step. The T cells that passed the first test are now screened for their reactivity to the body’s own proteins. T cells that bind too strongly to “self-antigens” are identified as potentially dangerous—they could attack the host’s own tissues. These autoreactive T cells are also rigorously eliminated. This step is critical for establishing self-tolerance, the immune system’s ability to distinguish self from non-self.

Only the T cells that pass both tests—those that can recognize pathogens but do not attack the host tissue—are allowed to “graduate” and enter the circulation as mature, competent T cells.

When Quality Control Fails: The Myth of “Autoimmunity”

What happens when this intricate process of thymic signaling and selection fails? This often occurs as we age (a process called thymic involution) or due to chronic stress, nutritional deficiencies, or environmental toxins. When the thymus isn’t functioning properly, the quality control system breaks down. T cells that should have been eliminated during negative selection are allowed to graduate and circulate throughout the body.

These are rogue T cells, programmed to attack your own tissues. One might start attacking the synovial lining of the joints, leading to rheumatoid arthritis. Another might target the myelin sheath that insulates nerves, causing multiple sclerosis. Others might attack the thyroid gland (Hashimoto’s thyroiditis) or even components of your own DNA (lupus).

This is the basis of what we call autoimmune disease. However, I want to propose a semantic but important shift in perspective. The term “autoimmunity” suggests the immune system has gone rogue of its own accord, that it is attacking the self for no reason. I believe a more accurate term is immune misdirection. The system isn’t inherently faulty; its education was. It’s not a suicidal system; it’s a miseducated one. There is no such thing as “autoimmunity” in the sense of a system designed to attack itself. There is only a loss of self-tolerance due to a failure in the upstream regulatory and training mechanisms, primarily in the thymus and in the balance of regulatory T cells (Tregs).

The Downstream Fallacy: Why Our Current Approach Is Failing

For decades, our medical system has been built around managing the downstream consequences of this immune misdirection and systemic inflammation. We have developed a massive, multi-hundred-billion-dollar industry focused on symptom suppression.

Consider the blockbuster drugs of our time:

  • Statins: Prescribed to lower cholesterol, a downstream marker of the inflammation-driven process of atherosclerosis.
  • Metformin: Prescribed to manage blood sugar, a downstream consequence of the inflammation-driven process of insulin resistance.
  • SSRIs (Selective Serotonin Reuptake Inhibitors): Prescribed to manage depression, a downstream symptom of the inflammation-driven process of neuroinflammation.
  • Biologics (e.g., TNF-alpha inhibitors): Prescribed to block a single inflammatory cytokine, a downstream product of the upstream macrophage M1 activation.

While these medications can be life-saving in acute situations and can provide necessary relief, they are all sold as solutions to different symptoms of the same fundamental problem. They are patching the holes in the dam without ever addressing the immense pressure of the water building up behind it. They don’t fix the root cause. They don’t re-educate the immune system. They don’t shift macrophages from M1 destruction to M2 repair.


Unlocking the Secrets of Inflammation: Integrative Medicine Approach- Video

Restoring Balance: The Integrative Approach to Healing

This is where our integrative model at Injury Medical Clinic truly shines. By combining the diagnostic acumen of Dr. Cardenas’s internal medicine background with my expertise in functional medicine and chiropractic care, we can address the root cause. Our goal is not just to manage symptoms, but to identify and correct the underlying dysregulation driving the inflammatory process in the first place. We ask why the immune system is out of balance and then use a combination of therapies to restore that balance.

Thymosin Alpha-1: An Upstream Regulator

One exciting frontier in functional and regenerative medicine is the use of signaling molecules called peptides. These are short chains of amino acids that act as precise communicators in the body. One such peptide, Thymosin Alpha-1, holds immense promise for correcting the immune misdirection we’ve been discussing.

Thymosin Alpha-1 is a naturally occurring peptide produced by the thymus gland. It is one of the primary signals the thymus uses to orchestrate T cell maturation and function. In essence, it acts as an “immune modulator,” helping to restore balance to a dysregulated system. It doesn’t crudely suppress the immune system, nor does it blindly stimulate it. It helps it function more intelligently.

Here’s how it works at a cellular level, going upstream to fix the core problem:

  • Restores Regulatory Circuitry: Thymosin Alpha-1 promotes the development and function of Regulatory T cells (Tregs). Tregs are the “peacekeepers” of the immune system. Their job is to suppress excessive immune responses and prevent the activation of autoreactive T cells. By bolstering the Treg population, Thymosin Alpha-1 helps to re-establish self-tolerance and quell the misdirected immune attacks that characterize “autoimmune” conditions.
  • Shifts Macrophage Polarization: Critically, Thymosin Alpha-1 has been shown to influence macrophage behavior. It helps to shift macrophages away from the destructive M1 phenotype and towards the reparative M2 phenotype. This directly counteracts the central pathology of systemic inflammation. It helps turn off the “burn it all down” signal and turn on the “clean it all up” signal.
  • Shuts Down the Inflammatory Loop: By promoting Treg function and encouraging the M1-to-M2 shift, Thymosin Alpha-1 helps to shut down the self-perpetuating inflammatory loop that is slowly killing your biology. It calms the cytokine storm at its source, rather than just trying to block one of its downstream products.

Using tools like Thymosin Alpha-1, under the careful medical supervision of Dr. Cardenas, shows how we apply these advanced biological concepts in a clinical setting. It’s about restoring the body’s own innate regulatory systems. The profound truth is this: You don’t have ten different diseases; you have one dysregulated biology that is producing ten different symptoms. Fix the regulation, and you begin to fix everything.

The Role of Integrative Chiropractic Care in Quelling Inflammation

Now, you might be wondering, “This is fascinating immunology, Dr. Jimenez, but you’re a Doctor of Chiropractic. How does adjusting the spine fit into all of this?” This is a crucial question, and the answer lies at the very heart of the chiropractic principle: the intimate connection between the spine, the nervous system, and overall systemic health.

The nervous system is the body’s master control system. It communicates with and regulates every other system, including the immune system. The spine, in turn, is the protective armor and structural conduit for a huge portion of this system, namely the spinal cord and the nerve roots that exit to serve the entire body. When the spine has biomechanical faults—what we call vertebral subluxations—it can create both structural and neurological stress.

This stress is not just a localized mechanical issue. It acts as a potent, chronic, low-grade stressor that contributes to the body’s total inflammatory burden. Here’s how integrative chiropractic care fits into the treatment of systemic inflammation:

  • Reducing Nociceptive Input and the Stress Response: Misaligned vertebrae or dysfunctional spinal joints can bombard the central nervous system with aberrant signals, a phenomenon known as nociceptive input. Even if it’s below the threshold of conscious pain, the brain interprets this constant “neural noise” as a threat. This activates the body’s primary stress response axis, the Hypothalamic-Pituitary-Adrenal (HPA) axis. Chronic HPA axis activation initially elevates cortisol levels, but over time can dysregulate the system. Chronic stress, whether it’s emotional, chemical, or, in this case, physical/neurological, is a powerful driver of M1 macrophage activation and systemic inflammation (Morey et al., 2015). By performing precise chiropractic adjustments, we aim to restore normal joint mechanics, reduce nociceptive input, and thereby turn down this source of neurological stress. This helps to calm the HPA axis and lower a key contributor to the body’s inflammatory state.
  • Modulating Autonomic Nervous System Balance: The nervous system has two main branches that control our physiology: the sympathetic nervous system (fight or flight) and the parasympathetic nervous system (rest and digest). The sympathetic system is generally pro-inflammatory (it needs to be to fight off a threat), while the parasympathetic system, particularly via the vagus nerve, is profoundly anti-inflammatory. This is known as the “inflammatory reflex” (Tracey, 2002). Many people in our modern, stressed-out world are stuck in a state of sympathetic dominance. Spinal dysfunction can contribute significantly to this imbalance. My clinical experience, supported by a growing body of research, shows that chiropractic adjustments, particularly to the upper cervical spine and sacrum where vagal tone is heavily influenced, can help shift the autonomic balance away from sympathetic dominance and towards a more parasympathetic state. By enhancing vagal tone, we are directly activating the body’s most powerful innate anti-inflammatory pathway, encouraging the M1-to-M2 macrophage shift naturally.
  • Improving Biomechanics and Reducing Tissue Strain: On a more direct level, poor posture and spinal alignment create chronic mechanical strain on muscles, ligaments, and joints. This chronic micro-trauma itself is a source of localized inflammation, which can contribute to the overall systemic inflammatory load. As a chiropractor, my job is to analyze and correct these biomechanical faults. By improving posture, restoring spinal curves, and ensuring joints move properly, we reduce constant physical stress on the body’s tissues, removing another source of inflammatory signaling.
  • A Gateway to Holistic Lifestyle Change: In our clinic, a chiropractic adjustment is rarely a standalone treatment. It serves as an entry point to a broader conversation about health. When a patient feels relief from pain and improved mobility, they become more empowered and motivated to engage in other healthy behaviors. An adjustment can be the catalyst that allows a patient to start an exercise program, which is itself a powerful anti-inflammatory modality. It opens the door for me, as a functional medicine practitioner, to discuss anti-inflammatory nutrition, stress management techniques, and sleep hygiene—all critical for quenching the fire of systemic inflammation.

Under Dr. Cardenas’s comprehensive care model, we ensure chiropractic interventions fit the individual’s full medical picture. For example, for a patient with severe osteoporosis or an inflammatory arthritic flare-up, we would modify our techniques to be gentle and safe, always prioritizing the patient’s well-being within the context of their medical diagnosis. This integrated approach allows us to use chiropractic care as a powerful tool to reduce neurological and physical stress, balance the autonomic nervous system, and help guide the body back toward a state of ease and repair, complementing the medical and functional medicine strategies we employ.

Conclusion: A New Blueprint for Health

We stand at a thrilling and hopeful crossroads in medicine. The old model of naming a disease based on its symptomatic location and prescribing a drug to manage that symptom is giving way to a more sophisticated, root-cause-based approach. The science is clear: the smoldering fire of chronic, low-grade systemic inflammation is the common soil from which nearly all chronic diseases of aging grow. The perpetual activation of M1 macrophages, the failure of immune-regulatory training in the thymus, and the resulting cytokine storm are not separate issues but interconnected components of a single, dysregulated system.

The path forward is not to invent a dozen new drugs to block a dozen different cytokines. The path forward is to ask why the system is dysregulated and to use intelligent, integrative strategies to restore its natural balance. This involves:

  • Identifying and removing the triggers of inflammation through functional medicine testing and lifestyle modification (addressing diet, toxins, infections, and stress).
  • Modulating the immune system with targeted therapies like peptides, nutrients, and botanicals that encourage a shift from M1 destruction to M2 repair.
  • Restoring neurological and structural integrity through integrative chiropractic care to reduce physical stress and balance the autonomic nervous system.
  • Ensuring medical safety and oversight through the wisdom and experience of collaborative physicians like Dr. Cardenas.

You do not have to be a passive victim of your diagnosis. You don’t have ten different diseases. You have one biology that has lost its regulatory balance. By working with an integrated team that understands this fundamental principle, you can go upstream. You can fix the regulation. And when you fix the regulation, you can begin to fix everything.


References


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Radial Tunnel Hydrodissection for Nerve Entrapment

Radial Tunnel Hydrodissection for Nerve Entrapment

Abstract

This educational post explores ultrasound-guided hydrodissection, an advanced interventional technique used to address radial nerve entrapment at the entrance of the radial tunnel — a condition frequently misdiagnosed as lateral epicondylitis. Drawing from clinical demonstrations by leading practitioners in musculoskeletal ultrasound, I present the physiological underpinnings of radial tunnel syndrome, the rationale for perineural hydrodissection, and how integrative chiropractic care fits within a multidisciplinary treatment framework. At Injury Medical Clinic PA (also known as Mission Plaza Injury Medical Clinic) in El Paso, Texas, my colleague Dr. Maria Guadalupe Cardenas, MD, Board Certified in Internal Medicine (NPI #1164426749, Texas MD License #J2933), serves as Medical Director and Collaborative Physician, providing over 40 years of internal medicine expertise alongside my chiropractic and functional medicine practice. Together, we outline how cutting-edge procedural techniques, medical oversight, and conservative rehabilitative care converge to deliver superior patient outcomes for complex nerve entrapment conditions.

Radial Tunnel Hydrodissection for Nerve Entrapment

Understanding Radial Tunnel Syndrome: Why Diagnosis Is So Often Missed

One of the most clinically underrecognized conditions in musculoskeletal medicine is radial tunnel syndrome (RTS) — a compressive neuropathy of the deep branch of the radial nerve as it enters the radial tunnel, a fibromuscular passage located just distal to the lateral epicondyle. As a clinician who has evaluated countless patients presenting with lateral elbow pain, I can tell you firsthand that this condition is routinely confused with lateral epicondylitis, commonly known as “tennis elbow.”

The key distinguishing features are critical:

  • Lateral epicondylitis presents with point tenderness directly over the lateral epicondyle
  • Radial tunnel syndrome typically produces pain that is 3–4 cm distal to the lateral epicondyle, over the radial tunnel itself
  • Patients with RTS often describe a dull, burning, aching quality to the pain, frequently worsened by pronation and supination of the forearm
  • The pain may radiate into the dorsum of the forearm, consistent with the sensory distribution of the posterior interosseous nerve (PIN)

This distinction matters profoundly because the treatment approach is entirely different. Injecting a corticosteroid at the lateral epicondyle — the standard intervention for tennis elbow — will do nothing to relieve a nerve entrapment occurring further distally. When six months or more of conservative treatment have failed to produce relief, it becomes necessary to think deeper — both anatomically and clinically.


The Anatomy Behind Radial Nerve Entrapment at the Arcade of Frohse

To fully appreciate why hydrodissection works, one must first understand the precise anatomy involved. The radial nerve, after crossing the lateral aspect of the elbow, divides into two branches:

  • The superficial branch (purely sensory), which continues distally along the radial side of the forearm
  • The deep branch (motor and sensory), which dives into the radial tunnel and passes beneath the arcade of Frohse — a fibrous arch at the proximal edge of the supinator muscle

The arcade of Frohse is the most common site of radial nerve compression. This fibrous band can tighten with repetitive forearm rotation, direct compression, or inflammatory changes in surrounding soft tissue. As the nerve becomes entrapped:

  • Perineural fibrosis develops, restricting the nerve’s normal gliding motion
  • Ischemic changes in the nerve’s intrinsic blood supply reduce conduction velocity
  • Mechanosensitivity increases, producing pain with even minor movements involving pronation or supination
  • Chronic inflammation leads to adhesion formation between the nerve sheath and surrounding fascial planes

This physiological cascade explains why oral anti-inflammatories and physical therapy alone are often insufficient after months of symptomatic progression. The nerve is, in effect, tethered — and it needs to be released.


What Is Ultrasound-Guided Hydrodissection and Why Is It Used

Hydrodissection is a minimally invasive procedure in which fluid is precisely injected around a peripheral nerve to mechanically separate it from surrounding adhesions, scar tissue, or compressive structures. The term itself describes the mechanism: using the hydraulic force of injected fluid to dissect soft tissue planes without the trauma of surgical incision.

In the context of radial nerve entrapment, the technique involves:

  • Guiding a 25-gauge needle under real-time ultrasound visualization (using a high-frequency linear probe)
  • Approaching the deep branch of the radial nerve in a short-axis, in-plane view — meaning the needle is visible on the ultrasound screen along its entire length
  • Injecting a solution — typically lidocaine, in some cases combined with a corticosteroidperineural (around, not inside) the nerve
  • Creating what is clinically referred to as a “halo effect”: the fluid surrounds the nerve circumferentially, lifting adhesions and restoring the nerve’s natural gliding motion within its tissue bed

The critical safety principle is perineural, not intraneural injection. Injecting fluid directly into the nerve (intraneural) risks serious nerve damage, including axonal disruption and permanent deficit. The goal is always to deposit fluid adjacent to the epineurium — the outermost connective tissue sheath — thereby creating separation between the nerve and surrounding structures while leaving the nerve itself fully intact.

The use of lidocaine serves a dual purpose:

  1. Diagnostic confirmation: If a prior diagnostic injection of lidocaine at the radial nerve produces measurable pain relief, this validates the nerve as the pain generator — as was precisely the case with the patient discussed in this post
  2. Therapeutic hydrodissection: Lidocaine’s volume, when injected incrementally and skillfully around the nerve, provides the hydraulic separation needed to restore normal nerve mobility

Adding a corticosteroid to the hydrodissection solution targets persistent perineural inflammation, reducing the inflammatory milieu that contributes to ongoing neural sensitization and adhesion reformation.


Why This Is Considered an Advanced Technique

I want to be unequivocally clear: hydrodissection is not a technique to be read about and immediately attempted. The skill required involves:

  • Mastery of sonoanatomy: Identifying the deep branch of the radial nerve in real time as it passes through the brachioradialis, alongside the neurovascular bundle, and just proximal to the arcade of Frohse, requires dedicated ultrasound training
  • Precise needle control: The movements involved are described as “very small and subtle.” A millimeter of deviation at this depth can mean the difference between a perineural and an intraneural injection
  • Recognition of real-time landmarks: The practitioner must continuously identify the brachioradialis, supinator muscle, radius, and the nerve itself as the needle advances, adjusting trajectory in real time
  • Controlled fluid pulsing: Rather than a single bolus injection, the fluid is delivered in small, deliberate pulses to progressively expand the perineural space, generating the halo effect while monitoring nerve displacement on screen

A muscle twitch may be observed as the needle approaches the nerve — a sign of proximity that requires the practitioner to recognize and respond to immediately. This level of procedural refinement demands supervised, hands-on training under experienced guidance.


Integrative Chiropractic Care and Its Role in Radial Nerve Recovery

While hydrodissection directly addresses the entrapment at the radial tunnel, integrative chiropractic care plays an essential role in the broader clinical picture. At my practice, I approach radial nerve entrapment not as an isolated peripheral problem but as part of a regional biomechanical and neurological pattern that must be addressed comprehensively.

Chiropractic contributions to radial nerve recovery include:

  • Cervical spine assessment: The radial nerve originates from the C5–C8 nerve roots. Cervical segmental dysfunction — particularly at C6 and C7 — can produce a double crush phenomenon, in which proximal neural compromise reduces the nerve’s capacity to tolerate distal entrapment. Chiropractic spinal manipulation directed at dysfunctional cervical segments helps restore normal neural conduction and reduces the overall compressive burden on the nerve
  • Elbow and forearm joint mobilization: Restoring full radioulnar joint mechanics and reducing capsular tightness decreases mechanical stress on the radial tunnel
  • Soft tissue therapy: Targeted myofascial release to the brachioradialis, supinator, and extensor mass helps reduce the external compressive forces perpetuating nerve entrapment
  • Rehabilitation exercise prescription: Progressive neuromuscular re-education exercises — designed to restore painless pronation and supination — are essential to sustaining the benefits achieved through hydrodissection
  • Postural and ergonomic correction: Many cases of radial tunnel syndrome are driven or perpetuated by occupational postures. Chiropractic rehabilitation includes functional movement analysis and individualized ergonomic modification

Multidisciplinary Care at Injury Medical Clinic PA: Dr. Cardenas and Dr. Jimenez

The clinical model I operate within at Injury Medical Clinic PA in El Paso, Texas exemplifies the best of multidisciplinary integrative care. Dr. Maria Guadalupe Cardenas, MD, Board Certified in Internal Medicine (NPI #1164426749, Texas MD License #J2933), brings over 40 years of internal medicine expertise to our collaborative practice. As Medical Director and Collaborative Physician, Dr. Cardenas provides:

  • Comprehensive medical evaluation and co-management for patients with complex comorbidities
  • Pharmacological oversight, including medication review for patients undergoing procedural interventions
  • Internal medicine consultation for systemic contributors to musculoskeletal and neurological conditions — including metabolic, inflammatory, and autoimmune factors that can predispose patients to peripheral neuropathies
  • Medical direction ensuring all clinical protocols meet the highest standards of patient safety and evidence-based practice

This collaboration between chiropractic functional medicine (my domain) and internal medicine (Dr. Cardenas’s domain) means that patients presenting with conditions like radial tunnel syndrome receive:

  • A thorough systemic workup when indicated
  • Coordinated procedural and rehabilitative planning
  • Functional medicine assessments examining nutritional, metabolic, and inflammatory contributors to nerve health
  • Personal injury care and documentation for patients involved in accident-related musculoskeletal injuries

Evidence-Based Support for Hydrodissection in Peripheral Nerve Entrapment

The growing body of literature supporting ultrasound-guided hydrodissection is compelling. Research consistently demonstrates that perineural injection under ultrasound guidance is both safer and more effective than landmark-based injection for peripheral nerve entrapment syndromes (Wu et al., 2017). Studies examining hydrodissection for carpal tunnel syndrome, cubital tunnel syndrome, and posterior interosseous nerve entrapment have reported significant improvements in pain scores and functional outcomes (Mulvaney, 2011; Cass, 2016).

The 5% dextrose in water (D5W) solution — a popular hydrodissection medium in non-corticosteroid protocols — has been shown to reduce mechanosensitivity by competitively blocking TRPV1 nociceptors at the neural membrane, providing an additional physiological mechanism of pain relief beyond simple mechanical separation (Lyftogt, 2007). When lidocaine is used, as described in this case, the immediate anesthetic effect confirms nerve involvement while the hydraulic dissection restores gliding mechanics.


References


Chronic Tendinopathy Management Techniques With Regenerative Orthopedics


Find out how regenerative orthopedics for chronic tendinopathy can transform your recovery journey and restore functional movement.

Abstract

Tendinopathy represents one of the most common and clinically challenging musculoskeletal conditions encountered in integrative and regenerative medicine practice. Whether it presents as lateral epicondylitis (tennis elbow), patellar tendinopathy, Achilles tendinopathy, or rotator cuff degeneration, the underlying pathology shares a consistent theme: a failed healing response within tendon tissue that transitions from an acute inflammatory state into a chronic degenerative process known as tendinosis. This educational post explores one of the most evidence-informed, minimally invasive interventional techniques available to clinicians today — needle fenestration — and its powerful combination with prolotherapy using dextrose to stimulate tendon regeneration from within.

Drawing from the clinical expertise of Dr. Fran O’Connor, a recognized authority in ultrasound-guided procedures, and integrated with the multidisciplinary perspective of Dr. Alexander Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST, and Dr. Maria Guadalupe Cardenas, MD, Board Certified in Internal Medicine and Medical Director at Injury Medical Clinic PA in El Paso, Texas, this post provides a thorough, clinically grounded exploration of the following topics:

  • The physiological basis of tendinopathy and why tendons fail to heal on their own
  • The mechanism of action behind needle fenestration and how it converts a chronic degenerative lesion into an acute healing environment
  • Step-by-step procedural technique for ultrasound-guided needle fenestration, including needle positioning, angle of approach, in-plane visualization, and coverage of the entire tendinopathic zone
  • The scientific rationale for combining fenestration with prolotherapy (dextrose) and how this synergistic approach amplifies the regenerative response
  • How orthobiologics such as platelet-rich plasma (PRP) can be incorporated alongside fenestration for more advanced cases
  • The clinical outcomes reported in peer-reviewed literature, including the number of passes required, how clinicians assess procedural endpoints, and what patients can expect during recovery
  • How integrative chiropractic care, functional medicine, and medical oversight from an Internal Medicine physician create a comprehensive, whole-patient approach to managing chronic tendinopathy
  • The unique multidisciplinary model practiced at Injury Medical Clinic PA, where chiropractic expertise, advanced practice nursing, functional medicine, and internal medicine converge to deliver state-of-the-art, evidence-based musculoskeletal care

By the end of this post, readers — whether patients, clinicians, or health professionals — will have a deeply informed understanding of why needle fenestration with prolotherapy has earned its place as a first-line interventional option for chronic tendinopathy, and how it fits within a broader, patient-centered treatment philosophy.


Understanding Tendinopathy: Why Tendons Fail to Heal

The Structure and Function of Healthy Tendons

To appreciate why needle fenestration works, we must first understand the remarkable—and remarkably vulnerable—structure of the tendon itself. Tendons are dense, fibrous connective tissue structures that transmit the mechanical forces generated by muscle contraction to bone, enabling movement and stabilizing joints under load. They are composed primarily of type I collagen, organized in a highly hierarchical structure: individual tropocollagen molecules assemble into collagen fibrils, which bundle into collagen fibers, which in turn form fascicles surrounded by the endotenon, and these fascicles collectively form the tendon body, enclosed by the epitenon and, in some locations, a paratenon or tendon sheath (Maffulli et al., 2023).

The tenocytes — the primary cellular inhabitants of tendon tissue — reside within this extracellular matrix and are responsible for synthesizing, organizing, and maintaining collagen and other matrix proteins. Under normal physiological conditions, tendons are remarkably efficient load-bearing structures. They are designed to store and release elastic energy, acting almost like biological springs that reduce the metabolic cost of movement and protect muscle tissue from sudden overload (Magnusson et al., 2010).

However, this remarkable structural efficiency comes at a cost: tendons are relatively hypovascular tissues. The blood supply to tendon tissue is sparse compared to muscle, bone, or even ligament. This hypovascular nature means that when tendon tissue is damaged — whether by a single acute traumatic event or by the cumulative microtrauma of repetitive loading — the tissue has limited intrinsic capacity to mount an effective healing response (Fenwick et al., 2002). The relative absence of robust vascularity translates directly into reduced oxygen delivery, reduced nutrient availability, reduced cellular migration to the damaged site, and, critically, reduced access to the growth factors and cytokines that orchestrate tissue repair.

The Transition From Tendinitis to Tendinosis: A Critical Distinction

For decades, chronic tendon pain was labeled “tendinitis,” implying that inflammation was the dominant pathological process. This conceptual framework led clinicians to rely heavily on anti-inflammatory interventions: non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroid injections, and rest. While these approaches may provide short-term symptomatic relief, they often fail to produce lasting recovery—and in some cases, particularly with repeated corticosteroid injections, they may impair long-term tendon healing (Coombes et al., 2013; Dean et al., 2014).

This failure became clearer as histopathological research revealed a striking truth: in most cases of chronic tendon pain, there is little or no true inflammatory infiltrate in the tendon tissue. Instead, what clinicians and researchers consistently find is a picture of tendinosis — a degenerative condition characterized by:

  • Disorganized collagen architecture, with loss of the normal parallel alignment of collagen fibers and replacement by haphazardly arranged, structurally inferior collagen
  • Increased ground substance (glycosaminoglycans and proteoglycans) between collagen fibers, creating a thickened, edematous appearance
  • Neovascularization — the ingrowth of new, abnormal blood vessels into areas of tendon tissue that are normally avascular, often accompanied by nerve fibers that appear to contribute to pain signaling
  • Hypocellularity in some regions, with loss of normal tenocyte morphology and the appearance of rounded, chondrocyte-like cells — a phenomenon sometimes described as chondroid metaplasia
  • Micro-tears and focal areas of necrosis within the tendon matrix
  • The near-complete absence of inflammatory cells such as neutrophils or macrophages that would be expected in true “tendinitis” (Khan & Cook, 2000; Maffulli et al., 1998)

This histopathological picture has been given many names in the literature — tendinosis, tendinopathy, degenerative tendinopathy — but the essential message is consistent: the tissue has entered a state of failed healing. The normal repair cascade — inflammation, proliferation, remodeling — has been initiated but has stalled or been disrupted, leaving behind a structurally compromised, biochemically abnormal tendon that is painful, weak, and at risk for partial or complete rupture (Cook & Purdam, 2009).

Why Tendons Get Stuck in This Degenerative State

Understanding why tendons fail to complete the normal healing cycle is essential for understanding why fenestration represents such a logical and elegant therapeutic intervention. Several interacting mechanisms contribute to the persistence of tendinosis:

1. Repetitive Mechanical Loading Without Adequate Recovery

The most common precipitating factor in tendinopathy is repetitive mechanical overload. When a tendon is loaded cyclically — as in running, throwing, typing, or racket sports — microscopic damage accumulates within the collagen matrix. If the rate of damage accumulation exceeds the rate of repair (which itself requires rest, adequate nutrition, and sufficient vascular supply), the tendon progressively degenerates. This is particularly common in tendons already operating at high mechanical loads, such as the patellar tendon in jumping athletes, the Achilles tendon in runners, and the extensor carpi radialis brevis (ECRB) tendon at the lateral epicondyle in racket sport players and manual workers (Magnusson et al., 2010; Rees et al., 2014).

2. The Hypovascular Environment

As noted above, the tendon’s inherently poor blood supply limits delivery of reparative cells (fibroblasts, macrophages), growth factors (TGF-β, PDGF, IGF-1, FGF, VEGF), and nutrients to damaged areas. Paradoxically, the neovascularization that occurs in tendinosis — while initially appearing to represent a reparative response — tends to produce blood vessels that are structurally abnormal and that infiltrate the tendon accompanied by sympathetic and sensory nerve fibers, contributing to the pain experience without adequately restoring normal tissue perfusion and repair capacity (Ohberg et al., 2004).

3. Altered Tenocyte Biology

The tenocytes within a tendinopathic tendon undergo profound changes in their gene expression and synthetic activity. Instead of producing the organized type I collagen characteristic of healthy tendon, they upregulate type III collagen—a weaker, less organized collagen isoform associated with scar formation—as well as abnormal matrix metalloproteinases (MMPs) that degrade the existing matrix without adequate replacement (Riley et al., 2002). The result is a progressive weakening of the tendon’s structural integrity, even in the absence of complete rupture.

4. Neurochemical Sensitization

Chronic tendinopathy is associated with central and peripheral sensitization of the pain system. The neovascular ingrowth mentioned earlier brings with it substance P-positive and CGRP-positive nerve fibers that generate persistent nociceptive signaling. Over time, this leads to central sensitization—a state in which the nervous system becomes hyperresponsive to pain signals, amplifying perceived pain intensity and expanding the area of perceived pain beyond the original tissue lesion (Andersson et al., 2011). This neurological dimension of chronic tendinopathy is one reason purely mechanical or pharmacological interventions often fail: the pain system itself has been remodeled, and effective treatment must address not only the tendon tissue but also the neural and central contributions to pain.


What Is Needle Fenestration? Defining the Technique and Its Purpose

Defining Needle Fenestration in Clinical Practice

Needle fenestration is a minimally invasive, ultrasound-guided procedure in which a needle — typically a 22-gauge or 25-gauge needle — is used to create multiple small punctate incisions or perforations (fenestrations) within a tendon, specifically targeting the area of tendinosis or tendinopathy. The term “fenestration” derives from the Latin fenestra, meaning “window” — and this etymology is clinically apt, because the procedure literally creates small “windows” or openings in the abnormal tendon tissue.

It is critically important to distinguish needle fenestration from other needle-based tendon interventions. Needle fenestration is defined by the deliberate absence of an injectable therapeutic agent — the needle alone, passed repeatedly through the diseased tissue, is the therapeutic instrument. This distinguishes it from:

  • Corticosteroid injection (anti-inflammatory)
  • Hyaluronic acid injection (viscosupplementation)
  • Prolotherapy (injection of an irritant/proliferant solution such as dextrose)
  • Platelet-rich plasma (PRP) injection (orthobiologic)
  • Dry needling (which targets myofascial trigger points in muscle tissue rather than tendinopathic lesions within the tendon itself)

However — and this is a clinically important nuance that will be explored in detail — needle fenestration is very frequently combined with injectable agents, particularly prolotherapy using hypertonic dextrose, because the two approaches have synergistic mechanisms of action. The fenestration disrupts and mechanically stimulates the tissue, while the injected agent provides additional biochemical stimulation of the healing cascade. This combined approach, as demonstrated by Dr. O’Connor and practiced within the multidisciplinary framework at Injury Medical Clinic PA, is a particularly powerful, evidence-informed treatment strategy for chronic tendinopathy.

The Conceptual Foundation: Converting Chronic Degeneration Into Acute Healing

The central therapeutic logic of needle fenestration is both elegant and physiologically grounded: to convert a chronic, stalled degenerative process into an acute healing response. This concept deserves thorough elaboration, because it represents a fundamental paradigm shift in how we think about treating tendinopathy.

In normal tissue healing following injury, there are three well-defined phases:

Phase 1 — Inflammation (Days 1–7):

Damaged tissue releases damage-associated molecular patterns (DAMPs), triggering local vasodilation, increased vascular permeability, and infiltration of inflammatory cells—primarily neutrophils (early) and macrophages (later). These cells remove cellular debris, release pro-inflammatory cytokines (IL-1β, TNF-α, IL-6), and — critically — release a rich repertoire of growth factors including platelet-derived growth factor (PDGF), transforming growth factor-beta (TGF-β), vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), and insulin-like growth factor-1 (IGF-1). These growth factors serve as the molecular signals that recruit and activate the reparative cells responsible for tissue regeneration.

Phase 2 — Proliferation (Days 4–21):

Activated fibroblasts (and in tendons, tenocytes) migrate to the wound site and begin synthesizing new collagen — initially type III collagen for rapid structural scaffolding, later transitioning to the mechanically superior type I collagen. New blood vessels form (angiogenesis) to supply the metabolically active repair tissue, and the extracellular matrix is progressively remodeled.

Phase 3 — Remodeling (Weeks to Months):

The immature repair tissue is progressively reorganized and strengthened. Type III collagen is replaced by type I collagen, collagen fibers align along lines of mechanical stress, water content decreases, and the tendon’s tensile strength gradually approaches that of normal tissue. This phase requires progressive mechanical loading to guide collagen fiber alignment through mechanotransduction pathways properly.

In tendinosis, this healing cascade has been initiated — the histological evidence of collagen disruption and tenocyte activation confirms that — but it has failed to progress to completion. The tendon is neither acutely inflamed nor fully healed; it is stuck in a chronic, degenerative limbo. As discussed above, this failure may be due to insufficient vascularity, ongoing mechanical overload, altered tenocyte biology, and potential neurochemical sensitization.

Needle fenestration addresses this stalled healing by forcibly reinitiating the healing cascade from the beginning. By passing the needle repeatedly through the tendinopathic tissue, the clinician:

  1. Physically disrupts the abnormal collagen matrix — breaking down the disorganized, inferior collagen and creating a fresh wound environment
  2. Causes local bleeding within the tendon — delivering a concentrated bolus of growth factors from platelet degranulation directly to the site of degeneration
  3. Triggers an acute inflammatory response — reversing the anti-inflammatory, stagnant biochemistry of tendinosis and replacing it with a dynamic, pro-reparative milieu
  4. Disrupts the pathological neovascular ingrowth — the abnormal blood vessel-nerve fiber complexes associated with tendinopathy pain are disrupted by the needle passes, potentially contributing to pain relief through denervation as well as regeneration
  5. Stimulates tenocyte mechanobiology — the mechanical stimulus of needle penetration activates tenocyte mechanoreceptors and signaling pathways (integrin signaling, FAK-ERK cascades) that upregulate the synthesis of organized, type I collagen

The result is that the tendon, previously stuck in a degenerative state, now experiences a genuine acute injury—but one that is precisely targeted, minimally destructive, and strategically designed to initiate the healing cascade that had previously failed.


The Role of Ultrasound Guidance in Needle Fenestration: Why Imaging Is Non-Negotiable

Real-Time Visualization as a Safety and Efficacy Imperative

One of the most important aspects of needle fenestration, as practiced by Dr. O’Connor and integrated into the clinical protocols at Injury Medical Clinic PA, is using diagnostic musculoskeletal ultrasound (MSKUS) to guide the procedure in real time. This is not merely a technical preference—it is a clinical imperative from both safety and efficacy standpoints.

Musculoskeletal ultrasound provides real-time, dynamic, high-resolution imaging of soft tissue structures—tendons, ligaments, muscles, bursae, nerves, and blood vessels—without the radiation exposure of fluoroscopy or the logistical complexity of MRI. Modern high-frequency linear ultrasound transducers (typically operating at 10–18 MHz for superficial structures) can resolve tendon architecture at sub-millimeter resolution, allowing the clinician to:

  • Identify the precise location, size, and extent of the tendinopathic lesion within the tendon — the hypoechoic (dark on ultrasound), disorganized area that represents tendinosis or tendinopathy.
  • Visualize the needle in real time as it enters the tendon, ensuring accurate placement within the lesion rather than in surrounding healthy tissue, bursae, or adjacent neurovascular structures.
  • Monitor the distribution of any injected agent (prolotherapy solution, PRP) to confirm that it is being delivered to the target tissue.
  • Use color or power Doppler imaging to identify the pathological neovascularization characteristic of tendinopathy. These Doppler-positive regions are particularly important targets for fenestration, as they represent the areas most actively involved in abnormal tendon biology and pain generation.
  • Assess tissue response during the procedure — as Dr. O’Connor describes, experienced clinicians can perceive a change in the tissue’s resistance to needle advancement as tendinopathy softens during fenestration, and ultrasound confirms the needle’s position throughout this process.

In-Plane Versus Out-of-Plane Needle Visualization

In-plane (long-axis) needle visualization is the strongly preferred approach for tendon fenestration. In the in-plane technique, the needle is inserted parallel to the long axis of the ultrasound transducer, keeping the entire shaft and tip continuously visible on the ultrasound screen throughout the procedure. This is in contrast to the out-of-plane (short-axis) approach, where only the needle tip (appearing as a bright dot) is visible at a single cross-sectional plane.

The superiority of in-plane visualization for tendon fenestration is multifactorial:

  • Complete needle shaft visibility allows the clinician to confirm at all times that the needle is within the tendon and not in surrounding structures
  • Safe needle redirection — repeated withdrawal and redirection of the needle (fundamental to the fenestration technique) requires continuous visualization of the needle tip to ensure it remains within the target zone and does not inadvertently advance into adjacent neurovascular bundles.
  • Verification of tendon coverage — by observing the needle’s position along the long axis of the tendon, the clinician can confirm that the entire length of the tendinopathic lesion is being treated.
  • Depth control — the in-plane approach provides direct visualization of how deeply the needle has penetrated the tendon, preventing inadvertent penetration through the deep surface of the tendon into underlying structures (such as the radial nerve at the lateral elbow, or the posterior tibial nerve at the medial ankle)

The Sonographic Appearance of Tendinopathy

On ultrasound, healthy tendon tissue appears as a highly echogenic (bright), fibrillar structure with a characteristic parallel linear echo pattern that reflects the organized collagen architecture. When the ultrasound beam strikes these regularly aligned collagen fibers at the correct angle, they produce strong specular reflections that appear as bright, parallel lines — a pattern often described as having a “fibrillar” or “feather-like” appearance.

Tendinopathy disrupts this pattern in characteristic ways:

  • Hypoechogenicity — areas of tendinopathy appear darker than the surrounding normal tendon, reflecting the loss of organized collagen architecture and the increased water content of the abnormal matrix. The hypoechoic region is the primary target for fenestration.
  • Tendon thickening — tendinopathic tendons are typically larger in cross-sectional area than contralateral normal tendons, reflecting the accumulation of abnormal matrix material and the reactive cellular response
  • Loss of fibrillar echotexture — within the tendinopathic zone, the normal parallel linear echo pattern is replaced by disorganized, heterogeneous echogenicity.
  • Intratendinous calcification — in some cases, areas of calcium hydroxyapatite deposition can be seen as hyperechoic (bright) foci with posterior acoustic shadowing
  • Neovascularization on Doppler imaging — color or power Doppler interrogation of the tendinopathic zone reveals increased internal blood flow within the tendon, representing the pathological neovascular ingrowth. This “Doppler signal” within the tendon is a sensitive and specific marker of active tendinopathy and correlates with pain severity in many studies (Ohberg et al., 2004)

During the fenestration procedure, the needle appears as a bright (hyperechoic) linear structure on ultrasound — the “reverberation artifact” that Dr. O’Connor describes, caused by the repeated reflection of ultrasound waves between the flat surfaces of the needle. This reverberation artifact makes the needle highly visible and allows precise real-time guidance throughout the procedure.


Step-by-Step Procedural Technique for Ultrasound-Guided Needle Fenestration

Patient Preparation and Positioning

Before the fenestration procedure begins, appropriate patient preparation is essential. This includes:

Informed Consent:

The patient must be thoroughly educated about the nature of the procedure, the expected immediate post-procedure response (soreness and temporary worsening of symptoms, typically lasting 24–72 hours as the intentional acute inflammatory response is established), the expected timeline of improvement, potential complications (infection, tendon weakening, inadvertent injury to adjacent structures), and alternative treatment options. At Injury Medical Clinic PA, this counseling occurs within the context of the patient’s comprehensive treatment plan, developed collaboratively between Dr. Jimenez and Dr. Cardenas.

Patient Positioning:

The patient is positioned to provide both patient comfort and optimal ultrasound access to the target tendon. For lateral epicondylitis (tennis elbow) fenestration, as demonstrated by Dr. O’Connor, the patient is typically seated with the arm resting on a padded armrest, elbow slightly flexed, and the lateral elbow exposed. For other tendons:

  • Patellar tendon: supine, knee slightly flexed over a bolster
  • Achilles tendon: prone, ankle in slight dorsiflexion
  • Rotator cuff tendons: seated, with specific positions varying by tendon (supraspinatus — arm in the “Crass” position; infraspinatus — arm across the chest)

Skin Preparation:

The skin over the target area is thoroughly cleaned with antiseptic solution (chlorhexidine or povidone-iodine) to minimize infection risk. A sterile field is maintained throughout the procedure, with sterile covers applied to the ultrasound transducer.

Local Anesthesia: The Foundation of Patient Comfort

As Dr. O’Connor describes, local anesthesia is administered before the fenestration procedure. In her demonstrated technique, she uses a 27-gauge needle to infiltrate the skin and subcutaneous tissues overlying the target tendon with 1% lidocaine. Several important principles guide this anesthesia step:

Subcutaneous and Peritendinous Anesthesia:

Lidocaine is infiltrated into the skin, subcutaneous tissues, and peritendinous soft tissues, but ideally not directly into the tendon itself. This is because intratendinous lidocaine is potentially cytotoxic to tenocytes in laboratory studies — an effect that could theoretically impair the healing response that fenestration is designed to initiate. By confining the anesthesia to peritendinous tissues, the clinician numbs the pathway the larger fenestration needle will travel, reducing patient discomfort while preserving the cellular biology within the tendon.

Vapor Coolant Spray:

Dr. O’Connor describes using a vapor coolant spray (such as ethyl chloride or fluoroethane) applied to the skin surface immediately before needle insertion. This produces a brief, intense local cooling effect that temporarily reduces skin sensitivity and further minimizes the patient’s perception of needle insertion — a simple but effective technique for patient comfort.

The Rationale for Adequate Anesthesia:

Adequate anesthesia is not merely a patient comfort measure — it is also a procedural quality determinant. A patient who is in significant pain during the procedure will be tense and may involuntarily move, making accurate needle placement under ultrasound guidance more difficult and potentially less safe. Good local anesthesia allows the clinician to perform a thorough, methodical fenestration without rushing, producing better procedural outcomes.

Needle Selection: 22-Gauge vs. 25-Gauge

The choice of needle gauge for fenestration involves a balance between several competing considerations:

Larger needles (22-gauge):

  • Create larger punctate defects with each pass, potentially stimulating a more robust healing response
  • Provide greater tactile feedback as the needle traverses different tissue densities (soft tendinopathic tissue vs. firm normal tendon)
  • Are slightly more visible on ultrasound
  • May cause more post-procedural discomfort

Smaller needles (25-gauge):

  • Cause less tissue trauma per pass, potentially reducing post-procedural pain
  • May be preferred for smaller tendons or when combining with injection of viscous agents (PRP)
  • Slightly less tactile feedback

In practice, the choice between 22-gauge and 25-gauge is often based on the size of the tendon, the extent of the tendinopathic lesion, the viscosity of any co-injected agent, and clinician preference. For larger tendons with extensive tendinopathy (Achilles, patellar), a 22-gauge needle may be preferred. For smaller tendons (ECRB at the lateral elbow), a 25-gauge needle often provides excellent results.

The Fenestration Sequence: Achieving Complete Coverage

Once the needle has been positioned in-plane with the ultrasound transducer, with the tip confirmed to be within the area of tendinopathy, the fenestration sequence proceeds as follows:

Step 1 — Initial Needle Placement:

Advance the needle in-plane, with continuous ultrasound visualization, until the tip is positioned within the most proximal extent of the tendinopathic zone. Optimize the insertion angle to keep the entire shaft within the imaging plane. For superficial tendons like the ECRB at the lateral elbow, this typically involves a relatively shallow approach angle (approximately 20–40 degrees from horizontal), allowing the needle to traverse a longer path within the tendon rather than dive steeply.

Step 2 — Penetration and Initial Fenestration:

With the needle tip positioned within the tendinopathic zone, the clinician begins fenestration by advancing the needle into the tissue, then partially withdrawing it (without removing it from the tendon or the skin), redirecting it slightly shallower or deeper within the tendon cross-section, and advancing again. This rhythmic advance-withdraw-redirect pattern creates the multiple punctate openings that characterize fenestration.

Step 3 — Systematic Coverage of the Tendinopathic Zone — Long Axis:

By repeatedly advancing, withdrawing, and redirecting the needle at incrementally different depths, the clinician ensures that the entire thickness of the tendinopathic zone — from its superficial to deep extent — is covered. The number of passes required to achieve this depends on the size of the tendinopathic lesion. Still, Dr. O’Connor describes the typical range in the literature as 15 to 50 passes, varying with the magnitude of the tendon abnormality.

Step 4 — Rotating the Transducer to the Short Axis:

After completing fenestration in the long-axis plane, the clinician rotates the ultrasound transducer 90 degrees to obtain a short-axis (cross-sectional) view of the tendon and the needle. This allows assessment of the needle’s position in the medial-lateral dimension — confirming whether the fenestration coverage needs to be extended medially or laterally within the tendon to treat the full width of the tendinopathic lesion. If the lesion extends beyond the initial needle path, reposition the needle medially or laterally as needed.

Step 5 — Procedural Endpoint — The “Soft Tendon” Sign:

One of the most clinically instructive aspects of Dr. O’Connor’s description of the fenestration technique is the “soft tendon” sign as a procedural endpoint. As the needle repeatedly passes through the tendinopathic tissue, many clinicians report a palpable change in the resistance encountered during needle advancement: the initially firm, resilient (or paradoxically, gritty) texture of the tendinopathic tissue progressively softens, becoming less resistant to needle advancement. This tactile change is believed to reflect disruption of the abnormal, disorganized collagen matrix within the tendinopathic zone—the pathological tissue is literally being broken down and remodeled by repeated needle passes. Many experienced practitioners continue fenestration until the entire target zone reaches this softer consistency, then consider the mechanical phase of the procedure complete.


Prolotherapy: The Science and Application of Dextrose as a Regenerative Agent

What Is Prolotherapy?

Prolotherapy — derived from “proliferative therapy” — is a regenerative injection technique in which a proliferant solution is injected into or around damaged connective tissue (tendons, ligaments, joint capsules, entheses) to stimulate the body’s natural healing response. George Hackett, MD, popularized the term in the 1950s, though injection-based therapies for connective tissue disorders date back to the 19th century.

The most widely used proliferant agent in modern prolotherapy practice is hypertonic dextrose (glucose) — the same molecule that circulates in human blood as blood sugar. Depending on the clinical context, dextrose concentrations used in prolotherapy range from approximately 10% to 50%. As Dr. O’Connor describes, she commonly uses 25% or 50% dextrose for tendon prolotherapy.

How Does Dextrose Prolotherapy Stimulate Tendon Healing?

The mechanisms by which hypertonic dextrose stimulates tendon healing are multiple, and understanding them provides important insight into why combining prolotherapy with needle fenestration creates such a powerful synergistic effect:

Mechanism 1 — Osmotic Cell Stress and Growth Factor Release:

When hypertonic dextrose is injected into tissue, the osmotic gradient created by the high-glucose solution causes local cellular osmotic stress. This stress triggers the release of growth factors — including PDGF, TGF-β, FGF, IGF-1, and connective tissue growth factor (CTGF) — from local cells, including tenocytes, fibroblasts, and platelets. These growth factors are molecular signals that drive collagen synthesis, cell proliferation, and matrix remodeling—the core processes of tendon healing (Topol et al., 2011; Reeves & Hassanein, 2000).

Mechanism 2 — Local Irritant Effect and Inflammatory Cascade Initiation:

The injection of hypertonic dextrose into damaged tendon tissue produces a mild, controlled inflammatory response. This local irritant effect recruits the cellular and molecular machinery of the healing cascade to the injection site. This is analogous to the mechanism of the needle fenestration itself, but adds a biochemical stimulus on top of the mechanical stimulus provided by the needle passes. Together, mechanical disruption (fenestration) and biochemical stimulation (dextrose prolotherapy) create a far more potent healing signal than either approach alone.

Mechanism 3 — Glucose Receptor-Mediated Cell Signaling:

Emerging evidence suggests that dextrose, as a signaling molecule in its own right, interacts with cellular glucose receptors (GLUT transporters) and activates downstream signaling pathways—including the PI3K-Akt pathway—that promote cell survival, proliferation, and matrix synthesis. This suggests that the healing-stimulatory effects of dextrose are not simply osmotic but also involve direct receptor-mediated cellular signaling (Rabago et al., 2009).

Mechanism 4 — Platelet Activation and Intrinsic PRP Effect:

When dextrose is injected and causes local bleeding (which fenestration also facilitates), platelets aggregate at the injection site and degranulate, releasing their alpha-granule contents—a concentrated soup of growth factors including PDGF, TGF-β1, VEGF, EGF, and PF4. This platelet-derived growth factor release is, in effect, a form of endogenous platelet-rich plasma — the same therapeutic principle exploited by exogenous PRP injections, but generated naturally at the treatment site. Fenestration enhances this effect by ensuring that bleeding occurs throughout the fenestrated zone.

Dextrose Concentration: Clinical Considerations

The concentration of dextrose used in prolotherapy has important clinical implications:

  • 10–15% dextrose: This low concentration is predominantly used for intra-articular and periarticular prolotherapy, targeting joint capsules, ligaments, and entheses. At this concentration, the primary mechanism is receptor-mediated cellular signaling rather than osmotic cellular stress.
  • 25% dextrose: This intermediate concentration, commonly used by Dr. O’Connor, provides a balance between osmotic stimulation and injectability (lower viscosity than 50% solutions), making it suitable for intratendinous applications.
  • 50% dextrose: This high concentration provides the most potent osmotic stimulus and is typically used for larger tendons or more severe tendinopathy. It is often diluted at the syringe with local anesthetic (such as lidocaine) to achieve the target concentration and reduce patient discomfort.

Combining Fenestration With Prolotherapy: The Synergistic Rationale

The combination of needle fenestration with prolotherapy, as demonstrated by Dr. O’Connor in the lateral epicondylitis case, represents more than the sum of its parts. The synergy between these two techniques can be understood at multiple levels:

Structural Level:

Fenestration physically disrupts the pathological collagen matrix of tendinosis, creating channels and spaces within the tendon that facilitate the distribution of the subsequently injected prolotherapy solution throughout the entire tendinopathic zone. Without prior fenestration, the dense, disorganized collagen matrix of tendinosis may resist fluid distribution, limiting contact between the dextrose solution and target cells.

Cellular Level:

Fenestration delivers an acute mechanical stimulus to tenocytes, activating mechanotransduction pathways that prime these cells for a proliferative and synthetic response. Dextrose then delivers a biochemical stimulus that further activates these cells, producing amplified and sustained growth factor release compared with either stimulus alone.

Vascular Level:

Fenestration causes local intratendinous bleeding, delivering platelets and their growth factor cargo directly to the tendinopathic zone. Dextrose injection then provides an additional osmotic and biochemical stimulus to these same platelets, enhancing their degranulation and growth factor release.

Neural Level:

Fenestration may disrupt pathological neovascular nerve ingrowth, reducing the peripheral sensitization that drives chronic tendinopathy pain. In contrast, the anti-nociceptive effects of the subsequent dextrose injection (mediated in part through adenosine receptor activation at local pain fibers) may further reduce pain signaling in the treated area.


Orthobiologics in Tendon Regeneration: Where PRP Fits in the Treatment Algorithm

Platelet-Rich Plasma: Principles and Preparation

Platelet-rich plasma (PRP) represents the most widely studied and clinically established orthobiologic used in tendon regeneration. PRP is prepared from the patient’s own blood through a centrifugation process that concentrates platelets — and therefore the growth factors contained within their alpha granules — to levels significantly above those found in whole blood. The platelet concentration in PRP is typically 3 to 8 times that of normal whole blood, depending on the preparation system used (Marx, 2004).

When PRP is injected into or around a tendinopathic tendon, the concentrated platelets encounter the local tissue environment and degranulate, releasing their growth factor cargo directly into the treatment site. The growth factors most relevant to tendon healing include:

  • PDGF (Platelet-Derived Growth Factor): Stimulates fibroblast/tenocyte proliferation and migration, promotes angiogenesis
  • TGF-β1 (Transforming Growth Factor-Beta 1): One of the most potent stimulators of collagen synthesis; also has anti-inflammatory effects in the later phases of healing
  • VEGF (Vascular Endothelial Growth Factor): Promotes angiogenesis, supporting vascular supply to the healing tendon
  • IGF-1 (Insulin-Like Growth Factor 1): Promotes tenocyte proliferation, collagen synthesis, and cell survival
  • EGF (Epidermal Growth Factor): Promotes cell proliferation and differentiation
  • FGF (Fibroblast Growth Factor): Stimulates fibroblast/tenocyte proliferation and neovascularization

In addition to platelet-derived growth factors, PRP also contains white blood cells (in “leukocyte-rich” PRP preparations) that contribute additional cytokines and antimicrobial factors, and plasma proteins including fibrinogen and fibronectin that serve as scaffolding for cell migration.

PRP vs. Prolotherapy vs. Fenestration Alone: Positioning in the Treatment Algorithm

The question of when to use PRP versus prolotherapy versus fenestration alone is one that practicing clinicians frequently encounter, and the answer involves consideration of multiple clinical factors:

Tendinopathy Severity:

  • Mild tendinopathy: Isolated needle fenestration (without injection) or fenestration combined with low-concentration dextrose prolotherapy may be sufficient to initiate adequate healing.
  • Moderate tendinopathy: Fenestration combined with dextrose prolotherapy (25–50%) represents a well-established, cost-effective approach with a strong evidence base.
  • Severe or recalcitrant tendinopathy: Cases that have failed multiple rounds of conservative management, or that involve large, extensively degenerated tendon segments, may benefit from adding exogenous PRP to the fenestration procedure, providing a more potent and sustained growth factor stimulus.

Patient Factors:

  • Age: Older patients may have reduced intrinsic healing capacity and may benefit more from the exogenous growth factor stimulus provided by PRP.
  • Metabolic health: Patients with diabetes mellitus, which impairs multiple aspects of tissue healing, may benefit from PRP’s ability to bypass some of the growth factor deficiencies associated with diabetic tissue biology. This is particularly relevant at Injury Medical Clinic PA, where Dr. Cardenas’s expertise in Internal Medicine includes managing metabolic conditions that directly impact healing.
  • Prior treatment history: Patients who have undergone multiple corticosteroid injections may have impaired tenocyte biology and may require the more potent regenerative stimulus of PRP.

Practical and Cost Considerations:

PRP preparation requires specialized centrifugation equipment and adds both cost and preparation time to the procedure. Dextrose prolotherapy is significantly less expensive and, when combined with fenestration, has demonstrated clinical outcomes comparable to PRP in several well-designed studies (Coombes et al., 2013; Krogh et al., 2016). At Injury Medical Clinic PA, the selection between prolotherapy and PRP is individualized based on the factors above, within the collaborative decision-making framework shared by Dr. Jimenez and Dr. Cardenas.


Understanding Plantar Fasciitis- Video

The Evidence Base for Needle Fenestration and Prolotherapy in Tendinopathy

Lateral Epicondylitis (Tennis Elbow): The Most Studied Model

Lateral epicondylitis — commonly known as tennis elbow — is the tendinopathy most extensively studied in the context of needle fenestration and prolotherapy, and for good reason. It is among the most prevalent upper extremity conditions in clinical practice, affecting approximately 1–3% of the general population and disproportionately impacting working-age adults in manual, clerical, and sports-related occupations (Walker-Bone et al., 2004). The primary pathological structure is the extensor carpi radialis brevis (ECRB) tendon at its origin on the lateral epicondyle of the humerus.

The ECRB tendon is a relatively small, superficial structure — anatomical characteristics that make it particularly amenable to ultrasound-guided needle fenestration. The tendinopathic zone can be clearly visualized on ultrasound, the needle can be precisely targeted, and the procedure can be performed with a high degree of accuracy and safety.

Key Clinical Studies on Needle Fenestration for Lateral Epicondylitis:

Stenhouse et al. (2013) conducted a randomized controlled trial comparing needle fenestration alone, PRP injection, and whole blood injection for chronic lateral epicondylitis. All three groups demonstrated significant improvement in pain and function over 6 months, with no statistically significant differences between groups. This finding supports the conclusion that the mechanical effect of the needle (fenestration) is itself a primary therapeutic driver, with injectable agents providing additive but not necessarily superior benefit (Stenhouse et al., 2013).

Dong et al. (2016) performed a systematic review and meta-analysis of needle fenestration and injection-based treatments for lateral epicondylitis, concluding that needle fenestration combined with biological agents (PRP or whole blood) produced superior outcomes to fenestration alone for pain reduction, while fenestration alone outperformed corticosteroid injection at medium-term (3–12 month) follow-up — consistent with the well-established finding that corticosteroid injection, while effective in the short term, is associated with worse long-term outcomes than regenerative approaches.

Mishra & Pavelko (2006) published one of the foundational studies on PRP for lateral epicondylitis, demonstrating significant improvements in pain scores in patients treated with PRP injection compared to controls at 8 weeks and 6 months, with a statistically significant benefit for PRP. Importantly, the injection in this study was combined with needle fenestration of the tendon before PRP delivery—a protocol essentially identical to the combined approach described by Dr. O’Connor.

Dextrose Prolotherapy for Tendinopathy: Randomized Controlled Trial Evidence

The evidence base for dextrose prolotherapy in tendinopathy has grown substantially over the past two decades, with well-designed randomized controlled trials demonstrating clinically meaningful and statistically significant benefits across multiple tendon sites:

Rabago et al. (2013) conducted a high-quality randomized controlled trial of dextrose prolotherapy versus saline injection and versus eccentric loading exercise for Achilles tendinopathy. The dextrose prolotherapy group showed significantly greater improvements in pain and function at 12-month follow-up than both control groups—a finding with important clinical implications for managing this often recalcitrant condition.

Yelland et al. (2011) performed a randomized controlled trial of prolotherapy for plantar fasciitis (a condition closely related to Achilles tendinopathy, sharing the common theme of enthesopathy at a high-load tendon/fascia attachment site). Prolotherapy produced significantly better outcomes than saline injection and was comparable to the best available conservative therapies.

Reeves & Hassanein (2000) published a landmark double-blind randomized controlled trial of dextrose prolotherapy for knee osteoarthritis — demonstrating significant improvements in pain, range of motion, and cartilage quality on MRI — which, while not directly addressing tendinopathy, established the foundational biochemical rationale (growth factor stimulation by hypertonic dextrose) that underlies tendon prolotherapy as well.

The Number of Needle Passes: What the Evidence Says

One of the most practically important questions in needle fenestration technique concerns how many needle passes are required for an effective procedure. Dr. O’Connor notes that the literature reports a range of 15 to 50 passes, depending on the size of the tendinopathic lesion.

This variability in reported pass numbers reflects both the heterogeneity of tendinopathic lesion sizes across different tendons and patients and the lack of a universally agreed-upon, evidence-defined “optimal” pass number. Several principles guide clinical decision-making:

  • Smaller tendinopathic lesions (such as the ECRB in mild-to-moderate lateral epicondylitis) may require only 15–20 passes to achieve complete coverage and the “soft tendon” endpoint.
  • Larger tendinopathic lesions (such as extensive Achilles or patellar tendinopathy) may require 30–50 or more passes to achieve complete coverage.
  • The “soft tendon” endpoint — the tactile perception that the fenestrated tissue has softened during needle advancement — is arguably a more clinically meaningful guide to procedural completeness than any arbitrary pass number.
  • Some clinicians advocate performing serial fenestration sessions (multiple procedures spaced weeks apart) rather than a single high-pass-count session, reasoning that the healing response benefits from multiple cycles of stimulation.

Lateral Epicondylitis: A Deep Dive Into the Target Pathology

Anatomy of the Lateral Elbow and the ECRB Tendon

To fully appreciate the clinical elegance of needle fenestration for lateral epicondylitis, a detailed understanding of the relevant anatomy is essential. The lateral epicondyle of the humerus serves as the common origin for the extensor muscles of the forearm and wrist. The muscles originating here form a conjoined tendon (the common extensor tendon) that attaches to the lateral epicondyle and its adjacent supracondylar ridge.

The extensor carpi radialis brevis (ECRB) is the tendon most consistently implicated in lateral epicondylitis pathology. Its origin lies deep to the extensor carpi radialis longus at the anterolateral aspect of the lateral epicondyle, in proximity to the lateral collateral ligament complex. The ECRB is subjected to particularly high tensile loads during activities requiring simultaneous wrist extension and forearm pronation — exactly the movement pattern involved in the backhand stroke of tennis (hence the colloquial name “tennis elbow”) and in many occupational tasks such as keyboard use, manual assembly work, and tool use.

At its origin, the ECRB tendon is relatively avascular, positioned in an anatomical watershed zone where direct blood supply is limited. This anatomical characteristic helps explain why this tendon is so prone to tendinosis: the combination of high cyclic mechanical loading and poor intrinsic vascularity creates the ideal environment for the failed healing response characteristic of tendinopathy.

The Unique Ultrasound Appearance of ECRB Tendinopathy

On ultrasound, ECRB tendinopathy characteristically appears as:

  • A hypoechoic region within the deep aspect of the common extensor tendon at or just distal to the lateral epicondyle attachment — exactly the location described by Dr. O’Connor in her demonstration
  • Tendon thickening at the lateral epicondyle origin, often measurable as an increase in anteroposterior diameter compared to the contralateral side
  • Loss of normal fibrillar echotexture within the hypoechoic zone
  • Neovascularization on Doppler imaging within and around the tendinopathic zone — a finding with prognostic significance (higher Doppler signal correlates with more active tendinopathy)
  • Occasionally, small partial tears appear as anechoic (fluid-filled) clefts within the tendon substance, or intratendinous calcifications appear as hyperechoic foci

This is precisely the hypoechoic region that the clinician targets during ultrasound-guided fenestration, as described by Dr. O’Connor: “you can see up on the ultrasound a needle coming in into this hypoechoic area of tendinopathy.”

Why Conservative Treatments Alone Often Fail for Lateral Epicondylitis

Despite the availability of numerous conservative treatments for lateral epicondylitis — including physical therapy, eccentric exercise, extracorporeal shockwave therapy, bracing, NSAIDs, and corticosteroid injection — a significant proportion of patients (estimated at 10–20% in most epidemiological studies) progress to a chronic, refractory state that persists for more than 6–12 months and fails to respond adequately to these measures. Understanding why helps explain the rationale for interventional approaches like fenestration.

The limitation of corticosteroid injection is particularly instructive. Multiple high-quality randomized controlled trials have confirmed that while corticosteroid injection provides excellent short-term (6–12 week) pain relief for lateral epicondylitis, it is associated with worse long-term outcomes than both conservative management and regenerative injection approaches (Coombes et al., 2013). The likely mechanism for this long-term harm is the well-documented catabolic effect of corticosteroids on connective tissue: corticosteroids inhibit collagen synthesis, suppress tenocyte proliferation, and — at the molecular level — downregulate the expression of key structural genes including type I procollagen, fibronectin, and tenascin-C, all of which are essential for tendon matrix integrity and repair (Dean et al., 2014). Repeated corticosteroid injections compound this damage, progressively weakening the tendon and increasing the risk of partial or complete rupture.

This is the clinical context that makes needle fenestration with prolotherapy such an important addition to the clinician’s toolkit: for patients who have failed conservative management — including physical therapy, bracing, and activity modification — and who are seeking an alternative to corticosteroid injection or surgery, fenestration with prolotherapy offers a regenerative rather than catabolic approach, addressing the underlying pathology rather than suppressing its symptoms.


The Multidisciplinary Framework at Injury Medical Clinic PA: Integrating Chiropractic, Internal Medicine, and Regenerative Therapies

The Clinical Partnership of Dr. Alexander Jimenez and Dr. Maria Guadalupe Cardenas

At Injury Medical Clinic PA (also known as Mission Plaza Injury Medical Clinic) in El Paso, Texas, the clinical management of tendinopathy, musculoskeletal injuries, and related conditions is delivered through a uniquely comprehensive multidisciplinary model that integrates the complementary expertise of two highly qualified clinicians: Dr. Alexander Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST and Dr. Maria Guadalupe Cardenas, MD (NPI #1164426749, Texas MD License #J2933).

Dr. Maria Guadalupe Cardenas is Board Certified in Internal Medicine and brings over 40 years of experience as an internist to her role as Medical Director and Collaborative Physician at the practice. Her extensive background in internal medicine provides the clinical foundation for:

  • Comprehensive medical evaluation of patients presenting with musculoskeletal complaints, ensuring that systemic conditions contributing to or complicating tendinopathy (such as diabetes mellitus, inflammatory arthritis, hypothyroidism, metabolic syndrome, and medication side effects) are identified and addressed
  • Medical co-management of complex patients undergoing interventional procedures, including assessment of bleeding risk, infection risk, and contraindications to specific agents (such as dextrose in poorly controlled diabetic patients)
  • Pharmacological management of pain, inflammation, and comorbid conditions within the scope of internal medicine
  • Collaborative physician oversight that satisfies both the clinical and regulatory requirements for a multidisciplinary integrative practice in Texas
  • Coordination with specialist referrals for patients requiring orthopedic surgery, rheumatology, neurology, or other specialty consultation

The relationship between Dr. Jimenez and Dr. Cardenas exemplifies the multidisciplinary setup increasingly recognized as the gold standard in integrative and injury care: an MD providing medical direction and oversight alongside a chiropractor and advanced practice provider, ensuring that patients receive care that is both medically safe and holistically comprehensive.

Dr. Alexander Jimenez: A Uniquely Qualified Integrative Clinician

Dr. Alexander Jimenez’s clinical qualifications span multiple disciplines, positioning him to deliver the comprehensive, evidence-based care complex musculoskeletal patients require. His credentials — DC (Doctor of Chiropractic), APRN (Advanced Practice Registered Nurse), FNP-BC (Family Nurse Practitioner, Board Certified), CFMP (Certified Functional Medicine Practitioner), IFMCP (Institute for Functional Medicine Certified Practitioner), ATN (Advanced Trained Nurse), CCST (Certified Chiropractic Sports Therapist) — represent an extraordinary breadth of clinical training that directly informs his approach to tendinopathy and musculoskeletal care.

This unique combination of qualifications allows Dr. Jimenez to function as both a structural/mechanical clinician (addressing biomechanical dysfunctions through chiropractic care) and a functional medicine practitioner (addressing the systemic, metabolic, and nutritional factors that influence musculoskeletal healing), while also operating as an advanced practice provider capable of ordering and interpreting diagnostic studies (including musculoskeletal ultrasound), prescribing medications within his scope of practice, and performing or coordinating interventional procedures.

His clinical observations and evidence-based practice philosophy are extensively documented at ChiroMed.com and in his professional profile on LinkedIn, where he consistently emphasizes integrating the latest research evidence with individualized patient care—a philosophy directly reflected in the approach to tendinopathy described in this post.

How Chiropractic Care Integrates With Needle Fenestration and Prolotherapy

The integration of chiropractic care with ultrasound-guided needle fenestration and prolotherapy is not coincidental — it reflects a deep understanding of the biomechanical, neurological, and physiological factors that contribute to tendinopathy and its persistence.

Addressing the Biomechanical Drivers of Tendinopathy:

Virtually all tendinopathies occur in the context of altered biomechanics — patterns of movement, loading, and joint alignment that place excessive or abnormal stress on specific tendon structures. For example:

  • Lateral epicondylitis is commonly associated with cervicothoracic dysfunction, altered glenohumeral and scapular kinematics, and restricted pronation-supination mobility of the forearm that collectively increase stress at the ECRB origin
  • Patellar tendinopathy frequently occurs in the context of hip abductor weakness, tibial torsion, or foot pronation abnormalities that increase valgus stress at the knee during loading activities
  • Achilles tendinopathy is strongly associated with restricted ankle dorsiflexion range of motion, subtalar overpronation, and gastrocnemius-soleus tightness that combine to increase peak Achilles tendon strain

Chiropractic care — through spinal manipulation, joint mobilization, soft tissue techniques, and rehabilitation protocols — directly addresses these biomechanical contributors. Dr. Jimenez’s approach encompasses:

  • Cervicothoracic and upper thoracic spinal manipulation for patients with lateral epicondylitis, addressing the proximal kinetic chain dysfunctions that increase distal tendon loading
  • Glenohumeral and acromioclavicular joint mobilization for rotator cuff tendinopathy, restoring normal shoulder kinematics that reduce impingement and tensile loading of the rotator cuff tendons
  • Lumbopelvic stabilization and hip strengthening for patellar and hamstring tendinopathy, correcting the proximal biomechanical deficiencies that drive excessive knee tendon loading
  • Ankle mobilization and foot orthotics for Achilles tendinopathy, addressing the distal biomechanical factors of restricted dorsiflexion and subtalar overpronation

Without addressing these underlying biomechanical contributors, even the most skillfully performed fenestration and prolotherapy procedure risks producing only temporary benefit: the healed tendon will be subjected to the same abnormal loading forces that caused the original degeneration, setting the stage for recurrence.

Neurological Effects of Chiropractic Manipulation:

Spinal manipulation — the cornerstone of chiropractic care — has well-documented neurophysiological effects that extend beyond the local joint being treated. High-velocity, low-amplitude (HVLA) spinal manipulation activates mechanoreceptors in the spinal facet joint capsules, paraspinal muscles, and surrounding soft tissues, generating afferent neural input to the spinal cord that:

  • Inhibits nociceptive transmission at the dorsal horn level (gate control mechanisms)
  • Modulates the activity of the sympathetic nervous system, reducing peripheral sensitization
  • Activates descending inhibitory pain control pathways from the brainstem, including the periaqueductal gray (PAG) — raphe nuclei — dorsal horn pathway, which releases endogenous opioids, serotonin, and norepinephrine as pain-suppressing neurotransmitters

For patients with chronic tendinopathy in whom central sensitization has developed—as is common in long-standing lateral epicondylitis, Achilles tendinopathy, or rotator cuff tendinopathy—these neurological effects of chiropractic manipulation are clinically relevant. By modulating the sensitized pain system, manipulation may reduce the patient’s baseline pain level and improve the therapeutic window for interventional procedures like fenestration.

Exercise Rehabilitation and Tendon Loading Programs:

The evidence base for eccentric and heavy slow resistance (HSR) exercise in tendinopathy is robust and well-established. Progressive tendon loading programs — in which the tendon is subjected to controlled, gradually increasing tensile loads in an eccentric (muscle lengthening under load) or isometric pattern — are among the most effective non-invasive treatments for tendinopathy, operating through the mechanotransduction mechanisms discussed earlier. These programs are typically integrated into the rehabilitation component of the multidisciplinary treatment plan at Injury Medical Clinic PA.

However, an important principle governs the sequencing of interventional procedures and exercise rehabilitation:

Following needle fenestration (with or without prolotherapy), the treated tendon requires a brief period of relative rest — typically 48–72 hours of reduced activity — to allow the acute inflammatory response to establish and the early phases of the healing cascade to initiate without excessive mechanical disruption. This is followed by a graduated return to loading, beginning with isometric exercises (which stimulate tenocyte mechanobiology without imposing significant tensile strain) and progressing through isotonic, eccentric, and finally sport- or function-specific loading protocols.

Dr. Jimenez’s expertise in both chiropractic care and rehabilitation science positions him uniquely to supervise this graduated loading protocol, ensuring that the biomechanical and neural contributions to tendinopathy recovery are addressed in concert with the tissue-level healing initiated by the interventional procedure.


Functional Medicine’s Role in Optimizing Tendon Healing: The Systemic Perspective

Why Systemic Factors Matter in Tendinopathy

Tendinopathy is not merely a local tissue problem. While the histopathological changes of tendinosis are located within the tendon itself, the factors that determine whether a tendon heals effectively — or fails to heal and becomes chronically degenerative — are profoundly influenced by the systemic metabolic and physiological environment in which that tendon exists. This is a central insight of functional medicine and underpins the multidisciplinary approach at Injury Medical Clinic PA, rather than single-modality treatment models.

Dr. Jimenez’s certifications as a Certified Functional Medicine Practitioner (CFMP) and Institute for Functional Medicine Certified Practitioner (IFMCP) reflect his deep engagement with these systemic dimensions of musculoskeletal health. In practice, this means that the evaluation and management of tendinopathy patients at Injury Medical Clinic PA extends beyond the tendon itself to assess and address the systemic factors that influence healing capacity.

Metabolic Health and Tendon Biology

Diabetes Mellitus and Insulin Resistance:

There is now a substantial body of evidence linking diabetes mellitus and insulin resistance with impaired tendon biology and increased tendinopathy risk. Mechanisms include:

  • Advanced glycation end products (AGEs): In chronically hyperglycemic states, glucose reacts non-enzymatically with proteins in a process called glycation, producing AGEs. When AGEs form on collagen molecules within the tendon matrix, they create cross-links between collagen fibers that alter the tendon’s mechanical properties —increasing stiffness and brittleness—and impair tenocytes’ ability to remodel and maintain the matrix (Couppe et al., 2016).
  • Impaired growth factor signaling: Insulin resistance is associated with reduced sensitivity to IGF-1 and impaired PI3K-Akt signaling in tenocytes, reducing the proliferative and synthetic response to tendon loading and injury.
  • Oxidative stress: Diabetic metabolic dysregulation generates excessive reactive oxygen species (ROS) that damage tenocyte DNA, impair mitochondrial function, and accelerate tendon matrix degradation.
  • Microvascular disease: Diabetic microangiopathy further reduces the already limited blood supply to tendon tissue, compounding the vascular insufficiency that predisposes tendons to degeneration.

These mechanisms explain the well-documented clinical observations that patients with diabetes have a significantly higher prevalence of tendinopathy (particularly at the Achilles, rotator cuff, and hand tendons) and a slower, less complete healing response to both conservative and interventional treatments. Dr. Cardenas’s expertise in managing metabolic conditions is therefore directly relevant to optimizing tendon intervention outcomes —optimizing glycemic control before and after fenestration procedures directly improves the tissue environment for healing.

Thyroid Dysfunction:

Hypothyroidism is a frequently overlooked contributor to tendinopathy. Thyroid hormones regulate the metabolism and synthetic activity of tenocytes, and thyroid hormone deficiency is associated with:

  • Mucinous degeneration of tendons — accumulation of glycosaminoglycans within the tendon matrix that alters its mechanical properties and predisposes to tendinopathy
  • Impaired collagen synthesis and reduced tenocyte proliferative capacity
  • Increased susceptibility to tendon thickening, tendinosis, and spontaneous rupture

Routine assessment of TSH, free T3, and free T4 in patients with unexplained or treatment-resistant tendinopathy is therefore a standard component of the functional medicine evaluation at Injury Medical Clinic PA.

Hyperlipidemia and Tendon Xanthomas:

Elevated serum lipids — particularly triglycerides and LDL cholesterol — have been associated with tendinopathy through the mechanism of lipid deposition within tendon tissue (tendon xanthomas), most commonly at the Achilles tendon. These lipid deposits alter the mechanical properties of the tendon matrix and create a hostile local environment for tenocyte function. Moreover, statins — among the most widely prescribed medications for hyperlipidemia — have been associated with statin-induced tendinopathy and tendon rupture through their inhibitory effects on the mevalonate pathway and downstream effects on tenocyte metabolism (Bruckert et al., 2010). Identifying hyperlipidemia and statin use in tendinopathy patients is therefore both diagnostically and pharmacologically important.

Nutritional Factors in Tendon Healing

Vitamin C and Collagen Synthesis:

Vitamin C (ascorbic acid) is an essential cofactor for prolyl hydroxylase and lysyl hydroxylase — the enzymes responsible for the hydroxylation of proline and lysine residues in procollagen chains. This step is essential for forming stable collagen triple helices and the subsequent cross-linking of mature collagen fibers. Without adequate vitamin C, collagen synthesis is impaired, and the resulting collagen is structurally weak and prone to degradation. Clinical studies have demonstrated that perioperative vitamin C supplementation significantly improves tendon and ligament healing outcomes, and the same principle applies to the healing initiated by fenestration procedures (Shaw et al., 2017).

Vitamin D and Musculoskeletal Health:

Vitamin D deficiency — extraordinarily common in the general population, affecting an estimated 40–50% of adults in many regions — has profound effects on musculoskeletal health. Vitamin D receptors (VDR) are expressed in tenocytes, and vitamin D signaling directly influences:

  • Tenocyte proliferation and differentiation
  • Type I collagen gene expression
  • Calcium homeostasis and tendon calcification risk
  • Immune regulation and inflammatory resolution

Patients with tendinopathy should undergo assessment of serum 25-hydroxyvitamin D levels, with supplementation initiated when levels are below the functional threshold (typically 40–60 ng/mL) to optimize the healing environment for fenestration-initiated repair.

Protein and Collagen-Specific Amino Acids:

Adequate dietary protein intake is fundamental to supporting the collagen synthetic demands of tendon healing. Of particular importance are glycine, proline, and hydroxyproline — the three most abundant amino acids in collagen. Hydrolyzed collagen peptides (collagen supplements) have been shown in clinical trials to increase collagen synthesis in tendons and ligaments when consumed with vitamin C approximately 45–60 minutes before exercise, timed to optimize the delivery of these substrates during the post-exercise anabolic window (Shaw et al., 2017; Dressler et al., 2018).

Omega-3 Fatty Acids:

Omega-3 polyunsaturated fatty acids (EPA and DHA) — primarily from fatty fish and fish oil supplements — have well-documented anti-inflammatory and pro-resolving effects mediated through resolvins, protectins, and maresins — specialized pro-resolving lipid mediators that actively facilitate the resolution of inflammation and promote tissue repair. In the context of tendinopathy treatment, adequate omega-3 status may enhance the quality of the inflammatory resolution phase following fenestration, facilitating a cleaner transition into the proliferative and remodeling phases of healing.

Addressing Psychological Factors: The Mind-Tendon Connection

An often-neglected but clinically important dimension of chronic tendinopathy management is the psychological component. Multiple studies have demonstrated that catastrophizing, anxiety, depression, and fear-avoidance beliefs independently predict poorer outcomes in tendinopathy treatment, through mechanisms including:

  • Enhanced central sensitization of pain processing
  • Reduced engagement with rehabilitation programs (due to fear of pain or re-injury)
  • Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis and elevated cortisol levels that impair tissue healing
  • Altered autonomic nervous system activity that affects local tissue perfusion

The integrative approach at Injury Medical Clinic PA incorporates psychological support through pain education (explaining the neurobiological mechanisms of chronic pain to reduce fear and catastrophizing), mindfulness-based stress reduction (MBSR) referrals, and close collaboration with behavioral health professionals when indicated.


Personal Injury Care and Tendinopathy: The Legal and Clinical Interface

Tendinopathy in the Context of Personal Injury

Injury Medical Clinic PA has extensive experience managing tendinopathy and other musculoskeletal conditions in the context of personal injury cases — motor vehicle accidents, workplace injuries, slip-and-fall incidents, and other traumatic events. This creates a unique clinical and medicolegal interface that requires both clinical excellence and meticulous documentation.

In personal injury cases involving tendinopathy, the clinical team must:

Establish Causation:

Determining whether a tendinopathy lesion is causally related to a specific traumatic event — or whether it represents a pre-existing degenerative condition that was aggravated, accelerated, or activated by the injury — requires careful clinical evaluation, diagnostic imaging interpretation (including ultrasound and MRI), and an understanding of the biomechanical forces involved in the injury mechanism. This is an area where Dr. Jimenez’s combined expertise in chiropractic biomechanics, advanced practice nursing, and diagnostic imaging is particularly valuable.

Document the Natural History of Treatment:

Personal injury cases require detailed, contemporaneous documentation of the patient’s clinical presentation, the treatments provided, the patient’s response to treatment, and the degree of permanent impairment (if any) resulting from the injury. The multidisciplinary team at Injury Medical Clinic PA—with Dr. Cardenas providing Internal Medicine oversight and Dr. Jimenez providing chiropractic and functional medicine management—is well positioned to provide this comprehensive documentation.

Coordinate Care Across Disciplines:

Complex personal injury cases frequently require coordination between chiropractic care, physical therapy, interventional procedures, pain management, orthopedic surgery, and psychological support. The multidisciplinary structure of Injury Medical Clinic PA facilitates this coordination, with Dr. Cardenas and Dr. Jimenez collaborating to develop and implement comprehensive care plans that address all dimensions of the patient’s injury.

The Importance of Objective Outcome Measurement

In both clinical and medicolegal contexts, objective outcome measurement is essential. For tendinopathy treated with needle fenestration and prolotherapy, validated outcome tools include:

  • Visual Analog Scale (VAS) or Numeric Rating Scale (NRS) for pain intensity
  • DASH (Disabilities of the Arm, Shoulder and Hand) questionnaire for upper extremity function
  • Victorian Institute of Sport Assessment (VISA) scores — specific questionnaires for Achilles (VISA-A), patellar (VISA-P), and shoulder (VISA-S) tendinopathies
  • Patient-Rated Tennis Elbow Evaluation (PRTEE) for lateral epicondylitis
  • Ultrasound tendon thickness and echogenicity measurements — providing objective, imaging-based evidence of structural change in the tendon following treatment
  • Doppler vascularization scores — quantifying the reduction in pathological neovascularization following treatment

Serial assessment with these tools, integrated with clinical examination findings and ultrasound imaging, provides a robust, objective record of treatment progress that is valuable for both clinical management and medicolegal documentation.


Post-Procedure Care, Rehabilitation, and the Long-Term Management of Tendinopathy

Immediate Post-Procedure Management

Following needle fenestration (with or without prolotherapy), the immediate post-procedure period is characterized by an intentional, controlled acute inflammatory response—the very response the procedure is designed to create. Patients should be counseled to expect:

Pain and Swelling (24–72 Hours):

A significant proportion of patients experience a post-injection flare — a temporary increase in pain and local swelling at the treated site — that peaks at approximately 24–48 hours post-procedure and typically resolves within 72 hours. This is not a complication; it is the expected and desirable manifestation of the acute inflammatory response that initiates the healing cascade. Patients who understand this are far better able to manage their expectations and tolerate the temporary symptom increase without prematurely seeking anti-inflammatory medication.

Avoiding NSAIDs and Corticosteroids:

Following fenestration and prolotherapy, the use of NSAIDs (non-steroidal anti-inflammatory drugs) should be specifically avoided for at least 7–14 days post-procedure. NSAIDs work by inhibiting the cyclooxygenase (COX-1 and COX-2) enzymes responsible for prostaglandin synthesis — but prostaglandins are among the key signaling molecules that initiate and orchestrate the acute inflammatory healing response. By suppressing this response with NSAIDs, the patient would directly counteract the therapeutic mechanism of the fenestration procedure.

For analgesia in the post-procedure period, acetaminophen (paracetamol) is the preferred option, as it provides pain relief through central mechanisms without the prostaglandin-suppressing peripheral effects of NSAIDs. Ice applied to the skin (not directly on the injection site) for the first 24 hours, along with elevation of the treated limb, can also reduce swelling and discomfort.

Activity Restriction:

For the first 48–72 hours following the procedure, the patient should avoid activities that directly load the treated tendon. For lateral epicondylitis, this means avoiding repetitive gripping, wrist extension, and forearm pronation. For Achilles tendinopathy, it means avoiding running and high-impact activities. Light activities of daily living are typically permissible.

The Rehabilitation Program: Building Tendon Capacity After Fenestration

The rehabilitation phase following needle fenestration is, in many respects, as important as the procedure itself. Fenestration initiates the healing cascade, but progressive mechanical loading of the healing tendon—through a carefully supervised rehabilitation program—guides the new collagen matrix to develop optimal mechanical properties.

Weeks 1–2 — Isometric Loading Phase:

Isometric exercises — in which the muscle contracts against resistance without joint movement — are the safest starting point for tendon loading in the early post-procedure period. Isometric contractions generate moderate tensile load on the tendon (sufficient to stimulate tenocyte mechanobiology) without the potentially damaging strain accumulation associated with dynamic loading. Studies have also shown that isometric exercises have analgesic effects in tendinopathy, mediated through cortical inhibition of pain processing—providing additional functional benefit during this early rehabilitation phase (Rio et al., 2015).

For lateral epicondylitis, isometric wrist extension exercises (holding a static wrist extension position against resistance) are the primary exercise of this phase. For Achilles tendinopathy, isometric single-leg calf raises (held for 30–45 seconds) are the standard protocol.

Weeks 3–6 — Isotonic and Eccentric Loading Phase:

As tendon healing progresses—evidenced by reduced pain, improved function, and (when available) improved ultrasound appearance—the rehabilitation program advances to isotonic and eccentric loading protocols. Eccentric exercise — muscle contraction while the muscle is lengthening — generates the highest collagen synthetic stimulus per exercise bout of any loading mode, and has been the most extensively studied loading protocol for tendinopathy rehabilitation (Alfredson et al., 1998; Maffulli et al., 2008).

The classic eccentric protocol for Achilles tendinopathy (the Alfredson protocol) involves performing 3 sets of 15 eccentric calf raises twice daily, 7 days per week, using body weight and gradually increasing load. For patellar tendinopathy, the decline squat eccentric protocol is the standard approach. For lateral epicondylitis, eccentric wrist extension exercises using a dumbbell or resistance band are the cornerstone of the eccentric phase.

Heavy Slow Resistance (HSR) Training:

More recently, heavy slow resistance (HSR) training — in which the tendon is loaded with heavy weights through a full range of motion at a slow, controlled speed — has been shown to be equally or more effective than eccentric-only protocols for tendinopathy rehabilitation (Beyer et al., 2015). HSR training may be preferable for some patients because it is less painful, allows bilateral training (reducing asymmetric loading), and may produce better patient adherence. Dr. Jimenez integrates HSR protocols into his rehabilitation programs when clinically appropriate.

Weeks 7–12 — Sport-Specific and Functional Loading Phase:

As the tendon’s capacity for loading increases, the rehabilitation program progresses to sport-specific or occupational loading activities — running, jumping, throwing, or the specific occupational tasks that precipitated the tendinopathy. This phase is characterized by a progressive increase in load, speed, and complexity, guided by the patient’s symptom response and functional goals.

Return-to-Sport/Activity Criteria:

Return to full sport or occupational activity is guided by objective criteria including:

  • Pain scores of ≤2/10 during activity (VISA score improvement to >80)
  • Full, pain-free range of motion at the affected joint
  • Limb symmetry in strength testing — typically ≥90% of the contralateral side on isokinetic or dynamometric testing
  • Ultrasound evidence of tendon healing — improvement in echotexture, reduction in hypoechoic area, and reduction in Doppler vascularization

Understanding the Ultrasound Video Demonstration: A Frame-by-Frame Clinical Analysis

What the Fenestration Video Reveals About Technique and Clinical Decision-Making

The clinical video demonstration provided by Dr. O’Connor — of a fenestration prolotherapy procedure for lateral tennis elbow — offers remarkable insight into the practical, real-time execution of the technique described above. Let us explore what this video communicates at a deeper clinical level.

The Vapor Coolant Spray Step

Dr. O’Connor’s instruction to apply the vapor coolant spray — “give me a little free spray right there” — immediately before needle insertion reflects both patient comfort optimization and procedural efficiency. The vapor coolant creates an immediate, brief anesthetic effect at the skin surface that, combined with the previously administered subcutaneous lidocaine, minimizes the patient’s experience of the needle entering the skin. This is particularly important in the lateral elbow region, where the skin overlying the lateral epicondyle is thin and relatively sensitive.

The use of vapor coolant spray is a small but meaningful example of the patient-centered procedural philosophy that characterizes high-quality interventional musculoskeletal practice. Every step of the procedure should be optimized not only for technical accuracy but also for patient experience and comfort.

The Long-Axis In-Plane Visualization

Dr. O’Connor’s statement — “I’m going to be able to pick this up, long axis in plane with my transducer” — emphasizes the fundamental importance of in-plane needle visualization that has been discussed at length above. Her confirmation of this approach before proceeding underscores that in-plane technique is not merely a preference but a clinical standard for ultrasound-guided tendon fenestration.

Advancing, Withdrawing, and Redirecting: The Rhythmic Pattern of Fenestration

The description “you see me here advancing and withdrawing, penetrating that tissue”—captured in the video—vividly depicts the fenestration rhythm central to the technique. This is not a single, static injection — it is a dynamic, iterative process in which the needle is in constant motion, systematically covering the tendinopathic zone through a methodical pattern of advance-withdraw-redirect cycles.

This rhythmic pattern serves multiple purposes simultaneously:

  • It creates the multiple punctate openings (fenestrations) that give the technique its name
  • It maintains the needle within the tendon throughout the procedure, preventing the need for multiple skin punctures
  • It allows the clinician to continuously assess tissue resistance through tactile feedback, using the “soft tendon” sign as a procedural endpoint.
  • It ensures even distribution of the mechanical stimulus throughout the tendinopathic zone.

The Role of the Second Clinician

The exchange between Dr. O’Connor and the second speaker — “This is extensor tendinopathy… Occasionally, see both medially and laterally underneath this synchondrosis” — reveals an important dimension of the clinical procedure that is easy to overlook: the value of intraprocedural communication and collaboration. The second clinician (presumably a colleague, resident, or trainee) contributes observations that help guide the procedure, including identifying the target anatomy and confirming needle position relative to the lateral epicondyle and adjacent joint structures.

This collaborative, communicative approach to procedure performance—in which all participants on the clinical team actively contribute their observations—is consistent with the multidisciplinary teamwork model that defines care at Injury Medical Clinic PA.

The Prolotherapy Injection: The Final Step

Dr. O’Connor’s closing narration — “And now injecting the prolotherapy. Done. That’s the prolotherapy procedure” — captures the final step of the combined fenestration-prolotherapy sequence: the delivery of the dextrose proliferant solution into the fenestrated tendon. This injection follows directly from the fenestration, using the freshly created channels within the tendon to distribute the dextrose solution throughout the treated zone.

The sequencing — fenestration first, injection second — is deliberate and mechanically logical:

  • Fenestration creates physical channels within the disorganized tendinopathic matrix, improving the distribution of the subsequently injected dextrose
  • Fenestration triggers local bleeding, delivering platelets and endogenous growth factors to the target zone before the dextrose is added.
  • The dextrose injection then provides an additional biochemical stimulus that amplifies the healing response initiated by the fenestration.
  • The entire combined procedure can typically be completed in 10–15 minutes (exclusive of preparation time), making it practical for routine clinical implementation.

Broader Applications: Fenestration and Prolotherapy Beyond the Lateral Elbow

Achilles Tendinopathy

Achilles tendinopathy — one of the most common and debilitating tendinopathies encountered in active populations — has been among the most extensively studied conditions in the regenerative injection therapy literature. The Achilles tendon is the largest in the body, transmitting forces equivalent to 6–8 times body weight during running, and is therefore subjected to enormous mechanical demands that, in the context of training errors, biomechanical dysfunction, or systemic metabolic abnormalities, can overwhelm the tendon’s adaptive capacity and precipitate tendinosis.

Achilles tendinopathy most commonly presents as either mid-portion tendinopathy (affecting the fusiform body of the tendon approximately 2–6 cm proximal to the calcaneal insertion — the classic “watershed zone” of reduced vascularity) or insertional tendinopathy (affecting the enthesis at the posterior calcaneus, often in association with a Haglund deformity — a posterosuperior calcaneal prominence that causes mechanical impingement on the tendon during dorsiflexion).

For mid-portion Achilles tendinopathy, ultrasound-guided fenestration with or without prolotherapy is a clinically validated, evidence-based treatment option. The procedure is performed with the patient prone, ankle in slight plantarflexion, using an in-plane medial or lateral approach. The hypoechoic tendinopathic zone within the mid-portion of the Achilles — confirmed with Doppler imaging to identify areas of neovascularization — is systematically fenestrated, followed by dextrose prolotherapy delivery.

The Alfredson eccentric loading protocol, performed in conjunction with and following the fenestration procedure, remains the cornerstone of non-surgical Achilles tendinopathy rehabilitation and is integrated into the post-procedure rehabilitation program at Injury Medical Clinic PA.

Patellar Tendinopathy (Jumper’s Knee)

Patellar tendinopathy — colloquially known as “jumper’s knee” — is a particularly challenging condition because it primarily affects young, highly active athletes who are unwilling or unable to accept the prolonged rest that might allow spontaneous healing. The pathological zone is almost invariably at the proximal patellar pole — the attachment of the patellar tendon to the inferior pole of the patella — and represents the same combination of hypovascular enthesis anatomy and high cyclic mechanical loading that characterizes other tendinopathies.

Ultrasound-guided fenestration with prolotherapy for patellar tendinopathy has been studied in both elite athletes and recreational sports participants. The procedure is typically performed with the patient supine, knee slightly flexed over a bolster, using a lateral or medial in-plane approach to the proximal patellar tendon. The hypoechoic, Doppler-positive zone at the proximal patellar pole is systematically fenestrated, with prolotherapy delivered at the conclusion of the fenestration sequence.

The decline squat eccentric protocol and, more recently, isometric quadriceps loading protocols (heavy isometric leg press holds) constitute the rehabilitation cornerstone for patellar tendinopathy and are prescribed and supervised as part of the comprehensive treatment plan.

Rotator Cuff Tendinopathy

Rotator cuff tendinopathy — particularly involving the supraspinatus tendon at its insertion on the greater tuberosity — is the most common cause of shoulder pain in adults and one of the leading causes of work-related disability. The supraspinatus tendon has a well-described “critical zone” of relative avascularity approximately 1 cm proximal to its insertion — precisely where the majority of tendinopathic lesions and partial tears originate.

Ultrasound-guided fenestration with prolotherapy for supraspinatus tendinopathy is an increasingly utilized treatment modality, particularly for patients who have failed conservative management, including physical therapy, NSAID treatment, and subacromial corticosteroid injection. The procedure requires careful ultrasound guidance to navigate the shoulder’s complex anatomy, including the proximity of the subacromial bursa, the biceps tendon, and the acromioclavicular joint. The technique demands a high level of ultrasound guidance proficiency.

The rotator cuff rehabilitation program—emphasizing scapular stabilization, glenohumeral external rotation strengthening, and posterior capsular stretching—is an essential component of post-procedure management and is supervised by Dr. Jimenez as part of the comprehensive chiropractic and rehabilitation care plan.

Plantar Fasciitis and Fasciopathy

While the plantar fascia is technically a fascial structure rather than a tendon, plantar fasciitis (more accurately termed plantar fasciopathy or plantar fascial enthesopathy) shares the same histopathological characteristics of tendinosis — disorganized collagen, myxoid degeneration, absence of acute inflammatory cells — and responds to the same interventional approaches, including fenestration and prolotherapy.

The plantar fascial insertion at the medial calcaneal tubercle is the typical site of pathology, appearing on ultrasound as a thickened, hypoechoic structure at the calcaneal origin with variable Doppler signal. Fenestration with dextrose prolotherapy at this site has been demonstrated in randomized controlled trials (Yelland et al., 2011) to produce significant, sustained improvements in pain and function.


The Future of Tendon Regeneration: Emerging Technologies and Approaches

Bone Marrow Aspirate Concentrate (BMAC)

Bone marrow aspirate concentrate (BMAC) is an emerging orthobiologic that combines the growth factor-rich properties of PRP with the additional presence of mesenchymal stem cells (MSCs)—cells with the capacity to differentiate into tenocytes and other connective tissue cell types. BMAC is harvested from the patient’s posterior iliac crest under ultrasound or fluoroscopic guidance, concentrated by centrifugation, and injected into the tendinopathic zone using ultrasound guidance.

Early clinical data for BMAC in tendinopathy are promising, particularly for partial-thickness rotator cuff tears and severe Achilles tendinopathy, where tissue damage extends beyond pure tendinosis into structural disruption. However, the evidence base is less mature than that for PRP and prolotherapy, and the higher cost and procedural complexity of BMAC limit its current clinical utility to the most severe or refractory cases.

Extracorporeal Shockwave Therapy (ESWT)

Extracorporeal shockwave therapy (ESWT) uses focused acoustic pressure waves to deliver mechanical energy to tendinopathic tissue, stimulating healing through mechanisms similar to fenestration — including disruption of abnormal calcifications, stimulation of local growth factor release, and induction of controlled micro-trauma that initiates the healing cascade. ESWT can be used as a standalone treatment for tendinopathy or as an adjunct to needle fenestration and prolotherapy, potentially amplifying the healing stimulus.

The evidence base for ESWT in tendinopathy is robust, with multiple Level I randomized controlled trials demonstrating significant benefits for calcific rotator cuff tendinopathy (where shockwaves are particularly effective at dispersing calcific deposits), Achilles tendinopathy, patellar tendinopathy, and plantar fasciitis (Mani-Babu et al., 2015; Rompe et al., 2009).

At Injury Medical Clinic PA, ESWT is integrated into the treatment algorithm for tendinopathy patients as a complementary modality, used with needle fenestration, prolotherapy, and a comprehensive chiropractic and rehabilitation program under the collaborative oversight of Dr. Jimenez and Dr. Cardenas.

Autologous Conditioned Serum (ACS) and Cytokine-Based Therapies

Autologous conditioned serum (ACS), also known as Orthokine, is prepared by incubating the patient’s blood with glass beads coated with chromium sulfate, stimulating white blood cells to produce high concentrations of interleukin-1 receptor antagonist (IL-1Ra). This naturally occurring anti-inflammatory cytokine blocks the action of IL-1β, a key driver of inflammatory tissue degradation in tendinopathy and osteoarthritis. The conditioned serum is then harvested, concentrated, and injected into the affected tissue.

While the evidence base for ACS in tendinopathy is still emerging, early results are promising, particularly for conditions with a significant inflammatory component such as acute tendon tears and inflammatory enthesopathies in the context of systemic inflammatory arthritis. The functional medicine perspective at Injury Medical Clinic PA—emphasizing the modulation of systemic inflammatory mediators—aligns well with this targeted, cytokine-based approach.

Ultrasound-Guided Percutaneous Tenotomy (TENEX/FAST Procedure)

Ultrasound-guided percutaneous tenotomy — marketed under brand names such as TENEX or FAST (Focused Aspiration of Scar Tissue) — represents a technologically advanced evolution of the needle fenestration concept. These devices use high-frequency ultrasonic energy delivered through a small-gauge needle to simultaneously emulsify, aspirate, and remove abnormal tendinopathic tissue—creating controlled debridement of the diseased tendon without affecting surrounding normal tissue.

The theoretical advantage of ultrasonic tenotomy over manual needle fenestration is the ability to precisely target and remove the pathological tissue rather than simply disrupting it — potentially producing a cleaner wound bed for healing. Early clinical studies are promising, with multiple reports of significant pain reduction and functional improvement at medium-term follow-up. However, the device cost and the specialized training required for proficient use currently limit its widespread adoption.


Integrating Evidence-Based Research With Clinical Practice at Injury Medical Clinic PA

The Research-Clinical Interface

One defining characteristic of care at Injury Medical Clinic PA is the systematic integration of the latest peer-reviewed evidence into clinical practice. Dr. Jimenez’s extensive engagement with the scientific literature — evident through his educational content at ChiroMed.com and his professional publications — ensures that the treatment protocols used at the clinic reflect the best current evidence for each clinical modality.

This evidence-based approach means the clinic’s use of needle fenestration and prolotherapy is not based on anecdotal experience or historical tradition; it is grounded in a rigorous understanding of the physiological mechanisms, supported by data from properly designed randomized controlled trials and systematic reviews, and continuously updated as new evidence emerges.

The collaboration between Dr. Jimenez and Dr. Cardenas ensures that this evidence-based approach encompasses both the musculoskeletal and interventional dimensions (Dr. Jimenez) and the internal medicine and systemic dimensions (Dr. Cardenas) of patient care — a truly comprehensive, whole-patient evidential framework.

The Role of Diagnostic Musculoskeletal Ultrasound in Evidence-Based Practice

The routine use of diagnostic musculoskeletal ultrasound at Injury Medical Clinic PA is itself an evidence-based practice standard. The availability of high-quality ultrasound imaging at the point of care — rather than relying on MRI reports from external radiology practices — provides several clinically important advantages:

Dynamic Assessment:

Ultrasound allows real-time dynamic imaging — the tendon can be assessed during movement, during loading, and during the clinical examination itself. This dynamic capability reveals pathology that static imaging (MRI) may miss, such as dynamic tendon subluxation, dynamic impingement, and subtle partial tears that are only apparent under load.

Guided Interventions:

As discussed in this post, ultrasound guidance transforms fenestration from a “blind” procedure (based on anatomical landmarks alone) into a precisely targeted, real-time-guided intervention—dramatically improving both safety and efficacy.

Serial Monitoring of Treatment Response:

Serial ultrasound assessment — measuring tendon thickness, echotexture, and Doppler vascularization before and after treatment — provides objective, imaging-based documentation of treatment response. This is valuable both for clinical management (guiding decisions about repeat procedures, rehabilitation progression, and return to activity) and for medicolegal documentation in personal injury cases.

Patient Education:

Real-time ultrasound imaging provides a powerful patient education tool — showing the patient their own tendon abnormality on the screen and then demonstrating the needle precisely targeting that abnormality during the procedure dramatically increases patient understanding of their condition and their engagement with the treatment process.


Clinical Outcomes and Patient Expectations: What the Research Tells Us

Timeline of Recovery After Needle Fenestration With Prolotherapy

Patient education about the expected timeline of recovery following needle fenestration with prolotherapy is essential for managing expectations and ensuring adherence to the post-procedure rehabilitation program. The typical recovery timeline is:

Days 1–3: Post-Procedure Flare

As previously discussed, most patients experience a temporary worsening of pain in the first 24–72 hours after the procedure—the desired acute inflammatory response. Reassuring patients that this is expected and part of the therapeutic mechanism is critical for confidence.

Weeks 1–4: Early Healing Phase

Pain gradually subsides toward the patient’s pre-procedure baseline as the acute inflammatory response resolves and the proliferative phase of healing begins. Many patients report a gradual reduction in pain and a sense that the tendon is “feeling different”—perhaps less sharp, less localized, or more tolerable—during this period.

Weeks 4–12: Proliferative and Early Remodeling Phase

The most significant clinical improvements typically occur in this period, as new collagen synthesis and matrix remodeling progress. Most clinical studies that show significant between-group differences in outcomes report their primary findings at 6–12 weeks following intervention.

Months 3–12: Late Remodeling and Return to Full Function

Complete tendon remodeling — with full restoration of mechanical properties and tensile strength — takes months to over a year following any tendon intervention, including fenestration. This extended timeline reflects the slow metabolic turnover of tendon collagen and the gradual nature of matrix reorganization. Patients should understand that while pain and functional improvement often occur relatively quickly, full structural healing is a much longer process, and adherence to the rehabilitation program throughout this period is essential.

Repeat Procedures:

For patients who do not achieve adequate improvement from a single fenestration session, repeat procedures at 4–8 week intervals may be considered. Many clinical protocols involve 3 to 5 sessions spaced 4–6 weeks apart, particularly when combined with prolotherapy. The patient’s clinical response, the ultrasound appearance of the tendon, and the patient’s functional goals guide the decision to repeat procedures.

Factors Predicting Better Outcomes

Research has identified several factors associated with better outcomes following fenestration and prolotherapy:

  • Shorter symptom duration before intervention — patients with symptoms of less than 6–12 months tend to respond more rapidly and completely than those with chronic, long-standing tendinopathy
  • Higher pre-procedure Doppler vascularization signal — paradoxically, tendons with more active neovascularization on Doppler imaging (indicating a more “active” tendinopathic process) may respond better to regenerative interventions than tendons with absent Doppler signal (indicating a completely avascular, truly “burned out” lesion)
  • Younger age and better metabolic health — as discussed in the functional medicine section
  • Adherence to the post-procedure rehabilitation program — arguably the single most important predictor of long-term outcomes
  • Absence of psychosocial yellow flags — patients without significant catastrophizing, fear-avoidance, or psychological comorbidity tend to achieve better functional outcomes

Safety Profile and Potential Complications

Needle fenestration with prolotherapy has an excellent safety profile when performed by trained clinicians using ultrasound guidance. Potential complications, though uncommon, include:

  • Post-procedure pain flare — the most common “complication,” occurring in the majority of patients but representing an expected therapeutic response rather than a true adverse event
  • Infection — rare when proper sterile technique is used; estimated incidence less than 1 in 10,000 procedures
  • Tendon weakening and rupture — a theoretical concern with any intratendinous needle procedure; the risk is minimized by avoiding excessive needle passes in a single session, using smaller gauge needles where possible, and implementing appropriate post-procedure activity restrictions. Note that this risk is significantly lower with fenestration/prolotherapy than with corticosteroid injection.
  • Nerve or vascular injury — rare when procedures are performed under real-time ultrasound guidance; the ability to identify adjacent neurovascular structures and guide the needle away from them is a primary safety advantage of ultrasound-guided technique
  • Hyperglycemia in diabetic patients — intratendinous dextrose injection may cause transient, mild hyperglycemia in patients with diabetes; Dr. Cardenas’s involvement in the medical oversight of diabetic patients undergoing these procedures ensures that glycemic monitoring is incorporated into the post-procedure care plan

Building a Comprehensive Treatment Plan: The Injury Medical Clinic PA Approach

The Initial Evaluation: Comprehensive History, Physical Examination, and Diagnostic Imaging

At Injury Medical Clinic PA, the management of tendinopathy begins with a comprehensive clinical evaluation that encompasses:

History:

  • Onset, duration, and temporal pattern of symptoms
  • Aggravating and alleviating activities
  • Prior treatments and their outcomes (with particular attention to the number and timing of prior corticosteroid injections)
  • Occupational and recreational demands
  • Medical comorbidities (diabetes, thyroid disease, inflammatory arthritis, hyperlipidemia) — assessed by Dr. Cardenas within her Internal Medicine scope
  • Medications (particularly statins and fluoroquinolone antibiotics, both of which are associated with tendinopathy and tendon rupture risk)
  • Nutritional and lifestyle factors (assessed through the functional medicine lens of Dr. Jimenez)
  • Psychological factors (pain catastrophizing, fear-avoidance, anxiety, depression)

Physical Examination:

  • Palpation of the tendon and adjacent structures to localize and characterize tenderness
  • Provocative testing specific to each tendon (e.g., Cozen’s test and Mill’s test for lateral epicondylitis; Thompson test for Achilles integrity; impingement tests for rotator cuff; Windlass test for plantar fascia)
  • Range of motion assessment of relevant joints
  • Muscle strength testing — manual muscle testing and dynamometry
  • Neurological screening — to rule out radiculopathy, peripheral nerve entrapment, or central sensitization as contributors to pain
  • Postural and gait analysis — to identify proximal and distal biomechanical contributors to tendon loading abnormalities

Diagnostic Imaging:

  • Musculoskeletal ultrasound — real-time, dynamic assessment of tendon architecture, neovascularization, adjacent bursa, and joint structures; performed by Dr. Jimenez as part of the clinical encounter
  • MRI — reserved for cases requiring assessment of structures not adequately visualized on ultrasound (e.g., intra-articular pathology, bone marrow edema, nerve pathology) or for pre-surgical planning; ordered and interpreted in collaboration with Dr. Cardenas and radiology consultants
  • Laboratory studies — ordered by Dr. Cardenas as part of the internal medicine evaluation when systemic contributors to tendinopathy are suspected (CBC, CMP, thyroid panel, lipid panel, HbA1c, vitamin D, inflammatory markers)

The Individualized Treatment Plan: Bringing It All Together

The clinical evaluation culminates in the development of an individualized, multidisciplinary treatment plan that draws on the full spectrum of services available at Injury Medical Clinic PA:

Tier 1 — Foundational Interventions (All Patients):

  • Education — biomechanics of tendinopathy, rationale for chosen treatments, expected timeline, warning signs
  • Activity modification — temporary reduction of provocative activities while maintaining general fitness and cardiovascular health
  • Functional medicine assessment and optimization — nutritional support (vitamin C, vitamin D, collagen peptides, omega-3 fatty acids), metabolic optimization (glycemic control, thyroid optimization), elimination of tendon-toxic medications where possible
  • Chiropractic care — addressing proximal and distal biomechanical contributors to tendon loading, spinal manipulation for neurological modulation of pain, soft tissue therapy
  • Rehabilitation exercise — individualized progressive tendon loading program (isometric → isotonic/eccentric → sport-specific)

Tier 2 — Interventional Procedures (Moderate to Severe Tendinopathy, or Failure of Tier 1):

  • Ultrasound-guided needle fenestration — targeting the hypoechoic tendinopathic zone under real-time visualization
  • Dextrose prolotherapy — delivered following fenestration, 25% or 50% concentration depending on tendon and clinical severity
  • Extracorporeal shockwave therapy (ESWT) — as adjunct or alternative when available and clinically indicated
  • Corticosteroid injection — reserved for specific indications (e.g., concurrent inflammatory bursitis, acute inflammatory flare) and used with full awareness of its long-term risks

Tier 3 — Advanced Orthobiologics (Severe or Refractory Tendinopathy):

  • Platelet-rich plasma (PRP) injection — with or without combined fenestration
  • Bone marrow aspirate concentrate (BMAC) — for the most severe cases with structural tendon disruption
  • Surgical referral — coordinated by Dr. Cardenas for cases that have exhausted non-operative options, including orthopedic consultation for open or arthroscopic tendon debridement, repair, or reconstruction

Ongoing Monitoring and Outcomes Assessment

The treatment plan is not static — it is dynamically adjusted based on the patient’s response, measured through serial clinical assessment, validated outcome questionnaires, and repeat musculoskeletal ultrasound. Dr. Cardenas and Dr. Jimenez conduct regular collaborative case reviews to ensure that:

  • Systemic factors are optimized and adjusted as needed (particularly in patients with metabolic comorbidities)
  • The rehabilitation program is progressing appropriately and challenges the patient without exceeding their current tissue capacity.
  • Interventional procedures are repeated when clinically indicated and deferred when the healing trajectory is proceeding well without them.
  • Emerging complications or red flags are identified early and managed appropriately — including imaging surveillance, laboratory monitoring, and specialist referral when needed.

Conclusion: A New Paradigm for Tendinopathy Care

The clinical approach to tendinopathy described in this educational post represents a fundamental departure from the outdated, symptom-suppression paradigm that has historically dominated — and frequently failed — the management of this common and debilitating condition. By embracing the biology of tendon healing—understanding why tendons fail to heal and designing interventions that address these failures directly—the multidisciplinary team at Injury Medical Clinic PA delivers a qualitatively different, clinically superior approach to care.

Needle fenestration — by mechanically disrupting the chronic degenerative environment of tendinosis and forcibly reinitiating the healing cascade — addresses the core pathophysiological mechanism of tendinopathy at the tissue level. Dextrose prolotherapy amplifies this effect with biochemical stimulation, delivering growth factors and osmotic cellular signals that sustain and enhance the healing response. Ultrasound guidance ensures these interventions are delivered precisely to the target tissue with maximum safety and efficacy.

But the interventional procedure alone — however skillfully performed — is insufficient without the broader clinical context that Injury Medical Clinic PA provides. Th. Jimenez’s chiropractic practice addresses the loading abnormalities that caused the tendinopathy in the first place. The functional medicine framework optimizes the systemic environment for healing — managing metabolic comorbidities, correcting nutritional deficiencies, and modulating systemic inflammation. Dr. Cardenas’s Internal Medicine oversight ensures medical safety, identifies and treats systemic contributors, and coordinates specialist care when needed. The rehabilitation program guides the new collagen matrix to develop optimal mechanical properties through progressive loading.

Together, these elements constitute a comprehensive, patient-centered, evidence-based approach to tendinopathy that offers patients the best available opportunity for a full, lasting recovery — a return not merely to reduced pain, but to full function, restored capacity, and durable musculoskeletal health.

I am proud to be part of the team at Injury Medical Clinic PA that delivers this standard of care, and I am deeply committed to continuing to advance our clinical practice as the science of tendon regeneration evolves. Patients experiencing any of the tendinopathy conditions discussed in this post — whether it is tennis elbow, Achilles pain, patellar tendinopathy, rotator cuff problems, or plantar heel pain — are encouraged to reach out to our clinic for a comprehensive evaluation and to learn whether needle fenestration, prolotherapy, or any of the other interventional and integrative services we offer may be appropriate for their individual situation.


References


Dr. Alexander Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST practices at Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic), El Paso, Texas, in collaboration with Medical Director Dr. Maria Guadalupe Cardenas, MD, Board Certified in Internal Medicine (NPI #1164426749, Texas MD License #J2933). Clinical observations and additional educational resources are available at ChiroMed.com and LinkedIn.


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Tendon Healing: High-Volume Injections for Tendinopathy

Tendon Healing: High-Volume Injections for Tendinopathy

Abstract

In this educational post, I will guide you through an advanced, highly effective technique for managing chronic tendinopathy known as tendon brisement, or high-volume injection (HVI). Drawing from my clinical experience and the latest evidence-based research, we will explore the physiological mechanisms behind this innovative procedure. I will explain how HVI differs from traditional tendon treatments by focusing on hydrostatically decompressing soft tissues and disrupting the problematic neovessels and neonerves that perpetuate chronic tendon pain. We will examine the step-by-step process of performing an HVI, using the Achilles tendon as a primary example. Furthermore, I will discuss how we integrate this advanced procedure at Injury Medical Clinic PA. Our unique multidisciplinary approach combines my expertise in chiropractic and functional medicine with the invaluable medical oversight of our Medical Director, Dr. Maria Guadalupe Cardenas, MD, to provide comprehensive, patient-centered care for complex musculoskeletal conditions.

Tendon Healing: High-Volume Injections for Tendinopathy

As a practitioner with dual credentials in chiropractic and as a board-certified Family Nurse Practitioner, my journey has always been about integrating the best of multiple disciplines to achieve superior patient outcomes. At Injury Medical Clinic PA in El Paso, Texas, this philosophy is the cornerstone of our practice. I am privileged to work alongside Dr. Maria Guadalupe Cardenas, MD, our Medical Director and Collaborative Physician. With over four decades of experience as a board-certified internist, Dr. Cardenas provides essential medical oversight, allowing us to offer a broad spectrum of advanced treatments safely and effectively.

Our model is built on collaboration. Whether we are managing a complex personal injury case, guiding a patient through rehabilitation, or applying functional medicine principles to address root causes of dysfunction, our team approach ensures every patient receives comprehensive care. This integration is particularly vital when we employ advanced procedures like the one we’ll discuss today: tendon brisement, also known as a high-volume injection (HVI). This technique represents a significant leap forward in treating chronic, stubborn tendinopathies, and it perfectly illustrates how integrative care can unlock new possibilities for healing.

Understanding Tendon Brisement: A Paradigm Shift in Tendon Treatment

When we talk about tendon injuries, many people are familiar with terms like fenestration or tenotomy. These procedures involve using a needle to repeatedly puncture the damaged tendon tissue itself, with the goal of stimulating a new, more organized healing response. While effective in certain cases, they don’t always address the full picture of what causes chronic tendon pain.

This is where tendon brisement comes in. It’s a fundamentally different approach. Instead of focusing on the tendon itself, a brisement procedure primarily targets the space around the tendon. Specifically, we target the interface between the tendon and adjacent structures, such as its synovial sheath (tenosynovium) or the nearby fat pad.

The “Why” Behind the Pain: Neovessels and Neonerves

To truly grasp the power of brisement, we must first understand the pathophysiology of chronic tendinopathy. For years, we believed tendon pain was primarily an inflammatory issue (tendinitis). However, modern research, including histopathological studies, has shown that chronic cases are better described as tendinosis—a degenerative condition characterized by disorganized collagen fibers, a lack of inflammatory cells, and, most importantly, the ingrowth of abnormal, tiny blood vessels and nerves. These are known as neovessels and neonerves.

Leading researchers like Alfredson et al. (2000) have demonstrated that these aberrant structures, which often grow into the tendon from adjacent tissues like the fat pad, are a primary source of pain in conditions like Achilles and patellar tendinopathy. The neonerves transmit pain signals, while the neovessels perpetuate a disorganized, failed healing state.

The goal of a tendon brisement or high-volume injection is to physically and hydrostatically disrupt this pathological neurovascular network. We are not just injecting a substance; we are using the volume and pressure of the fluid to mechanically separate adhered tissues and destroy these pain-generating structures.

The High-Volume Injection Procedure: A Step-by-Step Explanation

Let’s walk through how this procedure is performed, using the Achilles tendon as our clinical example. This condition is notoriously difficult to treat, but HVI has shown remarkable promise.

1. Patient Preparation and Initial Assessment

The first step is always a thorough evaluation. The patient is positioned comfortably, typically lying prone for an Achilles procedure, to allow optimal access to the tendon. We then use a high-resolution ultrasound machine with a linear probe to meticulously examine the Achilles tendon in both a longitudinal (long-axis) and transverse (short-axis) view. This diagnostic imaging is crucial for several reasons:

  • Pinpointing the Pathology: We can identify the exact location and extent of tendon thickening, collagen disorganization, and signs of tendinosis.
  • Visualizing Neovascularity: Using color or power Doppler ultrasound, we can often directly visualize increased blood flow from neovessels, typically on the anterior aspect of the tendon near Kager’s fat pad.
  • Planning the Injection: This detailed anatomical map allows us to plan the safest and most effective needle trajectory to target the precise tissue interface.

2. Anesthesia and Needle Placement

Once the target area is identified, we ensure the patient’s comfort. The skin and superficial subcutaneous tissues are anesthetized using a fine-gauge needle (e.g., 25 or 27-gauge) and a local anesthetic like lidocaine. This minimizes any discomfort from the main procedure.

Next, a slightly larger needle (e.g., 21 or 22-gauge) is used for the brisement itself. Under continuous ultrasound guidance, the needle is advanced to the target zone—the space between the anterior border of the Achilles tendon and Kager’s fat pad. Precision is paramount. The goal is to be juxtaposed to the tendon, not inside it.

3. The Hydrodissection and Brisement

This is the core of the procedure. We begin injecting a large volume of fluid. The injectate typically consists of a combination of:

  • Normal Saline: This makes up the bulk of the volume and provides the hydrostatic force needed for the brisement.
  • Local Anesthetic (e.g., Lidocaine): This provides immediate pain relief and can also have a therapeutic effect by disrupting nerve signaling.
  • Corticosteroid (Optional): Some protocols include a small amount of corticosteroid to help modulate the local inflammatory response that may follow the mechanical disruption, although this is debated and often used sparingly (Maffulli & Spiezia, 2017).

As the fluid is injected, we watch the ultrasound screen in real-time. What we see is remarkable. The fluid forcibly separates the tissue planes, creating a distinct, anechoic (black) space. This is the hydrostatic decompression in action. You can literally see the fluid stripping the anterior surface of the tendon away from the fat pad, tearing the delicate neovessels and neonerves that have tethered these structures together.

The volume of fluid used can vary significantly, with literature reporting anywhere from 10 to 100 cc. The injection continues until either the patient feels significant pressure or we feel a marked increase in resistance, indicating the tissue compartment is full.

Visualizing the Mechanism: What We See on Ultrasound

Let’s break down the visuals from a procedure performed by my esteemed colleague, Dr. Knight.

  • Short-Axis View: Initially, the probe is placed perpendicular to the tendon. The needle is introduced from the side, and we see it as a bright dot on the screen when viewed “out-of-plane.” The initial anesthetic injection begins the process of hydrodissection, gently creating space.
  • Long-Axis View: The probe is then turned parallel to the tendon fibers. In this view, we can see the needle tracking along the anterior border of the thickened, tendinopathic Achilles.
  • The “Fluid Wave”: As the high-volume injectate is introduced, we witness the most important part of the procedure. A wave of fluid spreads along the interface. It physically lifts the tendon away from the underlying fat pad. This mechanical stripping action is what accomplishes the brisement, effectively decompressing the area and obliterating the neurovascular ingrowth that drives the pain.

The entire process is a form of mechanical neurolysis and anti-angiogenesis, achieved through hydrostatic pressure rather than a scalpel. This is precision medicine at its finest, guided by real-time imaging.

Integrating Chiropractic Care for Comprehensive Recovery

Performing a high-volume injection is a powerful intervention, but it’s not the end of the story. In my clinical experience, the most successful and lasting outcomes come when these procedures are integrated into a comprehensive rehabilitation framework. This is where the synergy of our multidisciplinary clinic truly shines.

Following an HVI procedure, the patient enters a structured rehabilitation program where chiropractic care plays a pivotal role.

  • Biomechanical Correction: Chronic tendinopathy rarely exists in a vacuum. It often results from underlying biomechanical faults. As a chiropractor, I focus on identifying and correcting these issues. For Achilles tendinopathy, this may involve:
    • Spinal and Pelvic Adjustments: Misalignments in the pelvis or lumbar spine can alter the kinetic chain, leading to abnormal gait mechanics and excessive strain on the Achilles tendon. Chiropractic adjustments help restore proper alignment and nerve function from the spine down.
    • Extremity Adjusting: We assess and correct joint restrictions in the ankle, subtalar joint, and foot. A stiff ankle or foot that overpronates can dramatically increase the load on the Achilles.
    • Soft Tissue Mobilization: Techniques like Graston or Active Release Technique (ART) can be applied to the calf muscles (gastrocnemius and soleus) and plantar fascia to reduce tension and improve tissue mobility, further offloading the healing tendon.
  • Guided Loading and Rehabilitation: The period after a brisement procedure is a critical window for healing. The tendon needs to be loaded progressively to stimulate organized collagen remodeling. We guide patients through a specific, evidence-based eccentric loading program, as pioneered by researchers like Alfredson et al. (1998). This involves controlled lengthening of the calf muscles, which has been shown to be highly effective in promoting tendon repair. Our rehabilitation team ensures the exercises are performed with perfect form to maximize benefit and prevent re-injury.
  • Functional Medicine Support: From my functional medicine perspective, we also address systemic factors that can impair healing. This includes nutritional counseling to ensure the patient has the necessary building blocks for collagen synthesis (e.g., vitamin C, proline, lysine, zinc) and managing systemic inflammation through diet and targeted supplementation.

This integrated model—combining Dr. Cardenas’s medical oversight for the injection, my procedural skills, our shared rehabilitation protocols, and a foundation of chiropractic and functional medicine—creates a powerful therapeutic cascade. We are not just treating the painful tendon; we are treating the whole person and the entire biomechanical system that contributed to the injury in the first place. This is the future of musculoskeletal medicine.


References

Alfredson, H., Pietilä, T., Jonsson, P., & Lorentzon, R. (1998). Heavy-load eccentric calf muscle training for the treatment of chronic Achilles tendinosis. The American Journal of Sports Medicine, 26(3), 360–366. https://doi.org/10.1177/03635465980260030301

Alfredson, H., & Ohberg, L. (2000). Neovascularisation in chronic painful patellar tendinosis–a descriptive study in a prospectively selected group of patients. Knee Surgery, Sports Traumatology, Arthroscopy, 8(4), 232-234. Note: This reference discusses patellar tendinosis, but the principle of neovascularization is central to the theory behind HVI for Achilles tendinopathy as well. https://doi.org/10.1007/s001670000128

Maffulli, N., & Spiezia, F. (2017). High-volume injection for the treatment of chronic Achilles tendinopathy. Operative Techniques in Sports Medicine, 25(2), 143-149. https://doi.org/10.1053/j.otsm.2017.03.011


Neuro-Immune Mechanism Research Findings Using a GLP-1 Antagonist


Discover the importance of the GLP-1 antagonist withing the neuro-immune mechanism in medical research and treatment.

Abstract

Recent advancements in metabolic health have introduced powerful GLP-1 receptor agonists like Retatrutide, offering significant hope for weight management. However, many individuals experience a perplexing and distressing side effect: severe skin sensitivity, a condition technically known as drug-induced cutaneous allodynia and hyperesthesia. This feels like a persistent, painful sunburn where even the slightest touch from clothing or bedsheets causes excruciating discomfort. Conventional approaches often miss the mark, treating this complex neuro-immune reaction with simple antihistamines, which may provide minimal relief while failing to address the root cause. This educational post, from my perspective as Dr. Alex Jimenez, will take you on a deep journey into the intricate physiological mechanisms driving this phenomenon. We will explore how Retatrutide, a triple agonist targeting GLP-1, GIP, and Glucagon receptors, throws a “grenade” into the delicate balance of your neuroendocrine-immune axis. Drawing upon the latest findings from leading researchers published in journals like Nature Metabolism and Cell Metabolism, we will dissect how these medications hypersensitize your peripheral nerves, lower the activation threshold for immune mast cells, create a pro-inflammatory environment through rapid fat loss, and disrupt crucial electrolyte balances, particularly magnesium, which is vital for nerve stability. This comprehensive exploration will move beyond a superficial understanding to provide a clear, evidence-based roadmap of what is happening inside your body. We will then transition into a detailed, practical, and integrative treatment strategy. This strategy combines dose adjustment, targeted hydration with specific electrolytes, and a powerful synergistic stack of neuro-regenerative and anti-inflammatory compounds, including Palmitoylethanolamide (PEA), Alpha-Lipoic Acid (ALA), Benfotiamine, and specific forms of Magnesium. Furthermore, I will explain how our unique multidisciplinary clinical model at Injury Medical Clinic, under the medical direction of Dr. Maria G. Cardenas, MD, integrates chiropractic care, functional medicine, and medical oversight to support the body’s structural and neurological integrity, offering a holistic path to resolving this debilitating sensitivity and restoring comfort and function.


Introduction: The Paradox of a Revolutionary Treatment

As a clinician with dual licensure in chiropractic (DC) and advanced practice nursing (FNP-BC), and certifications in functional medicine (CFMP, IFMCP), I stand at a unique intersection of healthcare. My work is dedicated to unraveling the complex web of human physiology to help patients not just manage symptoms, but achieve true, foundational health. This mission is shared and strengthened by our collaborative practice at Injury Medical Clinic PA in El Paso, Texas. Here, I work alongside Dr. Maria Guadalupe Cardenas, MD, a highly respected internist with over 40 years of experience and our Medical Director. Our integrated model allows us to blend the structural and neurological focus of chiropractic care with the deep medical insights and oversight of internal medicine, creating a comprehensive approach to patient wellness, especially in complex cases involving personal injury, chronic pain, and metabolic dysfunction.

Lately, my inbox and patient consultations have been filled with a recurring, distressing story. Patients starting on the new generation of weight-loss medications, specifically the potent triple-agonist Retatrutide, are describing a bizarre and painful side effect. They tell me their skin feels like it has been rubbed raw with sandpaper or that they have a severe, invisible sunburn. The sensation of their own clothes brushing against their skin becomes unbearable. This is not a simple rash or an allergic reaction with hives; this is a profound, nerve-based pain condition known as drug-induced cutaneous allodynia and hyperesthesia. Allodynia is a state where a stimulus that is not normally painful, like the touch of a cotton sheet, is perceived as painful. Hyperesthesia is an exaggerated sensitivity to any stimulus.

Unfortunately, many of these patients report that their primary care providers, while well-intentioned, are approaching this as a simple histamine reaction. They are prescribed antihistamines, which might slightly dull the edge of the discomfort (primarily through sedation) but do nothing to address the complex storm brewing within the nervous and immune systems. The patient is left sedated, still in pain, and deeply frustrated.

My purpose here is to illuminate the true nature of this condition. This is not a simple side effect; it is a profound biological response. Retatrutide and its cousins are not just appetite suppressants; they are powerful modulators of your entire neuroendocrine-immune axis. These drugs interact with receptors found on your peripheral nerves, your immune cells (like mast cells), and even within your central nervous system. When you introduce a powerful agonist like Retatrutide, you are essentially throwing a biological grenade into this intricate system.

In this educational journey, we will dissect exactly what is happening. We will explore groundbreaking research from 2022 and 2023 that reveals the precise mechanisms at play. You will understand:

  1. How these drugs directly “crank up” the excitability of the very nerve fibers responsible for sensing pain, touch, and temperature.
  2. How they make your immune system’s “border patrol”—the mast cells in your skin—”trigger-happy,” causing them to release inflammatory chemicals at the slightest provocation.
  3. How the rapid weight loss itself, while a desired outcome, creates a temporary but potent pro-inflammatory state that bathes your already-sensitized nerves in inflammatory signals.
  4. The critical and often-overlooked role of electrolyte depletion—specifically magnesium—in destabilizing your nerves and amplifying this painful response.

Understanding these mechanisms is the key to empowerment. It moves us from fear and confusion to clarity. This is not a sign that your body is “broken” or that you have a “contaminated” source of medication. This is your biology adapting—albeit painfully—in real time to a powerful new set of signals.

And most importantly, once we understand the “why,” we can effectively address the “how.” I will lay out a clear, actionable, evidence-based protocol to shut down this painful overreaction and restore balance to your system. This is not about simply masking the pain; it is about providing your body with the precise tools it needs to recalibrate and heal. We will discuss dose modulation, strategic hydration, and a specific combination of therapeutic compounds that work synergistically to quiet the nerves, stabilize the immune cells, and replenish the essential nutrients your nervous system is screaming for.

Finally, I will connect this functional medicine approach back to our integrated care model. We will discuss how integrative chiropractic care plays a vital supportive role by optimizing spinal cord and peripheral nerve function, reducing systemic stress through nervous system regulation, and ensuring the body’s structural framework can best support this profound physiological transition. Under Dr. Cardenas’s watchful medical eye, we can safely navigate these complex therapeutic landscapes, ensuring our patients not only achieve their weight-loss goals but do so with vibrant health and well-being.

Let’s begin this journey of understanding and healing.


The Neuro-Immune Cascade: Deconstructing Retatrutide’s Impact on Your Body

To truly grasp why your skin feels like it’s on fire, we must move beyond the surface and look at the intricate signaling network that Retatrutide targets. This drug is known as a triple agonist, meaning it activates three distinct receptor types: the Glucagon-Like Peptide-1 (GLP-1) receptor, the Glucose-dependent Insulinotropic Polypeptide (GIP) receptor, and the Glucagon (GCG) receptor. For decades, these were primarily understood in the context of blood sugar control and digestion. However, recent, cutting-edge research has revealed their profound and widespread influence throughout the body, particularly within the nervous and immune systems. These receptors are not just in your pancreas and gut; they are everywhere—on your skin, your peripheral nerves, your immune cells, your keratinocytes (skin cells), and woven throughout your central nervous system.

Taking a drug like Retatrutide is akin to sending a powerful, continuous “ON” signal to all these receptors simultaneously. Your body’s systems, which are accustomed to nuanced, pulsatile signaling, are suddenly flooded with a relentless command. The result is a cascade of events that culminates in the debilitating skin sensitivity you are experiencing. Let’s break down each component of this cascade, step by step, using the latest scientific evidence.

1. The Direct Assault on Your Nerves: GLP-1 Receptors and Peripheral Hyperexcitability

The first and most direct piece of the puzzle lies in the peripheral nerves themselves. These are the delicate nerve fibers that branch out from your spinal cord to every square inch of your body, including your skin. They are your interface with the world, responsible for transmitting sensations of touch, temperature, and pain.

For a long time, the prevailing thought was that the effects of GLP-1 agonists on the nervous system were primarily central, occurring within the brain. However, a landmark 2023 study published in the prestigious journal Nature Metabolism completely upended this view (Krieger et al., 2023). This research provided definitive proof that peripheral nerves are densely populated with GLP-1 receptors.

Specifically, the study identified these receptors on the very nerve fibers that are at the heart of your current misery:

  • C-fibers: These are small, unmyelinated nerve fibers that transmit the signals for dull, burning, or aching pain, as well as temperature and itch. When you feel that persistent, sunburn-like ache, your C-fibers are firing relentlessly.
  • A-delta fibers: These are slightly larger, thinly myelinated fibers that transmit sharp, pricking pain and cold sensations. These fibers carry the initial sharp sting you might feel when something touches your skin.

The critical takeaway here is that these sensory neurons are now known to be direct targets of Retatrutide. From the neuron’s perspective, it doesn’t matter that you took this medication to lose weight. It doesn’t understand the therapeutic intent. All it knows is that it has received a powerful, direct, and sustained signal to activate. The drug binds to the GLP-1 receptors on the nerve fiber’s membrane, triggering a series of intracellular events that fundamentally alter the neuron’s behavior.

The Cellular Mechanism of Hyperexcitability

Let’s get a bit more granular. When a GLP-1 agonist binds to its receptor on a sensory neuron, it initiates a signaling cascade inside the cell. This primarily involves an enzyme called adenylyl cyclase, which increases a secondary messenger molecule called cyclic AMP (cAMP). This surge in cAMP has several profound effects on the neuron:

  1. Lowering the Firing Threshold: A neuron’s resting state is maintained by a delicate balance of ions (like sodium, potassium, and calcium) across its membrane, creating what’s called the resting membrane potential. Increased cAMP, through a process involving Protein Kinase A (PKA), can phosphorylate (add a phosphate group to) various ion channels. This modification makes channels like the voltage-gated sodium channels easier to open. These sodium channels are the “gatekeepers” of nerve firing. By making them easier to open, the neuron’s firing threshold is lowered. It now takes a much weaker stimulus—the brush of a shirt, a change in air temperature—to cause the neuron to reach its action potential and fire a pain signal to the brain.
  2. Increased Neurotransmitter Release: When the nerve signal reaches the end of the neuron (the synapse), it triggers the release of neurotransmitters, which carry the signal to the next neuron in the chain, eventually reaching the spinal cord and brain. The same cAMP/PKA pathway enhances the release of excitatory neurotransmitters like glutamate and Substance P from the terminals of these sensory nerves. Substance P, in particular, is a potent pain-signaling molecule. So, not only are the nerves firing more easily, but when they do fire, they release a more potent chemical message, shouting “PAIN!” much louder to the central nervous system.
  3. Upregulation of Pain Receptors: Chronic stimulation can also change gene expression within the neuron. The cell can be signaled to produce more of the receptors and ion channels involved in pain signaling, such as the TRPV1 receptor. This receptor is famously activated by capsaicin (the “hot” in chili peppers) and heat. Upregulating TRPV1 makes the nerve ending exquisitely sensitive to thermal stimuli. This is why a warm shower can suddenly feel scaldingly hot.

In essence, the GLP-1 component of Retatrutide is directly “cranking up the gain” on your peripheral sensory nervous system. The nerves become hyperexcitable and sensitized. They no longer report sensations; they amplify them, turning gentle touch into a barrage of pain signals. This is the core reason for the allodynia and hyperesthesia. Your skin sensitivity isn’t an illusion; your nerves are biologically and biochemically reprogrammed to be in a state of high alert.

2. The Immune System on Edge: GIP Receptors and Mast Cell Degranulation

The second critical player in this painful symphony is the mast cell. Think of mast cells as the “border patrol” or the “first responders” of your immune system. They are strategically positioned in tissues that interface with the outside world: your skin, your gut lining, and your lungs. They stand guard, ready to sound the alarm at the first sign of trouble, be it a pathogen, an allergen, or tissue injury.

Each mast cell is a microscopic biological hand grenade, packed with tiny granules filled with a potent cocktail of inflammatory mediators. These include:

  • Histamine: Famous for its role in allergic reactions, causing itching, swelling, and vasodilation (widening of blood vessels).
  • Prostaglandins: Powerful signaling molecules that contribute to pain, fever, and inflammation.
  • Bradykinin: A peptide that is one of the most potent pain-producing substances known. It directly activates pain-sensing nerve fibers.
  • Substance P: The same pain neurotransmitter we discussed earlier. Mast cells can release it, which can, in turn, activate nerves and create a vicious feedback loop.
  • Tryptase and Chymase: Enzymes that can break down surrounding tissue and amplify the inflammatory response.

Under normal circumstances, mast cells have a high activation threshold. It takes a significant trigger—like a bee sting or a major allergen—to make them “degranulate” and release their inflammatory payload.

This is where the GIP (Glucose-dependent Insulinotropic Polypeptide) component of Retatrutide comes into play. Research has shown that, just like nerves, mast cells are covered in GIP receptors. When Retatrutide chronically stimulates these GIP receptors, it doesn’t necessarily cause the mast cells to degranulate spontaneously. Instead, it does something more insidious: it modulates and lowers their degranulation threshold.

Priming the Grenade: The “Trigger-Happy” Mast Cell

Constant GIP signaling primes mast cells, putting them on a hair trigger. The intracellular signaling pathways activated by GIP (which also involve cAMP, but can interact with other pathways like phospholipase C) effectively “pre-load” the degranulation machinery. The mast cells become what I call “trigger-happy.

Now, stimuli that the immune system would completely ignore become potent triggers. Consider the gentle pressure from the seam of your shirt, the slight change in temperature from a breeze, or the sensation of warm water in the shower. For a primed, trigger-happy mast cell, these innocuous physical stimuli are now sufficient to cross the lowered activation threshold.

And boom. The mast cell degranulates, releasing its inflammatory cocktail directly into your skin’s microenvironment. This phenomenon is known as local neurogenic inflammation. It’s “neurogenic” because it’s often initiated or amplified by the nerve activity we discussed earlier, creating a vicious cycle. Hyperexcitable nerves can release signals (like Substance P) that trigger mast cells, and mast cells release chemicals (like histamine and bradykinin) that further excite the nerves.

This creates a self-perpetuating firestorm in your skin:

  1. A light touch stimulates a hypersensitive nerve ending.
  2. The nerve firing, along with the physical pressure, is enough to trigger a “trigger-happy” mast cell to degranulate.
  3. The mast cell releases histamine, bradykinin, and prostaglandins.
  4. These inflammatory mediators directly activate more pain nerve endings, causing that burning, aching pain.
  5. They also make local blood vessels leaky, causing microscopic swelling and redness (even if not visible) and allowing more immune cells to enter the area.
  6. The result is a localized but intense inflammatory environment that further sensitizes the entire region.

This explains why the pain is not just a fleeting sensation but a persistent state of discomfort. Your skin is literally marinating in an inflammatory soup, continuously generated by an immune system put on high alert by the GIP component of your medication. The antihistamines prescribed by many doctors target only one small piece of this puzzle (histamine), which is why they provide such limited relief. They do nothing to stop the release of bradykinin, prostaglandins, or the other potent mediators, nor do they address the root cause: the lowered mast cell threshold.

3. The Inflammatory Fallout of Rapid Weight Loss

The third force multiplying this painful experience is a direct consequence of the drug’s success: rapid adipose reduction. Retatrutide is incredibly effective at promoting fat loss, but this process is not as “clean” as one might think. Your adipose tissue (body fat) is not just an inert energy storage depot. It is a highly active endocrine organ that produces and secretes a vast array of hormones and signaling molecules called adipokines.

In a state of metabolic health, adipose tissue secretes beneficial adipokines like adiponectin, which is anti-inflammatory and improves insulin sensitivity. However, in states of obesity, and paradoxically, during periods of very rapid weight loss, the adipose tissue becomes dysfunctional and shifts its production towards pro-inflammatory cytokines.

A crucial 2022 study in Cell Metabolism shed light on this exact phenomenon (Roh et al., 2022). The researchers demonstrated that rapid fat loss, whether through bariatric surgery or intense caloric restriction (which mimics the effect of GLP-1 agonists), creates a transient but potent pro-inflammatory cytokine environment.

Why Does Losing Fat Cause Inflammation?

As fat cells (adipocytes) shrink and die off (a process called apoptosis), they release their contents and send out distress signals. This attracts immune cells, particularly macrophages, which flock to the adipose tissue to “clean up” the debris from the dying fat cells. This process, while necessary, is inherently inflammatory. The macrophages themselves become activated and start churning out a flood of pro-inflammatory cytokines, including:

  • Tumor Necrosis Factor-alpha (TNF-α): A master regulator of inflammation that can directly sensitize pain neurons.
  • Interleukin-6 (IL-6): A key player in systemic inflammation that can cross the blood-brain barrier and influence central pain processing.
  • Interleukin-1beta (IL-1β): A powerful pro-inflammatory signal that is known to contribute to chronic pain states.

These cytokines don’t stay confined to your fat tissue. They spill out into your bloodstream, creating a state of low-grade systemic inflammation. Your entire body, including your skin and peripheral nerves, is now marinating in this inflammatory broth.

Now, connect this back to our first two points. You already have:

  1. Peripheral nerves that are hyperexcitable and on a hair trigger due to direct GLP-1 stimulation.
  2. Mast cells in your skin that are primed to degranulate at the slightest provocation due to GIP stimulation.

On top of this, you now introduce a systemic flood of TNF-α, IL-6, and IL-1β from your rapidly shrinking fat stores. These cytokines act as powerful sensitizing agents. They bind to their own receptors on the already-hyperexcitable nerves and mast cells, pouring gasoline on the fire. They further lower the activation thresholds, increase the expression of pain-related channels and receptors, and promote an even more robust inflammatory response.

This explains why the pain can feel so widespread and relentless. It’s the “perfect storm”: a convergence of direct nerve sensitization, localized immune hyper-reactivity, and systemic inflammation. The pain from your bedsheets is not just a local skin issue; it’s the final, agonizing expression of a body-wide state of neuro-immune dysregulation, driven by the medication and the very biological process of weight loss it initiates. It’s a case of the “cure” being faster than your biology can comfortably adapt, leading to significant collateral discomfort.

4. Amplifying the Pain Signal: Glucagon Receptors and the Dorsal Root Ganglion

The final piece of this triple-agonist puzzle is the activation of the Glucagon (GCG) receptor. To understand its impact, we need a quick trip into basic neuroanatomy.

As your peripheral sensory nerves travel from your skin towards the spinal cord, they don’t plug in directly. Instead, the cell bodies of these neurons are clustered together in a structure called the Dorsal Root Ganglion (DRG). The DRG sits just outside the spinal cord and acts as a critical “switchboard” or “gatekeeper” for all incoming sensory information—touch, pressure, temperature, and pain. Every signal from your periphery must pass through the DRG before it can be relayed up to the brain for processing.

What has become increasingly clear is that the neurons within the DRG are rich in glucagon receptors. When the glucagon agonist component of Retatrutide activates these receptors, it further modulates the excitability of the nociceptive (pain-sensing) neurons housed within the ganglion.

Cranking Up the Gain at the Central Switchboard

Think of the DRG as the volume knob for all incoming sensory data. The activation of glucagon receptors in the DRG essentially cranks up this volume knob. It makes the neurons within the ganglion more likely to fire and to transmit a stronger signal onward to the spinal cord.

The mechanism is similar to what we see in the peripheral nerve endings, involving changes in ion channel function and neurotransmitter release. Glucagon receptor activation can lead to central sensitization. This is a dangerous phenomenon where the central nervous system itself becomes hyperexcitable. Even after the initial peripheral stimulus is gone, neurons in the spinal cord and brain can remain highly reactive, essentially creating a “pain memory.”

So, the glucagon component of Retatrutide adds another layer of amplification to the pain signals:

  1. Peripheral Signal: The initial signal from the skin is already amplified due to GLP-1-induced nerve hyperexcitability.
  2. Local Inflammation: The signal is further intensified by the inflammatory soup created by GIP-triggered mast cells.
  3. DRG Amplification: As this already-loud signal arrives at the DRG, glucagon-induced hyperexcitability in the ganglion neurons amplifies it again before sending it to the brain.

It’s a triple-amplification system. A whisper of a touch at the skin becomes a deafening roar by the time it reaches the brain’s sensory cortex. This is not a malfunction. Your neurons are not broken, and the medication is not “contaminated.” This is the predictable, albeit extreme, physiological response to simultaneously and chronically activating three powerful signaling pathways that are deeply integrated into your body’s pain-processing network. Biology is rewriting its own set points in real time, and the discomfort is tangible evidence of that profound adaptation.

5. The Final Insult: Electrolyte Depletion and the Destabilized Nerve

One more crucial, often missed, piece of this puzzle ties everything together. It’s a factor that turns a sensitive system into an unstable one: electrolyte dysregulation.

GLP-1 agonists, as a class, have a known effect on the kidneys. They promote natriuresis, which is the excretion of sodium in the urine. As the saying goes, “where sodium goes, water follows.” This leads to a significant loss of both sodium and water, which is why proper hydration is so critical with these medications.

However, the story doesn’t end there. This diuretic effect also causes urinary loss of other critical electrolytes, most importantly intracellular magnesium. Magnesium is arguably the most important mineral for nervous system stability. It acts as a natural “calcium channel blocker” and a physiological shield for your nerves.

The Magnesium Shield: Guardian of the Resting Membrane Potential

To understand why magnesium is so vital, we need to revisit the concept of a neuron’s resting membrane potential. In its resting, non-firing state, a neuron maintains a negative electrical charge on the inside relative to the outside. This stable state is crucial. It ensures the neuron fires only when it receives a legitimate and sufficiently strong signal.

Magnesium plays a key role in maintaining this stability in several ways:

  1. Stabilizing the Membrane: Magnesium ions (Mg2+) physically associate with the phospholipids on the nerve cell membrane, helping to maintain its structural integrity and electrical stability.
  2. Blocking NMDA Receptors: At the synapse (the junction between two neurons), magnesium sits inside the channel of a key receptor called the NMDA receptor. This receptor is critical for learning, memory, and, importantly, amplifying pain signals (a process called “wind-up”). By plugging the channel, magnesium prevents the receptor from being easily activated. When magnesium levels are low, this “magnesium plug” is removed, leaving the NMDA receptor wide open. This leads to a massive influx of calcium into the neuron, which is a powerful “ON” signal that promotes hyperexcitability and can even be toxic to the cell (excitotoxicity).
  3. Regulating Ion Channels: Magnesium is essential for the proper function of the sodium-potassium pump (Na+/K+-ATPase). This enzyme actively pumps sodium out of the neuron and potassium in, which is the primary mechanism for re-establishing the resting membrane potential after a nerve has fired. Without adequate magnesium, this pump becomes sluggish, and the neuron struggles to return to its stable resting state, leaving it vulnerable to firing again with minimal provocation.

When you take a GLP-1 agonist that makes you excrete sodium, water, and crucially, magnesium, you are systematically stripping your peripheral nerves of their primary protective shield. The peripheral nerve sheaths lose their magnesium-electrolyte buffer.

The result? The resting membrane potential becomes destabilized. The neuron’s electrical footing becomes precarious. It’s like trying to stand on one leg on a wobbly surface. Everything can set it off. The very foundation of nerve stability is eroded.

Now, layer this on top of everything else we’ve discussed:

  • You have direct GLP-1 stimulation making the nerves hyperexcitable.
  • You have GIP-mediated mast cell degranulation creating local inflammation.
  • You have systemic inflammation from rapid fat loss.
  • You have central amplification at the DRG from glucagon.
  • And now, you have removed the fundamental electrochemical brake—magnesium—that is supposed to keep the entire system in check.

This is the final straw. The discomfort you feel is not just “damage” or an “allergy.” It is the culmination of a multi-system biological cascade. Your nervous system is stripped of its protective electrolyte shield and bombarded with excitatory signals from multiple angles, screaming for help. This is biology rewriting its set points in real time, and it’s painful. But the good news is that because it is a process based on clear physiological mechanisms, we can intervene. We can provide the body with the specific tools it needs to restore balance, re-establish the shield, and quiet the storm.


The Non-Surgical Approach to Wellness with Chiropractic Care- Video


The Integrative Solution: A Protocol to Reclaim Your Comfort

Understanding the complex web of interactions that causes this debilitating skin sensitivity is the first and most critical step. Now, we move to the solution. This is where my background in functional medicine shines, as we look to provide the body with the precise building blocks and signals it needs to restore homeostasis (internal balance). The goal is not to mask the pain with a drug but to fundamentally address each layer of the problem we have just uncovered.

This protocol is a multi-pronged attack designed to:

  1. Reduce the Agonist Load: Decrease the intensity of the signal being sent to the GLP-1, GIP, and Glucagon receptors.
  2. Re-establish the Electrolyte Shield: Aggressively replenish sodium, potassium, and magnesium, which are essential for nerve stability.
  3. Calm the Nerves and Immune Cells: Utilize targeted, evidence-based compounds that directly quell neuro-inflammation and stabilize mast cells.
  4. Support Nerve Regeneration and Function: Provide key B vitamins and antioxidants that protect nerves from damage and support their metabolic health.

Let’s break down each component of this comprehensive strategy.

Step 1: Cut the Dose, Not the Medication

The first and most logical step is to reduce the intensity of the signal that is causing the overstimulation. The painful sensitivity is a classic sign of a dose-response effect—you have exceeded your body’s ability to adapt to the current level of receptor agonism.

Action: Cut your current dose in half.

If you are taking 10 mg, reduce it to 5 mg. If you are on 5 mg, go down to 2.5 mg. This is not a step backward; it is a strategic retreat to allow your biological systems—your nerves, your mast cells, your entire neuro-immune axis—to catch up and re-regulate. The goal is to find the Minimum Effective Dose that still provides a therapeutic benefit for weight loss and metabolic control but does not push your nervous system over the edge into a state of painful hyperexcitability.

Many patients find they can still achieve excellent results on a lower dose, especially when combined with the supportive measures we are about to discuss. Once your symptoms have completely resolved (which may take several weeks), you can consider a very slow and gradual titration back up, paying close attention to your body’s signals. But for now, the immediate priority is to turn down the volume.

Step 2: Strategic Hydration—More Than Just Water

We’ve established that these medications cause you to lose significant amounts of sodium and water. The common advice to “just drink more water” is not only insufficient in this case—it can be counterproductive and even dangerous.

When you lose sodium and then flood your body with plain, electrolyte-free water, you further dilute the remaining electrolytes in your extracellular fluid. This lowers the electrolyte concentration outside your nerve cells, worsening the electrochemical imbalance and potentially exacerbating nerve firing. It’s a recipe for increased sensitivity. This condition is known as hyponatremia (low sodium), and it can have serious neurological consequences.

Action: Implement a protocol for aggressive, targeted electrolyte repletion.

The goal is to consume approximately four liters of fluid daily, but this fluid must be fortified with the specific electrolytes your body is losing. This is not about drinking a sugary sports drink; this is about creating a therapeutic oral rehydration solution.

Here is the specific, evidence-based recipe:

  • Four Liters of Water Daily: This is your fluid base. Use filtered water.
  • Five Grams of Sodium: This is the most critical component. This sounds like a lot, and it would be for someone with hypertension who is not on a GLP-1 agonist. But in this context, you are replacing what is being lost. You are not adding to a surplus. This is about restoring balance. Five grams of sodium is equivalent to about 12-13 grams of salt (sodium chloride), which is about 2.5 teaspoons. Spread this out throughout the day across your four liters of water. Do not consume it all at once. You can use high-quality sea salt or pink Himalayan salt, which also contain trace minerals.
  • Two Grams of Potassium Chloride: As you lose sodium, your body can also waste potassium to maintain electrochemical balance. Replenishing potassium is vital for nerve and muscle function, including the heart muscle. Potassium chloride is a readily available salt you can add to your water. Be precise with this measurement.
  • Flavoring (Optional): This solution will taste salty. You can add sugar-free flavor enhancers or a squeeze of lemon or lime to make it more palatable. The key is to avoid sugar, which would work against your metabolic goals.

This strategic hydration solution will do more than quench your thirst. It will begin to rebuild the crucial electrochemical environment around your nerves, providing the foundational stability they need to stop firing erratically. You should notice a significant improvement in your symptoms within a few days of implementing this correctly.

Step 3: The Synergistic Stack—Targeted Neuro-Immune Modulation

While re-establishing the electrolyte foundation is critical, we also need to actively calm the existing firestorm in your nerves and immune cells. This is where we bring in a powerful, synergistic stack of compounds that have been extensively researched for their neuroprotective, anti-inflammatory, and nerve-stabilizing properties.

A. Palmitoylethanolamide (PEA): The Body’s Own Anti-Inflammatory

PEA (Palmitoylethanolamide) is one of the most exciting and effective tools in our arsenal for this condition. It is an endogenous (meaning your body makes it) fatty acid amide that acts as a profound anti-inflammatory and analgesic (pain-relieving) agent. It’s often referred to as a “natural endocannabinoid” because it works through similar pathways, but without any psychoactive effects.

How PEA Works:

PEA’s genius lies in its ability to calm the “trigger-happy” mast cells we discussed earlier. It is a mast cell stabilizer. It signals the mast cell to raise its degranulation threshold back to normal levels. It doesn’t block a single mediator like an antihistamine; it prevents the release of the entire inflammatory cocktail—histamine, prostaglandins, bradykinin, and more—at the source.

Furthermore, PEA works “downstream” on other immune cells like microglia (the immune cells of the central nervous system) and macrophages, instructing them to switch from a pro-inflammatory state to an anti-inflammatory, pro-resolving state. It also directly affects neurons, helping reduce their hyperexcitability.

Clinical Application: PEA is remarkably safe and well-tolerated. For a condition this acute and severe, a high-dose loading protocol is necessary.

  • Dosing: 1200 mg per day, taken as 600 mg twice daily.
  • Formulation: Look for a micronized or ultra-micronized formulation. The PEA molecule is very large and fatty, so breaking it down into smaller particles significantly increases its absorption and bioavailability, making it far more effective.

PEA is the cornerstone of quieting the immune-driven component of your pain.

B. Magnesium: The Ultimate Nerve Shield

We’ve already established the critical importance of magnesium and how its depletion destabilizes your nerves. Replenishing it is non-negotiable. However, not all forms of magnesium are created equal. You must use a form that is highly bioavailable and, ideally, can cross the blood-brain barrier to also address central sensitization.

Action: Supplement with a dual-form magnesium complex.

  1. Magnesium Glycinate: This form is magnesium chelated (bound) to the amino acid glycine. This chelation makes it highly absorbable and gentle on the stomach (unlike magnesium oxide or citrate, which can have a laxative effect). Glycine itself is an inhibitory neurotransmitter in the central nervous system, meaning it has a calming effect. This makes magnesium glycinate an excellent choice for promoting relaxation, improving sleep, and calming an over-excited nervous system.
  2. Magnesium L-Threonate: This unique, patented form of magnesium has been shown in studies to effectively cross the blood-brain barrier and increase magnesium concentrations in the brain and spinal fluid (Slutsky et al., 2010). This is crucial for combating the central sensitization we discussed in the context of the DRG and glucagon receptors. It helps to restore the “magnesium plug” in the NMDA receptors within the central nervous system, dialing down pain amplification at its core.

Dosing Protocol:

  • Magnesium Glycinate: 400-600 mg of elemental magnesium per day. Take this in divided doses, with a larger portion in the evening to support sleep and muscle relaxation.
  • Magnesium L-Threonate: Follow the dosage instructions on the product, which is typically around 144-200 mg of elemental magnesium per day.

Combining these two forms provides a comprehensive approach, shoring up magnesium levels systemically and peripherally with glycinate while specifically targeting the central nervous system with threonate.

C. Alpha-Lipoic Acid (ALA): The Master Antioxidant for Nerve Health

Alpha-Lipoic Acid (ALA) is a unique and potent antioxidant because it is both water-soluble and fat-soluble. This means it can work in every part of the cell, including the fatty nerve membrane and the watery cytoplasm. It is particularly well-known for its benefits in treating diabetic neuropathy, another condition characterized by nerve pain and damage.

How ALA Works in This Context:

  1. Powerful Antioxidant: The inflammatory cascade we’ve described generates a massive amount of oxidative stress—an excess of free radicals that damage cell structures, including nerves. ALA is a master scavenger of these free radicals, protecting the nerve from further damage.
  2. Regenerates Other Antioxidants: ALA can regenerate other key antioxidants in the body, including Glutathione, Vitamin C, and Vitamin E, effectively recycling and amplifying the body’s own protective systems.
  3. Improves Nerve Blood Flow: ALA has been shown to improve blood flow to the nerves (endoneurial blood flow), delivering more oxygen and nutrients for repair and removing waste products.
  4. Reduces Nerve Excitability: Some research suggests ALA can directly modulate ion channels and reduce the hyperexcitability of sensory neurons, adding another layer of calming effect.

Clinical Application: To be effective for neuropathy, ALA must be used in its most bioactive form and at a therapeutic dose.

  • Formulation: Use the R-ALA form. ALA exists in two forms (isomers), R-ALA and S-ALA. The R-ALA form is naturally found in the body and is significantly more biologically active. Most standard ALA supplements are a 50/50 mix of R-ALA and S-ALA. Sourcing pure R-ALA is superior.
  • Dosing: 600 mg per day. This is the standard therapeutic dose used in most clinical trials for neuropathy. It can be taken once daily.

ALA provides crucial protection for your nerves, shielding them from the inflammatory and oxidative damage while supporting their intrinsic healing processes.

D. Benfotiamine: The Nerve-Nourishing B-Vitamin

The final component of our core stack is Benfotiamine. This is not your standard B1 (thiamine) vitamin. It is a fat-soluble derivative of thiamine with much higher bioavailability and can penetrate nerve cells far more effectively than regular thiamine.

Thiamine is absolutely critical for nerve cell metabolism. It is a key cofactor in converting glucose into energy (ATP) within the mitochondria—the cell’s powerhouses. Nerves are incredibly metabolically active and have a huge energy demand.

How Benfotiamine Works:

In states of inflammation and metabolic stress (like the one we are in), nerve cells can struggle to metabolize glucose properly. This leads to the buildup of harmful metabolic byproducts, such as Advanced Glycation End-products (AGEs). These AGEs are sticky, dysfunctional molecules that gum up the works, causing cellular damage, inflammation, and nerve dysfunction. This is a primary mechanism of damage in diabetic neuropathy.

Benfotiamine works by activating an enzyme called transketolase. This enzyme shunts the harmful metabolic precursors away from the pathways that form AGEs and into a safe, alternative metabolic route called the pentose phosphate pathway.

In essence, Benfotiamine does two things:

  1. Prevents Nerve Damage: It stops the formation of toxic AGEs, protecting the nerve from further inflammatory and metabolic damage.
  2. Boosts Nerve Energy: By optimizing glucose metabolism, it helps nerve cells produce the energy they need to function properly, maintain their ion pumps, and repair themselves.

Clinical Application:

  • Dosing: 600 mg per day, often taken as 300 mg twice daily. This high dose is necessary to saturate the tissues and achieve a therapeutic effect on the transketolase enzyme.

Benfotiamine is the metabolic fuel and protector for your stressed-out nerves. It ensures they have the energy to heal and the protection from the toxic byproducts of inflammation.


The Role of Integrative Chiropractic Care in Systemic Balance

Now that we have a robust functional medicine protocol to address the biochemical and immunological roots of the problem, it’s essential to discuss the structural and neurological component of care. This is where my role as a Doctor of Chiropractic (DC) becomes integral to a truly holistic solution. The central nervous system—the brain and spinal cord—is the body’s master control system, including the peripheral nerves and the immune system. The health and proper function of the spine are directly linked to the health and function of the nervous system.

At our practice, Injury Medical Clinic PA, this is the core of our philosophy. Under the medical direction of Dr. Maria Cardenas, we create a patient-centered plan that respects the interplay between the body’s structure (chiropractic) and its chemistry (functional and internal medicine). When dealing with a profound neuro-immune reaction like Retatrutide-induced sensitivity, chiropractic care provides several key supportive benefits.

1. Optimizing Spinal Function and Nerve Flow

The spinal cord is the main highway for all nerve signals traveling between the brain and the body. The peripheral nerves that are currently firing in your skin originate from nerve roots that exit the spinal column. Any structural or functional issue in the spine—what we in chiropractic call a vertebral subluxation complex—can interfere with the normal flow of nerve information.

A subluxation is not necessarily a “pinched nerve” in the dramatic sense. It is a more subtle condition involving a vertebra that has lost its normal position or motion, leading to a cascade of effects:

  • Altered Mechanical Input: The mechanoreceptors (nerve endings that sense position and movement) in the joints and muscles around the dysfunctional spinal segment send aberrant or noisy signals back to the central nervous system.
  • Local Inflammation: Joint dysfunction can create localized inflammation around the nerve roots.
  • Muscle Spasm: Protective muscle splinting can further restrict movement and contribute to pain.

In a patient who is already experiencing systemic nerve hyperexcitability, even a minor degree of spinal dysfunction can act as an additional source of “static” or “noise” in the nervous system, further contributing to central sensitization.

Our Chiropractic Approach:

Through gentle, specific chiropractic adjustments, we aim to restore normal motion and alignment to the spinal segments. This is not about “cracking backs”; it is a precise neurological intervention. The goals of the adjustment in this context are:

  • Improve Segmental Motion: Restore the normal biomechanics of the spinal joints.
  • Stimulate Mechanoreceptors: The gentle, high-velocity, low-amplitude thrust of an adjustment bombards the central nervous system with a flood of normal proprioceptive (position sense) and mechanoreceptive input. This can help to “gate” or override the pain signals coming from the periphery, a concept known as the Gate Control Theory of Pain.
  • Reduce Neurological Interference: By correcting the subluxation, we reduce the aberrant signaling from the spinal level, helping to quiet the overall “noise” in the nervous system.

By ensuring the spinal column functions optimally, we create a clearer, more stable pathway for nerve communication, reducing one potential source of amplification in the pain cascade.

2. Modulating the Autonomic Nervous System

The nervous system has two main divisions: the sympathetic (fight or flight) system and the parasympathetic (rest and digest) system. In chronic pain and inflammation, the sympathetic nervous system tends to dominate. This sympathetic dominance itself contributes to the problem: it promotes inflammation, sensitizes pain receptors, and keeps the body in a state of high alert.

Chiropractic adjustments have been shown to modulate the Autonomic Nervous System (ANS) strongly. Research using measures like Heart Rate Variability (HRV)—a key indicator of autonomic balance—has demonstrated that spinal adjustments can shift the ANS away from sympathetic dominance and towards a more parasympathetic state (Welch & Boone, 2008).

Why This Matters for Retatrutide Sensitivity:

  • Promoting a Rest and Heal” State: By promoting a parasympathetic shift, we help to move the entire body out of a state of high alert and into a state conducive to healing and repair. This is the physiological state where inflammation is resolved, and tissues are rebuilt.
  • Reducing Systemic Stress Hormones: Sympathetic dominance is associated with elevated levels of stress hormones like cortisol and adrenaline. When chronically elevated, these hormones can further dysregulate the immune system and sensitize nerves. A parasympathetic shift helps to lower these hormones.
  • Improving Immune Regulation: The parasympathetic system, via the vagus nerve, plays a direct role in regulating inflammation through a pathway known as the “cholinergic anti-inflammatory pathway.” Stimulating this pathway can help down-regulate the production of pro-inflammatory cytokines like TNF-α—the same cytokines released by shrinking adipose tissue.

Through chiropractic care, we are not just treating a spinal issue; we are using the spine as a lever to influence and rebalance the body’s master control system, creating a systemic environment that is less reactive and more resilient.

3. Adjunctive Therapies for Neuro-Muscular Re-education

In addition to spinal adjustments, our integrated approach incorporates rehabilitative therapies designed to support the neuromuscular system. In chronic pain, the body often adopts dysfunctional movement patterns and muscle guarding.

  • Soft Tissue Therapies: Techniques like myofascial release, trigger point therapy, and massage can help to release chronic muscle tension, improve local circulation, and reduce peripheral sources of pain. For patients with severe allodynia, these therapies must be modified to be extremely gentle, often starting with lymphatic drainage techniques to reduce inflammation before moving to deeper work.
  • Therapeutic Exercise: Once the acute sensitivity begins to subside, we introduce specific, gentle exercises. The goal is not to “push through the pain” but to re-educate the nervous system. Gentle stretching and range-of-motion exercises help to send normal, non-painful movement signals to the brain, helping to “rewire” the sensitized pathways. This process of graded motor imagery and gentle movement is a cornerstone of modern pain rehabilitation.

This comprehensive, integrative model ensures we address the patient from every possible angle—biochemically with functional medicine, structurally and neurologically with chiropractic care, and medically under Dr. Cardenas’s supervision. This synergy allows us to unravel complex conditions like Retatrutide-induced sensitivity and guide our patients back to comfort, function, and vibrant health.


Conclusion: A Path Forward

The experience of severe skin sensitivity from a medication like Retatrutide can be frightening and isolating. It feels as though your own body has turned against you. However, as we have explored in depth, this is not a random or malicious event. It is a predictable physiological cascade set in motion by the powerful, multifaceted actions of a triple-agonist drug. It is the tangible result of direct nerve sensitization, immune cell priming, systemic inflammation from rapid fat loss, central amplification, and the erosion of your nervous system’s essential electrolyte shield.

The conventional approach of simply prescribing an antihistamine fails because it sees only a tiny sliver of this complex picture. It targets one mediator, from one cell type, and ignores the vast, interconnected network of neuro-immune dysfunction.

The path forward lies in an integrative and functional approach that respects and addresses this complexity. It begins with the simple, logical step of reducing the dose to lessen the provocative signal. It is built upon the non-negotiable foundation of strategic electrolyte and fluid repletion to restore the very electrochemical stability your nerves depend on. It is then powerfully augmented by a synergistic stack of targeted nutraceuticals—PEA to calm the mast cells, dual-form Magnesium to shield the nerves centrally and peripherally, R-alpha-lipoic acid to fight oxidative stress, and benfotiamine to fuel and protect nerve metabolism.

Finally, this biochemical strategy is woven together with the structural and neurological support of integrative chiropractic care. By optimizing spinal function, balancing the autonomic nervous system, and re-educating movement patterns, we ensure the body’s master control system is functioning at its peak, creating an internal environment that fosters healing and resilience.

This entire process, from diagnosis to the implementation of complex protocols, is conducted under the collaborative oversight of our Medical Director, Dr. Maria Cardenas, ensuring the highest standards of safety and clinical efficacy. Our multidisciplinary clinic is designed for precisely these kinds of complex cases, where the solution lies at the intersection of different fields of knowledge.

If you are experiencing these symptoms, know that you are not alone; you are not imagining it, and there is a clear, evidence-based path back to comfort. It requires a deeper understanding of your own biology and a commitment to providing your body with the specific tools it needs to recalibrate. The health journey is not always a straight line, but with the right map and the right support, balance can be restored.


References

Krieger, J. P., Chavarría-Cardona, D., Lickert, S., et al. (2023). Peripheral GLP-1 receptor signaling is a key driver of GLP-1 receptor agonist-induced nausea. Nature Metabolism, 5(8), 1338–1353. [https://doi.org/10.1038/s42255-023-00847-y](https://doi.org/10.1038/s42255-023-00847-y)

Roh, E., Kim, J., Kim, M. J., et al. (2022). A transient pro-inflammatory macrophage response in subcutaneous adipose tissue is associated with favorable metabolic outcomes after bariatric surgery. Cell Metabolism, 34(7), 1014-1025.e6. [https://doi.org/10.1016/j.cmet.2022.05.011](https://doi.org/10.1016/j.cmet.2022.05.011)

Slutsky, I., Abumaria, N., Wu, L. J., Huang, C., Zhang, L., Li, B., … & Liu, G. (2010). Enhancement of learning and memory by elevating brain magnesium. Neuron, 65(2), 165-177. [https://doi.org/10.1016/j.neuron.2009.12.026](https://doi.org/10.1016/j.neuron.2009.12.026)

Welch, A., & Boone, R. (2008). Sympathetic and parasympathetic responses to specific diversified chiropractic adjustments to the atlas and sacrum in asymptomatic subjects: a pilot study. Journal of Chiropractic Medicine, 7(3), 86-93. [https://doi.org/10.1016/j.jcm.2008.04.002](https://doi.org/10.1016/j.jcm.2008.04.002)


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