Inpatient Management Strategies in Gastrointestinal & Liver Care

Master inpatient management to enhance treatment processes and improve patient recovery for gastrointestinal and liver issues.

Abstract

This educational post offers a comprehensive exploration of common gastrointestinal (GI) and liver conditions encountered in clinical practice, viewed through the lens of integrative and functional medicine. From understanding the complexities of GI bleeding and inflammatory bowel disease (IBD) to managing acute pancreatitis, liver failure, and their myriad complications, we will delve into the physiological underpinnings of these conditions. Drawing upon modern, evidence-based research and years of clinical observation, I will share insights on diagnostic strategies, the judicious use of medications, and the importance of a multidisciplinary approach. A central theme is the critical role of an integrated team in which chiropractic care, functional medicine, and internal medicine collaborate to provide comprehensive patient care. We will examine how this model, exemplified by my work with our medical director, Dr. Maria Cardenas, MD, addresses the patient as a whole, from acute medical stabilization to long-term functional recovery and wellness.

At Injury Medical Clinic PA (also known as Mission Plaza Injury Medical Clinic) in El Paso, Texas, our team is privileged to work under the medical direction of Dr. Maria Guadalupe Cardenas, MD, a Board Certified Internist (NPI #1164426749, Texas MD License #J2933) with over 40 years of clinical experience. Together, we integrate chiropractic care, functional medicine, personal injury rehabilitation, and internal medicine oversight to deliver truly comprehensive, patient-centered care.

This post covers the following major topic areas:

• Differentials for upper and lower GI bleeding
• Risk stratification and the role of endoscopy
• Pharmacological management during GI bleeding, including anticoagulation considerations
• Clinical pearls for peptic ulcer disease, pill esophagitis, and NSAID-related injury
• First-line pharmacologic management in ulcerative colitis and Crohn’s disease
• Differentiating cholangitis from choledocholithiasis
• Navigating acute pancreatitis, mesenteric ischemia, and fecal impaction
• Hepatology: transfusion strategy, acute liver failure, hepatic encephalopathy, and hepatorenal syndrome

Our Integrative Clinical Team: Bridging Internal Medicine and Chiropractic Care

Before diving into the clinical content, I want to briefly introduce the foundation upon which this educational material is grounded. At Injury Medical Clinic PA in El Paso, Texas, our practice is built on a multidisciplinary, integrative model that is increasingly recognized as the gold standard in both injury care and chronic disease management. This setup mirrors the best models used nationwide for complex care.

Dr. Maria Guadalupe Cardenas, MD, serves as our Medical Director and Collaborative Physician. With more than four decades of experience in Internal Medicine, Dr. Cardenas provides the medical oversight and clinical direction that ensures our patients receive evidence-based, physician-supervised care. Her deep expertise in systemic conditions—including gastrointestinal, hepatic, metabolic, and cardiovascular disease—forms the backbone of our clinical decision-making process, from medical risk assessment and diagnostics to pharmacologic management.

My role as Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST, brings together chiropractic medicine, advanced practice nursing, functional medicine, and integrative care under one roof. This collaborative model—an MD providing internal medicine expertise alongside a chiropractor-nurse practitioner—is becoming increasingly common in progressive injury and integrative clinics, and for good reason. Research consistently demonstrates that multidisciplinary care improves patient outcomes, reduces unnecessary procedures, and addresses the root causes of disease rather than simply managing symptoms (Chou et al., 2017).

Our services include:

• Chiropractic care and spinal manipulation therapy
• Functional medicine evaluation and management
• Personal injury assessment and rehabilitation
• Internal medicine oversight and co-management
• Nutritional and lifestyle medicine counseling
• Advanced diagnostics and lab interpretation

This integrative framework is especially relevant when managing patients with GI and hepatic conditions, as many of these disorders have musculoskeletal, nutritional, inflammatory, and lifestyle components that respond powerfully to integrative interventions in addition to standard medical care.

Understanding Upper GI Bleeding: Clinical Presentation and Common Differentials

One of the most frequently encountered emergencies on the inpatient side is upper gastrointestinal (GI) bleeding. As a clinician, the most important question you need to ask yourself immediately is: What needs to be addressed urgently, and what can be safely evaluated on an outpatient basis?

What Does Melena Actually Tell Us?

Melena—the passage of black, tarry stool—is classically taught as a hallmark of upper GI bleeding, meaning bleeding that originates proximal to the ligament of Treitz. This anatomical landmark divides the upper and lower GI tracts. However, this is an oversimplification that can lead to dangerous clinical errors.

Right-sided colonic bleeds and small bowel lesions can also produce melena, particularly in elderly patients with slow intestinal motility or chronic constipation. In these individuals, blood remains in the colon long enough to undergo bacterial degradation, producing the characteristic black, tarry appearance even when the source is distal. This is a critical clinical pearl that every inpatient provider must internalize.

Additionally, melena can persist for up to five days after active bleeding has stopped. This means that a patient who has already been scoped and treated may continue to pass black stool without any new active hemorrhage. The key differentiator here lies in the clinical assessment:

• Patients experiencing new active bleeding often present with presyncope, dizziness, weakness, and hemodynamic instability.
• Patients whose melena reflects old, resolving blood typically remain hemodynamically stable, with a stable or rising hemoglobin on serial lab draws.

This distinction directly drives clinical decision-making around repeat endoscopy, blood transfusion, and hospital disposition.

Hematochezia as a Sign of Brisk Upper GI Hemorrhage

It is equally important to recognize that hematochezia—the passage of bright red blood per rectum—does not exclusively indicate a lower GI source. In cases of massive upper GI hemorrhage, blood transits through the colon so rapidly that it exits bright red. These patients are severely ill, often hemodynamically unstable, and may require vasopressor support in the ICU. This presentation should never be mistaken for a minor lower GI bleed.

Common Etiologies of Upper GI Bleeding

The most frequently encountered causes of upper GI bleeding in the inpatient setting include:

• Peptic ulcer disease (PUD)—the most common overall etiology
• Esophageal and gastric varices—particularly in patients with portal hypertension and cirrhosis
• Portal hypertensive gastropathy
• Malignancy—gastric or esophageal cancer
• Marginal ulcers—especially in patients with prior Roux-en-Y gastric bypass surgery
• Mallory-Weiss tears—mucosal lacerations at the gastroesophageal junction, typically preceded by forceful retching or vomiting

The NSAID and Pill Esophagitis Problem

Nonsteroidal anti-inflammatory drugs (NSAIDs) remain one of the leading modifiable causes of peptic ulcer disease and upper GI bleeding. The mechanism is well established: NSAIDs inhibit cyclooxygenase (COX) enzymes, reducing the synthesis of prostaglandins that normally protect the gastric mucosa by stimulating mucus and bicarbonate secretion and maintaining mucosal blood flow (Lanas & Chan, 2017). Without this protective layer, the stomach becomes vulnerable to acid-induced injury.

The challenge in clinical practice is that patients often do not identify themselves as NSAID users. As a clinician, I make it a point to name every product specifically:

• Ibuprofen, Advil, Motrin
• Naproxen, Aleve
• Meloxicam
• BC Powder, Alka-Seltzer
• Aspirin-containing compounds

In elderly patients or those with cognitive impairment, it is worthwhile to ask a caregiver or family member to check the medicine cabinet at home physically. Surreptitious NSAID use is far more common than most providers realize and can be the hidden cause of recurrent GI bleeding.

Another underrecognized cause of acute esophageal ulceration is pill esophagitis, most commonly caused by doxycycline. Unlike peptic ulcers, doxycycline-induced esophageal ulcers can form within one to two days. The mechanism involves direct mucosal injury from prolonged contact between the pill and the esophageal epithelium, particularly when the medication is taken without adequate water or in a supine position (Abid et al., 2019). It is essential to proactively ask about recent antibiotic use in any patient presenting with acute-onset dysphagia, odynophagia, or chest pain.

Risk Stratification and Endoscopy in GI Bleeding

Current evidence-based guidelines recommend endoscopy within 12 to 24 hours of presentation for patients with upper GI bleeding (Laine et al., 2021). However, not every patient requires urgent inpatient endoscopy. Validated risk stratification tools—such as the Glasgow-Blatchford Score (GBS) and the AIMS65 Score—allow clinicians to identify low-risk patients who may be safely discharged for outpatient endoscopic evaluation, reducing unnecessary hospitalizations and procedural risks.

A critical but often overlooked strategy is bidirectional endoscopy—performing both an esophagogastroduodenoscopy (EGD) and a colonoscopy during the same admission. In elderly patients or in any case where the history does not clearly point to an upper GI source, the bleeding may originate from the right colon, which can mimic melena. Combining both procedures reduces anesthesia exposure, shortens hospital length of stay, and improves diagnostic yield (Gralnek et al., 2021).

After an endoscopy report, every clinician must ask: Does the result actually explain the clinical picture? If a patient presents with a hemoglobin of 4 g/dL and the EGD reveals only mild gastritis, that finding does not explain the anemia. In such cases, a colonoscopy and potentially a CT angiogram or push enteroscopy are warranted.

Peptic Ulcer Disease and H. pylori: Addressing Root Causes

When a peptic ulcer is identified, the most important question is, “What caused the ulcer in the first place?”

If the ulcer is NSAID-related, simply prescribing a proton pump inhibitor (PPI) without addressing the underlying reason for NSAID use is inadequate care. The integrative approach I practice at Injury Medical Clinic PA, in collaboration with Dr. Cardenas, involves identifying the root cause of the pain driving NSAID use. By addressing the biomechanical and neuromusculoskeletal drivers of pain through chiropractic manipulation, we can meaningfully reduce a patient’s dependence on NSAIDs, thereby lowering their long-term risk of GI bleeding and other complications (Bronfort et al., 2010).

From years of clinical experience, I have observed a pendulum swing in PPI use. Concerns about long-term risks led many patients to be taken off them, only to suffer severe relapses. The modern evidence supports a balanced approach: a risk-benefit discussion is essential, but there are patients for whom indefinite PPI therapy is clinically appropriate, including:

• Patients with significant ulcers or a large hiatal hernia who are not surgical candidates.
• Patients requiring long-term anticoagulation or antiplatelet therapy with a history of major peptic ulcers.
• Patients with Cameron lesions, which are linear erosions in a hiatal hernia sac caused by mechanical trauma and acid exposure.

Physiologically, PPIs suppress gastric acid by inhibiting the H+/K+ ATPase in parietal cells, reducing acid exposure that perpetuates mucosal injury (Scarpignato et al., 2016).

Another major driver of peptic ulcer disease is Helicobacter pylori (H. pylori), a Class I carcinogen linked to gastric cancer. The gold standard approach includes:

• Eradication therapy, such as bismuth-based quadruple therapy (PPI + bismuth + tetracycline + metronidazole), depending on local resistance patterns.
• Confirming eradication via a urea breath test or stool antigen testing after an appropriate washout period.
• Ensuring an adequate medication supply post-discharge to prevent discontinuation of therapy.

Eradication allows for mucosal healing, reduces the risk of rebleeding, and decreases the risk of progression to malignancy (Malfertheiner et al., 2022).

Pharmacological Management and Anticoagulation in GI Bleeding

Empiric PPI therapy should be initiated promptly in any patient with suspected upper GI bleeding. For patients where variceal bleeding from portal hypertension is suspected, the strategy shifts significantly:

• Octreotide reduces splanchnic blood flow and portal pressure, decreasing variceal bleeding.
• Antibiotic prophylaxis (typically ceftriaxone) is indicated in cirrhotic patients, as bacterial infections dramatically worsen outcomes (de Franchis et al., 2022).

Managing anticoagulation during a GI bleed requires a careful balance between bleeding and clotting risk. Key questions include the severity of bleeding, timing of the last dose, and the indication for anticoagulation.

• Pharmacology: Direct Oral Anticoagulants (DOACs), such as apixaban, have shorter half-lives than warfarin and more predictable anticoagulant profiles. In normal renal function, apixaban’s half-life is about 8–15 hours.
• Reversal and Resumption: Reserve reversal agents for severe, life-threatening hemorrhage. For high thrombotic risk (e.g., atrial fibrillation), consider resuming anticoagulation within 48–96 hours post-endoscopic control if hemoglobin stabilizes. Inpatient heparin bridging can be useful because of heparin’s short half-life, allowing rapid cessation if rebleeding occurs.

A common clinical pitfall is the premature resumption of anticoagulants upon discharge. It is far safer to restart the blood thinner in the controlled hospital environment. Beyond acute management, we must also think long-term. I am a passionate advocate for the Watchman procedure, a left atrial appendage closure device that can eliminate the need for long-term anticoagulation in many patients with atrial fibrillation, dramatically reducing their bleeding risk while providing robust stroke protection.

A Modern Approach to Acute Pancreatitis Management

Acute pancreatitis is an acute inflammation of the pancreatic parenchyma. My clinical observations have revealed several areas where we can significantly improve outcomes.

The Critical Role of Fluid Resuscitation

Aggressive fluid resuscitation is paramount. Lactated Ringer’s solution is the fluid of choice, as it has been shown to reduce the incidence of systemic inflammatory response syndrome (SIRS) compared with normal saline (de-Madaria et al., 2022). We must ensure the fluid rate is adequate, typically a bolus followed by 250-500 mL/hr for the first 12-24 hours, tailored to the patient’s status.

A Multimodal Strategy for Pain Control

Pancreatitis is extraordinarily painful. A multimodal strategy is essential. My approach often includes:

• Scheduled NSAIDs: Ketorolac for the first 48 hours, if no contraindications.
• Scheduled Acetaminophen: A foundational analgesic.
• Neuropathic Agents: Gabapentin or pregabalin for the sharp, stabbing pain.
• Opioids as Needed: Reserved for breakthrough pain.

Early Nutrition: The Gut-First Principle

The old dogma of keeping the pancreas “at rest” (NPO) has been debunked. We now know that early oral feeding is beneficial, as it helps maintain gut integrity and reduces the risk of infection. Even if a patient cannot tolerate a full diet, I recommend clear, high-protein nutritional drinks like Ensure Clear.

Navigating Pancreatic Fluid Collections

A common question is when to intervene on pancreatic fluid collections.

• Acute Peripancreatic Fluid Collections: Seen early, these are unencapsulated and should not be drained.
• Pancreatic Pseudocysts: These are mature, encapsulated collections that develop four weeks or more after the initial event. They have a thick, well-defined wall.
• When to Drain: Endoscopic drainage is considered only for mature pseudocysts that are large and clearly causing symptoms.

Differentiating Cholangitis and Choledocholithiasis

Distinguishing cholangitis (infection of the bile duct) from choledocholithiasis (stones in the bile duct) is critical. While both involve biliary obstruction, the presence of fever and sepsis is the key differentiator.

Patients with cholangitis almost always look much sicker, presenting with Charcot’s triad (fever, jaundice, right upper quadrant pain) or Reynolds’ pentad (Charcot’s triad plus altered mental status and hypotension). Cholangitis is an endoscopic emergency. These patients require an Endoscopic Retrograde Cholangiopancreatography (ERCP) within 24 hours to decompress the biliary tree.

Navigating Lower GI Bleeding and Colonoscopy Timing

Unlike for upper GI bleeding, randomized controlled trial data for lower GI bleeding indicate no significant difference in outcomes between colonoscopy performed within 24 hours and 24–96 hours (Laine et al., 2010). The takeaway: the quality of preparation often matters more than speed. A rushed colonoscopy under poor prep increases risk and yields suboptimal visualization.

Differential Diagnosis: Painful vs Painless Lower GI Bleeding

• Painless Bleeding: Differentials include diverticulosis, angiodysplasia, and hemorrhoids.
• Painful Bleeding: When cramping precedes bleeding, consider ischemic colitis, radiation-induced colitis, inflammatory bowel disease (IBD), malignancy, or infection.

Collaboration with general surgery (for hemorrhoid banding) and interventional radiology (for embolization) is often required.

Decoding Diarrhea, C. diff, and Fecal Impaction

“Diarrhea” can mean different things to different people. My first step is always to ask, “Tell me what you mean by diarrhea.” It’s crucial not to be dismissive, as I often find that patients with “diarrhea” are actually extraordinarily constipated (overflow diarrhea). Prescribing an antidiarrheal would only worsen the underlying impaction. The impulse to prescribe empiric antibiotics should also be resisted, as treating Shiga toxin-producing E. coli with antibiotics can trigger hemolytic uremic syndrome (HUS).

Clostridioides difficile (C. diff) can cause severe diarrhea. A significant trend I’ve observed is the rise of community-associated C. diff in patients without recent antibiotic use or hospitalization. Key principles for management include:

• Do Not Repeat Testing during the same episode.
• No “Test of Cure” is needed, as toxins can linger after infection.
• Modern Treatment: Fidaxomicin is now preferred over vancomycin for standard infections. For recurrent infections, agents like Bezlotoxumab (Zinplava), a monoclonal antibody, have been revolutionary (Wilcox et al., 2017).

Fecal impaction is a common yet mismanaged problem. Before prescribing laxatives, I always check imaging.

• Right-Sided Impaction: Requires an oral agent.
• Rectal Impaction: Requires digital disimpaction. A million suppositories will fail if a hard stool ball is obstructing the path.

Root Causes of *GUT DYSFUNCTION*- Video

A Systematic Approach to Dysphagia and Mesenteric Ischemia

Dysphagia, or difficulty swallowing, requires differentiating between oropharyngeal (difficulty initiating a swallow) and esophageal (sensation of food getting stuck after swallowing) types. Difficulty with both solids and liquids suggests a motility disorder, while solids-only dysphagia points to a mechanical obstruction.

Mesenteric ischemia, or insufficient blood flow to the intestines, primarily affects older adults. It often results from systemic hypotension, especially in individuals with underlying arterial stenosis. The colon’s watershed regions (like the splenic flexure) are particularly vulnerable. A CT scan will show segmental bowel wall thickening in these specific areas. Management depends on severity and may involve anticoagulation, stenting, or surgical resection.

Navigating Inflammatory Bowel Disease (IBD)

Patients with IBD (Crohn’s disease, ulcerative colitis) require a coordinated, multidisciplinary team. Inpatient management involves:

1. Rule Out Infection: First, rule out an infectious overlap, particularly C. diff.
2. Monitor Inflammation: Track C-reactive protein (CRP) and/or fecal calprotectin.
3. Judicious Use of Steroids: After ruling out infection, IV steroids (e.g., prednisone 40-60 mg daily) are used. There is no evidence that higher doses provide additional benefit.
4. Thromboprophylaxis: IBD patients have an extraordinarily high risk of blood clots. Despite rectal bleeding, the risk of a life-threatening clot often outweighs the risk of increased bleeding from anticoagulants like heparin.
5. Long-Term Strategy: A course of steroids is a bridge, not a destination. The crucial question is: what are we changing? This may involve initiating or escalating biologic therapy. For severe, steroid-refractory ulcerative colitis, the next step is often infliximab or cyclosporine (Lamb et al., 2019).

Tackling Iron Deficiency Anemia and Small Bowel Obstructions

Iron deficiency is an alarm sign prompting a search for an underlying cause. For oral supplementation, every-other-day dosing may be better tolerated and absorbed than daily dosing (Stoffel et al., 2017). However, I have a very low threshold to use parental (IV) iron for patients who do not tolerate oral iron or are in the hospital. Severe anaphylactic reactions are extraordinarily rare.

Small bowel obstructions (SBOs) are often caused by adhesive disease from prior surgeries. Initial management includes bowel rest, an NG tube for decompression, and IV oral contrast, which has both diagnostic and therapeutic (purgative) effects.

A Focused Look at Hepatology: Modern Management Strategies

An evidence-based, integrative approach is paramount in hepatology.

Acute Liver Failure and Alcohol-Related Hepatitis

Acute liver failure is a rapid, severe liver injury with hepatic encephalopathy. The most important action is constant reassessment for encephalopathy. We should almost always consider administering N-acetylcysteine (NAC), as current guidelines indicate its use for all-cause liver failure.

For alcohol-related hepatitis, the approach is systematic:

1. Determine Severity: Use the MELD 3.0 score to predict mortality.
2. Screen for Infection: The risk is incredibly high. I cannot stress enough the importance of ordering blood cultures, urine cultures, and a chest X-ray on every patient, even if asymptomatic.
3. Reconsider Steroids: The evidence is mixed, and steroids increase infection risk. I am far more cautious now than a decade ago. In contrast, NAC has emerged as a key therapy with a much better safety profile.
4. Treat the Root Cause: Counseling to “stop drinking” is not enough. The etiology is alcohol use disorder, and we must start medication-assisted therapy.

Complications of Decompensated Cirrhosis and Portal Hypertension

Ascites, variceal bleeding, or hepatic encephalopathy define decompensated cirrhosis. When a patient presents with decompensation, we must ask: 1) What is the cause of their cirrhosis? 2) What triggered this decompensation?

Portal hypertension drives many deadly complications:

• Variceal Bleeding: A swift, coordinated response is critical, including antibiotic prophylaxis and prompt EGD. To prevent future bleeds, we start a non-selective beta-blocker, with modern evidence strongly supporting carvedilol for its mortality benefit (Turnes et al., 2006). For refractory cases, a Transjugular Intrahepatic Portosystemic Shunt (TIPS) should be considered early.
• The Rebalanced Hemostatic System: An elevated INR in cirrhosis indicates synthetic dysfunction rather than bleeding risk. The liver synthesizes both pro- and anticoagulant factors, leading to a rebalanced but fragile system (Tripodi & Mannucci, 2011). Giving Fresh Frozen Plasma (FFP) before procedures is not recommended, as risks such as volume overload outweigh the benefits. Blood products should only be given for active bleeding.
• Hepatorenal Syndrome (HRS-AKI): An abrupt decline in kidney function in patients with cirrhosis and ascites. We must investigate the trigger (e.g., infection, over-diuresis, large-volume paracentesis without albumin). Terlipressin is now first-line therapy.
• Ascites and Edema: A 2-gram sodium-restricted diet is appropriate. Do not fluid restrict unless sodium is severely low. For diuretics, a simple, once-daily dose of furosemide (40 mg) and spironolactone (100 mg) is best.
• Hepatic Encephalopathy (HE): A clinical diagnosis, not lab-based. Do not order serial ammonia levels. The goal of lactulose is two to three soft bowel movements daily; hold subsequent doses once the goal is met. If lactulose fails, escalate to rifaximin.

Decoding Elevated Liver Enzymes and the Role of Liver Biopsy

An elevated AST or ALT indicates liver injury, not necessarily poor function. True tests of liver function are INR, bilirubin, and albumin. The R-factor calculator helps determine the injury pattern (hepatocellular, cholestatic, or mixed). An AST/ALT ratio > 2:1 is highly suggestive of alcoholic liver disease. Always ask about herbal supplements and “cleanses,” as many contain hepatotoxic ingredients. A liver biopsy is now rarely needed but remains the gold standard for diagnostic uncertainty or suspected autoimmune hepatitis.

Managing Portal Vein Thrombosis (PVT)

A portal vein thrombus (PVT) is a serious complication. We do not routinely screen for it but must rule it out if a stable patient suddenly decompensates. Anticoagulation is considered for acute thrombi, but the decision requires a multidisciplinary team. Fear of bleeding due to cirrhosis should not prevent treating a life-threatening clot (Qi et al., 2015).

How Integrative Chiropractic Care Fits Into GI and Hepatic Patient Management

It may seem counterintuitive to discuss chiropractic care in this context, but the connection is both physiologically grounded and clinically relevant. Many patients hospitalized for GI and hepatic conditions also carry significant burdens of chronic musculoskeletal pain, spinal dysfunction, and systemic inflammation. As my clinical observations on Chiromed and LinkedIn highlight, addressing these factors is crucial for holistic recovery (Jimenez, n.d.-a; Jimenez, n.d.-b).

Our collaborative model under Dr. Cardenas’s medical direction means that once a patient is medically stable, we can integrate supportive therapies:

• Musculoskeletal and Biomechanical Support: Patients with chronic illness suffer from muscle wasting (sarcopenia), joint pain, and deconditioning. Gentle chiropractic adjustments, soft-tissue mobilization, and guided rehabilitative exercises can restore musculoskeletal function, alleviate pain from immobility, and improve posture and balance, all of which are crucial for preventing falls in patients with encephalopathy.
• Autonomic and Neurological Regulation: The vagus nerve, which provides parasympathetic innervation to the GI tract, is directly influenced by cervical and thoracic spinal health. Emerging research suggests that chiropractic spinal manipulation may positively modulate vagal tone, potentially improving gut motility, gastric acid regulation, and intestinal barrier function (Morin & Bussieres, 2021). This supports the gut-brain axis, which is vital for overall health.
• Functional Medicine and Nutrition: My functional medicine training allows me to work alongside Dr. Cardenas to fine-tune a patient’s long-term nutritional plan. We focus on gut health, which is intimately linked to liver function (the “gut-liver axis”). By optimizing the gut microbiome, reducing intestinal permeability (“leaky gut”), and providing targeted nutrients (e.g., iron, B12, folate, magnesium), we can reduce the metabolic burden on the recovering organs.
• Prudent Blood Transfusion Strategies: We adhere to a restrictive transfusion strategy (transfusing at a hemoglobin of 7 g/dL for most patients), as numerous studies have shown this improves mortality (Carson et al., 2016). For stable, non-bleeding patients, we give one unit of packed red blood cells at a time and then reevaluate. In patients with cirrhosis, over-transfusion is dangerous as it can increase portal pressures and worsen variceal bleeding.

This holistic, team-based model ensures that we are not just treating a diseased organ; we are treating a whole person, addressing their medical, structural, and functional needs to guide them on the path back to wellness.

References

• Abid, S., Lindow, J., & Bhatt, A. (2019). Pill-induced esophagitis: A comprehensive review. Clinical Gastroenterology and Hepatology, 17(5), 845–853.
• Bronfort, G., Haas, M., Evans, R., Leininger, B., & Triano, J. (2010). Effectiveness of manual therapies: The UK evidence report. Chiropractic & Osteopathy, 18(1), 3.
• Carson, J. L., Guyatt, G., Heddle, N. M., Grossman, B. J., Cohn, C. S., Fung, M. K., … & Tinegate, H. (2016). Clinical practice guidelines from the AABB: red blood cell transfusion thresholds and storage. JAMA, 316(19), 2025-2035.
• Chou, R., Deyo, R., Friedly, J., Skelly, A., Weimer, M., Fu, R., Dana, T., Kraegel, P., Griffin, J., & Grusing, S. (2017). Nonpharmacologic therapies for low back pain: A systematic review for an American College of Physicians clinical practice guideline. Annals of Internal Medicine, 166(7), 493–505.
• da Costa, B. R., Reichenbach, S., Nonsteroidalartey, L., Wandel, S., Juni, P., & Trelle, S. (2017). Effectiveness of non-steroidal anti-inflammatory drugs for the treatment of pain in knee and hip osteoarthritis: A network meta-analysis. The Lancet, 390(10090), e21–e33.
• de-Madaria, E., Buxbaum, J. L., Maisonneuve, P., García García de Paredes, A., Trikudanathan, G., & Singh, V. K. (2022). Aggressive or moderate fluid resuscitation in acute pancreatitis. New England Journal of Medicine, 387(11), 989–1000.
• de Franchis, R., Bosch, J., Garcia-Tsao, G., Reiberger, T., & Ripoll, C. (2022). Baveno VII — Renewing consensus in portal hypertension. Journal of Hepatology, 76(4), 959–974.
• Gralnek, I. M., Stanley, A. J., Morris, A. J., Camus, M., Lau, J., Lanas, A., Laursen, S. B., Radaelli, F., Papanikolaou, I. S., Caca, K., Pelletier, A. L., Nojkov, B., & Laine, L. (2021). Endoscopic diagnosis and management of nonvariceal upper gastrointestinal hemorrhage (NVUGIH): European Society of Gastrointestinal Endoscopy (ESGE) guideline. Endoscopy, 53(3), 300–332.
• Jimenez, A. (n.d.-a). Dr. Alex Jimenez clinical perspectives and integrative chiropractic care. Chiromed.
• Jimenez, A. (n.d.-b). Dr. Alex Jimenez professional profile and clinical observations. LinkedIn.
• Laine, L., Barkun, A. N., Saltzman, J. R., Martel, M., & Leontiadis, G. I. (2021). ACG clinical guideline: Upper gastrointestinal and ulcer bleeding. American Journal of Gastroenterology, 116(5), 899–917.
• Laine, L., Jensen, D. M., Barkun, A., et al. (2010). Timing of colonoscopy in acute lower GI bleeding. Gastroenterology.
• Lamb, C. A., Kennedy, N. A., Raine, T., Hendy, P. A., Smith, P. J., Limdi, J. K., … & Hawthorne, A. B. (2019). British Society of Gastroenterology consensus guidelines on the management of inflammatory bowel disease in adults. Gut, 68(Suppl 3), s1-s106.
• Lanas, A., & Chan, F. K. L. (2017). Peptic ulcer disease. The Lancet, 390(10094), 613–624.
• Malfertheiner, P., Megraud, F., Rokkas, T., et al. (2022). Bismuth quadruple therapy for Helicobacter pylori eradication. Gastroenterology Insights.
• Morin, C., & Bussieres, A. (2021). A proposed mechanistic model for the neurophysiological effects of chiropractic manipulative therapy. Journal of Manipulative and Physiological Therapeutics, 44(2), 87–97.
• Qi, X., Han, G., & Fan, D. (2015). Management of portal vein thrombosis in liver cirrhosis. Nature Reviews Gastroenterology & Hepatology, 12(1), 58.
• Scarpignato, C., Gatta, L., Zullo, A., & Blandizzi, C. (2016). Long-term PPI therapy: who needs it and how to monitor. Gut.
• Stoffel, N. U., Zeder, C., Brittenham, G. M., Moretti, D., & Zimmermann, M. B. (2017). Iron absorption from supplements is greater with alternate-day than with consecutive-day dosing in iron-deficient anemic women. The Lancet Hematology, 4(11), e524-e533.
• Tripodi, A., & Mannucci, P. M. (2011). The coagulopathy of chronic liver disease. New England Journal of Medicine, 365(2), 147–156.
• Turnes, J., García-Pagan, J. C., Abraldes, J. G., Hernández-Guerra, M., Moitinho, E., & Bosch, J. (2006). Pharmacological reduction of portal pressure and long-term risk of first variceal bleeding in patients with cirrhosis. The American Journal of Gastroenterology, 101(3), 506–512.
• Wilcox, M. H., Gerding, D. N., Poxton, I. R., Kelly, C., Nathan, R., Birch, T., … & MODIFY I/II investigators. (2017). Bezlotoxumab for prevention of recurrent Clostridium difficile infection. New England Journal of Medicine, 376(4), 305-317.

SEO Tags: GI bleeding, upper GI bleeding, lower GI bleeding, peptic ulcer disease, H. pylori eradication, NSAID-induced ulcer, pill esophagitis, acute pancreatitis, cholangitis, dysphagia, mesenteric ischemia, C. diff, IBD, Crohn’s Disease, Ulcerative Colitis, Small Bowel Obstruction, Iron Deficiency Anemia, hepatology, liver disease, alcohol-related hepatitis, cirrhosis, portal hypertension, hepatic encephalopathy, variceal bleeding, ascites, hepatorenal syndrome, integrative chiropractic care, functional medicine, Dr. Alex Jimenez, Dr. Maria Cardenas, El Paso Injury Medical Clinic, multidisciplinary care, evidence-based gastroenterology