Inpatient Management for Gastrointestinal & Liver Health

Discover best practices for inpatient management and improve clinical results in gastrointestinal and liver function.

Abstract

In this comprehensive educational post, I will guide you through the complex, high-stakes world of inpatient gastroenterology and hepatology. I’m Dr. Alex Jimenez, and from a first-person clinical perspective, we will journey through the latest evidence-based findings from leading researchers, translating them into clear, actionable insights. We will explore the management of critical conditions including upper and lower GI bleeding, the nuances of anticoagulation management, severe inflammatory bowel disease flares, acute pancreatitis, and the full spectrum of advanced liver disease complications like hepatic encephalopathy, variceal bleeding, and hepatorenal syndrome. This post will also clarify the subtleties of interpreting liver labs, managing challenging issues like fecal impaction, and developing a structured approach to dysphagia. A central theme is the power of our integrative and multidisciplinary approach at Injury Medical Clinic PA. I will detail how we combine advanced chiropractic care, functional medicine, and personalized rehabilitation with the expert medical oversight of our Medical Director, Dr. Maria Guadalupe Cardenas, MD. This collaborative model is essential for managing the systemic effects of these complex conditions, ensuring our patients in El Paso, Texas, receive holistic, modern, and effective care.

Our Integrated Care Model: Chiropractic, Medical, and Functional Medicine Synergy

At Injury Medical Clinic PA, also known as Mission Plaza Injury Medical Clinic, our philosophy is rooted in a deeply collaborative and integrative approach to healthcare. My journey and extensive training across multiple disciplines—from a Doctor of Chiropractic (DC) to an Advanced Practice Registered Nurse (APRN) and a Board-Certified Family Nurse Practitioner (FNP-BC), along with certifications in Functional Medicine (CFMP, IFMCP) and other specialized fields—have shaped my understanding that the human body is an interconnected system. No single specialty holds all the answers.

This is why I am proud to work alongside Dr. Maria Guadalupe Cardenas, MD (NPI #1164426749, Texas MD License #J2933), our esteemed Medical Director and Collaborative Physician. Dr. Cardenas is a highly respected, board-certified Internist with over 40 years of invaluable experience. Her role is crucial; she provides the hospital-grade medical oversight that allows us to safely and effectively manage a wide range of conditions, from acute injuries to chronic diseases. This multidisciplinary partnership, in which an MD provides medical direction alongside a chiropractor, is a cornerstone of modern integrative and injury-care clinics.

Our team at Injury Medical Clinic integrates:

• Internal Medicine Oversight (Dr. Maria Cardenas, MD): Providing medical diagnosis, prescription management, supervision of care protocols, and complex case supervision for GI and hepatic patients needing high-acuity coordination.
• Integrative Chiropractic and Functional Medicine (Dr. Alex Jimenez, DC, APRN, FNP-BC): Focusing on musculoskeletal alignment, nervous system function, biomechanics, and investigating the root causes of disease through a functional lens.
• Gastroenterology/Hepatology Consultation Pathways: For urgent endoscopy and inpatient protocols.
• Personal Injury and Rehabilitation: Offering specialized care for accident-related injuries and restoring function safely.

This structure allows us to bridge the gap between different disciplines. For a patient with chronic GI issues, I might provide chiropractic adjustments to improve spinal function and autonomic balance, while Dr. Cardenas manages their medical conditions and medications. Our functional medicine approach would then guide us in creating a nutritional and lifestyle plan to address underlying inflammation. It’s a holistic model designed for optimal patient recovery and wellness, with insights and collaborative pathways often shared via my LinkedIn and the educational resources at healthcoach.clinic.

Part 1: Navigating Gastrointestinal Bleeding

Upper GI Bleeding: Recognizing Urgency, Stabilizing Physiology, and Choosing the Right Path

Upper GI bleeding is one of the most common and high-stakes inpatient scenarios. I start with one decisive question: Which cases demand immediate scope and intensive care, and which can be stabilized and transitioned to outpatient evaluation?

• Key Clinical Distinctions:

• • Melena (dark, tarry stools) usually indicates bleeding proximal to the ligament of Treitz (upper GI), but slow transit in older adults can make right-sided colon bleeding appear as melena.
  • Melena can persist for up to 5 days after bleeding stops, so patient status matters more than stool color after endoscopy.
  • Hematochezia (bright red blood per rectum) in an unstable patient can reflect a brisk upper GI bleed—these patients may be hypotensive, tachycardic, and require ICU-level resuscitation.

• Immediate Stabilization:

• • • Assess hemodynamics, orthostatic symptoms, and serial hemoglobin
    • Start Proton Pump Inhibitors (PPIs) empirically; low risk, potentially high yield in suspected ulcer bleeding.
    • If portal hypertension is suspected (cirrhosis with variceal risk), initiate octreotide and antibiotic prophylaxis (e.g., ceftriaxone) to reduce infection-triggered variceal bleeding morbidity.
    • Arrange urgent endoscopy within 12–24 hours when criteria are met—this window is key to diagnostic accuracy and therapeutic intervention.

• Physiologic Underpinnings:

• • In ulcer bleeding, gastric acid perpetuates mucosal injury. PPIs stabilize the clot by raising gastric pH, reducing pepsin activity, and enhancing platelet aggregation at the site of bleeding, as detailed in Laine’s 2009 review on Proton pump inhibitor therapy in upper GI bleeding.
  • Portal hypertensive bleeding results from elevated portal venous pressures. Octreotide decreases splanchnic blood flow, reducing portal pressure and active bleeding, an effect demonstrated in randomized trials on Octreotide in variceal hemorrhage.

• My Bedside Decision-Making Pearls:

• • Evaluate whether the endoscopic finding matches the clinical situation. A tiny non-bleeding gastric ulcer does not explain a hemoglobin of 4 g/dL—broaden the search.
  • Use risk stratification scores, such as the Glasgow-Blatchford Score, to identify low-risk patients suitable for outpatient pathways, thereby minimizing unnecessary admissions.

Rethinking Long-Term Proton Pump Inhibitor (PPI) Therapy

For years, PPIs have been lifesavers, but growing concern over long-term risks has led some clinicians to de-prescribe them, sometimes with serious consequences. In my practice, I always emphasize a risk-benefit discussion.

There are specific scenarios where the benefits of indefinite PPI therapy unequivocally outweigh the risks:

• Patients with Significant Ulcers: Especially those who are asymptomatic and lack warning signs.
• Patients with Large Hiatal Hernias: Particularly those who are not surgical candidates. The mechanical defect creates a persistent risk. A large hiatal hernia containingCameron’ss ulcers (linear ulcers in the hernia sac) is a classic cause of profound iron deficiency anemia.
• Patients on Long-Term Anticoagulation or Antiplatelet Therapy: If they have a history of a significant peptic ulcer, a PPI is a crucial protective measure.

Medication History That Saves Lives: NSAIDs, Hidden Aspirin, and Pill Esophagitis

I regularly find preventable causes in the medication cabinet. Many patients do not know what “NSAID” stands for.

• Practical Approach: Ask specifically about ibuprofen, naproxen, meloxicam, Aleve, Advil, BC powder, Alka-Seltzer, and any combination cold-or-pain products.
• Pill Esophagitis: Doxycycline is a common culprit and can cause pill esophagitis, leading to rapid ulcer formation within 1–2 days. Ask about recent antibiotic use and administration habits (taking pills with minimal water or lying down quickly).
• Physiologic Perspective: NSAIDs inhibit COX-1, reducing prostaglandin synthesis and impairing mucosal blood flow, as described in the literature on the mechanisms of NSAID-induced gastropathy. Doxycycline’s local caustic effect is amplified by prolonged esophageal contact.
• Integrative Alternatives: Do not simply command: “Stop NSAIDs.” Provide viable pain strategies such as topical NSAIDs, chiropractic care for biomechanical pain, and evidence-based nutraceuticals like curcumin (Curcumin anti-inflammatory evidence) and boswellia, always coordinated with Dr. Cardenas for safety.

The Critical Role of H. pylori Eradication

Helicobacter pylori is a primary cause of gastric cancer and recurrent ulcers. It is imperative to test for and treat it effectively. The standard of care is now quadruple therapy, and it is equally important to perform eradication testing to confirm that the infection is gone. A crucial aspect of care is ensuring that patients are discharged with an adequate supply of medication, as treatment gaps can lead to recurrence.

Endoscopy Strategy: When to Add Colonoscopy and Advanced Imaging

When melena persists without a clear upper GI source, I consider colon prep early, especially in elderly patients, to reduce anesthesia exposure if a colonoscopy is ultimately needed.

• Bidirectional Endoscopy: If an EGD shows only mild gastritis that doesn’t account for severe anemia, proceed with colonoscopy.
• Advanced Imaging: If both scopes are nondiagnostic, obtain CT angiography in GI bleeding to evaluate for ectopic varices or small-bowel masses.
• Push Enteroscopy: When necessary, repeat the upper endoscopy with push enteroscopy to visualize deeper portions of the duodenum and proximal jejunum.

Pharmacologic Management During GI Bleeding: Anticoagulation Strategies

This is one of the most delicate balancing acts we face. The modern literature supports a balanced approach.

• Immediate Steps:

• • Hold anticoagulants temporarily; reverse based on agent and severity.
  • Warfarin: vitamin K and prothrombin complex concentrate (PCC).
  • Direct oral anticoagulants (DOACs): use specific reversal agents like idarucizumab or andexanet alfa in life-threatening situations. Reviewing Anticoagulant reversal strategies is key.
  • Evaluate thromboembolic risk (e.g., CHA2DS2-VASc, recent stents) to plan early resumption. A heparin drip, with its short half-life, is a safe way to “pressure test” the system before resuming long-acting agents.

• Case Study Example: A 72-year-old male on apixaban for atrial fibrillation presents with melena and a hemoglobin of 6.8 g/dL. An EGD reveals a large hiatal hernia with Cameron’s ulcers. This patient needs lifelong PPI therapy. The most delicate part is resuming his anticoagulant. I would consider restarting it within 48-72 hours after his hemoglobin stabilizes, often using a heparin bridge to provide thrombotic protection while minimizing bleeding risk. I have seen patients suffer devastating strokes because their anticoagulation was held for too long. Stopping a blood thinner is an active decision with its own set of potentially fatal consequences.
• The Watchman Procedure: This scenario also presents an opportunity to ask a crucial question: Can we find a safer, long-term alternative? For many individuals on blood thinners for atrial fibrillation, I am a strong advocate for the Watchman procedure, a left atrial appendage closure device that reduces stroke risk without the need for long-term anticoagulation.

Lower GI Bleeding: Differentials, Risk, and Timely Intervention

Lower GI bleeding differentials include diverticular hemorrhage, angiodysplasia, colitis (infectious/ischemic/IBD), hemorrhoids, and malignancy. The approach emphasizes hemodynamic assessment first, followed by early CTA in brisk bleeding to enable interventional radiology embolization, and colonoscopy after bowel prep when stabilized.

• Timing the Colonoscopy: Unlike upper GI bleeds, the urgency for a colonoscopy in lower GI bleeds is different. A randomized trial in Gastroenterology found no significant difference in outcomes between urgent colonoscopy (<24 hours) and elective colonoscopy (24-96 hours). This gives us time to optimize the bowel prep, which is far more beneficial than rushing into an inadequate procedure.
• Painless vs. Painful Bleeding: The presence or absence of pain is a critical diagnostic clue.

• • Painless: Think diverticulosis, angiodysplasias (Angiodysplasia pathophysiology), or internal hemorrhoids.
  • Painful: Consider ischemic colitis (pain often precedes bleeding), radiation-induced colitis, IBD, malignancy, or infectious colitis.

• Multidisciplinary Management: Lower GI bleeds often require collaboration with interventional radiology and general surgery. Getting the surgical team involved early, even for potential outpatient follow-up, is always a good strategy.

Part 2: Complex GI and Hepatobiliary Conditions

Decoding Patient Symptoms: Diarrhea or Constipation?

A patient might report “diarrhea,” but it’s our job to dig deeper. I always start by asking, “Tell me what you mean by diarrhea.” It’s crucial to understand frequency, consistency (using the Bristol Stool Chart), and urgency.

You might be surprised how often severe constipation masquerades as diarrhea. This is overflow diarrhea, where liquid stool leaks around an impacted mass. In this case, prescribing an anti-diarrheal medication would be the worst possible course of action. When true diarrhea is present, we must consider infectious causes, ischemia, and IBD.

Navigating C. Difficile and the Prudent Use of Antibiotics

Clostridioides difficile, or C. diff, can cause debilitating colitis. I am now seeing a significant rise in community-associated C. diff in patients with no recent antibiotic history, so do not let a lack of exposure dissuade you from testing.

A critical point is the danger of empirically prescribing antibiotics for undiagnosed diarrhea. If caused by a Shiga toxin-producing organism, antibiotics can trigger hemolytic uremic syndrome (HUS). For a confirmed C. diff diagnosis, Fidaxomicin is now preferred over vancomycin. There is no role for repeat testing during the same episode or for a “test of cure” after treatment.

The Overlooked Problem of Fecal Impaction

The key to management is understanding the location. Before ordering laxatives, I always pull up the patient’s imaging.

• Right-Sided Impaction: This patient needs an oral osmotic laxative, such as Miralax, to push the stool through from above.
• Rectal Impaction: No amount of oral laxatives will work until the distal obstruction is cleared. This is where digital disimpaction is essential. Many clinicians hesitate, but it is often the most critical step.

A common clinical error is holding laxatives because a patient with a known impaction is having “diarrhea.” This is almost always overflow diarrhea. Holding laxatives only worsens the underlying problem.

Dysphagia: Oropharyngeal Versus Esophageal – How I Differentiate

Clarifying the dysphagia subtype guides testing, as per Dysphagia evaluation standards.

• Oropharyngeal Dysphagia: Difficulty initiating the swallow, with coughing, choking, or nasal regurgitation. This often points to a neurologic issue. Order a videofluoroscopic swallow study.
• Esophageal Dysphagia: Sensation of food sticking after initiation.

• • Solids-only suggests a mechanical obstruction (stricture or ring).
  • Both solids and liquids suggest a motility disorder (achalasia). Evaluate with EGD, barium esophagram, and high-resolution manometry.

Acute Pancreatitis: Fluids, Pain, and Feeding

The cornerstones of management are:

1. Aggressive Fluid Resuscitation: Lactated RRinger’sis the fluid of choice. Proper resuscitation helps prevent progression to necrotizing pancreatitis.
2. Multimodal Pain Control: Layering different medications is the gold standard. I use scheduled NSAIDs (if kidney function allows), scheduled acetaminophen, and neuropathic agents like gabapentin, reserving opioids for breakthrough pain.
3. Early Enteral Nutrition: The old dogma of keeping the pancreas “at rest” is debunked. Early feeding helps maintain gut barrier integrity. Aim to start oral feeding as soon as tolerated.

Intervention for pancreatic fluid collections is only considered if they are mature pseudocysts (>4 weeks) and causing symptoms.

Cholangitis Versus Choledocholithiasis: How I Differentiate

• Choledocholithiasis: A stone in the common bile duct, which may be stable.
• Acute Cholangitis: Biliary obstruction plus infection. The key differentiator is often fever and signs of sepsis. Charcot’s triad (fever, jaundice, RUQ pain) is classic, but in the elderly, subtle signs like new-onset confusion or diaphoresis should raise suspicion. Cholangitis is an endoscopic emergency requiring ERCP within 24 hours for decompression, as per the Tokyo Guidelines for cholangitis.

Understanding Mesenteric Ischemia

This serious condition predominantly affects older adults, often in the context of systemic hypotension. The colon’s watershed regions (splenic flexure, rectosigmoid junction) are most susceptible. A CT scan often shows bowel wall thickening in these specific areas, a major clue pointing toward ischemia.

Part 3: The Spectrum of Liver Disease

Rationalizing Lab Draws and Differentiating Liver Injury from Function

One of the most underappreciated aspects of inpatient care is managing lab draws. Fragmented, scattered draws reduce circulating red blood cell mass and increase the risk of iatrogenic anemia. I teach clinicians to consolidate draws and to separate “liver injury” from “liver function” markers.

• Liver Injury Markers: Elevated ALT/AST reflect hepatocellular damage. ALP and GGT rise with cholestasis.
• Liver Function Markers: Bilirubin, albumin, and INR reflect the liver’s synthetic and excretory functions. Worsening bilirubin and INR suggest declining hepatic function, not merely injury. As outlined in reviews on liver test interpretation, this distinction is crucial for prognosis.

The R-factor (ALT / ULN) ÷ (Alk Phos / ULN) is a simple calculation that helps determine the pattern of injury: hepatocellular, cholestatic, or mixed, which dramatically narrows the differential diagnosis.

The Hidden Culprits: Supplements, Herbs, and Medications

A meticulous patient history is one of the most powerful diagnostic tools. I ask my patients very specifically: “What are you putting into your body that isn’t food or water?” This includes juices, shakes, powders, and teas. Unregulated “liver cleanse” products are a common cause of severe drug-induced liver injury (DILI).

Acute Liver Failure: Criteria and Rapid Response

ALF is defined by the acute onset of hepatic injury, coagulopathy (INR> 1.5), and encephalopathy in a patient without preexisting cirrhosis. Immediate steps include identifying the etiology (acetaminophen, viral hepatitis, etc.), managing complications, and making an early referral to a transplant center. N-acetylcysteine (NAC) is indicated for all-cause liver failure, not just acetaminophen toxicity, as it replenishes glutathione stores and improves microcirculatory blood flow. Further reading can be found in reviews on Acute liver failure management.

Alcohol-Related Hepatitis: Severity, Infection Risk, and Treatment

This is among the most common diagnoses in adult inpatient medicine. An AST: ALT ratio greater than 2:1 is highly specific for alcohol-mediated injury. We use the MELD score to stratify severity. A key principle is to screen all patients for infection (blood/urine cultures, chest X-ray), as the risk of infection exceeds 20% and hepatitis itself mimics infection.

The role of steroids is evolving. Multiple trials have shown mixed results, and steroids increase infectious risk. N-acetylcysteine is now strongly favored. Most importantly, counseling a patient to stop drinking is not treatment. Effective management requires medication-assisted therapy (MAT) and psychiatric support.

Decompensated Cirrhosis and Its Complications

Decompensation is the development of ascites, variceal hemorrhage, or hepatic encephalopathy. Every case demands an inquiry into its precipitating cause (alcohol recidivism, DILI, portal vein thrombosis, or hepatocellular carcinoma).

Hepatic Encephalopathy (HE): Triggers, Treatment, and Clinical Pearls

HE is a neuropsychiatric complication from the accumulation of ammonia and other neurotoxins. Common precipitants include GI bleeding, infection, constipation, electrolyte disturbances, and sedative use.

• Lactulose and Rifaximin: Lactulose traps ammonia in the gut, but over-administration must be avoided. Set clear hold parameters (e.g., hold if >3 bowel movements/day). Rifaximin reduces ammonia production by gut bacteria and is a key add-on therapy. A review of the pathophysiology of hepatic encephalopathy is highly recommended.
• Ammonia Levels: Serum ammonia is highly sensitive to pre-analytical errors and should not be used as a routine screening test.
• Driving Safety: Patients with a history of HE must be formally evaluated by their local DMV before driving.

Portal Hypertension and Variceal Bleeding

Portal hypertension is a direct consequence of cirrhotic scarring.

• Prophylaxis and Management: For an active variceal bleed, start antibiotics immediately and perform an EGD with banding within 12 hours. To prevent future bleeds, eradicate varices with repeated banding and start a non-selective beta-blocker.
• Carvedilol: This is the preferred agent. Its dual beta and alpha-1 blockade leads to a greater reduction in portal pressure and a mortality benefit.
• TIPS (Transjugular Intrahepatic Portosystemic Shunt): For patients with recurrent bleeding, consider TIPS early. The best candidates have a MELD score of less than 18.

A Paradigm Shift in Managing Coagulopathy in Cirrhosis

An elevated INR in cirrhosis reflects synthetic dysfunction, not necessarily a high bleeding risk. The liver also produces fewer anticoagulant proteins, resulting in a rebalanced hemostatic system. These patients are just as likely to clot as they are to bleed. Giving Fresh Frozen Plasma (FFP) to “correct the INR” is not recommended and can be harmful by increasing portal pressure.

Ascites Management: Diuretics, Diet, and Paracentesis

• Diet and Fluid: A 2,000 mg sodium-restricted diet is appropriate. Fluid restriction is rarely necessary unless serum sodium is <120 mEq/L.
• Diuretics: Start with furosemide 40 mg and spironolactone 100 mg. This combination minimizes electrolyte disturbances.
• Paracentesis: For large-volume paracentesis, albumin must be administered (6-8 g per liter removed) to prevent circulatory dysfunction and subsequent renal injury.

Hepatorenal Syndrome (HRS): Recognition and Evidence-Based Therapy

HRS results from extreme splanchnic vasodilation and renal vasoconstriction. Management includes volume assessment with albumin, vasoconstrictors like terlipressin, and evaluation for TIPS/transplant.

Portal Vein Thrombosis (PVT): A Serious Complication

A clot in the portal vein should be ruled out in any patient with a new decompensation. Remember, patients with high INRs can and do clot. Management requires a multidisciplinary approach with a hepatologist, radiologist, and hematologist. Anticoagulation is often necessary for acute, symptomatic PVT.

The Inflammatory Bowel Disease (IBD) Flare

When a patient with Crohn’s or ulcerative colitis is admitted for a flare, the approach is systematic.

• Workup: Rule out infectious overlap (especially C. diff) and use inflammatory markers like CRP and fecal calprotectin.
• Steroids: Once infection is ruled out, IV corticosteroids (e.g., methylprednisolone) are first-line. There is no evidence that doses higher than 60 mg/day of prednisone provide additional benefit.
• Biologics: For severe or steroid-refractory cases, plan for biologics such as infliximab (anti-TNF), vedolizumab (anti-integrin), or ustekinumab (anti-IL-12/23), as their mechanisms of action in IBD are distinct.
• Thromboprophylaxis is Non-Negotiable: IBD creates a hypercoagulable state. The risk of a life-threatening clot usually outweighs the risk of increased bleeding from anticoagulants.

Judicious Use of Blood Transfusions and Iron

• Restrictive Transfusion Strategy: Multiple studies, including a landmark trial on Restrictive transfusion in GI bleeding, have shown that a restrictive strategy (transfusing when hemoglobin <7 g/dL) leads to better outcomes. In cirrhosis, over-transfusion can increase portal pressures and worsen variceal bleeding.
• Iron Deficiency Anemia: This is an alarm sign, especially in men and post-menopausal women, as it can indicate an occult GI malignancy. Oral iron is poorly tolerated. I have a very low threshold for administering parenteral (IV) iron for hospitalized patients. The risk of anaphylaxis with modern formulations is extraordinarily rare, and the improvement in patient energy and well-being is remarkable.

Root Causes of *GUT DYSFUNCTION*- Video

The Role of Integrative Chiropractic Care in GI and Hepatic Health

You might be wondering how chiropractic care fits into this picture. The connection lies in the intricate relationship between the spine, the nervous system, and the gut—the gut-brain axis.

• Neurological Connection: The autonomic nervous system, with control centers around the spinal column, directly regulates gut motility, secretion, and blood flow. Spinal misalignments, or subluxations, can potentially interfere with these nerve signals. As a chiropractor, I use specific adjustments to restore proper spinal mechanics and optimize nerve function, which can help normalize autonomic tone.
• Pain Modulation and Musculoskeletal Support: Patients with chronic GI distress often develop compensatory postural changes and musculoskeletal pain. For example, mechanical pain in the thoracolumbar regions can worsen sympathetic tone, elevating splanchnic vasoconstriction and impairing gut perfusion. My role is to address these secondary issues with manual therapies, alleviating pain, improving posture, and reducing the overall stress load on the body, which can be a trigger for GI flares. All interventions are medically cleared by Dr. Cardenas and sequenced after stabilization.
• Autonomic Regulation: Techniques that target parasympathetic balance (e.g., breathing mechanics coaching, rib cage mobility) can improve diaphragmatic excursion and vagal tone, thereby supporting gut motility and post-illness recovery.
• Holistic, Functional Medicine Perspective: As a functional medicine practitioner, I also focus on diet, stress, and lifestyle. We work with patients to identify food sensitivities, correct nutritional deficiencies (such as iron), implement stress-management techniques, and use targeted nutrition for mucosal healing (e.g., adequate protein, glutamine, zinc, and carnosine) under Dr. Cardenas’s oversight. This integration of medical diagnosis with structural, neurological, and functional care is our standard at Injury Medical Clinic.

References

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