Discover key practices in inpatient management to optimize gastrointestinal and liver function in healthcare settings.

Abstract

Welcome to our educational series. In this comprehensive post, I will explore the latest evidence-based findings in the inpatient management of common and complex gastroenterology and hepatology conditions. As a clinician with extensive experience in chiropractic, functional medicine, and advanced practice nursing, I will take you on a journey through the complexities of upper and lower GI bleeding, the critical role of risk stratification, and the nuanced management of anticoagulants. We will examine the diagnostic puzzles of dysphagia, diarrhea, and constipation, the urgent nature of cholangitis, the challenges of mesenteric ischemia, and the practicalities of treating fecal impactions. II’llalso cover first-line treatments for severe inflammatory bowel diseases such as ulcerative colitis and Crohn’s disease, the management of Clostridioides difficile (C. diff), and strategies for managing small bowel obstructions. The discussion will then shift to hepatology, where we will explore the criteria for diagnosing acute liver failure, the management of alcohol-related hepatitis, and the intricate care required for complications of decompensated cirrhosis, including hepatic encephalopathy, portal hypertension, ascites, and hepatorenal syndrome. A central theme will be the power of an integrative, multidisciplinary approach, showcasing how our team at Injury Medical Clinic PA provides comprehensive, patient-centered care.

Our Multidisciplinary Team: A Collaborative Approach to Health

Hello, I’m Dr. Alex Jimenez. My journey in healthcare has been one of continuous learning and integration, leading me to hold credentials in chiropractic (DC), advanced practice nursing (APRN, FNP-BC), and certified functional medicine (CFMP, IFMCP, ATN, CCST). This unique blend of expertise allows me to view patient health through multiple lenses—structural, physiological, and biochemical.

At our practice, Injury Medical Clinic PA (also known as Mission Plaza Injury Medical Clinic) in El Paso, Texas, we believe in the power of collaboration. This is why I am proud to work alongside Dr. Maria Guadalupe Cardenas, MD. With over 40 years of experience as a board-certified internist, Dr. Cardenas serves as our Medical Director and Collaborative Physician. Her NPI is #1164426749, and her Texas MD License is #J2933. Her profound medical knowledge provides essential oversight and complements our integrative services, a model common in modern injury and integrative clinics. Together, we lead a team that offers a spectrum of care:

• Medical Oversight (Internal Medicine): Led by Dr. Cardenas for comprehensive medical diagnosis, medication management, and direction on complex medical conditions, ensuring all treatments are medically sound and safe.
• Integrative Chiropractic Care (Dr. Jimenez): Focused on the neuromusculoskeletal system, spinal health, and its impact on overall physiological function. This includes addressing compensatory pain, improving nervous system regulation, and optimizing biomechanics.
• Functional Medicine: Investigating the root causes of disease by looking at genetics, lifestyle, and environment to uncover underlying imbalances contributing to illness.
• Personal Injury and Rehabilitation: Aiding recovery from trauma with a focus on restoring function, mobility, and strength through tailored physical rehabilitation programs.

This synergy allows us to address the patient as a whole person rather than a collection of symptoms, ensuring that all aspects of their health—from acute medical needs to long-term functional wellness—are managed cohesively.

Gastroenterology: Unraveling Upper GI Bleeding

One of the most frequent and urgent situations we encounter in a clinical setting is upper gastrointestinal (GI) bleeding. When a patient presents with symptoms, my first critical task is to determine the urgency of the case. Does this patient need an immediate endoscopic evaluation, or can we safely manage them in an outpatient setting?

A common sign of an upper GI bleed is melena, which refers to black, tarry stools. This typically indicates that bleeding has occurred somewhere proximal to the ligament of Treitz, the anatomical landmark that divides the upper and lower GI tracts. However, a crucial clinical observation I’ve made over the years is that we must not anchor ourselves to this classic definition. While melena often points to an upper GI source, it can also originate from the small bowel or even the right side of the colon, especially in elderly patients. These individuals often have slower gut motility and may be constipated, allowing blood to remain in the colon long enough for bacteria to break it down, turning it black.

Conversely, hematochezia (bright red blood per rectum) is usually associated with lower GI bleeding. Still, in rare, severe cases, it can be a sign of a very brisk upper GI bleed. These patients are profoundly ill, often hemodynamically unstable, and may require intensive care with vasopressor support.

It’s also vital to remember that melena can persist for up to five days after the bleeding has actually stopped. If a patient has undergone an endoscopy, had an ulcer treated, but continues to pass melena, we look at the whole patient:

• Assess Hemodynamics: Are their vital signs stable?
• Evaluate Symptoms: Do they feel dizzy, weak, or presyncopal when passing the stool? This is a red flag for new or ongoing bleeding.
• Monitor Labs: Is their hemoglobin stable or, even better, trending upward? This is a reassuring sign that we are likely seeing old, residual blood making its way out.

Common Causes and Clinical Pearls for Upper GI Bleeding

Several conditions commonly cause upper GI bleeds. Understanding these is the first step in effective diagnosis and management.

• Peptic Ulcer Disease (PUD): This remains a leading cause, often linked to H. pylori infection or NSAID use.
• Esophageal Varices: Swollen veins in the esophagus, typically a complication of severe liver disease and portal hypertension.
• Portal Hypertensive Gastropathy: Changes in the stomach lining due to high pressure in the portal vein system.
• Malignancy: Tumors in the esophagus, stomach, or duodenum can bleed.
• Marginal Ulcers: These can occur at the anastomosis site after surgeries like a Roux-en-Y gastric bypass.
• Mallory-Weiss Tears: Lacerations in the mucosal lining at the junction of the esophagus and stomach, classically caused by forceful retching or vomiting.
• Cameron Lesions: Ulcerations that form within a large hiatal hernia sac, where the gastric mucosa is chronically traumatized at the diaphragmatic pinch point.

One of the most impactful clinical pearls I can share is about investigating NSAID (non-steroidal anti-inflammatory drug) use. Simply asking, “Do you take NSAIDs?” is often not enough. I find it much more effective to list them by name: “Are you taking ibuprofen, Aleve, Advil, naproxen, meloxicam, BC Powder, or Alka-Seltzer?” The last two are particularly important, as many people don’t realize they contain aspirin. In my practice, I often ask a family member to physically check the medicine cabinets at home, which has solved many cases of what we call surreptitious NSAID use.

Another critical factor to consider is pill esophagitis. With doxycycline now being a first-line antibiotic for many conditions, I am seeing it cause pill-induced esophagitis more and more frequently. A doxycycline-induced ulcer can develop within one or two days.

The Role of Endoscopy and Risk Stratification

Once we suspect an upper GI bleed, the next step is to determine if and when to perform an endoscopy. The standard of care is to provide access to an endoscopy within 12 to 24 hours. We use validated risk stratification tools to help with this decision.

Here’s an integrative strategy I’ve incorporated into my practice: if the patient’s history doesn’t strongly suggest an upper GI source and we have time, I often consider preparing them for a colonoscopy at the same time. By considering a bidirectional scope from the outset, we can potentially reduce the patient’s length of stay and their exposure to anesthesia. Of course, if the clinical picture screams “upper GI bleed,” starting with an EGD (esophagogastroduodenoscopy) is perfectly reasonable. But even then, we must always ask: Does the endoscopic finding match the clinical picture? For instance, if a patient presents with a hemoglobin level of 4 and the EGD shows only mild gastritis, that finding does not adequately explain the severity of the anemia. A follow-up colonoscopy is essential.

If both scopes are unrevealing, a CT angiogram can help identify ectopic varices or a mass in the small intestine, or a push enteroscopy can examine the small intestine more deeply.

Managing Peptic Ulcers and Long-Term PPI Therapy

When an ulcer is found, our job isn’t done. The most important question to ask is, “What caused this ulcer?” Simply treating the ulcer without addressing the root cause is a recipe for recurrence.

If the cause is H. pylori, it must be eradicated. H. pylori is a Group 1 carcinogen associated with peptic ulcer disease and gastric cancer.

• Treatment: Use bismuth-based quadruple therapy (PPI + bismuth + tetracycline + metronidazole) or non-bismuth concomitant therapy, depending on local resistance patterns.
• Confirm Eradication: Perform a urea breath test or stool antigen test at least 4 weeks after antibiotics and 2 weeks after stopping PPIs to confirm cure (Chey et al., 2017).

Indiscriminately deprescribing proton pump inhibitors (PPIs) can lead to preventable complications. There are clear situations where indefinite PPI therapy is appropriate and protective:

• Complicated Peptic Ulcers: For large or complicated ulcers, long-term acid suppression supports healing and reduces the risk of rebleeding by stabilizing clot formation.
• Large Hiatal Hernias and Cameron Lesions: PPIs reduce acid exposure, allowing the chronically traumatized mucosa to recover.
• High-Risk Patients on Anticoagulants: For patients on long-term anticoagulation or antiplatelet therapy with a prior significant ulcer, PPIs are crucial to reduce the risk of bleeding.

If the cause is NSAID use, we must provide reasonable alternatives. This is where our integrative and functional medicine approach becomes crucial.

• Chiropractic Care: For musculoskeletal pain, such as osteoarthritis or migraines, chiropractic adjustments can be profoundly effective. By correcting spinal misalignments, we can reduce nerve interference and decrease the inflammatory load, directly reducing thepatient’ss need for pain-relieving NSAIDs.
• Functional Medicine: We can explore natural, gut-sparing anti-inflammatory agents like curcumin, boswellia, and fish oil.
• Lifestyle Modifications: We work with patients on anti-inflammatory diets, stress management techniques, and targeted physical rehabilitation to address the underlying drivers of their pain.

By offering effective, safe alternatives, we not only help the ulcer heal but also address the patient’s primary complaint and significantly reduce the risk of a future bleed.

Navigating Lower GI Bleeding

Unlike upper GI bleeding, which often requires urgent endoscopy, lower GI bleeding requires a more nuanced approach to the timing of colonoscopy.

Optimizing Colonoscopy Timing and Preparation

A randomized controlled trial found no significant differences in outcomes between colonoscopy performed within <24 hours and 24–96 hours for acute lower GI bleeding (Laine & Shah, 2010). This supports prioritizing adequate preparation over rushed timing when a patient is clinically stable. A poor prep reduces diagnostic yield and risks anesthesia without benefit.

Strategy: When hemodynamically stable, use the time to achieve adequate prep. For suspected distal sources (rectum or sigmoid), consider targeted enemas. Gradual administration of prep can also help monitor for ongoing bleeding.

Differential Diagnosis in Lower GI Bleeding: Pain Matters

• Painless Lower GI Bleeding:

• • Diverticulosis: Brisk, often painless hematochezia.
  • Angiodysplasias: Fragile, dilated submucosal vessels, often in the right colon.
  • Hemorrhoids: Typically painless bleeding with defecation.

• Painful Lower GI Bleeding:

• • Ischemic Colitis: Crampy pain followed by bleeding.
  • Radiation Proctitis/Colitis: Telangiectasias and friable mucosa.
  • Inflammatory Bowel Disease (IBD): Significant cramping, urgency, and systemic features.
  • Malignancy and Infection: May present with pain, weight loss, or fevers.

For ongoing brisk bleeding not amenable to endoscopy, a CT angiogram can localize the source for interventional radiology (IR) embolization. Surgery is reserved for refractory, life-threatening hemorrhage.

Anticoagulation in GI Bleeding: Balancing Risks

Managing patients with GI bleeding who are on anticoagulants requires careful, individualized decision-making. Restarting a blood thinner while the patient is still in the hospital allows for monitoring in a controlled environment.

Pharmacology and Reversal

• Direct Oral Anticoagulants (DOACs): Have shorter half-lives (e.g., apixaban, approx. 8–15 hours). Renal impairment prolongs effects.
• Warfarin: Has longer kinetics but established reversal with Vitamin K and prothrombin complex concentrate (PCC).
• Heparin: A short half-life makes it a valuable tool in acute settings; stopping the infusion is often the most effective reversal.
• Reversal Agents: Should be reserved for severe, life-threatening bleeding. Overuse exposes patients to thrombotic risk without clear benefit (Tomaselli et al., 2020).

Resumption of Anticoagulation

Early resumption after GI bleeding (often within a 2–7-day window) reduces thromboembolic events and overall mortality compared with prolonged interruption, though it may slightly increase the risk of rebleeding (Qureshi et al., 2014; Witt et al., 2012). For patients with atrial fibrillation, the Watchman procedure, which permanently seals off the left atrial appendage, is a phenomenal long-term option that can allow many to discontinue anticoagulation.

Managing Other Common and Complex GI Conditions

Acute Pancreatitis: A Deep Dive into Management

Acute pancreatitis management hinges on a few key principles.

• Aggressive Fluid Resuscitation: Lactated Ringer’s (LR) is the fluid of choice because it reduces systemic inflammation more effectively than normal saline (Nishida et al., 2021). A rate of 150-250 mL/hour is more appropriate than lower “maintenance” rates.
• Multimodal Pain Management: Relying solely on opioids is ineffective. My approach includes scheduled NSAIDs (like ketorolac), scheduled acetaminophen, and neuropathic agents like gabapentin or pregabalin to calm hyperexcited nerves, with opioids used for breakthrough pain only.
• Early Oral Feeding: The old dogma of keeping the pancreas “at rest” (NPO) has been debunked. Early feeding is associated with better outcomes. If a full diet isn’t tolerated, use high-protein clear nutritional drinks.
• Patience with Fluid Collections: Early collections are common and usually resolve on their own. Endoscopic drainage is generally not considered until at least four weeks have passed, allowing the collection to mature into a pseudocyst.

Cholangitis vs. Choledocholithiasis: A Critical Distinction

While both involve stones in the common bile duct, cholangitis is an infection of the biliary tree and is an endoscopic emergency. The most reliable differentiator is the presence of fever and signs of sepsis. Patients with cholangitis often have that “toxic” appearance, presenting with Charcot’s triad (fever, jaundice, right upper quadrant pain). They require an Endoscopic Retrograde Cholangiopancreatography (ERCP) within 24 hours to decompress the obstructed duct and prevent a significant increase in mortality.

Understanding Mesenteric Ischemia

Mesenteric ischemia, or insufficient blood flow to the intestines, primarily affects older people. It often occurs in”watershed” areas of the colon (e.g., splenic flexure) vulnerable to hypoperfusion. Patients present with cramping abdominal pain and sometimes bloody diarrhea. A CT scan shows bowel wall thickening in these specific regions. Management includes restoring perfusion, supportive care with gentle laxatives like Miralax to keep stool soft, and consultation with vascular or general surgery.

The Diagnostic Challenge of Dysphagia and Diarrhea

• Dysphagia (Difficulty Swallowing): Differentiate between oropharyngeal (difficulty initiating a swallow) and esophageal causes (food getting stuck after swallowing). Dysphagia to solids only often suggests a mechanical obstruction, while dysphagia to both solids and liquids suggests a motility disorder.
• Diarrhea: My first question is always: “Could this be constipation?” Overflow diarrhea is incredibly common. When a hard stool mass obstructs the colon, liquid stool from further up leaks around it. Reviewing imaging is key before treating what is reported as “diarrhea.”

Fecal Impaction: A Hands-On Approach

Before prescribing laxatives, review imaging to determine where the stool is. If it’s packed in the rectum, oral laxatives will only work once the distal obstruction is cleared. This is where digital disimpaction becomes indispensable. No amount of suppositories can break up a rock-hard rectal impaction. Once the path is cleared manually, other laxatives can work effectively.

Decoding GI Symptoms and C. difficile Management

Always ask patients to define symptoms like “diarrhea” and “constipation.” A change in bowel habits does not always meet the clinical definition. If true diarrhea is present, an infectious workup is the next step. Avoid empiric antibiotics for GI infections unless the patient is septic, immunocompromised, or has a severe IBD flare, as they can worsen conditions like Shiga toxin-producing E. coli infection.

Clostridioides difficile, or C. diff, is a major concern. I am seeing a rise in community-associated C. diff without recent antibiotic use, so a lack of antibiotic history should not dissuade you from considering the diagnosis.

• No Role for Repeat Testing: Do not “test for cure.” The test can remain positive long after the infection has resolved.
• Modern Treatment: Fidaxomicin is now preferred over vancomycin. For recurrent infections, Bezlotoxumab (Zinplava), a monoclonal antibody, has shown incredible effectiveness.

Root Causes of *GUT DYSFUNCTION*- Video

A Multidisciplinary Approach to Inflammatory Bowel Disease (IBD)

Patients with Inflammatory Bowel Disease (IBD), including Crohn’s disease and ulcerative colitis, require a well-coordinated team.

• Rule Out Infection: Before starting steroids, it is essential to rule out an overlapping infection, especially C. diff.
• Appropriate Steroid Dosing: High-dose IV steroids are a mainstay, but doses exceeding 60 mg per day of prednisone (or its equivalent) offer little extra benefit while increasing risks.
• Thromboprophylaxis: IBD patients are at an extraordinarily high risk for venous thromboembolism (VTE). Prophylactic heparin is often life-saving and rarely worsens rectal bleeding.
• Long-Term Strategy: Don’t just send a patient home on steroids. Ask: What are we changing to prevent the next hospitalization? This involves evaluating and adjusting their maintenance therapy.

Managing Small Bowel Obstructions and Iron Deficiency

The most common cause of small bowel obstructions (SBOs) is adhesive disease from prior surgery. Initial management includes bowel rest and NG tube decompression. IV oral contrast is a fantastic tool; it helps track resolution on X-ray and has a purgative effect that can help clear the blockage.

Iron deficiency is an alarm sign. Oral iron is poorly tolerated; research shows every-other-day dosing can improve absorption (Stoffel et al., 2017). However, I have a very low threshold for using parental (IV) iron. You can completely replete a patient’s iron stores in one session, and the fear of anaphylaxis is overstated with modern formulations.

A Restrictive Approach to Blood Transfusions

A restrictive transfusion strategy (transfusing only when hemoglobin drops below 7 g/dL) improves mortality and reduces complications compared to a more liberal approach (Carson et al., 2016). The right answer is almost always to give one unit of blood at a time and then re-evaluate. In patients with liver disease and portal hypertension, over-transfusion can be dangerous, as it can increase portal pressures and precipitate worse variceal bleeding.

The Role of Integrative Chiropractic in GI Recovery

While chiropractic is not a primary treatment for active GI bleeding or acute IBD flares, it plays a vital supportive role in recovery and long-term management.

• Biomechanics and Pressure Regulation: Faulty breathing mechanics and poor posture (e.g., hyperkyphosis) can increase intra-abdominal pressure, exacerbating reflux and hernia-related mucosal trauma. Through targeted breathing retraining, manual therapy for rib cage mobility, and corrective exercises, we can optimize diaphragm function and distribute pressure more evenly.
• Pain Modulation and Medication Minimization: By addressing musculoskeletal pain with manual therapy and exercise, we reduce reliance on NSAIDs—a major contributor to ulcer formation and rebleeding.
• Autonomic Nervous System Balance: Spinal misalignments can impact the nerve supply to digestive organs. Chiropractic adjustments can help restore proper autonomic balance, improve gut motility, reduce stress, and support the gut-brain axis.
• Rehabilitation During Anemia Recovery: Anemia decreases exercise tolerance and postural stability. We implement gradual conditioning, balance training, and orthostatic tolerance drills to reduce fall risk and safely restore function.

Understanding and Managing Complex Liver Conditions

Our integrative team approach is crucial for managing the complexities of liver disease. We focus on optimizing inpatient care by minimizing blood draws, proactively supplementing with iron, folate, and B12, and providing aggressive nutritional support.

Acute Liver Failure and Alcohol-Related Hepatitis

Acute liver failure is a rapid deterioration of liver function in someone without preexisting liver disease. A key concern is hepatic encephalopathy. The most common causes are viral hepatitis and drug-induced liver injuries (DILI).

• N-acetylcysteine (NAC): This is a critical intervention for all-cause acute liver failure. As a precursor to glutathione, NAC replenishes the liver’s master antioxidant, protecting it from further injury. Start it early.

Alcohol-related hepatitis carries an incredibly high risk of infection. A critical pearl is to screen for asymptomatic infection. Every patient should have blood cultures, a urine culture, and a chest X-ray, regardless of symptoms. The evidence for steroids is mixed; my current practice favors using NAC. It is also crucial to identify a potential “second hit” from co-existing metabolic-associated steatotic liver disease (MASLD) (Loomba et al., 2021) and to offer medication-assisted therapy (MAT) for the underlying alcohol use disorder.

Decoding Elevated Liver Enzymes and Liver Function

It’s a common point of confusion: AST and ALT are enzymes that indicate liver injury or inflammation. They do not measure liver function. True measures of the liver’s synthetic and metabolic function are the INR and bilirubin level. To characterize the pattern of injury, I use the R-factor:

R = (Patient’s ALT / ALT Upper Limit of Normal) / (Patient’s ALP / ALP Upper Limit of Normal)

• R > 5: Suggests a hepatocellular
• R < 2: Suggests a cholestatic
• R between 2 and 5: Suggests a mixed

This calculation focuses the differential diagnosis. Also, always perform a deep dive into the patient’s history, including all prescriptions, over-the-counter drugs, and herbal supplements or “cleanses,” which can be a hidden cause of severe DILI.

The Complications of Decompensated Cirrhosis

When a patient develops decompensated cirrhosis (ascites, variceal hemorrhage, or HE), I always ask two questions:

1. What is the underlying cause of their cirrhosis, and are we treating it?
2. What was the trigger for this decompensation? (e.g., infection, DILI, portal vein thrombosis, HCC, return to alcohol use).

Portal Hypertension: The Driving Force

Portal hypertension is the engine behind most of cirrhosis’s deadly complications.

• Hepatopulmonary Syndrome (HPS): A lung complication. The pathognomonic symptoms are platypnea (shortness of breath worse when upright) and orthodeoxia (drop in oxygen when upright). The only curative treatment is a liver transplant.
• Hepatorenal Syndrome (HRS-AKI): Functional kidney failure. We must rule out other triggers, such as infection, overdiuresis, or large-volume paracentesis without albumin replacement (Salerno et al., 2018). Treatment involves vasoconstrictors like terlipressin.
• Ascites: First, calculate the Serum-Ascites Albumin Gradient (SAAG) to confirm that portal hypertension is the cause (SAAG> 1.1 g/dL). Management includes a 2-gram sodium diet and diuretics, typically a combination of furosemide (40 mg) and spironolactone (100 mg).
• Variceal Bleeding: An acute bleed is a medical emergency. The protocol includes antibiotic prophylaxis (to prevent SBP), urgent endoscopy (EGD) within 12 hours for banding, and starting a non-selective beta-blocker. Carvedilol is the preferred agent due to its dual alpha- and beta-blocking properties, which more effectively reduce portal pressure and improve survival (Reiberger et al., 2013).

Blood Products in Cirrhosis: A Paradigm Shift

The elevated INR in cirrhosis is a marker of synthetic dysfunction, not a predictor of bleeding risk. The hemostatic system is rebalanced but fragile. Giving Fresh Frozen Plasma (FFP) to “correct” the INR in a non-bleeding patient is fundamentally wrong and can increase portal pressure, provoking a bleed (Garcia-Tsao et al., 2007). Adhere to a restrictive transfusion strategy with a hemoglobin goal around 7 g/dL.

Hepatic Encephalopathy (HE)

HE is a clinical diagnosis of exclusion. Do not use serial ammonia levels to guide therapy. Always identify the precipitating cause (e.g., infection, GI bleed, constipation, electrolyte imbalance).

• Treatment: Lactulose is a cornerstone. Set a clear goal of two to three soft bowel movements per day and implement “hold” parameters to prevent over-treatment. If lactulose is insufficient, add rifaximin, a gut-specific antibiotic that reduces ammonia-producing bacteria (Bass et al., 2010).
• Nutrition: The myth of protein restriction for HE is debunked. These patients are hypercatabolic and need adequate protein to prevent muscle wasting (sarcopenia), which worsens outcomes (Tsoris & Marlar, 2024).
• Safety: Advise patients to avoid driving until their local DMV has formally evaluated them.

Portal Vein Thrombosis (PVT)

A portal vein thrombosis (PVT), or blood clot in the portal vein, can trigger acute decompensation. If a stable patient suddenly decompensates, PVT should be included in the differential diagnosis. The decision to anticoagulate is complex and multidisciplinary. An elevated INR should not scare you from anticoagulating a patient with an acute, symptomatic PVT who needs it.

Closing Thoughts

GI and liver diseases demand clear reasoning, patience with preparation, and a focus on both acute stabilization and long-term protection. In our El Paso-based integrative clinic, we use the best available evidence alongside disciplined clinical observation to create safe, effective, and personalized plans. When integrated with chiropractic, functional nutrition, and rehabilitation under medical direction, patients not only survive the event—they regain strength and resilience for the long term.

References

• Bass, N. M., Mullen, K. D., Sanyal, A., Poordad, F., Neff, G., Leevy, C. B., … & TARGET Study Group. (2010). Rifaximin treatment in hepatic encephalopathy. The New England Journal of Medicine, 362(12), 1071–1081.
• 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. Annals of Internal Medicine, 165(11), 784–791.
• Chávez-Tapia, N. C., Barrientos-Gutiérrez, T., Téllez-Ávila, F. I., Soares-Weiser, K., & Uribe, M. (2011). Meta-analysis: antibiotic prophylaxis for cirrhotic patients with upper gastrointestinal bleeding – an updated Cochrane review. Alimentary Pharmacology & Therapeutics, 34(5), 509–518.
• Chey, W. D., Leontiadis, G. I., Howden, C. W., & Moss, S. F. (2017). ACG clinical guideline: Treatment of Helicobacter pylori infection. American Journal of Gastroenterology, 112(2), 212–239.
• Garcia-Tsao, G., Sanyal, A. J., Grace, N. D., & Carey, W. (2007). Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology, 46(3), 922–938.
• Gibson, C. M., Mehran, R., Bode, C., et al. (2016). Prevention of bleeding in patients with atrial fibrillation undergoing PCI. New England Journal of Medicine, 375(25), 2423–2434.
• Laine, L., & Shah, A. (2010). Randomized trial of urgent vs. elective colonoscopy in lower GI bleeding. Gastroenterology, 138(1), 239–244.
• Loomba, R., Lim, J. K., Patton, H., & El-Serag, H. B. (2021). AGA Clinical Practice Update on Screening and Surveillance for Hepatocellular Carcinoma in Patients with Nonalcoholic Fatty Liver Disease: Expert Review. Gastroenterology, 161(5), 1689–1699.
• Malfertheiner, P., Megraud, F., Rokkas, T., et al. (2022). Management of Helicobacter pylori infection—the Maastricht VI/Florence consensus report. Gut, 71(9), 1724–1762.
• Nishida, Y., Kataoka, K., Takeda, K., Tanaka, H., Nakamura, Y., Ohtsuka, T., Ito, H., Tanaka, T., Kawabe, K., Ishida, T., & Tanaka, M. (2021). Randomized clinical trial of lactated Ringer’s versus normal saline for acute pancreatitis. Pancreatology, 21(4), 790–797.
• Qureshi, W., Mittal, C., Patsias, I., et al. (2014). Restarting anticoagulation and antiplatelet agents after gastrointestinal bleeding. Journal of the American Heart Association, 3(5), e000846.
• Reiberger, T., Ulbrich, G., Ferlitsch, A., Payer, B. A., Schwabl, P., Pinter, M., … & Trauner, M. (2013). Carvedilol for primary prophylaxis of variceal bleeding in cirrhotic patients with hemodynamic non-response to propranolol. Gut, 62(11), 1634–1641.
• Salerno, F., Angeli, P., Cárdenas, A., Møller, S., & Wiest, R. (2018). Diagnosis, prevention and treatment of hepatorenal syndrome in cirrhosis. Gut, 67(7), 1310-1320.
• Stoffel, N. U., Zeder, C., Brittenham, G. M., Moretti, D., & Zimmermann, M. B. (2017). Iron absorption from oral iron supplements given on consecutive versus alternate days and as single morning doses versus twice-daily split doses in iron-depleted women: two open-label, randomized controlled trials. The Lancet Hematology, 4(11), e524–e533.
• Tomaselli, G. F., Mahaffey, K. W., Cuker, A., et al. (2020). 2020 ACC expert consensus decision pathway on management of bleeding in patients on oral anticoagulants. Journal of the American College of Cardiology, 76(5), 594–622.
• Tsoris, A., & Marlar, C. A. (2024). Hepatic Encephalopathy. In StatPearls. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK539716/
• Witt, D. M., Delate, T., Garcia, D. A., et al. (2012). Risk of thromboembolism, recurrent hemorrhage, and death after warfarin therapy interruption for gastrointestinal tract bleeding. Annals of Internal Medicine, 156(10), 668–674.
• Zhang, W., Jones, A., & Doherty, M. (2004). Does paracetamol (acetaminophen) reduce the pain of osteoarthritis? A meta-analysis of randomized controlled trials. Annals of the Rheumatic Diseases, 63(8), 901-907.

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gastroenterology, hepatology, upper GI bleeding, lower GI bleeding, peptic ulcer disease, H. pylori, proton pump inhibitors, PPIs, melena, hematochezia, cirrhosis, hepatic encephalopathy, portal hypertension, ascites, variceal bleeding, hepatorenal syndrome, acute liver failure, alcohol-related hepatitis, acute pancreatitis, cholangitis, mesenteric ischemia, fecal impaction, dysphagia, C. difficile, inflammatory bowel disease, IBD, small bowel obstruction, iron deficiency anemia, blood transfusion, integrative medicine, chiropractic care, functional medicine, Dr. Alex Jimenez, Dr. Maria Guadalupe Cardenas, El Paso Texas, Injury Medical Clinic PA, internal medicine oversight