Inpatient Management: Key Considerations in Gastrointestinal & Liver Care

Understand the importance of inpatient management in improving patients’ liver health and gastrointestinal wellness.

Abstract

In this educational post, I present a modern, evidence-based journey through the inpatient management of gastrointestinal and hepatologic conditions, written from my first-person perspective as Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST. Drawing on leading research and my clinical observations, I address upper and lower gastrointestinal bleeding, peptic ulcer disease, pill esophagitis, dysphagia, inflammatory bowel disease, acute pancreatitis, cholangitis versus choledocholithiasis, mesenteric ischemia, severe fecal impaction, iron deficiency anemia, anticoagulation management, portal hypertension, variceal bleeding, hepatic encephalopathy, hepatorenal syndrome, acute and alcohol-related liver disease, portal vein thrombosis, and core inpatient nutrition principles. I explain why we choose specific therapies, how physiology guides decision-making, and where integrative chiropractic care and functional medicine fit alongside internal medicine oversight. I also describe our multidisciplinary model at Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic) in El Paso, Texas, where I collaborate with our Medical Director, Dr. Maria Guadalupe Cardenas, MD (Board Certified in Internal Medicine; NPI #1164426749; Texas MD License #J2933), who brings over 40 years of experience as an internist to co-manage complex cases safely and effectively. This post is designed to be easy to read, clinically practical, and thoroughly referenced with APA-7 style citations.

About Our Multidisciplinary Clinic and Team-Based Care

At Injury Medical Clinic PA (also known as Mission Plaza Injury Medical Clinic) in El Paso, Texas, I practice within a multidisciplinary, integrative framework that is increasingly recognized as best practice in injury and complex care settings. Our structure pairs comprehensive chiropractic care and functional medicine with internal medicine oversight for safe, coordinated care.

• I, Dr. Alex Jimenez (DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST), provide:

• • Integrative chiropractic care focused on biomechanical alignment, neuromuscular function, and autonomic nervous system modulation
  • Advanced practice nursing services and clinical decision-making
  • Functional medicine assessment, nutrition optimization, and rehabilitation strategies
  • Personal injury care and recovery planning

• Dr. Maria Guadalupe Cardenas, MD, Board Certified in Internal Medicine (NPI #1164426749; Texas MD License #J2933), serves as:

• • Medical Director and Collaborative Physician
  • Co-manager of complex medical conditions requiring systemic, pharmacologic, or procedural oversight
  • Internal medicine anchor ensuring safety, guideline adherence, and interdisciplinary communication

• Our integrated services include:

• • Chiropractic adjustments, soft tissue work, and spinal rehabilitation
  • Functional medicine diagnostics and targeted nutrition
  • Personal injury recovery and physical reconditioning
  • Internal medicine protocols, pharmacotherapy, and inpatient-style care pathways

This collaborative model aligns structural health with systemic physiology, allowing us to treat the whole person. In my clinical experience and as supported by literature, combining musculoskeletal care with internal medicine management creates synergy—improving pain, autonomic balance, mobility, and resilience while safely addressing acute medical issues (Meeker & Haldeman, 2002).

Upper Gastrointestinal Bleeding: Physiology, Triage, and Endoscopy Timing

When I evaluate upper gastrointestinal bleeding (UGIB), physiology guides urgency. Melena—black, tarry stools—usually indicates bleeding proximal to the ligament of Treitz, but slow transit in older adults can cause right-sided colonic bleeds that mimic melena. Melena can persist for up to five days after bleeding stops, so I differentiate residual blood from ongoing hemorrhage by clinical trajectory: stability and rising hemoglobin suggest residual blood; presyncope, hypotension, and falling hemoglobin indicate ongoing bleeding.

Hematochezia (bright red blood per rectum) can represent brisk UGIB when transit is rapid, and blood does not have time to oxidize. These patients are often unstable and need ICU-level care, vasoactive support, and urgent endoscopy.

• Common UGIB etiologies:

• • Peptic ulcer disease
  • Esophageal and gastric varices
  • Portal hypertensive gastropathy
  • Malignancy
  • Marginal ulcers post-bariatric surgery
  • Mallory-Weiss tears after retching

I use validated risk tools and clinical signs to determine endoscopy timing:

• Hemodynamically stable with low-risk features: early inpatient EGD within 12–24 hours
• Uncertain source in older adults: consider bidirectional endoscopy (EGD and colonoscopy) with coordinated prep to avoid repeat anesthesia and reduce length of stay
• If EGD shows gastritis thatdoesn’tt explain severe anemia, I proceed to colonoscopy; endoscopic findings must match the clinical picture.
• If bidirectional endoscopy is non-diagnostic, I consider CT angiography or push enteroscopy to evaluate for ectopic varices, small-bowel lesions, or vascular malformations.s

For suspected varices, I initiate octreotide to reduce splanchnic blood flow and portal pressure, and provide antibiotic prophylaxis to prevent spontaneous bacterial peritonitis (SBP) (Garcia-Tsao et al., 2017; Saltzman, 2021).

NSAIDs and Peptic Ulcer Disease: Mechanisms, Detection, and Integrative Alternatives

I have learned never to accept “I don’t take NSAIDs” at face value. Patients rarely equate “BC Powder,” “Alka-Seltzer,” or brand-name ibuprofen or naproxen with NSAIDs. I ask specifically and involve family to check home medications. NSAIDs inhibit COX-1/COX-2, reducing prostaglandin production that defends the gastric mucosa—less mucus, less bicarbonate, less mucosal blood flow—thereby creating vulnerability to erosions, ulcers, and bleeding (Lanas & Chan, 2017).

• Why stop NSAIDs? To restore prostaglandin-mediated mucosal protection and reduce ulcer risk
• Why integrative alternatives?

• • Chiropractic care and rehabilitative exercise reduce musculoskeletal pain, often curbing NSAID reliance (Bronfort et al., 2010)
  • Omega-3s, curcumin, and anti-inflammatory nutrition can lower systemic inflammatory load with fewer GI side effects.

When a peptic ulcer is identified, I ask “why did it form?”—NSAIDs, H. pylori, stress ulcers, gastric acid hypersecretion (Zollinger–Ellison), or pill injury. I initiate PPIs to suppress the H+/K+ ATPase pump in parietal cells, raise intragastric pH, and promote healing. In variceal contexts, I add octreotide; in H. pylori infection, I use guideline-based eradication regimens and confirm cure (Lanas & Chan, 2017; Strand et al., 2017; Laine & Jensen, 2012).

In select cases, indefinite PPI therapy is necessary—large hiatal hernias with Cameron’s ulcers, severe recurrent ulcers without surgical options, or patients needing lifelong anticoagulation/antiplatelets after a prior ulcer bleed. I strongly advocate adequate discharge supplies due to real-world follow-up delays; sending only 30 days of a vital medication risks therapy lapses and readmission.

Pill Esophagitis and Doxycycline: Rapid-Onset Mucosal Injury

When patients present with sudden dysphagia, odynophagia, or chest pain without cardiac findings, I ask about recent antibiotics. Doxycycline is acidic, and when taken with insufficient water or lying down, it can lodge in the esophagus and cause pill esophagitis within 24–48 hours. Direct chemical mucosal injury is rapid and severe. Prevention is simple—take pills upright with water, avoid bedtime dosing—while management includes PPI therapy and supportive care.

Lower Gastrointestinal Bleeding: Pain Pattern, Prep Quality, and Multidisciplinary Coordination

In lower GI bleeding (LGIB), the urgency differs from that in UGIB. Rushing colonoscopy with poor inpatient prep often yields inconclusive exams under anesthesia. I target high-quality prep based on patient tolerance and timing. A randomized trial found no differences in outcomes between colonoscopy within 24 hours versus 24–96 hours, underscoring why prep quality and patient readiness matter (Laine et al., 2021).

• Pain framing changes differential:

• • Painless bleeding: diverticulosis, angiodysplasia, internal hemorrhoids
  • Painful bleeding: ischemic colitis (pain first, then bleeding), IBD flares, radiation colitis, malignancy, infectious colitis

• Practical strategies:

• • If rectosigmoid bleeding is likely, enemas can suffice for prep
  • I use prep output diagnostically: clearing suggests bleeding cessation (common in diverticular bleeds); persistent maroon/red output with dropping hemoglobin suggests ongoing bleeding—once prepped, proceed to therapeutic colonoscopy.

LGIB often benefits from early collaboration with interventional radiology and surgery. Hemorrhoid banding or selective IR therapy bridges the gap between inpatient stabilization and outpatient definitive care.

Anticoagulation in GI Bleeding: Balancing Hemorrhage and Thrombosis

Managing anticoagulation during GI bleeding is one of the most nuanced decisions I make. I consider:

• Severity of bleeding and hemodynamics
• Last anti-coagulant dose
• Indication (atrial fibrillation, mechanical valve, recent DVT/PE)
• Concomitant aspirin or NSAIDs

I weigh bleeding risk against thrombotic risk. Holding anticoagulation too long has caused devastating strokes in hospitalized patientsI’vee treated. DOACs have shorter half-lives than warfarin; warfarin reversal is straightforward (vitamin K, prothrombin complex concentrates), but reversal agents are reserved for life-threatening bleeds (Abraham, 2022).

When resuming, I often bridge with heparin due to its short half-life; if rebleeding occurs, stopping heparin causes rapid dissipation—operating as a physiologic “stress test” of hemostasis.

I also advocate device-based solutions where appropriate. In patients with non-valvular atrial fibrillation and recurrent bleeding, Watchman left atrial appendage occlusion can reduce the need for long-term anticoagulation by eliminating the primary cardiac thrombus source. While I do not perform this procedure, I coordinate with cardiology to evaluate candidacy and create individualized plans that reduce bleeding risk while preserving stroke prophylaxis.

Case Integration: Hiatal Hernia and Cameron’s Ulcers with Anticoagulation

Consider a 72-year-old on apixaban presenting with melena and hemoglobin 6.8 g/dL. EGD reveals a large hiatal hernia with Cameron’s ulcers and a small nonbleeding gastric ulcer. Chronic slow bleeding from these erosions can drive severe anemia. Given the mechanical reality of the hernia, I recommend lifelong PPI therapy to minimize acid-mediated injury, even if surgical repair is considered. After stabilization, I resume anticoagulation within 48–72 hours, often bridging with heparin to test tolerance and minimize rebleed risk.

My integrative role includes:

• Root-cause analysis of inflammation, nutrition gaps, and healing barriers
• Musculoskeletal care addressing deconditioning, stiffness, and pain after hospitalization
• Coordinated care with Dr. Cardenas and consulting teams to unify medical and integrative plans

Acute Pancreatitis: Fluid Resuscitation, Pain Modulation, and Early Nutrition

Acute pancreatitis is driven by premature trypsinogen activation within acinar cells—autodigestion and systemic inflammation ensue. Aggressive fluids are essential early due to capillary leak and third spacing. I favor Lactated Ringer’s to reduce hyperchloremic acidosis and support acid-base stability. Under-dosing fluids (e.g., 50–75 mL/hr) in a large patient can precipitate hypovolemia and renal injury; I titrate to clinical response and laboratory markers (American College of Gastroenterology, 2024).

• Pain control: multimodal therapy targeting multiple pathways reduces opioid needs

• • Ketorolac for COX-mediated inflammation
  • Acetaminophen for central modulation
  • Gabapentin/pregabalin for neuropathic components
  • Opioids for breakthrough only

• Nutrition: I initiate early enteral feeding with clear protein formulations to preserve mucosal barrier integrity, reduce bacterial translocation, and improve outcomes. Prophylactic antibiotics are rarely indicated; SIRS is usually sterile inflammation.
• Fluid collections: I avoid early drainage; walls are immature. I await maturation into a pseudocyst (≥4 weeks) with a thick wall—the “orange rind” sign—before considering endoscopic drainage if symptomatic.

Biliary Emergencies: Cholangitis Versus Choledocholithiasis

I differentiate cholangitis (infected obstruction) from choledocholithiasis (obstruction without infection) by the presence of systemic toxicity and sepsis physiology. In cholangitis, elevated ductal pressures drive bacteria into the bloodstream—prompting high fever (which may be blunted in the elderly), rigors, and clinical toxicity. ERCP within 24 hours decompresses the duct, treats the source, and reduces mortality. For choledocholithiasis, ERCP remains critical to clear the duct, ideally before cholecystectomy, to prevent retained stones and surgical injury.

Mesenteric Ischemia: Watershed Vulnerability and Post-Event Care

Older adults, dialysis patients, and those with profound hypotension are at risk for mesenteric ischemia—especially at watershed areas like the splenic flexure (Griffiths’ point) and rectosigmoid junction (Sudeck’s point). Systemic hypoperfusion shunts blood away from splanchnic circulation; anaerobic metabolism and lactic acidosis follow, leading to mucosal necrosis. Pain is often disproportionate to the exam. CT angiography shows localized wall thickening. Management includes stabilization, vascular evaluation, and anticoagulation when microthrombi are suspected; surgical resection if nonviable bowel forms.

Post-recovery, edema and dysmotility impair peristalsis; I use gentle osmotic laxatives (polyethylene glycol) to maintain soft stool and prevent painful stretching.

Root Causes of *GUT DYSFUNCTION*- Video

Severe Fecal Impaction: Overflow Diarrhea and Practical Mechanics

I am vigilant for overflow diarrhea—liquid stool bypassing a hard impaction. Staff may misinterpret liquid stool as diarrhea and hold laxatives, worsening constipation. I localize the impaction anatomically:

• Proximal impaction (ascending colon): enemas are ineffective; use high-volume oral osmotics
• Distal impaction (rectal vault): begin with digital disimpaction, lubrication, and glycerin suppositories, then follow with pharmacologic agents

This mechanical-first approach transforms outcomes and prevents ischemic complications from pressure.

Dysphagia: Oropharyngeal Versus Esophageal, and Diagnostic Pathways

I differentiate oropharyngeal dysphagia (neuromuscular initiation failure, drooling, nasopharyngeal regurgitation) from esophageal dysphagia (seconds after swallow; food stuck” lower chest). Solids-only dysphagia suggests structural narrowing (stricture, ring, malignancy), while solids and liquids together suggest motility disorders (achalasia). Odynophagia points toward infectious or pill-induced esophagitis (often doxycycline).

• Barium esophagram maps anatomy and is helpful in high-risk patients, but EGD offers immediate diagnosis and therapy—dilation of strictures brings instant relief and functional improvement.

Inflammatory Bowel Disease: Flare Management, Thrombosis Risk, and Long-Term Planning

When hospitalized for an IBD flare, I rule out C. difficile and other infections, trend CRP/ESR daily, and leverage fecal calprotectin to quantify inflammation. CT/MR enterography delineates the extent of disease and complications. Intravenous steroids are standard, but dosing beyond 40–60 mg prednisone equivalent daily is not supported and raises adverse effects without added benefit. I avoid overly aggressive dosing (Papa et al., 2016; Mullish & Williams, 2018).

I am aggressive about VTE prophylaxis; IBD patients have high thrombosis risk—even with rectal bleeding. Heparin prophylaxis seldom worsens bleeding and reduces the risk of life-threatening clot events.

Before discharge, I optimize maintenance therapy—check antidrug antibodies, adjust biologic frequency, or add immunomodulators. A short steroid course without changing long-term control is inadequate care.

C. difficile: Modern Testing, Treatment, and Recurrence Prevention

I see increasing community-associated C. difficile infections without recent antibiotic use. I do not repeat tests in the same episode, nor do I perform tests of cure; they mislead. Fulminant disease is clinically obvious—distension, toxic appearance, altered bowel sounds. I favor fidaxomicin for initial therapy due to lower recurrence rates, advocate for early coordination to address insurance barriers, and use bezlotoxumab to prevent recurrence in high-risk patients (Mullish & Williams, 2018).

Iron Deficiency Anemia and Restrictive Transfusion Strategy

I treat iron deficiency anemia as an alarm sign to find hidden bleeding. I use ferrous sulfate with vitamin C and increasingly favor every-other-day dosing to improve absorption and reduce GI side effects. Many patients cannot tolerate or absorb oral iron; I maintain a low threshold for IV iron in hospital settings—anaphylaxis is exceedingly rare, and replenishment dramatically improves function and well-being.

I follow a restrictive transfusion strategy (e.g., hemoglobin target ~7 g/dL in stable patients). In cirrhosis, over-transfusion raises portal pressure and worsens bleeding risk. I transfuse one unit at a time and reassess (Carson et al., 2016).

Portal Hypertension and Variceal Bleeding: Prevention and Procedural Timing

In acute variceal bleeding, I initiate antibiotic prophylaxis, perform urgent EGD (within 12 hours) for banding, and plan serial EGDs to eradicate varices. For prevention, I prefer carvedilol—a non-selective beta-blocker with alpha-1 blockade—to reduce portal pressure more effectively than selective agents. I coordinate with cardiology to switch from metoprolol when appropriate.

I consider TIPS early in recurrent bleeds or when beta-blockers are intolerable—ideally with MELD < 18 and without severe encephalopathy—to reduce risk and improve survival (Garcia-Tsao et al., 2017; North-Lewis, 2018).

Hepatic Encephalopathy: Practical Dosing and Cognitive Safety

I set clear lactulose goals—two to three soft bowel movements daily. I include “hold parameters” when goals are met to avoid dehydration and electrolyte imbalances; holding applies only to that dosing interval, not to indefinite cessation. I add rifaximin for refractory cases.

I advise patients not to drive until formal assessment; cognitive impairment can be subtle and unsafe despite normal bedside testing (Vilstrup et al., 2014).

Coagulation in Cirrhosis: Rethinking INR and Blood Products

Cirrhosis rebalances hemostasis—patients lose both pro- and anticoagulant factors. Elevated INR reflects synthetic dysfunction, not direct bleeding risk. I avoid routine FFP for INR correction; it carries risks of volume overload and increased portal pressure. I transfuse platelets for severe thrombocytopenia with active bleeding, and cryoprecipitate only if fibrinogen is low during a significant bleed. Restrictive RBC transfusion reduces the risk of rebleeding by avoiding portal pressure surges (Garcia-Tsao et al., 2017; Carson et al., 2016).

Acute Liver Failure and Alcohol-Related Hepatitis: NAC, Infection Screening, and Discharge Criteria

In acute liver failure, I start N-acetylcysteine (NAC) early—even in non-acetaminophen cases—to replenish glutathione, improve microcirculatory flow, and reduce oxidative stress. I monitor for hepatic encephalopathy and dynamic changes in INR; new-onset encephalopathy prompts engagement with the transplant center (Jalan & Williams, 2018).

In alcohol-related hepatitis, I calculate MELD/MELD 3.0, screen for asymptomatic infections (blood cultures, urine culture, chest X-ray), and differentiate lactulose-induced diarrhea from infectious diarrhea. I have become more cautious with steroids due to infection risk and limited short-term benefit, and I increasingly use NAC for its favorable risk-benefit profile (Singal & Shah, 2022; Crabb et al., 2020). Discharge focuses on trend improvement (not normalization), completion of NAC, and initiation of medication-assisted therapy for alcohol use disorder.

Decompensated Cirrhosis: Ascites, HRS-AKI, and Pulmonary Syndromes

I confirm ascites etiology with SAAG. I recommend a 2-gram sodium diet, avoid fluid restriction unless sodium < 120 mEq/L, and simplify diuretics with once-daily furosemide plus spironolactone titrated together to maintain potassium. After large-volume paracentesis (>5 L), I replace albumin to prevent circulatory dysfunction and HRS-AKI.

For HRS-AKI, I use terlipressin when available (contraindications: hypoxia, severe vascular disease) or combine norepinephrine or midodrine plus octreotide. Dialysis is typically a bridge to transplant (Biggins et al., 2021).

I recognize hepatopulmonary syndrome and portopulmonary hypertension with platypnea and orthodeoxia; a bubble echocardiogram confirms shunt physiology. The only definitive cure is transplantation; oxygen supports symptoms.

Elevated Liver Enzymes: Pattern Recognition and Targeted Workup

I use the R-factor to classify injury patterns (hepatocellular, cholestatic, or mixed). AST: ALT > 2:1 suggests alcoholic liver disease. Enzymes in the thousands narrow the differential to ischemia, acute viral hepatitis, and acetaminophen toxicity. I distinguish injury markers (AST/ALT) from function markers (INR, bilirubin).

I am judicious about liver biopsy—reserved for diagnostic uncertainty or suspected autoimmune hepatitis (e.g., high-titer ANA, AMA positivity). I collaborate closely with pharmacists and ask about all ingested substances—antibiotics taken months ago, herbal supplements,”“cleanses,” juices—because idiosyncratic DILI is common and often overlooked (Chalasani et al., 2014).

Portal Vein Thrombosis: Imaging, Risk Assessment, and Anticoagulation Decisions

If a previously compensated patient acutely decompensates, I rule out portal vein thrombosis (PVT). I start with Doppler ultrasound; if limited, I proceed to CT/MRI for extent and rule out malignant thrombus. Hypercoagulable workups are usually unhelpful in cirrhosis.

• I avoid anticoagulation in chronic, occlusive PVT with cavernous transformation.
• I consider anticoagulation in acute/extending PVT or when intestinal ischemia is suspected.d
• I individualize therapy and monitoring with hepatology, hematology, and pharmacy, tailoring DOAC or LMWH dosing and surveillance imaging (European Association for the Study of the Liver, 2016)

Where Integrative Chiropractic Care Fits

Integrative chiropractic care complements internal medicine in several ways:

• Autonomic modulation: Targeted spinal adjustments may influence vagal tone and sympathetic outflow to the GI tract, potentially affecting acid secretion, motility, and mucosal blood flow. Emerging evidence suggests spinal manipulation can alter heart rate variability, a proxy for autonomic balance (Budgell & Polus, 2006).
• Pain reduction and functional recovery: By addressing biomechanical dysfunction, soft tissue restrictions, and neuromuscular imbalance, chiropractic care reduces pain and enhances mobility—often decreasing reliance on NSAIDs and opioids (Bronfort et al., 2010).
• Rehabilitation and resilience: Hospitalization often leads to deconditioning. Integrative rehabilitation rebuilds strength, improves posture and breathing mechanics, supports lymphatic return, and aids GI motility through movement.
• Functional medicine synergy: I integrate anti-inflammatory nutrition, targeted micronutrient therapy, and gut-restorative protocols alongside medical therapy to reduce systemic inflammatory burden and support recovery.

Under Dr. Cardenas’s medical direction, these therapies are safely combined with pharmacologic and procedural care, creating a unified plan that treats both symptom and system.

Clinical Observations and Practice Philosophy

From my clinical work and communications shared on my website and professional profile, I advocate for:

• Clear discharge planning with adequate medications, especially PPIs and iron, recognizing real-world follow-up delays in rural and underserved settings
• Physiology-first protocols—timing colonoscopy for optimal prep quality, using heparin bridges to test anticoagulation tolerance, and adopting restrictive transfusion strategies to reduce portal pressure
• Education and empowerment—teaching patients and staff about overflow diarrhea, lactulose hold parameters, and the risks/benefits of steroids versus NAC in alcohol-related hepatitis.

My commitment is to evidence-based, integrative care that respects the realities ofpatients’’ lives and supports long-term healing.

References

• Abraham, N. S. (2022). Management of anti-coagulants in patients with acute gastrointestinal bleeding. UpToDate.
• American College of Gastroenterology. (2024). Clinical guidelines for the management of acute pancreatitis. The American Journal of Gastroenterology.
• Biggins, S. W., Angeli, P., Garcia-Tsao, G., Ginès, P., Ling, S. C., Nadim, M. K., … & Wong, F. (2021). Diagnosis, evaluation, and management of ascites, spontaneous bacterial peritonitis and hepatorenal syndrome: 2021 practice guidance by the American Association for the Study of Liver Diseases. Hepatology, 74(1), 399–424.
• Bronfort, G., Haas, M., Evans, R., Leininger, B., & Triano, J. (2010). Effectiveness of manual therapies: The UK evidence report. Chiropractic & Osteopathy, 18(1), 3.
• Budgell, B., & Polus, B. (2006). The effects of thoracic manipulation on heart rate variability: A controlled crossover trial. Journal of Manipulative and Physiological Therapeutics, 29(8), 603–610.
• Carson, J. L., Guyatt, G., Heddle, N. M., Grossman, B. J., Cohn, C. S., Fung, M. K., … & Tondon, R. (2016). Clinical practice guidelines from the AABB: Red blood cell transfusion thresholds and storage. JAMA, 316(19), 2025–2035.
• Chalasani, N., Hayashi, P. H., Bonkovsky, H. L., Navarro, V. J., Lee, W. M., & Fontana, R. J. (2014). ACG clinical guideline: The diagnosis and management of idiosyncratic drug-induced liver injury. The American Journal of Gastroenterology, 109(7), 950–966.
• Crabb, D. W., Im, G. Y., Szabo, G., Mellinger, J. L., & Lucey, M. R. (2020). Diagnosis and treatment of alcohol-associated liver diseases: 2019 practice guidance from the AASLD. Hepatology, 71(1), 306–333.
• European Association for the Study of the Liver. (2016). EASL clinical practice guidelines: Vascular diseases of the liver. Journal of Hepatology, 64(1), 179–202.
• Garcia-Tsao, G., Abraldes, J. G., Berzigotti, A., & Bosch, J. (2017). Portal hypertensive bleeding in cirrhosis: Risk stratification, diagnosis, and management: 2016 practice guidance by the AASLD. Hepatology, 65(1), 310–335.
• Jalan, R., & Williams, R. (2018). The role of N-acetylcysteine in acute liver failure. Current Opinion in Critical Care, 24(2), 114–119.
• Laine, L., Shah, A., & Bemanian, S. (2021). A randomized controlled trial of urgent vs elective colonoscopy in patients with acute lower gastrointestinal bleeding. Gastroenterology, 160(5), 1572–1581.e4.
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• Meeker, W. C., & Haldeman, S. (2002). Chiropractic: A profession at the crossroads of mainstream and alternative medicine. Annals of Internal Medicine, 136(3), 216–227.
• Mullish, B. H., & Williams, H. R. T. (2018). Clostridioides difficile infection and inflammatory bowel disease: A review. Journal of Basic and Clinical Medicine, 5(2), 27–38.
• North-Lewis, P. (2018). The Baveno VI guidelines for management of portal hypertension: A game-changer for hepatologists? United European Gastroenterology Journal, 6(5), 637–640.
• Papa, A., Gasbarrini, A., & Tursi, A. (2016). Inflammatory bowel disease and thrombosis. World Journal of Gastroenterology, 22(5), 1819–1827.
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• Singal, A. K., & Shah, V. H. (2022). Alcoholic hepatitis: Pathogenesis, evaluation, and treatment. Gastroenterology, 162(3), 748–763.
• Strand, D. S., Kim, D., & Peura, D. A. (2017). 25 years of proton pump inhibitors: A comprehensive review. Gut and Liver, 11(1), 27–37.
• Vilstrup, H., Amodio, P., Bajaj, J., Cordoba, J., Ferenci, P., Mullen, K. D., … & Wong, P. (2014). Hepatic encephalopathy in chronic liver disease: Practice guideline by AASLD and EASL. Hepatology, 60(2), 715–735.

SEO tags: upper GI bleeding, melena vs hematochezia, peptic ulcer disease, NSAID-induced GI injury, doxycycline pill esophagitis, colonoscopy timing, diverticular bleeding, anticoagulation in GI bleed, Watchman device, heparin bridge, Cameron’s ulcers, proton pump inhibitors, acute pancreatitis fluids, Lactated Ringer’s pancreatitis, early enteral feeding, cholangitis ERCP, mesenteric ischemia watershed, overflow diarrhea impaction, dysphagia EGD dilation, IBD flare CRP calprotectin, C. difficile fidaxomicin, bezlotoxumab recurrence, iron deficiency IV iron, restrictive transfusion cirrhosis, variceal bleeding carvedilol, TIPS MELD, lactulose hold parameters, hepatic encephalopathy rifaximin, coagulation cirrhosis INR, acute liver failure NAC, alcohol-related hepatitis infection screen, SAAG ascites, HRS-AKI terlipressin, portal vein thrombosis anticoagulation, integrative chiropractic autonomic modulation, functional medicine GI, Injury Medical Clinic PA, Dr. Alex Jimenez DC APRN FNP-BC, Dr. Maria Guadalupe Cardenas MD El Paso Texas