What is the best course of treatment for a 56-year-old chronic alcoholic (long-term heavy drinker) with a history of liver disease, presenting with hematemesis (vomiting blood), melena (black tarry stools), hypotension (low blood pressure), tachycardia (rapid heart rate), impaired renal function (elevated blood urea nitrogen), coagulopathy (elevated international normalized ratio), and anemia (low hemoglobin), with icteric sclerae (yellowing of the eyes) and spider angioma (skin lesions)?

Management of Acute Variceal Hemorrhage in Decompensated Alcoholic Cirrhosis

This patient requires immediate resuscitation with vasoactive therapy (octreotide or terlipressin) started before endoscopy, urgent upper endoscopy for diagnosis and endoscopic band ligation or sclerotherapy, prophylactic antibiotics, restrictive transfusion strategy, and intensive care monitoring for complications including hepatorenal syndrome and infection. 1

Immediate Resuscitation and Stabilization

Vasoactive Therapy - Start Immediately

• Begin octreotide or terlipressin immediately upon suspicion of variceal bleeding, without waiting for endoscopic confirmation. 1
• This patient's presentation (hematemesis, melena, hypotension, tachycardia, stigmata of chronic liver disease) strongly suggests variceal hemorrhage from portal hypertension. 1, 2
• Vasoactive drugs reduce portal pressure and control bleeding while preparing for endoscopy. 1

Avoid Beta-Blockers in Acute Hemorrhage

• Beta-blockers like propranolol are contraindicated during active bleeding as they worsen hypotension (BP already 88/56 mmHg) and increase acute kidney injury risk (BUN already elevated at 28 mg/dL). 1
• Beta-blockers are reserved for secondary prophylaxis after stabilization, not acute management. 1

Blood Product Strategy

• Use restrictive transfusion approach - target hemoglobin 7-8 g/dL rather than aggressive correction. 3
• Despite INR 2.0 and low platelets (implied by cirrhosis), routine correction with FFP or platelet transfusions is not indicated as these patients have rebalanced hemostasis and such products may worsen portal pressure. 3
• Prohemostatic therapy is not first-line management even with markedly abnormal coagulation parameters, as bleeding is mechanical (variceal rupture) not coagulopathic. 3

Prophylactic Antibiotics - Critical

• Start broad-spectrum antibiotics immediately (typically ceftriaxone or norfloxacin). 4, 1
• Patients with alcoholic cirrhosis and variceal bleeding have extremely high infection risk, and bacterial infections can trigger bleeding and worsen outcomes. 4, 5
• Antibiotic prophylaxis reduces mortality in this population. 4

Urgent Endoscopy and Definitive Hemostasis

Timing and Approach

• Perform urgent upper endoscopy within 12 hours after initial resuscitation to confirm variceal source and provide endoscopic therapy. 1, 6
• Important caveat: While varices are most likely (60-70% of upper GI bleeding in alcoholic cirrhosis), 30-40% of bleeding in alcoholic liver disease is non-variceal (peptic ulcer disease, Dieulafoy's lesion, Mallory-Weiss tear). 6
• Patients with alcoholic cirrhosis have increased risk and severity of peptic ulcer bleeding, which carries worse outcomes than in non-cirrhotics. 6

Endoscopic Treatment

• If varices confirmed: endoscopic variceal ligation (banding) is preferred, or sclerotherapy if banding not feasible. 1
• If non-variceal source found: standard hemostatic techniques (clips, thermal therapy, injection) as appropriate. 6

Critical Monitoring and Complications

Renal Function Surveillance

• Monitor creatinine and urine output closely - this patient already has elevated BUN (28 mg/dL) suggesting early renal dysfunction. 4
• Hepatorenal syndrome is a major cause of death in severe alcoholic hepatitis with variceal bleeding. 4
• Avoid nephrotoxic agents and maintain adequate but not excessive volume status. 4

Infection Monitoring

• Check for infections daily - spontaneous bacterial peritonitis, pneumonia, urinary tract infections are common and deadly in this population. 4, 1
• Low threshold for diagnostic paracentesis if ascites present (globular tense abdomen suggests significant ascites). 4

Prognostic Assessment and Disease Severity

Calculate Severity Scores

• Maddrey Discriminant Function (MDF) = 4.6 × (PT patient - PT control) + total bilirubin (mg/dL). 4
  • With INR 2.0 (PT ~24 seconds if control is 12) and bilirubin 5.2: MDF ≈ 60, indicating severe alcoholic hepatitis with very high mortality risk. 4
• MELD score should also be calculated - likely >20 given INR 2.0, bilirubin 5.2, and elevated creatinine (implied by BUN 28). 4
• MDF ≥32 or MELD ≥11 indicates poor prognosis requiring intensive management. 4

Mortality Risk

• This patient has extremely high short-term mortality - 28-day mortality of 30-50% with variceal bleeding in alcoholic cirrhosis. 1
• Combination of variceal bleeding with severe ascites (suggested by globular tense abdomen) carries 20-64% one-year mortality. 1
• The presence of hematemesis with shock requiring >1000 mL rapid transfusion within one hour defines massive bleeding with grave prognosis. 7

Specific Therapies to Avoid

Proton Pump Inhibitors - Not Effective

• PPIs are not indicated for variceal bleeding as this is portal hypertension-related, not acid-related mucosal injury. 1
• PPIs may be considered only if non-variceal source (peptic ulcer) is confirmed on endoscopy. 1

Corticosteroids - Timing Matters

• While severe alcoholic hepatitis (MDF ≥32) may warrant corticosteroids, do not start steroids during active bleeding or active infection. 4
• First-line therapy for severe alcoholic hepatitis is corticosteroids, but with ongoing sepsis, pentoxifylline is preferred. 4
• Stabilize bleeding and rule out infection before considering steroids. 4

Long-Term Management After Stabilization

Alcohol Cessation - Most Critical Intervention

• Absolute alcohol abstinence is the single most important intervention for survival. 4, 1
• Continued alcohol use results in 100% 3-year mortality versus 75% survival with complete abstinence in Child-Pugh C alcoholic cirrhosis. 1
• Patients who continue drinking have markedly increased risk of rebleeding and death. 4
• Initiate addiction counseling and pharmacotherapy (naltrexone, acamprosate) after acute stabilization. 4

Nutritional Support

• Patients with alcoholic cirrhosis are severely malnourished (albumin 2.5 g/dL indicates protein depletion). 4
• Provide thiamine supplementation immediately to prevent Wernicke's encephalopathy. 6
• Monitor for alcohol withdrawal syndrome requiring benzodiazepines. 6

Secondary Prophylaxis

• After bleeding controlled: initiate non-selective beta-blocker (propranolol or carvedilol) plus repeat endoscopic variceal ligation sessions until varices eradicated. 1
• Consider transjugular intrahepatic portosystemic shunt (TIPS) if rebleeding occurs despite medical and endoscopic therapy. 1