Upper Gastrointestinal Hemorrhage (UGIB, UGIH) Management: Variceal Bleeding vs. Non-Variceal Bleeding
- Mayta
- Sep 15, 2024
- 4 min read
Managing upper gastrointestinal (GI) hemorrhage requires distinguishing between variceal and non-variceal bleeding, both of which present unique challenges and treatment approaches. Let's explore the clinical presentation, diagnostic criteria, and management protocols, integrating insights from clinical standing orders and guidelines.
1. History Taking
Chief Complaint: Patients with UGIB typically present with:
Hematochezia: Bright red blood in stools.
Melena: Black, tarry stools, indicative of slower bleeding higher up in the GI tract.
Hematemesis: Vomiting blood, often seen in significant or acute bleeding episodes.
Associated Symptoms:
Dizziness, fatigue, syncope (due to anemia and hypovolemia).
Abdominal pain: May indicate underlying ulcer disease or gastritis.
Past Medical History:
Variceal bleeding risk: History of cirrhosis, chronic liver disease, alcohol abuse, or viral hepatitis.
Non-variceal bleeding risk: History of peptic ulcer disease, NSAID use, or gastric tumors.
Medications:
Use of NSAIDs, aspirin, anticoagulants, or alcohol, all of which increase bleeding risk.
2. Physical Examination
General Appearance: Patients may exhibit pallor, tachycardia, or hypotension, all signs of significant blood loss.
Abdominal Examination:
Ascites or hepatomegaly: Indicate chronic liver disease and portal hypertension, suggestive of variceal bleeding.
Epigastric tenderness: Could point to peptic ulcer disease or gastritis.
Signs of Liver Disease:
Jaundice, spider angiomas, caput medusae, and palmar erythema (indicative of portal hypertension).
Rectal Exam:
Detect melena (indicative of slower, higher-up bleeding) or hematochezia (suggestive of brisk lower GI bleeding or massive UGIB).
3. Diagnostic Criteria
Endoscopy (Crucial in 90% of cases):
Variceal bleeding:
Identification of esophageal or gastric varices with signs of active bleeding (red wale marks).
Non-variceal bleeding:
Typically from peptic ulcers, visualized during endoscopy with active bleeding, a visible vessel, or adherent clot.
Laboratory Tests:
Hemoglobin (Hgb): Significant blood loss often presents with a sharp drop in Hgb levels.
Platelet count: Commonly decreased in variceal bleeding due to liver disease.
Liver Function Tests (LFTs): Elevated bilirubin, AST/ALT, and INR point toward impaired liver function and a higher risk of variceal bleeding.
BUN/Creatinine ratio: An elevated ratio may indicate an upper GI bleed due to digestion of blood in the stomach.
4. Orders and Management
Laboratory Investigations (Standing Order):
CBC (Complete Blood Count), PT, PTT, INR: To assess hemoglobin levels, coagulopathy, and general bleeding risk.
BUN, Creatinine, Electrolytes, LFTs: To monitor kidney function and liver status, which is crucial for patients with variceal bleeding.
Serial Hematocrit and DTX: Monitored every 4, 6, or 8 hours to observe for ongoing blood loss and glycemic control (DTX 80-180 mg%).
Transfusion Protocols
Packed Red Cells (PRC): Ordered in multiple units to restore hemoglobin levels after significant blood loss.
Platelet Transfusion: Administered if thrombocytopenia is present, particularly common in variceal bleeding due to liver disease.
Fresh Frozen Plasma (FFP): To correct coagulation abnormalities in liver disease (common in cirrhotic patients).
Medication Management
For Variceal Bleeding:
Octreotide (Somatostatin Analog):
Type: Vasoactive agent.
Mechanism: Reduces portal venous pressure by vasoconstriction of the splanchnic circulation.
Dosage: 50 mcg IV bolus, followed by 500 mcg in 5% dextrose solution over 20 minutes, then continuous infusion at 50 mcg/hour.
Ceftriaxone 1g IV OD:
Type: Broad-spectrum third-generation cephalosporin antibiotic.
Use: Prophylaxis against spontaneous bacterial peritonitis (SBP), common in cirrhotic patients with variceal bleeding.
Beta-Blockers (Propranolol):
Type: Non-selective beta-blocker.
Mechanism: Reduces portal pressure by decreasing heart rate and blood pressure in the portal system.
Vitamin K 10 mg IV OD:
Use: To correct coagulopathy, especially in cirrhotic patients with elevated INR.
Thiamine 100 mg IV OD:
Used in chronic alcohol users to prevent Wernicke’s encephalopathy.
For Non-Variceal Bleeding:
Proton Pump Inhibitors (PPIs):
Pantoprazole 80 mg IV bolus followed by 8 mg/hour continuous infusion: Reduces gastric acid secretion, aiding in clot stabilization and ulcer healing.
Epinephrine:
Type: Sympathomimetic agent.
Mechanism: Used during endoscopic injection therapy to cause localized vasoconstriction, stopping the bleeding at the ulcer site.
H. pylori Eradication:
Clarithromycin 500 mg BID, Amoxicillin 1g BID, and a PPI for 14 days to treat underlying H. pylori in ulcer disease.
Oxygen Supplementation:
Oxygen via cannula at 3 L/min: To maintain oxygenation in patients at risk of hypoxemia due to significant blood loss.
IV Fluids and Inotropic Support:
Normal Saline (NSS): Typically 500-1000 ml bolus followed by 1000-2000 ml at 80-120 ml/hour for volume resuscitation.
Vasopressors (e.g., Levophed): Used to maintain blood pressure in hemodynamically unstable patients.
Key Differentiation in Drug Management:
Variceal bleeding focuses on reducing portal pressure through systemic vasoconstriction (e.g., octreotide, beta-blockers).
Non-variceal bleeding is primarily treated with PPIs and endoscopic therapies (e.g., epinephrine injections, clips, or thermal coagulation).
Conclusion:
The comprehensive management of upper GI hemorrhage involves:
Early resuscitation with fluids and blood products.
Specific drug therapies based on whether the bleeding is variceal or non-variceal.
Endoscopy for diagnosis and immediate treatment (band ligation, injection therapy).
Monitoring and continuous reassessment of hemodynamic stability and lab parameters.
Understanding the differences in the pathophysiology and treatment strategies for variceal and non-variceal bleeding ensures optimal care, reducing complications and improving patient outcomes.
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