2025 PACUPrep BCCCP Preparatory Course Acute Upper Gastrointestinal Bleeding Management of Acute Upper Gastrointestinal Bleeding
Supportive Care and Monitoring in Acute Upper GI Bleeding

Supportive Care and Monitoring in Acute Upper GI Bleeding

Objectives Icon A checkmark inside a circle, symbolizing achieved goals.

Learning Objective

Recommend appropriate supportive care and monitoring to manage complications associated with acute upper gastrointestinal bleeding and its treatment.

I. Overview of Supportive Care in Acute UGIB

In acute upper gastrointestinal bleeding (UGIB), supportive care is crucial for ensuring adequate oxygenation, maintaining perfusion, and protecting end-organ function while definitive hemostasis is pursued. This care is integrated with ongoing resuscitation efforts, endoscopic interventions, and transfusion strategies. Effective management requires multidisciplinary coordination among pharmacy, critical care, gastroenterology, and nursing teams.

Goals of Supportive Care:

  • Secure and maintain a patent airway, especially in patients with altered mental status or massive hematemesis.
  • Maintain mean arterial pressure (MAP) ≥ 65 mmHg to ensure adequate tissue perfusion.
  • Preserve end-organ function by optimizing oxygen delivery and addressing metabolic derangements.
Key Pearls
  • Supportive care is dynamic—reassess patient status in real time as bleeding and hemodynamics evolve.
  • Consider early ICU admission for patients with ongoing bleeding, high-risk scores (e.g., Glasgow-Blatchford, Rockall), or evidence of organ dysfunction.

II. Mechanical Ventilation

A. Indications

  • Airway protection in patients with encephalopathy, massive hematemesis, or significant risk of aspiration.
  • To facilitate large-volume resuscitation or urgent endoscopy without compromising airway patency.
  • Respiratory failure secondary to aspiration pneumonia or transfusion-related acute lung injury (TRALI).

B. Ventilation Strategies

  • Tidal volume: Employ lung-protective ventilation with 4–6 mL/kg ideal body weight.
  • Permissive hypercapnia: Generally tolerated unless contraindicated by conditions such as intracranial hypertension.
  • PEEP (Positive End-Expiratory Pressure): Use the lowest level necessary to maintain PaO₂ > 60 mmHg and SpO₂ > 90%, while minimizing barotrauma and adverse effects on venous return and splanchnic perfusion.

C. Sedation and Analgesia

  • Preferred agents: Propofol or dexmedetomidine are often favored due to their rapid offset, facilitating neurological assessments and daily sedation interruptions.
  • Caution: Avoid benzodiazepines in patients with hepatic encephalopathy. Adjust doses of all sedatives and analgesics in the presence of renal or hepatic dysfunction.
  • Monitoring: Continuously monitor for oversedation, hypotension (especially with propofol), and potential drug interactions with vasopressors or other critical care medications.
Key Pearls
  • Excessive PEEP can worsen hypotension by reducing venous return and may impair splanchnic perfusion—titrate carefully based on oxygenation and hemodynamic response.
  • Implementing daily sedation interruptions and using validated sedation scales can reduce ventilator days and associated complications like ventilator-associated pneumonia (VAP).

III. Hemodynamic Support

A. Monitoring

  • Arterial line: Essential for continuous MAP monitoring; aim for MAP ≥ 65 mmHg.
  • Dynamic indices: Utilize pulse pressure variation (PPV) or stroke volume variation (SVV) in mechanically ventilated patients without arrhythmias to guide fluid responsiveness.
  • Perfusion markers: Monitor lactate clearance (aim for normalization or significant reduction) and urine output (> 0.5 mL/kg/hr) as indicators of adequate tissue perfusion.

B. Pharmacotherapy

Vasopressors are indicated if hypotension persists despite adequate fluid resuscitation.

Vasopressor Agents in UGIB-Related Shock
Agent Mechanism Dose Monitoring Notes
Norepinephrine Potent α₁-agonist with β₁ activity—increases SVR, modest increase in CO. Start 0.05–0.1 μg/kg/min; titrate to achieve MAP ≥ 65 mmHg. MAP, digital/extremity perfusion, lactate trend, arrhythmias. First-line agent; generally less arrhythmogenic than dopamine. Use with caution if mesenteric ischemia is suspected.
Vasopressin V₁–receptor vasoconstriction—causes splanchnic and systemic vasoconstriction. Fixed infusion, typically 0.03–0.04 units/min. Not titrated. Serum sodium, signs of ischemia (digital, myocardial, splanchnic). Often used as an adjunct to norepinephrine (catecholamine-sparing effect) to help reach MAP goals or reduce norepinephrine dose.

C. Fluid Management

  • Fluid type: Use balanced crystalloids (e.g., Lactated Ringer’s, Plasma-Lyte). Avoid overzealous boluses that can dilute clotting factors and worsen coagulopathy.
  • Target endpoints: Guide fluid administration using dynamic indices (if applicable), urine output, lactate clearance, and overall clinical assessment.
  • Avoid fluid overload: Excessive fluid administration increases the risk of transfusion-associated circulatory overload (TACO), pulmonary edema, and can potentially increase portal pressure in cirrhotic patients, exacerbating variceal bleeding.
Key Pearls
  • Goal-directed fluid therapy, rather than empiric large-volume resuscitation, helps prevent dilutional coagulopathy and organ edema.
  • Reassess volume status and perfusion frequently, especially after each fluid bolus. Consider early initiation of vasopressors if hypotension persists despite initial fluid challenges.

IV. Prevention of ICU-Related Complications

A. Venous Thromboembolism (VTE) Prophylaxis

1. Pharmacologic Prophylaxis

  • Low-Molecular-Weight Heparin (LMWH): Enoxaparin 40 mg subcutaneously daily is commonly used. Contraindicated in active, uncontrolled bleeding or severe thrombocytopenia (e.g., platelets < 50×10⁹/L).
  • Unfractionated Heparin (UFH): 5,000 units subcutaneously every 8 hours may be preferred in patients with significant renal impairment (CrCl < 30 mL/min).
  • Monitoring: Consider anti-Xa level monitoring for LMWH in patients with severe renal dysfunction or obesity, if used.

2. Mechanical Prophylaxis

  • Intermittent pneumatic compression (IPC) devices should be used when pharmacologic anticoagulation is contraindicated due to active bleeding or high bleeding risk.

B. Stress-Related Mucosal Damage (SRMD) Prophylaxis

1. Proton Pump Inhibitors (PPIs)

  • Pantoprazole 40 mg intravenously daily is often used to maintain an intragastric pH > 4, which is thought to reduce stress ulceration.
  • Risks: Prolonged use is associated with an increased risk of Clostridioides difficile infection and potentially pneumonia. Limit to high-risk patients (e.g., mechanical ventilation >48h, coagulopathy).

2. Histamine-2 Receptor Antagonists (H₂RAs)

  • Famotidine (as ranitidine is largely unavailable) 20 mg IV q12hr.
  • Tachyphylaxis (diminishing effect over time) can occur. Some studies show comparable bleeding prevention to PPIs for SRMD in certain ICU populations.

C. Infection Prevention

  • Ventilator-Associated Pneumonia (VAP) bundles: Implement measures such as head-of-bed elevation (30–45 degrees), daily sedation breaks and assessment of readiness to extubate, and regular oral care with chlorhexidine.
  • Central Line-Associated Bloodstream Infection (CLABSI) bundles: Adhere to strict aseptic technique during insertion (full barrier precautions, chlorhexidine skin prep), and perform daily assessment of line necessity to facilitate prompt removal.
  • Antibiotic stewardship: In patients with cirrhosis and UGIB, short-course prophylactic antibiotics (e.g., ceftriaxone) are recommended to reduce infection rates and mortality. For other ICU infections, use narrow-spectrum antibiotics based on local susceptibility patterns and de-escalate when possible.
Key Pearls
  • Carefully balance the risk of VTE against the risk of rebleeding. Resume pharmacologic VTE prophylaxis as soon as it is deemed safe after hemostasis is achieved.
  • Early initiation of enteral nutrition, when feasible, may provide some mucosal protection and potentially reduce the need for pharmacologic stress ulcer prophylaxis in select patients.

V. Management of Iatrogenic Complications

A. Drug-Induced Organ Dysfunction

  • Nephrotoxicity: Vasopressors (especially at high doses) and intravenous contrast agents can contribute to acute kidney injury. Monitor serum creatinine and urine output closely; adjust drug doses based on renal function. Ensure adequate hydration pre- and post-contrast exposure if possible.
  • Hepatotoxicity: While less common with agents used in UGIB, some drugs like somatostatin analogs (octreotide, terlipressin) used for variceal bleeding can have effects on liver function or splanchnic circulation. Periodic monitoring of liver function tests (LFTs) may be warranted with prolonged use.

B. Transfusion-Related Events

  • Transfusion-Related Acute Lung Injury (TRALI): Characterized by acute hypoxemia and noncardiogenic pulmonary edema developing within 6 hours of transfusion. Management is primarily supportive, including mechanical ventilation if necessary.
  • Transfusion-Associated Circulatory Overload (TACO): Occurs due to rapid or large-volume transfusion, leading to hydrostatic pulmonary edema. Management includes diuretics, fluid restriction, and oxygen support. Monitor central venous pressure (CVP) or other volume indicators if available.
Key Pearls
  • Adherence to a restrictive transfusion strategy (targeting a hemoglobin threshold of 7 g/dL in most stable patients without massive bleeding) has been shown to reduce the risk of TRALI/TACO and may improve overall outcomes in UGIB.

VI. Multidisciplinary Goals-of-Care Discussions

  • Identify patients at high risk for poor prognosis, prolonged ICU stay, or treatment futility early in their admission. This includes those with severe comorbidities, advanced age, refractory shock, or irreversible organ damage.
  • Utilize structured communication frameworks (e.g., SPIKES: Setting, Perception, Invitation, Knowledge, Emotions, Strategy/Summary) for conducting family meetings to discuss prognosis, treatment options, and patient preferences.
  • Clearly document agreed-upon goals of care, including limitations of treatment if applicable (e.g., Do Not Resuscitate/Do Not Intubate orders), and ensure these are communicated to the entire care team. Revisit these discussions after major interventions or significant clinical changes.
Key Pearls
  • Early involvement of palliative care specialists can be beneficial in complex cases to help align medical interventions with patient values, manage symptoms, and support families, potentially preventing futile or non-beneficial care.

VII. Monitoring and Reassessment

Continuous and vigilant monitoring is key to managing patients with acute UGIB effectively.

  • Hemodynamics: Track MAP, heart rate, CVP (if available), and signs of peripheral perfusion. Monitor lactate clearance and urine output as indicators of resuscitation adequacy.
  • Laboratory Parameters: Obtain serial hemoglobin/hematocrit levels to assess ongoing bleeding or response to transfusion. Monitor coagulation profile (INR, PTT, fibrinogen, platelets), renal function (creatinine, BUN), and hepatic panels.
  • Triggers for Escalation of Care:
    • Persistent hypotension despite fluid and vasopressor support.
    • Rising lactate levels or failure of lactate to clear.
    • Clinical evidence of rebleeding (hematemesis, melena, hemodynamic instability after initial stabilization).
    • Worsening organ dysfunction (e.g., declining renal function, worsening encephalopathy, respiratory failure).
  • Triggers for De-escalation of Care:
    • Stable hemodynamics off vasopressors or on weaning doses.
    • No further evidence of bleeding for a defined period (e.g., 24-48 hours).
    • Improving organ function and laboratory parameters.
    • Successful endoscopic hemostasis with low-risk stigmata.
Key Pearls
  • Frequent reassessment of the patient’s clinical status, coupled with protocolized triggers for intervention or changes in management, ensures timely adjustment of supportive measures and can improve outcomes.

References

  1. Laine L, Barkun AN, Saltzman JR, Martel M, Leontiadis GI. ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding. Am J Gastroenterol. 2021;116(5):899–917.
  2. Villanueva C, Colomo A, Bosch A, et al. Transfusion Strategies for Acute Upper Gastrointestinal Bleeding. N Engl J Med. 2013;368(1):11–21.
  3. Pantoprazole Trial Investigators. Pantoprazole in Patients at Risk for Gastrointestinal Bleeding in the ICU. N Engl J Med. 2018;379(23):2199–2208.
  4. Toews I, Hussain S, Nyirenda JLZ, et al. Pharmacological Interventions for Preventing Upper Gastrointestinal Bleeding in People Admitted to ICUs: A Network Meta-Analysis. BMJ Evid Based Med. 2024;0(0):1.
  5. Huang HB, Jiang W, Wang CY, et al. Stress Ulcer Prophylaxis in ICU Patients Receiving Enteral Nutrition: A Systematic Review and Meta-Analysis. Crit Care. 2018;22(1):20.
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