Description
Intensive care management in Acute Liver Failure (ALF) is critical due to its rapid progression and high mortality risk. It involves close monitoring and support of multiple organ systems, particularly neurological function to prevent or manage cerebral edema. Key components include maintaining hemodynamic stability, managing coagulopathy, preventing infections, and ensuring adequate nutrition. Early identification of candidates for liver transplantation is vital, as it remains the definitive treatment in many cases. A multidisciplinary approach, including hepatology, critical care, and transplant teams, is essential for optimal outcomes.
Summary Listen
- Acute Liver Failure (ALF) is a medical emergency in the ICU, requiring swift recognition, coordinated care, and protocol-driven management. Optimal outcomes involve risk stratification, cerebral protection, hemodynamic management, infection control, and timely transplant referral. ICU involvement can be the deciding factor between recovery, transplant, or tragedy.
- ALF is characterized by rapid onset liver injury, typically in the absence of pre-existing chronic liver disease. Massive hepatocyte necrosis is a hallmark, leading to abrupt jaundice, coagulopathy, and encephalopathy. Systemic inflammatory response syndrome (SIRS) triggers cerebral edema and multi-organ dysfunction. While ICU advancements have improved outcomes, liver transplantation is often the definitive treatment.
- ALF is sub-classified based on the time from jaundice onset to encephalopathy onset. Hyperacute ALF occurs within 7 days, acute ALF within 8-28 days, and subacute ALF within 28 days to 3 months. The etiology of ALF varies by geography and age, with viral causes dominating in regions like India, while acetaminophen toxicity is more common in Western countries.
- The pathophysiology of ALF involves a primary liver injury, often from viruses or toxins, that triggers hepatocyte cell death. This leads to an exaggerated immune response, with Kupffer cells releasing cytokines and recruiting more immune cells, worsening liver damage. The resulting cytokine storm induces systemic effects like vasodilation, hypotension, cerebral edema, hyperammonemia, and coagulopathy.
- Clinical presentation of ALF is multi-systemic, affecting the brain (encephalopathy, edema), heart (high output state), lungs (acute lung injury), liver (impaired gluconeogenesis, coagulopathy), and kidneys (AKI). Recognizing red flags early, such as altered mental status, hemodynamic instability, or signs of cerebral edema, is critical for guiding ICU interventions and transplant decisions.
- Initial ICU assessment involves confirming the diagnosis, ruling out chronic liver disease, and identifying the etiology of ALF. Investigations include liver panel, coagulation profile, renal panel, metabolic profile (lactate, ammonia), virology (HAV, HBV, HEV), autoimmune markers, toxicology screen (if suspected), and imaging (ultrasound, CT/MRI brain).
- Organ-specific management prioritizes neuroprotection, especially in hyperacute cases. Strategies include frequent neurological assessments, head elevation, minimizing stimulation, and judicious sedation (avoiding benzodiazepines). Invasive ICP monitoring is less common, with non-invasive methods like optic nerve sheath diameter measurement guiding interventions. CRRT is considered for ammonia control and cerebral edema reduction.
- Cardiovascular management in ALF addresses systemic vasodilation and low central volume. Fluid resuscitation with balanced crystalloids is essential, guided by dynamic assessment. Vasopressors, such as norepinephrine, are used to maintain adequate mean arterial pressure. Adrenal insufficiency should be considered, and low-dose hydrocortisone may be beneficial.
- Respiratory management often involves early intubation to protect the airway and manage hypoxia. Ventilation strategies include lung-protective settings with low tidal volumes and positive end-expiratory pressure (PEEP). Nutrition is often overlooked, with early enteral feeding prioritized to maintain gut integrity. Parenteral nutrition is considered if enteral feeding is inadequate.
- Metabolic management focuses on glucose control, maintaining a target range of 150-180 mg/dL. Sodium levels should be managed to prevent hyponatremia or hypernatremia. Low phosphate levels may indicate liver regeneration and warrant supplementation. AKI is a common complication, requiring preventative strategies and CRRT if necessary.
- Coagulopathy in ALF should be managed cautiously, avoiding overcorrection with FFP. Instead, interventions like thromboelastography (TEG) or rotational thromboelastometry (ROTEM) can guide transfusion decisions. Sepsis is a frequent complication, necessitating prompt broad-spectrum antibiotics and consideration of fungal infections.
- Bridging therapies are used to support patients awaiting liver transplantation. Molecular Adsorbent Recirculating System (MARS) and Prometheus have not shown consistent mortality benefits. Plasma exchange, however, has demonstrated improved transplant-free survival by removing toxins and modulating the immune response.
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About the Speakers
Dr. Himanshu Sharma
Consultant Critical Care Medicine, Zydus Hospital, Gujarat
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