Acute liver failure causes quick liver function deterioration and coagulopathy. It impacts young individuals with high mortality rates.
It has two types as:
Fulminant
Sub-fulminant
Fulminant hepatic failure is when encephalopathy develops within 8 weeks of symptom onset in a patient with healthy liver. While sub-fulminant hepatic failure is for patients with liver issues lasting up to 26 weeks.
Patients with acquired hepatitis B and autoimmune hepatitis may be included if their disease is for <26 weeks.
It occurs within days or weeks and can be life-threatening thus Identify the cause of acute liver failure is necessary for immediate and specific treatment.
Good intensive care support is crucial as treatment phase and the focus should be on fluid management and hemodynamics.
Monitoring of infection surveillance, nutrition maintenance, and identification of bleeding these are essential parameters in treatment phase.
Epidemiology
Anatomy
Pathophysiology
Cerebral edema development leads to high morbidity and mortality in liver failure. Brain cytotoxic edema from cellular osmoregulation issues causes astrocyte swelling. Astrocyte swelling common in brain edema study of acute liver failure.
Glutamate detoxified to glutamine through synthetase. Accumulation in astrocytes causes swelling and brain edema.
Increased intracranial blood volume and cerebral blood flow due to disrupted autoregulation factor in acute liver failure.
Fulminant hepatic failure can lead to multisystem organ failure in a hyperdynamic circulatory state.
Etiology
Atypical causes of viral hepatitis and fulminant hepatic failure as follows:
Cytomegalovirus
Hemorrhagic fever viruses
Epstein-Barr virus
Herpes simplex virus
Paramyxovirus
Several causes for liver failure are:
Hepatic failure in pregnancy
hepatotoxicity due to acetaminophen and idiosyncratic drug
Toxin-related hepatotoxicity
Vascular and metabolic causes
Malignancies
Genetics
Prognostic Factors
Etiology and complications determine outcome in acute liver failure. Acetaminophen-induced cases have better prognosis than those with indeterminate.
Stage 3 or 4 encephalopathy patients face poor prognosis. Mortality risk rises with complications such as cerebral edema, renal failure, and infections.
Pre-transplantation lowest pH and body mass index are preoperative prognostic factors for liver transplant survival.
Fulminant hepatic failure due to viral hepatitis has poor patient outcomes. Patient in deep coma on admission correlates with higher mortality rates.
Clinical History
Clinical History:
Acute liver failure affects individuals of all age groups, but in the age group of 10 to 40 years old it occurs more.
Physical Examination
Vital Signs assessment
Neurological examination
Cardiovascular examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Fast onset of bleeding observed due to decreased clotting factors synthesis.
Severity varies from confusion to coma due to rapid onset and fluid accumulation in hypoalbuminemia.
Brain swelling causes high pressure and rapidly develops into life-threatening conditions.
Differential Diagnoses
Drug-Induced Liver Injury
Metabolic Diseases
Viral Hepatitis
Autoimmune Hepatitis
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Patients with hepatic failure in coma have decreasing airway protection.
Stage III coma patients require both NGT for stomach decompression and intubation for further treatment.
Low-dose short-acting benzodiazepines may be given before intubation and continued.
Propofol reduces cerebral blood flow, it may cause intracranial hypertension, lidocaine recommended for suctioning.
Avoid sedation and use low-dose benzodiazepines for agitation treatment if needed.
Cerebral edema is rare in grades I-II encephalopathy but increases to 25% to 35% in grade III and 65% to 75% in grade IV.
Hemodynamic issues in acute liver failure can lead to multiple organ failure while hypotension affects 15% of patients.
Fresh frozen plasma correction unnecessary for clotting abnormalities without bleeding, unless invasive procedure planned or profound coagulopathy present.
Avoid aminoglycosides and NSAIDs in acetaminophen hepatotoxicity due to nephrotoxicity risk.
Patients should be managed in ICU with facilities for continuous monitoring and advanced supportive care.
Individual should increase dietary intake with fruits and vegetables to promote metabolic needs. Proper fluid intake on daily basis to maintain electrolyte balance.
Regular monitoring of blood glucose levels should be done to prevent hypoglycemia condition.
Proper education and awareness about liver failure should be provided and its related causes with management strategies.
Appointments with a gastroenterologist and preventing recurrence of disorder is an ongoing life-long effort.
Use of Antidotes
Silibinin:
It is a water-soluble derivative of silymarin that has antioxidant properties that may benefit liver disease management.
N-acetylcysteine:
It is used in acetaminophen overdose cases, and it restores depleted intrahepatic glutathione levels.
Use of Osmotic Diuretic
Mannitol:
It is effective in the short term for decreasing cerebral edema. It is administered through intravenous route to treat intracranial hypertension in acute liver failure.
Airway Management and Mechanical Ventilation is required for patients with severe hepatic encephalopathy, respiratory failure, or inability to protect the airway.
Central Venous Catheterization is required for administration of medications, fluids, and for hemodynamic monitoring.
Patients with poor prognosis, not responsive to treatment, and meeting criteria for transplant are eligible for liver transplantation.
use-of-phases-in-managing-acute-liver-failure
In the initial diagnosis phase, evaluation of medical history, laboratory tests and imaging studies to confirm diagnosis.
Pharmacologic therapy is very effective in the treatment phase as it includes use of antidotes, osmotic diuretic, barbiturate, and surgical intervention.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and rehabilitation.
The regular follow-up visits with the gastroenterologist are schedule to check the improvement of patients along with treatment response.
Acute liver failure causes quick liver function deterioration and coagulopathy. It impacts young individuals with high mortality rates.
It has two types as:
Fulminant
Sub-fulminant
Fulminant hepatic failure is when encephalopathy develops within 8 weeks of symptom onset in a patient with healthy liver. While sub-fulminant hepatic failure is for patients with liver issues lasting up to 26 weeks.
Patients with acquired hepatitis B and autoimmune hepatitis may be included if their disease is for <26 weeks.
It occurs within days or weeks and can be life-threatening thus Identify the cause of acute liver failure is necessary for immediate and specific treatment.
Good intensive care support is crucial as treatment phase and the focus should be on fluid management and hemodynamics.
Monitoring of infection surveillance, nutrition maintenance, and identification of bleeding these are essential parameters in treatment phase.
Cerebral edema development leads to high morbidity and mortality in liver failure. Brain cytotoxic edema from cellular osmoregulation issues causes astrocyte swelling. Astrocyte swelling common in brain edema study of acute liver failure.
Glutamate detoxified to glutamine through synthetase. Accumulation in astrocytes causes swelling and brain edema.
Increased intracranial blood volume and cerebral blood flow due to disrupted autoregulation factor in acute liver failure.
Fulminant hepatic failure can lead to multisystem organ failure in a hyperdynamic circulatory state.
Atypical causes of viral hepatitis and fulminant hepatic failure as follows:
Cytomegalovirus
Hemorrhagic fever viruses
Epstein-Barr virus
Herpes simplex virus
Paramyxovirus
Several causes for liver failure are:
Hepatic failure in pregnancy
hepatotoxicity due to acetaminophen and idiosyncratic drug
Toxin-related hepatotoxicity
Vascular and metabolic causes
Malignancies
Etiology and complications determine outcome in acute liver failure. Acetaminophen-induced cases have better prognosis than those with indeterminate.
Stage 3 or 4 encephalopathy patients face poor prognosis. Mortality risk rises with complications such as cerebral edema, renal failure, and infections.
Pre-transplantation lowest pH and body mass index are preoperative prognostic factors for liver transplant survival.
Fulminant hepatic failure due to viral hepatitis has poor patient outcomes. Patient in deep coma on admission correlates with higher mortality rates.
Clinical History:
Acute liver failure affects individuals of all age groups, but in the age group of 10 to 40 years old it occurs more.
Vital Signs assessment
Neurological examination
Cardiovascular examination
Fast onset of bleeding observed due to decreased clotting factors synthesis.
Severity varies from confusion to coma due to rapid onset and fluid accumulation in hypoalbuminemia.
Brain swelling causes high pressure and rapidly develops into life-threatening conditions.
Drug-Induced Liver Injury
Metabolic Diseases
Viral Hepatitis
Autoimmune Hepatitis
Patients with hepatic failure in coma have decreasing airway protection.
Stage III coma patients require both NGT for stomach decompression and intubation for further treatment.
Low-dose short-acting benzodiazepines may be given before intubation and continued.
Propofol reduces cerebral blood flow, it may cause intracranial hypertension, lidocaine recommended for suctioning.
Avoid sedation and use low-dose benzodiazepines for agitation treatment if needed.
Cerebral edema is rare in grades I-II encephalopathy but increases to 25% to 35% in grade III and 65% to 75% in grade IV.
Hemodynamic issues in acute liver failure can lead to multiple organ failure while hypotension affects 15% of patients.
Fresh frozen plasma correction unnecessary for clotting abnormalities without bleeding, unless invasive procedure planned or profound coagulopathy present.
Avoid aminoglycosides and NSAIDs in acetaminophen hepatotoxicity due to nephrotoxicity risk.
Gastroenterology
Patients should be managed in ICU with facilities for continuous monitoring and advanced supportive care.
Individual should increase dietary intake with fruits and vegetables to promote metabolic needs. Proper fluid intake on daily basis to maintain electrolyte balance.
Regular monitoring of blood glucose levels should be done to prevent hypoglycemia condition.
Proper education and awareness about liver failure should be provided and its related causes with management strategies.
Appointments with a gastroenterologist and preventing recurrence of disorder is an ongoing life-long effort.
Gastroenterology
Silibinin:
It is a water-soluble derivative of silymarin that has antioxidant properties that may benefit liver disease management.
N-acetylcysteine:
It is used in acetaminophen overdose cases, and it restores depleted intrahepatic glutathione levels.
Gastroenterology
Mannitol:
It is effective in the short term for decreasing cerebral edema. It is administered through intravenous route to treat intracranial hypertension in acute liver failure.
It is a short-acting benzodiazepine sedative-hypnotic used in patients for acute or short-term sedation.
Gastroenterology
Propofol:
It decreases cerebral blood flow and intracranial hypertension.
Gastroenterology
Airway Management and Mechanical Ventilation is required for patients with severe hepatic encephalopathy, respiratory failure, or inability to protect the airway.
Central Venous Catheterization is required for administration of medications, fluids, and for hemodynamic monitoring.
Patients with poor prognosis, not responsive to treatment, and meeting criteria for transplant are eligible for liver transplantation.
Gastroenterology
In the initial diagnosis phase, evaluation of medical history, laboratory tests and imaging studies to confirm diagnosis.
Pharmacologic therapy is very effective in the treatment phase as it includes use of antidotes, osmotic diuretic, barbiturate, and surgical intervention.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and rehabilitation.
The regular follow-up visits with the gastroenterologist are schedule to check the improvement of patients along with treatment response.
Acute liver failure causes quick liver function deterioration and coagulopathy. It impacts young individuals with high mortality rates.
It has two types as:
Fulminant
Sub-fulminant
Fulminant hepatic failure is when encephalopathy develops within 8 weeks of symptom onset in a patient with healthy liver. While sub-fulminant hepatic failure is for patients with liver issues lasting up to 26 weeks.
Patients with acquired hepatitis B and autoimmune hepatitis may be included if their disease is for <26 weeks.
It occurs within days or weeks and can be life-threatening thus Identify the cause of acute liver failure is necessary for immediate and specific treatment.
Good intensive care support is crucial as treatment phase and the focus should be on fluid management and hemodynamics.
Monitoring of infection surveillance, nutrition maintenance, and identification of bleeding these are essential parameters in treatment phase.
Cerebral edema development leads to high morbidity and mortality in liver failure. Brain cytotoxic edema from cellular osmoregulation issues causes astrocyte swelling. Astrocyte swelling common in brain edema study of acute liver failure.
Glutamate detoxified to glutamine through synthetase. Accumulation in astrocytes causes swelling and brain edema.
Increased intracranial blood volume and cerebral blood flow due to disrupted autoregulation factor in acute liver failure.
Fulminant hepatic failure can lead to multisystem organ failure in a hyperdynamic circulatory state.
Atypical causes of viral hepatitis and fulminant hepatic failure as follows:
Cytomegalovirus
Hemorrhagic fever viruses
Epstein-Barr virus
Herpes simplex virus
Paramyxovirus
Several causes for liver failure are:
Hepatic failure in pregnancy
hepatotoxicity due to acetaminophen and idiosyncratic drug
Toxin-related hepatotoxicity
Vascular and metabolic causes
Malignancies
Etiology and complications determine outcome in acute liver failure. Acetaminophen-induced cases have better prognosis than those with indeterminate.
Stage 3 or 4 encephalopathy patients face poor prognosis. Mortality risk rises with complications such as cerebral edema, renal failure, and infections.
Pre-transplantation lowest pH and body mass index are preoperative prognostic factors for liver transplant survival.
Fulminant hepatic failure due to viral hepatitis has poor patient outcomes. Patient in deep coma on admission correlates with higher mortality rates.
Clinical History:
Acute liver failure affects individuals of all age groups, but in the age group of 10 to 40 years old it occurs more.
Vital Signs assessment
Neurological examination
Cardiovascular examination
Fast onset of bleeding observed due to decreased clotting factors synthesis.
Severity varies from confusion to coma due to rapid onset and fluid accumulation in hypoalbuminemia.
Brain swelling causes high pressure and rapidly develops into life-threatening conditions.
Drug-Induced Liver Injury
Metabolic Diseases
Viral Hepatitis
Autoimmune Hepatitis
Patients with hepatic failure in coma have decreasing airway protection.
Stage III coma patients require both NGT for stomach decompression and intubation for further treatment.
Low-dose short-acting benzodiazepines may be given before intubation and continued.
Propofol reduces cerebral blood flow, it may cause intracranial hypertension, lidocaine recommended for suctioning.
Avoid sedation and use low-dose benzodiazepines for agitation treatment if needed.
Cerebral edema is rare in grades I-II encephalopathy but increases to 25% to 35% in grade III and 65% to 75% in grade IV.
Hemodynamic issues in acute liver failure can lead to multiple organ failure while hypotension affects 15% of patients.
Fresh frozen plasma correction unnecessary for clotting abnormalities without bleeding, unless invasive procedure planned or profound coagulopathy present.
Avoid aminoglycosides and NSAIDs in acetaminophen hepatotoxicity due to nephrotoxicity risk.
Gastroenterology
Patients should be managed in ICU with facilities for continuous monitoring and advanced supportive care.
Individual should increase dietary intake with fruits and vegetables to promote metabolic needs. Proper fluid intake on daily basis to maintain electrolyte balance.
Regular monitoring of blood glucose levels should be done to prevent hypoglycemia condition.
Proper education and awareness about liver failure should be provided and its related causes with management strategies.
Appointments with a gastroenterologist and preventing recurrence of disorder is an ongoing life-long effort.
Gastroenterology
Silibinin:
It is a water-soluble derivative of silymarin that has antioxidant properties that may benefit liver disease management.
N-acetylcysteine:
It is used in acetaminophen overdose cases, and it restores depleted intrahepatic glutathione levels.
Gastroenterology
Mannitol:
It is effective in the short term for decreasing cerebral edema. It is administered through intravenous route to treat intracranial hypertension in acute liver failure.
It is a short-acting benzodiazepine sedative-hypnotic used in patients for acute or short-term sedation.
Gastroenterology
Propofol:
It decreases cerebral blood flow and intracranial hypertension.
Gastroenterology
Airway Management and Mechanical Ventilation is required for patients with severe hepatic encephalopathy, respiratory failure, or inability to protect the airway.
Central Venous Catheterization is required for administration of medications, fluids, and for hemodynamic monitoring.
Patients with poor prognosis, not responsive to treatment, and meeting criteria for transplant are eligible for liver transplantation.
Gastroenterology
In the initial diagnosis phase, evaluation of medical history, laboratory tests and imaging studies to confirm diagnosis.
Pharmacologic therapy is very effective in the treatment phase as it includes use of antidotes, osmotic diuretic, barbiturate, and surgical intervention.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and rehabilitation.
The regular follow-up visits with the gastroenterologist are schedule to check the improvement of patients along with treatment response.
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