Robert J. Wong and Glen A. Lutchman
Acute liver failure (ALF) is a rare condition characterized by a rapid decline in hepatic synthetic function, marked hepatocellular inflammation, and a high mortality rate. The incidence of ALF is approximately 2,000 cases per year in the United States; it accounts for 6% of all liver-related deaths and 6% of liver transplantations.1–3 Differentiating acute from acute-on-chronic liver failure can be difficult, but is important when assessing patient prognosis and need for transfer to a liver transplant center. Early recognition of ALF allows for targeted supportive therapy, early evaluation for liver transplantation, and timely involvement of multidisciplinary specialties, including hepatologists, intensivists, and transplant surgeons.
ALF is a general term used to define the development of jaundice, hepatic encephalopathy, and coagulopathy (international normalized ratio [INR] ≥ 1.5) in an individual without underlying liver disease with a disease course of <26 weeks. More accurate subclassifications are differentiated by elapsed time from development of jaundice to development of hepatic encephalopathy1,3:
While popular, these terms are not particularly useful since they do not have prognostic significance. For example, “hyperacute” disease generally carries a better prognosis because of a high prevalence in this cohort of acetaminophen-related disease, which tends to have better outcomes.1,3–5 For the remainder of this chapter, we will use the more general definition of ALF.
The initial approach to ALF (Fig. 25.1) involves determining the underlying etiology of disease and the implementing etiology-specific targeted therapy (Tables 25.1 and 25.2). A thorough patient history, including interviews with family and friends, can provide clues to specific ingestions, drugs, or toxins that may be implicated in the patient's disease and enables a review of the patient's prescribed medications for possible drug–drug interactions. The physical exam should focus on an assessment of the patient's mental status and degree of encephalopathy, with specific attention paid to airway patency and need for early intubation for airway protection. This is particularly important if transfer to another hospital is being considered. Initial emergency department (ED) evaluation includes comprehensive laboratory testing aimed at assessing the severity and identifying the underlying etiology of the liver failure (Table 25.3).
FIGURE 25.1 Initial evaluation of ALF.
TABLE 25.1 Common Etiologies of Acute Liver Failure
Data from the Acute Liver Failure Study Group Registry, 1998–2008. From Stravitz RT, Kramer DJ. Management of acute liver failure. Nat Rev Gastroenterol Hepatol. 2009;6:542–553.
TABLE 25.2 Etiology-Specific Targeted Therapy
TABLE 25.3 Laboratory Evaluation in Patients with Acute Liver Failure
Abdominal ultrasound with Doppler flow, if available, is helpful in the evaluation of vascular etiologies of ALF (i.e., Budd-Chiari syndrome) and should also be initiated in the ED. Finally, if possible, a social worker should interview the patient and family in the ED, especially if transfer to a liver transplant center is being considered, as information gained in these interviews can have significant bearing on liver transplant candidacy (e.g., recent alcohol or drug use, social support mechanisms, financial/insurance information).
SYSTEM-SPECIFIC CLINICAL COMPLICATIONS
A common presenting symptom of ALF is hepatic encephalopathy (see Hepatic Encephalopathy). With more severe forms of encephalopathy, maintenance of airway protection may be compromised, necessitating endotracheal intubation. As a result, all patients presenting with ALF should be assessed for the need for ventilatory support. In addition to providing airway protection in patients with severe hepatic encephalopathy, mechanical ventilation also allows for targeted hyperventilation (i.e., hypocapnia) for treatment of cerebral edema and intracranial hypertension (see Neurologic Complications).6,7There are currently insufficient data to recommend a standard mode of mechanical ventilation in ALF patients. However, tidal volume and plateau pressure should be limited to prevent development of acute lung injury. As a result, respiratory rate should be adjusted to ensure adequate minute ventilation to prevent increasing PCO2, which can further exacerbate intracranial hypertension.8,9
One of the most feared complications of ALF, and a leading cause of mortality among these patients, is neurologic impairment—specifically, cerebral edema and intracranial hypertension. Both of these conditions are more common among patients with hyperacute liver failure and can result in hypoxic brain injury, permanent neurologic deficits, and death.1,8,9 Failure to clinically recognize cerebral edema can lead to treatment delays and progression of neurologic complications, including uncal herniation. While the exact etiology of cerebral edema is unclear, it is hypothesized that ALF-induced systemic inflammation and hormonal dysregulation lead to osmotic disturbances in the brain and to heightened cerebral blood flow from autoregulation.10 The risk of cerebral edema and subsequent herniation has been shown to correlate with both the severity of a patient's hepatic encephalopathy and the degree of serum ammonia elevation (see Hepatic Encephalopathy).10–12
Patients with ALF and evidence of neurologic impairments (e.g., cerebral edema) should be monitored in the intensive care unit (ICU). Management of cerebral edema and intracranial hypertension consists of endotracheal intubation when indicated for mental status compromise, close monitoring of intracranial pressure (ICP), and medical therapy to minimize further elevation in ICP. ICP should be maintained at <20 mm Hg and cerebral perfusion pressure (CPP) at >60 mm Hg. CPP is determined by the difference between mean arterial pressure (MAP) and ICP. The role of invasive ICP monitoring in ALF is under study and is only to be undertaken in collaboration with an intensivist and transplant hepatologist.1,13–15 Alternative methods of ICP monitoring, such as transcranial Doppler, are under evaluation.16
In patients with ALF suspected of developing intracranial hypertension, several steps can be taken to treat the elevated pressures and prevent further deterioration. Minimizing patient stimuli, elevating the head of bed to 30°, and avoiding placement of central access in the neck region are initial precautions that can be taken.1,8,9 Medical intervention includes osmotic therapy with either mannitol or hypertonic saline; this increases blood osmolality and induces fluid shift from the brain intracellular space to the intravascular space, thereby decreasing brain edema and pressure. An early randomized control trial of 34 patients with ALF evaluated the effect of intravenous mannitol (given as a rapid infusion of 1 g/kg body weight) in the treatment of patients with intracranial hypertension (ICP ≥30 mm Hg for >5 minutes). Compared to the 17 patients who did not receive mannitol therapy, those who underwent mannitol infusions had significantly higher overall survival (47.1% vs. 5.9%).17 In a randomized controlled trial of 30% hypertonic saline in the management of 45 patients with ALF (using a target serum sodium level of between 145 and 150 mmol/L), a significantly lower incidence of intracranial hypertension was seen among the treatment group.18
For patients requiring mechanical ventilation, hyperventilation to a goal PaCO2 of 25 to 30 mm Hg results in vasoconstriction and decreased ICP and cerebral edema. While mechanical hyperventilation has not been proven effective in the prevention of cerebral edema, it is commonly used for treatment of acute rises in ICP/cerebral edema.6,7
The role of hypothermia in the management of ALF patients is complex; it likely affects multiple factors responsible for the development of encephalopathy and intracranial hypertension.19–21 An early clinical study evaluated the role of hypothermia in seven patients with uncontrolled intracranial hypertension despite the aforementioned therapies. Patients who were cooled to 32°C demonstrated a significant decline in ICP, from 45 to 16 mm Hg, with subsequent improvements in CPP.21 Other studies have reported that hypothermia used as adjunct to standard therapy may be helpful in patients with persistent uncontrolled intracranial hypertension, especially as a bridge toward liver transplantation19–21; however, well-designed randomized clinical trials for this application are lacking.
Pharmacologic coma and sedation, another adjunctive therapy, reduce ICP by suppressing cerebral metabolic activity and decreasing CPP. Phenobarbital has been traditionally used for this purpose, but propofol has become the preferred sedative agent in many centers.22,23
Hepatic encephalopathy is a neurologic complication of ALF that requires early identification and aggressive treatment. Accurate assessment (see grading system, below) of degree of encephalopathy helps inform the decision to initiate definitive ventilatory support and protect the patient's airway; prompt treatment helps prevent worsening cerebral edema. Serum ammonia will be elevated in ALF and is hypothesized play a role in the pathogenesis of worsening cerebral edema and intracranial hypertension. Lowering ammonia levels with lactulose and early dialysis may help treat or prevent the development of cerebral edema.1,11,24,25 The U.S. Acute Liver Failure Study Group retrospectively evaluated the role of lactulose in the management of encephalopathy among ALF patients.25 While the severity of encephalopathy did not differ between patients in the treated and untreated groups, overall survival was slightly higher for patients receiving lactulose therapy.25 Care should be taken, however, to avoid lactulose therapy–associated dehydration and electrolyte disturbances. The role of nonabsorbable antibiotics (e.g., rifaximin) in the management of encephalopathy in patients with ALF is not well studied26; as a result, rifaximin is not considered standard of care, but may be considered on a case-by-case scenario in consultation with the hepatology service.
Hepatic Encephalopathy Grading System
The systemic inflammation and hormonal dysregulation that result from ALF can lead to systemic vasodilation, contributing to decreased MAP and CPP. Adequate maintenance of cardiovascular perfusion directly affects the CPP and overall neurologic complications. Initial management with intravascular volume repletion is aimed at maintaining MAP > 80 mm Hg and CPP > 60 mm Hg. Patients should be resuscitated with normal saline first and switched to half-normal saline with 75 mEq/L of sodium bicarbonate if acidosis is present. Adjunctive therapy with vasopressor therapy may be needed to maintain/reach MAP and CPP targets. Norepinephrine is the vasopressor of choice, with the addition of vasopressin to permit titration of the norepinephrine infusion.1,4
Coagulopathy is another common feature of ALF and correlates with a patient's degree of hepatic synthetic dysfunction. Aggressive correction of thrombocytopenia and elevated INR is not necessary if there is no evidence of bleeding.27 Prior to invasive diagnostic or therapeutic interventions, however, coagulopathy may be corrected with fresh frozen plasma and platelets; goals for correction, however, are not well established.
In the setting of active gastrointestinal bleeding, more aggressive transfusion of cryoprecipitate may also be instituted. Recombinant factor VIIa is an option for life-threatening bleeding but carries risk of thrombosis.28 Given the increased risk of gastrointestinal tract bleeding in the setting of coagulopathy and the risk of developing stress-induced ulcers, routine prophylactic acid suppression therapy is indicated. In a multicenter, randomized placebo-controlled trial of 1,200 mechanically ventilated patients, acid suppression therapy was associated with significantly reduced risk of gastrointestinal bleeding (relative risk 0.44).29 While the study cohort was not limited to patients with ALF, the findings of this study have been used to support the routine use of acid suppression in ALF.
Acute renal failure is a common complication in ALF. Hemodynamic alterations affecting adequate renal perfusion coupled with the direct nephrotoxicity of drugs and toxins such as acetaminophen and amanita poisoning contribute to worsening renal function. ALF-induced acidosis, electrolyte abnormalities, and uremia can further contribute to renal impairment. The renal failure, in turn, can exacerbate the systemic inflammatory response triggered by the ALF.
Fluid resuscitation to achieve optimal intravascular volume, coupled with vasopressor therapy to achieve MAP goals, can improve hypoperfusion-induced renal failure. Early recognition of renal failure and, when indicated, initiation of renal replacement therapy with continuous venovenous hemodialysis (CVVH) can also assist significantly in the overall management of ALF.30,31 Early initiation of dialysis allows for more aggressive management of encephalopathy and elevated ICP by forced hypernatremia and lowering of blood ammonia levels. Furthermore, CVVH has been demonstrated to improve cardiovascular stability in patients with ALF.30,31 In one study, 32 critically ill patients with ALF and acute renal failure were randomized to receive either intermittent or continuous modes of renal replacement therapy.31 Patients treated with CVVH had improved overall cardiovascular parameters, as measured by cardiac output and tissue oxygen delivery.
Ninety percent of ALF patients develop some degree of infection, a result of the confluence of invasive monitoring and immune system dysfunction. Severe bacterial or fungal infections can preclude liver transplantation and/or complicate the posttransplantation recovery.1,32–35 Pneumonia is the most common infection experienced by ALF patients, followed by urinary tract infections and catheter-related infections. Gram-positive organisms are the most common infectious culprits, followed by gram-negative organisms and fungi.34,35
Surveillance cultures of blood, urine, and sputum and chest radiography should be routinely evaluated in patients with ALF. In the absence of suspected infection, empiric prophylactic antibiotic or antifungal therapy has not been shown to provide a survival benefit.32,33 In one study, ALF patients without evidence of acute infection were randomized to receive or not to receive prophylactic parenteral and enteral antimicrobial therapy.33 While the treated group showed a significant reduction in the development of infections, overall survival was not significantly different between the treated and untreated groups. Gut decontamination with poorly absorbable antibiotics has also not been shown to improve survival outcomes among ALF patients.36 Antibiotic or antifungal therapy should, however, be initiated if there is a clinical suspicion of infection or deteriorating clinical status (e.g., worsening hepatic encephalopathy or systemic inflammatory response syndrome).
Severe metabolic and electrolyte abnormalities are common in patients with ALF, a result of multiorgan dysfunction. Early recognition and correction of these derangements can prevent further deterioration.1 Some of the common metabolic complications that result from ALF include the following:
TABLE 25.4 King's College Criteria for Assessment of Liver Failure Prognosis
From O'Grady JG, Alexander GJM, Hayllar KM, et al. Early indicators of prognosis in fulminant hepatic failure. Gastroenterology. 1989;97:439–455. Patients meeting the criteria are identified has having a poor prognosis.
Acetaminophen toxicity is by far the most common cause of ALF in the United States, accounting for over 50% of all cases in the United States.1,3,5 A detailed patient history is essential to diagnosing a deliberate or accidental overdose, especially given the multitude of both prescription and nonprescription medications that include acetaminophen. Acetaminophen-related hepatotoxicity is a dose-related adverse event; while ingestion of >10 to 15 g over a period of 24 hours is typically needed to induce ALF, concurrent disease or individual variations in hepatic metabolism may allow significant damage from ingestion of only 3 to 4 g.41–43
In toxic acetaminophen ingestions, aminotransferase levels are characteristically elevated several hundred-fold above normal values, with a peak in the rise of aminotransferases typically occurring 48 to 72 hours following ingestion. Use of the Rumack-Matthew acetaminophen nomogram can assist in prognosticating the risk of ALF in patients with less severe aminotransferase abnormalities.3,43 The nomogram plots the serum concentration of acetaminophen against last known ingestion time in an attempt to prognosticate hepatotoxicity and guide administration of therapy with N-acetylcysteine (NAC). Recently, acetaminophen–protein adducts, which have a longer half-life than acetaminophen, have been proposed as a means of identifying the cause of ALF in patients presenting without an identifiable etiology or undetectable acetaminophen levels.43,44 A recent study evaluated sera from 110 subjects with indeterminate ALF enrolled in the Acute Liver Failure Study Group.43 The sera of these patients, along with 199 positive controls of sera from patients with known acetaminophen-related ALF, were evaluated for acetaminophen–cysteine adducts. Over 94.5% of controls demonstrated levels of adducts that confirmed acetaminophen toxicity; 18% of the indeterminate cases tested positive, which confirmed previous reports citing the high prevalence of unrecognized acetaminophen toxicity among patients with indeterminate liver failure.43
If ingestion occurs within 3 to 4 hours, administration of activated charcoal at a dose of 1 g/kg orally may be of some benefit,45 however, NAC therapy remains the most beneficial intervention.46,47 One of the original studies evaluating the benefit of NAC in the treatment of acetaminophen-related ALF described the outcomes of 2,540 acetaminophen-toxic patients treated with oral NAC.47 Patients treated with oral NAC had significantly lower rates of hepatotoxicity and significantly reduced mortality; patients treated within 8 hours of last ingestion had better outcomes that those who were treated at later intervals. NAC can be administered orally or intravenously; however, the intravenous route is preferred given the lower risk of aspiration. The dosing regimen for both oral and intravenous NAC is presented in Table 25.2.
Given the multitude of potentially hepatotoxic prescription and nonprescription drugs, a thorough patient history is essential. Common culprits of mixed-etiology ALF include antibiotics, antifungals, antituberculosis medications, sulfa-containing drugs, and psychiatric and neurologic medications including antiepileptics. In addition to pharmaceutical agents, nutritional and herbal supplements need to be carefully evaluated for potential hepatotoxicity. Early identification and removal of the offending agent, along with supportive care, are the mainstay of therapy in these cases.48,49
While NAC therapy has demonstrated greatest utility in patients with acetaminophen toxicity, it may also benefit patients with non–acetaminophen-related ALF.50 In a prospective, double-blinded trial of 173 ALF patients without evidence of acetaminophen toxicity, a 72-hour infusion of NAC was compared to placebo (dextrose) in affecting survival outcomes. While there was no statistically significant difference in overall 3-week survival seen between the NAC group and the placebo group (70% vs. 66%), patients treated with NAC had significantly better 3-week transplant-free survival (40% vs. 27%).50 The survival advantage was, however, limited to patients with less severe hepatic encephalopathy (grade 1 to 2).
Mushroom poisoning with Amanita toxin is a potentially lethal cause of ALF. As there is no serologic test to confirm exposure, a careful patient/observer history is essential, both to identify the fungus and to estimate the timing of exposure. Patients presenting with recent ingestion may benefit from nasogastric lavage to attempt removal of remaining toxic material. Silibinin and penicillin are accepted antidotes to mushroom poisoning. While greater evidence supports the efficacy of silibinin, this treatment is not available as a licensed drug in the United States.51,52 However, when Amanita poisoning is suspected, an application to the Food and Drug Administration for emergency use of this agent is possible. Silibinin is administered orally or intravenously at a dose of 30 to 40 mg/kg/d for 3 to 4 days. Penicillin is an acceptable alternative in conjunction with NAC treatment. Amanita toxin is excreted in the bile, and the use of nasobiliary drainage or aspiration of the second portion of the duodenum (ideally performed in an ICU) may decrease enterohepatic circulation of the toxin.53
Acute viral hepatitis accounts for approximately 12% of all cases of ALF in the United States.54,55 Several viruses have the potential to induce liver failure, each with its own unique risk factors, routes of transmission, diagnostic workup, and targeted treatment regimen. Acute hepatitis A infection (HAV) is a common ailment spread primarily through fecal–oral transmission. The diagnosis can be confirmed with positive anti-HAV IgM. Most HAV infections resolve with supportive therapy that includes fluid resuscitation and correction of electrolyte disturbances. However, any signs of hepatic dysfunction, including encephalopathy or coagulopathy, or signs of multiorgan dysfunction (e.g., renal failure or respiratory failure) require hospital admission and monitoring for development of ALF.
Acute hepatitis B infection (HBV) most often occurs as a result of intravenous drug use or sexual transmission. Acute HBV is confirmed by the presence of anti-HBV core Ab IgM. HBV antigen and HBV viral DNA may also be present. As in acute HAV, patient evaluation in acute HBV centers on assessment of organ function and identification of early symptoms of ALF that would require hospital admission. Following an initial diagnostic workup and appropriate resuscitation in the ED, inpatient treatment is generally guided by the hepatology service. First-line treatment for HBV consists of tenofovir 300 mg/d or entecavir 0.5 mg/d.56 A randomized, placebo-controlled trial of patients with ALF secondary to HBV demonstrated that treatment with tenofovir was associated with significantly lower HBV viral DNA levels and improved liver disease severity, as measured by the model for end-stage liver disease (MELD) score and Child-Pugh score.56 In addition, patients who were treated with tenofovir had significantly higher 3-month survival compared to patients who received placebo (57% vs. 15%).56
Acute hepatitis C infection (HCV) in the United States is associated primarily with intravenous drug use in the United States; the diagnosis can be confirmed with anti-HCV Ab and HCV viral RNA. ALF secondary to acute HCV is rare. The timing of antiviral therapy for acute HCV is unclear; current studies lack definitive data, and recently developed anti-HCV therapies have not undergone well-designed clinical trials. In patients with uncomplicated acute HCV, monitoring for spontaneous clearance of HCV RNA over a 12- to 16-week period is reasonable. The evidence for antiviral therapy in the setting of HCV-induced ALF is less clear, and general supportive measures should be instituted instead.57
Acute hepatitis D infection (HDV) is rare and occurs either as a coinfection with HBV or as superimposed acute HDV in a patient with chronic HBV. Diagnosis is conferred with the anti-HDV Ab and HDV antigen; supportive care occurs concurrently with treatment of the HBV infection. Acute hepatitis E infection (HEV) is transmitted via fecal–oral route, and diagnosis is confirmed with anti-HEV IgM and IgG. Treatment is supportive. With all the acute viral hepatitis infections, the initial evaluation and management in the ED focus on supportive care, including fluid and electrolyte resuscitation. The appropriate laboratory workup as previously described should be initiated; treatment is usually guided by the diagnosis and initiated by the inpatient team.
Autoimmune hepatitis can present with a wide spectrum of clinical disease severity. While it is often diagnosed in the workup of mild elevations in aminotransferase levels and vague systemic complaints, autoimmune hepatitis can also present in a fulminant course with ALF.58,59 A suspicion for autoimmune hepatitis is gleaned from a complete patient history of potential comorbid autoimmune disease states. Initial evaluation in the ED should include antinuclear antibodies (ANA), anti–smooth muscle antibodies (ASMA), and total serum IgG.
A thorough workup to exclude viral hepatitis and alcoholic liver disease further supports the diagnosis of autoimmune hepatitis. In patients with negative serologic markers in whom the suspicion for this etiology remains, liver biopsy may help to confirm diagnosis. Once ALF secondary to autoimmune hepatitis is confirmed, timely initiation of immunosuppressive therapy is critical and may reduce the progression of disease and need for liver transplantation.59 The initial evaluation in the ED should focus on ensuring that the diagnostic workup is sufficient to evaluate for this process.
Wilson disease is a rare cause of liver disease; it is caused by a defect in copper metabolism and characterized by Kayser-Fleischer rings (secondary to copper deposition at the corneoscleral junction of the eye) and neuropsychiatric disease (secondary to copper deposition in the brain). Coombs-negative hemolytic anemia is a common associated presentation. A characteristic biochemical finding is an extremely low alkaline phosphatase (ALK) in the setting of marked elevation of aminotransferases. Early identification is important for prompt initiation of liver transplant evaluation. Initial diagnostic tests that can be sent from the ED include serum ceruloplasmin and routine liver function tests. Further diagnostic testing with urinary copper levels and liver biopsy with quantitative copper concentration in patients with high suspicion of Wilson disease can help confirm the diagnosis. The hepatology service should be consulted to evaluate the need for liver biopsy. In the setting of ALF, treatment in the ED should be supportive while the patient is rapidly evaluated for liver transplantation.1
“Shock liver” is a relatively common syndrome of ischemic hepatitis, characterized by acute elevation of aminotransferase levels. Precipitated by severe hypotension or hypovolemia resulting in hepatic ischemia, this syndrome is common in patients with underlying cardiac disease or severe congestive heart failure. Post–cardiac arrest patients who experience a period of hepatic hypoperfusion will often present with some degree of ischemic hepatitis. Correction of the underlying etiology and prompt initiation of cardiovascular support generally lead to recovery of hepatic function and usually prevent the need for liver transplant.1,60 Overall prognosis, however, depends on the etiologies that precipitate the ischemic event.
Budd-Chiari syndrome is a rare disease precipitated by hepatic venous outflow obstruction resulting in hepatic decompensation and ALF.60,61 Hepatic vein obstruction is generally secondary to thrombosis, and an underlying hypercoagulable state should be evaluated for. Acute abdominal pain, new-onset ascites, and marked hepatomegaly are often found on clinical presentation. The diagnostic approach relies on radiographic evidence of obstructive disease, preferably obtained through abdominal ultrasonography with Doppler flow. Contrast-enhanced computed tomography and magnetic resonance venography are alternative diagnostic tools, but should be used with caution, as many patients presenting with ALF have impaired renal function.
A diagnosis of Budd-Chiari requires a comprehensive workup to determine the underlying prothrombotic disorder. Potential culprits include hematologic disorders and hematologic malignancy (which, if diagnosed, may preclude the option of transplantation). Anticoagulation therapy and venous decompression (i.e., transjugular intrahepatic portosystemic shunting) have a role in the management of Budd-Chiari syndrome, but patients presenting with ALF as a result of this disease have a poorer prognosis, and liver transplantation may be the preferred therapeutic option.60,61 In the ED, initial workup involves early resuscitation and the initiation of appropriate laboratory and radiographic diagnostic evaluation.
Pregnancy-related liver disease is relatively rare, and the development of ALF in pregnant patients is even more rare.62 Both acute fatty liver of pregnancy and HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) generally occur during the third trimester of pregnancy and can result in progressive hepatic injury leading to liver failure. In addition to abnormal aminotransferase levels and thrombocytopenia, jaundice, coagulopathy, preeclampsia, and hypoglycemia are often seen in the setting of pregnancy-related ALF. Treatment is supportive, and prompt delivery of the fetus in consultation with a high-risk obstetrics team generally results in rapid recovery of hepatic function.62 While rare, liver transplantation may need to be considered in postpartum patients with persistent or progressively worsening hepatic dysfunction.
ALF is a significant cause of morbidity and mortality in the United States. Prompt recognition of ALF is important to initiate the appropriate diagnostic workup and to triage the patient toward an appropriate critical care setting. While the diagnostic evaluation and subsequent management of ALF are complicated, the emergency physician plays a key role in assessing the severity of disease and initiating the appropriate diagnostic testing required to confirm the underlying etiology. Severely ill ALF patients should always be admitted to an ICU or transferred to a liver transplantation center as needed.
CI, confidence interval; RR, relative risk.
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