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Acute Liver Failure Treatment & Management

  • Author: Gagan K Sood, MD; Chief Editor: BS Anand, MD  more...
 
Updated: Feb 04, 2016
 

Approach Considerations

The most important aspect of treatment in patients with acute liver failure is to provide good intensive care support.[1, 2, 3, 4]  Patients with grade II encephalopathy should be transferred to the intensive care unit (ICU) for monitoring. As encephalopathy progresses, protection of the airway becomes increasingly important.

Most patients with acute liver failure tend to develop some degree of circulatory dysfunction. Careful attention should be paid to fluid management and hemodynamics. Monitoring of metabolic parameters, surveillance for infection, maintenance of nutrition, and prompt recognition of gastrointestinal bleeding are crucial.

Coagulation parameters, complete blood cell count, and metabolic panel should be checked frequently. Serum aminotransferases and bilirubin are generally measured daily to follow the course of the disease.

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Airway Protection

As patients with fulminant hepatic failure drift deeper into coma, the ability to protect their airway from aspiration decreases. Patients who are in stage III coma should have a nasogastric tube (NGT) inserted for stomach decompression. When patients progress to stage III coma, intubation should be performed.

Short-acting benzodiazepines in low doses (eg, midazolam, 2-3 mg) may be used before intubation, or propofol (50 mcg/kg/min) may be initiated before intubation and continued as an infusion. Propofol is also known to decrease the cerebral blood flow and intracranial hypertension (ICH). It may be advisable to use endotracheal lidocaine before endotracheal suctioning.

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Management of Encephalopathy and Cerebral Edema

Patients with grade I encephalopathy may sometimes be safely managed in a medicine ward. Frequent mental status checks should be performed, and transfer to an ICU is warranted with progression to grade II encephalopathy.

Sedation should be avoided if possible. Unmanageable agitation may be treated with short-acting benzodiazepines in low doses.

Patients should be positioned with the head elevated at 30°. Efforts should be made to avoid patient stimulation. Maneuvers that cause straining or, in particular, Valsalva-like movements may increase intracranial pressure (ICP).

There is increasing evidence that ammonia may play a pathogenic role in the development of cerebral edema. Reducing elevated ammonia levels with enteral administration of lactulose might help prevent or treat cerebral edema. In the late stages of encephalopathy, to reduce the risk of aspiration, avoid providing lactulose by mouth or nasogastric tube in the absence of endotracheal intubation.

The occurrence of cerebral edema and ICH in patients with acute liver failure is related to the severity of encephalopathy. Cerebral edema is seldom observed in patients with grades I-II encephalopathy. The risk of edema increases to 25-35% with progression to grade III and increases to 65-75% (or more) in patients reaching grade IV coma.

Patients in the advanced stages of encephalopathy require close follow-up care. Monitoring and management of hemodynamic and renal parameters, as well as glucose, electrolytes, and acid/base status, become critical. Frequent neurologic evaluation for signs of elevated ICP should be conducted.

Intracranial pressure monitoring

In patients with grade III or IV encephalopathy, consider placement of an ICP monitor. ICP monitoring helps in the early recognition of cerebral edema.

The clinical signs of elevated ICP, including hypertension, bradycardia, and irregular respirations (Cushing triad), are not uniformly present; these and other neurologic changes, such as papillary dilatation or signs of decerebration, are typically evident only late in the course. CT scanning of the brain does not reliably detect edema, especially in the early stages.

The primary purpose of ICP monitoring is to detect elevations in ICP and reductions in cerebral perfusion pressure (CPP; calculated as mean arterial pressure [MAP] minus ICP) so that interventions can be made to prevent herniation while preserving brain perfusion. The ultimate goal of such measures is to maintain neurologic integrity and to prolong survival while awaiting the receipt of a donor organ or recovery of sufficient functioning hepatocyte mass. Additionally, refractory ICH and/or decreased CPP are considered contraindications to liver transplantation in many centers.

If an ICP monitor is placed, ICP should be maintained below 20-25 mm Hg, if possible, with CPP maintained above 50-60 mm Hg. Support of systemic blood pressure may be required to maintain adequate CPP.

Management of intracranial hypertension

ICH is managed initially with the use of mannitol. Osmotic diuresis with IV mannitol is effective in the short term in decreasing cerebral edema. Administration of IV mannitol (in a bolus dose of 0.5-1 g/kg or 50-100 g) is recommended to treat ICH in acute liver failure. The dose may be repeated once or twice, as needed, provided that serum osmolality has not exceeded 320 mOsm/L. Volume overload is a risk with mannitol use in patients with renal impairment and may necessitate the use of dialysis to remove excess fluid.

If life-threatening ICH is not controlled with mannitol infusion and other general management as outlined above, hyperventilation may be instituted temporarily in an attempt to acutely lower the ICP and to prevent impending herniation. Hyperventilation to reduce the partial pressure of carbon dioxide in the blood (PaCO2) to 25-30 mm Hg can quickly lower ICP via vasoconstriction, causing decreased cerebral blood flow, but this effect is short-lived.

Other therapies used to decrease ICH but not routinely recommended may be considered in refractory ICH. These include hypertonic saline, barbiturates, and hypothermia.

A controlled trial of administration of 30% hypertonic saline, 5-20 mL/h, to maintain serum sodium levels of 145-155 mmol/L in patients with acute liver failure and severe encephalopathy suggested that induction and maintenance of hypernatremia may be used to prevent the rise in ICP values.[31]

Barbiturate agents (thiopental or pentobarbital) may also be considered when severe ICH does not respond to other measures; administration has been shown to effectively decrease ICP. Significant systemic hypotension frequently limits their use and may necessitate additional measures to maintain adequate mean arterial pressure. Doses of barbiturates for ICH are as follows:

  • Thiopental: 5-10 mg/kg loading dose followed by 3-5 mg/kg IV infusion
  • Pentobarbital: 3-5 mg/kg IV loading dose followed by 1-3 mg/kg/h infusion

Moderate hypothermia (32-34°C) may prevent or control ICH in patients with acute liver failure. An external cooling blanket may be used to achieve this goal. Potential deleterious effects of hypothermia include increased risk of infection, coagulation disturbance, and cardiac arrhythmias.

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Hemodynamic Monitoring

Hemodynamic derangements consistent with multiple organ failure occur in acute liver failure. Hypotension (ie, systolic blood pressure < 80 mm Hg) may be present in 15% of patients. Most patients will require fluid resuscitation on admission. Intravascular volume deficits may be present on admission due to decreased oral intake or gastrointestinal blood loss.

Hemodynamic derangement resembles that of sepsis or cirrhosis with hepatorenal syndrome (low systemic vascular resistance [SVR] with normal or increased cardiac output). An arterial line should be placed for continuous blood pressure monitoring.

A Swan-Ganz catheter should be placed, and fluid replacement with colloid albumin should be guided by the filling pressure. If needed, dopamine or norepinephrine can be used to correct hypotension.

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Management of Coagulopathy

In the absence of bleeding, it is usually not necessary to correct clotting abnormalities with fresh frozen plasma (FFP). The exception is when an invasive procedure is planned or in the presence of profound coagulopathy (INR >7).[32]

Prothrombin time (PT) and partial thromboplastin time (PTT) become prolonged when plasma coagulation components are diluted to less than 30%, and abnormal bleeding occurs when they are less than 17%. One unit of FFP increases the coagulation factor by 5%; 2 units increase it by 10%. An FFP infusion of 15 mL/kg of body weight or 4 units will correct the deficiency. If the fibrinogen level is very low (< 80 mg/dL), consider administering cryoprecipitate.

Recombinant factor VIIa may be used in patients whose condition is nonresponsive to FFP. It is used in a dose of 4 µg/kg IV push over 2-5 minutes. PT is normalized in 20 minutes and remains normalized for 3-4 hours.

Platelet transfusions are not used until the count is less than 10,000/µL or if an invasive procedure is being done and the platelet count is less than 50,000/µL. Six to 8 units of random donor platelets (1 random donor unit platelet/10 kg) will increase the platelet count to greater than 50,000/µL. The platelet count should be checked after 1 hour and 24 hours. Transfused platelets survive 3-5 days.

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Management of Acetaminophen Toxicity

Treat acetaminophen (paracetamol, APAP) overdose with N-acetylcysteine (NAC).[33] Researchers theorize that this antidote works by a number of protective mechanisms. Early after an overdose, NAC prevents the formation and accumulation of N -acetyl-p-benzoquinone imine (NAPQI), a free radical that binds to intracellular proteins, nonspecifically resulting in toxicity.

NAC increases glutathione stores, combines directly with NAPQI as a glutathione substitute, and enhances sulfate conjugation. NAC also functions as an anti-inflammatory and antioxidant and has positive inotropic and vasodilating effects, which improve the microcirculatory blood flow and oxygen delivery to tissues. These latter effects decrease morbidity and mortality once hepatotoxicity is well established.

The protective effect of NAC is greatest when administered within 8 hours of ingestion; however, when indicated, administer regardless of the time since the overdose. Therapy with NAC has been shown to decrease mortality in late-presenting patients with fulminant hepatic failure (in the absence of acetaminophen in the serum).

If patients present within 4 hours of overdosing on acetaminophen, give activated charcoal just prior to starting NAC.[1]

Never administer aminoglycosides or nonsteroidal anti-inflammatory drugs (NSAIDs) to patients with acetaminophen hepatotoxicity, because the potential for nephrotoxicity is exaggerated greatly in this setting.

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Mushroom Poisoning

Treat Amanita phalloides mushroom intoxication with IV penicillin G, even though its mode of action is unclear. Silibinin, a water-soluble derivative of silymarin, may be administered orally, and oral charcoal may be helpful by binding the mushroom toxin.

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Liver Transplantation

Liver transplantation is the definitive treatment in liver failure, but a detailed discussion is beyond the scope of this article. For more information on liver transplantation, see the Medscape articles Liver Transplants and Pediatric Liver Transplantation. The American Association for the Study of Liver Diseases has produced guidelines on the evaluation of patients for liver transplantation.[34, 35] Preoperative management is emphasized in this section.

In selected patients for whom no allograft is immediately available, consider support with a bioartificial liver. This is a short-term measure that only leads to survival if the liver spontaneously recovers or is replaced.[5, 6, 7, 8]

Artificial liver support systems can be divided into 2 major categories: biologic (bioartificial) and nonbiologic.

The bioartificial liver is composed of a dialysis cartridge with mammalian or porcine hepatocytes filling the extracapillary spaces. These devices have undergone controlled trials. One multicenter trial reported improved short-term survival for a subgroup of patients with acute liver failure who were treated with a porcine hepatocyte-based artificial liver.[8]

Nonbiologic extracorporeal liver support systems, such as hemodialysis, hemofiltration, charcoal hemoperfusion, plasmapheresis, and exchange transfusions, have been used; however, no controlled study has shown long-term benefit.

These modalities permit temporary liver support until a suitable donor liver is found. Although extracorporeal hemoperfusion of charcoal and other inert substances provide some measure of excretory function, this technique provides no synthetic capacity.

Among the liver support systems currently available, albumin dialysis using the molecular adsorbent recirculating system (MARS) is the one that has been most extensively investigated. In this device, blood is dialyzed across an albumin-impregnated membrane against 20% albumin. Charcoal and anion exchange resin columns in the circuit cleanse and regenerate the albumin dialysate. Clinical studies have shown that this system improves hyperbilirubinemia and encephalopathy.

Two other systems based on the removal of albumin bound toxins—the Prometheus, using the principle of fractionated plasma separation and adsorption (FPSA), and the single pass albumin dialysis (SPAD)—are also undergoing clinical studies for acute liver failure.[36]

Currently available liver support systems are not routinely recommended outside of clinical trials. In the future, hepatocyte transplantation, which has shown dramatic results in animal models of acute liver failure, may provide long-term support, but this approach remains investigational.

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Diet

Patients with acute liver failure are, by necessity, on nothing by mouth (NPO) status. They may require large amounts of IV glucose to avoid hypoglycemia.

When enteral feeding via a feeding tube is not feasible (eg, as in a patient with paralytic ileus), institute total parenteral nutrition (TPN). (See also Nutritional Requirements of Adults Before Transplantation and Nutritional Requirements of Children Prior to Transplantation.) Restricting protein (amino acids) to 0.6 g/kg body weight per day was previously routine in the setting of hepatic encephalopathy. However, this may not be necessary.

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Long Term Monitoring

Bed rest is recommended.

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Consultations

Managing fulminant hepatic failure is a team effort. Consultations with specialists in intensive care, gastroenterology, infectious diseases, hematology, neurology, neurosurgery, and transplantation surgery may be needed to address the myriad complex issues that can confront the medical staff.

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Contributor Information and Disclosures
Author

Gagan K Sood, MD Associate Professor, Department of Medicine and Surgery, Baylor College of Medicine

Gagan K Sood, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association

Disclosure: Nothing to disclose.

Coauthor(s)

Mark S Slabinski, MD, FACEP, FAAEM Vice President, EMP Medical Group

Mark S Slabinski, MD, FACEP, FAAEM is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Ohio State Medical Association

Disclosure: Nothing to disclose.

Steven A Conrad, MD, PhD Chief, Department of Emergency Medicine; Chief, Multidisciplinary Critical Care Service, Professor, Department of Emergency and Internal Medicine, Louisiana State University Health Sciences Center

Steven A Conrad, MD, PhD is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American College of Emergency Physicians, American College of Physicians, International Society for Heart and Lung Transplantation, Louisiana State Medical Society, Shock Society, Society for Academic Emergency Medicine, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Lemi Luu, MD, RDMS, FACEP, FAAEM Attending Physician, Department of Emergency Medicine, Bridgeport Hospital, Yale-New Haven Health System

Lemi Luu, MD, RDMS, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Institute of Ultrasound in Medicine

Disclosure: Nothing to disclose.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Acknowledgements

David Eric Bernstein, MD Director of Hepatology, North Shore University Hospital; Professor of Clinical Medicine, Albert Einstein College of Medicine

David Eric Bernstein, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Oscar S Brann, MD, FACP Associate Clinical Professor, Department of Medicine, University of California at San Diego; Consulting Staff, Mecklenburg Medical Group

Oscar S Brann, MD, FACP is a member of the following medical societies: American Gastroenterological Association

Disclosure: Nothing to disclose.

Blake A Jones, MD New Hampshire Gastroenterology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Carin M Van Gelder, MD Assistant Professor, Department of Emergency Medicine, Yale University; EMS Medical Director, NHSHP and EMS Physician, SHARP Team; Attending Physician, Emergency Medicine, Yale-New Haven Medical Center

Carin M Van Gelder, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Massachusetts Medical Society, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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Ultrasonogram shows a hyperechoic mass representing hepatocellular carcinoma.
Subacute subdural hematoma with extension into the anterior interhemispheric cistern. Note that the sutures do not contain the spread of these hemorrhages.
Table. Grading of Hepatic Encephalopathy
Grade Level of Consciousness Personality and Intellect Neurologic Signs Electroencephalogram (EEG) Abnormalities
0 Normal Normal None None
Subclinical Normal Normal Abnormalities only on psychometric testing None
1 Day/night sleep reversal, restlessness Forgetfulness, mild confusion, agitation, irritability Tremor, apraxia, incoordination, impaired handwriting Triphasic waves (5 Hz)
2 Lethargy, slowed responses Disorientation to time, loss of inhibition, inappropriate behavior Asterixis, dysarthria, ataxia, hypoactive reflexes Triphasic waves (5 Hz)
3 Somnolence, confusion Disorientation to place, aggressive behavior Asterixis, muscular rigidity, Babinski signs, hyperactive reflexes Triphasic waves (5 Hz)
4 Coma None Decerebration Delta/slow wave activity
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