Hepatic failure

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Hepatic failure
ICD-10 K72.9
DiseasesDB 5728
MeSH D017093

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Roghayeh Marandi[2]


Synonyms and keywords: Liver failure; fulminating hepatic failure

Overview

Liver failure is the inability of the liver to perform its normal synthetic and metabolic function as part of normal physiology.

Historical Perspective

Classification

Three forms are recognized:

Pathophysiology

The pathophysiology of ALF can be divided into cause‐specific liver injury pathophysiologies and pathophysiology related to the occurrence of secondary multi-organ failure.




Causes

Causes for Acute liver failure[13][14]:

Category Etiology of Acute liver failure
Viruses
Drugs
Metabolic diseases
Toxins
Vascular diseases
Malignant Infiltration
Autoimmune disease
Indeterminate
  • Unknown

Drug-induced acute liver injury

Viral hepatitis

Mushroom poisoning

Causes of chronic liver failure

Differential Diagnosis

Epidemiology and Demographics

Etiology of ALF in Adults.jpg

Risk factors

Screening

Not applicable

Natural History, Complications and Prognosis

Natural History

Clinical features in Hepatic failure and complications

Brain

Liver

Kidney and adrenal

System

Heart

  • High output state
  • Subclinical myocardial injury
  • Hepatocardiac syndrome

Pancreas

Lungs

Bone marrow

Prognosis

prognosis of Acute liver failure

  • The prognosis in patients with acute liver failure is highly variable and depends on the etiology, subtypes (hyperacute, acute,...), age, and the degree of coagulopathy. Determining the prognosis for these patients is vital. The overall mortality of ALF is currently between 30% to 40%.[13] Liver transplantation has dramatically improved short-term survival in patients with acute liver failure. Still, 25% to 45% of patients will survive with medical treatment.[22]
  • Identification of patients who will eventually require liver transplantation should be addressed through continuous medical assessment. The most widely accepted prognostic tool for patients who present with ALF is King's College Criteria (KCC) .Although his scoring system is generally quite accurate in predicting poor prognosis and, along with clinical judgment, is useful for ensuring timely transfer to a liver transplant center in adults, but data suggest they may not reliably predict outcomes in the pediatric population.[23][19][24][22]

Prognosis of chronic liver failure

  • Patients with compensated cirrhosis have a median survival of 6–12 years. Decompensation and end stage liver disease occurs in 5%–7% annually; median survival then declines to 2 years.[25]

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | Chest X Ray | CT | MRI | Echocardiography or Ultrasound | Other Imaging Findings | Other Diagnostic Studies | Clinical prediction rules

History and symptoms

Social history

Past Medical history

Menstrual history

Family history

Medication history

  • History of use of all medications used over the last 6 months, including prescription medications, over-the-counter agents, herbal supplements, wild mushrooms, or other alternatives/complementary therapies;

Symptoms

Physical Examination

  • Complete physical examination should be performed.

Appearance of the patient

  • Patients with hepatic failure have any degree of Hepatic encephalopathy.[28][29]

Vital signs

In patients with hepatic failure vital signs include:[30]

Skin

Signs of liver disease may be seen, such as:[31]

HEENT

Neck

Physical examination of neck is usually normal but in Hepatic failure due to CHF,Jugular vein distention may be seen.

Lungs

Heart

Physical examination of heart is usually normal unless the cause of hepatic failure is Heart disease such as Right heart failure.

Abdomen

Signs of liver disease may be seen such as:

Back

Physical examination of back is usually normal

Genitourinary

Neuromuscular

Extremities

Laboratory Findings



Imaging

Treatment

The most important part of the management of hepatic failure involves the timely diagnosis of it. Making a timely diagnosis in a patient who presents with liver dysfunction and an altered mental state remains the single most important management step for the clinician, as a delay can lead to substantial morbidity and mortality. Although there is no proven therapy for ALF, understanding the progression of ALF, from loss of hepatocytes to the development of multiorgan failure, helps the clinician in disease-specific complication management.

The management of Hepatic failure should involve

  1. Specific Treatment
  2. Supportive and symptomatic management
  3. Management of complications
  4. Emergency therapies
  5. Liver transplantation

1. Specific treatment:

  • Identification of the etiology and initiation of specific treatment.

Acetaminophen intoxication

  • Oral NAC: 140 mg/kg loading dose, then 70 mg/kg every 4 hours until discontinued by hepatology or transplantation surgery attending physician
    • Or
  • IV NAC: 150 mg/kg loading dose, then 50 mg/kg IV over 4 hours, then 100 mg/kg IV over 16 hours as a continuous infusion until discontinued by hepatology or transplantation surgery attending physician

Amanita phalloides(mushroom poisoning)

  • Charcoal: via NGT every 4 hours alternating with silymarin
  • Penicillin G: 1 g/kg/day IV and
  • NAC (Dosing as for acetaminophen overdose.),
  • Silymarin: 300 mg PO/NGT every 12 hours,
  • Legalon-SIL: 5 mg/kg/day IV (given in 4 divided doses) or 5 mg/kg IV loading dose followed by 20 mg/kg/day via continuous infusion

Herpes simplex virus infection

  • Acyclovir: 10 mg/kg IV every 8 hours (using IBW) adjusted for kidney function

Cytomegalovirus infection

  • Ganciclovir: 5 mg/kg IV every 12 hours (using IBW) adjusted for kidney function

Autoimmune hepatitis

Hepatitis B virus infection

Acute fatty liver of pregnancy /HELLP

  • Delivery of the fetus

2. Supportive and symptomatic management

3. Management of Complications:

Treatment of Hepatic encephalopathy:

Even minimal hepatic encephalopathy may benefit from treatment.[43]

Traditionally it has been presumed that excessive protein intake leads to increased generation of ammonia, which, in the setting of severe liver impairment, will accumulate and worsen the hepatic encephalopathy. While very large protein loads (such as gastrointestinal hemorrhage, because blood is rich in protein) are known to precipitate encephalopathy, the need for patients with chronic liver disease patients to be protein restricted has been disproven.[44] Indeed, because chronic liver disease is a catabolic state, a protein restricted diet would lead to protein malnutrition and a negative nitrogen balance.

Concomitant hypokalemia should be corrected as hypokalemia increases renal ammonia production and may promote conversion of ammonium into ammonia which can cross the blood-brain barrier.[45]

Lactulose is a compound that will cause osmotic diarrhea, thus lessening the time available for intestinal bacteria to metabolize protein into ammonia within the bowel. Further, it acidifies the environment in the lumen of the bowel. This promotes the conversion of lumenal ammonia (NH3) to ammonium (NH4+) which, by which virtue of its net charge, should be less readily absorbed into the bloodstream from the bowel lumen. Despite this theoretical and appealing mechanism, a meta-analysis of randomized controlled trials by the international Cochrane Collaboration found benefit, but suggests there is little evidence for its preferred use to treat hepatic encephalopathy.[46] Indeed, any drug (laxative) which speeds up transit through the bowel thereby lessening the time available for bacteria to metabolize protein into ammonia, works just as well.

Lactulose can be given rectally for patients who cannot take oral medications.[47][48][49] One regimen is 300 mL (200 gm) of lactulose syrup (10 gm/15 ml) in 1 L of water which is retained for 1 hour, with the patient in the Trendelenburg position.[50]

Antibiotics may be given to kill bacteria present in the bowel thereby decreasing bacterial conversion of protein to ammonia (and other toxic substances) there. Although effective, neomycin, a non-absorbable aminoglycoside antibiotic, is essentially contraindicated; it has been found that a proportion of the ingested dose is indeed absorbed due to increased gut permeability, thus increasing the risk of renal failure and hearing loss (i.e. two of the potential side effects of neomycin). The former side-effect, in particular, is especially worrisome given the already increased likelihood of renal failure in cirrhosis and portal hypertension (i.e. hepatorenal syndrome). Metronidazole has also been studied.[51]

Rifaximin , receieved orphan drug status in 2005 for the treatment of hepatic encephalopathy. In contrast to neomycin, its tolerability profile is comparable to placebo.[52] Multiple clinical trials have demonstrated that rifaximin at a dose of 400 mg taken orally 3 times a day was as effective as lactulose or lactilol at improving hepatic encephalopathy symptoms.[53] Similarly, rifaximin was as effective as neomycin and paromomycin.[54] Rifaximin was better tolerated than both the cathartics and the other nonabsorbable antibiotics. A number of concerns remain regarding rifaximin's role in the treatment of hepatic encephalopathy. It remains to be determined if rifaximin can improve severe encephalopathy symptoms as rapidly as lactulose. There are also concerns regarding the cost-effectiveness of the medication.

A meta-analysis of randomized controlled trials by the international cochrane collaboration found benefit from flumazenil.[55] The doses of flumazenil varied around a median of 2 milligrams over 10 minutes: flumazenil was given as a continuous infusion (12 trials), preceded by bolus injections in two trials. One trial used only bolus injections. Patients received flumazenil at a total dose ranging from 0.2 to 19.5 milligram (median 2 milligram). The median duration of treatment was 10 minutes (range one minute to 72 hours)'. However, the benefit was short.

L-ornithine-L-aspartate stimulates the urea cycle, and has shown encouraging results in randomized controlled trials.[56][57][58]

Contraindicated medications

Hepatic coma is considered an absolute contraindication to the use of the following medications:

Treatment of cerebral edema:

The goal in the management of ICH is to lower the ICP to less than 20 to 25 mm Hg and maintain the cerebral perfusion pressure above 50 to 60 mm Hg. This is mainly performed by increasing the mean arterial pressure (MAP) and decreasing the ICP by the methods mentioned below:[59]

Treatment of hepatorenal syndrome:

Because of the high mortality associated with hepatorenal syndrome, emphasis is on prevention in patients who are at risk for the condition. Strategies for avoiding hepatorenal syndrome include appropriate and non-aggressive use of diuretics, identification and early treatment of infection and hemorrhage, and avoidance of other toxins that can affect both the liver and kidney.[60]

The definitive treatment for hepatorenal syndrome is liver transplantation, and all other therapies can best be described as bridges to transplantation. These treatment strategies include the following:[61]

Albumin

All major studies showing improvement in renal function in patients with hepatorenal syndrome have involved expansion of the volume of the plasma with albumin given intravenously [62][63] One regimen is 1 gm albumin per kg of body weight intravenously on day one followed by followed by 20-40 grams daily.[64]

Midodrine and octreotide

Midodrine is an alpha-agonist and octreotide is an analog of somatostatin. The medications are respectively systemic vasoconstrictors and inhibitors of vasodilators, and were not found to be useful when used individually in the treatment of the hepatorenal syndrome.[65] However, one study of 13 patients with hepatorenal syndrome showed significant improvement when the two were used together (with midodrine given orally, octreotide given subcutaneously and both dosed according to blood pressure), with three patients surviving to discharge.[66] A nonrandomized, observational study used "100 μg subcutaneously TID, with the goal to increase the dose to 200 μg subcutaneous TID" and "midodrine administration started at 5, 7.5, or 10 mg TID orally, with the goal to increase the dose to 12.5 or 15 mg if necessary" and found that "octreotide/midodrine treatment appears to improve 30-day survival".[67]

Vasopressin analogues

The vasopressin analogue ornipressin was found in a number of studies to be useful in improvement of renal function in patients with hepatorenal syndrome,[62][68] but has been limited by ischemic complications[62]. Terlipressin is a vasopressin analogue that has been found in one study to be useful for improving renal function in patients with hepatorenal syndrome with a lesser incidence of ischemia.[63] Neither medication is available for use in North America.

Transjugular intrahepatic portosystemic shunt

TIPS, shown in progress here, has been shown to improve renal function in individuals with HRS if portal pressures decrease after the procedure.

Transjugular intrahepatic portosystemic shunts (TIPS) involve decompression of the high pressures in the portal circulation by placing a small stent between a portal and hepatic vein. They have also been shown to improve renal function in patients with hepatorenal syndrome.[69][70]

Liver dialysis

Liver dialysis involves extracorporeal dialysis to remove toxins from the circulation. The molecular adsorbents recirculation system (MARS) has shown some utility as a bridge to transplantation in patients with hepatorenal syndrome.[71]

Hemodialysis

Renal replacement therapy may be required to 'bridge' the patient to liver transplantation, although the condition of the patient may dictate the modality used.[72]

Other medications

Other agents used in treatment include

Management of Coagulopathy[5]

  • Routine correction of thrombocytopenia or elevated INR by plasma infusion, in the absence of bleeding, is not indicated in acute liver failure, because of the low incidence of bleeding manifestations in ALF and the risk of volume expansion with plasma replacement. In addition, INR is an important prognostic indicator in ALF, correction of coagulopathy would alter the INR and interfere in the assessment of prognosis.
  • Routine administration of vitamin K (5 to10 mg subcutaneously)
  • plasma or clotting factor replacement therapy in clinically significant bleeding or the need for a procedure with a high bleeding risk such as ICP monitor insertion. Recombinant activated factor VII is used if INR is still high to correct coagulopathy in these patients.
  • Patients with thrombocytopenia with platelet count less than 50,000 cells/mm3 with clinically significant bleeding should receive platelet transfusion. In the absence of bleeding, there is no need to initiate platelet transfusion.[5]

Management of metabolic abnormalities

Treatment of hemodynamic instabilty

4. Emergency therapies

5. Liver transplantation

  • Early consultation with liver transplant specialists and transfer of patients to a liver transplant center when necessary

Contraindicated medications

Severe hepatic failure is considered an absolute contraindication to the use of the following medications:

The ALFSG index is a newer option that may be more accurate.[75]

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