Liver failure

Hepatic Encephalopathy in Dogs and Cats

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Episode based on:

Lidbury JA, Cook AK, Steiner JM. Hepatic encephalopathy in dogs and cats. J Vet Emerg Crit Care 2016. 26 (4):471-487.

“The aims of this article are to comparatively review the pathogenesis, clinical presentation, diagnosis, and management of HE in dogs and cats. Gaps in the understanding of HE in dogs and cats and areas worthy of future study are also highlighted.”

What is Hepatic Encephalopathy?

“the spectrum of neuropsychiatric abnormalities seen in patients with liver dysfunction after exclusion of other known brain disease” from Hepatic encephalopathy – definition, nomenclature, diagnosis, and quantification: final report of the working party at the 11th World Congresses of Gastroenterology, Vienna 1998 (Hepatology, 2002).

Hepatic Encephalopathy – Classification

Three types in human medicine:

  • Type A: due to acute liver failure in the absence of pre-existing liver disease.
  • Type B: associated with portal systemic bypass without intrinsic hepatocellular disease; e.g. congenital portosystemic shunting in dogs and cats.
  • Type C: associated with cirrhosis and portal hypertension or acquired portal systemic shunting. Subcategorised according to duration and characteristics. Distinction made in people between ‘overt HE’ (signs of impaired mental status) and ‘covert HE’ (no altered mental status).

“can be applied to dogs and cats if the definition of type C HE is broadened to include cases associated with all intrinsic hepatocellular disease and portal hypertension or acquired portal systemic shunting.”

Covert HE currently not recognised in dogs and cats – likely exists but challenging to diagnose.

Schemes for grading severity exist in human medicine. No universally accepted guidelines to grading in dogs or cats. Some authors have adapted human grading schemes for use in dogs, e.g. Proot et al, 2009.

Hepatic Encephalopathy – Pathogenesis


Evidence (more and better quality in people) for central role of ammonia dysmetabolism.
Gastrointestinal tract is main source of ammonia. Especially via breakdown of nitrogenous products (e.g. urea) by urease producing gastrointestinal microbial organisms; but also via conversion of glutamine to ammonia within intestinal mucosa.

Ammonia and the liver:

Liver is main site of ammonia detoxification (kidneys and skeletal muscle much less so): failure of hepatic detoxification leads to hyperammonaemia and higher cerebral exposure.

Main causes of inadequate hepatic detoxification:

1) Portosystemic shunting (PSS):

Most common reason in dogs and cats
Ammonia-rich splanchnic blood from the gastrointestinal tract bypasses hepatic uptake and flows directly into systemic circulation.
Two types of portosystemic shunt, extrahepatic and intrahepatic
Congenital vascular anomalies or acquired collateral blood vessels secondary to prehepatic or hepatic portal hypertension



2) Intrinsic liver dysfunction despite receiving ammonia-rich blood:

Due to acute liver failure or potentially chronic cirrhotic changes

Ammonia and the brain:

Brain is involved and active in ammonia handling
Ammonia passes freely across the blood brain barrier (BBB) in healthy individuals
Ammonia and pathogenesis of hepatic encephalopathy:

  • One of the most appealing theories is ammonia causes astrocyte swelling
  • Other potential mechanisms too
  • May also contribute to neurological dysfunction by increasing BBB permeability

“Dogs and cats with HE are often hyperammonemic, and successful treatment of HE is usually associated with a reduction in serum ammonia concentrations. However, patients may have HE despite a blood ammonia concentration within the reference interval suggesting that other mechanisms also play a role in the pathogenesis of HE.” (authors cite Rothuizen, van den Ingh, 1982).

Other pathogenic mechanisms of HE:

Infection and inflammation may play a role:

Clinical evidence in people
Non-infectious or infection systemic inflammatory response syndrome (SIRS) is common in people with both acute liver failure and cirrhosis
Inflammatory mediators may trigger HE by exacerbating cerebral effects of ammonia

Systemic inflammation also a potential phenomenon in dogs and cats with acute liver failure…“However, the relationship between inflammation and canine HE needs to be better defined. To the authors’ knowledge, this relationship has not been studied at all in cats.”


Neurosteroids found in high concentrations in the brain
Oxidative stress
Amino acid balance

Hepatic Encephalopathy – Precipitating factors


At least one trigger identified in 88 to 90% of those affected
Individuals with one or more triggers have a worse prognosis than those without
Most commonly reported include: gastrointestinal bleeding, constipation, diarrhoea, infection, hypokalaemia, hyponatraemia, and excess dietary protein.

Number of same factors can potentially precipitate HE in dogs and cats; some have been described in the veterinary literature. “However, the evidence base to support the role of many of these factors in veterinary species is weak or nonexistent.” Further investigation of the factors that may predispose dogs and cats to HE is needed.

Hepatic Encephalopathy – Clinical presentation

Signalment reflects most common causes of HE in dogs and cats, namely congenital or acquired portosystemic shunts.

Canine breeds most likely to be have congenital PSS (in descending order): Havanese, Yorkshire Terrier, Maltese, Dandy Dinmont Terrier, Pug, Miniature Schnauzer, Standard Schnauzer, and Shi Tzu. (Tobias, Rohrbach, 2003)

No studies evaluating which breeds are most likely to develop acquired shunting. Probably most likely in breeds predisposed to chronic hepatitis. Wide age range but typically older than dogs presenting for congenital PSS.

Congenital PSS reported in several cat breeds; unclear which – if any – are predisposed.
The authors say that although congenital shunts have been reported in a number of cat breeds, it is not clear which if any cat breeds are predisposed to HE and large-scale epidemiological studies will be needed to ascertain this.

Clinical signs:

Initially often subtle and episodic; can progress in intensity and frequency
May be exacerbated by eating
In one study (Lidbury et al, 2012)):

  • Most common historical findings: obtundation, altered behaviour, head pressing, ataxia, apparent seizures, vomiting, lethargy, ptyalism, apparent blindness, and shaking.
  • Most common neurological findings: obtundation, ataxia, weakness, conscious proprioceptive deficits, seizures, circling, cranial nerve deficits, stupor, and tremor.

Signs of HE in cats reportedly broadly similar to those in dogs. 

Hepatic Encephalopathy – Diagnosis

In veterinary medicine, based on:

  • Presence of consistent clinical signs
  • Exclusion of other causes of encephalopathy
  • Laboratory findings
  • Imaging studies, and
  • Response to treatment

Currently no way to evaluate dogs and cats that have HE but without impaired mental status.

Measuring blood ammonia concentration:

May or may not be elevated in dogs with HE

“In individual dogs, fasting ammonia concentrations poorly predict the severity of HE.” (Rothuizen, van den Ingh, 1982)

When accessible, seems to be performed routinely or at least commonly in veterinary patients suspected of having HE; not the case in human medicine.

Appropriate sample handling is critical:

  • Ammonium ions are extremely labile in plasma and ammonia may be released by red blood cells ex vivo.
  • Samples should be collected in a lithium heparin or EDTA tube, placed immediately on ice, and the plasma separated from the red blood cells as soon as possible.
  • Plasma must be kept cooled and should be analysed within 30 minutes of collection.

In-house and point of care analysers available: Reliability? Validation in dogs and cats?

“Measurement of pre- and postprandial serum bile acid concentrations is a useful test for diagnosing hepatobiliary disease, including portosystemic shunting, in dogs and cats. A definitive diagnosis of portosystemic-shunting requires diagnostic imaging or surgical exploration. Several imaging modalities are useful for this purpose, including angiography, abdominal ultrasonography, portal scintigraphy, computed tomography angiography, and MRI angiography. These imaging modalities, apart from portal scintigraphy, frequently allow the anatomic characterization of the shunt vessel(s)….For patients with acquired liver disease, a histological diagnosis is often necessary to define the underlying cause.”

Hepatic Encephalopathy – Treatment

Treating the underlying cause:

Various techniques for attenuation of congenital PSS
“Generally, signs related to HE improve after shunt attenuation…although incomplete closure can lead to persistent compromise. Dogs with a poorly developed portal vasculature may develop portal hypertension after shunt closure. This triggers the development of [acquired collateral circulation] with possible recurrence of HE. Postoperative seizures can also occur, the pathogenesis of which is unknown.”

Post-attenuation seizures “can occur in dogs and cats that do not have HE or other metabolic causes of seizures….Typical histological changes of the cerebrum in animals undergoing necropsy include selective “ischemic” neuronal necrosis and other changes that are consistent with ischemia or hypoxia. Withdrawal of endogenous benzodiazepines [post-congenital shunt] attenuation has also been proposed as a potential mechanism.”

Attenuation of acquired shunts contraindicated; these shunts are a compensatory response to portal hypertension and closure results in an acute exacerbation of portal hypertension.

General supportive care and treatment of precipitating factors:

Standard practice around:

  • Maintenance of fluid and electrolyte balance
  • Routine care of the comatose or stuporous patient
  • Management of suspected intracranial hypertension
  • Antimicrobial therapy for confirmed or highly suspected infection
  • Gastroduodenal ulcer treatment and prophylaxis

Warm water enemas:

Advised in this review to be performed in severely affected dogs and cats with HE until signs improve (reference is a single author book chapter).
Help remove blood and faecal matter from colon; therefore decrease bacterial ammonia production.
Also indicated for constipated patients with HE of all severity grades.


Typical recommendation is protein-restricted diet containing specific types of protein sources.
Cats reportedly have a higher dietary protein requirement than dogs.
Diets recommended for HE also tend to have other modifications including reduction in some substances and supplementation with others.

“Although several commercially available diets are marketed for dogs and cats with HE, the optimal diet formulation has not been established.”


A non-absorbable disaccharide
Potential beneficial effects:

  • Trapping of ammonium ions within the colon leading to decreased absorption of ammonia into the portal circulation
  • Inhibition of ammonia production by colonic bacteria
  • Stimulation of incorporation of ammonia within bacterial proteins
  • Reduced intestinal transit times leading to decreased bacterial ammonia release
  • Increased faecal excretion of nitrogenous compounds

Placebo controlled studies in humans support efficacy for treating overt HE. While lactulose is “commonly used to treat HE in dogs and cats [both acutely and chronically]…there are no studies that have critically evaluated the efficacy of this drug.”

Can be given per rectum after a cleansing warm water enema in acutely compromised patients but “it has not been proven that this has any benefits over a plain warm water enema.”

Antimicrobial therapy:

Aim to reduce ammonia production by altering intestinal microbiome

  • Poor gastrointestinal absorption
  • Use no longer recommended in people as inadequate evidence of efficacy and risk of serious renal injury and ototoxicity
  • No good quality information about its use for HE in dogs and cats.

Metronidazole and vancomycin have also been used to treat HE in people; may be better tolerated in people than neomycin but their efficacy has not been rigorously established. Clinical trials have not been reported describing the efficacy of metronidazole for HE in dogs and cats.

Rifaximin (semisynthetic derivative of rifampicin) is US Food and Drug Administration approved for maintaining remission of HE in people. “The pharmacokinetics of rifaximin has been reported for dogs and this drug has been reported to be well tolerated in this species…The lack of apparent adverse effects is a potential benefit compared to neomycin and metronidazole. However, the safety and efficacy of this drug in dogs and cats with HE have not been established. Current costs are also likely to be prohibitive.”

Intravenous ampicillin (or potentiated amoxicillin) may be used in dogs or cats that cannot receive oral medications
Use of oral ampicillin also been reported


“Anticonvulsant drugs should be administered to patients with HE if seizures occur and in patients that seizure after attenuation of a congenital portosystemic shunt. Additionally, they are sometimes given to patients prior to shunt attenuation in an attempt to reduce the occurrence of postoperative seizures.”

“The use of diazepam and midazolam to treat seizures due to HE is controversial and there are no clinical trials that have evaluated the efficacy of these drugs in this setting. As diazepam is hepatically metabolized its half-life may be prolonged in dogs and cats with HE. Therefore, the dose and frequency that is used should be reduced in order to avoid causing profound sedation…In people benzodiazepine administration is considered to be a precipitating factor for HE.”


  • Rapidly acting anticonvulsant with few side effects identified so far
  • Can be given intravenously or orally to dogs and cats
  • Principal route of excretion is renal so suitable for patients with hepatic compromise.
  • Use in dogs undergoing congenital PSS attenuation may be well tolerated and may reduce occurrence of postoperative seizures (Fryer et al, 2011).

Phenobarbital and propofol may also be used if required in acute situations
Potassium bromide can be used as an adjunct to other anticonvulsant drugs in dogs; of little use in emergency scenario due to very long half-life and delayed onset of action.

Other potential treatment options in people:

  • Flumazenil (intravenous benzodiazepine receptor antagonist): role of endogenous benzodiazepines in the pathogenesis of HE is controversial; only consensus is that flumazenil is useful when treating human patients with HE who have taken benzodiazepines.
  • L-ornithine-L-aspartate (or LOLA): thought to increase the rate of ammonia detoxification; early positive findings with clinical use in people with overt HE but further work is needed.
  • L-carnitine: several potentially beneficial mechanisms of action have been proposed in ammonia toxicity; some positive early findings in people but more work is needed. 
  • Prebiotics, probiotics and synbiotics: controversy in the evidence base in people and further well-designed large-scale clinical trials are needed.

Application to veterinary emergency and critical care

“HE is a relatively common but potentially life-threatening complication of hepatobiliary disease in dogs and cats. Veterinarians working in emergency or critical care settings must be able to promptly recognize, diagnose, and manage this condition. Although increased blood ammonia concentrations strongly suggest HE, it is important for clinicians to be aware of the limitations of this diagnostic tool. It is also essential that predisposing factors are quickly identified and addressed and that appropriate supportive care is provided.”

“Although there are several well-established treatments for HE in dogs, none of them are supported by robust scientific evidence. Clinical trials of the drugs currently used to treat HE are needed to help optimize treatment protocols.”

Papers mentioned in this episode:

Fryer KJ, Levine JM, Peycke LE, et al. Incidence of postoperative seizures with and without levetiracetam pretreatment in dogs undergoing portosystemic shunt attenuation. J Vet Int Med 2011. 25(6):1379–1384.

Lidbury JA, Cook AK, Steiner JM. Hepatic encephalopathy in dogs and cats. J Vet Emerg Crit Care 2016. 26 (4):471-487.

Lidbury JA, Ivanek R, Suchodolski JS, Steiner JM. Clinical feature of hepatic encephalopathy in dogs: 80 cases (1991–2011). J Vet Int Med 2012. 26(3):781 (Abstract).

Mehl ML, Kyles AE, Hardie EM, et al. Evaluation of ameroid ring constrictors for treatment for single extrahepatic portosystemic shunts in dogs: 168 cases (1995–2001). J Am Vet Med Assoc 2005. 226(12):2020–2030.

Proot S, Biourge V, Teske E, Rothuizen. Soy Protein Isolate versus Meat-Based Low-Protein Diet for Dogs with Congenital Portosystemic Shunts. J Vet Int Med 2009. 23(4):794-800.

Rothuizen J, van den Ingh TS. Arterial and venous ammonia concentrations in the diagnosis of canine hepato-encephalopathy. Res Vet Sci 1982. 33(1):17-21.

Taboada J, Dimski DS. Hepatic encephalopathy: clinical signs, pathogenesis, and treatment. Vet Clin North Am Small Anim Pract 1995. 25(2):337–355.

Tobias KM, Rohrbach BW. Association of breed with the diagnosis of congenital portosystemic shunts in dogs: 2,400 cases (1980–2002). J Am Vet Med Assoc 2003. 223(11):1636–1639.

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Acute liver failure

*** If you find these podcasts useful and interesting, PLEASE click on the iTunes icon below, then the "View in iTunes" blue link, and then rate and/or review the podcast. That will be really great and much appreciated. Thank you! ***

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Episode based on:

Weingarten MA, Sande AA. Acute liver failure in dogs and cats. J Vet Emerg Crit Care 2015. 25(4):455-473.

Get in touch if you would like a copy of the paper.

1. Injury versus failure:

Acute liver injury: acute hepatocellular damage but liver function is retained; damage may resolve without any impact on function
Failure implies reduced liver function due to severe and extensive damage

2. More common causes:


Cycad Palms or Sago Palms:

  • Found throughout the USA, especially in the South; also in other countries but not native to the UK
  • Primary toxin is cycasin
  • No specific treatment or antidote

Blue-green algae*
Amanita mushrooms*

(* No specific antidotes or therapies)

Xylitol – see episode 6

Drug/Drug reactions:

Dose-dependent predictable hepatotoxic drugs versus idiosyncratic non-dose dependent hepatotoxicity
Paracetamol (acetaminophen):

  • Used therapeutically in dogs; wide safety margin in this species
  • Cats are very susceptible to its dose-dependent toxicity so it should not be used in this species

Infectious – especially leptospirosis
Hepatic lipidosis in cats
Fatal acute hepatic necrosis in cats due to oral administration of diazepam and zolazepam – idiosyncratic

3. Clinical findings and consequences:

Clinical signs:

Often non-specific, e.g. vomiting, diarrhoea, anorexia, lethargy etc.
May progress toward sepsis and multiple organ dysfunction
May be due to primary cause of ALF and/or consequences of ALF

Icterus/jaundice due to hyperbilirubinaemia:

  • Three types: pre-hepatic due to red cell haemolysis; hepatic and post-hepatic which often occur to some extent concurrently

“Due to the large reserve capacity of the liver, icterus due to intrahepatic cholestasis is only apparent when the liver is severely and diffusely affected.”


ALF has multifactorial and complex effects on coagulation

“Some patients with ALF may show no evidence of hemorrhage, others may hemorrhage only after invasive procedures including placement of IV catheters, while others may have spontaneous hemorrhage”

Both primary (thrombocytopenia, thrombopathia, endothelial dysfunction) and secondary (clotting factor deficiency) clotting abnormalities may be present

ALF may result in altered production of both procoagulant and anticoagulant factors
Patients with ALF often have functional defects in vitamin K-dependent coagulation factors
May have evidence of dysfibrinogenaemia or hyperfibrinolysis in the absence of DIC

“The end result of these alterations in primary hemostasis, secondary hemostasis, and fibrinolysis is a “rebalanced,” but often unstable, system that can result in either hemorrhage or thrombosis.”

Hepatic encephalopathy:

Neuropsychiatric disorder subdivided into 3 types based on chronicity, aetiology and presentation:

  • Type A: acute form, associated with acute liver failure
  • Type B: bypass form, associated with portal-systemic shunts
  • Type C: chronic form, associated with cirrhosis and portal hypertension

Signs of type A HE often manifest suddenly and progress rapidly; spectrum from mild to very severe neurological signs
Ammonia likely plays a crucial role in the development of type A HE; further complicated by cerebral oedema, intracranial hypertension, hypoglycaemia, hyponatraemia, and systemic inflammatory response syndrome (SIRS). 


In health, the liver plays a key role in the body's innate and acquired immune systems. Through the portal circulation, the liver is exposed to bacteria from the gastrointestinal tract and the liver also synthesises factors involved in the complement cascade. In ALF, the liver is unable to effectively remove or neutralise pathogens prior to the blood passing into systemic circulation, resulting in bacteraemia.

“In people with ALF, bacteremia has been reported in up to 80% of the patient population, most commonly with gram-negative enteric organisms, staphylococci species, and fungal organisms, such as Candida albicans. Iatrogenic sources of bacteremia are common and include indwelling intravenous and urinary catheters, as well as skin contamination.”

4. Diagnosis:

Clinical pathology:

Need to demonstrate hepatic dysfunction or insufficiency rather than just injury
Intracellular ‘leakage’ enzymes – ALT, AST – increase first signifying hepatocellular injury
Inducible membrane-bound ALP and GGT may also increase – typically to much less extent but depends on presence of concurrent biliary tract obstruction

“Increase in both ALT and AST activities are sensitive indicators of acute liver damage, but the degree of increase in these values above the reference interval does not necessarily correlate with the degree of hepatocellular damage.”

Subsequent evidence of dysfunction:

  • Hyperbilirubinaemia
  • Prolonged prothrombin time
  • Hypoglycaemia
  • Hypoalbuminaemia – typically end-stage

But sequence and development of these findings can vary.

“There are several electrolyte and acid-base derangements that either occur as a result of ALF or complicate management of ALF patients. These abnormalities include hypokalemia, hypophosphatemia, hyperphosphatemia, hyponatremia, hyperlactatemia, and refractory metabolic acidosis”.

“Patients with ALF often develop hyperlactatemia and an associated metabolic acidosis. Causes of hyperlactatemia include hypotension, poor tissue perfusion, and tissue hypoxia with subsequent anaerobic metabolism and lactate production at the level of the tissue…Hyperlactatemia has been associated with a poor prognosis in human patients with ALF and HE as well as people with ALF secondary to acetaminophen toxicity.”


“plasma ammonia concentrations remain difficult to interpret as it is the actual exposure of the brain to ammonia, not the concentration of ammonia in circulation, that leads to the development of HE. Therefore, the health of the blood–brain barrier, an immeasurable quantity, plays a significant role in the clinical interpretation of ammonia concentration and the development of HE….However, serum ammonia concentration may be useful for prognosis as hyperammonemia at presentation as well as persistent hyperammonemia in spite of treatment has been associated with both increased rates of cerebral herniation as well as an increased mortality rate” in people.

Performance of in-house point-of-care analysers can be very unpredictable/unreliable
Submitting samples to external laboratories is possible – must heed sample-handling guidelines including keeping on ice

Diagnostic imaging:

Routine imaging will not evaluate liver function but may demonstrate gross abnormalities in liver structure; these vary depending on the cause of the pathology, in particular between focal and diffuse conditions.
Ultrasonography will also allow guided samples to be obtained for histopathology

“when diagnosing ALF, sonography is a useful, but not definitive, tool and must be paired with appropriate history, physical examination findings, biochemistry results, and histopathology.”

5. Treatment:

“Aggressive treatment for ALF should be initiated as soon as possible. If the underlying cause is known, it should be removed and an antidote, if available, administered. Unfortunately, the inciting cause of ALF is often unknown and thus the cornerstone of therapy in veterinary patients remains supportive care while the liver is allowed time to recover. Generalized supportive care includes intravenous fluid therapy, liver supplemental medications, nutritional management, and management of any complications that may arise.”

Supportive care:

Fluid therapy:

Standard approach in terms of correcting hypovolaemia/hypoperfusion and dehydration and subsequent maintenance of fluid balance

Avoid lactate-containing fluids?

“Lactated Ringer's solution should be avoided as it contains lactate as a buffer, which requires a functioning liver for proper metabolism”; remember that this lactate would be converted by the liver to bicarbonate which according to the traditional model of acid-base is why Hartmann’s or lactated Ringer’s is considered an alkalinising solution.

“it seems to me that the recommendation to use 0.9% sodium chloride is based on theoretical reasoning to avoid the administration of lactate; the sodium concentration is higher than that in Hartmann’s which may be helpful because as I mentioned earlier these patients may be hyponatraemic, but this solution may also promote a metabolic acidosis in a patient that is potentially already acidaemic. What patient-centred clinical relevance all this has, well, I don’t think we can say for sure.” (Shailen)

“In patients who remain hypotensive (systolic blood pressure < 90 mm Hg, MAP < 65 mm Hg) despite correction of intravascular volume depletion with fluid therapy, vasopressor therapy may be required….In patients who are persistently hypotensive despite volume resuscitation and the use of vasopressors, relative adrenal insufficiency, and a trial of a supraphysiologic dose of a corticosteroid could be considered.”

For more on critical illness-induced corticosteroid insufficiency see “Steroids and Shock” episode, number 17

Maintain normoglycaemia – avoid hyperglycaemia – and normal electrolyte status
Avoid hyponatraemia


“Patients in ALF typically exist in a hypermetabolic state with a higher than normal energy requirement, leading to a catabolic state characterized by a negative nitrogen balance….Provision of adequate dietary protein is essential as catabolism of skeletal muscles leads to increased ammonia production, decreased capacity for muscle detoxification of ammonia, and increased potential for HE.”

Preferred protein sources may vary between patients with HE and those without in terms of keeping ammonia production low
Also consider carbohydrates, lipids, vitamins

“Hepatoprotective” medications:

“There are numerous “hepatoprotective” medications on the market, including SAMe, NAC, silymarin, and vitamins C and E, which decrease oxidative stress. In health, hepatocytes have potent intrinsic antioxidant systems including glutathione (GSH). In damaged livers, GSH may be less available, resulting in increased ROS concentrations leading to hepatocyte death.”

Lack of evidence in terms of efficacy (except for N-acetylcysteine in paracetamol toxicity)
Considerable uncertainty in terms of therapeutic dosing regimens

“I think the perspective with these agents in acute liver failure is that they may do some good, we don’t know for sure, but are unlikely to harm the patient. Of course we have to factor any patient stress caused by administration of oral medications and any financial costs into our risk and cost to benefit assessment.” (Shailen)

Management of complications:


“In human patients with ALF, the most common sites of infection are the lung, urinary tract, and blood and the most commonly isolated organisms include Staphylcocci, Streptococci, and enteric gram-negative bacilli…Infection prevention is crucial and cleanliness should be strictly maintained by doctors and nursing staff through thorough hand washing and barrier nursing protocols…The use of prophylactic antimicrobials in all ALF patients is controversial, as prophylactic parenteral and enteral antimicrobials have not been shown to improve outcome or survival in these patients….Empirical antimicrobial therapy is recommended when suspicion for infection or the likelihood of sepsis is high, such as when there is progression of HE, refractory hypotension, or the presence of SIRS…The choice for empiric antimicrobial therapy should include broad spectrum coverage for gram-positive and gram-negative bacteria, such as a third-generation cephalosporin.”

Coagulation disorders:

Spontaneous haemorrhage uncommon
Plasma therapy not recommended solely on the basis of a prolonged PT or aPTT
No clear benefits to the use of plasma in patients without evidence of haemorrhage; need to be cognoscente of potential risks (albeit less than with red cell administration)/costs

What about giving plasma before an invasive procedure?

“This recommendation is empirically derived, as there are no evidence-based data showing that the treatment of coagulopathies results in less risk of hemorrhage during invasive procedures, and there are no data showing an appropriate standard end-point of therapy.”

Treat all ALF patients with vitamin K1?
Consider H2 blockers or proton pump inhibitors as gastrointestinal bleeding is a potential complication?

Hepatic encephalopathy, cerebral oedema, and increased ICP:

“Unlike with patients with type C [chronic] HE, there are currently insufficient data to recommend therapy with lactulose or nonabsorbable antimicrobials such as rifaximin and neomycin in patients with ALF.” Not sure of the evidence base for this.

Correction of cerebral oedema via mannitol or hypertonic saline is a mainstay of therapy in acute liver failure patients with hepatic encephalopathy
For more on intracranial hypertension detection and management see traumatic brain injury episode, episode 22.

6. Prognosis:

Varies considerably depending on:

  • Underlying aetiology
  • Degree of hepatocellular damage
  • Capacity of liver to regenerate
  • Stage of disease when treatment is initiated
  • Presence and rapidity of development of disease sequelae such as HE
  • Response to therapy

“Unfortunately, the prognosis of ALF in dogs and cats is generally considered to be poor” 


Auzinger G, Wendon J. Intensive care management of acute liver failure. Curr Opin Crit Care 2008; 14(2):179–188.

Weingarten MA, Sande AA. Acute liver failure in dogs and cats. J Vet Emerg Crit Care 2015. 25(4):455-473.

Tweet: Check out FREE audio podcasts from @VetEmCC Also available in iTunes/Stitcher. #veterinary #podcast