What's Magnesium Got To Do With It?

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This episode is based on:

Humphrey S, Kirby R, Rudloff E. Magnesium physiology and clinical therapy in veterinary critical care. J Vet Emerg Crit Care 2015. 25(2):210-225.

“Magnesium (Mg) is a cation with an escalating role in critical care medicine.”

Is this true?
If it is, is it a good thing?
Is the evidence base supporting this escalating role theoretical, experimental or clinical? 

Background theory

“magnesium plays a pivotal role in cellular energy production and cell-specific functions in every organ of the body. Excess or deficiency of this important cation can result in life-threatening complications.”

Majority (99%) intracellular, especially bone
Plasma magnesium: protein-bound, complexed (anions e.g. citrate, phosphate), ionised
Ionised Mg physiologically active form

Plasma [Mg] may not reflect cellular environment
Changes in plasma [Mg] may not reflect changes in total body [Mg]

Intracellular [Mg] maintained at 0.5–1 mmol/L despite significant fluctuations in extracellular [Mg].

Cellular functions:

“Magnesium plays a pivotal role in the electrophysiology and ion flux across cell and mitochondrial membranes” ultimately impacting on energy production and release.
Affects cellular functions via relationship with intracellular calcium; in general competes with or otherwise influences calcium movement.

Various other functions mentioned in article.

Total body magnesium content dependent upon intestinal and renal absorption and excretion

Measuring Magnesium

“Accurate measurement of total body magnesium is a challenge due to its intracellular location and activity. The current clinical standard is to quantitate serum total or ionized magnesium concentrations…Monitoring the biologically active serum ionized magnesium concentration is preferred over total serum magnesium concentration.”

Serum quantitation may not accurately reflect total body magnesium content – unresolved
Research methodologies that allow intracellular magnesium to be measured may become available for clinical use

Magnesium disorders

“Total body magnesium concentration is affected by dietary intake, gastrointestinal function, hormonal balance, redistribution of the magnesium cation, and excretion into a third body space or urine. Magnesium disorders can manifest with a multitude of clinical signs, none of which are specific for the magnesium disorder.”

Article includes summary of mechanisms, causes, clinical signs, and treatment recommendations for magnesium excess and deficiency.

*Patient may have clinical signs that are compatible with a magnesium disorder – but they will not be pathognomic for one
*Abnormal plasma [Mg] may support that signs are due to a magnesium disorder – but not necessarily
*Decision to treat: empirical; based on risk-benefit assessment

Magnesium excess

“The two most commonly reported causes of magnesium excess in both human and veterinary patients are renal failure and iatrogenic causes…Hypermagnesemia can occur when magnesium-containing drugs such as antacids, laxatives, or enemas are administered to patients with underlying renal disease….Hypotension is one of the key clinical complications of magnesium excess.”

[Martin LG, Matteson VL, Wingfield WE, et al. Abnormalities of Serum Magnesium in Critically III Dogs: Incidence and Implications. J Vet Emerg Crit Care 1994. 4(1):15-20]

  • Naturally occurring total hypermagnesaemia reported to occur in up to 13% of critically ill dogs admitted to the ICU of one teaching hospital
  • Found that dogs with hypermagnesaemia were 2.6 times more likely to die of their underlying disease than dogs with normal serum magnesium
  • Dogs with renal disease had the highest median values for serum magnesium 

Remember to critique the paper methodology yourself before attributing any significance to these reported results!

“The concept that naturally occurring hypermagnesaemia may have prognostic value warrants further study”
Magnesium deficiency

Total body magnesium deficiency can exist despite normal serum magnesium concentration.
“A diagnosis of ionized hypomagnesemia has been associated with a prolonged hospital stay in dogs…ileus in horses following colic surgery…as well as a prolonged hospital stay and a higher incidence of mortality in hospitalized cats…The hospital length of stay for critically ill dogs with hypomagnesemia was reported to be twice as long as those with normal serum magnesium….Hypomagnesemia was also associated with concurrent hyponatremia and hypokalemia in dogs.” Reference canine paper above, one equine paper and one feline paper.

“Hypomagnesemia is common in critically ill human patients”
“Although magnesium-depleted patients may represent a subset of patients with more severe disease, hypomagnesemia appears to be an independent predictor of outcome”. Reference one human study.
If there is good quality evidence that hypomagnesaemia is common in critically ill human patients, does the same apply to critically ill dogs, and what about critically ill cats?

Keep an evidence-based perspective to all this…..

  • Hypokalaemia can become refractory to standard potassium replacement therapy as a consequence of magnesium deficiency. Magnesium replacement may be necessary before potassium supplementation is effective.
  • Magnesium also apparently serves as a cofactor for insulin release and function, as well as in maintenance of appropriate cellular sensitivity to insulin. Insulin resistance may develop secondary to magnesium deficiency.
  • Diabetic ketoacidosis: “hypomagnesemia is a common finding in diabetic ketoacidotic people. Ketoaciduria and glucosuria promote urinary magnesium excretion, which can be exacerbated with fluid diuresis. In addition, significant cellular redistribution of magnesium occurs as it moves from the extracellular space to the intracellular compartment with insulin therapy. Close monitoring for clinical signs of a magnesium deficit is necessary since a total body deficit may not be reflected in the measured serum magnesium concentration.”
  • Calcium and magnesium are affected in a similar manner by hormones. As many as one-third of human patients with low serum magnesium may concurrently have low serum calcium. Correction of magnesium deficiencies may be required with refractory hypocalcaemia.
  • Magnesium deficiency has been shown to affect gastrointestinal function and motility.  Magnesium deficiency should be considered a differential in any patient with decreased stomach or intestinal motility.
  • “Magnesium has been successfully used in the treatment of preeclampsia and eclampsia in women since 1912…The anticonvulsant of choice for treating seizures due to eclampsia is magnesium…Hypomagnesemia may also be a factor in dogs presenting with eclampsia and should be considered when managing dogs with signs of eclampsia.”
  • "Cardiac conduction abnormalities are one of the most common and serious manifestations of magnesium deficiency. Cardiac arrhythmias associated with hypomagnesemia include ventricular tachycardia, ventricular fibrillation, supraventricular tachycardia, atrial fibrillation, digitalis toxicity associated arrhythmias, and torsades de pointes (TdP).” But the authors point out that “Magnesium's role in the pathogenesis of arrhythmias is difficult to ascertain since magnesium deficits often coexist with potassium and calcium deficiencies….Multiple studies in both human and veterinary patients have documented resolution of TdP after magnesium sulfate infusion… Magnesium supplementation decreases the incidence of ventricular arrhythmias and atrial fibrillation following cardiopulmonary bypass and coronary artery bypass in humans with magnesium deficiency.” Some human medics use magnesium in the treatment of ventricular dysrhythmias.

Treatment of magnesium disorders

“The decision to treat a suspected or diagnosed magnesium disorder will depend on the severity of the clinical signs and the magnitude of change from normal range of the serum magnesium level of the patient.”
Provide some more detailed treatment recommendations with mostly human medicine references

Magnesium excess

Hypermagnesaemia treated by replacing magnesium-containing medications or fluids with magnesium-free ones.
Promoting urinary excretion and inhibiting renal tubular reabsorption of magnesium are mainstays of treatment for moderate to severe hypermagnesaemia and when clinical signs are apparent (e.g. cardiac arrhythmia, hypotension). Use IV sodium chloride +/- diuretics.
Acute magnesium toxicity from iatrogenic overdose treated with additional calcium gluconate
“Hemo- or peritoneal dialysis using magnesium-free dialysate may be necessary to treat symptomatic magnesium excess resulting from kidney disease or iatrogenic overdose.” 

Magnesium deficiency

“If the magnesium deficit is mild, dietary changes and oral magnesium salts such as magnesium carbonate or oxide may be sufficient to increase magnesium intake….Oral magnesium supplementation…should be considered in small animal patients at risk for chronic mild magnesium deficit, for example, those with GI malabsorptive diseases or chronic digoxin or loop diuretic therapy.”

“Animals symptomatic for low magnesium should be treated with an IV infusion of magnesium sulfate or magnesium chloride” and they recommend accounting for the magnesium content of any IV fluids being used when calculating magnesium supplementation doses.”

“the optimum dosage and rate of magnesium administration has not been defined for veterinary patients”

Reportedly a single experimental canine study has been the basis of the magnesium sulfate dose recommendation in dogs and cats.

Magnesium Infusion as an Adjunct to Therapy

“The multifaceted role of magnesium in cells has led researchers and clinicians in human medicine to explore the effects of infusing magnesium as an adjunct to therapy for various conditions.”
Cite a reference from 1974 for potential use in shock resuscitation
“Current studies of brain injury, spinal injury, pain, sepsis and systemic inflammatory response syndrome, hypercoagulable states, eclampsia, tetanus, and ischemia have demonstrated potential beneficial effects from magnesium administration. In these situations, magnesium administration is not given to replace a documented magnesium deficiency but instead given for its beneficial effects in specific cells. Though all syndromes reported in people may not be common in veterinary patients, knowledge of the possible mechanisms of action of magnesium infusion on various tissues may allow extrapolation into the veterinary population of patients.”

The authors say that current studies have demonstrated potential beneficial effects in a variety of scenarios. We should explore the evidence for that statement further to ensure that we are happy that it is legitimate.
And, is extrapolating from humans to veterinary patients a legitimate practice?

“Magnesium sulfate has been utilized in the treatment of autonomic dysfunction associated with severe generalized tetanus in both people and dogs.” Reference a single case report from JVECC in 2011. Much greater anecdotal experience exists but to date use of magnesium in tetanus remains inconclusive.

Risk-benefit assessment:

“The administration of magnesium as an adjunctive therapy in the tetanus patient has not been associated with adverse side effects” – may not help but unlikely to do any harm so maybe give it a go?
Potential to actually induce hypermagnesaemia


  • “Magnesium is an important intracellular cation required for energy production and cell function in every organ.
  • Changes in magnesium homeostasis have consistently been correlated with increases in morbidity and mortality in veterinary and human critical patients.
  • Assessment of serum magnesium concentration should become a routine part of critical patient evaluation since the clinical signs and conditions associated with magnesium disorders can be nonspecific and varied.
  • Equipment to measure serum ionized or total magnesium is readily available in-hospital.
  • However, measurement of serum magnesium may not reflect total body magnesium concentration.
  • The serum magnesium concentration combined with clinical signs and conditions associated with magnesium disorders are used to make the diagnosis and to monitor treatment.
  • Research is exploring the role of magnesium infusions as an adjunct to standard therapy for clinical disorders such as head trauma, reperfusion injury, and vascular disease.
  • Future studies are expected to better define the role of magnesium in critical illness and investigate potential benefits of magnesium infusion in veterinary patients.”

SJ: “I guess my position is that when it comes to the clinical aspects and recommendations that the authors make, I don’t necessarily disagree, however I am also not sure that there is the evidence base in dogs and cats to support the statements at this time. So for me it is most definitely an area of on-going interest to see what more comes to light going forward.”

Please do get in touch if you have any comments or questions using the contact form, via email at shailenjasani@gmail.com, via Twitter @VetEmCC or via Facebook at the Veterinary ECC Small Talk page.

[This podcast is closely aligned with the MedEdLIFE Research Collaborative's Quality Checklist for Podcasts.]

I mention my Small Animal Emergency Medicine App for iPhone/iPad in this episode which you can find HERE. An Android version is in development.

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Journal Papers Episode: JVIM 2015

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In this episode of the podcast I discuss some of the papers that were published in the Journal of Veterinary Internal Medicine during 2015. Remember that this journal is now freely available via open online access. The papers I mention are as follows:

Van Meervenne SAE, Volk HA, Van Ham ML. Association between Estrus and Onset of Seizures in Dogs with Idiopathic Epilepsy. J Vet Int Med 2015. 29(1):251-253.

Hoehne SN, Hopper K, Epstein SE. Accuracy of Potassium Supplementation of Fluids Administered Intravenously. J Vet Int Med 2015. 29(3):834-839.

Fullagar B, Boysen SR, Toy M, et al. Sound Pressure Levels in 2 Veterinary Intensive Care Units. J Vet Int Med 2015. 29(4):1013-1021.

Hu H, Barker A, Harcourt-Brown T, Jeffery N. Systematic Review of Brain Tumor Treatment in Dogs. J Vet Int Med 2015. 29(6):1456-1463.

Goggs R, Dennis SG, Di Bella A, et al. Predicting Outcome in dogs with Primary Immune-Mediated Hemolytic Anemia: Results of a Multicenter Case Registry. J Vet Int Med 2015. 29(6):1603-1610.

[This podcast is closely aligned with the MedEdLIFE Research Collaborative's Quality Checklist for Podcasts.]

I mention my Small Animal Emergency Medicine App for iPhone/iPad in this episode which you can find HERE. An Android version is in development.

Tweet: Check out FREE audio podcasts from @VetEmCC http://ctt.ec/UqL8b+ Also available in iTunes/Stitcher. #veterinary #podcast

Managing Dog Bite Injuries

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In this episode I am joined by my good friend and European Specialist in Small Animal Surgery, Nicola Kulendra.

Apologies for the sound quality of this episode which is poorer than usual and not produced in stereo sound! Ooops.

I mention my Small Animal Emergency Medicine App for iPhone/iPad in this episode which you can find HERE. An Android version is in development.

[This podcast is closely aligned with the MedEdLIFE Research Collaborative's Quality Checklist for Podcasts.]

Tweet: Check out FREE audio podcasts from @VetEmCC http://ctt.ec/UqL8b+ Also available in iTunes/Stitcher. #veterinary #podcast

Patient Handovers/Rounds

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This episode is the first in this series to feature guests! In today's episode I am joined by Liz Hughston and Charlotte Rosenthal, two specialist ECC nurses from the USA.

Liz mentions "The Checklist Manifesto" by Atul Guwande and during the podcast we also refer to my ECC In-Patient Checklist.

This is a great human medicine blog post relating to handoffs in the Emergency Department that clearly has relevance to veterinary settings too. "ED HANDOFFS – THE PROBLEM AND WHAT WE CAN DO TO IMPROVE"

January 2016: something else that we did not discuss during this podcast episode was the I-PASS handoff system ("I-PASS this patient to you"!) reported in human medicine. See more here and here.

Tweet: Check out FREE audio podcasts from @VetEmCC http://ctt.ec/UqL8b+ Also available in iTunes/Stitcher. #veterinary #podcast

Acute liver failure

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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 http://ctt.ec/UqL8b+ Also available in iTunes/Stitcher. #veterinary #podcast