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.

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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 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.

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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.

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Traumatic Brain Injury (TBI) Management

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Key points and main potentially contentious areas.

1. Address potentially life-threatening problems:

Priorities as for any emergency patient: triage, address potentially life-threatening problems, implement stabilisation measures, provide analgesia
The most urgent problems may be extra-cranial; their treatment may have beneficial effects on the brain too (e.g. draining severe pneumothorax may systemic and cerebral oxygenation, reduce patient distress etc.).

2. Primary and Secondary TBI:

Primary injury, e.g.

  • Concussion
  • Contusion – parenchymal haemorrhage and oedema
  • Laceration
  • Extra-axial haemorrhage

Immediate result of traumatic event; will already have occurred by presentation.

Prime aim is to LIMIT SECONDARY BRAIN INJURY due to e.g.

  • Hypoxia
  • Ischaemia from hypoperfusion
  • Raised intracranial pressure (ICP)
  • Active haemorrhage
  • Blood brain barrier compromise
“The priority is to ensure that the brain receives an adequate supply of well-oxygenated…arterial blood in a patient with adequate ventilation.”

Treatment for possible raised ICP is one part of this therapy.
Secondary injury also affected by hypo/hypercapnia, hyperthermia, hypo/hyperglycaemia

3. Ensuring adequate oxygenation and ventilation:

Adequate brain oxygen supply depends on:

  • Adequate cerebral blood flow
  • Adequately oxygenated cerebral blood supply

Adequately oxygenated cerebral blood supply:


Routine approach to monitoring and supplementing systemic arterial oxygenation
Failure to achieve adequate oxygenation non-invasively necessitates intubation and ventilation +/- anaesthesia depending on patient’s status; practical and financial implications may be preclusive.

Note that excessive oxygenation may also be harmful by promoting oxidative injury; oxidative injury is one of the main mechanisms of secondary injury in TBI. Hyperoxia only really of concern in intubated patients on high FiO2 supplementation.

“if you have any doubt about the patient’s oxygenation status, then take a liberal approach to supplementation.”


Carbon dioxide status predominantly determined by ventilation

Hyperventilation lowers arterial CO2 levels causing cerebral vasoconstriction and potentially reducing ICP; but cerebral vasoconstriction also reduces cerebral perfusion which could be more harmful than the raised ICP attempting to be addressed.
Hyperventilation may worsen morbidity and mortality and inducing hypocarbia is no longer recommended
Hyercarbia should also be avoided; recommended target PaCO2/end-tidal CO2 approximately 35-45 mmHg, i.e. within normal range.
Requires access to arterial blood gas analysis or capnograph/capnometer
Difficult to influence ventilation too much unless patient is intubated but nevertheless, e.g. drain pneumothorax, treat pain etc.

4. Ensuring adequate cerebral perfusion:

Other key component to ensuring brain receives adequate supply of well-oxygenated blood Cerebral perfusion pressure (CPP) = Mean systemic arterial blood pressure (MAP) – Intracranial pressure (ICP)
In healthy brain autoregulatory homeostatic mechanisms protect cerebral blood flow over a range of MAP values
Autoregulation may be lost in injured brain; cerebral blood flow becomes even more dependent on CPP

“So this means that one of our key goals in the management of a traumatic brain injury patient is to try and maintain adequate cerebral perfusion pressure which we do by optimising the mean systemic arterial pressure and potentially trying to manipulate the intracranial pressure.”

Optimising mean systemic arterial pressure:

Head trauma patient may present with systemic hypoperfusion/hypotension due to blood loss +/- SIRS
Suggested targets include MAP 80 mmHg or systolic BP 100 mmHg; based on what evidence?
As always, priorities physical perfusion assessment and correction over BP readings
Standard approach to intravenous fluid resuscitation; replacement crystalloid typical first choice but hypertonic saline has a definite role (see below)
Vasopressor therapy if hypotension persists despite adequate fluid resuscitation (if available)
‘Conservatively aggressive’ approach: MUST RESUSCITATE SYSTEMIC PERFUSION but try to avoid overdoing it which may exacerbate cerebral oedema/raised ICP especially with a damaged blood-brain barrier.

5. Raised intracranial pressure:

Monroe-Kellie doctrine: intracranial volume = brain parenchyma + cerebral blood volume + CSF
Skull is a rigid structure so if one compartment increases in size, one or both of the other compartments has to shrink to compensate (intracranial compliance) or you will get an increase in intracranial pressure.
Parenchymal damage and blood leakage in TBI may exceed intracranial compliance capacity; raised ICP may occur.
Raised ICP will eventually compromise cerebral perfusion causing ischaemia; eventually global brain ischaemia and subsequent brain death results.

Detecting raised ICP:

Not as simple as it sounds
ICP measurement (invasive, non-invasive) is available in some human hospitals – but not veterinary centres
Measurement of optic nerve sheath diameter using ultrasonography has also been explored in human medicine; retrobulbar optic nerve sheath is continuous with the subarachnoid space so its diameter may reflect intracranial pressure.
Also some investigations into whether there is any clinically useful correlation between intraocular pressure and intracranial pressure in people.
On-going debate in human medicine is whether managing brain injury patients using ICP measurement results in better patient-centred outcomes than using clinical judgment alone; should be seen as complementary rather than independent means of patient assessment.

Cerebral ischaemic response (Cushing reflex):

Sufficient increase in ICP triggers systemic arterial hypertension as a response to try and maintain cerebral perfusion; subsequently you get reflex bradycardia.
May be reasonable to presume Cushing reflex is present in a patient with head trauma and raised ICP despite absence of bradycardia; latter is likely to ensue shortly.
Late onset phenomenon; increase in ICP likely to be substantial and potentially life-threatening when Cushing reflex detected

Other findings potentially suggestive of raised ICP:


  • Unexplained deterioration in mental status
  • Dilated non-responsive pupils
  • Loss of physiological nystagmus
  • Decerebrate posturing
  • Any animal with significant head trauma??

Medical therapy for raised ICP:

Don’t overlook measures to promote venous drainage from the brain, e.g. keeping head elevated 15-30 above horizontal, minimising jugular compression.

But…most effective intervention involves medical therapy for cerebral oedema “basically trying to shrink the brain by exposing it to the dehydrating effects of hypertonic saline or mannitol”.

Both are likely to have multiple other mechanisms of action although osmotic effects most likely predominate. 

Hypertonic saline vs. mannitol?

What do you have available?!

“If you do have both then you should note that at the present time, the evidence base that exists does not support one of these fluids being more effective than the other for the reduction of intracranial hypertension. You should note that the evidence base is either experimental animal models or clinical human patients.”

Normovolaemic patient: choose either first; can try the other one after if inadequate response
Hypoperfused hypovolaemic patient:
Choose hypertonic saline: restores intravascular volume and reduces intracranial pressure concurrently (albeit transiently)
Mannitol contraindicated – osmotic diuretic, may exacerbate volume status

Mannitol may require warming to dissolve crystals; hypertonic saline more convenient to use


Loop diuretic, could be used for raised ICP and may be equipotent to mannitol for this; maybe even synergistic if used with mannitol concurrently.
Avoid if hypovolaemic

“It is my understanding that the reason furosemide is not usually used instead of or in addition to mannitol is that it is more likely to cause potentially severe electrolyte abnormalities.”

When should medical therapy be used?

Not always clear but:

  • Cushing response – absolute indication
  • Relative indications:
    • Progressive neurological signs
    • Moderate-to-severe head injury refractory to aggressive extracranial stabilisation

6. Neurological examination:

Details can be found in other resources
Be careful not to draw premature conclusions, i.e. until effects of other factors (e.g. hypoperfusion, hypoxaemia, hypothermia, hypoglycaemia) influencing neurological status excluded.
Detailed neurological exam after patient stabilised; then repeat this on a regular basis for monitoring and prognostication.

7. Diagnostic imaging:

Point-of-care ultrasound evaluations of abdomen and thorax
Possible additional indications for imaging down the line e.g. fractures

Plain radiography:

  • Not routinely indicated
  • May reveal skull fractures but can be really difficult to obtain radiographs of interpretable quality
  • Does not provide clinically useful information with respect to brain injury

Advanced imaging:

“Now when it comes to more advanced imaging then aside from the issue of availability, we get into a bit of a can of worms. Some of you will be aware of the history of head CT in human trauma patients and I am not going to elaborate on that suffice to say that there is some concern about its overuse and constant discussion about what criteria should trigger a head CT to be performed. And those points apply equally to veterinary patients, likewise when we consider the use of MRI in brain injury.”

CT and MRI have relative strengths and weaknesses
MRI may provide prognostic information by detecting subtle parenchymal damage not evident on CT (e.g. Beltran et al, 2014)
Must consider risk-benefit profile of requisite patient chemical restraint – if needed

8. Other treatment considerations:

Minimise increases in cerebral metabolic rate:

Increase may worsen secondary injury
Treat seizures immediately – no evidence supporting prophylactic anticonvulsant use
Judicious sedation if distressed (flailing, constant vocalisation): opioids; anticonvulsants; conservative acepromazine or (dex)medetomidine use?

Address hyperthermia:

  • May occur due to e.g. direct trauma to hypothalamic thermoregulatory centre; seizure activity
  • Increases cellular metabolism and vasodilation leading to increased ICP

Therapeutic hypothermia:

  • May be neuroprotective
  • Has been used in people with TBI but no consensus position about risk-benefit assessment and suitability to different patient populations
  • Also logistical challenges to staff: can you actually do it? Can you provide the patient with the relevant monitoring and care they need?

(At least) One published veterinary case report (Hayes, 2009)

“I guess my take on what we should do at the moment is if the head trauma patient presents hypothermic then I would not actively warm them but take steps to prevent them getting even colder. If they are normothermic then I would maintain this. If they are hyperthermic then I would cool them to normothermia but I would not be inducing hypothermia. Having said that if I had a patient with severe brain injury where the prognosis was considered very poor-to-grave and I was working in an advanced referral setting and the pet’s carers understood the implications and lack of evidence, I would be willing to give induced hypothermia a go on the basis that in this individual patient in these clinical circumstances, the potential benefit could be justified. But I stress that is a very unfounded personal position.”


**Should be one of the first considerations after rapid baseline neurological exam!**
Alleviating pain is a key aim in all clinical patients from a welfare point of view; may have to assume its presence and treat empirically with TBI patients.
May allow more reliable rather than less reliable neurological exam to be performed (e.g. by relieving pain-induced distress)

Use pure (mu-agonist) opioid
NSAIDs contraindicated in hypovolaemic patients
Possible role for ketamine as analgesic +/- sedative. More in this podcast episode


“The use of methylprednisolone succinate for central nervous system injury was a longstanding practice in both human and veterinary medicine. However it was not one based on sound clinical evidence. More recent clinical trials in humans have not shown positive effects on outcome and some have suggested possible increases in morbidity and/or mortality. Considering the potential adverse effects (e.g. gastrointestinal ulceration, increased risk of infection/immunosuppression, hyperglycaemia, increased catabolism) of these agents, current recommendations are that methylprednisolone or indeed any other steroid should not be used for traumatic brain injury.”

Recommendation extrapolated from human medicine…

“But it seems to me that if there is no good evidence showing that steroids are beneficial for CNS injury in dogs and cats and if the current consensus is not to use them in people, who after all are another mammalian species, then we should not be using them in dogs and cats either at the moment.”

Potential role of steroids in patients with other types of brain problems is a separate discussion
Anti-inflammatory dose corticosteroids (e.g. dexamethasone 0.1 mg/kg) occasionally indicated for significant soft tissue swelling due to head trauma

Hyperglycaemia following traumatic brain injury:

Relatively common
Likely due to (at least in part) to sympathetic catecholamine response
Generally said to be associated with increased mortality or at least worsened neurological outcomes in humans and experimental animals; some more recent potentially discordant evidence.
Does hyperglycaemia actually worsen the brain injury, is it just a marker of injury severity, or both?

“Even if the hyperglycaemia is detrimental, maintaining normal blood glucose levels within tight limits is controversial in human patients with severe TBI, because hypoglycaemia, a common complication of tight glucose control, can induce and aggravate underlying brain injury. As far as I am aware the majority of currently available clinical evidence in people does not support tight glucose control during the acute care of patients with severe TBI.”

Veterinary clinical evidence very poor
Hyperglycaemia likely to be marker of severity of TBI at least
No current evidence showing detrimental effect on outcome; same risks associated with tight glucose control apply as for people

“Therefore specific therapy to try and lower blood glucose is not indicated but it is important to try and avoid iatrogenic hyperglycaemia if possible – e.g. don’t use corticosteroids!”

“….even if there is a correlation between the severity of traumatic brain injury and the level of hyperglycaemia that does not mean that we can use the blood glucose prognostically. It may be that there is some prognostic value in watching how the glucose trends but this has not been shown as yet and we certainly should not use a single blood glucose measurement prognostically.” (See BestBET)

“Bearing in mind what I have just said, someone had in fact asked me about the potential administration of glucose to traumatic brain injury patients. I am not sure but I think this may have been on the back of some experimental work suggesting that there may be a benefit of providing exogenous energy substrates for the brain during periods of increased cerebral metabolic demand. But it is my understanding that the current consensus is that in clinical patients we would only administer glucose if they were hypoglycaemic which can worsen the secondary injury and we would aim to maintain normal blood glucose concentration not to induce hyperglycaemia.”

9. Prognostication:

Challenging in both human and veterinary patients
Desired end-point is for a live patient with a good quality of life
Avoid making too hasty judgments; avoid dragging things out when there is no point

Clinically-derived prognostic calculators (e.g. IMPACT Prognostic calculator (International Mission for Prognosis and Analysis of Clinical Trials in TBI;; CRASH Prognosis model ( can help to at least guide prognostication in people.

“Level of consciousness is the most reliable empirical measure of impaired cerebral function and it provides information about the functional capabilities of the cerebral cortex and the ascending reticular activating system (RAS) in the brainstem. In human and veterinary patients signs of slow but steady improvement are likely to be the most practical guide.”

Modified Glasgow Coma Scale (The Small Animal Coma Scale):

Quantitative way of grading and monitoring brain injury by scoring three categories from 1-6; the categories are motor activity; brainstem reflexes; and, level of consciousness.

In Platt et al, 2001 it suggested that:

  • MGCS 3-8 implies grave prognosis
  • MGCS 9-14 implies guarded prognosis
  • MGCS 15-18 implies good prognosis

But note:

  • Only included dogs
  • Dogs with polysystemic trauma excluded – common in head trauma patients and may affect prognosis

“As far as prognosticating on the basis of a specific MGCS score I don’t think it can be argued that this study is adequate for that purpose when critiqued from an evidence-based point of view. But as long as we keep that in mind we definitely can use the MGCS as a tool to monitor our patients and objectively assess progression rather than as a prognostic indicator. So perform an assessment early on and then repeat it at regular intervals to monitor progress. Undoubtedly the lower the score the poorer the prognosis but be careful about over-committing on the basis of this single study.”

“And in fact very recently in 2014 the MGCS has been modified further and made available for free as an app for iOS and Android. The app allows users to use the MGCS to assess their patient’s neurological status and prognosticate – bearing in mind the caveats – but it also allows this data to be submitted to a server database. Furthermore two weeks later the user is asked to submit further information for the same patient in terms of progression and outcome. In this way it is hoped that real clinical data can be collected, contribute to an evidence base and allow refinement of the MGCS especially with regard to prognostication.”

See here for more about the MGCS app.

Beltran et al, 2014 suggested that MRI could be helpful in predicting the prognosis in dogs with TBI.

Other topics not covered include nutritional support, nursing care, decompressive surgical therapy, monitoring and so on.

Please do get in touch using the contact form on website, via email at, via Twitter @VetEmCC or via Facebook at the Veterinary ECC Small Talk page. I would love to hear what you think of my views expressed in this episode, what you agree with and indeed what you might disagree with.


Beltran E, Platt SR, McConnell JF, et al. Prognostic value of early magnetic resonance imaging in dogs after traumatic brain injury: 50 cases. J Vet Int Med 2014. 28(4):1256-1262.

Crossley S, Reid J, McLatchie R, et al. A systematic review of therapeutic hypothermia for adult patients following traumatic brain injury. Critical Care 2014, 18:R75

Eiichi S, Hiroyasu K, Hirosuke F, et al. Diverse Effects of Hypothermia Therapy in Patients with Severe Traumatic Brain Injury Based on the Computed Tomography Classification of the Traumatic Coma Data Bank. J Neurotrauma 2015. 32(5):353-358.

Hayes GM. Severe seizures associated with traumatic brain injury managed by controlled hypothermia, pharmacologic coma, and mechanical ventilation in a dog. J Vet Emerg Crit Care 2009. 19(6):629-634.

Platt SR, Radaelli ST, McDonnell JJ. The Prognostic Value of the Modified Glasgow Coma Scale in Head Trauma in Dogs. J Vet Int Med 2001. 15(6):581-584. 

Yanai H, Tapia-Nieto R, Cherubini GB, Caine A. Results of magnetic resonance imaging performed within 48 hours after head trauma in dogs and association with outcome: 18 cases (2007–2012). J Am Vet Med Assoc 2015. 246(11):1222-1229.

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