Traumatic Brain Injury
World Small Animal Veterinary Association Congress Proceedings, 2019
A. Bersenas
Ontario Veterinary College, University of Guelph, Clinical Studies, Guelph, ON, Canada

Patients with traumatic brain injury (TBI) must be appropriately assessed to determine the extent of their injuries, to localize the lesion and to determine prognosis. Crucial elements for evaluating the TBI patient are: level of consciousness, cranial nerve examination (particularly pupillary light response, and physiologic nystagmus), motor activity, and systemic signs.1

Modified Glasgow Coma Score (MGCS) assesses neurological function in 3 categories (motor activity, brainstem reflexes, level of consciousness) and attributes a score 1–6 for each category with a maximum score of 18 (no neurologic dysfunction) to a minimum score of 3 (abysmal neurologic function). The MGCS has shown a strong association with survival in dogs up to 48 hours after hospital admission,2,3 and is a good tool for assessing, and trending, TBI patients.

Systemic Signs

Cushing’s reflex - Defined as hypertension and bradycardia associated with markedly elevated ICP and impending brain herniation. In the face of elevated ICP and poor perfusion to the pons and medulla, massive sympathetic discharge causes marked elevation in blood pressure with ensuing baroreceptor mediated bradycardia.

Respiratory pattern - The respiratory centers are located within the brainstem. Markedly abnormal respiratory patterns suggest a brainstem lesion and carry a poorer prognosis.


Normotension - Cerebral blood flow is critical for patient survival. The goal for the brain injured patient is to maintain systolic blood pressure at least ≥90–100 mm Hg.4 Blood pressure should be supported with crystalloid, colloid or hypertonic saline. Low volume resuscitation is recommended, large volumes of crystalloid solutions should be avoided as fluid overload may exacerbate brain edema.1

Oxygenation - For patients with concurrent respiratory compromise, oxygen should be supplemented using the lowest fraction of inspired oxygen to achieve pulse oximetry (SpO2) of 94–98%.1 Hyperoxia (paO2>150 mm Hg) should be avoided due to deleterious effects of excessive oxygen.1

Optimized venous drainage - Elevate the head - approximately 15–30° degree angle. Ensure that the jugulars are not kinked. Prevent coughing, sneezing, or vomiting. Provide smooth induction by premedicating the patient and using lidocaine spray on the larynx. Avoid nasal cannulas. Consider antiemetic therapy to prevent nausea.

Pain management - Opioids are the mainstay of therapy for TBI patients.5 These should be titrated to effect to decrease the risk of hypoventilation or nausea. Short-acting opioids, i.e., injectable fentanyl, are preferred. Alternatively, buprenorphine or mu agonist opioids (morphine, hydromorphone) are administered in incremental doses to avoid unwanted side effects. Only once the patient is stabilized are NSAIDs considered. Gabapentin is an analgesic option recommended in human medicine.6

Glucose control - Normoglycemia is optimal. Hyperglycemia should be avoided as it has been associated with worsening neurological outcome.1 Conversely, hypoglycemia should be fiercely avoided as hypoglycemia in the TBI patient will have deleterious cerebral metabolic effects.

Seizure regulation - Patients presenting with TBI may exhibit seizures. Approximately 14% of TBI patients have early onset seizures within 24 hours of injury, or develop seizures within 1 week of injury.7 Seizures should be aggressively managed with diazepam bolus (0.5 mg/kg IV) followed by diazepam infusion (0.5–1.0 mg/kg/hr). Preferentially levetiracetam (20 mg/kg PO TID), or phenobarbital (2–4 mg/kg q 12 hours) should be initiated for continued seizure management.1,7 TBI patients are predisposed to post traumatic epilepsy (PTE) generally noted within one year of injury.7 The risk of PTE increases with TBI severity with an overall incidence of 6.6%, increasing to 14.3% in dogs with skull fractures.

Temperature regulation - Studies have failed to demonstrate improved outcome with active cooling of the TBI patient.8,9 However, hyperthermia/pyrexia will cause vasodilation which can worsen ICP and should be avoided.

Nursing care - Extensive nursing care may be required for these patients. Regular turning and physiotherapy are necessary for the recumbent patient. Eye-lube may be necessary for patients unable to blink. Suctioning of the mouth may be required for patients with difficulty swallowing. Nutritional requirements should be addressed.

Placement of a feeding tube - Esophagostomy tube or gastrostomy tube should be considered if there is an inability or lack of voluntary intake.

Glucocorticoid therapy - No benefit has been noted with the addition of glucocorticoid therapy in the TBI patient, and glucocorticoids are not recommended.1,8

Frequent re-evaluation of the TBI patient is necessary, as changes in neurological status can happen abruptly.

Treatment of Elevated Intracranial Pressure

Any patient showing a combination of ≥2 clinical signs: Decreased level of consciousness, abrupt change in pupil size, absent physiologic nystagmus/PLR (unilateral or bilateral), or the Cushing’s reflex should be treated for elevated ICP and imminent brain herniation.

Hyperosmolar therapy - Mannitol or hypertonic saline (HTS) both provide an osmotic gradient to draw edema fluid from the brain parenchyma. Mannitol and HTS can be used interchangeably. Reviews in the literature slightly favour HTS.10 The duration of effect following administration is variable and repeat dosing is necessary.

Mannitol should be administered at 0.5 g/kg intravenously over 10 minutes for impending brain herniation.1 Higher doses of mannitol 1–2 g/kg may be required and have recently shown improved effect in comatose patients. Constant rate infusion (CRI) of mannitol should be avoided.

Hypertonic saline dose recommendations vary based on the concentration of HTS used. A 3% solution is administered intravenously at 5–10 ml/kg over 10–30 minutes depending on acuity. This can be followed by an infusion at 0.5–1.5 ml/kg/hr, which is titrated to effect. Other recommendations include 4–6 ml/kg of 5% HTS at a rate of 1 ml/kg/min or 4 ml/kg of 7.5% HTS administered slowly.5 Concerns when using hypertonic saline include hypernatremia. Sodium levels should be maintained under 160 mmol/L.

General anesthesia/intubation/ventilation Anesthesia will decrease cerebral metabolic oxygen consumption. In addition, intubation with mechanical ventilation allows manipulation of carbon dioxide (CO2) levels. Hyperventilation and hypocapnia (PaCO2 30–35 mm Hg) promote vasoconstriction and may temporarily alleviate elevations in ICP while other treatment options (e.g., hyperosmolar solutions/surgical intervention) take effect. Hypercarbia should be avoided in the TBI patient, optimal PaCO2 is near 40 mm Hg.5 With normal lung function, this coincides with an end tidal CO2 around 35.

Decompressive craniectomy should be considered in veterinary patients failing aggressive medical therapy or with a compressive lesion from fracture or hemorrhage.1

Sedative and anesthetic considerations - Sedation and pain management should be provided to TBI patients to treat agitation and sympathetic stimulation. Note that sedation can make patient assessment more difficult. The benzodiazepines have no effect on ICP and are good sedatives for the TBI patient. The alpha-2-agonists at high doses cause decreased cardiac output and the potential for decreased cerebral perfusion, and should only be used at ultra-low doses if selected e.g., dexmedetomidine 1–2 μg/kg/hr.5,6 For general anesthesia, propofol and the barbiturates are good choices. Hypotension and respiratory depression must be anticipated and addressed when using propofol.5 If ICP is already elevated, inhalant anesthetics should be excluded and propofol infusion selected instead.


Poor prognostic indicators for dogs presenting with TBI include signs of shock, severe concurrent injuries, and decreased MGCS or requirement for endotracheal intubation or HTS administration.3 Patients with significant brainstem injury have a grave prognosis. However, for patients with thalamocortical injury, and minimal brain stem injury, prognosis is excellent. Prognosis improves markedly once patients have survived the 24 hours following their initial insult. Patients can change neurological status abruptly and >72 hours are necessary before the patient is considered to be ‘out-of-the-woods’. Overall prognosis is dependent on the site and extent of neurological damage. Time and extensive nursing care may be required. These patients may require prolonged hospitalization and time for return to normal function.


1.  Kuo KW, Bacek LM, Taylor AR. Head trauma. Vet Clin Small Anim 2018; 48:111–128.

2.  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.

3.  Sharma D, Holowaychuk MK. Retrospective evaluation of prognostic indicators in dogs with head trauma: 72 cases. J Vet Emerg Crit Care 2015;25:631–639.

4.  Spaite DW, Chengcheng H, Bobrow BJ, et al. Mortality and prehospital blood pressure in patients with major traumatic brain injury, implications for the hypotension threshold. JAMA Surg 2017;152:360–368.

5.  Armitage-Chan EA, Metmore LA, Chan DL. Anesthetic management of the head trauma patient. J Vet Emerg Crit Care 2007;17(1):5–14.

6.  Oddo M, Crippa IA, Mehta S, et al. Optimizing sedation in patients with acute brain injury. Crit Care 2016;20:128.

7.  Steinmetz S, Tipold A, Loscher W. Epilepsy after head injury in dogs. A natural model of posttraumatic epilepsy. Epilepsia 2013;54(4):580–588.

8.  Carney N, Totten A, O’Reilly C, et al. Guidelines for the management of severe traumatic brain injury, 4th ed. Neurosurg 2016;1–10.

9.  Andrews PJD, Sinclair HL, Rodriguez A, et al. Hypothermia for intracranial hypertension after traumatic brain injury. N Engl J Med 2015;373:25.

10.  Torre-Healy A, Marko NF, Weil RJ. Hyperosmolar therapy for intracranial hypertension. Neurocrit Care 2012;17:117130.


Speaker Information
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A. Bersenas
Clinical Studies
Ontario Veterinary College
University of Guelph
Guelph, ON, Canada

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