Head trauma is a common emergency presentation; it has been estimated that up to 20% of traumatized dogs and cats present with traumatic brain injury (TBI). It is important that the emergency clinician recognizes rapidly the clinical signs and presentation of TBI and initiates rapidly the stabilization of the patient to limit any further axonal damage.

Traumatic brain injury in the small animal patient may be the result of a variety of traumatic events. Primary brain injury will result in concussion, contusion, and laceration of the brain parenchyma. There is little that we, as veterinarians, can do about the primary injury once the patient is brought to us (excluding surgical management of large hematoma and depressed skull fractures); minimizing the incidence or impact of secondary brain injury is the focus of the emergency medical management of the patient with TBI.

Secondary brain injury refers to a cascade of pathophysiologic processes that culminate in progressive neuronal damage. Insufficient oxygen delivery to neuronal tissue, accumulation of lactate and depletion of ATP levels are only some of the pathophysiological mechanism behind the secondary damage. Aggressive resuscitation of the trauma patient will minimize the occurrence of secondary brain injury from decreased oxygen delivery.

The approach to the small animal TBI patient should follow the ABCDs (cardiovascular, respiratory, and central nervous system) used to triage and to evaluate every emergency patient as multisystemic abnormalities, besides the TBI, could be present in a traumatized animal and they should be recognized and addressed accordingly. Clinical signs that can suggest a traumatic brain injury are altered level of consciousness, seizures, cranial nerve deficits, head tilt, circling, and nystagmus blood loss via ear canal. Inappropriate bradycardia, associated with a mild generalized hypertension, should alert the clinician to the possibility of severely increased intracranial pressure

Oxygen is always useful in a traumatized hypoperfused patient. In the patient with TBI we should keep in mind some important considerations: we must avoid unnecessary patient's restrain and we should try not to stimulate sneezing or coughing to avoid further increase of the intracranial pressure. Oxygen provided through flow or mask is usually easily accepted and without complications.

In these patients we should not restrict IV fluids for the fear of worsening the cerebral edema, but we should also avoid excessive administration of isotonic crystalline solution, since overzealous administration of crystalloid solutions can lead to increased cerebral oedema as they redistribute rapidly in the interstitial space Therefore, IV fluids in patient with TBI deserve special attention and adequate monitoring. The topic of IV fluids in patient with TBI is particularly controversial, since it can have a dramatic impact on the patient's prognosis. When using isotonic crystalloids (for example, Ringer's lactate solution), the recommended initial doses are small bolus of 10–20 ml/kg in 30 minutes, repeated if necessary until the stabilization of the vital signs. The use of hypertonic saline is considered by many authors the fluid of choice for the treatment of hypovolaemia in patient with TBI. Hypertonic saline has a great capacity for expansion of intravascular volume requiring a reduced volume of fluids, compared to the volume required when crystalloids solutions are used (3–5 ml of solution NaCl/kg at 7% in 10–15 minutes). Furthermore, as it is administered quicker, it will minimize the length of time that the cerebral perfusion pressure (CPP) is not optimal; the hypertonic effect of this fluid offers an additional osmotic effect at the brain interstitial level and it can help reduce intracranial pressure. Hypertonic saline was also shown to modulate the proinflammatory mediators and mitigate the in vitro cytotoxicity of polymorphonuclear neutrophils. However, there is some evidence that the hypertonic saline solutions can alter the blood-brain barrier and worsen an intracranial hemorrhage.

Hypertonic saline may be administered at a dose of 4 ml/kg of a 7.5% solution by slow IV infusion. Colloids have been suggested in the management of patients with TBI, because of the small amount of colloids required to reach an effective volume expansion. The use of colloids should be weighed against their possible side effects, also in light of what has been recently published in human medicine. Hypotonic fluids should never be administered to the head trauma patient, because they can easily cross into the interstitium and equilibrate with the intracellular space, thus perpetuating cellular edema

The most commonly used and "abused" medications in patients with TBI are the glucocorticoids. Both the human and veterinary literature has taken its distance from the use of steroids in the treatment of head trauma. In addition to the lack of any positive effect, glucocorticoids promote or worsen hyperglycemia, cause polyuria and delay the healing of skin wounds. Hyperglycemia can result in the provision of additional substrate for anaerobic metabolism and thus the production of lactic acid. Intracellular acidosis may result in ongoing cellular injury.

A more acceptable treatment if the presence of cerebral edema is suspected is the use of mannitol. Mannitol is a powerful osmotic agent, able to decrease the ICP and cerebral edema after TBI and it is considered the drug of choice in patients that are cardiovascular stable. In addition to its osmotic effect, mannitol is also known for its effect against free radicals and its rheological properties, which could limit the secondary cerebral lesion. The recommended dose is 0.5–1 g/kg of mannitol in 20–30 minutes.

Hypoventilation in traumatized patients with TBI and altered state of consciousness may be a significant problem, especially when it leads to the development of hypercapnia. The increase of CO₂ causes cerebral vasodilatation and increase in ICP. Traumatic brain injury patients who suffer from a sudden neurological deterioration, that are not responsive to mannitol, should be intubated and ventilated, as long as we don't reach a stable clinical situation and stabilization of PaCO₂ (ETCO₂) around 35 mm Hg. Hyperventilation, until you reach hypocapnia (< 30 mm Hg) will cause cerebral vasoconstriction and a decrease in perfusion and it should be used only temporarily if you have the risk of a brain herniation.

The use of analgesics is strongly recommended in these subjects, because both pain and anxiety cause an increase in ICP. Opioid drugs are the drugs of choice; however, because they may cause respiratory depression, it is important to use low dosages and increase the dose until we reach the desired effect. Alternatively, drugs such as fentanyl (3–5 µg/kg/h) can be used in a continuous rate infusion, ensuring the achievement of a more stable plasma concentration and safest analgesics effect.

Another important aspect to consider in these patients is to position their head slightly elevated by 30 degrees, being very careful not to compress the jugular veins (or partial occlusion of the jugular veins can lead to increased intracranial pressure).

The patient that is affected by TBI should be closely monitored for the following 24–48h after the trauma; the use of the Glasgow modified coma scale will allow us to monitor over time the patient with TBI and to have at 24–48 h a more precise prognosis. The neurological damage following TBI can be reversible; it is important to give your patient enough time to improve, if there is a positive trend in their neurological status.

References

1.  Sande A, West C. Traumatic brain injury: a review of pathophysiology and management. J Vet Emerg Crit Care. 2010;20(2):177–190.

2.  Platt SR, Radaelli ST, McDonnell JJ. The prognostic value of the modified Glasgow coma scale in head trauma in dogs. J Vet Intern Med. 2001;15:581–584.

3.  Syring RS, Otto CM, Drobatz KJ. Hyperglycemia in dogs and cats with head trauma: 122 cases (1997–1999). J Am Vet Med Assoc. 2001;218:1124–1129.