The trauma patient

28 The trauma patient


Trauma is one of the most common reasons for emergency presentation and can also be one of the most stressful to the patient, owner and veterinary personnel. A calm and rational approach is therefore paramount. Trauma is especially common in cats, amongst which motor vehicle accidents (road traffic accidents) are very common, and more so than dogs, severely injured cats can decompensate very easily without appropriate management. The majority of this chapter therefore focuses on cats although most of the principles and information provided are equally applicable to dogs.


The most common causes of trauma in companion animals are motor vehicle accidents, animal (especially dog) bite injuries, tail pull injuries and falls from a height (especially feline high-rise syndrome). Puppies and kittens are also relatively commonly trodden on and dogs may be kicked by horses. The most common injuries that occur following motor vehicle accidents are listed in Box 28.1. Cranial, thoracic and pelvic injuries are especially common in cats.




Traumatic Brain Injury



Theory refresher





Minimizing secondary brain injury


The prime aim in the management of traumatic brain injury (TBI) is to limit secondary brain injury that may occur as a result of various mechanisms including hypoxia, ischaemia due to hypoperfusion, raised intracranial pressure (ICP) or active haemorrhage. Earlier discussions of TBI tended to focus on the detrimental effects of raised ICP via impairment of cerebral blood flow and the potential for brainstem compression and herniation. However, secondary brain injury is significantly perpetuated by hypoxia and systemic hypoperfusion, and the priority is therefore to ensure that the brain receives an adequate supply of well-oxygenated arterial blood. Treatment for possible raised ICP is just one part of this therapy.




Ensuring adequate cerebral perfusion


Cerebral blood flow, and hence oxygen and nutrient delivery to the brain, is driven by the cerebral perfusion pressure (CPP) gradient between mean arterial pressure (MAP) and ICP:



image



Normal homeostatic mechanisms protecting cerebral blood flow may be lost in TBI and cerebral blood flow becomes largely dependent on systemic blood pressure. Maintenance of an adequate CPP is a cornerstone of modern brain injury therapy.





Neurological examination


Once potentially life-threatening extracranial abnormalities have been addressed, a thorough baseline neurological examination should be performed.










Treatment


Treatment of TBI is summarized in Table 28.1 and illustrated further in Case example 1.


Table 28.1 Treatment of traumatic brain injury
























Treatment Comments
Oxygen supplementation


Intravenous fluid therapy



Intracranial hypertension therapy

Minimize increases in cerebral metabolic rate


Analgesia


Nutritional support



ICP, intracranial pressure; SpO2, percentage saturation of haemoglobin with oxygen.




Case example 1







Case management




Hypertonic saline was not available and a 20 ml/kg bolus of 0.9% sodium chloride (normal, physiological saline) was therefore administered intravenously over 15 minutes. No warming measures were implemented at this time and the cat was kept in sternal recumbency with his head elevated at a 30° angle to the table. A more thorough baseline neurological evaluation was performed at this time. Anisocoria was present with the right pupil larger than the left but a menace response could not be elicited in either eye. Bilateral pupillary light responses, both direct and consensual, were intact. Blink and gag reflexes were present and jaw tone was adequate. The cat’s posture seemed appropriate. Oculocephalic reflex was not tested at this time.


A low dose (0.1 mg/kg slow i.v.) of methadone was administered during the initial fluid bolus. At the end of the bolus the cat’s perfusion had improved but he remained mildly hypovolaemic. A further conservative bolus of 5 ml/kg was administered over 10 minutes, after which the cat was assessed as euvolaemic.


Despite the improved perfusion, the cat’s mentation remained inappropriately reduced and it was therefore suspected that this was the result of raised intracranial pressure secondary to traumatic brain injury. Mannitol (0.5 g/kg i.v. bolus over 20 minutes) was therefore administered, following which a slow but notable clinical improvement was detected. The anisocoria resolved and the cat was able to raise his head voluntarily. Systolic blood pressure at this time was within normal limits (105 mmHg). No free peritoneal fluid was detected on abdominal ultrasound. Thoracic radiographs were not taken because it was felt that the index of suspicion for significant intrathoracic injury was too low to justify the additional stress involved for the cat.


Sep 3, 2016 | Posted by in SMALL ANIMAL | Comments Off on The trauma patient
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