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

Clinical Tip

• The prime aim in the management of traumatic brain injury (TBI) is to limit secondary brain injury. This is done by ensuring that the brain receives an adequate supply of well-oxygenated arterial blood.

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 oxygenation and ventilation

Hypoxia must be avoided at all costs and pulse oximetry (and arterial blood gas analysis if available) should be used. A percentage saturation of haemoglobin with oxygen (SpO₂) on room air of more than 95% is satisfactory. Animals with low SpO₂ should be provided with oxygen supplementation immediately and a liberal ‘if in doubt, supplement oxygen’ approach is strongly encouraged. In addition, any processes that may interfere with adequate ventilation (e.g. pneumothorax, pain) must be addressed appropriately.

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:

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.

Mean arterial pressure

The head trauma patient may well present with systemic hypotension (i.e. decreased MAP). Mean arterial pressure can be measured noninvasively using an oscillometric device and a reasonable target MAP is 80 mmHg. If only Doppler sphygmomanometry is available, then a systolic blood pressure of 100 mmHg is considered equivalent.

Clinical Tip

• Regardless of whether blood pressure monitoring is or is not available, it is essential to ensure that hypoperfusion identified on the basis of physical examination is corrected. Blood pressure monitoring is not a substitute for regular assessment of physical perfusion parameters.

Raised intracranial pressure

ICP is the pressure exerted between the skull and the three intracranial compartments – brain parenchyma, blood and cerebrospinal fluid. Direct measurement of ICP is not practical in veterinary medicine at this time and the presence of elevated ICP is therefore inferred. The Cushing response is the most specific marker available – intracranial hypertension causes systemic hypertension and a consequent reflex bradycardia. These findings should prompt aggressive treatment for raised ICP. Other less specific findings that may suggest intracranial hypertension include otherwise unexplained deterioration of mental status, dilated nonresponsive pupils, loss of physiological nystagmus and decerebrate posturing.

Neurological examination

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

1 Mentation: normal, depressed/obtunded, stuporous, comatose; hysterical.

2 Pupils: symmetry; size; pupillary light reflexes (PLR), direct and consensual

(a) Normal size pupil with slow PLR (least severe)

(b) Miotic pupil with intact PLR

(c) Pinpoint pupil with no PLR

(d) Mydriatic pupil with no PLR (most severe).

3 Other cranial nerves: especially menace responses, blink and gag reflexes and jaw tone.

4 Oculocephalic reflex: in a normal animal, moving the head from side to side and up and down elicits physiological nystagmus. At the end of each movement, the head should be stabilized and cessation of nystagmus noted. An abnormality of this reflex following head trauma is typically due to a lesion of the brainstem (Box 28.2).

5 Respiratory pattern: irregular respiratory patterns may be seen due to brain injury, including:

(a) Hyperventilation

(b) Cheyne–Stokes respiration

(c) Ataxic respiration (irregular rate, rhythm and excursion)

6 Motor function and posture: animals that are not comatose should maintain voluntary motor activity unless trauma has occurred to the brainstem, the spinal cord, or a peripheral nerve.

(a) Hemiparesis/plegia: unilateral brainstem damage (also some spinal cord lesions)

(b) Tetraparesis/plegia: more diffuse brainstem damage (also cervical spinal cord lesion)

(c) Decerebrate rigidity: extreme extensor rigidity of all four limbs with no periods of relaxation; lateral recumbency and possible opisthotonos; marked changes in mentation and very grave prognosis

(d) Decerebellate rigidity: extensor rigidity of all 4 limbs but with periods of relaxation and flexion of the pelvic limbs; mentation may be normal; better prognosis than decerebrate rigidity.

(e) Schiff–Sherrington phenomenon: decerebrate and decerebellate rigidity must be distinguished from this phenomenon which may occur as a result of an acute severe lesion of the spinal cord between T2 and L3. Pelvic limb paralysis accompanied by extensor rigidity of the thoracic limbs is seen when the animal is in lateral recumbency.

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	Liberal approach encouraged Maintain SpO₂ above 95% Ideally intubate and ventilate if SpO₂ remains below 90% but there may be practical and financial considerations
Intravenous fluid therapy	Early fluid resuscitation to correct systemic hypoperfusion and ensure adequate cerebral blood flow Isotonic crystalloid typical first choice; may need synthetic colloid if inadequate response Hypertonic saline appropriate choice in some cases (see below) Avoid hypervolaemia as may increase intracranial pressure – but only be conservative once hypovolaemia corrected
Intracranial hypertension therapy	Promote venous drainage from the brain – keep head elevated 15–30° above horizontal; minimize jugular compression (e.g. avoid jugular venepuncture, do not restrain around the neck area) Medical therapy for cerebral oedema: • Mannitol: hyperosmolar; induces osmotic diuresis reducing cerebral oedema; other potential beneficial effects; contraindicated in hypovolaemic patients • Hypertonic saline (e.g. 7.5% sodium chloride): especially indicated in hypovolaemic patients with suspected raised ICP to both restore intravascular volume and reduce cerebral oedema; osmotically active; other potential beneficial effects
Minimize increases in cerebral metabolic rate	Antiseizure therapy if indicated Sedate if distressed (flailing, constant vocalization) – use opioids and anticonvulsant medications preferentially Treat hyperthermia secondary to brain injury and/or seizure activity
Analgesia	Rapid baseline neurological examination first Pure opioid May also contribute to sedation
Nutritional support	Important once patient is stable and improving – do not start too soon Avoid syringe feeding – provides inadequate calorific intake; potential for aspiration and interference with head injuries Oesophagostomy tube preferred once stable for anaesthesia

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

Prognosis

Some clinicians use a Modified Glasgow Coma Scale (The Small Animal Coma Scale) as a quantitative way of grading and monitoring brain injury and assisting with prognosis. Ultimately, signs of slow but steady improvement on repeat neurological evaluation may be the most practical guide.

Nursing Aspect

Patients with traumatic brain injury may be recumbent for prolonged periods and the value of adequate nursing in such cases should not be underestimated. The most important measures are as follows:

• TLC, gentle handling (independent of interventions)

• Minimize stress: be calm and quiet around the patient, provide a dimly lit quiet environment, use gentle restraint and minimize/group interventions

• Use well-padded bedding to prevent pressure sores and ensure bedding is dry, clean and comfortable

• Turn every 2–4 hours if recumbent to prevent atelectasis (lung collapse)

• Lubricate eyes every 4–6 hours to prevent corneal drying and ulceration

• Appropriate bladder management: express or catheterize if necessary and prevent urinary soiling

• Tempt to eat if appropriate

• Perform regular physiotherapy in patients that are likely to be recumbent for prolonged periods

Case example 1

Presenting Signs and Case History

A 3-year-old male neutered domestic long hair cat presented shortly after a presumed motor vehicle accident. The cat had been healthy prior to going out that evening but had returned home some time later in respiratory distress. Notable deterioration had occurred in the time it had taken the owners to bring the cat to the clinic. No other significant preceding history was reported.

Major body system examination

On presentation the cat was stuporous. Heart rate was 160 beats per minute with no murmur or gallop sound heard and femoral pulses could not be palpated. Mucous membranes were pale pink with a prolonged capillary refill time and extremities were cold. The cat was tachypnoeic but lung sounds were appropriate for the rate and effort. Percentage saturation of haemoglobin with oxygen (SpO₂) on room air was 97%. Abdominal palpation was unremarkable but the cat was mildly hypothermic (rectal temperature 36.5°C). There were palpable skull fractures in the region of the left frontal bone and left-sided scleral and nasal haemorrhage was identified. Blood pressure could not be obtained initially by sphygmomanometry.

Assessment

The cat was assessed as moderately to severely hypovolaemic and the presence of hypothermia was not considered unusual in a cat with this presentation. Although the cat’s mental status could in part be attributed to the hypovolaemia, it was felt to be too severely altered and, given the clear evidence of head injury, a component of TBI was therefore suspected. The cat’s respiratory status seemed appropriate and neither significant intrathoracic injury nor a central effect on respiration was suspected. At this stage it was not possible to make a reliable assessment of the cat’s pain status.

Emergency database

An intravenous catheter was placed in a cephalic vein and blood obtained via the catheter for an emergency database. This revealed low–normal manual packed cell volume (PCV) (32%, reference range 31–45%) with low serum total solids (TS) (50 g/l, reference range 61–80 g/l) suggestive of recent haemorrhage. The cat was moderately hyperglycaemic (15.0 mmol/l, reference range 4.2–6.6 mmol/l).

Clinical Tip

• Jugular vein occlusion for venepuncture should be avoided as far as possible in patients with raised intracranial pressure as impaired drainage from the brain may significantly exacerbate intracranial hypertension.

Clinical Tip

• Hyperglycaemia may be identified in dogs and cats following head trauma and is thought to result from a response involving the sympathetic nervous system and the adrenal medulla. The degree of hyperglycaemia often correlates with the severity of traumatic injury but a relationship with outcome has not been shown in dogs and cats.

Case management

Clinical Tip

• Treatment of extracranial potentially life-threatening abnormalities is the immediate priority in the management of patients with traumatic brain injury (TBI). In reality, treatment of such abnormalities often concurrently achieves the prime aim with respect to intracranial trauma management which is to limit secondary brain injury, i.e. as primary brain injury (including disruption of blood vessels and tearing/crushing of parenchyma) will already have occurred at the time of presentation.

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.

Clinical Tip

Animals with traumatic brain injury must be monitored very closely, in particular for the following three developments.

• Seizure activity: seizure activity will increase cerebral metabolic rate, increasing cerebral oxygen demand and therefore the risk of hypoxic injury. It may also worsen cerebral oedema, thereby exacerbating raised intracranial pressure (ICP), and can cause hyperthermia. Antiseizure medication must therefore be administered at the first sign of seizure activity.

• Bradycardia: the onset of previously undetected bradycardia may signal an increase in ICP and should prompt immediate treatment.

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Tags: Saunders Solutions in Veterinary Practice Small Animal Emergency

Sep 3, 2016 | Posted by admin in SMALL ANIMAL | Comments Off

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