Head Trauma: Assessment & Management
World Small Animal Veterinary Association World Congress Proceedings, 2005
Simon R. Platt, BVM&S, DACVIM (Neurology), DECVN, MRCVS
Animal Health Trust
Newmarket, Suffolk, UK

Severe head trauma is associated with high mortality in human beings and animals.Although there is no standard of care for head trauma in human medicine, a series of guidelines have been developed centered around maintaining adequate cerebral perfusion (The Brain Trauma Foundation 2000). The appropriate therapy for head trauma patients remains controversial in veterinary medicine due to a lack of objective information on the treatment of dogs and cats with head injuries. Treatment of affected animals must be immediate if the animal is to recover to a level that is both functional and acceptable to the owner. Many dogs and cats can recover from severe brain injuries if systemic and neurological abnormalities that can be treated are identified early enough.

Primary Patient Assessment

As with all types of acute injury, the "ABCs" (airway, breathing, cardiovascular status) of emergency care are extremely important.

Initial physical assessment of the severely brain-injured patient focuses on imminently life threatening abnormalities. It is important not to focus initially on the patient's neurological status as many patients will be in a state of hypovolaemic shock following a head injury, which can exacerbate a depressed mentation. Hypovolemia and hypoxemia need to be recognised and addressed immediately. In addition, a minimum essential data-base includes a PCV, total protein level, a blood urea level, glucose and electrolyte levels as well as a urine specific gravity. Respiratory system dysfunction can be common after head injury. The most dramatic respiratory abnormality seen following head injury can be neurogenic pulmonary oedema (NPO). Neurogenic pulmonary oedema is usually self-limiting if the patient survives, and will resolve in a matter of hours to days, but can cause severe dyspnoea, tachypnea and hypoxemia. Hypoxemia exacerbates the development of secondary tissue damage. There is no clinical localising value to specific breathing patterns and these patterns may vary over time.

Secondary Patient Assessment

Once normovolemia and appropriate oxygenation and ventilation are established (see below), the patient should be thoroughly assessed for traumatic injuries. These include skull, vertebral and long bone fractures as well as splenic torsions and ruptured bladder and ureters. The neurological examination, cranial imaging and ICP measurement can then be considered.

Neurological Assessment

Neurological assessment should be repeated every 30 to 60 minutes in severely head injured patients to assess the patient for deterioration or to monitor the efficacy of any therapies administered. This requires an objective mechanism to 'score' the patient so that treatment decisions could be made logically.

The Modified Glasgow Coma Scoring System

In humans, traumatic brain injury is graded as mild, moderate or severe on the basis of an objective scoring system, the Glasgow coma scale (GCS). A modification of the GCS has been proposed for use in veterinary medicine (Table 1.). The scoring system enables grading of the initial neurological status and serial monitoring of the patient. Such a system can facilitate assessment of prognosis, which is crucial information for both the veterinarian and owner. The modified scoring system incorporates 3 categories of the examination (i.e., level of consciousness, motor activity, brainstem reflexes),which are assigned a score from 1 to 6 providing a total score of 3 to 18, with the best prognosis being the higher score.

Diagnostic Imaging

Imaging of the patient's head is often indicated, especially in those animals that fail to respond to aggressive medical therapy or deteriorate after initially responding to such therapy. Skull radiographs are unlikely to reveal clinically useful information about brain injury but may occasionally reveal evidence of calvarial fractures.

Computed tomography (CT) is the preferred modality for imaging the head in cases of severe head injury. Even patients with 'mild' head trauma can exhibit abnormalities on the CT scan and so the initial decision to image the patients head should not be based on the neurological examination alone. CT image acquisition time is faster and often less expensive than MRI and CT also demonstrates acute haemorrhage and bone detail better than MR. However, MR imaging has been shown to provide key information relevant to the prognosis based upon its ability to detect subtle parenchymal damage not evident on CT imaging.

Cervical spinal radiographs are also advised at the time of any skull imaging to rule out concurrent spinal lesions. As for spinal trauma, thoracic radiographs will help to evaluate for evidence of thoracic and cardiac trauma.

Intracranial Pressure Monitoring

Medical and surgical decisions based on ICP measurements rather than on gross neurologic findings have decreased morbidity and mortality in human head trauma victims. ICP monitoring is a standard procedure for human head trauma management but has only recently been investigated in dogs and cats. Unfortunately, the extremely high cost of the fibreoptic system is likely to limit its use in veterinary medicine, however other systems may become available to enable ICP monitoring to become an integral part of head trauma management in dogs and cats.

Urinary Tract Assessment

Urinary output should be monitored and if it is elevated (>2-3 mL/kg/hour) for at least 2 consecutive hours, the patient should be considered for possible central diabetes insipidus (DI), which may suggest severe damage to the hypothalamic area. Diagnosis is based upon the presence of high serum sodium as well as low urine sodium and low urine osmolality. However, polyuria due to fluid overload, hyperglycaemia, and therapeutic osmotic diuresis must be ruled out in the diagnosis of central DI. Oliguria (in the absence of hypovolemia), may indicate the syndrome of inappropriate antidiuretic hormone secretion, if it is accompanied by hyponatraemia and increased urine sodium; however hypotension, pain and even stress can cause a similar situation. The most important consideration in head injury is maintenance of cerebral perfusion by treatment of hypotension and elevated ICP. As well as ensuring adequate cerebral perfusion, head injury management is aimed at measures to prevent and limit the development of secondary nervous system damage, as in the case of spinal cord trauma.


1. Minimising increases in ICP

Simple precautions can be taken in positioning the animal with its head elevated at a 30° angle from the horizontal to maximize arterial supply to and venous drainage from the brain. It is also important to ensure that there is no constrictive collar obstructing the jugular veins as this immediately elevates ICP.

2. Fluid therapy

The basic goal of fluid management of head trauma cases is to maintain a normovolaemic to slightly hypervolaemic state. There is no support for attempting to dehydrate the patient in an attempt to reduce cerebral oedema and this is now recognized to be deleterious to cerebral metabolism. In contrast immediate restoration of blood volume is imperative to ensure normotension and adequate CPP.

Initial resuscitation usually involves intravenous administration of hypertonic saline and or synthetic colloids. Use of these solutions allows rapid restoration of blood volume and pressure while limiting volume of fluid administered. In contrast, crystalloids will extravasate into the interstitium within an hour of administration and thus larger volumes are required for restoration of blood volume. As a result this could lead to exacerbation of oedema in head trauma patient. Hypertonic saline administration (4-5 ml/kg over 3-5 minutes) draws fluid from the interstitial and intracellular spaces into the intravascular space which improves blood pressure and cerebral blood pressure and flow, with a subsequent decrease in intracranial pressure. However, this should be avoided in presence of systemic dehydration or hypernatraemia and it should be noted that the effects of this fluid only last up to an hour. Colloid solutions, such as Dextran-70 or Hetastarch should be administered after hypertonic saline is used, to maintain the intravascular volume. Hypertonic solutions act to dehydrate the tissues, thus it is essential that crystalloid solutions are also administered after administration of HSS to ensure dehydration does not occur. The sole use of colloids will not prevent dehydration; in addition, the co-administration of hypertonic solutions and colloids are more effective at restoring blood volume than either alone.

3. Osmotic diuretics

Osmotic diuretics such as mannitol are very useful in the treatment of intracranial hypertension. Mannitol has an immediate plasma expanding effect that reduces blood viscosity, and increases cerebral blood flow and oxygen delivery. This results in vasoconstriction within a few minutes causing an almost immediate decrease in ICP. The better known osmotic effect of mannitol reverses the blood-brain osmotic gradient, thereby reducing extracellular fluid volume in both normal and damaged brain.

Mannitol should be administered as a bolus over a 15 -minute period, rather than as an infusion in order to obtain the plasma expanding effect; its effect on decreasing brain oedema takes approximately 15-30 minutes to establish and lasts between 2 and 5 hours. Administering doses of 0.25 g/kg appear equally effective in lowering ICP as doses as large as 1.0 g/kg, but may last a shorter time. Repeated administration of mannitol can cause an accompanying diuresis, which may result in volume contraction, intracellular dehydration and the concomitant risk of hypotension and ischaemia. It is therefore recommended that mannitol use is reserved for the critical patient (Glasgow coma score of < 8) or the deteriorating patient. There has been no clinical evidence to prove the theory that mannitol is contraindicated in the presence of intracranial haemorrhage. There is evidence that the combination of mannitol with frusemide (0.7 mg/kg) may lower ICP in a synergistic fashion, especially if frusemide is given first.

4. Arterial blood pressure support

Presence of arterial hypotension despite fluid resuscitation (see above) may require administration of vaso-active agents such as dopamine (2-10 µg/kg/min). Conversely, arterial hypertensive episodes ("Cushing's response") may be managed with calcium channel blockers such as amlodipine (0.625 to 1.25 mg/cat every 24 hours; 0.5 to 1.0 mg/kg in dogs every 24 hours). However, the author recommends treating the increased ICP aggressively before using drugs to assist blood pressure regulation.

5. Oxygenation and ventilation

Hyperoxygenation is recommended for most acutely brain-injured animals. Partial pressure of oxygen in the arterial blood (PaO2) should be maintained as close to normal as possible (at or above 80 mm Hg). Supplemental oxygen should be administered initially via face-mask as oxygen cages are usually ineffective as constant monitoring of the patient does not allow for a closed system. As soon as possible, nasal oxygen catheters or transtracheal oxygen catheters should be used to supply a 40% inspired oxygen concentration with flow rates of 100 ml / kg / min and 50 ml / kg / min respectively. If the patient is in a coma, immediate intubation and ventilation may be needed if blood gas evaluations indicate. A tracheostomy tube may be warranted in some patients for assisted ventilation.

Hyperventilation has traditionally been known as a means of lowering abnormally high ICP through a hypocapnic cerebral vasoconstrictive effect. However, hyperventilation is a double-edged sword. Besides reducing the ICP, it induces potentially detrimental reductions in the cerebral circulations if the pCO2 level is less than 30-35 mmHG. The major difficulty with hyperventilation is our present inability to monitor the presence and effects of ischaemia on the brain. It is important that animals do not hypoventilate, and such animals should be ventilated to maintain a PaCO2 of 30-40mmHg. Aggressive hyperventilation can be used for short periods in deteriorating or critical animals.

6. Seizure prophylaxis

Although the role of prophylactic anticonvulsants in preventing post-traumatic epileptic disorders remains unclear, seizure activity greatly exacerbates intracranial hypertension in the head injury patient. For this reason, it is recommended to treat all seizure activity in these patients aggressively. As most cases need to be treated parenterally, phenobarbitone (2 mg/kg IM q 6-8hrs) is recommended. This can be continued for 3-6 months after the trauma and can then be slowly tapered off if there have been no further seizures. Phenobarbitone will have the additional benefit of reducing cerebral metabolic demands and therefore acts as a cerebral protectant.

7. Corticosteroids

Corticosteroids, known to be beneficial in brain oedema attributed to a tumour, have been studied extensively in head injury. Clinical trials in people have not shown a beneficial effect of corticosteroids, including MPSS, in the treatment of head injury. In addition, they have been associated with increased risks of infection, are immunosuppressive, cause hyperglycemia and other significant effects on metabolism.

8. Nutritional support

Nutritional support is essential in the management of the head injured patient. Such support has been shown to improve the neurological recovery as well as shorten the time to recovery. On a short-term basis, a nasogastric tube can be used to deliver peptide rich compounds; caution should be used when placing and maintaining these tubes as they may cause sneezing, which may elevate intracranial pressure. For medium to long-term management, pharyngostomy or oesophagostomy tubes should be used. If there is brain stem damage, a gastrostomy tube should be inserted, in case of poor oesophageal function. Care should be taken to avoid hyperglycaemia, which may promote cerebral acidosis in brain-damaged individuals. For details on the above procedures and on diet selection, the reader is directed to more comprehensive descriptions.


A description of the surgical techniques for intracranial surgery can be found elsewhere. Although it is rare that surgery is indicated in head injury cases, there are several specific abnormalities that can be associated with an episode of head trauma that may warrant the consideration of surgical treatment:

1. Acute Extra-axial Haematomas

Generous craniotomies are generally indicated once these abnormalities have been diagnosed with imaging. If the haematoma is due to a fracture across a venous sinus, there may be profuse bleeding associated with surgical intervention. The need for blood transfusions should be expected. Haematoma removal also risks the chance of bleeding from previously compressed vessels.

2. Calvarial Fractures

A skull fracture per se may or may not have significant implications for patient management. Skull fractures are typically differentiated based upon:

 Pattern--depressed, comminuted, linear.


 Type--open, closed

A fracture is generally classed as depressed if the inner table of the bone is driven in, to a depth equivalent to the width of the skull. All but the most contaminated, comminuted and cosmetically deforming depressed fractures can be managed without operative intervention.

3. Acute Intraparenchymal Haematoma

In contrast to acute extra-axial haematomas, acute intraparenchymal clots may be conservatively managed, unless subacute enlargement of initially small intraparenchymal clots is identified with repeat MR scanning.

4. Haemorrhagic Parenchymal Contusions

Most haemorrhagic contusions do not require surgical management. The main indication for surgery with these types of lesions is limited to cerebellar contusions with compression of the 4th ventricle and brain stem; surgery aims to reduce the potential for further compression and herniation, which can develop over the initial 24-48 hours.

5. Intracranial Hypertension (ICH)

Benefit can be found when decompressive procedures are carried out before irreversible bilateral papillary dilation has developed. Conversely, "prophylactic" decompressive surgery seems inappropriate before non-surgical management of elevated ICH has been carefully maximized.

Table 1. Modified Glasgow Coma Scale

Motor Activity


Normal gait, normal spinal reflexes


Hemiparesis, tetraparesis or decerebrate activity


Recumbent, intermittent extensor rigidity


Recumbent, constant extensor rigidity


Recumbent, constant extensor rigidity with opisthotonus


Recumbent, hypotonia of muscles, depressed or absent spinal reflexes


Brain Stem Reflexes


Normal pupillary light reflexes and oculocephalic reflexes


Slow pupillary light reflexes and normal to reduced oculocephalic reflexes


Bilateral unresponsive miosis with normal to reduced oculocephalic reflexes


Pinpoint pupils with reduced to absent oculocephalic reflexes


Unilateral, unresponsive mydriasis with reduced to absent oculocephalic reflexes


Bilateral, unresponsive mydriasis with reduced to absent oculocephalic reflexes


Level of consciousness


Occasional periods of alertness and responsive to environment


Depression or delirium, capable of responding but response may be inappropriate


Semicomatose, responsive to visual stimuli


Semicomatose, responsive to auditory stimuli


Semicomatose, responsive only to repeated noxious stimuli


Comatose, unresponsive to repeated noxious stimuli


Speaker Information
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Simon R. Platt, BVM&S, DACVIM (Neurology), DECVN, MRCVS
Animal Health Trust
Newmarket, Suffolk, UK

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