Karol A. Mathews, DVM, DVSc, DACVECC
It is important to classify head injury into mild, moderate or severe as specific therapeutic interventions are guided by this classification. Prognosis depends on degree of head injury and other injuries. Mild and moderate head injured animals recover well; the severely head injured patient may also recover. Time should be given to fully assess the injuries and treat appropriately.The physical damage that occurred at the time of the accident cannot be changed. The goal of therapy is to minimize secondary brain insults and increased intracranial pressure (ICP) due to systemic causes. Hypotension (systolic blood pressure <95 mm Hg), hypoxia (PaO2 <60 mm Hg), hyperthermia, hypercapnia, hypocapnia, electrolyte imbalances, hyperglycemia, hypoglycemia and acid-base abnormalities are detrimental and impact significantly on outcome. Intracranial hemorrhage, cerebral edema and seizures are more difficult to control but should be anticipated. Maintaining adequate cerebral perfusion pressure (CPP) and oxygen delivery to brain tissue by manipulation of the mean arterial pressure (MAP) and ensuring adequate oxygenation have the most impact on reducing secondary brain injury. An increase in MAP to 'drive' cerebral blood flow should be provided (CPP = MAP-ICP) to reduce further brain injury, cell death/swelling/edema and further increases in ICP. Previous recommendations of keeping head injury patients somewhat dehydrated should be discarded. Normovolemia, should be the goal. Perfusion pressures of <70mmHg maybe associated with poor outcome following head injury. Maintaining cerebral perfusion is a priority in the management of animals with severe head injury. CPP = 80 mmHg should be the goal. With adequate volume expansion, hypertonic saline is the next most useful therapeutic modality to reduce ICP in severe brain injury. The use of mannitol should be reserved for impending cerebral or cerebellar herniation and certainly not used in mild to moderate head injured animals. Decompressive craniotomy is indicated in expanding hemorrhage.
The key to optimizing outcome from head injury is constant monitoring of vital signs and neurological status, recognition of deterioration and rapid therapeutic intervention. This monitoring is imperative because compensation for expanding tissue does occur and ICP usually remains constant until a critical mass is reached. To compensate for this increase in 'mass', cerebrospinal fluid (CSF) and venous blood exit the cranial vault rapidly to maintain CPP (it is for this reason, that jugular veins must not be occluded). Obviously, this compensation is finite; an exponential rise in ICP occurs due to increasing edema or hemorrhage and arterial blood flow to the brain decreases. It is important to note the subtle neurological changes that occur as this is approaching. As CPP rises, tentorial herniation of a cerebral hemisphere or herniation of the cerebellum through the foramen magnum may occur. If rapid intervention occurs prior to, or at this time, the animal may still recover. As an increase in ICP tends to occur for 48 hours, it is recommended that this period of time be given to trend and treat the animal to avoid secondary brain insult and assess prognosis. Other life-threatening injuries also have to be considered.
Emphasis will be placed on severe head injury. Supportive hypotensive management and neurological assessment will be discussed in lecture but not included in this manuscript due to space restriction.
A Primary Survey observing the Airway, Breathing, Circulation rule of triage must be conducted in all patients. Manipulation of the head and neck must be kept to a minimum. In addition, observe level of consciousness (LOC). Alert; responds to vocal stimuli; responds only to painful stimuli; unresponsive to all stimuli. Animal with massive blood loss, moderate-severe hypothermia or hypoxia may have an altered LOC without head injury. The LOC in head injured animals worsens with hypoxia and reduced perfusion pressure. Once corrected, the LOC improves. If hypoxia/hypovolemia are excluded, the altered LOC is likely due to traumatic central nervous system injury. The rectal temperature should be taken and the animal warmed or cooled to ~37°C, 98.7°F. Follow rules of triage for concurrent injuries.
The Secondary Survey will focus on the head injury only. While secondary survey is being conducted, it may be necessary for you to commence management, especially oxygen. Not all head injured animals require aggressive management.
Mild head injury may be associated with mild concussion, a detectable degree of temporary neurologic dysfunction may be observed. In animals, this degree of injury may go unnoticed but an owner may report that their pet has an 'odd' behaviour following the accident. Short-term amnesia in people may be experienced with slightly more severe injury; thus, a similar occurrence may happen to animals. This injury is reversible and not associated with major sequelae. However, 3% of humans deteriorate, therefore, close observation is required for 24 hours. No immediate therapy required. Mild to moderate head injury may be associated with classic cerebral concussion that results in loss of consciousness. Mild injury results in transient behavioural changes. Many humans have no residual effects, however, dizziness, nausea, anosmia, may exist and is referred to as a post-concussion syndrome. This may occur in animals. When awake, people are still able to follow simple commands but are confused (in animals, this behaviour may be noted as 'demented'), or somnolent and may have focal neurologic deficits (this also occurs in animals). Supportive care with constant neurological assessment is required. With moderate injury an animal may be awake but appear very demented. If the animal presents unconscious but responds to voice, touch or painful stimuli (stupor) it can be considered as having a moderate head injury; whereas those that progress to loss of response (coma), should be managed as severely-head injured patients. With severe brain trauma diffuse neuronal injury resulting in deep coma, not due to a mass lesion or ischemic insult, may be present. These animals may exhibit decerebration.
A minimum data base should be obtained, including ACT as injured brain tissue is a trigger for DIC which may occur and stick glucose as hyperglycemia contributes to morbidity. Venous blood gases to assess metabolic status as an indicator of perfusion (adjusted base excess < -4 mEq/L, HCO3 <16mEq/L suggests inadequate oxygen delivery due to anemia / poor perfusion / inadequate oxygenation; a PO2< 65mmHg on arterial blood indicates inadequate oxygenation potentially associated with pulmonary injury; lactate levels if >2.5 indicate anaerobic metabolism due to poor perfusion or increased muscle activity. Oxygen saturation of <95% requires oxygen supplementation. Blood pressure monitoring is essential to maintain adequate arterial and cerebral perfusion pressures. (systolic blood pressure <95mmHg, MAP <65 mmHg associated with head trauma suggests decreased CPP). ECG monitoring is essential due to potential for head trauma associated cardiac arrhythmias (brain-heart syndrome), or other trauma associated arrhythmias. Once the patient is stabilized radiographic imaging of the skull (fractures that are open or depressed greater than the thickness of the skull, require surgical intervention), and chest radiographs to identify if pulmonary contusions are present.
Management will depend on severity of head injury and accompanying injuries. Only animals with severe head injury require aggressive therapy. For most animals initially oxygen flow-by at 100 mL/kg/min is required. Hoods and other head covers are contraindicated without very high flows to prevent re-breathing of CO2. Avoid pressure on the neck as it causes an increase in the ICP. Keep the forequarters in a normal to slightly elevated (30°) position. Avoid nasal cannula as injury to cribriform plate may exist. If the patient is unconscious or severely dyspneic and unable to achieve 90%, or greater, oxygen saturation on nasal oxygen or flow-by, if PaCO2 is >50mmHg, if total CO2 is > normal range, or if the patient is apneic, mechanical ventilation will be required. If mechanical ventilation is necessary, give 1.0 mg/kg lidocaine IV prior to intubation to prevent elevation in ICP. A combination of fentanyl 10-30mcg/kgand propofol 0.5-2 mg/kg or thiopental 5-10 mg/kg (both may cause hypotension), may be required to facilitate intubation. A major concern with the opioids is that vomiting may occur with too much, which increases ICP, and conversely, too little may result in 'traumatic' intubation, also increasing ICP. The lowest dose possible to facilitate a non-traumatic intubation is advised. Prior to extubation, lidocaine 1.0 mg/kg IV (dogs & cats) should be repeated. If narcotic-induced hypoventilation is of concern, titrate naloxone (0.4mg/mL) 0.1mL or 0.25mL added to 10 mLs saline and titrate to effect. Avoid hyperventilation hypocapnia (PaCO2 <35mmHg, or PaCO2 <40mmHg) unless profound neurological dysfunction has occurred; 2-3 minutes of hyperventilation hypocapnia may decrease ICP temporarily.
Head injury alone (unless large scalp wound with evident blood loss) does not cause hypotension; if present, severe blood loss elsewhere is occurring and must be identified. If no visible injuries are present, consider blood loss into a fracture or cavity, or spinal injury. Normovolemia must be attained prior to assuming that neurological deficits are due to head trauma. If mean arterial 40-50 mmHg or systolic pressure < 90 mm Hg, and warm > 36°C (97°F) resuscitate with crystalloid/colloid boluses, or blood products as indicated. Hypertonic saline (HS) may exacerbate intracranial and other areas of hemorrhage but has shown benefit in head injury. The risk to benefit ratio must be considered for the individual patient. Caution with pulmonary contusions or fluid overload. Maintain serum sodium levels < 160mmol/L. For 3% HS bolus 2mL/kg/min (6-10mL/kg max), OR 5% (6-10mL/kg max), OR 7% (4-8mL/kg max) at 1mL/kg/min for dogs, quarter of this for cats, [respiratory arrest and/ or vagal reflex bradycardia may occur, treat with 0.02mg/kg atropine].
The administration of glucocorticoids in head trauma, as well as the particular glucocorticoid to use, is controversial. If acute trauma with abnormal neurological findings, the author suggests dexamethasone sodium phosphate at 0.25 mg/kg q24 for one or two days. Maintain blood glucose between within normal range.
Frequent neurological and cardiovascular evaluations are necessary to monitor the animal's progress. Bradycardia and other cardiac arrhythmias can be associated with brainstem lesions (brain-heart syndrome), are usually transient, and should be differentiated from the Cushing's reflex. Severe bradycardia with extremely high blood pressure (Cushing's reflex) in the presence of deteriorating mental status suggests severe increase in intracranial pressure with impending herniation and requires immediate treatment.
If anemic due to blood loss, administerblood or hemoglobin-based oxygen carrying solution (HBOCS) (caution with pulmonary contusions).Furosemide is required if fluid overload exists prior to HBOCS administration. An indication for hypertonic saline administration is a comatose, or deteriorating patient who initially has normal, reactive pupils but then develops unilateral pupillary dilation. Mannitol may be required if hypertonic saline is not successful. With rapid deterioration, mannitol may be the drug of choice. Mannitol 0.25 g/kg IV (volumes greater than this are usually not necessary) should be given over 5-10 minutes; repeat immediately if no improvement. A clear indication for mannitol administration in human patients is a comatose patient who initially has normal, reactive pupils but then develops unilateral pupillary dilation. Mannitol is also indicated in comatose patients with bilaterally dilated and non-reactive pupils who are not hypotensive. Another sign of impending herniation is the patient who develops dilated pupils, unilateral down-and-out strabismus, vocalization, opisthotonus with rapidly developing coma. While mannitol may exacerbate hemorrhage, it may be the drug of choice in this situation regardless of whether hemorrhage is suspected or not as hemorrhage may not be a cause of this deterioration. Hemorrhage may be a cause for deterioration occurring >24 hours after the traumatic incident, but edema is also highly likely (a CT scan or MRI is recommended for definitive diagnosis). In patients without such focal neurologic deficits or clear evidence of neurologic deterioration, the indications for the acute administration of mannitol are less clear and likely should be withheld. Mannitol can be repeated q4h as needed for 3-4 times in a 24-hour period, based on the neurological assessment. Do not administer by constant rate infusion. Extensive diuresis may occur, reassess fluid status. Mannitol is contraindicated in congestive heart failure, volume overloaded, hyperosmolar or anuric renal failure patients. Furosemide 0.5-2.0 mg/kg may be considered in these cases; however lidocaine (below) should be tried first, unless fluid overload is the cause for deterioration. Extensive diuresis with hypovolemia / hypotension may occur secondary to furosemide administration which may worsen CPP. Reassess fluid status frequently. Furosemide combined with mannitol have previously been suggested; however, this combination results in extreme fluid loss through diuresis and is not routinely recommended. Lidocaine 2% 1mg/kg IV has been used by the author to halt and reverse clinical neurological signs of tentorial herniation.
1. Mathews KA, Parent J. Head Trauma. Veterinary Emergency & Critical Care Manual 2nd. Mathews KA ed In Press. Guelph, Ontario, Canada, Lifelearn Inc.