Head trauma is commonly seen in veterinary emergency clinics. Animals sustain head trauma in numerous ways, including road traffic accidents, falling from heights, kicks from horses, being stepped on by owners (Figure 1). Animals with head trauma require immediate medical attention. The patient may also have concurrent injuries, such as circulatory or respiratory problems, which need to be addressed during the initial treatment and stabilisation period.
There are two types of head trauma or brain injury: primary and secondary. Primary head trauma, such as a skull fracture or cerebral haemorrhage, describes the injury to the brain tissue from direct trauma and the forces applied to the brain at impact, these forces include acceleration, deceleration and rotational forces (Freeman and Platt, 2012). The brain is unable to tolerate these forces because of its composition and lack of internal support. Secondary head trauma occurs following the primary trauma; following impact, a cascade of biomolecular events occur causing continued and progressive brain pathology. The presence of haematomas and oedema from the primary injury distorts normal brain parenchyma and decreases cerebral blood flow. In addition, a series of cellular reactions occur at the time of impact, and continue after the injury (Freeman and Platt, 2012). An important goal of treating head trauma is to limit or prevent secondary trauma.
Basic anatomy
The brain is encased within the skull, which does not allow any room for inflammation or swelling. The skull cavity contains parenchymal tissue (the brain, 80% contents), blood (10%) and cerebrospinal fluid (CSF, 10%). The main sections of the brain are the cerebrum, cerebellum, and brainstem.
Pathophysiology
Like all organs, the function of the central nervous system (CNS) is dependent on sufficient blood flow and oxygen and energy supply. The brain is a very active organ with a particularly high oxygen and energy demand (Sigrist, 2011). It consumes about 20% of the total body oxygen and more than 25% of the glucose (Sokoloff, 1981). Neurones are also not able to retrieve their energy anaerobically to a sufficient extent for them to function effectively. Since the brain has only very limited storage capacity for glucose and oxygen, a minimal lack of energy can lead to brain damage.
Cerebral blood flow depends on the ratio between cerebral perfusion pressure (CPP), and the cardiovascular resistance. In a healthy brain, the CPP is monitored closely to maintain the oxygen and energy supply to the nerve cells (Guyton and Hall, 2000). Through this autoregulation, cerebral blood flow is kept constant despite changes in blood pressure and cerebral vascular resistance. Cerebral blood flow is effectively self regulated, with CPP somewhere between 50–150 mmHg (Sigrist, 2011). At CPPs above or below this range, the cerebral blood flow becomes directly proportional (Busija, 1980). In various diseases of the brain, including traumatic brain injury (TBI), autoregulation may be impaired focally or generally, which will also lead to direct dependence of cerebral blood flow on mean arterial pressure (MAP):
Intracranial pressure (ICP) is the pressure exerted between the skull and the intracranial tissues, normal intracranial pressure being 5–10 mmHg (Bagley, 1996). Where there is inflammation or bleeding in the brain, intracranial venous blood and CSF are shunted into the body in an attempt to compensate for increasing ICP. If the body has done everything it can to compensate but the ICP continues to increase, intracranial hypertension (ICH) can develop. An increase in ICP results in decreased CPP and cerebral blood flow, decreased oxygen flow, and diminished supply of brain cells with oxygen and glucose. This leads to secondary changes and cell damage. ICH will lead to alterations in levels of consciousness, respiratory and circulatory abnormalities, and may cause death of the patient by brain herniation.
Severe, acute increases in ICP will trigger the ‘Cushing's reflex’, a characteristic rise in MAP and reflex decrease in heart rate. Briefly, this occurs due to an initial drop in CPP caused by the increase in ICP at a given MAP The resulting decrease in CPP triggers massive catecholamine release, which increases MAP, restoring CPP (Fletcher, 2012). The increase in MAP triggers baroreceptors in the carotid body and aortic arch, which causes reflex vagal stimulation, slowing the heart rate. The presence of the Cushing's reflex in a patient with head trauma is a sign of a potentially life threatening increase in ICP and should be treated promptly (Fletcher, 2012).
Initial assessment, diagnostics and monitoring
Initial assessment should involve evaluation of the patient's respiratory and cardiovascular systems:
- A — Is the airway patent? Ensure that the airway is patient and there is no debris or swelling in the oral cavity
- B — Is the patient breathing normally? If the patient is unconscious and has apnoea or dyspnoea, intubate the patient and perform manual ventilation, if needed
- C — How is the circulation? What are the heart rate, pulse rate and blood pressure? Ensure that the heart and pulse rates are synchronous. If there is a discrepancy, electrocardiography should be performed to check for arrhythmias. If the heart rate or blood pressure is not within normal limits, notify the veterinary surgeon. Emergency intervention, which may consist of fluid resuscitation and/or pain management, may be indicated (Terry, 2010).
Physical examination
Once stable, a complete physical examination should be performed to document the patient's condition at presentation. Patients with severe head trauma can deteriorate quickly; therefore, it is extremely important to note all changes in the patient's condition. The head and neck should be manipulated minimally during the physical examination. Manipulation can displace fractures, worsen spinal cord injuries, or occlude the jugular vein, which can decrease venous return from the brain and, in turn, increase ICP, leading to ICH. Patients with head trauma should receive supplemental oxygen until proper oxygenation is confirmed.
A physical examination should start with the assessment of the patient's level of consciousness, changes to which can reveal the severity and progression of the injury. The levels of consciousness are as follows:
- Alert and responsive — the patient exhibits normal behaviour
- Obtunded — the patient is awake but responds less to stimuli
- Stuporous — the patient responds only to painful/noxious stimuli
- Comatose — the patient is unconscious and does not response to any stimuli (Sigrist, 2011).
Examination of the eyes can provide important information about the severity of brain injury. Any deviation from the normal eye position is called strabismus, which usually is caused by damage to the cranial nerves or brainstem (Terry, 2010).
It is extremely important to check normal eye position. Rhythmic eye movement that is vertical, rotary or horizontal, fast or slow, is called nystagmus. Physiologic nystagmus (or oculocephalic reflex) can be initiated in healthy patients by moving the head horizontally or vertically, resulting in rapid eye movement (also called fast phase) towards where the head is positioned (Terry, 2010). Absence of physiologic nystagmus indicates severe brainstem damage and correlates with a poor prognosis (MacIntyre et al, 2005). Any other type of nystagmus is considered abnormal.
In addition the pupils' response to light (the pupillary light reflex (PLR)) should be assessed. Shining a bright light into the eyes should cause the pupils to constrict they should dilate when the light is removed. A slow PLR suggests a guarded to poor response (MacIntyre et al, 2005). Absence of a PLR suggests a grave response. Continual monitoring of the PLR can help assess the ICP Checking the size of the pupils is also important. With head trauma, the pupils can be normal, constricted (miosis), dilated (mydriasis), or asymmetric (anisocoria). Miotic (pinpoint) pupils are usually due to cerebral injury or oedema, indicating a guarded to fair prognosis, but they can be associated with ocular causes, such as ocular injury, so this cause should be investigated (Platt, 2012). Mydriasis can be associated with stress, medications, ophthalmic disease, decreased cerebral perfusion and impending cardiopulmonary arrest, but also may indicate permanent midbrain damage or brain herniation and is associated with a poor prognosis. Mydriasis is not directly associated with brain injury, but is important to recognise in debilitated patients because it can be associated with cardiopulmonary arrest. Progression from miosis to mydriasis indicates deteriorating neurological status and is an indication for immediate, aggressive therapy (Freeman and Platt, 2012). Anisocoria (Figure 2) has several causes, including oculomotor nerve damage or compression, direct eye injury, and uveitis (inflammation of the uvea) (Terry, 2010). Mid-size pupils that are unresponsive to light usually indicate a brainstem injury and grave prognosis. Changes in the pupils' size should be closely monitored and recorded in the medical history/chart.
The menace response is the involuntary blink of the eyelids in response to movement towards the eyes. If the menace response is intact, the patient will then blink when something approaches the face, indicating sight. The staff member who evaluates this response should be careful not to move air towards the face, which can cause the eyes to blink, possibly leading to a false-positive test result. Neonates can be difficult to assess because they may not yet have developed a menace response (Terry, 2010).
Blindness may indicate that either the nerves to the eyes and brain are too inflamed to work or there is a problem with the eye(s). Vision problems usually indicate major nerve problems with the head. Treatment decisions are not made based only on blindness. In many cases of blindness due to trauma, vision can be restored (Terry, 2010).
The patient's body position can be used to help the veterinary surgeon determine the severity of the brain injury and the prognosis. In a position called opisthotonus or decerebrate rigidity, the patient is recumbent and comatose with all limbs rigidly extended, and the head back. Opisthotonus indicates severe brainstem injury and usually carries a grave prognosis (Sturges and LeCouter, 2009). Decerebellate posture (Figure 3), which has a more favourable prognosis than decerebrate rigidity, may indicate an acute cerebellar lesion or herniation (MacIntyre et al, 2005). In decerebellate posture, the patient's forelimbs are extended and hindlimbs flexed. Patients with this posture are usually conscious and have responsive pupils. Close monitoring of the patient is important because subtle changes in posture can indicate progression of the injury. Schiff-Sherrington syndrome, which may appear similar to decerebrate posture, is characterised by extended, rigid forelimbs and paralysed, flaccid hindlimbs. This syndrome indicates a thoracolumbar spinal lesion. It is extremely important to carefully assess the patient to avoid confusion and misdiagnosis (Terry, 2010).
Neurological assessment
The Modified Glasgow Coma Scale score (MGCS) is a quantitative measure that has been shown to be associated with survival to 48 hours in dogs with TBI (Fletcher, 2010), and provides a score that can be used to assess initial neurologic status as well as progression of signs. This scale incorporates three domains: level of consciousness, posture, and pupillary size/response to light, with a score of 1-6 assigned to each domain. The final score ranges from 3–18, with lower scores indicating more severe neurologic deficits. The initial neurological examination should be interpreted bearing in mind the patient's systemic status, as shock can cause significant neurologic dysfunction (Fletcher, 2012).
Initial diagnostics
Because patients with head trauma can deteriorate quickly, they must be closely monitored. After the initial assessment, an intravenous (IV) catheter should be placed and blood drawn for an extended database (venous and arterial blood gas values, complete blood count. Collection of blood from the jugular vein is contraindicated because occlusion of the vein decreases venous outflow from the brain, therefore increasing ICP (Fletcher, 2012). The packed cell volume (PCV) and total solids (TS) value are used to check for haemorrhage. The blood glucose level is monitored to ensure that the patient is not hypoglycaemic and is supplemented only until the level is normal. Hyperglycaemia (iatrogenic or related to brain trauma) is associated with severe head injuries in animals (Terry, 2010). To avoid hyperglycaemia, the blood glucose level should be maintained in the normal range. Blood gas analysis is used to check ventilation, oxygenation, perfusion, and acid-base status. The carbon dioxide (CO2) level should be monitored because an increase in it can induce cerebral vasodilation and increase blood flow to the brain, thereby increasing ICP and possibly causing ICH (Terry, 2010). The CO2 levels should be maintained in the low normal range (40–45 mmHg (venous); 35–40 mmHg (arterial). Hypercapnia (arterial CO2 levels above 50 mmHg) can increase ICP, which may necessitate mechanical ventilation of the patient. Hypercapnia should also be avoided because it can cause cerebral vasoconstriction, which can lead to cerebral ischaemia (Terry, 2010).
Serial monitoring of the following is recommended: mucous membranes; capillary refill time; heart rate; respiratory rate and effort; pulse rate and quality; lung sounds; temperature; the heart's electrical activity; oxygenation (by pulse oximetry or arterial blood gas measurement); and blood pressure. By closely monitoring these parameters, veterinary nurses can detect changes in a patient's status and notify the veterinary surgeon before they become life threatening.
Based on extensive research on head trauma and hypotension, blood pressure should be maintained at100–150 mmHg and MAP at 80–110 mmHg (Fletcher, 2007). Hypotensive patients have decreased cerebral perfusion, which may lead to brain ischaemia.
In the past, it was thought that the administration of IV fluids would increase ICP, causing more brain trauma. Research has found that early and rapid establishment of euvolaemia and avoidance of overhydration are essential. There has been much discussion about whether crystalloid or colloid fluid therapy is better for rehydrating head trauma patients. Either therapy can be used as long as hypovolaemia is treated and blood pressure is maintained in the normal range (Terry, 2010).
Monitoring
The duration and frequency of episodes of hypoperfusion have been associated with poorer outcomes in people with TBI (Fletcher, 2010). Serial monitoring of perfusion is essential for successful management. Frequent qualitative assessment of tissue perfusion via mucous membrane colour, capillary refill time, heart rate and pulse quality, as well as quantitative assessment of blood pressure, oxygenation, and ventilation are crucial (Terry, 2010). A minimal MAP of 80 mmHg should be targeted to decrease the risk of inadequate CPP. If the Doppler technique is used for monitoring, a minimum of 100 mmHg should be the target, as it most closely reflects systolic pressure in small animals (Fletcher, 2012). Continuous electrocardiogram (ECG) monitoring should also be employed if possible; if episodes of sinus bradycardia are noted, blood pressure should be assessed for evidence of the Cushing's reflex, which warrants aggressive therapy directed at lowering ICP (Fletcher, 2010).
When the ICP is dangerously high, it can trigger the Cushing's reflex, in which the patient's blood pressure is increased and heart rate decreased (bradycardia). The Cushing's reflex is life threatening, so immediate identification and treatment are important. Affected patients should be monitored by continuous electrocardiography and regular blood pressure monitoring (Terry, 2010).
Treatment
There are two main hyperosmolar treatments for an increase in ICP: mannitol or hypertonic saline therapy. Mannitol is an effective therapy for patients with increased ICP, and has been shown to reduce cerebral oedema, increase CPP and cerebral blood flow, and improve neurologic outcome in TBI. It has a rapid onset of action, with clinical improvement occurring within minutes of administration, and these effects can last as long as 1.5–6 hours. Mannitol boluses of 0.5–1.5 g/kg have been recommended for treatment of increased ICP in dogs and cats. The diuretic effect of mannitol can be profound and can cause severe volume depletion; therefore, treatment must be followed with isotonic crystalloid solutions and/or colloids to maintain intravascular volume. Mannitol crystallises easily at room temperature, so it should be warmed before administration through a 0.22 μm filter.
Hypertonic saline may be used as an alternative to mannitol in patients with TBI. Hypertonic saline has similar osmotic effects to mannitol, and can also improve haemodynamic status via volume expansion and positive inotropic effects, as well as beneficial vasoregulatory and immunomodulatory effects (Fletcher, 2012). In euvolemic patients with evidence of intracranial hypertension, both mannitol and hypertonic saline can have beneficial effects. If an individual patient is not responding to one drug, the other may yield a beneficial response (Fletcher, 2010).
Frusemide, a diuretic, has been used to help manage cerebral oedema. However, frusemide can deplete intravascular fluid volume, resulting in systemic hypotension and a decrease in CPP, leading to cerebral ischaemia. Because frusemide can adversely affect the patient outcome, it is one of the least used diuretics for treating an increase in ICP (Terry, 2010). Frusemide can be used alone or with mannitol, but it is normally given once, whereas mannitol can be given several times.
The use of corticosteroids is not recommended for treating head trauma patients. Research in humans has found that the use of corticosteroids is detrimental to recovery. In a clinical study involving more than 10 000 people who sustained head injuries, corticosteroid therapy was associated with worse outcomes (Fletcher and Syring, 2009). The Human Brain Trauma Foundation recommends that corticosteroids not be given to patients with TBIs. Veterinary medicine has followed this recommendation.
Sedatives and analgesia are recommended if a patient is anxious, may worsen through their injury through self trauma, or seems painful. The sedative or analgesic that is used ideally should be reversible with flumazenil (a benzodiazepine antagonist) or naloxone (an opiate antagonist). Buprenorphine is ideal for treating pain because it does not depress the respiratory system or CNS as much as fentanyl. Seizures are a common complication of head trauma. If a patient has seizures, traditional anticonvulsants (e.g. diazepam, midazolam) should be administered (Terry, 2012). If the seizures are not controlled with these medications, administration of propofol is recommended. Propofol, which includes anaesthesia, can be given as a one off bolus (to see if the seizures stop) or a constant rate infusion (Figure 4). If propofol is needed for long periods of time, the patient should be intubated and given supplemental oxygen. The respiratory rate and effort, and heart rate, should be monitored closely while the patient is under anaesthesia. An arterial blood gas reading should be obtained to ensure adequate ventilation until the patient is awake. Monitoring the end-tidal CO2 level is helpful if the clinic is not able to check the blood gas values.
Recent treatment developments
Polyethylene glycol is an inorganic hydrophilic polymer that has a white matter sparing effect after induced traumatic CNS injury when injected intravenously. It has also been shown to have antioxidant effects and to decrease free radical production. In experimental studies of TBI, it reduced cellular damage and compromise of the blood brain barrier, and improved behavioural recovery in rats when administered within 2–4 hours after brain injury (Fletcher, 2012). This drug shows promise as a therapeutic agent for the treatment of TBI.
Controlled hypothermia and induction of coma reduce the metabolic rate and have been reported in human head trauma patients, and recently in veterinary patients. Hypothermia can be achieved by cooling a patient to a rectal temperature of 32–35°C, which reduces cerebral metabolic rate and oxygen consumption and leads to a decreased cerebral blood flow and ICP (Platt, 2012). This technique is not without its problems as it may result in the development of cardiac arrhythmias, coagulopathies, electrolyte disturbances, hypovolaemia and insulin resistance (Freeman and Platt, 2012).
Patient care
Patient care is an important part of what veterinary nurses can do for a head trauma patient, that is usually recumbent. It is very important to turn these patients at least every 4 hours. Patients should be maintained on a clean, dry, padded area to prevent decubital ulcers. While the patient is recumbent, it is very important to elevate the cranial end of the body to 30° to 40°C to decrease the ICP and thereby help prevent ICH. Elevating the head alone may restrict the jugular veins, decreasing blood flow from the brain and thereby increasing the ICP (Terry, 2010).
Because patients may not be able to blink, their eyes should be flushed with ocular wash and lubricated with artificial tears at least every 4 hours to prevent dry eyes and formation of ulcers.
Obtunded or comatose patients may have difficulty swallowing, causing saliva and debris to accumulate in their mouths; therefore, the mouth should be wiped out every 4 to 6 hours, as needed, to remove secretions and keep it moist (Terry, 2010). An oral cleaning spray or solution can be used to clean the mouth, and diluted glycerine can be used to keep the mouth moist. Rarely, the mouth and oral pharynx may require suctioning to remove a large amount of secretions.
If the patient cannot walk or stand or use a litter tray, the bladder should be expressed at least every 3 to 6 hours or an indwelling urinary catheter and closed system should be placed to keep the patient clean and dry and to avoid development of an atonic bladder (Terry, 2010).
Recovery time can be prolongerd and nutrition is an important part of recovery. If the patient can eat they should be helped into sternal and encouraged to eat every 4 to 6 hours. If the patient is obtunded or comatose, a feeding tube, e.g. oesophageal or gastrotomy tube, should be placed or the patient be given parenteral nutrition. Nasooesophogeal tubes are generally contraindicated as they may stimulate sneezing, which can cause a transient increase in ICP (Platt, 2012).
Muscle wasting can occur in non-ambulatory patients, therefore, passive range of motion exercises (PROM) may be indicated for all the limbs every 6 to 8 hours. PROM should be performed with caution, or not at all, in patients that also have a spinal injury or a broken limb (Terry, 2010). Consult the veterinary surgeon before starting PROM.
Conclusion
While head trauma patients can be difficult to manage, these patients are highly rewarding and allow the nursing team to develop their nursing skills. Successful outcome for these patients is very much dependent on close monitoring, attention to detail and focusing on changes in the patient clinical signs, which may detect early deterioration and allow changes to be made to the treatment plan.
Key Points
- An important goal of treating head trauma is to limit or prevent secondary trauma.
- The duration and frequency of episodes of hypoperfusion have been associated with poorer outcomes in people with traumatic brain injury.
- Cerebral blood flow depends on the ratio between cerebral perfusion pressure (CPP), and the cardiovascular resistance.
- The use of corticosteroids is detrimental to recovery.
- Severe, acute increases in intracranial pressure will trigger the ‘Cushing's reflex’, a characteristic rise in mean arterial pressure and reflex decrease in heart rate.
- In a healthy brain, the CPP is monitored closely to maintain the oxygen and energy supply to the nerve cells.