Initial assessment of a head trauma patient should include identification and management of imminently life-threatening injuries. Following this primary evaluation, a neurological examination can be performed to decide whether a neurological lesion is present, give a preliminary prognosis and grade its severity using the Modified Glasgow Coma Scale (MGCS). These steps were covered in a previous article (Lowrie, 2013) alongside the important pathophysiology on which treatment is based. The present article describes the next steps in patient management, which can be broadly categorised into two components: extracranial and intracranial stabilisation. Extracranial stabilisation defines the correction of tissue perfusion, usually as a result of hypovolaemia, and the improving of systemic oxygenation and ventilation. Intracranial stabilisation centres on optimising cerebral perfusion pressure (CPP), decreasing intracranial pressure (ICP) and minimising increases in cerebral metabolic rate.
Treatment
The distinction between assessment, stabilisation, diagnosis and treatment is blurred as treatment should begin from the moment the patient enters the hospital and continue throughout the period that diagnostic procedures are performed. Attempts to treat such patients should focus on systemic support rather than specific neurological therapies.
Traumatic brain injury is made up of the primary injury (a consequence of the direct trauma) and secondary injury. The importance of this lies in the fact that primary injury is not treatable, whereas secondary injury is the one we aim to minimise through management. Secondary injury is the result of a biochemical cascade initiated by excitatory neurotransmitter release, intracellular calcium influx, hypoperfusion with possible ischaemia and inflammation. Management of the secondary injury is divided into extracranial and intracranial stabilisation. Extracranial stabilisation aims to reduce the systemic consequences of trauma (e.g. hypotension, hypoxia, acidosis) to maintain cerebral perfusion and provide adequate blood supply to the brain. Failing to do this can worsen both the clinical signs and secondary injury. Intracranial stabilisation attempts to control intracranial events such as intracranial hypertension, a compromised blood–brain barrier and cerebral oedema. Resuscitation of the patient with traumatic brain injury must address all of these aspects; the focus for treatment should be on the perfusion parameters and ICP, which will help minimise secondary injury and speed recovery.
The mainstay of treatment is to maintain systemic mean arterial blood pressure (extracranial stabilisation) and decrease ICP (intracranial stabilisation). A guide for managing any animal with traumatic brain injury follows.
Steroids are no longer recommended in head trauma patients. Their use was studied in a prospective trial in humans, involving 20 000 patients, that had to be abandoned because the detrimental effects of steroids showed an 18% increased risk of mortality. (CRASH Collaborators, 2004). Veterinary literature supports these findings (Evans and Fernandez, 2019).
Stage 1: extracranial stabilisation
The most important consideration in head trauma is maintenance of cerebral perfusion by treating systemic hypotension and elevated ICP. The initial approach to head trauma is to focus on extracranial stabilisation followed by an attempt to manage intracranial abnormalities. Careful assessment of pulse, respiratory rate, blood pressure and neurological status are important during this initial period (Figure 1). All animals should be given oxygen and fluid therapy. Table 1 summarises the main parameters that should be stabilised and monitored, and some of the methods employed to correct them.
Table 1. Guidelines for monitoring head trauma patients
| Monitoring parameters | Parameters |
|---|---|
| Neurological examination | Modified Glasgow Coma Scale >15 |
| Blood pressure | Mean arterial pressure80–120 mmHg |
| Blood gases | PaO2 ≥90 mmHgPaCO2 <35–40 mmHg |
| Pulse oximetry | SpO2 ≥95% |
Patient ventilation
Cerebral blood flow is an important contributor to ICP. Blood flow alters in response to blood concentrations of oxygen and carbon dioxide in the brain, so abnormalities in these parameters will alter blood flow, which directly affects ICP. Therefore, control of PaO2 and PaCO2 affect ICP. Oxygen saturation is easily monitored using pulse oximetry (to measure SpO2) and the amount of carbon dioxide within the blood can be assessed using capnography.
Oxygen supplementation is recommended in all patients following head trauma. The goal of oxygen therapy is to maintain the partial pressure of oxygen in the arterial blood supply (PaO2) 90 mmHg. If the patient is unable to ventilate spontaneously and effectively, mechanical ventilation should be employed.
Fluid therapy
There is controversy regarding the best type of fluid to use when resuscitating a patient with traumatic brain injury. However, it is now widely accepted that it is the rate and quantity of fluid given that is more important than the type of fluid chosen (Chesnut, 1998; Armitage-Chan et al, 2007). Restoring blood volume immediately is imperative to ensure a normal blood pressure and adequate CPP. Failure to do so has been associated with increased mortality (Chesnut, 1998). An important point of note is that hyperglycaemia is a negative prognostic indicator, so dextrose solutions are to be avoided.
The rate and amount of fluid given is dictated by the blood pressure and ‘shock’ status of the animal. Indicators of shock include tachycardia, poor pulse quality, pale or grey mucous membranes and a delayed capillary refill time.
Hypotension (mean arterial blood pressure <80 mmHg or systolic blood pressure <110 mmHg) is most likely the result of shock unless another significant life-threatening injury is present, e.g. haemorrhage. Crystalloid boluses should be given initially to achieve a normal mean arterial blood pressure (80–120 mmHg). If crystalloid alone is ineffective then colloid boluses may be considered. Persistent hypotension is dangerous because it leads to decreased cerebral perfusion with subsequent cerebral vasodilation and an increase in ICP.
Hypertension (mean arterial blood pressure >120 mmHg; systolic blood pressure >140 mmHg) is undesirable because it causes reflex vasoconstriction and decreases cerebral perfusion.
Normal blood pressure (mean arterial blood pressure 80–100 mmHg) in a patient that is not in shock necessitates starting maintenance fluid therapy and monitoring blood pressure every 2–4 hours. The reason for this is that hypovolaemic shock causes a significant reduction in organ perfusion. However, blood pressure is usually normal during this compensatory shock phase as it is maintained by homeostatic mechanisms that respond to reduced tissue perfusion. These homeostatic mechanisms include heart rate, peripheral vasoconstriction, reduced urine production and shifts of fluid from the interstitial space to the intravascular space. Once the fluid deficit exceeds the ability of the body to compensate (decompensatory shock) the blood pressure will fall.
If this management stabilises the patient and the MGCS is greater than eight, then resuscitation is often sufficient and monitoring should continue. Re-examination every 6–8 hours is recommended to ensure the improvements are sustained and continuing. In patients with a MGCS of less than eight or in those that continue to deteriorate, further intervention should be considered as outlined in stage 2.
Analgesia
Failure to provide adequate analgesia can increase ICP as pain and anxiety can increase cerebral blood flow thus increasing ICP. Opioids are most commonly used following head trauma because of their minimal impact on the cardiovascular system (and therefore minimal impact on CPP) and the ease of reversing their effects. The major disadvantages of this class of drug are their potential for respiratory depression and hypotension. Short-acting opioids such as fentanyl and remifentanil are advantageous as they have a fast onset of action and short duration, meaning continuous rate infusions can be given and titrated to effect. Naloxone can be used to reverse these drugs if significant respiratory or cardiovascular effects are seen.
Stage 2: intracranial stabilisation
Focus transfers to intracranial abnormalities once the initial assessment is complete and blood pressure and hypoxaemia are stabilised. This is not indicated in every head trauma case and is reserved for those patients with moderate-to-severe head injury that are not responding to aggressive extracranial stabilisation therapy, and those with progressive neurological signs. Essentially this means those patients with a MGCS of less than 8 and those that have a deteriorating MGCS score. The aims of intracranial stabilisation are to decrease intracranial pressure using the following three principles:
- Reducing cerebral oedema associated with head trauma
- Optimising cerebral blood volume
- Removing any space occupying mass.
The first step in trying to reduce ICP is the use of hyperosmolar agents such as mannitol or hypertonic saline.
Hyperosmolar agents
Mannitol has an immediate plasma-expanding effect that reduces blood viscosity, subsequently increasing cerebral blood flow and oxygen delivery and resulting in vasoconstriction (Freeman and Platt, 2012). In doing this it reduces cerebral blood volume and rapidly lowers ICP. Mannitol also reduces extracellular fluid volume by causing fluid to move out of tissues and into the blood. The dose is 0.25–1 g/kg intravenously, slowly over 10–20 minutes. Repeated administration of mannitol will cause diuresis and hypovolaemia. This will then result in hypotension and the increased risk of ischaemia, which is why mannitol is contraindicated in hypovolaemia. The author recommends using mannitol cautiously and only in critical patients i.e. those patients with a MGCS score of less than 8, or those that are deteriorating despite initial management.
Hypertonic saline offers certain advantages over mannitol in that sodium is actively reabsorbed by the kidneys and so repeated administration does not cause depletion of the intravascular volume over time and rebound hypertension. It improves CPP and blood flow by rapidly restoring intravascular blood volume. Additionally, the high sodium content of hypertonic saline draws fluid from the brain parenchyma, which subsequently reduces ICP. Hypertonic saline should not be used if a patient is hypovolaemic or hypernatraemic. A dose of 5–6 ml/kg (dogs) and 2–4 ml/kg (cats) of 7.5% sodium chloride (NaCl) should be given slowly over 5–10 minutes.
Seizure therapy
Seizure activity greatly exacerbates intracranial hypertension in patients with head injuries resulting in hypoxia and oedema. Seizure activity may occur immediately following trauma or may be delayed in onset. Seizures at presentation should be initially treated with a short-acting benzodiazepine such as diazepam (0.5–2 mg/kg) or midazolam (0.2–0.5 mg/kg) given intravenously. If this is successful in ceasing seizure activity, but additional seizures subsequently occur, additional boluses or a constant rate infusion may be administered (diazepam 0.5–2.0 mg/kg/hour or midazolam 0.2 mg/kg/hour in 0.9% saline). Refractory seizures may require additional therapy such as a continuous infusion of propofol (4–8 mg/kg bolus intravenously to effect followed by a constant rate infusion of 1–5 mg/kg/hour) with a long acting anticonvulsant medication such as phenobarbitone (maintenance dose: 3 mg/kg every 12 hours; loading dose: 20–24 mg/kg over 24 hours given to effect). The problem with this approach is that these medications cause varying degrees of sedation in a patient with an already abnormal mentation. Intravenous levetiracetam is gaining favour as an anticonvulsant that can be administered parenterally without causing such severe sedation. The dose for dogs and cats is 20 mg/kg as an intravenous bolus and this can be repeated every 8 hours.
It is uncertain whether anti-convulsant medication should be administered prophylactically to all patients following head trauma (Steinmetz et al, 2013). In people it has been shown that patients treated with anti-convulsant medication in the first 7 days following head trauma have a significantly lower risk of post-traumatic seizures. However, beyond this time there appears to be no beneficial effect of prophylactic treatment.
Stage 3
Failure of fluid therapy, oxygenation and ventilation strategies, and osmotic diuretics to resuscitate the patient and/or improve the neurological status significantly warrants radical therapy, and such cases should be considered for advanced imaging (see Surgery below). The efficacy of the treatments discussed in the following sections have not been evaluated in veterinary medicine and they remain controversial or unproven in people with traumatic brain injury. The treatments outlined are the current thinking on the best way to manage veterinary patients with traumatic brain injury (Garosi and Adamantos, 2011).
Patient ventilation revisited
Cerebral blood volume is a component of ICP. A low PaCO2 (<35 mmHg) will cause cerebral vasoconstriction and thus reduce cerebral blood volume and ICP. A low PaCO2 can be achieved by hyperventilation, although excessive or chronic hyperventilation can be accompanied by a reduction in global cerebral blood flow, which increases the risk of brain ischaemia. For this reason it is not a recommended therapy unless the PaCO2 can be closely monitored with capnography or arterial blood gas analysis. The aim of ventilation is to ensure that the PaCO2 remains below 35–40 mmHg and that PaO2 remains above 90 mmHg. Patients with severe head injury require mechanical ventilation to maintain these arterial blood gas concentrations at their optimal levels. The absolute indications for mechanical ventilation include loss of consciousness, rising PaCO2 of >50 mmHg and falling SpO2 despite appropriate treatment.
Surgery
Surgical intervention is uncommonly required for the majority of head trauma patients. In those in which it is performed, it is done because of a failure to improve or deterioration despite aggressive medical therapy. Advanced imaging, computed tomography (CT) or magnetic resonance imaging (MRI), is always necessary before considering this method and, as previously mentioned, these imaging modalities are reserved for a similar subset of poor responders (Figure 2).
Surgery is aimed at reducing ICP and this is achieved by removal of severely depressed calvarial fractures or large haematomas.
Imaging diagnosis
Head trauma can be associated with all manner of brain injuries. The main injuries that occur secondary to head trauma include skull fractures, intracranial haemorrhage and brain contusion. It is important to determine what the aims of imaging are before commencing such a study. For example, if a skull fracture was observed in a patient that was improving with initial therapy, would this finding be an indication to perform surgery? Given the patient was already improving then the answer would likely be no. The need for surgery is determined on response to initial therapy. Advanced imaging of the brain using MRI or CT should be reserved for those patients that fail to improve following aggressive medical therapy or show deterioration despite initial treatment. This form of imaging requires heavy sedation or anaesthesia so it should be performed prudently following head trauma because it can destabilise the patient. Occasionally it is possible to perform these procedures without chemical restraint, when the patient is severely stuporous or comatose.
Skull radiographs are of limited value in the evaluation of traumatic brain injury as they may identify calvarial fractures but rarely give information on whether they are compressing the brain significantly. CT is preferred to evaluate bony abnormalities but can also identify haemorrhage in the acute stages. However, MRI is more sensitive at detecting haemorrhage and may also detect contusion in severe cases (Figure 3). Patients with brain contusion do not always have identifiable changes on MRI and so it is possible to have a patient with traumatic brain injury that has a normal MRI scan.
Prognosis
The prognosis depends on severity of neurological signs at presentation and response to treatment. The association between a patient's score using the MGCS and prognosis has been evaluated (Platt et al, 2001; Beltran et al, 2014). The first study revealed an almost linear correlation between score and probability of survival within the first 72 hours (Platt et al, 2001). Therefore, patients with a high score had a high probability of survival while patients with a low MGSC were less likely to survive. A score of 8 was associated with a 50:50 chance of survival. A second study looked at association between MGSC at presentation and long-term survival (at 1 and 6 months) and a similar trend was noted (Beltran et al, 2014).
MRI evaluation of head trauma patients has also been assessed in conjunction with the MGCS to determine patient outcome (Beltran et al, 2014). MRI changes were graded from I to IV, i.e. mild to severe, according to modified established criteria from human head trauma imaging. The imaging grade was significantly associated with patient outcome at both 1 and 6 months. The presence of a midline shift on MRI was also found to be significantly associated with decreased survival at 1 month following injury. However, as mentioned earlier, the risk of performing MRI is high in many patients and so this should not be performed if the only aim is to establish a prognosis.
Overall, the best way to establish prognosis is to perform MGCS scoring daily. Doing this allows the clinician to inform the owner of the potential for recovery. For example, if the MGCS score is low then a cautious approach to expectations is required, whereas a higher MGCS score carries a better prognosis. Similarly, if serial assessment shows an increasing trend in the MGCS then it would be reasonable to expect a better prognosis. If the score remains the same or deteriorates, this raises concern that the problem is progressing and intervention is likely needed to allow recovery.
Conclusions
It is important to cater the treatment of traumatic brain injury to the individual patient. Often less is more and the main skill in managing these difficult situations is in knowing when to intervene with more aggressive therapy. Not all patients require mannitol and few need advanced imaging in order to achieve a successful outcome. Initial treatment of traumatic brain injury should be achievable in all veterinary practices regardless of available equipment.
KEY POINTS
- Osmotic diuretics such as mannitol should never be used for correcting intracranial pressure without being certain that the patient has been successfully volume resuscitated.
- Rarely do calvarial fractures require surgical intervention. Indications for surgery include those that are contaminated, severely depressed or open. The majority of fractures can be managed conservatively provided neurological status is stable or improving.
- Advanced imaging is reserved for severely affected patients (those with a Modified Glasgow Coma Scale of <8 or those that deteriorate despite treatment).