Intubation should occur if the patient is unable to maintain an adequate airway, oxygen saturation over 95% or has a GCS under 9. It is essential to avoid hypoxia and hypercapnia. Hyperventilation should be avoided, except in unusual circumstances in which prior consultation via ARV is advised. Aim to keep the end-tidal carbon dioxide (ETCO2) reading around 35–40 mmHg. Blood gas analysis should be used to assist setting ventilation parameters (if available). ETCO2 monitoring (if available) should also be used to assess respiratory status and the adequacy of ventilation. Always have emergency airway equipment by the bedside.
CT scanning is the preferred method of imaging if available and should be performed early in the severe to moderate TBI group. Except for an uncomplicated minor head injury, ideally all patients with a significant head injury should have a CT scan. If it appears that the patient will require transfer to an MTS, the decision as to whether to conduct a CT prior to retrieval must be considered. In virtually all situations the CT scan will be repeated upon admission to the MTS, therefore whether the imaging will alter care in the early stages may be debatable. Any critical trauma patient must be very carefully monitored and attended while in the CT scanner.
Definite indications for CT scanning are:
Where CT facilities do not exist, the use of plain skull x-rays is controversial but may provide important information. They should not delay a retrieval consultation or transfer. If performed, the views required are lateral, anteroposterior and Towne’s and a view tangential to the point of impact to show a depressed fracture.
Ensure cervical spine x-rays or CT scans are performed.
Consider the need for FAST if available and if staff are trained in its use. In haemodynamically stable patients, FAST can be delayed until the secondary survey and is ideally performed by a second operator while the remainder of the secondary survey is completed.
Difficulties arise with accurate assessment of the GCS in patients who present with potential head trauma and intoxication due to alcohol or prescribed or illicit medications. The reliability of the GCS can be made problematic, particularly in the eye-opening component. Assuming that an altered conscious state is due only to intoxication is particularly risky and places the patient and clinician at risk.15
CT imaging of the brain and cervical spine is recommended in all patients who are intoxicated and have signs of an injury to the head. Agitated patients with signs of head injury may require sedation and intubation to facilitate appropriate management with CT imaging. CT of the facial bones may also be required where there is evidence of facial injuries.
Intoxicated patients without signs of head injury should be observed until they are clinically not intoxicated. If there is still doubt in relation to a brain/spine injury at this stage based on clinical examination then CT imaging should be performed.
High-risk groups for intracranial injury include chronic alcoholics, older people and any patient on anticoagulation. These patients are at risk of missed chronic and acute on chronic subdural haematomas.16
While these patients can be challenging to care for in the emergency department, it is vital to maintain close observation and prevent any further injury from occurring. Consultation with regional hospitals, trauma services or ARV may be appropriate to obtain advice or where necessary to arrange transfer or retrieval.
Any patient who is taking an anticoagulant such as warfarin or other oral anticoagulants (dabigatran, rivaroxaban, apixaban) is at high risk of developing a significant intracranial haemorrhage from minor head injury mechanisms. CT imaging of the brain should be performed on all patients with a history of head injury.
Platelet inhibitor therapy (aspirin (e.g. Astrix, Cartia), dipyridamole (Asasantin, Persantin), clopidogrel (Iscover, Plavix), prasugrel (Effient), ticagrelor (Brilinta)) also increases the risk for haemorrhagic injuries but to a lesser degree.
These patients often have significant comorbidities also, all of which will have a direct impact on surgical and intensive care decision making and treatment. The effects of anticoagulation and antiplatelet drugs may require their reversal, with consideration of the risks of exacerbation of the underlying condition.
Where intracranial haemorrhage is present, patients on anticoagulation medication may deteriorate because of extension of their bleed leading to mass effect, brain compression and herniation. In these patients, reversal of medications should be commenced with appropriate reversal agents. Consultation with ARV should take place prior to administration.
For immediate reversal of anticoagulation in patients with bleeding due to warfarin, prothrombin complex concentrates (Prothrombinex-VF in Australia) are preferred over fresh frozen plasma (FFP). The dose for prothrombin complex concentrates is 35–50 units/kg IV. This aims to achieve complete reversal of an excessive INR within 15 minutes. The dose for life-threatening bleeding should be the maximum 50 units/kg.17
Fresh frozen plasma (FFP) is not routinely needed in combination with prothrombin complex concentrates (PCC) unless there is life-threatening bleeding. If life-threatening bleeding is present the dose of FFP is 150–300 mL by IV infusion. Where Prothrombinex-VF is unavailable the dose for FFP is 15 mL/kg IV infusion. Time is required for determining the patient’s blood type (or use group AB plasma), thawing of the product and subsequent infusion.
Vitamin K is essential for sustaining the reversal achieved by PCC or FFP. IV administration produces a more rapid response than oral administration in the short term. The dose is 5–10 mg IV.
Specialist haematological advice should be sought for guidance on reversal of anticoagulation due to new novel anticoagulants such as dabigatran, rivaroxaban and apixaban. For such patients, consult with MTS emergency, trauma and haematology staff via ARV.
Idarucizumab is a monoclonal antibody fragment which binds free and thrombin-bound dabigatran and neutralises its activity, resulting in complete reversal of the anticoagulant effect. Its effect is immediate and lasts for 24 hours18.
The complete dose of 5g should be given as two consecutive IV infusions over 5-10 minutes each. As it is a fairly new drug on the scene, its availability is limited and in Victoria is only located at The Alfred and Royal Melbourne Major Trauma Services (MTS). In consultation with ARV and the MTS, there may be the possibility of prearranged reversal agents being taken to site for administration by retrieval staff in urgent situations.
In the initial acute resuscitation it is best to maintain the patient in a supine position. If there is a delay in transferring the patient to a metropolitan neurological service and the patient has an adequate volume and hypotension is not an ongoing problem, nor are there concerns for thoracolumbar injury then consideration can be given to adjusting the position. Elevating the head of the bed by 30% while maintaining a neutral spine alignment has been shown to reduce ICP without significantly changing cerebral blood flow.19 It also aids in promotion of venous drainage.
Anticonvulsants are indicated in the early stages following moderate to severe TBI in order to reduce the incidence of seizures. Recurrent seizures may increase ICP as well as place a large metabolic demand on damaged brain tissue that in turn may aggravate secondary brain injury. Effectiveness in reducing seizure activity has been shown up to the first week post injury.20
Phenytoin is recommended to decrease the incidence of early post traumatic seizures (within 7 days of injury) when the overall benefit is thought to outweigh the complications of such treatment. At the present time there is insufficient evidence to recommend Levetiracetam (Keppra) compared with Phenytoin regarding efficacy in preventing early post traumatic seizures and toxicity21.
In patients with prolonged seizures, midazolam or diazepam should be administered in addition to phenytoin. Ongoing seizure activity increases the likelihood of secondary brain injury.
In a ventilated patient, arterial blood gasses (ABG) provide important information, especially in an intubated patient. Ventilation targets should be based on blood gas analysis and adjusted accordingly, aiming for a PaCO2 of 35–40 mmHg and a Sa02 94-98%.
Lab tests should be taken for FBC (full blood count), UEC (urea electrolytes and creatinine) and glucose as a baseline. Consider taking a group and cross-match as well if the patient is involved in a trauma presentation with a high index of suspicion for further injuries. Coagulation studies should be done if there is a possibility of intracranial haemorrhage or if the patient is on anticoagulation.
Prevention of thermal extremes is the goal in initial management of TBI. A rise in core body temperature is common in the first few days after injury, which can then increase the likelihood of secondary brain injury due to a rise in ICP and carbon dioxide production. Hypothermia should also be avoided as it may aggravate acute traumatic coagulopathy.
Recent studies have looked at induced mild hypothermia (32–35 °C) in severe TBI, cooling the patient as soon as possible post presentation to the emergency department. Hypothermia may be beneficial for an injured brain as it may be neuroprotective and assists in reducing ICP and cerebral metabolic demands.22 At this point, there is no conclusive evidence to support its mainstream use and trials are currently underway.
For patients suffering a head injury, analgesia should be carefully considered. The drug of choice will be considerate upon clinical signs, the need for analgesia and the provider’s skilled decision making. When using opiates it is important to adequately monitor the patient’s neurological status; titrate the dose so it is effective in pain management but also so that it does not make determining the GCS almost impossible. Short-acting agents are the best choice; avoid continuous infusions at this stage. Pupil size and reactivity can be affected by the administration of opiates and barbituates, therefore they become unreliable. When assessing GCS keep this in mind.
Providing a dark and quiet environment can also help an agitated patient though this is not often able to be achieved in the emergency environment.
Consider antiemetics at this stage, especially if transfer and retrieval is likely.
Drowsy, confused or agitated TBI patients should not be sedated in the initial resuscitation. It makes assessment of their GCS difficult and can alter their response to examination, complicating assessment and diagnosis.
In a ventilated patient, however, paralysis and sedation are essential to management. Appropriate sedation may lower ICP by reducing metabolic demand. Further beneficial effects of sedation include a reduction in hypertension and tachycardia as well as improved patient–ventilator synchrony. Propofol has become a widely used sedative with neurological injuries as it has a rapid onset and short duration of action that allows the provider to evaluate the neurological response when required. It has been shown to depress cerebral metabolism and oxygen consumption, therefore having a neuroprotective effect.
SBP should remain above 110 mmHg and Sp02 between 94-98% to avoid secondary brain injury. Monitoring of the heart rate, respiration rate, blood pressure and oxygen saturation should take place at 15-minute intervals or less if indicated. All monitoring should be maintained until the retrieval team arrives. A baseline ECG should be taken if time permits and facilities exist prior to transfer.
Initial management of the wound in the emergency department is aimed toward controlling bleeding with either bandaging or direct external pressure. If bleeding is unable to be controlled, then stapling or suturing the wound may be required as a form of temporary closure. Discussion with ARV and a neurosurgical specialist should take place to guide treatment.
In a patient with a moderate to severe TBI with an open wound, it is best to leave definitive treatment to the care of the neurosurgical facility upon transfer. The wound will require exploration and debridement.
A urinary catheter should be inserted in the patient with a severe head injury and urine output measured hourly. A urinalysis should be performed also to check for blood. The desired urine output for adults is 0.5–1.0 mL/kg/hr.
All patients should be kept nil orally in the initial post-resuscitation phase of injury. The placement of a nasogastric tube in head injury cases is controversial due to the risk of possible intracranial insertion. In suspected base of skull fractures or with any maxillofacial injuries, insertion should be avoided until the patient is transferred to the neurosurgical centre. Alternatively, an orogastric tube can be placed under careful direct visualisation.
Tetanus prophylaxis should be administered in any penetrating brain injury patients.23
Antibiotic prophylaxis should occur in all cases of open and penetrating injuries as well as when there is suspicion of any base of skull fractures. The risk of local wound infections is particularly high in patients with a penetrating injury due to the presence of contaminated foreign objects such as skin, hair and bone fragments.24 The prophylactic use of antibiotics where there is a CSF leak leading to possible meningitis remains controversial. Consultation with the ARV clinicians and neurosurgical specialists is advised.
Studies have determined that steroids should no longer be used in the acute management of TBI.
The importance of frequent reassessment cannot be overemphasised. Deterioration in a patient’s neurological status can be swift, leading to devastating further secondary brain injury if not caught in time. Patients should be re-evaluated at regular intervals as guided by the clinician. GCS ideally should be performed every 15/60 in moderate to severe head injury cases. If in doubt about any aspect of patient care, repeat ABCDE.