In the out-of-hospital environment, paramedics and EMRs/FRs can encounter three different types of head injuries: scalp injuries; cranial fractures; and traumatic brain injuries. These can occur in isolation, but are commonly associated with each other and are the result of blunt or penetrating trauma to the head. Head injuries are the most common cause of death and severe disability in trauma. Immediate post-injury management can have a profound effect on the patient’s long-term prospects for both survival and recovery.
Hypoxia and hypotension, in conjunction with traumatic brain injury, are universally lethal conditions. It is imperative that paramedics and EMRs/FRs work to maintain a normal blood pressure and oxygen saturation.
Use intravenous fluids to target a mean arterial pressure of at least 80 mmHg (or a systolic blood pressure of at least 110 mmHg).
Patients must not be hypo- or hyperventilated; paramedics and EMRs/FRs must take all appropriate measures to protect the airway and ensure adequate oxygenation and ventilation at all times, up to and including supraglottic airway devices and endotracheal intubation.
Seizures and vomiting are common complications of head injuries. Prepare to intervene as necessary.
Except in the case of isolated penetrating trauma, head injuries are seldom isolated. Identify and manage other injuries concurrently.
Additional Treatment Information
Select conveyance destinations in accordance with provincial and local trauma triage guidelines or clinical pathway. In general, convey patients to facilities that have neurosurgical capabilities. Consider the use of Autolaunch or Early Fixed-Wing Activation where appropriate.
Endotracheal intubation in head injuries remains fraught. The risk of hypotension and hypoxia in the peri-intubation period is significant and adversely affects mortality. Paramedics electing to intubate patients with traumatic brain injuries must choose an induction strategy with those goals in mind.
Moderate to severe traumatic brain injuries are often accompanied by injuries to other parts of the body. In these cases, other injuries must not be neglected.
Temperature control of patients with traumatic brain injuries can be challenging. Although the hazards of hypothermia in the context of trauma are relatively well understood, the injured brain is at equal risk from hyperthermia. Patients should be kept normothermic. If the patient is, or becomes hyperthermic, passive heat loss should be promoted. Do not undertake active cooling.
All patients with head trauma should be conveyed to the closest appropriate trauma receiving hospital as per local trauma destination guidelines or clinical pathway.
Traumatic brain injuries can be further classified based upon the degree of disability, as measured by the Glasgow Coma Scale:
A GCS ≥ 13 is indicative of mild injury
A GCS that falls between 9 and 12 is suggestive of a moderate injury
A GCS ≤ 8 is defined as a severe traumatic brain injury
“Concussion” is a term that has been used synonymously with “mild traumatic brain injury” but more accurately describes the signs and symptoms experienced by an individual who has suffered a mild traumatic brain injury.
Signs and symptoms of a concussion include, but are not limited to: grossly observable loss of coordination; vacant stare; disorientation; delayed or difficult responses to questions; slurred speech; inappropriate emotional responses; and memory deficits. Headache, dizziness, nausea, and vomiting are common. These symptoms may immediately follow the traumatic injury or may take hours to fully evolve.
Differentiating between mild traumatic brain injuries that require imaging and hospital evaluation and those that do not is extremely difficult in the out-of-hospital environment and carries significant risk for paramedics and EMRs/FRs. Therefore, as a general rule, patients who are “concussed” – who have experienced an alteration in mental status that may not necessarily be associated with a loss of consciousness – should be conveyed for further evaluation.
Scalp lacerations are associated with extensive bleeding because the blood vessels of the scalp lack the ability to vasoconstrict as effectively as elsewhere in the body. Direct pressure is usually sufficient to control these types of wounds. but awareness needs to be undertaken as open scalp wounds are occasionally the only indication of deeper, more serious injuries.
Caution should be exercised in elderly patients or individuals taking anticoagulant medications: relatively minor mechanisms of injury can cause significant (and catastrophic) hemorrhage that may be undetected during the initial assessment.
The skull is a relatively strong body part and so cranial injuries, including basilar skull fractures, require a significant amount of force. Battle’s sign is a late finding in these patients; its absence does not exclude the possibility of a basilar skull fracture.
Cerebral herniation is a complication of traumatic brain injury where the rising intracranial pressure begins to push the cerebrum caudally, obstructing the flow of cerebrospinal fluid and compressing the brainstem. Signs include a falling level of consciousness, unilateral pupil dilation and lateral-inferior deviation of the eye on the affected side, paralysis of the arm and leg on the opposite side, and decerebrate posturing. Patients may yawn, sigh, take intermittent deep breaths, or progress to Cheyne-Stokes respirations.
Trismus is commonly seen following severe traumatic brain injuries. In the majority of cases, these patients can be effectively ventilated using good bag-valve mask techniques, though suctioning can be difficult and adjunct placement may be impossible.
Mean arterial pressure can be calculated by the formula ([DBP x 2] + SBP) / 3, and is in general a more meaningful measure of cerebral perfusion than systolic blood pressure alone.
First Responder (FR) Interventions
Protect and maintain the patient’s airway; consider potential for vomiting based on level of consciousness; provide supplemental oxygen as required
Hypertension associated with traumatic brain injury should generally not be treated in the out-of-hospital setting with anti-hypertensive drugs; if severe hypertension occurs with a sustained systolic blood pressure > 160 mmHg, contact CliniCall for LABETalol or hydrALAzine
Call ETP prior to administration of LABETalol or hydrALAzine
If hemoglobin is < 90 g/L, transfuse PRBC if available
Optimize cerebral venous out-flow:
Raise head of bed to 30°
Promote venous drainage (e.g., cervical collars, ETT ties loose, trans-pulmonary PEEP of 0 cmH2O, trans-pulmonary plateau pressure < 25 cmH2O)
Maintain neck neutrality
If no esophageal balloon in place, set PEEP 5-10 cmH2O
Decompress stomach if required
Mechanical ventilation strategies:
BVM with PEEP valve: maintain adequate oxygenation while preserving adequate cerebral venous drainage
Ensure oxygenation goals are being met (SpO2 > 97%, PaO2 100-150 mmHg)
Ensure ventilation goals are being met (EtCO2 35-40 mmHg, PaCO2 35-40 mmHg)
Minimize Pplats while maintaining ventilation goals
Control seizure activity:
Consider etiology and patient presentation when selecting appropriate agent:
Consider the side effect of hypotension: vasopressors may be required to maintain hemodynamic goals
Consider the utility of phenyTOIN or phenobarbital for seizing and seizure prophylaxis; treat based on the etiology, patient presentation, and conveyance context (prophylaxis indicated for penetrating head injuries, depressed skull fractures, or a seizing patient)
Monitor for signs of raised ICP:
ONSD of > 6 mm after patient optimization
If > 6 mm treat with osmotic therapy
If Na < 150 mEq/L: hypertonic saline or mannitol/HTS 100 mL every 5-10 minutes with continuous monitoring of ICP
If Na > 150 mEq/L: Mannitol 0.5 g/kg with continuous monitoring of ICP
Watch for diuretic effects; be prepared to replace volume loss at 1:1 ratio
Call ETP prior to use of hypertonic saline
Monitor for signs of cerebral herniation:
EVD monitoring if in situ, or maintain intracranial pressure monitoring
Neurological exam findings:
Unilateral pupillary dilation considered to be related to a rise in intracranial pressure