Chapter 7 – Head Trauma


Head trauma is a significant cause of death around the world, especially in patients 1–45 years old.15 Close to 80% of patients are managed in the emergency department (ED).1.2 Head injury not only causes initial primary injury, but it is associated with several secondary injuries.15

Chapter 7 Head Trauma

Brit Long

Head trauma is a significant cause of death around the world, especially in patients 1–45 years old.15 Close to 80% of patients are managed in the emergency department (ED).1.2 Head injury not only causes initial primary injury, but it is associated with several secondary injuries.15

Neurologic Injuries

The goal of resuscitation and management of the patient with head trauma is to target normal ICP, while preserving cerebral blood flow and perfusion.2, 610

Cerebral Perfusion Pressure (CPP) = Mean Arterial Pressure (MAP) − Intracranial Pressure (ICP)
Cerebral Perfusion Pressure (CPP) = Mean Arterial Pressure (MAP) − Intracranial Pressure (ICP)

  • ICP is a function of the brain parenchyma, blood, and cerebrospinal fluid (CSF).2, 713 An increase of one component requires a decrease in another.2, 713

  • Once compensatory methods are exhausted, further volume leads to increases in ICP.

  • Increases in ICP and decreases in cerebral perfusion are difficult to measure directly in the ED, and physicians should assess for clinical findings.

  • An increase in ICP may result in herniation and decreased blood flow (Table 7.1, Figures 7.1 and 7.2).2, 7, 14, 15

  • Head injury is classified most commonly based on the Glasgow Coma Scale (GCS). Mild (GCS 14–15) is most common, followed by moderate TBI (GCS 9–13) and severe (GCS ≤8), which has mortality approaching 40% (Table 7.2).2, 7, 14, 15

  • Blunt impact to the head causes acceleration and deceleration of the brain, resulting in compression, distortion, and shearing of the tissues.2, 7, 10, 1417

  • Penetrating injury is less common, though it has a more severe mortality, with 9% survival.2, 7, 14, 15, 18, 19 Most penetrating TBI is due to firearm projectiles, which not only penetrate brain matter but are associated with a wavelike pattern of tissue injury (Figures 7.9 and 7.10).2, 15, 18, 19

  • Blast injury is rare in civilians, with the majority occurring in war. Any explosion can cause energy transmission through the cranium and central vasculature.18, 19 Cerebral edema may occur, which occurs within one hour of injury. Vasospasm occurs in 50% of patients.2, 14, 15, 18, 19

Table 7.1 Herniation syndromes

Herniation Pathophysiology Presentation

  • Parasympathetic fibers of cranial nerve III compression

  • Pyramidal tract compression

  • Ipsilateral fixed and dilated pupil

  • Contralateral motor paralysis

Subtype: Kernohan’s notch

  • Compression of cerebral peduncle in uncal herniation

  • Secondary condition caused by primary injury on opposite hemisphere

  • Ipsilateral hemiplegia/hemiparesis, called Kernohan’s sign

  • False localizing sign

Central transtentorial

  • Midline lesion with compression of midbrain

  • Bilateral nonresponsive midpoint pupils, bilateral Babinski, increased muscular tone


  • Cerebellar tonsil herniation through foramen magnum

  • Pinpoint pupils, flaccid paralysis, sudden death

Upward posterior fossa/transtentorial

  • Cerebellar and midbrain movement upwards through tentorial opening

  • Pinpoint pupils, downward conjugate gaze, irregular respirations

  • Death

Figure 7.1 Brainstem herniation. Illustration of an epidural hematoma with acute mass effect and compression of the ipsilateral cerebral peduncle resulting in uncal herniation and compression of the brain stem (arrow)

(illustration by Robert Amaral, reproduced with permission from Color Atlas of Emergency Trauma, Second Edition)

Figure 7.2 Brainstem herniation. (A) Patient with transtentorial herniation from blunt head trauma. The right pupil is constricted normally; the left pupil is fixed and dilated. (B) CT scan shows a large left subdural hematoma (arrow) with midline shift. This compression resulted in brainstem herniation

(reproduced with permission from Color Atlas of Emergency Trauma, Second Edition)

Table 7.2 Head injuries

Injury Pathophysiology Common locations Characteristics
Contusion (Figure 7.3)

  • Coup and contrecoup injury from trauma

  • Orbitofrontal region

  • Anterior temporal region

  • Up to one third may expand

Epidural hematoma (Figure 7.4)

  • Middle meningeal artery and vein injury

  • Close to site of skull fracture

  • Convex shape

  • Does not cross suture lines

  • Commonly not associated with brain injury

Subdural hematoma (Figure 7.5)

  • Bridging vein injury

  • Cerebral convexities

  • Tentorium and falx

  • Concave shape

  • Crosses suture lines

  • Associated with brain injury

  • More common in those with brain atrophy

Subarachnoid hemorrhage (Figure 7.6)

  • Pial vessel injury or laceration

  • Cerebral convexities

  • Interpeduncular cisterns

  • Ventricles

  • May be present in a few sulci or fissures, more diffuse if severe

  • Most common CT finding in moderate TBI

Diffuse axonal injury (Figure 7.7)

  • Shearing mechanism results in white matter damage

  • Diffuse axonal swelling

  • Gray-white matter junction in hemispheres

  • Severe injuries may affect corpus callosum and midbrain

  • May present in profound coma without elevated ICP

  • Poor outcome common

Depressed skull fracture (Figure 7.8)

  • Fracture through cranial vault

  • Any site of cranial trauma

  • Often associated with underlying damage to central vasculature or parenchyma

Figure 7.3 Cerebral Contusion. (A) CT right frontal lobe contusion (large arrow) with surrounding edema (small arrow). (B) Axial CT scan showing a left temporal lobe contusion (arrow) with surrounding edema. (C) Axial CT scan with large left hemispheric contusion (large arrow) and surrounding edema (small arrow)

(reproduced with permission from Color Atlas of Emergency Trauma, Second Edition)_

Figure 7.4 Epidural hematoma. CT scans of epidural hemorrhages progressing in size and mass effect. (A) Subtle left parietal EDH without mass effect; arrow reveals lenticular space occupying hyperdense lesion. (B) EDH in the right parietal area (arrow) with narrowing of right ventricle and midline shift. (C) Massive acute right parietal EDH with a mass effect and increased intracranial pressure. (D) Intraoperative appearance of a large EDH. The hematoma is on top of the dura mater

(reproduced with permission from Color Atlas of Emergency Trauma, Second Edition)

Figure 7.5 Subdural hematoma. Axial CT scans of subdural hemorrhages. (A) Small right parieto-occipital acute SDH without mass effect (arrow). (B) Right SDH (arrow) with left cephalohematoma demonstrating coup–contrecoup injury. Note the significant midline shift

(reproduced with permission from Color Atlas of Emergency Trauma, Second Edition)

Figure 7.6 Subarachnoid hemorrhage. (A) CT scan of SAH appears like fingerlike projections of hyperdense blood as it tracks along the sulci of the posterior parietal lobe (arrow). (B) CT scan showing left parietal SAH (lower arrow), acute left SDH (upper arrow). Note the effacement of the posterior horn of the left lateral ventricle and midline shift. (C) Bloody CSF drainage from a ventriculostomy catheter in a patient with SAH. (D) Autopsy specimen of a brain with SAH seen here tracking along the sulci of the brain beneath the arachnoid membrane

(reproduced with permission from Color Atlas of Emergency Trauma, Second Edition)

Figure 7.7 Diffuse axonal injury. (A) CT showing focal petechial hemorrhages in the frontal lobes at the gray–white matter junction (arrows) in a patient with diffuse axonal injury. (B) MRI showing multiple high-intensity focal hemorrhages (arrows) including those at the gray–white matter interface in a patient with diffuse axonal injury

(reproduced with permission from Color Atlas of Emergency Trauma, Second Edition)

Figure 7.8 Depressed skull fracture. (A) Lateral radiograph of the skull showing hyperdensity due to overlapping bone fragments (arrow) at the apical–parietal skull. (B) CT scan bone windows showing right temporoparietal comminuted depressed fracture (arrow) and associated soft tissue swelling. This patient suffered a concomitant epidural hematoma. (C) CT scan showing depressed fracture of the left parietal bone (large arrow) with underlying epidural hematoma (small arrow). (D) CT scan showing 3-D reconstruction of a skull with left parietal depressed comminuted skull fracture (arrow)

(reproduced with permission from Color Atlas of Emergency Trauma, Second Edition)

Figure 7.9 Gunshot wound to the head. Gunshot wounds to the brain. (A) Patient with multiple gunshot wounds to the head. Note the cephalohematoma and periorbital ecchymosis. (B) CT scan of a gunshot wound showing a SDH, intraparenchymal hemorrhage (arrow A) and intraparenchymal bullet fragments (arrow B), and an open frontotemporal skull fracture (arrow C)

(reproduced with permission from Color Atlas of Emergency Trauma, Second Edition)

Figure 7.10 Knife wound to the head. Knife injuries to the head. Foreign bodies should be removed only after an angiogram or in the operating room. (A) Stab wound to the head with an embedded knife in the frontal area. The patient was awake and alert. (B) Anteroposterior radiograph revealing the knife blade within the cranium. The knife was pulled out in the operating room without any complication

(reproduced with permission from Color Atlas of Emergency Trauma, Second Edition)

Physiologic Goals

A goal systolic blood pressure of at least 100 mm Hg (ages 50–69) and 110 mm Hg for 15–49 years and >70 years is recommended per the Brain Trauma Foundation.2, 7, 8, 14 Otherwise, a MAP of 70–80 mm Hg is advised (Box 7.1).14, 15 Normal oxygen saturation is vital, as hypoxemia results in a significant increase in mortality.

Box 7.1 Goal Physiologic Parameters

  • Pulse oximetry 94–98% (avoid hypoxemia and hyperoxemia)

  • PaCO2 35–45 mm Hg

  • SBP ≥100 mm Hg (50–69 years), and ≥110 mm Hg (15–49, >70 years)

  • pH 7.35–7.45

  • ICP ≤20 mm Hg

  • Glucose 80–180 mg/dL

  • CPP ≥60 mm Hg

  • Serum Na 135–145, (Hypertonic saline goal is 145–160)

  • INR ≤1.4

  • Platelets ≥75 × 103/mm3

  • Hgb >8 mg/dL

Secondary Injuries

Secondary injuries must be prevented to avoid worsened patient outcome.2, 7, 15, 2023

  • Hypotension: Occurs in 1/3 of patients, resulting in worse outcome (OR = 2.67).

  • Hypoxia: Occurs in 50% of patients, resulting in worse outcome (OR = 2.14).

  • Hyperoxia: PaO2 levels above 300–470 mm Hg are associated with worse outcome.

  • Fever: Elevated body temperature furthers central brain injury.

  • Coagulopathy: May cause worsening of the neurologic injury and death.

  • Glucose: Hyper- and hypoglycemia are predictors of poor neurologic status.

ED Evaluation and Management

Focus on airway, breathing, circulation, disability, and exposure in the primary survey, with spinal precautions.2, 14, 24, 25 Avoid secondary complications (Box 7.2).2, 14

  • Markers of worse outcome include poor GCS motor score, pupillary dysfunction, and increased ICP. Abnormal pupillary response and altered motor function are markers of severity.2, 7, 14, 15

  • Decorticate posturing (arm flexion and leg extension) is due to injury above the midbrain, and decerebrate posturing (arm extension and internal rotation, wrist and finger flexion, leg internal rotation and extension) is a sign of midbrain injury.2, 14

  • Abnormal pupils, decreased mental status, abnormal GCS, penetrating injury, abnormal motor status, and severe injury require neuroimaging after initial stabilization.

  • Severe head trauma requires consultation with neurosurgery.2, 7, 10, 14

  • Constant reassessment is required due to the risk of intracranial pathology worsening, especially with intracerebral hemorrhage. If worsening, emergent neuroimaging is required.14, 2628

Box 7.2 ED Management Goals

  • Maintain spinal precautions

  • Conduct primary and secondary surveys; address life-threatening injuries

  • Advanced airway management may be needed for airway protection, hypoxia, and control of ventilation

  • Obtain rapid IV access

  • Optimize oxygenation, blood pressure, and ventilation

  • Target oxygen saturation >94%, with systolic blood pressure >100–110 mm Hg

  • Focused neurologic exam: GCS, motor function, and pupillary function

  • Obtain head CT noncontrast

  • Any sign of worsening neurologic status warrants hyperosmolar therapy

Tiers of ICP management are suggested per the Brain Trauma Foundation (Table 7.3).2, 7, 14, 15 Tier 0 therapies should be initiated immediately, with head of bed elevation and pain and agitation treatment. Hyperventilation should only be used in patients with concern for active herniation.2, 7, 14

Table 7.3 Management tiers

Tier Options

  • Head of bed elevation

  • Control fever, pain, and agitation

  • Optimize physiologic parameters such as blood pressure and oxygen

  • Target PaCO2 to 35–38 mm Hg


  • Osmotic therapy includes mannitol, hypertonic saline, or sodium bicarbonate

  • External ventricular drainage system should be placed if acute obstruction is present


  • Propofol drip titration

  • Optimize other parameters


  • Barbiturate coma

  • Surgical decompression if ICP refractory to treatment

  • Therapeutic hypothermia

  • Moderate hyperventilation (only if active herniation)

Airway Management

  • Airway protection and blood pressure support for severe head trauma with first pass success are priorities.

  • Rapid sequence intubation with in-line stabilization of the cervical spine may be necessary (Box 7.3).2, 11, 1820

  • Preoxygenation is important to avoid desaturation.21, 22

Box 7.3 Keys in Airway Management

  • Preparation: Proper positioning, preoxygenate, and use apneic oxygenation with nasal cannula, facemask, or noninvasive positive pressure ventilation

  • Elevate head of bed to improve CPP and decrease aspiration

  • Premedication regimens are controversial. Fentanyl at 2–5 µg/kg IV or esmolol 1.5 mg/kg IV may decrease catecholamine surge and control the hemodynamic response to intubation

  • Induction agents may include ketamine or etomidate – these agents have less hemodynamic effects

  • Propofol has neuroprotective effects, but hypotension may occur

  • Post-intubation analgesia and sedation are essential – have your drips ready to go at the time of intubation29,30


Eighty percent of patients experience hypertension to laryngoscopy or suctioning. Lidocaine does not reduce ICP or improve neurologic outcome.25, 31, 32 Fentanyl (2–5 µg/kg IV prior to intubation) can reduce the hyperdynamic response to intubation, as can esmolol at 1.5 mg/kg IV. Esmolol should be avoided in patients with hypotension, hemorrhagic shock, or signs of multiple trauma.25, 31, 32


Ketamine, propofol, or etomidate can be used. The key for an induction agent is utilizing lower doses in patients with hypotension, as any agent at full dose will worsen hypotension.3337

  • Ketamine can be used for induction, as it improves cerebral blood flow, and evidence suggests it does not raise ICP.33, 34

  • Etomidate may result in less hypotension and cardiac dysfunction. It can reduce ICP and maintain CPP, but it also may lower the seizure threshold and increase the risk of vomiting and myoclonic movements.33, 35

  • Propofol has high lipid solubility and rapid onset of action that can reduce ICP and oxidative stress, though it may cause hypotension.33, 36, 37


Improves first pass success, including succinylcholine or rocuronium. Succinylcholine allows faster time to recovery and neurologic status assessment. Both are safe and efficacious.14, 33, 3840 Defasciculating doses of paralytics do not reduce ICP and are not recommended.33, 40

Post Intubation

Inadequate analgesia and sedation may increase ICP due to sympathomimetic response.2, 14, 33 Post intubation medications should be ordered at the same time as paralytic and induction agents.41, 42

  • Analgesics including fentanyl (1 mcg/kg IV) and remifentanil are fast and predictable. Hydromorphone and morphine have a longer duration of effect but may accumulate with longer infusions.

  • Sedative medications include propofol, which possesses fast onset and offset. Side effects include hypotension. Infusion rather than bolus will decrease the risk of hypotension. Benzodiazepines are less reliable and will decrease BP and respiratory status.41, 42 Tolerance may develop and accumulation may occur. Dexmedetomidine is a selective alpha-2 receptor agonist with anxiolytic and sedative effects.42

Target oxygen saturations 94–98% with PaCO2 levels of 35–40 mm Hg, or end tidal CO2 30–40 mm Hg.2, 14, 33, 43

Blood Pressure Control

Maintaining adequate MAP is vital to patient outcome.


Defined by SBP less than 90 mm Hg, hypotension increases mortality two-fold.2, 14, 4346 Hypotension does not occur until herniation is imminent. Permissive hypotension is not recommended. ATLS recommends MAP >80 mm Hg. Minimum SBP should be 100 mm Hg.5

For treatment, IV fluids should be started with NS. Albumin and hypo-osmotic fluid should be avoided. Start first with fluids, specifically normal saline or blood.2, 14, 4346 Avoid hypo-osmotic fluids, which can increase cerebral edema and ICP.14, 43

Neurogenic Shock

Neurogenic shock occurs with injury above T6 spinal level, caused by a loss of sympathetic tone.4749 This presents with hypotension and bradycardia, though hypovolemic shock should be assumed in the trauma patient. Management includes IV fluids and vasopressors as needed in neurogenic shock, with goal MAP above 80 mm Hg.4749


SBP of at least 100–110 mm Hg is recommended by the Brain Trauma Foundation.14 Patients with neurogenic shock require a higher MAP target for spinal cord perfusion.4749 Norepinephrine will increase afterload and inotropy, while phenylephrine will improve vascular tone and can be used in patients who are not bradycardic.


Hypertension is common as the body attempts to autoregulate. A rapid decrease in blood pressure is not advised. Levels less than 180/100 mm Hg are recommended (target 140–180/70–100 mm Hg), and lower target levels do not improve outcomes. Options for blood pressure management include nicardipine (bolus and infusion) and labetalol.2, 14, 43

Hyperosmolar Therapy

This reduces ICP and improve cerebral blood flow.2, 7, 14, 5058 These agents should be used with signs of increased ICP, pupillary change, a decrease in GCS ≥2 points, or posturing.2, 7, 14, 43, 50 For ICP reduction, a 2015 meta-analysis finds no difference in neurologic outcome or mortality between mannitol and HTS.50


Administered as a 20% solution, 0.25–1 g/kg IV over 5 minutes. Mannitol deforms RBCs and decreases blood viscosity. The blood–brain barrier should be intact if using mannitol. If not intact, mannitol will worsen outcomes. Following mannitol, rebound increases in ICP may occur. However, mannitol can result in significant diuresis and hypotension. Fluids should be provided and a Foley catheter placed to monitor mannitol’s diuretic effect.2, 14, 43, 5058


Concentrations range from 2% to 23.4%, which also improves cerebral blood flow and reduces brain water content. The most common solution is 3% HTS 250 mL over 10 minutes (23.4% 30 mL can be used through central line). In patients with hypotension, HTS can improve blood pressure as a volume expander. Risk of rebound ICP is less with HTS. Hyperchloremic metabolic acidosis is the most common side effect.2, 14, 43, 5058

ICP Monitoring

Placement of an ICP monitor allows continuous assessment of ICP and may assist in management. This should be completed in consultation with a neurosurgeon.2, 7, 14, 59, 60 Invasive placement of a ventricular catheter or intraparenchymal monitor is most reliable (Box 7.4). Ventriculostomy or external ventricular drain (EVD) allows drainage of CSF, which can be therapeutic.2, 14, 59, 60

Box 7.4 Indications For ICP Monitor Placement

  • GCS 3–8 with abnormal CT scan

  • GCS 3–8 with normal CT and two of the following: Age >40 years, motor posturing, SBP <90 mm Hg

  • GCS 9–15 with CT showing mass lesion (>1 cm contusion, ICH >3 cm), effaced cisterns, or midline shift >5 mm

  • Following craniectomy for ICP monitoring

  • Inability to follow neurologic examination (such as with sedation)

Utility of US in ICP Evaluation

Optic nerve sheath diameter (ONSD) correlates with ICP, evaluated by US. Normal ONSD is up to 5 mm in diameter, and values greater than 5 mm suggest increased ICP (sensitivity and specificity >90%). This should be measured 3 mm posterior to the globe.6163

Surgical Indications

Decompressive craniectomy may be needed for refractory intracranial hypertension, though it does not improve functional outcome (DECRA, RESCUE-ICP trials) (Table 7.4).6468

Table 7.4 Surgical interventions for specific injuries

Lesion Surgical Indication
Epidural hematoma

  • GCS <9 with anisocoria

  • EDH >30 cm3

Subdural hematoma

  • SDH thickness >10 mm or midline shift >5 mm regardless of GCS

  • GCS decline by >2

  • Fixed and dilated or asymmetric pupils

  • ICP >20 mm Hg

Parenchymal lesion

  • Lesion ≥50 cm3

  • GCS 6–8 with midline shift ≥5 mm, cistern compression, or frontal/temporal contusion ≥20 cm3

  • Continued neurologic decline, refractory intracranial hypertension, or mass effect on CT due to lesion

Posterior fossa lesion

  • Mass effect on CT

  • Neurologic decline due to lesion

Depressed skull fracture

  • Open fracture greater than cranium thickness

  • Open fracture with dural penetration, significant associated intracranial hematoma, depression >1 cm, frontal sinus involvement, gross deformity, wound infection, pneumocephalus, gross wound contamination

Coagulopathy Reversal in Traumatic Intracerebral Hemorrhage

Close to one third of patients will have a coagulopathy.2, 7, 14 Coagulation panel and TEG or ROTEM are recommended. Vitamin K, PCC/FFP, and novel antidotes may be required.6972 Platelet transfusion for ICH in patients on antiplatelet medication with ICH may be harmful and should be discussed with neurosurgery.73

Seizure Management

Seizures occur in close to 30% of patients. Early posttraumatic seizures occur within 7 days of injury, with late seizures beyond 7 days.2, 7, 14, 74, 75

  • Benzodiazepines should be provided as first line therapy for active seizure.

  • Prophylaxis is recommended for GCS < 10, cortical contusion, any intracranial hematoma, depressed skull fracture, penetrating head injury, or seizure within 24 hours of injury.14

  • Levetiracetam is recommended as first line for prophylaxis.74, 75

Tranexamic Acid in Head Trauma

CRASH-2 and MATTERs studies show survival benefit within three hours of trauma for TXA.76, 77 The CRASH-2 Intracranial Bleeding Study suggests a trend towards reduction in ICH size and lower mortality, with another study finding reduced bleeding.78 CRASH-3 evaluating TXA in head trauma is ongoing.79

Hypothermia and pharmacologically-induced coma (barbiturates) may be used for extreme refractory ICP elevations, but no improvement in outcomes has been suggested in the literature.8082

Pitfalls in ED Evaluation and Management

  • Several medications have not demonstrated improvement in outcomes in head trauma, including corticosteroids, progesterone, magnesium, hyperbaric oxygen, and cyclosporine.2, 7, 14

  • Hyperventilation can reduce ICP for short periods, but hyperventilation may result in secondary ischemia, increasing the risk of cerebral edema. A PaCO2 less than 30 mm Hg for six hours up to five days is associated with worse outcome.2, 7, 14, 43

Key Points

  • Head trauma is common. Primary and secondary injuries result in severe morbidity and mortality.

  • Injuries include head contusion, epidural hematoma, subdural hematoma, subarachnoid hemorrhage, diffuse axonal injury, skull fracture, and traumatic spinal cord injury.

  • Cerebral perfusion pressure requires adequate cerebral blood flow.

  • Evaluation and management in the emergency department entails initial stabilization and resuscitation while assessing neurologic status.

  • Targeting MAP, oxygen levels, and neurologic status are key components. ICP management should follow a tiered approach.

  • Intubation of the patient with head trauma should be completed with several considerations.

  • Hyperosmolar treatments include HTS and mannitol.


1.Faul M, Xu L, Wald MM, et al. Traumatic Brain Injury in the United States: Emergency Department Visits, Hospitalizations and Deaths 2002–2006. Atlanta, GA: Centers for Disease Control and Prevention, National Center for Injury Prevention and Control; 2010. CrossRef | Find at Chinese University of Hong Kong Findit@CUHK Library | Google Scholar

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Jan 10, 2021 | Posted by in EMERGENCY MEDICINE | Comments Off on Chapter 7 – Head Trauma
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