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Head Trauma
Authors

Faizan Shaikh1; Muhammad Waseem2.

Affiliations
1 St Mary Mercy Hospital
2 Lincoln Medical Center / SGU

Last Update: December 6, 2019.

Introduction
Traumatic brain injury (TBI) is a common presentation in emergency departments, which accounts for more than one
million visits annually. It is a common cause of death and disability among children and adults.[1]

Based on the Glasgow Coma Scale (GCS) score, it is classified as:

Mild = GCS 14 to 15, also called concussion

Moderate = GCS 9 to 13

Severe = GCS 3 to 8

Etiology
The leading causes of head trauma are (1) motor vehicle-related injuries, (2) falls, and (3) assaults.[2][3]

Based on the mechanism, head trauma is classified as (1) blunt (the most common mechanism), (2) penetrating (most
fatal injuries), (3) blast.

Most severe TBIs result from motor vehicle collisions and falls.

Epidemiology
Head trauma is more common in children, adults up to 24 years, and those older than 75 years.[4][5][6]

TBI is 3 times more common in males than in females.

Although only 10% of TBI occurs in the elderly population, it accounts for up to 50% of TBI-related deaths.

Pathophysiology
The following concepts are involved in the regulation of blood flow and should be considered.

1) Monroe-Kellie Doctrine

Related to the understanding of intracranial pressure (ICP) dynamics.

Any individual component of the intracranial vault may undergo alterations, but the total volume of intracranial
contents remains constant since the space within the skull is fixed. In other words, the brain has a compensatory
mechanism to maintain an equilibrium thereby maintaining normal intracranial pressure.

According to this, the displacement of cerebrospinal fluid (CSF) or blood occurs to maintain normal ICP. A rise
in ICP will occur when the compensatory mechanisms are exhausted.

2) Regulation of Cerebral Blood Flow (CBF) (Autoregulation)

 Under normal circumstances, the brain maintains CBF via auto-regulation which maintains equilibrium
between oxygen delivery and metabolism.

Autoregulation adjusts Cerebral perfusion pressure (CPP) from 50 to 150 mm Hg. Beyond this range,
autoregulation is lost, and blood flow is only dependent on blood pressure.

Severe brain injury may disrupt autoregulation of CBF.

3) Cerebral Perfusion Pressure (CPP)

The difference between the mean arterial pressure (MAP) and the ICP (CPP = MAP – ICP)

Target CPP is 55 mm Hg to 60 mm Hg

An increase in ICP can decrease the CPP

A decrease in ICP may improve CPP

Remember, lowering MAP in a hypotensive patient may lower CPP.

A minimum CPP should be maintained to avoid cerebral insult. It is age-dependent and is as follows: Infants -
50 mm Hg, Children - 60 mm Hg, and Adults - 70 mm Hg.

CBF is quite sensitive to oxygen and carbon dioxide.

Hypoxia causes vasodilation and therefore increases CBF and may worsen ICP.

Hypercarbia also results in vasodilation and can alter ICP via effects on CSF pH and increases CBF.

4) Mean arterial pressure (MAP)

Maintain = 80 mm Hg

60 mm Hg = cerebral vessels maximally dilated

< 60 mm Hg = cerebral ischemia

> 150mmHg = increased ICP

5) Intracranial pressure (ICP)

An increase in ICP can decrease CPP.

ICP is dependent on the volume of the following compartments:

Brain parenchyma (< 1300 mL)

Cerebrospinal fluid (100 - 150 mL)

Intravascular blood (100 - 150 mL)

Cushing reflex (hypertension, bradycardia, and respiratory irregularity) due to an increase in ICP

Normal ICP is age-dependent (adult younger than ten years old, child 3-7 years old, infant 1.5-6 years old)

> 20 mm Hg= increased morbidity and mortality and should be treated. It is perhaps more important to maintain
an adequate CPP.

TBI can be classified as primary injury and secondary injury:

Primary Injury

Primary injury includes injury upon the initial impact that causes displacement of the brain due to direct impact, rapid
acceleration-deceleration, or penetration. These injuries may cause contusions, hematomas, or axonal injuries.

Contusion (bruise on the brain parenchyma)

Hematoma (subdural, epidural, intraparenchymal, intraventricular, and subarachnoid)

Diffuse axonal injury (stress or damage to axons)

Secondary Injury/Secondary Neurotoxic Cascade

Secondary injury consists of the changes that occur after the initial insult. It can be due to:

Systemic hypotension

Hypoxia

Increase in ICP

After a primary brain injury, a cascade of cellular and biochemical events occurs which include the release of
glutamate into the presynaptic space resulting in activation of N-methyl-D-aspartate, a-amino-3-hydroxy-5-methyl-4-
isoxazole propionic acid, and other receptors. This ionic shift may activate cytoplasmic and nuclear enzymes,
resulting in mitochondrial damage, and cell death and necrosis.

Brain Herniation

Herniation occurs due to increased ICP. Following are the types of herniations.

1) Uncal transtentorial

The uncus is the most medial portion of the hemisphere, and the first structure to shift below the tentorium.

Compression of parasympathetic fibers running with the third cranial nerve

Ipsilateral fixed and dilated pupil with contralateral hemiparesis

2) Central transtentorial

Midline lesions, such as lesions of the frontal or occipital lobes or vertex

Bilateral pinpoint pupils, bilateral Babinski signs, and increased muscle tone. Fixed midpoint pupils follow
along with prolonged hyperventilation and decorticate posturing

3) Cerebellar tonsillar

Cerebellar tonsils herniate in a downward direction through the foramen magnum

Compression on the lower brainstem and upper cervical spinal cord

Pinpoint pupils, flaccid paralysis, and sudden death

4) Upward posterior fossa/cerebellar herniation

The cerebellum is displaced in an upward direction through the tentorial opening

Conjugate downward gaze with an absence of vertical eye movements and pinpoint pupils

History and Physical

A good history concerning the mechanism of injury is important. Follow trauma life support protocol and perform
primary, secondary, and tertiary surveys. Once the patient is stabilized, a neurologic examination should be
conducted. CT scan is the diagnostic modality of choice in the initial evaluation of patients with head trauma.
The GCS is used to describe the level of consciousness. Patients who are intubated are only evaluated for motor
scores and eye-opening and the suffix T is added to the final score. The maximal GCS score is 10T and the lowest is
2T.

Classification of TBI is as follows:

Clouding of consciousness where there is a mild deficit in processing by the brain. It may persist for many months
and the patient may have a loss of recent memory, but long term memory remains intact.

Lethargy is a state of depressed alertness and can result in an inability to perform tasks that are usually done without
any effort. The patient may be aroused by stimuli but then settles back into a state of inactivity. Awareness of the
environment is present.

Obtundation is a state of decreased alertness and awareness. The patient will briefly respond to stimuli and only
follow simple commands; but will not be aware of the surroundings.

Stupor is when the patient cannot communicate lucidly and requires panful stimuli to be aroussed. Once the
stimulation is wihdrawn, the patient returns to the inactive state.

Coma is when the patient is not able to respond to any type of stimuli

Evaluation
CT scan is required in patients with head trauma

Moderate (GCS score 9 to 12)

Severe (GCS score < 8)

For patients who are at low risk for intracranial injuries, there are two externally validated rules for when to obtain a
head CT scan after TBI.[7][8]

It is important to understand that no individual history and physical examination finding can eliminate the possibility
of intracranial injury in head trauma patients.

Skull x-rays are only used to assess for foreign bodies, gunshots or stab wounds

New Orleans Criteria

Headache

Vomiting (any)

Age > 60 years

Drug or alcohol intoxication

Seizure

Trauma visible above clavicles

Short-term memory deficits

Canadian CT Head Rule

Dangerous mechanism of injury

Vomiting = two times

Age > 65 years

GCS score < 15, 2-hours post-injury

 Any sign of basal skull fracture

Possible open or depressed skull fracture

Amnesia for events 30 minutes before injury

Level A Recommendation

With the loss of consciousness or posttraumatic amnesia only if one or more of the following symptoms are present:

Headache

Vomiting

Age > 60 years

Drug or alcohol intoxication

Deficits in short-term memory

Physical findings suggestive of trauma above the clavicle

Posttraumatic seizure

GCS score < 15

Focal neurologic deficit

Coagulopathy

Level B Recommendation

Without loss of consciousness or posttraumatic amnesia if one of the following specific symptoms presents:

Focal neurologic deficit

Vomiting

Severe headache

Age > 65 years

Physical signs of a basilar skull fracture

GCS score < 15

Coagulopathy

Dangerous mechanism of injury

Ejection from a motor vehicle (such as Pedestrian struck or a fall from a height > three feet or five stairs)

The risk of intracranial injury when clinical decision rule results are negative is less than 1%.

For children, Pediatric Emergency Care Applied Research Network (PECARN) decision rules exist to rule out the
presence of clinically important traumatic brain injuries. However, this rule applies only to children with GCS > 14.

Treatment / Management
The most important goal is to prevent secondary brain injuries. This can be achieved by the following:

Maintain airway and ventilation

Maintain cerebral perfusion pressure

 Prevent secondary injuries (by recognizing and treating hypoxia, hypercapnia, or hypoperfusion)

Evaluate and manage for increased ICP

Obtain urgent neurosurgical consultation for intracranial mass lesions

Identify and treat other life-threatening injuries or conditions (if they exist)

A relatively higher systemic blood pressure is needed:

Increase in intracranial pressure

Loss of autoregulation of cerebral circulation

Priorities remain the same: the ABC also applies to TBI. The purpose is to optimize perfusion and oxygenation.[1][9]
[10]

Airway and Breathing

Identify any condition which might compromise airway, such as pneumothorax.

For sedation, consider using short-acting agents having minimal effect on blood pressure or ICP:

Induction agents: Etomidate or propofol

Paralytic agents: Succinylcholine or Rocuronium

Consider endotracheal intubation in the following situations:

Inadequate ventilation or gas exchange such as hypercarbia, hypoxia, or apnea

Severe injury (GCS score of = 8)

Inability to protect airway

Agitated patient

Need for patient transport

The cervical spine should be maintained in-line during intubation.

Nasotracheal intubation should be avoided in patients with facial trauma or basilar skull fracture.

Targets:

Oxygen saturation > 90

PaO2 > 60

PCO at 35 - 45

Circulation

Avoid hypotension. A normal blood pressure may not be adequate to maintain adequate flow and CPP if ICP is
elevated.

Target

Systolic blood pressure > 90 mm Hg

MAP > 80 mm Hg

Isolated head trauma usually does not cause hypotension. Look for another cause if the patient is in shock.
Increased ICP

Increased ICP can occur in head trauma patients resulting in the mass occupying lesion. Utilize a team approach to
manage impending herniation.

Signs and symptoms:

Change in mental status

Irregular pupils

Focal neurologic finding

Posturing: decerebrate or decorticate

Papilledema (may not be apparent with rapid elevation of ICP)

CT scan findings:

Attenuation of sulci and gyri

Poor gray/white matter demarcation

General Measures

Head Position: Raise the head of the bed and maintain the head in midline position at 30 degrees: potential to improve
cerebral blood flow by improving cerebral venous drainage.

Lower cerebral blood volume (CBV) can lower ICP.

Temperature Control: Fever should be avoided as it increases cerebral metabolic demand and affects ICP.

Seizure prophylaxis: Seizures should be avoided as they can also worsen CNS injury by increasing the metabolic
requirement and may potentially increase ICP. Consider administering fosphenytoin at a loading dose of 20mg/kg.

Only use an anticonvulsant when it is necessary, as it may inhibit brain recovery.

Fluid management: The goal is to achieve euvolemia. This will help to maintain adequate cerebral perfusion.
Hypovolemia in head trauma patients is harmful. Isotonic fluid such as normal saline or Ringer Lactate should be
used. Also, avoid hypotonic fluid.

Sedation: Consider sedation as agitation and muscular activity may increase ICP.

Fentanyl: Safe in intubated patients

Propofol: A short-acting agent with good sedative properties, potential to lower ICP, possible risk of
hypotension and fatal acidosis

Versed: sedative, anxiolytic, possible hypotension

Ketamine: Avoid as it may increase ICP.

Muscle relaxants: Vecuronium or Rocuronium are best options for intubation; Succinylcholine should not be
used as ICP may rise with fasciculations.

ICP monitoring:

Severe head injury

Moderate head injury with increased risk factors such as abnormal CT scan finding

Patients who cannot be evaluated with serial neurological examination

 ICP monitoring is often done in patients with severe trauma with a GCS less than 9. The reference range for
normal CIP is 2-15 mmHg. In addition, the waveform of the tracing is important.

Hyperventilation:

Normocarbia is desired in most head trauma patients. The goal is to maintain PaCO between 35-45 mmHg. Judicious
hyperventilation helps to reduce PaCO2 and causes cerebral vasoconstriction. Beware that, if extreme, it may reduce
CPP to the point that exacerbation of secondary brain injury may occur. Avoid hypercarbia: PaCO > 45 may cause
vasodilatation and increases ICP.

Mannitol:

A potent osmotic diuretic with net intravascular volume loss

Reduces ICP and improves cerebral blood flow, CPP, and brain metabolism

Expands plasma volume and can improve oxygen-carrying capacity

Onset of action is within 30 minutes

Duration of action is from two to eight hours

Dose is 0.25-1 g/kg (maximum: 4 g/kg/day)

Avoid serum sodium > 145 m Eq/L

Serum sodium > 145 m Eq/L

Serum osmolality > 315 mOsm

Relative contraindication: hypotension does not lower ICP in hypovolemic patients.

Hypertonic saline:

May be used in hypotensive patients or patients who are not adequately resuscitated.

Dose is 250 mL over 30 minutes.

Serum osmolality and serum sodium should be monitored.

Hypothermia may be used to lower cerebral metabolism but it is important to be aware that hypothermia also makes
the patient susceptible to infections and hypotension.

Mild Head Trauma

The majority of head trauma is mild. These patients can be discharged following a normal neurological examination
as there is minimal risk of developing an intracranial lesion.

Consider observing at least 4 to 6 hours if no imaging was obtained.

Consider hospitalization if these other risk factors are present:

Bleeding disorder

Patient taking anticoagulation therapy or antiplatelet therapy

Previous neurosurgical procedure

Provide strict return precautions for patients discharged without imaging.

Prognosis
The outcomes after head trauma depend on many factors. The initial GCS score does provide some information on the
outcome; the motor score is most predictive of outcome. Patients with a GCS of less than 8 at presentation have high
mortality. Advanced age, comorbidity, respiratory distress, and a comatosed state are also associated with poor
outcomes.

Complications
DVT rates are higher in head trauma patients

Neurological deficits

CSF leak

Hydrocephalus

Infections

Seizures

Cerebral edema

Pearls and Other Issues

Hyperglycemia may worsen the outcome.

An elevated temperature may increase ICP and worsen outcome.

Increase metabolic demand

Increase glutamate release

A prolonged seizure may worsen secondary brain injuries.

Enhancing Healthcare Team Outcomes

Head trauma is a major public health problem accounting for thousands of admissions each year and costing the
healthcare system billions of dollars. The majority of patients with head trauma are seen in the emergency
department; the head injury is often associated with other organ injuries as well. The care of a patient with head
trauma is by an interprofessional team that is dedicated to managing head trauma patients.

Most patients require admission and monitoring in an ICU setting. The outcome of these patients depends on the
severity of the head trauma, initial GCS score, and any other organ injury. Data indicate that those patients with an
initial GCS of 8 or less have a mortality rate of 30% within 2 weeks of the injury. Other negative prognostic factors
include advanced age, elevated intracranial pressure, and the presence of a gross neurologic deficit on presentation.
ICU nurses play a vital role in the managing of these patients; from providing basic medical care, monitoring, DVT
and ulcer prophylaxis and monitoring the patient for complications and reporting concerns to the team. The dietitian
manages the nutrition and physical therapists provide bedside exercises to prevent muscle wasting.

Patients with a GCS less than 9 often require mechanical ventilation, tracheostomy, and a feeding tube. With
prolonged hospital stay, there are prone to pressure ulcers, aspiration, sepsis, failure to thrive and deep vein thrombus.
Patients deemed to be brain dead are assessed by the entire team that includes specialists from end of life care.

Recovery in most patients can take months or even years. Even those who are discharged often have residual deficits
in executive function or neurological deficits. Some require speech, occupational and physical therapy for months. In
addition, the social worker should assess the home environment to make sure it is safe and offers amenities for the
disabled person. Only through such a team approach can the morbidity of head trauma be lowered.

Outcomes

Unfortunately, despite education of the public, many young people still lead a lifestyle that predisposes them to head
injury. Young people still drink and drive, text while driving, abuse alcohol and illicit drugs, and are often involved in
high-risk sporting activities, which makes them susceptible to head trauma.[11][12]

Questions
To access free multiple choice questions on this topic, click here.

References
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