Head Injury – Causes, Symptoms, Diagnosis, Treatment - Health

A Head Injury is any injury that results in trauma to the skull or brain. The terms traumatic brain injury and head injury are often used interchangeably in the medical literature. Because head injuries cover such a broad scope of injuries, there are many causes including accidents, falls, physical assault, or traffic accidents that can cause head injuries.

Head injuries include injuries to the brain and those to other parts of the head, such as the scalp and skull. Head injuries can be closed or open. A closed (non-missile) head injury is where the dura mater remains intact. The skull can be fractured, but not necessarily. A penetrating head injury occurs when an object pierces the skull and breaches the dura mater. Brain injuries may be diffuse, occurring over a wide area, or focal, located in a small, specific area. A head injury may cause a skull fracture, which may or may not be associated with injury to the brain. Some patients may have linear or depressed skull fractures. If intracranial hemorrhage occurs, a hematoma within the skull can put pressure on the brain. Types of intracranial hemorrhage include subdural, subarachnoid, extradural, and intraparenchymal hematoma. Craniotomy surgeries are used in these cases to lessen the pressure by draining off the blood.

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.[rx]

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

Mild = GCS 13 to 15, also called concussion
Moderate = GCS 9 to 12
Severe = GCS 3 to 8

Types of Head Injury

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. The 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

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 the 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 cerebrospinal fluid (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.

Causes of Head Injury

The leading causes of head trauma are

(1) motor vehicle-related injuries,
(2) falls, and
(3) assaults.[rx][rx]

Based on the mechanism, head trauma is classified as

(1) blunt (the most common mechanism),
(2) penetrating (most fatal injuries),
(3) blast.

Specific problems after a head injury can include

Skull fracture
Lacerations to the scalp and resulting hemorrhage of the skin
Traumatic subdural hematoma, bleeding below the dura mater which may develop slowly
Traumatic extradural, or epidural hematoma, bleeding between the dura mater and the skull
Traumatic subarachnoid hemorrhage
Cerebral contusion, a bruise of the brain
Concussion, a loss of function due to trauma
Dementia pugilistica, or “punch-drunk syndrome”, caused by repetitive head injuries, for example in boxing or other contact sports
A severe injury may lead to a coma or death
Shaken baby syndrome – a form of child abuse

Symptoms of Head Injury

Three categories used for classifying the severity of brain injuries are mild, moderate or severe.

Mild brain injuries

Symptoms of a mild brain injury include

headaches,
confusion
ringing ears
fatigue
changes in sleep patterns, mood, or behavior.
the trouble with memory,
concentration,
attention or thinking.
Mental fatigue is a common debilitating experience and may not be linked by the patient to the original (minor) incident.
Narcolepsy and sleep disorders are common misdiagnoses.

Moderate/severe brain injuries

Cognitive symptoms include

confusion
aggressive
abnormal behavior
slurred speech, and coma or other disorders of consciousness.
headaches that do not go away or worsen,
vomiting or nausea,
convulsions or seizures,
abnormal dilation of the eyes,
inability to awaken from sleep,
weakness in the extremities and loss of coordination
neurocognitive deficits,
delusions (often, to be specific, monothematic delusions),
speech or movement problems, and intellectual disability.
There may also be personality changes.
The most severe cases result in a coma or even persistent vegetative state.

Diagnosis of Head Injury

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.[rx][rx] It is important to understand that no individual history and physical examination findings 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.

CT Scan

If the patient is hemodynamically stable, obtain a Computed Tomography (CT) scan of the head to evaluate for the presence of a mass lesion (hematoma) or cerebral edema. It can be obtained when the patient is stabilized and ready to be transported to the radiology department.
A CT scan can adequately identify the extent of the intracranial injury and can also determine the relationship between the penetrating object and the intracranial structures. However, a radiolucent object, such as a wooden object, maybe missed by the CT scan.
In patients with penetrating head trauma, a large mass or hematoma may be evident. If ICP is increased, aqueductal stenosis is present, and the third but not fourth ventricle is enlarged.

Certain factors are important in critical decision making and have prognostic implications. These may include the following:

Sites of entry and exit wounds
Presence of intracranial fragments
Missile track and its relationship to both blood vessels and air-containing skull-base structures
Presence of intracranial air
Trans-ventricular injury
Basal ganglia and brain stem injury
Whether the missile track cross the midline
Presence of multi-lobar injury
Presence of basal cistern effacement
Brain parenchymal herniation
Presence of any associated mass effects

Plain Radiograph

Maybe useful as it provides information about the following:

Shape of the penetrating object
Skull fractures (if present)
An intracranial foreign object (if present)

Computed Tomographic Angiography (CTA)

If a vascular injury is suspected, noninvasive investigative CTA should be obtained after patient stabilization.

Magnetic Resonance Imaging (MRI) Scan

MRI Scan may be obtained if penetrating objects are suspected to be wooden objects. It should not be performed if intracranial metallic fragments are present. Such a procedure is contraindicated. However, if no bullets or intracranial metallic fragments are present, then an MRI scan of the brain can be performed in a stable patient. This can provide information about the posterior fossa structures and the extent of possible shared injuries.

Treatment of Head Injury

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.[rx][rx][rx]

Positioning

Though it is unclear whether elevating the head of the bed is clearly beneficial, elevation to 30 degrees is recommended in the setting of suspected increased ICP.[rx]

Airway and Breathing

Identify any condition which might compromise the 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 the 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. 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 a 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, the 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 the 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 of 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
The 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.

The 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.

Initial treatment should focus on the ABCs with the goal of maintaining cerebral perfusion and oxygenation.

Glucose

In patients with moderate to severe TBI, avoiding hyperglycemia is recommended. An insulin drip may be needed to maintain a goal of 100-180 mg/dL.[rx]

Temperature

As fever can increase the metabolic demand of the brain, and may increase ICP, treat fever aggressively with a goal of normothermia. At this time, therapeutic hypothermia for TBI is not recommended.

Seizures

Since seizures are a common sequela of CHI and may worsen secondary injury, treat acute seizures with benzodiazepines. Seizure prophylaxis is more controversial but is recommended in patients with GCS <10, penetrating injury, depressed skull fracture, cortical contusion, intracranial hematoma, or seizure within the first 24 hours of head injury. Levetiracetam has shown to be as effective as phenytoin, but there is currently no recommendation as to the superiority of either agent to prevent seizures.[rx][rx]

Elevated ICP and Herniation

Early consultation with neurosurgery in the setting of moderate to severe TBI is recommended. Neurosurgery will help to direct surgical interventions and ICP assessment and monitoring with devices such as an intracranial bolt or external ventricular drain (EVD).

A sustained ICP >20 mmHg is associated with increased morbidity and mortality, The Brain Trauma Foundation lists the following indications for invasive intracranial pressure monitoring:

1) Moderate to severe TBI in patients who cannot be accurately serially assessed by physical examination (for example intubated patients);
2) Severe head injury with abnormal CT scan;
3) Severe head injury with a normal CT if 2 of the following: age >40, systolic BP <90 mmHg, or abnormal motor posturing.

References

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