Head Injury: Classifications, Diagnosis and Treatment

Head injury refers to trauma to the head causing alteration in mental or physical functioning (neurological functions)

Etiology

The most common causes include:

  • Motor vehicle accidents (eg, collisions between vehicles, pedestrians struck by motor vehicles, bicycle accidents),
  • Falls,
  • Assaults,
  • Sports-related injuries, and
  • Penetrating trauma.

The male-to-female ratio for traumatic brain injury is nearly 2:1, and traumatic brain injury is much more common in persons younger than 35 years.

Classification of head injury

Head injuries can be classified according to;
1. The severity of the injury.
2. Anatomical classification
3. Pathological classification-penetrating or blunt injury
4. Primary and secondary brain injury.

A. The severity of the head injury

Severity is assessed by the following methods notably:

Glasgow Coma Scale.

A score below 8 is considered to represent severe head injury while 8 to 12 is assessed as a moderate head injury. 13 to 15 is a mild head injury.

B. Anatomical classification

Injury can involve one or more of the following structures.

Use the mnemonic  Scalp to remember them.

This consists of five layers; the first three layers are bound together and moved as a unit. The layers are:
S -Skin

C -Connective tissue: Dense
This is a fibro-fatty layer. The fibrous septa unite the skin to the underlying aponeurosis of the fronto-occipitalis muscle. The scalp vessels lie within this layer.

A- Aponeurosis of Galea 
This is a thin fibrous sheath attached to the bellies of the Fronto-occipitalis muscle. Deep to it is the sub aponeurotic space.

L- Loose connective(areolar) layer
Occupying the sub aponeurotic space. This layer contains emissary's veins. It is a large potential space and can contain a large amount of bleeds or pus following skull injury.

P Pericranium
Pericranium is the periosteum of the skull bone.

The scalp is very vascular and laceration can cause severe loss of blood. The vessels within the scalp do not constrict when injured because the wall is adherent to the surrounding fiber fatty tissue in the dense connective tissue layer. Bleeding can be controlled by applying pressure or suturing the scalp.

B. Skull Injuries

Skull fractures are simple or compound. Simple if there is no communication between the fracture and the atmosphere, while the fracture is compound if there is such communication. Skull fractures are classified as follows:

Simple/Closed Fractures

1. Linear or fissure fracture.

This involves the skull vault and can extend down to the base of the skull. The linear fracture indicates that there have been significant injuries to the head. Management is usually hospital admission and close observation for any complications.

2. Comminuted fracture

3. Cracked pot fracture

4. Ping-pong fracture

This is a greenstick fracture of the skull, it occurs in the first few months of life when the skull bones are still soft. It is caused after falls when the skull hits the edge of a blunt structure as the edge of a table. It shows as a deformity of the skull, it looks like a shallow trench on the surface of the skull.

If large and showing as a significant deformity it can be easily treated by elevating the depressed bone fragment

5.Depressed fracture

Skull fragment pushed below the level of the skull. Significant depression is depression twice the thickness of the diploe. This can result in dural tear and laceration of the underlying brain.
Skull fragments should be replaced to avoid the creation of skull defect and the need for cranioplasty.

The underlying dura should be repaired and any bleeding controlled. This is important in children below the age of 4 to avoid the complication of growing skull fracture.

Bone fragments should be replaced even in compound fractures and wound debrided.

Compound Fracture/open fracture e.g. Fracture Skull Base.

This starts as a vault linear fracture and extends into the skull base. It follows the weak points in the skull as the Cribriform plate, foramina, and internal ear. Nerve injury can result in involving the olfactory nerve, the facial nerve. etc

If the fracture extends into the Cribriform plate and is associated with dural tear CSF leak can result and this is called rhinorrhea. If the fracture extends into the internal ear and the middle ear we can get otorrhea, which is CSF leak from the ear.

C.Brain Injury

Injury to the brain is either localized or diffuse and can be either primary or secondary.

Primary Brain Injury

Injury directly due to the insult and occurring at the time of the injury

Brain concussion is a temporary physiological disruption of brain function.
A brain contusion is a Small petechiae and hemorrhages
Brain laceration-obvious deformity

Localized injury is a deformation of the brain at the point of impact. It is associated with dural laceration and underlying brain contusion or laceration. Usually, there is localized surrounding edema around the site of the impact.

Diffuse injury carries a greater risk of damage to the brain and the mechanisms involved in this injury are:
Acceleration/deceleration injury.

In acceleration injury, the head is put into motion from a standstill position, as a result of which the different layers of the brain travels at different velocities with shearing effects and rotation of the brain within the skull.

The shearing stresses between different layers of the brain result in petechial hemorrhages as well as diffuse axonal injury involving the white matter and brain stem. In deceleration injury, the head is brought to a standstill from a moving position as in falls. The same mechanism applies.

The extent of the diffuse injury and the axonal damage determines the outcome.
The more severe the injury is, the more brain damage occurs with more axonal injury. This would be associated with higher morbidity and mortality.

Penetrating injury

High velocity or slow velocity injury as a result of penetration with sharp objects. The base of the skull is thin bone and could easily be penetrated especially in children. This result in skull base fracture and damage to the brain overlying that area.

Compression injury 
The head is compressed between two solid objects as in motor vehicle accidents. The result is multiple linear fractures particularly in the weak areas of the skull base resulting in multiple cranial nerve injuries.

Secondary brain injury

This results as a consequence of the primary brain injury and this includes :

A. Intracranial hematomas.

These Include

1 Epidural hematoma

Epidural hematomas are located between the inner table of the skull and the dura. Usually due to laceration of the middle meningeal artery.

They are typically biconvex (lentiform) in shape because their outer border follows the inner table of the skull and their inner border is limited by locations at which the dura is firmly adherent to the skull.

Up to 10% of epidural hematomas may be venous in origin. In about 60 or 70% of cases, there is an associated skull fracture.

Usually located in the temporal area. Occasionally it is in the frontal, parietal or posterior fossa region.

As it is an arterial bleed the clot can get to a significant size within a short period of time with a rapid rise in the intracranial pressure. If untreated there is a high rate of morbidity and mortality but effective and early treatment can result in complete recovery. In these cases, there is no diffuse brain injury and the injury is localized to the area where the fracture and the hematoma is.

The aim of the management is to evacuate the clot as soon as possible and control the bleeding meningeal vessel.
In most cases this is an acute condition, however, occasionally the bleeding is a result of venous tear and the blood clot develops slowly. This is particularly the case in the frontal and occipital regions.

The clot is evacuated through a craniotomy but in acute situations where there are no facilities for the major neurosurgical procedure a burr hole should be done to release the intracranial clot and reduce the intracranial pressure.

Only 1/3 pts present with Classic "lucid interval,” normal brain function after the insult followed by focal neurologic deficits later.

2 Subdural hematoma

This is the result of a tear in one of the bridging veins between the surface of the cortex and the dural sinuses. The blood collects gradually and slowly as the bleed is of Acute subdural hematomas.

They are rare in children. Subdural hematomas are more common in alcoholics and patients > 50 yr, in whom the head injury may have been relatively trivial, even forgotten.

As the brain atrophies over time, the bridging veins become more exposed and, as a result, are more easily injured. These hematomas are usually a part of severe and diffuse brain injury. It causes significant morbidity and mortality because of associated diffuse brain injury.

Causes increased intracranial pressure with transtentorial or tonsilar herniation, widening pulse pressure, pupils in mid-position or dilated and fixed, spastic hemiplegia with hyperreflexia, quadrispasticity, decorticate rigidity, or decerebrate rigidity (due to progressive rostral-caudal neurologic deterioration).

Chronic subdural hematomas may not produce symptoms until several weeks after trauma. Although early diagnosis (2 to 4 weeks after trauma) may be suggested by delayed neurologic deterioration, later diagnosis can be overlooked because of the time-lapse between trauma and the onset of symptoms and signs.

Subdural hematomas are more common in alcoholics and patients > 50 yr. Increasing daily headache, fluctuating drowsiness or confusion (which may mimic early dementia), and mild-to-moderate hemiparesis are typical.

In infants, chronic subdural hematomas can cause head circumference to enlarge, suggesting hydrocephalus. MRI scans are diagnostic; CT scans are less consistently

3. Subarachnoid hemorrhage

The subarachnoid bleeding itself does not usually cause neurologic damage, but hydrocephalus and cerebral vasospasm, which are delayed complications typically seen days to weeks following subarachnoid hemorrhage, can lead to neurologic impairment.

Subarachnoid hemorrhages that occur because of trauma are typically located over gyri on the convexity of the brain. The subarachnoid hemorrhages that result from a ruptured cerebral aneurysm are usually located in the subarachnoid cisterns at the base of the brain.

4.Intraventricular hemorrhage

B. Brain edema

Children are prone to develop significant edema and this does not always occur as a result of severe head injury.
Brain edema could be localized around an area of brain damage or diffuse as seen in diffuse axonal brain injury.

Intracranial Pressure - Normal ~ 0-10mmHg (5-18 cmH2O)

Monro-Kellie Doctrine states that the total volume of intracranial contents must remain constant" The cranial cavity normally contains a brain weighing approximately 1400gm, 75mL of blood, and 75mL of cerebrospinal fluid.

The addition of a mass e.g. a hematoma results in the squeezing out of an equal volume of cerebrospinal fluid and venous blood to maintain the intracranial pressure. However, when this compensatory mechanism is exhausted, there is an exponential increase in ICP for even a small additional increase in the volume of the hematoma

Cerebral Perfusion Pressure = MAP - ICP = ~≥70mmHg

 Mean Arterial Pressure (MAP) = DBP + ⅓ Pulse pressure

Pulse pressure = SBP - DBP = ~50mmHg (<~½ SBP)

Cerebral Blood Flow - ~ 50mL/100gm of brain/minute; <5mL/100gm of brain/minute - there is cell death or irreversible damage.

venous origin. Their outer edge is convex, while their inner border is usually irregularly concave. Subdural hematomas are not limited by the intracranial suture lines; this is an important feature that aids in their differentiation from epidural hematomas.

C. Infection

This can occur in compound skull fractures and skull base fractures. Rhinorrhea and otorrhea prophylactic 3rd generation Cephalosporin

D. Hydrocephalus

Hydrocephalus can be caused by blockage of the ventricular system by a blood clot in cases of intraventricular hemorrhage or due to cicatrization and fibrosis of subarachnoid space or the arachnoid villi along the sagittal sinus from the deposition of blood products.

F.cerebrospinal fluid Leakage

This is a result of skull fractures crossing the nasal sinuses. In the case of ethmoid sinuses -rhinorrhea and fracture internal ear and the middle ear with rupture of tympanic membrane cause otorrhea.

Often these leaks are temporary and spontaneous closure within one leak occurs. If it persists then surgical intervention should be considered.

Diagnosis of Head Injury

History

Detail description of the event leading to injury to the head either from the relatives or from the patient.

  • Etiology such as road traffic accident, Assault, Fall, Missiles, Explosive. Detail of exact mechanism leading to head injury.
  • Site of trauma, any wounds
  • Any history of bleeding
  • Signs of shock such as dizziness, confusion, sweating
  • Any history of loss of consciousness
  • History of headache, vomiting, Blurring of vision are features of increased intracranial pressure,
  • History of otorrhea or rhinorrhea
  • Any lateralizing signs-loss of power in the limbs or loss of sensation.
  • History of alcohol or other drug consumption raise the risk of intracranial bleeding and cloud the mental status assessment.
  • The history of previous head injuries-Premorbid illness like diabetes mellitus, hypertension or Epilepsy

Physical examination

Suspect significant head trauma in any traumatized patient with cranial hematomas or lacerations or with altered sensorium with or without focal neurologic findings.
Obtain complete vital signs, including core temperature.

The GCS is the mainstay for rapid neurologic assessment in acute head injury. Both initial and worst GCS post-resuscitation scores have correlated significantly with 1-year outcomes following severe head injury

A. Examine the scalp carefully for evidence of trauma .

Inspect the head, and palpate carefully for scalp lacerations, subgaleal hematomas, ecchymoses, and deformity.

Inspect neck, chest, abdomen, back, and extremities-tenderness, pain, and deformity are often signs of associated injuries that require specific early treatment

B. Any clear fluid in the ear canal or coming from the nares must be assumed to be cerebrospinal fluid.

If the Autoregulation maintains CPP between 50-160mmHg. <50mmHg, the CBF declines steeply, & >160mmHg, there is passive dilatation of the cerebral vessels & an increase in CBF

Neurologic Examination

CN Exam-Systemic exam

Anosmia -shearing of the olfactory nerves at the cribriform plate. If accompanied by rhinorrhea, risk of ascending meningitis.

Abnormal post-resuscitation pupillary reactivity correlates with a poor 1-year outcome. A unilaterally dilated pupil with or without ipsilateral cranial nerve (CN) III paralysis may indicate impending herniation.

CN VI palsies may indicate raised intracranial pressure. CN VII palsy, particularly in association with decreased hearing, may indicate a fracture of the temporal bone.

Dysphagia raises the risk of both aspiration and inadequate nutrition.

Focal motor findings may be manifestations of a localized contusion or, more ominously, an early herniation syndrome.

Flexor or extensor posturing obviously implies extensive intracranial pathology or raised intracranial pressure. In the chronic phase, motoric manifestations typically include spasticity or, more unusually, akinesia and rigidity

Dilated or constricted pupils-Pupillary dilatation may occur when transtentorial compression occurs and parasympathetic tone of the pupil is totally lost.

Conversely, pinpoint pupils after a head injury may indicate loss of sympathetic tone resulting from a lesion in the brain stem caudal to the oculomotor nuclei (eg, pontine hemorrhage).
2. Deep reflexes
3. Sensory exam
4.Muscle tone

Investigations in head injury patient

1 Plain skull x-ray

This is useful in screening head injuries. It is indicated if there is a loss of consciousness or localized contusion or swelling over the head. Plain skull x-ray shows skull fractures and intracranial air.

Patients with skull fractures should be admitted to the hospital for observation. AP, lateral and Town views-OccipitoFrontal

2 CT scan

The Indications for ordering a CT scan are;

  • All moderate to Severe head injury GCS below 12
  • History of loss of consciousness or decreasing level of consciousness
  • Post-traumatic seizure
  • Lateralizing signs-weakness of a limb or unreactive pupil
  • Type of injury-Penetrating injury Or Skull fractures
  • Otorrhea and rhinorrhea

3. MRI

This examination is useful to show long term effects of head injury. Depending on the availability it also could be used in investigating acute cases.

4. Beta transferrin

This is a test for an enzyme that is only found in CSF. It is the optimum test for CSF leak.
Other Important Baseline Tests are;

1.PCV
2.Urea and electrolytes
3.Arterial blood gases
4.Blood alcohol level

The fluid is cerebrospinal fluid, a dipstick glucose test will usually be positive since cerebrospinal fluid contains glucose and mucus does not. False-negative results may occur in patients with hypoglycemia.

C. Blood behind the eardrum, a postauricular hematoma (Battle's sign), suggest basilar skull fracture or bilateral circumorbital hematomas ("raccoon eyes")

Management of head injury

Initial Management

Primary Survey

1st is A, B, C, D of resuscitation plus vital signs

1. Airway and cervical spine.

Maintain cervical spine immobilization in all unconscious or symptomatic (neck pain or tenderness) patients.

i)-Inspect mouth remove debris by sweeping through.

ii)Chin lift/jaw thrust (tongue is attached to the jaw) and always airway in tongue falling back.

To perform a chin lift, place two fingers under the mandible and gently lift upward to bring the chin anterior. During this maneuver, be careful not to hyperextend the neck. Care should be given to neck stabilization, if appropriate.

The jaw thrust is performed by manually elevating the angles of the mandible to obtain the same effect.

iii) Guedel airway/nasopharyngeal airway to secure airway. Insert the oral airway into the mouth behind the tongue; it is usually inserted upside down until the palate is encountered and is then rotated 180 degrees.

iv) Intubations; keep the neck immobilized in a neutral position. Intubate all unconscious patients (GCS < 9) to secure the airway.

Use sedation and short-acting neuromuscular blockade if necessary. If not possible

v)Tracheostomy

vii)cricothyrotomy

2. Breathing:

Oxygenation and ventilation.

LOOK OUT for the five major problems that may impair breathing -ie

1. Tension pneumothorax-put through a needle
2. Massive pneumothorax-chest tubes insertion
3. Sucking wounds-strap the open wound
4. Flail chest-positive pressure ventilation
5. Cardiac tamponade
6. Airway obstruction

1 Inspect (LOOK)
The inspection of the respiratory rate is essential. Are any of the following present?

  • Cyanosis
  • Any signs of respiratory distress- Use of accessory muscles, flaring of alae nasae, subcostal recession
  • Inspect Chest- movements, Penetrating injury, Presence of flail chest, Sucking chest wounds

2 Palpate (FEEL)

  • Tracheal shift
     
  • Broken ribs
  • Subcutaneous emphysema.
  • Chest expansion

3.Percussion

For dullness is useful for the diagnosis of haemothorax and pneumothorax.

4 Auscultate (LISTEN)

Pneumothorax (decreased breath sounds on site of injury)

If available, maintain the patient on oxygen until complete stabilization is achieved
If you suspect a tension pneumothorax, introduce a large-bore needle into the pleural cavity through the second intercostal space, midclavicular line, to decompress the tension and allow time for the placement of an intercostal tube

 If intubation in one or two attempts is not possible, a cricothyroidotomy should be considered a priority

5.Random blood glucose

3. Circulation and arrest of bleeding.

“Shock” is defined as inadequate organ perfusion and tissue oxygenation. In the trauma patient, it is most often due to hemorrhage and hypovolaemia.

The diagnosis of shock is based on clinical findings:

1) Hypotension
2) Hypothermia
3) Tachycardia
4) Tachypnoea
5) Cool extremities
6) Decreased capillary refill
7) Pallor
8) Decreased urine production

Haemorrhagic (hypovolaemic)

Shock is due to an acute loss of blood or fluids. The amount of blood loss after trauma is often poorly assessed and in blunt trauma is usually underestimated.

Remember:

Large volumes of blood may be hidden in the abdominal and pleural cavity
Femoral shaft fracture may lose up to 2 liters of blood
Pelvic fracture often loses in excess of 2 liters of blood.

Cardiogenic shock

Cardiogenic shock is due to inadequate heart function.

This may result from

  • Myocardial contusion (bruising)
  • Cardiac tamponade
  • Tension pneumothorax (preventing blood returning to heart)-
  •  Penetrating wound of the heart
  • Myocardial infarction.

Assessment of the jugular venous pressure is essential in these circumstances and an ECG should be recorded, if available.

Neurogenic shock

This is due to the loss of sympathetic tone, usually resulting from spinal cord injury. The classical presentation is hypotension without reflex tachycardia or skin vasoconstriction.

Septic shock

This is rare in the early phase of trauma but is a common cause of late death (via multi-organ failure) in the weeks following injury. It is most commonly seen in penetrating abdominal injury and burns patients.

Resuscitation

The first priority is to stop any obvious bleeding by Subfascial gauze pack placement and Manual compression on the proximal artery. Carefully applied a compressive dressing of the entire injured limb can be done. Then vascular access with 2 large bore size 16 on the 2-basilic veins

Detection of abnormal sounds in the chest.

Resuscitation action

Insert an intercostal drainage tube as a matter of priority, and before chest X-ray, if respiratory distress exists, to drain the chest pleura of air and blood.

When indications for intubation exist but the trachea cannot be intubated, consider using a laryngeal mask airway or direct access via a cricothyroidotomy.

Resuscitate to the goal of mean arterial pressure (MAP)>90 mmHg to maintain a presumptive cerebral perfusion pressure (CPP)>70-80mmHg

Urinary catheter insertion and monitor the input and output chart at least 30-50 ml/hour or 0.5/kg/hour of urine flow

Asses by vital signs, pallor, sweating, anxiety, skin warmth clammy, input and output

Blood transfusion must be considered when the patient has persistent hemodynamic instability despite fluid (colloid/crystalloid) infusion.

If type-specific or cross-matched blood is not available, use group O negative packed red blood cells.

Transfusion should, however, be seriously considered if the hemoglobin level is less than 7 g/dl and the patient is still bleeding.

4.Neurological dysfunction

Establish a preliminary level of consciousness by AVPU
A –Awake, V -Verbal response, P- Painful response
U –Unresponsive and any focal neurologic deficits.

5.Exposure and environmental modification

Cover the patient in case of shock and shivering.

Secondary survey

Head to toe exam with emphasis on the evaluation of head injury

Head examination

Scalp and ocular abnormalities-Racoon eye and battle signs, wounds, bleeding around the head, the external ear and tympanic membrane and periorbital soft tissue injuries

Neurological examination

1. Glasgow coma scale-Is the Gold standard for the evaluation of the severity of the head injury.
Used for monitoring the improvement or deterioration of the head injury.

a)Minimal head injury-GCS-15
b) Mild head injury GCS-14-15 history of loss of consciousness for less than 5 minutes.
c)Moderate head injury 9-13 with a history of loss of consciousness more than 5 minutes
d) Severe head injury GSC 5-8
c) critical head injury GSC 3-5

2.All cranial Nerve examination

3. Peripheral sensory and motor examination

Neck examination

Penetrating wounds and bleeds
Subcutaneous emphysema
Tracheal deviation
Neck vein appearance.

Chest examination

Clavicles and all ribs

Fluids: infuse 0.9% NaCl initially 2L to run as fast as possible through 2 large-bore IV lines in the antecubital fossa then re-assess

Abdominal Examination

Penetrating abdominal wound requiring surgical exploration
Blunt trauma: insert a nasogastric tube (not in the presence of facial trauma)
Rectal examination
Insert urinary catheter (check for meatal blood before insertion)

Pelvis and limbs

Fractures
Peripheral pulses
Cuts, bruises, and other minor injuries.
X-RAYS (if possible and where indicated)

Chest, C-spine and pelvis X-rays may be needed during the primary survey
NB-Cervical spine films (must see all 7 vertebrae)
Pelvic and long bone X-rays

Head injury observation chart

Monitoring the following in half, hourly or 2 hourly

1.Continuous monitor of level of consciousness

  • Best eye-opening score
  • Best verbal response score
  • Best motor response

2.Vital signs

  • Pulse
  • Temperature
  • BP
  • Respiratory rate

3.Pupillary reflexes

  • Reaction to light
  • Size of the pupil

4.Motor examination of limbs

  • The spontaneous movement of all the limbs
  • Paralysis

5.Monitor danger signs

  • Severe headache
  • Vomiting
  • Convulsions/seizures.
  • Drainage of fluids ear or nose
  • Presence of other injuries like Chest, Abdomen, Neck, Spine, Arm or leg

Complications of head injury

1.Cranial nerve palsies and Focal neurological signs
3.Infections
4.Hydrocephalus
5.Convulsive disorder/epilepsy
6.Psychiatric disorders
7.Cerebrospinal fluid fistulae, either in the form of rhinorrhea or otorrhea
8.Posttraumatic movement disorders Tremor, dystonia, parkinsonism, myoclonus, and hemiballism
9.Vascular injuries.
Arterial injuries that occur following head trauma include arterial transactions, thromboembolic phenomena, posttraumatic aneurysms, dissections, and carotid-cavernous fistulae (CCF).
9. Post-concussional symptoms e.g. Transient LOC, Bradycardia, Hypertension
10.Cumulative brain damage ('Punch-drunk syndrome')
11.Neurological & neuropsychological deficits e.g. Parkinsonism, Dementia
12. Neuroendocrine & metabolic disturbances e.g. Diabetes insipidus.

author

Daniel Ogera

Medical educator, passionale about pharmacology, physiology and pathophysiology.

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