La competencia disciplinaria de la ITRC. Reiteración 67

deaths.

• It is the leading cause of death and disability in young adults.

• The principal causes of head injury are road traffic accidents, assaults, falls, sport injuries and industrial accidents.

PATHOPHYSIOLOGY OF HEAD INJURY

Primary Injury

It is the damage occurring at the time of initial impact. It consists of diffuse axonal injury and focal contusions. It is not treatable and can only be prevented, e.g. by wearing seat belts and crash helmets.

Secondary Injury

It is the additional insult imposed on normal tissue following primary injury (Box 17.1). The focus of medical management is to prevent the secondary damage.

Box 17.1: Causes of secondary brain damage

• Hypotension • Hypoxia • Hyperthermia • Convulsions

• Raised intracranial pressure • Hyperglycemia

MECHANISMS OF HEAD INJURY • Closed injury: Due to blunt trauma.

• Open injury: Due to penetrating trauma, there is communication between intradural contents and atmosphere.

• Acceleration/Deceleration injuries: Due to mass movement of brain within closed cranial cavity. • ‘Coup’ injury: Brain injury occurring at the site of

blow.

• ‘Contre-coup’ injury: Injury to the brain surface opposite to the site of blow.

CLASSIFICATION OF HEAD INJURY

Anatomically, head injury can be classified starting from skin and going to the brain (Box 17.2).

Box 17.2: Classification of head injury

Scalp Laceration, contusion

Skull Fracture (simple, comminuted,

depressed, compound)

Dura Laceration

Brain

Primary injury: Diffuse axonal injury, concussion, contusion, laceration

Secondary injury: Edema, ischemia, hematoma, coning, infection, epilepsy

Blood vessels Extradural, subdural, intracerebral or intraventricular bleed

Supra/Infra-tentorial bleed CSF CSF rhinorrhea/otorrhea

Infection (meningitis) Obstruction (hydrocephalus) Cranial nerves Avulsion, compression

Associated injuries To eye, ear, paranasal sinuses, cervical spine

SCALP LACERATION

• It causes profuse bleeding because of:  Rich vascularity

 Blood vessels lie in dense fibrous layer superficial to epicranial aponeurosis and remain open once transected.

• In infants, scalp bleeding may cause hypovolemic shock.

• The deep lacerations in the scalp should always be palpated with gloved finger for any evidence of depressed fracture.

• The scalp laceration should be repaired as follows:-  Shaving of hair adjacent to wound.

 Apply soap on adjoining hair so that they get matted and do not fall in clean area.

 Clean the wound.

 Intradermal injection of 1% lignocaine for local anesthesia.

 Trimming of devitalized skin tags.

 In case of fresh bleeding, apply artery forceps on galea deep to artery and evert skin edges.  Apply interrupted skin stitches including a bite of

galea so as to control bleeding.

• Although rare, infection can occur deep to galea and it spreads rapidly due to presence of loose areolar tissue. Infection can reach intracranial sinuses through emissary veins. Osteomyelitis of skull is associated with subperiosteal swelling and edema of scalp called as ‘Potts’ puffy tumor (Box 17.3A). SKULL FRACTURES

Head injury can cause following types of skull fractures:- i. Simple linear fracture: It is the most common type of fracture and indicates severe head injury. A linear fracture of squamous temporal bone may lacerate middle meningeal artery and can cause extradural hematoma. Such patient should be hospitalized and closely observed for 48 hours. A

linear fracture on skull X-ray can be confused with vascular markings and suture lines.

ii. Depressed fracture: It is considered significant if on skull X-ray/CT scan, degree of depression is greater than depth of inner table of skull (Fig. 17.1). The complications likely to be seen in depressed fracture are shown in Box 17.3B.

In infants and children, depressed fracture is seen as concave depression of the skull and is called as Pond fracture (Figs 17.2A and B).

In compound depressed fracture causing dural tear, there is risk of CSF leak and air entering into the cranial cavity (pneumocranium) (Fig. 17.3). Here, the scalp wound should be debrided, bone fragments elevated and dural tear repaired. iii. Base of skull fracture: It is usually not evident on

routine skull X-ray and is diagnosed on clinical grounds.

Anterior fossa fractures present with:

• CSF rhinorrhea—if nasal discharge contains glucose, then the fluid is CSF and not the mucin.

Fig. 17.1: CT scan of the head showing

depressed fracture of skull

Box 17.3B: Complications of depressed fracture

• Dural tear • Pneumocranium • Intracranial hematoma

• Infection (meningitis) in compound fracture • Epilepsy

• Cosmetic deformity

• Raised intracranial pressure (due to pressure on venous sinuses)

Box 17.3A: Pott’s puffy tumor

• Subperiosteal infection of vault.

• Cause—osteomyelitis of skull, infected subperiosteal hematoma.

• Dumb bell abscess—pus in subperiosteal space and extradural space communicating with each other. • Pitting edema of scalp.

• Severe headache, vomiting, blurred vision. • CT scan is diagnostic.

• Treatment:

Burr hole and pus drainage. Antibiotics.

• ‘Raccoon’ or ‘panda’ eyes—there is periorbital hematoma limited to orbital margin. It indicates subgaleal hemorrhage that tracks down in eyelids (Fig. 17.4). Also there is subconjunctival hemorrhage extending beyond posterior limit of sclera indicating bleed tracking down from orbital cavity.

• I, III, IV and V cranial nerves may be involved. Middle fossa fractures present with:

• CSF otorrhea.

• VII and VIII cranial nerve palsy. Posterior fossa fractures present with:

• Battle’s sign—bruising over the mastoid (behind the ear) that develops 24-48 hours after injury.

• IX, X and XI cranial nerves may be involved. In base of skull fractures, there is potential risk of meningitis due to CSF leak, so prophylactic antibiotics should be given.

BRAIN INJURY

It can be primary or secondary brain injury.

Primary Brain Injury

It is the injury occurring at time of impact. The various types are:

a. Diffuse axonal injury: It is due to shearing at junction of grey matter with white matter. Its severity may

Fig. 17.2A: Pond fracture of skull in an infant

Fig. 17.2B: X-ray skull showing Pond depressed fracture

Fig. 17.3: CT scan head showing massive pneumocranium

of anterior cranial fossa