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INDIAN DENTAL ACADEMY Leader in continuing dental education

INTRODUCTION Head injury is the major cause of preventable death in the world in adults under 45 years and in those who survive a significant head injury, a leading cause of chronic disability. Most head injuries occur following falls, vehicular road accidents, pedestrian road accidents and assaults.

AIM To prevent or reduce the number of head injuries suffered. To provide optimum care for those unfortunate enough to suffer a head injury, preventing secondary brain injury from further compounding primary brain injury. To produce an optimum environment in which rehabilitation from head injury can occur.

SEVERITY OF HEAD INJURY The severity of head injury is usually classified according to the best post-resuscitation GCS. Minor head injury

GCS score 15

Mild head injury

GCS score 13 – 14

Severe head injury GCS score 3 – 8




IMPORTANCE OF GCS Prior to the development of GCS a series of loosely defined terms such as obtunded, lethargy, stupor and coma were employed to categorize the degree of unconsciousness. The development of the GCS permitted a reliable and reproducible assessment, with little interobserver variability across all classes of healthcare workers.

HEAD INJURY It can be classified into: Scalp lacerations Skull fractures 

simple linear fracture

depressed skull fracture

base of the skull fracture

 Brain injury 

Primary brain injury

Secondary brain injury

DEPRESSED SKULL FRACTURES Usually the result of blunt trauma If pericranium breached technically compound Surgery undertaken to prevent the risk of infection, to alleviate the mass effect and for cosmetic purposes. Contaminated wounds require extensive debridement, a duraplasty and irrigation before closure followed by course of I.V antibiotics.

BASE OF THE SKULL FRACTURES Ant. fossa fractures present with subconjunctival hematomas, anosmia, epistaxis and CSF rhinorrhea and may occasionally be assoc. with carotico-cavernous fistulae.

BASE OF THE SKULL FRACTURES Middle cranial fossa fractures present with CSF otorrhea or rhinorrhea, heamotympanum, ossicular disruption, battle sign or VII and VIII nerve palsies.

BRAIN INJURY Primary brain injury is that which occurs at the time of injury and is regarded as irreversible. Secondary brain injury occurs following the primary insult Mechanisms of secondary brain injury are : Hematoma formation Brain swelling and cerebral herniation Cerebral infection Extracranial complications such as hypotension, hypoxia and metabolic complications leading to cerebral ischemia.
















CEREBRAL CONCUSSION It is a clinical diagnosis and is manifested by temporary dysfunction that is most severe following the injury and resolves after a variable period. May be accompanied by Bradycardia, hypotension and sweating. Sometimes loss of consciousness. Amnesia for the event. Varying degrees of temporary lethargy, irritability and memory dysfunction.

CEREBRAL CONTUSION Cerebral contusions result from trauma to the brain causing localized hemorrhagic swelling. Usually found on the undersurface of frontal and temporal lobes when the brain is damaged by the rough bony edges found in the region of the ant. and middle cranial fossa. May swell over days leading to raised ICP or bleeding into a contusion may lead to intracranial hematoma.

DIFFUSE AXONAL INJURY Occurs as a result of mechanical shearing following deceleration, causing disruption and tearing of axons, esp. at grey / white matter interface. Severity may vary from mild confusion to coma and even death.

SECONDARY BRAIN INJURY Extradural hematoma Usually occurs as a result of squamous temporal bone fractures with laceration of MMA. Can also arise from fractured bone edges and rarely from the dural venous sinuses. Present as a convex configuration on the CT.

SECONDARY BRAIN INJURY Subdural hematoma Most common intracranial mass lesions resulting from head injury. Torn bridging veins draining blood from the cortex or dura. Cortical lacerations or bleeding from the dural venous sinuses. Usually present with multiple bleeding points.

SECONDARY BRAIN INJURY Chronic subdural hematoma Origin is uncertain, most probably arises following minor and often repeated insignificant head injury. With time the vol. of the hematoma enlarges, either through repeated episodes of bleeding or bec. the high osmotic potential of the blood attracts water.

SECONDARY BRAIN INJURY Brain swelling May be caused by an increase in the brain water content, as occurs in cerebral edema, or incd. blood due to cerebral hyperemia or dev. of an intracerebral mass lesion.

Brain herniation The skull is divided into various compartments by the infolding of the dura to form the cerebral falx and cerebral tentorium. A mass lesion such as intracerebral / extradural hematoma creates a pressure gradient across the compartments and leads to herniation of brain.

SECONDARY BRAIN INJURY Cerebral infection Compound fractures represent a potential route of infection through which organisms may track and cause meningitis or later cerebral abscess.

Cerebral ischemia This is common after severe head trauma and is caused by a combination of either hypoxia or impaired cerebral perfusion.

CLINICAL EXAMINATION Full examination of the patient has to be delayed until the immediate threats to life have been countered. Level of response should now be reassesed. Pupils : The vital sign, an ipsilateral dilating pupil indicates rising intracranial pressure from a compressing supratentorial lesion. Unilateral dilation may be caused bv direct injury to the eye, optic nerve damage or oculomotor nerve compression.

CLINICAL EXAMINATION If a head injured patient is admitted with equal reacting pupils and then develops dilatation of a pupil, provided there is also evidence of a deterioration in the level of response, a compressing extracerebral hematoma may be incriminated.

Direct injury to the third nerve is the usual cause of a unilateral dilated pupil immediately following head injury.

CLINICAL EXAMINATION MOTOR FUNCTION Absence of movement, either spontaneous or on painful stimulation, of either lower limb while there is movement in both upper limbs strongly suggests a spinal lesion. Hemiparesis is usually attributable to direct injury to the cerebral hemisphere. When it is accompanied by a deteriorating level of response with or without a dilating pupil, such hemiparesis may be caused by a compressing extracerebral haematoma.

CLINICAL EXAMINATION Other vital functions: The pulse, blood pressure, the rate and character of the breathing, and the temperature must all be noted. Progressive slowing of the pulse, a rising blood pressure and slowing of the respiratory rate are classic indicators of a rising intracranial pressure. Slowing of the pulse is the first of these three signs, with respiratory slowing occurring last.

CLINICAL EXAMINATION The head and face : It is important to note any areas of bruising, laceration and swelling as these may help to lateralise and localise an ensuing extracerebral haematoma. Epistaxis may indicate a fracture of the floor of the anterior cranial fossa and there mav be associated subconjunctival haemorrhage, Bleeding from the ear is usually indicative of a fractured petrous bone.

CLINICAL EXAMINATION A bruise may become apparent, 24-48 hours later, over the mastoid process. This is Battle's sign, indicating a fracture involving the petrous bone. Leakage of CSF, with rhinorrhoea and/or otorrhoea, suggests not only a fracture of the base of the skull but also a tear of the overlying dura. Meningitis is a possible consequence of this injury.

INITIAL MANAGEMENT Ensure adequate resuscitation of the patient. Airway control, ventilation, adequate respiration and circulation should be established prior to dealing with the head injury. Following resuscitation and stabilization of the patient, the history of the injury should be established.

INITIAL MANAGEMENT Important points to determine from history are: Period of loss of consciousness. Period of post-traumatic amnesia. Cause and circumstances of injury. Presence of headache and vomiting. Whether a seizure has occurred and the presence or absence of a focal neurological deficit.

INITIAL MANAGEMENT Important to determine the initial GCS, pupillary reaction and size, whether the patient’s condition is improving or deteriorating, BP and pulse rate and any associated injuries.

MANAGEMENT The overriding aim of the management of a patient who has suffered a head injury is to minimize the morbidity and mortality related to secondary brain injury. This requires rapid evaluation and triage of patients presenting with head injuries.


MANAGEMENT Mass lesions within the skull, such as intracranial hematomas, may cause a rise in the ICP and therefore reduction in cerebral perfusion, may also cause cerebral herniation. Treatment for raised ICP should be directed at removing the cause of raised ICP, IC vol. can be mechanically decd. by removing an intracranial mass or hematoma, reducing intracranial venous blood vol. by facilitating venous outflow via jugular veins, ventilating to bring PCO2 4 – 4.5 or by draining CSF thru a ventriculostomy.

MANAGEMENT Steroids are effective in decreasing ICP resulting from vasogenic edema (dexamethasone 4mg 6 hourly). They act by stabilising the blood brain barrier and reducing the oxygen radical injury. Frusemide reduces ICP by reducing cerebral edema and CSF production.

MANAGEMENT Mannitol, an osmotic dehydrating agent (1gm/kg 4-6 hourly) works by drawing water from parts of the brain with an intact BBB. Recurrent early seizures are managed with a loading dose of an anticonvulsant, usually valproate or phenytoin, followed by regular oral or I.V. doses. Following control of early seizures, anticonvulsant medications are given for about 6 weeks and the dose tailed of thereafter.

Intraop. appearance of extradural hematoma following craniotomy

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