HEAD INJURY Brain oxygen consumption is about 3

HEAD INJURY

Brain oxygen consumption is about 3. 5 ml 100 g -1 min -1 The brain relies on blood borne glucose for 90% of its energy requirements Normal cerebral blood flow is approximately 55 ml 100 g -1 min -1.

PRIMARY BRAIN INJURY It occcurs at the time of impact It includes injuries such as brainstem & hemi spheric contusions, diffuse axonic injuries & cortical lacerations SECONDARY BRAIN INJURY Occurs at some time after the moment of impact Often preventable Mainly caused by hypoxia, hypotension, raised ICP, reduced cerebral perfusion pressure & pyrexia

CLASSIFICATION OF HEAD INJURIES Based on Glasgow Coma Scale Best eye response There are 4 grades starting with the most severe: No eye opening Eye opening in response to pain. (Patient responds to pressure on the patient’s fingernail bed; if this does not elicit a response, supraorbital and sternal pressure or rub may be used. ) Eye opening to speech. (Not to be confused with an awaking of a sleeping person; such patients receive a score of 4, not 3. ) Eyes opening spontaneously

Best verbal response There are 5 grades starting with the most severe: No verbal response Incomprehensible sounds. (Moaning but no words. ) Inappropriate words. (Random or exclamatory articulated speech, but no conversational exchange) Confused. (The patient responds to questions coherently but there is some disorientation and confusion. ) Oriented. (Patient responds coherently and appropriately to questions such as the patient’s name and age, where they are and why, the year, month, etc. )

Best motor response (M) There are 6 grades starting with the most severe: 1) No motor response 2) Extension to pain (abduction of arm, external rotation of shoulder, supination of forearm, extension of wrist, decerebrate response) 3) Abnormal flexion to pain (adduction of arm, internal rotation of shoulder, pronation of forearm, flexion of wrist, decorticate response) 4) Flexion/Withdrawal to pain (flexion of elbow, supination of forearm, flexion of wrist when supra-orbital pressure applied ; pulls part of body away when nailbed pinched) 5) Localizes to pain. (Purposeful movements towards painful stimuli; e. g. , hand crosses mid-line and gets above clavicle when supra-orbital pressure applied. ) 6) Obeys commands. (The patient does simple things as asked. )

Based on this it is classified as : – ü MINOR HEAD INJURY : GCS 15 with no loss of consciousness ü MILD HEAD INJURY : GCS 14 or 15 with LOC ü MODERATE HEAD INJURY : GCS 9 to 13 ü SEVERE HEAD INJURY : GCS 3 to 8

CLASSIFICATION (CONT) 2) BLUNT VS PENETRATING Penetrating injuries are further classified into ü Low velocity such as stab injury ü High velocity such as gun shot injury

CLASSIFICATION (CONT) 3)MORPHOLOGICAL a) Skull fractures maybe divided into: ü Vault or ü Base of skull fractures. Vault fractures maybe open or closed, linear or communited, depressed or non depressed Intracranial haematomas maybe: 1) Extradural 2) Subdural, 3) Sub arachnoid 4) Intracerebral

MECHANISM 1. 2. 3. 4. 5. 6. 7. Distortion of the brain Mobility of the brain in relation to the skull Configuration of the interior of the skull Deceleration & acceleration injuries Cerebral concussion Cerebral contusion Cerebral laceration

DISTORTION OF THE BRAIN Brain is a soft structure, has mobility & distorts readily This distortion & mobility is accentuated by CSF & vascular components Any impact creates shearing forces in the brain causing damage to the neurons, supporting tissues & blood vessels This leads to loss of consciousness & focal neurological defects

MOBILITY OF THE BRAIN Causes cerebral damage & bleeding in dural spaces from torn vessels in the dura, commonly the veins In old age the brain shrinks, as a result of which ‘mobility’ of the brain increases favouring rupture of the veins which cross the subdural space

CONFIGURATION OF THE INTERIOR OF SKULL Damage is less severe over the smooth areas as compared to the rough So the damage is severe over anterior cranial fossa, over the falx & over the tentorium DECELERATION & ACCELERATION INJURIES Deceleration injury occurs when the moving head strikes an immovable object (RTA’s) Acceleration injury when stationary skull is struck by moving object (like an assault)

CEREBRAL CONCUSSION It is the slight distortion causing temporary physiological changes leading to transient loss of consciousness with complete recovery CEREBRAL CONTUSION It is more severe degree of damage with bruising & cerebral edema leading to diffuse or localised changes CEREBRAL LACERATION It is the tearing of the brain surface with collection of blood in different places with displacement of dural parts

EFFECTS OF BRAIN INJURIES 1) BRAIN EDEMA: accumulation of fluid, both intracellular & extracellular. Due to the congestion & dilatation of blood vessels 2) BRAIN NECROSIS: due to haemorrhagic infarction 3) EXTRADURAL HAEMATOMA: occurs usually in the temporo-parietal region commonly due to tear in middle meningeal veins & middle meningeal artery

CONTD……. 4) SUBDURAL HAEMATOMA: due to tear of veins between cerebrum & dura due to shearing forces 5)INTRACEREBRAL HAEMATOMA : occurs in different parts of the cerebrum 6) BRAIN ISCHAEMIA: due to increased pressure. This leads to alteration in the perfusion of brain which itself aggravates the ischaemia 7)COUP INJURY occurs on the side of the blow to the head. Contre-coup injury occurs on the side opposite to the side of the blow on th head

9) CONING It is due to raised intracranial pressure causing either: 1) Herniation of contents of supratentorial compartment through the tentorial hiatus 2) Herniation of the contents of infratentorial compartment through the foramen magnum 10) Respiratory failure 11)Fluid electrolyte imbalance 13)Hyperpyrexia 14) Convulsions 15) CSF rhinorrhea

CLINICAL APPROACH 1) 2) 3) ü ü ü ü ü Detailed history of injury History of alcohol intake- alcohol intake mimics head injury & may mask the features of head injury Neurological assessment by: - Level of consciousness Glasgow coma scale Pupillary reaction to light Pulse Temperature Blood pressure Respiratory rate Reflexes Limb movements

4) Status & protection of airway 5)General assessment of other injuries 6)Presence of any scalp haematoma, fractures of skull bone 7)Any blood from nose, ear, CSF rhinorrhea or CSF otorrhea

INVESTIGATIONS X-Ray Skull: to look for fracture, relative position of the calcified pineal gland, presence of intracranial air Serum electrolyte measurement Blood grouping & cross matching CT scan: To look for cerebral edema, hematomas, midline shift, fractures, ventricles, brain stem injury Carotid arteriography Usg abdomen Monitoring intracranial pressure

TREATMENT GENERAL 1) Environment-best managed in a neurointensive setting. Patient should be positioned head up 30 degrees 2) Protection of airway using mouth gag, endotracheal intubation, tracheostomy 3) Circulation & cerebral perfusion: ü Hypotension sits along hypoxia as a major cause of secondary brain injury ü Cerebral perfusion pressure= mean arterial pressueintracranial pressure ü CPP= MAP – ICP ü If ICP is 20 mmhg, it follows that MAP should be > 85 mmhg

Throat suction, bladder & bowel care Nasal oxygen or ventilator support IV fluids initially followed by Ryles tube feeding Electrolyte maintainence

CONTROL OF ICP Normal ICP is 8 -12 mm. Hg. A sustained ICP of >20 mm. Hg is associated with poor outcome. Measures include: ü ü ü Sedation with or without muscle relaxants Use of diuretics-frusemide, mannitol Thermoregulation as pyrexia will increase the brain metabolic rate & should be avoided Use of barbiturates like thiopentone to reduce brain metabolic rate Maintaining fluid & electrolyte balance Seizure control

DRUGS Analgesics & anticonvulsants like phenytoin or phenobarbitone is started Diuretics are given to reduce cerebral edema- either 20% mannitol, 200 ml iv 8 th hourly or frusemide 40 mg IV 8 th hourly. It should not be given in case of intra cranial hematoma Antibiotics like penicillins, ampicillin are given to prevent onset of meningitis Cortico steroids, either dexamethasone or betmethasone is used commonly

INDICATIONS FOR SURGERY Acute extradural hematoma Acute subdural hematoma Depressed skull fracture

MANAGEMENT OF MILD HEAD INJURY (GCS 14 -15) These patients are usually discharged from emergency dept based on the following criteria: ü GCS of 15/15 No focal neurological deficit Patient must not be under the influence of alcohol Patient must be accompanied by a responsible adult Verbal & written head injury advice must be given to the patient ü ü

Some patients with mild head injury are at significant risk of intracranial hematoma & require CT scan. The basis for selection of patient for CT scan is the NICE guidelines: ü GCS <13 at any point GCS 13 or 14 at 2 hours Suspected open, depressed or basal skull fracture Seizure Vomiting > 1 episode ü ü ü ü URGENT CT IF NONE OF THE ABOVE BUT: Age > 65 years Coagulopathy (e. g on warfarin) Dangerous mechanism of head injury (CT within 8 hrs) Antegrade amnesia

COMPLICATIONS OF HEAD INJURY Brainstem injury – due to coning Compression over cerebellum & medulla CSF rhinorrhea- due to communication between intracranial cavity & nose Meningitis Pituitary damage & endocrine failure Aerocele CSF otorrhea Depressed fractures

ACUTE EXTRADURAL HAEMORRHAGE It is the collection of blood in the extra dural space between the dura & the skull Most common site is temporo-parietal region It can be unilateral or bilateral Most commonly associated with skull fracture Vessels commonly involved are: 1) Middle meningeal veins 2) Anterior branch of middle meningeal artery 3) Posterior branch of middle meningeal artery

PATHOLOGY H/o fall or RTA Fracture of the thin temporal bone Tear of vessels Bleeding initially outward towards the scalp & under temporalis muscle Formation of hematoma Gradual stripping of dura from the skull In 6 -12 hrs extra dural hematoma occurs which raises the intracranial pressure

Coning of the supratentorial content(uncus of temporal lobe) through tentorial hiatus Shift of midbrain towards opposite side which gets injured by sharp edge of tentorial cerebelli Corticospinal tract before decussation on opposite side gets injured So hemiparesis & pupillary changes occur on the same side of hematoma This is called KERNOHANS EFFECT

Immediately after the injury there is transient loss of consciouness & the patient soon becomes normal Later after 6 -12 hours, he again falls ill & the condition deteriorates. This is the time taken to develop raised intracranial pressure, coning, & its effects. This crucial time gap which is unnoticed & often missed is called lucid interval

CLINICAL FEATURES H/O transient loss of consciousness Patient soon regains consciousness & again after 612 hours starts deteriorating(lucid interval) Confusion, irritability, drowsiness, hemiparesis on the same side of injury Initially pupillary constriction & later pupillary dilatation occurs on the same side, finally becomes totally unconscious –Hutchinsonian pupils Death can occur immediately Features of raised intracranial pressure like high blood pressure, bradycardia, vomiting is also seen

INVESTIGATIONS X-ray skull may show fracture of the temporal bone Electrolyte estimation CT head is diagnostic. Extra dural hematoma shows biconvex lesion Craniotomy is done & cranial flaps are raised. The dura is opened & the clot is evacuated. The dura is fixed to galea using interrupted sutures- hitch stitches Antibiotics & anticonvulsants are given post operatively

TREATMENT Earliest surgery & evacuation is needed 5 cm vertical incision in parietal region above the zygoma Galea is incised. Skull is opened using perforator & burr Meninges are kept aside Black currant jelly clot is evacuated Bleeding vessels are cauterized Dural hitch stitch are placed Opposite side if needed is evacuated Antibiotics, anticonvulsants, analgesics

CEREBRAL CONTUSION It is common in head injury It results from the brain being damaged by impacting against the skull either at the point of impact(coup) or on the other side of the head(contre coup) Also when the brain slides forwards & backwards over the ridged cranial fossa floor(most often affecting the inferior frontal lobes & temporal lobes

CT APPEARANCE Cerebral contusions appear heterogenous with mixed areas of high & low density There maybe an associated mass effect A contusion maybe described as an intracerebral hematoma if lesion contains large amount of fresh hemorrhage & therefore appears uniformly hyperdense

TREATMENT Cerebral contusions rarely require immediate surgical treatment A head injured patient with cerebral contusions must be admitted for observation as these lesions tend to mature & expand for 48 to 72 hours following injury Sometimes they may require delayed surgical evacuation to reduce mass effect.