4th lecture - Craniocerebral Traumas

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Craniocerebral Traumas:

Craniocerebral Traumas György T. Szeifert, M.D., Ph.D. Department of Traumatology, Semmelweis University, Budapest 2008.09.30

Traumatic brain injury:

Traumatic brain injury Primary : penetrating injuries through the cranial bone can cause direct brain damage locally, or at the opposite (contralateral) side (contrecoup) Secondary : brain edema, extradural hematoma, subdural hematoma (brain compression)

Consequences of cranial traumas:

Consequences of cranial traumas Brain edema Skull fractures Extradural (epidural) hematomas Subdural hematomas Intracerebral hematomas Subarachnoid hemorrhage

Clinical presentation of brain damage:

Clinical presentation of brain damage Cerebral concussion: transient loss of consciousness following a blow to the head, quick recovery, amnesia Cerebral contusion: morphological damage to cerebral tissue from focal bleeding or edema, slower recovery, may be incomplete with neurological deficit Cerebral compression: bleeding into the skull spaces (epidural, subdural, subarachnoid, intracerebral, intraventricular)

Signs and symptoms of head traumas :

Signs and symptoms of head traumas Galea lesions: bruising or laceration of the skin, scalp wounds, galeal hematomas Meningeal irritation: neck stiffness, Kernig´s sign Increasing intracranial pressure: headaches, nausea, vomiting, optic disc edema Impaired conscious level: amnesia, drowsy, reacts to movement, reacts to painful stimulus, no reaction Glasgow Coma Scale (GCS) Pupil differences, ocular movement disorders

Raised intracranial pressure:

Raised intracranial pressure Normal ICP < 10 mmHg Mild ICP increase 10-20 mmHg Moderate > 20 mmHg Severe > 40 mmHg « Monro-Kellie » doctrine: - rigid skull bone - CSF, blood, brain are incompressible, an increase in one constituent results in an increase in the intracranial pressure

Raised ICP: brain edema:

Raised ICP: brain edema Mechanism: - vasogenic: impairment of blood-brain barrier, fluid escapes to the extracellular space - cytotoxic: damage of cell metabolism, intracellular Na + increases, fluid accumulates within cells Signs and symptoms: meningeal irritation, headaches, nausea, vomiting, papilledema, impaired conscious level Treatment: - diuretics (Furanthral) - hyperosmotic infusions (Mannitol) - hyperventilation (drop in PCO2 >> vasoconstriction >> reduction in cerebral blood volume) - CSF drainage (ventricular puncture and CSF withdrawal) - barbiturate therapy (reduces neuronal activity and depresses cerebral metabolism) - steroids (cell membranes are stabilised >> decrease in perifocal peritumoral edema, no benefit in traumatic brain swelling)

Raised ICP: cerebral blood flow (CBF):

Raised ICP: cerebral blood flow (CBF) Systemic blood flow = blood pressure / vascular resistance CBF = cerebral perfusion pressure / cerebral vascular resistance Cerebral perfusion pressure = systemic blood pressure – ICP

Raised ICP: symptoms and signs :

Raised ICP: symptoms and signs Headaches Nausea, vomiting Optic disc swelling (papilledema) Pupil difference (tentorial herniation, irritation and compression of the III. nerve): pupils initially small (excitement), later dilated and fixed to light (palsy) Gaze disturbances (upward gaze is initially lost) Deterioration of conscious level (tentorial or tonsillar herniation >> compression of ascending reticular activating system in the brainstem and midbrain) Respiratory and circulatory irregularities, arrest Cushing-reflex: initial increase in blood pressure and a fall in pulse rate (bradycardia) associated with expanding intracranial mass

Conscious level assessment:

Conscious level assessment Historically used vague terms: - stupor, semicoma, deep coma Glasgow coma scale (GCS; 1974): - eye opening - verbal response - motor response

Conscious level assessment: Glasgow coma scale (GCS):

Conscious level assessment: Glasgow coma scale (GCS) Eye opening: spontaneous 4 to voice 3 to pain 2 none 1 Verbal response: orientated 5 confused 4 inappropriate words 3 incomprehensible sounds 2 none 1

Glasgow Coma Scale (GCS):

Glasgow Coma Scale (GCS) Motor response: obeys command 6 localizes pain 5 withdrow (pain) 4 flexion (pain) 3 extension (pain) 2 none 1

Glasgow Coma Scale (GCS):

Glasgow Coma Scale (GCS) Score - 5: 14-15 – alert, oriented - 4: 11-13 - drowsy - 3: 8-10 - stupor - 2: 5-7 – semicoma (reacts to pain) - 1: 3-4 – deep coma (no reaction to pain)

ICP monitoring:

ICP monitoring Mandatory at GCS 8 or less Types of ICP monitoring: - epidural - intraparenchymal - intraventricular (CSF drainage as well)

Management of raised ICP:

Management of raised ICP Conservative (non invasive): - Diuretics (Mannitol) - hyperventilation - barbiturate coma Operative (invasive): - ventricular puncture (CSF drainage, ICP monitoring) - evacuation of subdural, epidural or intracerbral hematomas (space-occupying lesions) - malignant i. c. hypertension (>40 Hgmm): decompressive craniectomy

Skull fractures:

Skull fractures Closed fractures: the scalp (skin and galea) intact Open fractures: penetration of skin and galea, open scalp wound (risk of infection) Linear fractures: no dislocation between fractured bony edges (usually single) Depressed fractures: dislocated bone fragments into the cranial space (single or multiple)

Skull fractures: diagnostic approach:

Skull fractures: diagnostic approach Examination of scalp wound (palpable bone fragments or foreign body) Skull X-ray: AP and lateral CT scan: bone window

Skull fractures: management:

Skull fractures: management Scalp wound: toilette, removal of foreign material, suture Linear fractures: conservative management Depressed fractures: operative treatment, elevation of dislocated bone fragments, fixation (suture, wire) Skull base fractures: usually conservative treatment (antibiotics, prevention of infection); permanent liquorrhoea needs CSF drainage (lumbar puncture), exploration, reconstructive operation

Skull fractures: complications:

Skull fractures: complications Early complications: extradural, subdural, intracerebral hematomas infection (meningitis, cerebral abscess) neurological deficit (palsy, speech arrest) conscious level deterioration Late (permanent) complications: amnesia personality changes liquorhoea epilepsy neurological deficit, disabilties

Cerebral concussion: management :

Cerebral concussion: management Skull X-ray, CT scan observation pain killers (headaches) diuretics

Cerebral contusion: management:

Cerebral contusion: management skull X-ray, CT scans (repeated controls) reduction of cerebral edema observation, GCS chart GCS 8 or less: ICP monitoring - epidural - intraparenchymal - intraventricular

Extradural (epidural) hematoma:

Extradural (epidural) hematoma Pathophysiological mechanism: - head injury, fracture of the temporal bone, rupture of the middle meningeal artery, arterial bleeding, rapidly growing hematoma, brain compression Symptoms: headache, nausea, vomiting Signs: meningeal irritation, focal neurological signs (localization), rapid deterioration of conscious level Diagnostic approach: skull X-ray: cranial fracture, bone displacement CT scan (bone window as well): fracture, lentil-shape hematoma, midline shift (position of the falx) Management: - urgent operation (craniotomy, evacuation of the hematoma, coagulation of the bleeding artery)

Subdural hematoma:

Subdural hematoma Pathophysiological mechanism: venous bleeding (head trauma, stretching and rupture of bridging veins, gradual subdural accumulation of blood) Forms: acut: severe skull injury, young adults, contusion and laceration of brain surface chronic: mild head trauma, occur predominantly in infancy and in the elderly, cerebral atrophy, alcoholism, coagulation disorder Presentation: slow, gradual evolution focal neurological signs (especially limb weakness) deterioration in conscious level, often with fluctuating course dementia Diagnostic approach: CT scan: subdural collection, midline shift (acut: hyperdens, chronic: isodense with capsule) Management: no midline shift: observation space occupying hematoma (midline shift): 1. burr holes + drainage (acut liquid hematomas without a capsule) 2. craniotomy and resection of the membrane + drainage (chronic collection with capsule)

Intracerebral hematoma :

Intracerebral hematoma Pathophysiological mechanism: hypertensive vasculopathy, (atherosclerotic wall changes, rupture of small perforating arteries) Presentation: focal neurological signes (limb weakness, speech problems) impairment of conscious level Diagnostic approach: CT scan: i.c. high density lesions Management: i.c. hematoma without a mass effect: conservative treatment (reduce perifocal edema, diuretics, ensure patent airway and adequate blood oxygenation) space-occupying hematoma: craniotomy + evacuation of hematoma stereotactic puncture + drainage (liquid hematomas) intraventricular hematoma: drainage + hematoma lysis (Urokinase)

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