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These are summarized in Table 24 7 along with comments about treatment Increased intracranial pressure may result from ventilatory obstruction, abnormal neck position, seizures, dilutional hyponatremia, or cerebral edema; an intracranial hematoma requiring surgical evacuation may also be responsible Other measures that may be necessary to reduce intracranial pressure include induced hyperventilation, intravenous mannitol infusion, and intravenous furosemide; corticosteroids provide no benefit in this context
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HEAD INJURY
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Trauma is the most common cause of death in young people, and head injury accounts for almost half of these traumarelated deaths The prognosis following head injury depends on the site and severity of brain damage Some guide to
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Table 24 7 Acute cerebral sequelae of head injury
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Sequelae Concussion Clinical Features Transient loss of consciousness with bradycardia, hypotension, and respiratory arrest for a few seconds followed by retrograde and posttraumatic amnesia Occasionally followed by transient neurologic deficit Loss of consciousness longer than with concussion May lead to death or severe residual neurologic deficit Headache, confusion, somnolence, seizures, and focal deficits occur several hours after injury and lead to coma, respiratory depression, and death unless treated by surgical evacuation Similar to epidural hemorrhage, but interval before onset of symptoms is longer Treatment is by surgical evacuation Generally develops immediately after injury Clinically resembles hypertensive hemorrhage Surgical evacuation is sometimes helpful Pathology Bruising on side of impact (coup injury) or contralaterally (contrecoup injury)
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Cerebral contusion or laceration Acute epidural hemorrhage Acute subdural hemorrhage Cerebral hemorrhage
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Cerebral contusion, edema, hemorrhage, and necrosis May have subarachnoid bleeding Tear in meningeal artery, vein, or dural sinus, leading to hematoma visible on CT scan Hematoma from tear in veins from cortex to superior sagittal sinus or from cerebral laceration, visible on CT scan Hematoma, visible on CT scan
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2 Scalp Injuries & Skull Fractures
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Scalp lacerations and depressed or compound depressed skull fractures should be treated surgically as appropriate Simple skull fractures require no specific treatment The clinical signs of basilar skull fracture include bruising about the orbit (raccoon sign), blood in the external auditory meatus (Battle s sign), and leakage of cerebrospinal fluid (which can be identified by its glucose content) from the ear or nose Cranial nerve palsies (involving especially the first, second, third, fourth, fifth, seventh, and eighth nerves in any combination) may also occur If there is any leakage of cerebrospinal fluid, conservative treatment, with elevation of the head, restriction of fluids, and administration of acetazolamide (250 mg four times daily), is often helpful; but if the leak continues for more than a few days, lumbar subarachnoid drainage may be necessary Antibiotics are given if infection occurs, based on culture and sensitivity studies Only very occasional patients require intracranial repair of the dural defect because of persistence of the leak or recurrent meningitis
General Considerations
While spinal cord damage may result from whiplash injury, severe injury usually relates to fracture-dislocation causing compression or angular deformity of the cord either cervically or in the lower thoracic and upper lumbar regions Extreme hypotension following injury may also lead to cord infarction
Clinical Findings
Total cord transection results in immediate flaccid paralysis and loss of sensation below the level of the lesion Reflex activity is lost for a variable period, and there is urinary and fecal retention As reflex function returns over the following days and weeks, spastic paraplegia or quadriplegia develops, with hyperreflexia and extensor plantar responses, but a flaccid atrophic (lower motor neuron) paralysis may be found depending on the segments of the cord that are affected The bladder and bowels also regain some reflex function, permitting urine and feces to be expelled at intervals As spasticity increases, flexor or extensor spasms (or both) of the legs become troublesome, especially if the patient develops bed sores or a urinary tract infection Paraplegia with the legs in flexion or extension may eventually result With lesser degrees of injury, patients may be left with mild limb weakness, distal sensory disturbance, or both Sphincter function may also be impaired, urinary urgency and urgency incontinence being especially common More particularly, a unilateral cord lesion leads to an ipsilateral motor disturbance with accompanying impairment of proprioception and contralateral loss of pain and temperature appreciation below the lesion (Brown-S quard syndrome) A central cord syndrome may lead to a lower motor neuron deficit and loss of pain and temperature appreciation, with sparing of posterior column functions A radicular deficit may occur at the level of the injury or, if the cauda equina is involved, there may be evidence of disturbed function in several lumbosacral roots
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