Management of Intracranial Injuries

• Basilar Skull Fracture
• Usually suggested by Battle's sign, raccoons eyes, or CSF leak
• Frequently not evident on skull films or head CT
• Significant if accompanied by CSF rhinorrhea/otorrhea, cranial nerve disruption, pneumocephalus, vascular disruption
• Most CSF leaks seal without intervention within several days
• Prophylactic antibiotics are controversial if patient is leaking CSF; may only select out resistant organisms
• If leak persists, surgical repair may be needed
• Occasionally patients develop delayed peripheral VIIth nerve palsy, which generally resolves spontaneously
• Cerebral contusion
• Hemorrhagic bruise to cortical tissue
• Uncontrasted head CT shows parenchymal usually spotty areas of increased density
• Frequently "blossom" (enlarge) over first 24 to 48 hours, and are associated with surrounding brain edema
• Steroids have no benefit in this type of edema
• Large contusions with mass effect require surgical intervention
• Increased ICP is frequently seen
• Serve as a potential seizure focus, so patients should be prophylactically loaded with anticonvulsant
• Depressed skull fracture
• Generally, if the fracture is depressed further than a full thickness of the skull, there is evidence of dural laceration, or creates a cosmetic defect, it needs to be elevated
• Fractures over dural sinuses carry risk of hemorrhage if manipulated and are usually not corrected
• Patients with open fractures should be placed on prophylactic abx (naf or vanco and gent)
• Length of abx therapy depends on amount of contamination and time to presentation, but is generally 1 week (not necessarily entirely IV)
• Bone from highly comminuted or contaminated fractures is generally removed
• Cranioplasty for repair can be performed 6 months later
• Diffuse malignant cerebral edema
• Massive, usually irreversible, cerebral swelling seen 24 to 72 hrs after head injury
• Generally seen in the pediatric population
• Does not require a massive head injury -even relatively minor injuries can progress in this fashion
• Even patients with good mental status initially can develop
• In patients with declining neurologic status, must consider this diagnosis and place ICP monitor early
• Diagnosis:
• Uncontrasted head CT may be normal, but usually shows diffuse cerebral swelling with loss of basal cisterns, compressed gyri, and small ventricles
• Increased ICP by intracranial pressure monitor
• Treatment: See section on treating increased ICP
• Epidural hematoma
• History: Classic triphasic presentation – initial LOC followed by lucid interval, then progressive obtundation – is only seen in 10%
• Occur in approximately 2% of severe head injuries
• Etiology:
• Usually arterial in origin – laceration of a branch of the middle meningeal
• Almost always associated with a skull fracture
• Occasionally associated with a tear of a venous sinus
• Location:
• 70% lateral, 10% frontal, 5% posterior fossa, 5% occipital
• Posterior fossa more common in children and elderly who tend to fall backwards
• Diagnosis: Head CT shows lens-shaped biconvex hyperdense extra-axial collection
• Treatment: Emergent surgical decompression
• Gunshot wound to the head
• Frequently fatal injuries, especially if projectile traverses both hemispheres or enters ventricle
• Injury is frequently followed by massive cerebral edema
• Surgical debridement may be needed in selected cases (i.e., fragments confined to single non-dominant hemisphere or single lobe)
• Angiogram should be obtained to rule out arterial injury
• Seizures frequent in survivors
• Presenting neurologic status is best indicator of prognosis
• <20% mortality in those awake/alert at presentation
• 90-100% mortality in those unresponsive at presentation
• Traumatic subarachnoid hemorrhage
• Trauma is the most frequent cause of subarachnoid hemorrhage
• Location over the cerebral hemispheres
• Diagnosis: Head CT shows gyri form bright attenuation
• Rarely leads to vasospasm since basal cisterns are not involved
• Can lead to delayed hydrocephalus weeks to months after injury
• Resolves without intervention
• Subdural hematoma
• May be acute, subacute, chronic, or any combination of these
• History:
• Acute: Declining LOC with hemiparesis
• Chronic: HA, seizures, slowly declining mental status, with or without focal neuro deficit
• Occurs in approximately 5% of significant head injuries
• 15-20% are bilateral
• Etiology:
• Venous origin, usually tear of a bridging cortical vein
• Chronic clots form subdural neomembranes with marked vascularization susceptible to rehemorrhage spontaneously or with even minor trauma
• Diagnosis: Head CT shows extra-axial collection following contours of brain
• Acute: hyperdense
• Subacute: isodense (mass effect makes it evident)
• Chronic: hypodense
• Treatment: Surgical evacuation of clot
• Acute clots are gelatinous and can only be removed by formal craniotomy
• Chronic clots have liquified and can frequently by removed by burr hole or twist drill
• Load with anticonvulsant given risk for seizures
• Outcome:
• 30-50% mortality
• Poor prognostic factors: advanced age, unconscious at time of injury, delay in treatment
• Mortality increases to 90% if surgical decompression delayed greater than 4 hours from injury