Basilar Skull Fracture

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Classification and Treatment

As the treatment and prognosis of brain tumors depend on their histological type and degree of malignancy, the first step of management is tissue diagnosis (see Table 31, p. 377). The subsequent clinical course may differ from that predicted by the histological grade because of "sampling error" (i.e., biopsy of an unrepresentative portion of the tumor). Other factors influencing prognosis include age, the completeness of surgical resection, the preoperative and postoperative neurological findings, tumor progression, and the site of the tumor.

■ Incidence (adapted from Lantos et al., 1997)

The most common primary intracranial tumors in patients under 20 years of age are medullo-blastoma, pilocytic astrocytoma, ependymoma, and astrocytoma (WHO grade II); from age 20 to age 45, astrocytoma (WHO grade II), oligodendroglioma, acoustic neuroma (schwannoma), and ependymoma; over age 45, glioblastoma, meningioma, acoustic neuroma, and oligoden-droglioma. The overall incidence of pituitary tumors (including pituitary metastases), craniopharyngioma, and intracranial lymphoma and sarcoma is low.

The Karnofsky scale (Karnofsky et al., 1951) is a commonly used measure of neurological disability, e. g., due to a brain tumor. Its use permits a standardized assessment of clinical course.

The initial treatment is often neurosurgical, with the objective of removing the tumor as completely as possible without causing a severe or permanent neurological deficit. The resection can often be no more than subtotal because of the proximity of the tumor to eloquent brain areas or the lack of a distinct boundary between the tumor and the surrounding tissue. The overall treatment plan is usually a combination of different treatment modalities, chosen with consideration of the patient's general condition and the location, extent, and degree of malignity of the tumor.

Symptomatic treatment. Edema: The an-tiedematous action of glucocorticosteroids takes effect several hours after they are administered; thus, acute intracranial hypertension must be treated with an intravenously given osmotic agent (20% mannitol). Glycerol can be given orally to lower the corticosteroid dose in chronic therapy. Antiepileptic drugs (e. g., pheny-toin or carbamazepine) are indicated if the patient has already had one or more seizures, or else prophylactically in patients with rapidly growing tumors and in the acute postoperative setting. Pain often requires treatment (headache, painful neoplastic meningeosis, painful local tumor invasion; cf. WHO staged treatment scheme for cancer-related pain). Restlessness: treatment of cerebral edema, psychotropic drugs (levomepromazine, melperone, chlor-prothixene). Antithrombotic prophylaxis: Subcutaneous heparin.

Grade I tumors. Some benign tumors, such as those discovered incidentally, can simply be ob-served—for example, with MRI scans repeated every 6 months—but most should be surgically resected, as a total resection is usually curative. Residual tumor after surgery can often be treated radiosurgically (ifindicated by the histo-logical diagnosis). Pituitary tumors and craniopharyngiomas can cause endocrine disturbances. Meningiomas and craniopharyn-giomas rarely recur after (total) resection. Grade II tumors. Five-year survival rate is 50-80%. Complete surgical resection of grade II tumors can be curative. As these tumors grow slowly, they are often less aggressively resected than malignant tumors, so as not to produce a neurological deficit (partial resection, later resection of regrown tumor if necessary). Observation with serial MRI rather than surgical resection may be an appropriate option in some patients after the diagnosis has been established by stereotactic biopsy; surgery and/or radiotherapy will be needed later in case of clinical or radiological progression. Chemotherapy is indicated for unresectable (or no longer resectable) tumors, or after failure of radiotherapy

Grade III tumors. Patients with grade III tumors survive a median of 2 years from the time of diagnosis with the best current treatment involving multiple modalities (surgery, radiotherapy, chemotherapy). Many patients, however, live considerably longer. There are still inadequate data on the potential efficacy of chemotherapy against malignant forms of meningioma, plexus papilloma, pineocytoma, schwannoma, heman-giopericytoma, and pituitary adenoma. Grade IV tumors. Patients with grade IV tumors survive a median of ca. 10 months from diagnosis even with the best current multimodality treatment (surgery, radiotherapy, chemotherapy). The 5-year survival rate of patients with glioblastoma is no more than 5 %. PNET (including medulloblastoma) and primary cerebral lymphoma have median survival times of a few years.

Cerebral metastases: Solitary, surgically accessible metastases are resected as long as there is no acute progression of the underlying malignant disease, or for tissue diagnosis if the primary tumor is of unknown type. Solitary metastases of diameter less than 3 cm can also be treated with local radiotherapy, in one of two forms: interstitial radiotherapy with surgically implanted radioactive material (brachytherapy), or stereotactic radiosurgery. The latter is a closed technique, requiring no incision, employing multiple radioactive cobalt sources (as in the Gamma Knife and X-Knife) or a linear accelerator. Solitary or multiple brain metastases in the setting of progressive primary disease are generally treated with whole-brain irradiation. Chemotherapy is indicated for tumors of known responsiveness to chemotherapy in patients whose general condition is satisfactory. Meta-static small-cell lung cancer, primary CNS lymphoma, and germ cell tumors are treated with radiotherapy or chemotherapy rather than surgery.

Spinal metastases: Resection and radiotherapy for localized tumors; radiotherapy alone for diffuse metastatic disease.

Leptomeningeal metastases: Chemotherapy (systemic, intrathecal, or intraventricular); irradiation of neuraxis.

Follow-up examinations are scheduled at shorter or longer intervals depending on the degree of malignity of the neoplasm and on the outcome of initial management (usually involving some combination of surgery, radiotherapy, and chemotherapy), with adjustment for individual factors and for any complications that may be encountered in the further course of the disease. A single CT or MRI scan 3 months post-operatively may suffice for the patient with a completely resected, benign tumor, while patients with malignant tumors should be followed up by examination every 6 weeks and neuroimaging every 3 months, at least initially. Later visits can be less frequent if the tumor does not recur.

Traumatic Brain Injury (TBI)

The outcome of traumatic brain injury depends on the type and extent of the acute (primary) injury and its secondary and late sequelae. Direct/indirect history. A history of the precipitating event and of the patient's condition at the scene should be obtained from the patient (if possible), or from an eyewitness, or both. Vomiting or an epileptic seizure in the acute aftermath of the event should be noted. Also important are the past medical history, current medications £ (particularly anticoagulants), and any history of alcoholism or drug abuse. ^ Physical examination. General: Open wounds, to fractures, bruises, bleeding or clear discharge O from the nose or ear. Neurological: Respiration, C circulation, pupils, motor function, other focal g signs.

"5 Diagnostic studies. Laboratory: Blood count, coagulation, electrolytes, blood glucose, urea, S creatinine, serum osmolality, blood alcohol, drug levels in urine, pregnancy testing if indicated. Essential radiological studies: Head CT with brain and bone windows is mandatory in all cases un less the neurological examination is completely normal. A cervical spine series from C1 to C7 is needed to rule out associated cervical injury. Plain films of the skull are generally unnecessary if CT is performed.

Additional studies, as indicated: Cranial or spinal MRI or MR angiography, EEG, Doppler ultrasonography, evoked potentials. In multiorgan trauma: Blood should be typed and cross-matched and several units should be kept ready for transfusion as needed. Physical examination and ancillary studies for any fractures, abdominal bleeding, pulmonary injury.

■ Primary Injury

The primary injury affects different parts of the skull and brain depending on the precipitating event. The traumatic lesion may be focal (hematoma, contusion, infarct, localized edema) or diffuse (hypoxic injury, subarachnoid hemorrhage, generalized edema). The worse the injury, the more severe the impairment of consciousness (pp. 116 ff). The clinical assessment of impairment of consciousness is described on pp.378 f (Tables 33 and 34).

Region

Type of Injury

Scalp

Cephalhematoma (neonates), laceration, scalping injury

Skull

• Fracture mechanism: Bending fracture (caused by blows to the head, etc.), burst fracture (caused by broad skull compression)

• Fracture type: Linear fracture (fissure, fissured fracture, separation of cranial sutures), impression fracture, fracture with multiple fragments, puncture fracture, growing skull fracture (in children only)

• Fracture site: Convexity (calvaria), base of skull

• Basilar skull fracture: Frontobasal (bilateral periorbital hematoma ("raccoon sign"), bleeding from nose/mouth, CSF rhinorrhea) or laterobasal (hearing loss, eardrum lesion, bleeding from the ear canal, CSF otorrhea, facial nerve palsy)

• Facial skull fracture: LeFort I-III midface fracture; orbital base fracture

Dura mater

Open head trauma1, CSF leak, pneumocephalus, pneumatocele

Blood vessels

Acute epidural, subdural, subarachnoid or intraparenchymal hemorrhage; carotid-cavernous sinus fistula; arterial dissection

• Diffuse axonal injury (clinical features: coma, autonomic dysfunction, decortication or decerebration, no focal lesion on CT or MRI)

• Penetrating (open or closed3) injury, or perforating (open) injury

• Brainstem injury

1 Wound with open dura and exposure of brain (definition). 2 Excluding cranial nerve lesions. 3 Without dural penetration (definition).

1 Wound with open dura and exposure of brain (definition). 2 Excluding cranial nerve lesions. 3 Without dural penetration (definition).

Open Depressed Skull Fracture

Lacerations

Head injuries

Head injuries

Hemorrhagic contusion

Inner dural layer

Cranial impression

Depressed skull fracture, hematoma dural opening

Gunshot-

wound, hematoma along trajectory

Brain herniation, edema

Inner and outer dural layer

Cranial impression

Steps For Subdural Hematoma

Head trauma (schematic) Subdural hematoma

Inner dural layer

Inner and outer dural layer

Head trauma (schematic) Subdural hematoma

Retroauricular Ecchymosis
Retroauricular ecchymosis (due to basilar skull fracture)

Traumatic intracranial hematoma

(Duration of unconsciousness)

24 h

Mild HT

GCS: 13-15

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  • magnus
    What does a basilar skull fracture effect in motor skills?
    7 years ago

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