F Intracranial hypertension
Definition and etiology
Intracranial hypertension occurs with a sustained increase in ICP above 15 to 20 mmHg. Intracranial hypertension develops with expanding tissue or fluid mass, interference with normal CSF absorption, excessive cerebral blood flow (CBF), or systemic disturbances promoting brain edema. Often, multiple factors are responsible for the development of intracranial hypertension. Head injury, stroke, intracranial hemorrhage, infection, tumor formation, postischemic or posthypoxic states, hydrocephalus, osmolar imbalances, and pulmonary disease can all cause increases in ICP.
Diagnostic and laboratory findings
Magnetic resonance imaging and CT are the two most prominent tests to evaluate tumors, hemorrhage, stroke, and areas of ischemia. Lumbar puncture is used to diagnose infections and hydrocephalus.
Clinical manifestations
Symptoms of increased ICP include headache, nausea, vomiting, papil-ledema, focal neurologic deficits, altered ventilatory function, decreasing consciousness, seizures, and coma. When ICP exceeds 30 mmHg, CBF progressively decreases, and a vicious cycle is established: ischemia produces brain edema, which in turn increases ICP and further precipitates ischemia. Cushing’s triad is associated with excessively high ICP and includes hypertension, bradycardia, and irregular respirations. If this cycle remains unchecked, progressive neurologic damage or catastrophic herniation may result.
Treatment
The major methods for the treatment of elevated ICP are listed in the box below.
Methods for the Treatment of Elevated Intracranial Pressure
