title: Prevention and treatment of intracranial hypertension.
abstract: Intracranial pressure (ICP) is the pressure exerted by cranial contents on the dural envelope. It comprises the partial pressures of brain, blood and cerebrospinal fluid (CSF). Normal intracranial pressure is somewhere below 10 mmHg; it may increase as a result of traumatic brain injury, stroke, neoplasm, Reye's syndrome, hepatic coma, or other pathologies. When ICP increases above 20 mmHg it may damage neurons and jeopardize cerebral perfusion. If such a condition persists, treatment is indicated. Control of ICP requires measurement, which can only be performed invasively. Standard techniques include direct ventricular manometry or measurement in the parenchyma with electronic or fiberoptic devices. Displaying the time course of pressure (high-resolution ICP tonoscopy) allows assessment of the validity of the signal and identification of specific pathological findings, such as A-, B- and C-waves. When ICP is pathologically elevated--at or above 20-25 mmHg--it needs to be lowered. A range of treatment modalities is available and should be applied with consideration of the underlying cause. When intracranial hypertension is caused by hematoma, contusion, tumor, hygroma, hydrocephalus or pneumatocephalus, surgical treatment is indicated. In the absence of a surgically treatable condition, ICP may be controlled by correcting the patient's position, temperature, ventilation or hemodynamics. If intracranial hypertension persists, drainage of CSF via external drainage is most effective. Other first-tier options include induced hypocapnea (hyperventilation; paCO2 < 35 mmHg), hyperosmolar therapy (mannitol, hypertonic saline) and induced arterial hypertension (CPP concept). When autoregulation of cerebral blood flow is compromised, hyperoncotic treatment aimed at reducing vasogenic edema and intracranial blood volume may be applied. When intracranial hypertension persists, second-tier treatments may be indicated. These include 'forced hyperventilation' (paCO2 < 25 mmHg), barbiturate coma or experimental protocols such as tris buffer, indomethacin or induced hypothermia. The last resort is emergent bilateral decompressive craniectomy; once taken into consideration, it should be performed without undue delay.
authors.affiliation: Johannes Gutenberg University Medical School at Mainz. jan-peter@jantzen.net
authors.forename: Jan-Peter A H
authors.initials: JP
authors.lastname: Jantzen
mesh_terms: D001929:Brain Edema / Q000209:etiology / Q000517:prevention & control; D001930:Brain Injuries / Q000150:complications / Q000628:therapy; D004322:Drainage; D006801:Humans; D006849:Hydrocephalus / Q000209:etiology / Q000517:prevention & control; D019586:Intracranial Hypertension / Q000209:etiology / Q000517:prevention & control* / Q000628:therapy*; D007427:Intracranial Pressure; D019635:Neurosurgical Procedures / Q000009:adverse effects*; D011007:Pneumocephalus / Q000209:etiology / Q000517:prevention & control; D011182:Postoperative Care; D012121:Respiration, Artificial