Cerebral protection: pathophysiology and treatment of increased intracranial pressure.

I ncreased pressure within the cranial cavity is a common and important problem in the care of patients with serious injuries and diseases of the central nervous system. Elevated intracranial pressure (ICP) is most commonly associated with severe head injury; some degree of increased ICP was found in 80 percent of all patients with a major head injury and in over one half of these patients the pressure was significantly elevated.’ Increased ICP accounts for 50 percent ofall head injury deaths.2 While the majority of cases of increased ICP are due to head injury, elevated pressure is seen as a secondary effect of a variety of other conditions including brain tumors, subarachnoid hemorrhage, spontaneous intracerebral hemorrhage, and Reye’s syndrome. A number of toxic and viral encephalopathies are also accompanied by intracranial hypertension. The mortality rate in head injury is roughly proportional to the ICE Normal ICP is 0 to 10 mm Hg. If ICP rises to 40 mm Hg, the mortality rate is 65 percent; when ICP reaches 60 mm Hg, the mortality rate is 100 percent. Approximately 15 percent of severe head injury patients develop elevated pressure which cannot be controlled; all of these patients eventually succumb.2 The relationship of ICP and morbidity in head injuries is not as clear. Patients with moderately elevated (25 to 40 mm Hg) ICP which is successfully lowered are often left with severe neurologic residuals. The ability to normalize ICP is not a guarantee of a good clinical result. The direct measurement of ICP is a relatively new technique. Until Lundberg’ demonstrated the feasibility and clinical usefulness of direct long-term measurement in 1960, the measurement of ICP was obtamed through lumbar puncture. Spinal subarachnoid space pressure thus obtained did not necessarily represent the pressure in the cranial cavity. The technique was dangerous in the presence of focal intracranial masses and was not applicable to prolonged monitoring. Lundberg’s monitoring technique used a catheter placed in the lateral ventricle, a common neurosurgical procedure. The catheter was connected by a fluidfilled tube to a pressure transducer and a chart recorder. Reliable ICP measurement was now possible for days at a time. Techniques ofICP monitoring and control were first applied to head injuries, and the great majority of clinical information has been developed from this source. A number of reports have demonstrated a significant decrease in head injury deaths, from approximately 52 percent to nearly 40 percent, when aggressive monitoring and control of ICP has been applied. 1.4-7 Difficulties with patient classification and differences in treatment protocol make scrupulous comparison between series difficult. The incidence and severity of ICP elevation is greater if an intracranial focal mass is present. The severity of the immediate parenchymal injury is also a powerful force determining outcome, irrespective of the level of ICP elevation. Despite these problems, it is generally agreed that monitoring and control of intracranial pressure favorably affects the outcome of severe head injuries. Similar aggressive treatment has become widely used in Reye’s syndrome. Here its value can be better appreciated since there is no appreciable underlying brain damage to influence results. The mortality of severe (grade 4) cases has been decreased from 80 percent to near 10 percent by stringent control of ICE89 It is clear that intracranial hypertension is a secondary effect of a number of pathologic processes and not a disease of itself. The most careful control of ICP will not reverse the brain damage caused by the primary disease or injury. The goal ofICP control is to permit the recovery of damaged tissue and to prevent secondary injury caused by intracranial hypertension.