Consultation with the Specialist: Increased Intracranial Pressure

1. Gitte Y. Larsen, MD* 2. Brahm Goldstein, MD† 1. 2. *Assistant Professor of Pediatrics, Division of Pediatric Critical Care, Doernbecher Children’s Hospital, Oregon Health Sciences University, Portland, OR. 3. 4. †Editorial Board. Increased intracranial pressure (ICP) may result from multiple etiologies, including cerebral edema associated with head trauma, hypoxic-ischemic events, infection, metabolic derangement, hydrocephalus, and space-occupying lesions. If unrecognized and untreated, increased ICP results in significant morbidity and mortality by causing irreversible neurologic injury. The intracranial cavity contains three components: blood, brain, and cerebrospinal fluid (CSF). CSF accounts for 10% of the total volume, blood for 10%, and brain for approximately 80%. CSF provides 70% of the intracranial buffering capacity. As the brain swells following an insult, CSF is displaced initially into the arachnoid space, cerebral blood flow (CBF) is altered, and ICP rises. The autoregulation of CBF is relatively constant at 50 to 150 mm Hg mean arterial pressure in adults. However, CBF is highly responsive to various metabolic factors, including Paco2, Pao2, and pH. For example, CBF rises linearly with increases in Paco2 of 20 to 70 torr and increases when the Pao2 falls below 50 torr. The ability to autoregulate blood flow often is altered or lost following a variety of insults, including head trauma. This may result in inappropriately high blood flows and an even higher ICP. As the compliance of the brain decreases, a relatively small change in volume will result in a large change in ICP. Infants were believed to be relatively protected against increases in ICP compared with older children, but little protection is afforded by an infant’s cranial and cerebral anatomy. Despite the presence of open sutures and larger subarachnoid spaces and cisterns, which serve to decompress expanding brain tissue, the smaller neural axis results in a less compliant pressure-volume relationship. Pathophysiology following brain injury occurs in two phases: primary and secondary. Primary brain injury refers to the initial insult, whether it be ischemic, anoxic/hypoxic, or shear injury …