Pseudotumor cerebri Craniosynostosis Venous sinus thrombosis routinely measured at the time spinal taps are performed, this technique is not appropriate for long-term ICP monitoring.

Because clinical signs of elevated ICP, such as the Cushing response (systemic hypertension, bradycardia, and irregular respirations), '401 are usually a late finding and may never even occur,[41] it is important to directly measure ICP with an invasive device in appropriate settings. Furthermore, because increases in ICP may result in a decrease in cerebral perfusion pressure (CPP) if autoregulation fails, early intervention can be hastened by the direct measurement of ICP. Normal intracranial pressures range from approximately 10 to 20 cm H2 O (or about 5 to 15 mm Hg). Cerebral perfusion pressure is calculated by subtracting the ICP from the mean arterial pressure (MAP) (CPP = MAP - ICP). Cerebral vasculature autoregulation cannot maintain appropriate cerebral blood flow and perfusion at CPP levels below 50 mm Hg. Long-term ICP monitoring was initiated in the 1950s and 1960s with the introduction of ventricular catheterization. This procedure involves insertion of a sterile catheter into the lateral ventricle that is guided by either skull-based landmarks or through stereotactic placement. Once within the ventricle, CSF may be drained and the ICP can be monitored. The latter may be completed by either direct visualization of the height of the CSF column generated outside the body or through its measurement by an external transducer. Possible complications of the ventricular catheter include subdural, epidural, or intracerebral hematomas and infection. A risk of so-called upward herniation exists if an infratentorial mass is present and CSF is quickly removed from the supratentorial lateral ventricles. Other systems for the measurement of ICP do not involve direct entry into the ventricles. Collectively, these devices are termed intracranial bolts, although this is a misnomer, and historically, they consist of hollow screws that are inserted through the skull and extend into the subarachnoid space. After the placement of these devices, tubing filled with sterile saline is attached to the bolt and a pressure monitor. True bolts are rarely used today, yet multiple systems are available that may use a hollow screw-like device. These devices usually use a pressure transducer or a fiber-optic cable inserted through the hollow bolt that directly measures the pressure within the subdural or subarachnoid space or in the brain parenchyma. Compared with the ventriculostomy, the risk of hemorrhage and ventriculitis is lower with this procedure.

After the ICP monitoring device is inserted, a waveform may be generated. Because the ICP varies with both respirations and the cardiac cycle, positive deflections of 2 to 10 mm H2 O can be observed in a patient who is not receiving positive pressure ventilation immediately after systole and during exhalation. Maneuvers to test the function of the ICP monitor include asking patients to increase their intrathoracic pressure (by using the Valsalva technique), which causes an increase in the ICP. Alternatively, a modified Queckenstedt test may be performed in which the jugular veins are lightly compressed. Because this maneuver causes a decrease in the venous drainage from the brain, an increase in the ICP occurs, and if the intracranial compliance is low this is rapidly observed. Neither of these tests should be performed in patients with critically elevated ICP. In these patients, evidence for plateau waves (acute elevations in ICP [600 to 1300 mm H 2 O] that last 5 to 20 minutes and then return to baseline) may be present.






Increased capillary permeability

Cellular swelling

Increased intraventricular fluid


White matter

Gray and white matter

Ventricular, periventricular white matter

Edema fluid

Plasma filtrate

Intracellular H2 O and sodium

Cerebrospinal fluid

Extracellular fluid volume





Tumor, abscess, infarction, hemorrhage, lead encephalopathy, ischemia, meningitis

Hypoxia, osmolality, ischemia, meningitis, Reye's syndrome

Communicating and noncommunicating hydrocephalus

Adapted from Fishman RA: Cerebrospinal Fluid in Diseases of the Nervous System. Philadelphia, W.B. Saunders, 1992.






Hvpocarbia by hyperventilation

pCO2 25 to 33 mm Hg RR 10 to 16/min

Immediate onset, well tolerated

Hypotension, barotrauma, duration usually hours or less


Mannitol 0.5 to 1 g/kg

Rapid onset, titratable, predictable

Hypotension, hypokalemia, duration hours or days


Pentobarbital 1.5 mg/kg

Mutes BP and respiratory fluctuations

Hypotension, fixed pupils (small), duration days


Timing critical

Large sustained ICP reduction

Surgical risk, tissue herniation through wound

RR, respiratory rate.

These waves may represent an autoregulatory response to insufficient cerebral blood flow (secondary to elevated ICP) that produces vasodilatation, an increased cerebral blood flow, and, in turn, further elevations of the ICP. y Because of the presumed underlying pathophysiology, the presence of plateau waves suggests a poor prognosis.

The clinical conditions for performing ICP monitoring or ventricular drainage are limited. In severe head trauma with diffuse intracerebral edema, ICP monitoring may aid in guiding therapeutic interventions; however, no randomized, controlled studies exist to determine if ICP monitoring affects long-term outcome. Other conditions that may require ICP monitoring to guide interventions include large intracranial hemorrhages or strokes, encephalitis or bacterial meningitis, acute and fulminant hepatic encephalopathy, intracranial tumors, and Reye's syndrome. In patients with normal pressure hydrocephalus, transient elevations in ICP (similar to plateau waves) may be present during rapid-eye-movement sleep, and documentation of these waves may aid in determining which patients could improve with shunting.

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