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ICP However, it should be kept in mind that the main neurologic signs of a large intracranial mass (pupillary dilatation, abducens palsies, drowsiness, and the Cushing response, as discussed in Chap 17) are due to displacement of brain tissue and therefore do not bear a strict relationship to ICP As a rule, patients with normal BP retain normal mental alertness with ICP of 25 to 40 mmHg unless there is concurrent shift of brain tissue Stated another way, coma generally cannot be attributed to elevated ICP alone Only when ICP exceeds 40 to 50 mmHg do cerebral perfusion pressure (CPP) and cerebral blood ow diminish to a degree that results in loss of consciousness Any further elevations are followed imminently by global ischemia and brain death Nonetheless, high levels of ICP that are often found under conditions of brain distortion, as discussed in Chaps 17 and 35, in the context of head injury From our own observations, it appears that the brain shift and herniation that causes the pupil to dilate on the side of a mass lesion generally corresponds to an ICP of 28 to 34 mmHg (Again, this is an association, not a direct effect of the elevated ICP) However, there are many exceptions, as, for example, when the mass in the medial temporal lobe is contiguous to the third nerve, and with slowly growing lesions, which may raise the ICP with few clinical signs Likewise, unilateral or bilateral abducens palsies do not bear a strict relationship to the degree of elevation of ICP This sign is more frequent when raised ICP is due to diffusely distributed brain swelling, hydrocephalus, meningitic processes, or pseudotumor states The consequences of increased intracranial pressure differ in infants and small children, whose cranial sutures have not closed Then the clinical problem involves differentiation from other types of enlargement of the head with or without hydrocephalus, such as constitutional macrocrania or an enlarged brain (megalencephaly; or hereditary metabolic diseases such as Krabbe disease, Alexander disease, Tay-Sachs disease, Canavan spongy degeneration of the brain), and from subdural hematoma or hygroma, neonatal ventricular hemorrhage, and various cysts and tumors.

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There is considerable evidence that the outcome in patients with intracranial mass lesions is favorably in uenced by maintaining the intracranial pressure at levels well below those which compromise cerebral perfusions An ICP below 20 mmHg is given as a target, since the compliance curve becomes steep beyond this level and small increments in cerebral volume may cause large elevations in pressure Unfortunately, the direct measurement of ICP and aggressive measures to counteract high pressures have not yielded uniformly bene cial results, and after several decades of popularity the routine use of such devices remains controversial The problem may be partly a matter of the time at which monitoring is instituted and the proper selection of patients for aggressive treatment of raised ICP Only if the ICP measurements are to be used as a guide to medical and surgical therapy is their use justi ed Also guring in the decision to institute monitoring are the prospects of ameliorating the underlying lesion, the patient s age, and the associated medical disease(s) Our practice has been to measure ICP with an indwelling beroptic monitor or intraventricular drain in otherwise salvagable patients who are stuporous or comatose and in whom a traumatic or other intracranial mass has caused either a shift of intracranial structures or severe generalized brain swelling The monitor is generally placed on the same side as a mass lesion

Clinical Features of Raised ICP (See also Chap 17) The clinical manifestations of increased ICP in children and adults are headache, nausea and vomiting, drowsiness, ocular palsies, and papilledema After several days or longer, papilledema may result in periodic visual obscurations If papilledema is protracted, optic atrophy and blindness may follow (see Chap 13 for further discussion) The practice of monitoring ICP with a pressure device inserted within the cranial cavity has permitted approximate correlations to be made between clinical signs and the levels of

The emergency management of raised ICP is considered in greater detail in Chaps 34 and 35, where it is discussed in relation to stroke and cerebral trauma A comprehensive discussion can also be found in the monograph on intensive care (Ropper) listed in the references

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