INCREASED INTRACRANIAL PRESSURE
ESSENTIALS OF DIAGNOSIS
Headache, nausea, and vomiting, with progression to obtundation and coma with or without localizing signs
Brain imaging showing a space-occupying lesion, edema, blood, or hydrocephalus
Increased intracranial pressure (ICP) is a pathologic state common to a variety of serious neurologic illnesses, all of which are characterized by the addition of volume to the intracranial vault. According to the Monro Kellie doctrine, the intracranial contents include brain, blood, and cerebrospinal fluid (CSF), all of which are relatively incompressible. Expansion of any one of these compartments must take place at the expense of the others and therefore will produce an increase in ICP. The normal ICP range oscillates between 5 and 20 cm H2O or 3–15 mm Hg. Because elevations beyond these levels can rapidly lead to brain injury and death, rapid acute identification and treatment of the primary cause of elevated ICP is paramount.
The most appropriate way to diagnose increased ICP is to measure it directly. A depressed level of consciousness in all its stages and reflex hypertension are probably the most consistent clinical signs. In principle, they both reflect the effects of globally reduced cerebral blood flow. Marked hypertension with bradycardia and irregular respiration is characteristic of the Kocher-Cushing reflex due to a rapid rise in ICP in the posterior fossa and impending cerebral herniation. However, in clinical practice, hypertension is most commonly associated with initial tachycardia before the bradycardic effect.
Headache, nausea, projectile vomiting, fourth and sixth cranial nerve palsies, and pupillary dilatation are also frequent signs seen in patients with increased ICP. Nevertheless, they do not correlate well with the severity of the disease. Although papilledema is a specific indicator of intracranial hypertension, it is present only in a minority of patients.
Localized mass lesions or diffuse increase in ICP can cause coma due to herniation of brain structures beyond the confines of the supratentorial-infratentorial compartments. Supratentorial lesions are associated with uncal and central herniation depending on the location of the lesion. Infratentorial structural lesions may also cause herniation, either transtentorially upward, producing midbrain compression, or downward through the foramen magnum with distortion of the medulla by the cerebellar tonsils. These syndromes must be recognized and rapidly managed medically and surgically as appropriate (Table 25–1).
Table Graphic Jump Location Table 25–1.Herniation syndrome. ||Download (.pdf) Table 25–1. Herniation syndrome.
|Type ||Lesion ||Injured Structure ||Clinical Presentation |
|Uncal ||Hemispheric or lateral middle fossa mass ||Ipsilateral CN III compression and cerebral peduncle || |
Initially: ipsilateral pupil dilated with preserved or sluggish reaction to light
Advanced stage: complete internal and external ophthalmoplegia, hemiparesis (50% ipsilateral and 50% contralateral)
|Central ||Supratentorial diffuse brain edema, hemorrhage, or midline brain tumors ||Initial obstructive hydrocephalus and displacement of thalamus and hypothalamus || |
Initially: decreased consciousness, small ...