This patient is clearly demonstrating clinical signs of herniation. The comatose examination with loss of airway protection requiring mechanical ventilation as well as the neurologic signs such as dilation and loss of reactivity of the right pupil and flexor posturing of the left arm/leg are strong indicators that the patient is suffering from right-sided brainstem compression. This constellation of neurologic signs is the most concerning issue in this patient's presentation and, as such, requires the most immediate attention from the treating physician.
A stat CT of the head (Figure 8-1) will demonstrate location of the mass, extent of midline shift, edema, hydrocephalus, lesional (with possible intraventricular) hemorrhage, and type of herniation. In this case, a large (5.5 × 5.6 × 5.7 cm), calcified, hyperdense mass is noted along the superior anterior falx associated with moderate surrounding edema and causing mass effect upon the right greater than left frontal horns. There is no associated hemorrhage or hydrocephalus. There is loss of sulcation indicative of elevated intracranial pressure (ICP), as well as acute infarcts in the bilateral occipital lobes, right greater than left, suggesting an ongoing process of transtentorial (uncal) herniation.
(Left) Noncontrast head CT revealing the large, midline hyperdense mass with calcifications along the anterior falx. Also noted is associated edema, bilateral compression of the frontal horns (right greater than left), and loss of sulcation suggestive of elevated ICP. (Right) Crowding of the ambient cisterns with medial displacement of the R temporal horn suggestive of downward (uncal) herniation. There are also bilateral hypodensities in the medial occipital lobes that may be an indicator of bilateral PCA infarction from herniation.
The immediate medical interventions are directed toward lowering the patient's elevated ICP. First, raising the head of the bed to at least 30 degrees will prevent cerebral venous outflow obstruction. Second, hyperventilating the patient to a goal Paco2 of 25 to 30 mm Hg will provide transient lowering of ICP by inducing vasoconstriction of cerebral arteries and arterioles, which will lower cerebral blood volume (CBV). Third, administration of sedatives, analgesics, and potentially paralytic agents helps to control agitation and in particular cases, such as propofol (beginning at 10 mg/kg per minute), reduces CBV and slows cerebral metabolism, actions that contribute to lowering ICP.1
The next major intervention is the use of hyperosmolar therapy, typically with continuous infusion of 3% hypertonic saline coupled with boluses of 23.4% hypertonic saline (in 30-mL pushes), along with standard mannitol administration (25% solution given at 0.25 to 1 g/kg). Such agents work by increasing serum osmolality, which brings water from the extracellular space into the serum, thereby reducing brain swelling. The goal serum osmolality is typically greater than 320 mOsm/L and the goal plasma sodium level in such a patient is typically 150 to 155 with sodium checks every 4 to 6 hours, as a sodium level above 155 has not been shown to be of proven clinical benefit.2 The side effects of hyperosmolar therapy include electrolyte imbalances (eg, hypokalemia), pulmonary edema (resulting from rapid intravascular volume expansion), coagulopathy, and intravascular hemolysis.3 Despite the radiographic features of this lesion, which point to it being an extra-axial mass such as a meningioma, it is still causing significant vasogenic edema that should be treated with intravenous steroids. An immediate bolus of 10 mg IV dexamethasone (Decadron), followed by a maintenance dose of 8 to 32 mg/day, should be implemented.4 Dexamethasone works by reducing the permeability of the cerebral capillaries.
Given the recent seizure, which likely precipitated the herniation event (seizures transiently elevate ICP, likely from increasing cerebral blood flow [CBF]), the patient should be maintained on antiepileptic medication, either phenytoin (Dilantin) (following a 20-mg/kg loading dose) or Keppra (following a 1-g loading dose).
There is also a discussion to be had regarding insertion of an ICP monitor in this patient. Typically, for patients with clinical signs of elevated ICP and a Glasgow Coma Scale (GCS) score less than 8 warrant direct, invasive monitoring of ICP.5 Since this patient presented with a known intracranial mass causing elevated ICP, the indication for an ICP monitor is less cogent given that imminent surgery will remove the source of the elevated ICP. If the patient were to be stabilized and supported for an extended period of time, for example, in the case of an unresectable lesion or in the obvious case of traumatic brain injury, then the utility of an ICP monitor becomes clear. In this case, therefore, an ICP monitor was not inserted immediately given the plan for urgent operative decompression.