Intracranial Hypertension

Intracranial HypertensionNormal intracranial contents include brain parenchyma, cerebrospinal fluid and intracranial blood. Since intracranial volume is fixed, volume changes in of any of components affect intracranial pressure (ICP). The pressure-volume curve described by Langfitt and coworkers demonstrates a curvilinear relationship between intracranial volume and changes in ICP. As intracranial volume increases, so does intracranial pressure. Initially, the rise in ICP is barely noticeable and the slope of the curve approximates zero. As intracranial volume accumulates, the curve becomes increasingly steeper, eventually approaching the vertical. Thus, ICP varies exponentially with intracranial CSF, brain, or blood volume. The treatment of intracranial hypertension essentially relies on this relationship and aims at lowering intracranial CSF, brain, and blood volume. It follows that ICP management mandates the use of intracranial pressure monitors.

Two basic types of ICP monitors are currently available: drainage and nondrainage types. The former can be placed in the ventricle, subarachnoid, or subdural space. The latter is usually placed within the parenchyma, though it can be placed in virtually any intracranial compartment. Because of its potential therapeutic role, the external ventricular drain is the ICP monitor of choice at our institution. Not only does it provide information on ICP, it also allows the physician to drain ventricular CSF, thus lowering ICP. If the ventricular catheter cannot be placed, then a nondraining ICP monitor is used. We use fiberoptic ICP monitors at our institution due to their ease of placement.

The major risks associated with these monitors are infection and hemorrhage. The infection rates for external ventricular drain versus fiberoptic catheters are 0–27% (average, 8%) and 0–1.7%, respectively. The risk of hemorrhage with either type is similar. The incidence of malfunction, on the other hand, is considerably higher with fiberoptic technology. Malfunction or obstruction rates for intraventricular, subdural, and subarachnoid drains are 2.5%, 2.7%, and 16%, respectively. The risk of malfunction with the fiberoptic catheter, on the other hand, is 10–30%. In addition, the cost difference between fiberoptic and drainage catheters is enormous, with nondraining monitors costing an order of magnitude more than external ventricular drains. All things considered, the accuracy, reliability, therapeutic value, and cost make the external ventricular drain the most useful ICP monitor available.

Though the risk of placing either hydrostatic or fiberoptic monitors is small, it is clear that not all traumatic brain injury patients require invasive monitoring.

Treatment of Intracranial Hypertension

Intracranial hypertension is treated by decreasing intracranial CSF, brain, or blood volume. Both surgical and nonsurgical approaches are available.

Cerebrospinal Fluid Volume

Cerebrospinal fluid volume is generally lowered via use of a ventriculostomy. This can be done by keeping the drain constantly open or by keeping it to monitor, draining only if the ICP reaches a set threshold. For most trauma situations, the author finds it most useful to keep the drain to monitor with intermittent drainage, as this allows for close monitoring of ICP spikes that otherwise might not be captured by leaving the drain constantly open. When no amount of drainage controls ICP, other ICP-lowering modalities should be started. Medical management of CSF volume is impractical in the trauma setting, as medications such as steroids or acetazolamide are slow in acting and have side effects that make their use undesirable.

Brain Volume

The surgical approach to decreasing brain volume is crude and generally unsatisfactory, as it requires the performance of a lobectomy. This is sometimes necessary in order to buy some extra space into which the remaining brain can swell, but generally, lobectomies are bloody affairs to be avoided if possible. Medical management of brain volume is more satisfying as it essentially boils down to giving IV mannitol and keeping serum sodium (Na+) at or slightly above the high end of normal. There are two practical limits to mannitol: hypotension and serum osmolality. Mannitol not only draws water across the blood-brain barrier, but it also is a powerful osmotic diuretic that can drop a patient’s blood pressure. Hypotension, therefore, is a contraindication to mannitol infusion. The second limit is serum osmolality—as it increases, so does viscosity. At levels above 320 mosm/kg, its deleterious effects on blood viscosity supersede the benefits of giving mannitol to lower ICP.

Hypernatremia helps control cerebral edema by normalizing the Na+ gradient across cellular membranes. As noted earlier, glutamate initiates a series of biochemical changes thought to be mediated through NMDA receptors. One of these changes involves intracellular Na+ accumulation, which leads to cellular swelling. Increasing serum Na+ presumably decreases cerebral (cytotoxic) edema by ameliorating intracellular water accumulation. The main issues of concern associated with hypernatremia are two—hyperchloremia and diabetes insipidus. The former results from infusion of large volumes or 0.9% NaCl solution. High serum chloride facilitates renal excretion of serum bicarbonate, which then leads to a metabolic acidosis. This can be reversed somewhat by changing from sodium chloride to a sodium bicarbonate solution.

Blood Volume

Of the three components, intracranial blood volume is the most interesting and challenging to manage. The surgical approach is fairly straightforward—its aim is to evacuate intracranial blood clots. Nonsurgical management focuses on the intravascular compartment. This is comprised of arterial, capillary, and venous volumes, which we will deal with individually.

Capillary Volume

This compartment is passive and cannot be manipulated to any significant degree.

Venous Volume

Though also passive, intracranial venous volume can be altered in a number of ways. The main goal is to lower ICP by decreasing venous volume. This can be accomplished simply by elevating the head of the bed. This facilitates intracranial venous drainage by increasing the pressure differential between intracranial venous pressure and central venous pressure. Another approach is simply to prevent increased intrathoracic pressure, as this would inhibit intracranial venous outflow and increase ICP. Causes of increased intrathoracic pressure include Valsalva maneuvers (ie, seizures, coughing, agitation, vomiting, straining) and primary pulmonary issues (ie, ARDS, pneumonia). By treating the underlying cause of each, we can sometimes control ICP. Sedatives, paralytics, anticonvulsants, and stool softeners all decrease Valsalva maneuvers; and optimizing ventilator parameters and treating pneumonias can also help control ICP.

Arterial Volume

This compartment is essentially manipulated by taking advantage of cerebral autoregulatory mechanisms. These couple cerebral blood flow to cerebral metabolic demands. First, metabolic autoregulation alters local cerebral blood flow to match changes in local cerebral metabolism. Second, pressure autoregulation is designed to keep a constant cerebral blood flow over a wide range of blood pressures. Third, osmotic autoregulation keeps blood flow constant with changes in blood viscosity—all other things being equal. They all essentially work through tissue pH as a means of detecting ischemia. As tissue pH drops, autoregulatory mechanisms see this as the tissue becoming ischemic and respond by vasodilating upstream arterioles in order to increase local blood flow. Though vasodilatation increases local tissue perfusion, it also increases arterial blood volume—which increases ICP. Conversely, increasing tissue pH leads to vasoconstriction and, consequently, lowers ICP.

The most common way of inducing cerebral vasoconstriction is to decrease serum PCO2 though mechanical hyperventilation. Serum PCO2 and pH are closely interrelated—decreasing PCO2 increases serum pH—and by hyperventilating, we essentially fool the cerebral vasculature into believing that the local cerebral blood flow is too high, thus causing vasoconstriction and decreased ICP. It is easy to see that this approach has the theoretical disadvantage that it can actually cause cerebral ischemia—a notion supported by data suggesting that hyperventilation below a PCO2 of 30 leads to worse neurologic outcome.

As long as autoregulation remains intact, we can also decrease ICP through induced systemic hypertension. This maneuver transiently increases cerebral blood flow and causes the brain to respond by inducing cerebral vasoconstriction. This then leads to a lowering of ICP. Finally, we can decrease cerebral metabolism through medications such as barbiturates and propofol. As the cerebral metabolic rate falls, so does metabolic demand. In response, the cerebral vasculature naturally constricts, thus lowering ICP. The biggest problem with the last approach is that both barbiturates can lower blood pressure and decrease cardiac function.

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