13.1 What Is Intracranial Pressure?

Elevated intracranial pressure (ICP) remains a frequently encountered dilemma in the neurosurgical intensive care unit (NICU). Few other pathologies challenge clinicians’ insight and vigilance as does intracranial hypertension. Elevated ICP results in secondary brain injury and poor neurologic outcome. ¹ Furthermore, intracranial hypertension is found in 40 to 60% of severe head injuries and is a major factor in the deaths of 50% of all fatalities. ²

The beneficial effects of removing pieces of the skull in cases of brain swelling have been known since the time of Hippocrates, Galen, and the ancient Egyptians. ² However, the dynamics governing intracranial pressure were not fully understood until the early 19th century. When Alexander Monro and George Kellie postulated that “anything new or exuberant cannot be intruded” within the cranium “without an equivalent displacement.” ² This would later become known as the Monro–Kellie doctrine or hypothesis, stating that “the sum of volumes of brain, CSF, and intracranial blood is constant.” ³

ICP is therefore a function of the contents of the cranial vault. The sum of the volumes of blood, brain, cerebrospinal fluid (CSF), and other elements (tumor, hematoma, abscess, edema), which are incompressible liquids and solids in the inelastic bony cranial vault together constitute the ICP.

An increase in any of the intracranial elements causes a concomitant decrease in the other elements. This principle does not apply to children with unfused sutures or to patients with comminuted skull fractures, both of whose cranial vaults are not a fixed space.

13.2 Cerebral Blood Flow, CSF Dynamics, and Intracranial Pressure

Cerebral autoregulation of blood flow has long been studied and is still not completely understood. As far back as 1939 Fog showed pial arteries to demonstrate compensatory dilatation and constriction in reaction to changes in blood pressure. ⁴ , ⁵ Later studies and reviews by Lassen ⁶ and Kontos et al ⁷ showed that, despite a wide range of systemic systolic blood pressures (60–140 mm Hg) the cerebral perfusion pressure remained relatively constant. In a more recent review by Koller and Toth it appears that the vasomotor response in cerebral vessels is regulated not only at large vessel on a pressure-sensitive myogenic mechanism but also regionally by flow signal metabolites, such as 20-HETE, nitric oxide, potassium, and transient receptor potential (TRP) channels. ⁸ Metabolic variables, such as PaCO₂, cerebral hyperemia resulting in nitric oxide (NO) production, K⁺ and H⁺ ion concentrations, and cerebral metabolic activity resulting in elevated adenosine levels have all been shown to affect cerebral blood flow ⁹ and are available to monitor and manipulate in the neurosurgical intensive care unit (NICU).

Tenets are based on knowledge of the cardiopulmonary system, specifically, cardiac output. In this, adjustments of vasopressors, inotropes, chronotropes, and other medication are made to optimize cerebral perfusion. Though usually requiring invasive monitoring, cardiac output may be approximated with a simple calculation:

where SV is stroke volume, HR is heart rate, VO₂ is oxygen consumption, and AVDO₂ is arteriovenous oxygen content difference.

Newer advances in hemodynamic monitoring systems, such as the FloTrac sensor (Edwards), allow continuous monitoring of cardiac output, cardiac index, stroke volume, stroke volume index (SVI), and stroke volume variance (SVV). This is done though monitoring via a standard arterial line connected to the FloTrac sensor, which uses an algorithm to calculate these hemodynamic variables. The physician can direct therapy in terms of preload, afterload, and cardiac contractility to optimize these parameters based on the patient’s condition. For example, SVV was shown to be a significantly better predictor of fluid responsiveness as compared to central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP). ¹⁰ The treatment algorithm shown in ► Fig. 13.1 can guide therapy in an attempt to improve stroke volume and in turn cardiac output.

The effect of cardiac output (CO) on cerebral blood flow (CBF) is controversial. Deegan et al showed that dynamic autoregulation of CBF remained constant with induced changes in CO via thigh cuff. ¹¹ Bouma and Muizelaar ¹² found no relationship between CO and CBF in head-injured patients. Conversely, Ogawa et al ¹³ showed that increases in CO via saline infusion increased CBF without a change in mean arterial pressure (MAP). Ogawa et al ¹³ also showed changes in CO via thigh cuff, and albumin infusion showed a linear increase or decrease in CBF without a change in MAP. Ultimately, CO likely has an effect on CBF, especially in cases when autoregulation is impaired.

CBF is measurable with neuroimaging modalities, including xenon CT, positron emission tomography (PET) scanning, transcranial Doppler, and functional magnetic resonance imaging (fMRI). These techniques are usually unavailable on a continuous basis to most clinicians. CBF is dependent on cerebral perfusion pressure (CPP). Normal adult CPP is > 50 mm Hg.

CBF is related to CPP via Poiseuille’s law. Using this formula, CPP is directly proportional to CBF and also to vessel radius; it is inversely proportional to blood viscosity and vessel length. Shown mathematically, Poiseulle’s law is

where r is vessel radius, n is viscosity, and l is vessel length.

where MAP is mean arterial pressure.

where DBP is diastolic blood pressure and SBP is systolic blood pressure.

Optimization of CPP at 60 to 70 mm Hg has been more reliably shown to be associated with an improved neurologic outcome. ¹⁴ Normal ICP is age dependent (► Table 13.1).

Although many definitions for a pathological threshold of ICP have been given, 20 to 25 mm Hg is generally accepted as truly pathological. ³