The cranium is a rigid structure. The major intracranial contents are the brain (to include the neuroglial elements and interstitial fluid), blood (arterial and venous), and cerebrospinal fluid (Table 19.1). When a new intracranial mass is introduced, a compensatory change in volume must occur through a reciprocal decrease in venous blood or cerebrospinal fluid (CSF) to keep the total intracranial volume constant. This is the Monro-Kellie doctrine (Fig. 19.1), which has been confirmed by many experimental and clinical observations. Only in children, with open fontanelles and whose sutures have not yet fused, can the cranium itself expand to physically accommodate extra volume.

TABLE 19.1 Intracranial Contents and Their Respective Volumes

Component	Volume	Percentage of Total Volume
Brain (70%) and interstitial fluid (10%)	1400 mL	80%
Blood	150 mL	10%
Cerebrospinal fluid	150 mL	10%
TOTAL	1700 mL	100%

FIGURE 19.1 Monro-Kellie doctrine holds that total intracranial volume remains constant. A, Physiological state with normal intracranial pressure (ICP). The major intracranial components are brain (80%), arterial and venous blood (10%), and cerebrospinal fluid (CSF) (10%). The cranium is a rigid container, the intracranial volume is constant, and the normal intracranial contents are shown with ICP within physiological range (10 to 15 mm Hg). B, Intracranial mass with compensation (normal ICP). This patient has an intracranial mass (space-occupying lesion) of moderate size. Because intracranial volume is constant, the increasing volume caused by the mass is compensated by a decrease in the intracranial content. Venous volume decreases through egress of venous blood from the intracranial cavity into the jugular veins. CSF volume decreases because of egress of CSF through the foramen magnum into the spinal canal. The brain itself is nearly incompressible, and thus no significant change in its volume occurs; neither is there change in arterial volume. Intracranial volume is constant and there is no net rise in ICP (pressure buffering). C, Intracranial mass with decompensation and elevated ICP. The intracranial mass is much larger, beyond the pressure-buffering capacity of venous blood and CSF; there is a net rise in ICP.

Compliance (dV/dP) is the change in volume observed for a given change in pressure. This represents the accommodative potential of the intracranial space. In clinical practice, however, what is actually measured is elastance (dP/dV). Elastance is the inverse of compliance and is the change in pressure observed for a given change in volume. It represents the resistance to outward expansion of an intracranial mass. The elastance curve (not compliance) is what is plotted in Figure 19.2. Although technically a misnomer, the term compliance is actually entrenched in the literature to describe the aforementioned phenomenon instead of using the proper term elastance. Because of this we, too, will conform to the traditional nomenclature for the rest of this chapter.

FIGURE 19.2 Pressure-volume curve. If an intracranial balloon is expanded slowly in a laboratory animal and the intracranial pressure (ICP) and the balloon’s volume are plotted, an exponential curve results. In the initial phase there is virtually no increase in ICP because of the compensatory decrease in cerebrospinal fluid (CSF) and venous volumes; the compliance is high (elastance low). With further expansion of the balloon, the ICP begins to rise; compliance is low (elastance high). In the terminal stages, when the compensatory mechanisms are exhausted, there is a steep rise in pressure (no compliance, highest elastance).

In accordance with the Monro-Kellie doctrine, several innate homeostatic mechanisms exist in an attempt to maintain intracranial pressure within the physiological range—generally considered less than 20 mm Hg in the acute inpatient setting. First, the venous system collapses easily and squeezes venous blood out through the jugular veins or through the emissary and scalp veins. Likewise, CSF can be displaced from the ventricular system through the foramina of Luschka and Magendie into the spinal subarachnoid space.¹ When these compensatory mechanisms have been exhausted, small changes in volume produce precipitous increases in pressure. This effect can be demonstrated experimentally by inserting a Foley catheter into the epidural space of a rat and gradually inflating a balloon with increasing volumes. The curve produced by plotting intracranial pressure against volume is the so-called compliance curve in Figure 19.2. The innate homeostatic pressure-buffering mechanism offered by displacement of CSF and venous blood keeps this curve flat until a “critical volume” is reached. After this critical volume, small volumetric changes result in precipitous increases in pressure, and intracranial hypertension naturally ensues. Brain parenchyma and arterial blood do not participate, to any significant extent, in the innate intracranial pressure-buffering mechanisms.

Acute Intracranial Hypertention

Symptoms and Signs

The symptoms and “sine qua non” of acute increased intracranial pressure are altered levels of consciousness with progressive neurological decline and decreasing wakefulness, usually followed by obtundation. The obtundation is usually due to one of two causes: (1) compression of the suprameduallary reticular activating system or (2) bithalamic or bicortical damage. This is typically manifested by a Glasgow Coma Scale (GCS) score less than 8, irregular breathing patterns, posturing, and possibly pupillary inequality.

Cerebral Blood Flow

Normal cerebral blood flow averages 55 to 60 mL/100 g brain tissue per minute. In the gray matter the blood flow is 75 mL/100 g brain tissue per minute, whereas in the white matter it is around 45 mL/100 g brain tissue per minute. This flow is sufficient to meet the metabolic needs of the brain. The brain usually begins to show signs of ischemia at 20 mL/100 g/minute and permanent damage usually results when the blood flow drops below 10 mL/100 g/minute in most models. The most significant factor that determines cerebral blood flow at any given time is the cerebral perfusion pressure (CPP). The CPP is the effective blood pressure gradient across the brain. CPP is the difference between the incoming mean arterial pressure (MAP) and the opposing intracranial pressure (ICP): CPP = MAP − ICP. The mean arterial pressure can be calculated in two ways: (1) the diastolic pressure plus one third of the pulse pressure (DP + 1⁄3PP) or (2) two thirds of the diastolic pressure plus one third of the systolic pressure (2⁄3DP + 1⁄3SP). The ICP has to be measured directly, which can be done with various devices and will be discussed later in this chapter. With increased ICP there is an obvious tendency for the cerebral perfusion pressure to decrease.

Three major factors regulate cerebral blood flow under physiological conditions: CPP, concentration of arterial CO₂, and arterial PO₂. The ability to maintain constant blood flow to the brain over a wide range of CPPs (50-150 mm Hg) is called cerebral autoregulation. When the CPP is low, the cerebral arterioles dilate to allow adequate flow at the decreased pressure. Conversely, an increase in CPP causes the arterioles to constrict and maintain the flow within physiological range (Fig. 19.3). Decreases in CO₂ tension in the blood (i.e., hyperventilation) causes diffuse vasoconstriction.² Vasoconstriction decreases both cerebral blood flow and cerebral blood volume in the brain. The risks and benefits of inducing hyperventilation are discussed under the treatment section at the end of this chapter. Lastly, severe hypoxia causes cerebrovascular dilatation. This effect only becomes apparent when the oxygen tension in the blood drops to 50 mm Hg and becomes maximal around 20 mm Hg.

FIGURE 19.3 Three major factors regulate cerebral blood flow (CBF) under physiological conditions: cerebral perfusion pressure (CPP), concentration of arterial CO₂, and arterial PO₂. This graph can be read in regard to CPP to CBF, or PaO₂ and PaCO₂ to CBF. The ability to maintain constant blood flow to the brain over a wide range of CPPs (50-150 mm Hg) is called cerebral autoregulation. Patients with hypertension have their autoregulatory curve shifted to the right. Trauma or stroke patients can have a loss of the normal sigmoidal shape to the autoregulatory curve. Additionally, decreases in CO₂ tension in the blood causes diffuse vasoconstriction. This decreases both cerebral blood flow and thus cerebral blood volume in the brain. Severe hypoxia causes cerebrovascular dilatation. This only becomes apparent when the oxygen tension in the blood drops to 50 mm Hg, and becomes maximal around 20 mm Hg.

Under certain pathological conditions cerebral blood flow cannot always be autoregulated.³ When the CPP exceeds 150 mm Hg, such as in hypertensive crisis, the autoregulatory system fails. In this case there would be a passive increase in blood flow proportionate to the increase in systemic pressure, causing an exudation of fluid from the vascular system with resultant vasogenic edema.⁴ Additionally, certain toxins such as carbon dioxide can cause diffuse cerebrovascular dilatation and inhibit proper autoregulation.⁵ Lastly, during the first 4 to 5 days of head trauma, many patients can experience a disruption in cerebral autoregulation; this is often observed in the pediatric population and may result in hyperemia.⁶

Disruption of cerebral blood flow autoregulation in the setting of trauma could potentially lead to severe alterations in CPP when a patient’s brain is acutely injured.⁷ When disrupted, cerebral blood flow would be directly proportional to CPP under a much larger range than normal. This is likely one of the contributing reasons why even one episode of hypotension in the patient with acute head injury may lead to significantly worse outcomes.⁸ Thus, many institutions have adopted protocols to maintain a minimal CPP in the acute setting—usually around 50 to 60 mm Hg—and perhaps a maximum threshold of CPP if the intracranial hypertension can be linked directly to hyperemia.

Various ways to evaluate a patient’s autoregulatory abilities have been developed to include computed tomography (CT) perfusion scans and transcranial Doppler (TCD) studies. Interpreting these studies, however, is a matter of current debate. Although still somewhat in its infancy, knowing the status of a patient’s autoregulatory capacity in traumatic brain injury is beginning to shape individualized care in the intensive care unit (ICU).

Monitoring Intracranial Pressure

The most significant factor determining morbidity and mortality risk in patients with acute cranial neurosurgical disorders continues to be increased ICP. Continuous ICP monitoring is very useful for assessing intracranial dynamics in patients with suspected intracranial hypertension. There are no clinical indicators that can be used in the early stage of rising ICP to forestall a further rise. Classical clinical indicators described in the literature (cranial nerve abnormalities, posturing, etc.) occur in the end stage and they are not sensitive enough to show subtle changes in pressure. The two most common indications for ICP monitoring are closed head injury and spontaneous subarachnoid hemorrhage.

Indications for Monitoring Intracranial Pressure

The advent of continuous ICP monitoring has improved outcomes in traumatic brain injury ^9,¹⁰ by reducing the effects of secondary injury occurring after the initial brain insult. In the modern intensive care unit ICP monitoring in the adult patient with severe head injury is a recommended practice guideline based on available clinical evidence. Indications of ICP monitoring following head injury include a GCS score between 3 and 8 and an abnormal CT scan. Unfortunately, no class I evidence is available regarding the use of ICP monitors in pediatric head injury patients. Nevertheless, strong evidence supports the association between elevated ICP and poor outcomes,¹¹ and aggressive treatment of elevated ICP is associated with the best clinical outcomes. ICP monitoring provides valuable data that can inform medical management.

Techniques of Monitoring Intracranial Pressure

Intracranial pressure is best measured directly and continuously from the cranial cavity. Although lumbar puncture can indirectly indicate ICP, it is neither safe nor accurate in the setting of intracranial hypertension as it might precipitate tonsillar/transtentorial herniation by increasing the pressure gradient between the cranial and spinal subarachnoid compartments.

There are two commonly used pressure-monitoring systems in contemporary neurosurgical practice. An intraventricular catheter connected to a manometer and a drainage system is the standard against which all other systems are compared.¹²^–¹⁴ The ventricular catheter ideally should be tunneled under the skin and brought out through a separate stab wound, well away from the ventricular entry site, to minimize the risk of infection. Infection is the most significant complication of intraventricular pressure monitoring. With the use of an electronic transducer, the waveform can also be monitored (Fig. 19.4). The major advantage of the method is that the ventricular catheter is used not only to measure the pressure, but also as a therapeutic modality allowing intermittent or continuous drainage of CSF when the pressure exceeds physiological limits.

FIGURE 19.4 Intracranial pressure (ICP) monitoring system using ventricular catheter, pressure transducer, manometer, and drainage bag.

A second method is the use of the fiberoptic transducer-tipped catheter system. The transducer-tipped catheter can be placed within the brain parenchyma or in the subdural space, depending on the surgeon’s choice and the clinical situation.¹⁵^–¹⁷ The pressure monitor gives both digital readout and a waveform. The advantages of this system are that the zero point does not have to be reset with changes in head position because the pressure-sensing transducer is within the cranial cavity, and it is not susceptible to blockage by debris because it is not a fluid-coupled system. Also, insertion of a fiberoptic cable into the brain parenchyma is not affected by ventricular size or shift, which can make insertion of a ventricular catheter in the setting of intracranial hypertension quite trying. Lastly, the infection rates with fiberoptic probes are significantly lower than with ventriculostomy catheters, reported as less than 1% in one of the the largest reported series.¹⁸ The disadvantages of this system, however, are (1) higher cost and (2) baseline drift, which means there is evidence that with prolonged fiberoptic monitoring the indicated pressures may become less accurate in an unpredictable fashion.^19,²⁰