Increased Intracranial Pressure

Physiologic Considerations
The intact cranium and vertebral canal, together with the relatively inelastic dura,
form a rigid container, such that an increase of any of its contents—brain, blood,
or CSF—will elevate the ICP. Furthermore, an increase in volume of any one of
these three components must be at the expense of the other two, a relationship that
is known as the Monro-Kellie doctrine. Small increments in brain volume do not
immediately raise the ICP because the of the countervailing buffering effect of
displacement of CSF from the cranial cavity into the spinal canal. To a lesser
extent there is deformation of the brain and limited stretching of the infoldings of
the relatively unyielding dura, specifically, the falx cerebri between the
hemispheres and the tentorium between the hemispheres and cerebellum. Once
these compensating measures have been exhausted, a mass within one dural
compartment leads to displacement, or “herniation of brain,― from that
compartment into an adjacent one. Any further increment in brain volume
necessarily reduces the volume of intracranial blood contained in the veins and
dural sinuses. Also, the CSF is formed more slowly in circumstances of raised
ICP. These accommodative volume-pressure relationships occur concurrently and
are subsumed under the term intracranial compliance (the change in ICP for a
given change in intracranial volume). As the brain, blood, or CSF volumes
continue to increase, the accommodative mechanisms fail and ICP rises
exponentially, as in the idealized compliance curve. The normal compliance curve
begins its steep ascent at an ICP of approximately 25 mmHg. After this point,
small increases in intracranial volume result in marked elevations in ICP.
The numerical difference between ICP and mean blood pressure within the
cerebral vessels is termed cerebral perfusion pressure (CPP). Besides the
aforementioned brain tissue shifts, which are discussed more fully in relation to
their clinical signs in Chap. 17, elevation in ICP that approaches the level of mean
systemic blood pressure eventually causes a widespread reduction in cerebral
blood flow/perfusion. In its most severe form, this global ischemia produces brain
death. Lesser degrees of raised ICP and reduced cerebral circulation cause
correspondingly less severe, but still extensive, cerebral infarction of a type quite
similar to what arises after cardiac arrest. In all circumstances, not only the
severity but also the duration of reduction of CPP are the main determinant of the
degree of cerebral damage.
Lundberg is credited with recording and analyzing intraventricular pressures
over long periods of time in patients with brain tumors. He found ICP to be
subject to periodic spontaneous fluctuations, of which he described three types
of pressure waves designated as A, B, and C. Only the A waves have proved to
be separable from arterial and respiratory pulsations and of clinical
consequence. They consist of rhythmic rises of ICP, up to 50 mmHg, occurring
every 15 to 30 min and lasting about 1 min, or of smaller but more protracted
elevations. These plateau waves, as they have come to be known, coincide with
an increase in intracranial blood volume, presumably as a result of a temporary
failure of cerebrovascular autoregulation. Rosner and Becker have observed that
plateau waves are sometimes preceded by a brief period of mild systemic
 hypotension. In their view, this slight hypotension induces cerebral vasodilation
in order to maintain normal blood flow. Upon recovery of the blood pressure,
the response in cerebrovascular tone is delayed, thereby allowing intracranial
blood volume to accumulate in the dilated vascular bed and raising ICP. In
support of this explanation is the observation that a brief period of induced
elevation of blood pressure paradoxically restores the normal cerebrovascular
tone and leads to an abrupt cessation of a plateau wave.
It has been demonstrated that the high mortality and morbidity of acute cerebral
mass lesions is in large part related to uncontrolled elevation in ICP. In a normal
adult reclining with the head and trunk elevated to 45 degrees, the ICP is in the
range of 2 to 5 mmHg. Levels up to 15 mmHg are not in themselves hazardous; in
fact, adequate cerebral perfusion can be maintained at an ICP of 40 mmHg
provided blood pressure (BP) remains normal. A higher ICP or a lower BP may
combine to reduce cerebral perfusion pressure and cause diffuse ischemic damage,
as discussed further on.
Causes of Raised ICP
In clinical practice, one of several general mechanisms causing elevated ICP can
be identified:

 A cerebral or extracerebral mass such as brain tumor; massive infarction

with edema; extensive traumatic contusion; parenchymal, subdural, or
extradural hematoma; or abscess, all of which tend to be localized and
deform the adjacent brain. The brain deformation is greatest locally, being
compartmentalized to a varying degree by dural partitions as already
noted.
 Generalized brain swelling, as occurs in ischemic-anoxic states, acute
hepatic failure, hypertensive encephalopathy, hypercarbia, and the Reye
hepatocerebral syndrome. Here the increase in pressure reduces the
cerebral perfusion pressure, but tissue shifts are minimal because the mass
effect is widely distributed throughout the cranial contents.
 An increase in venous pressure due to cerebral venous sinus thrombosis,
heart failure, or obstruction of the superior mediastinal or jugular veins.
 Obstruction to the flow and absorption of CSF. If the obstruction is within
the ventricles or in the subarachnoid space at the base of the brain,
hydrocephalus results. Extensive meningeal disease from any number of
causes (infectious, carcinomatous, granulomatous, hemorrhagic) is another
mechanism. If the block is confined to the absorptive sites adjacent to the
cerebral convexities and superior sagittal sinus, the ventricles remain
normal in size or enlarge only slightly, because the pressure over the
convexities approximates the pressure within the lateral ventricles (see
further on).
 Any process that expands the volume of CSF (meningitis, subarachnoid
hemorrhage) or, less commonly, increases CSF production (choroid plexus
tumor).

Clinical Features of Raised ICP (See also Chap. 17)

The clinical manifestations of increased ICP in children and adults are headache,
nausea and vomiting, drowsiness, ocular palsies, and papilledema. After several
days or longer, papilledema may result in periodic visual obscurations. If
papilledema is protracted, optic atrophy and blindness may follow (see Chap. 13
for further discussion). The practice of monitoring ICP with a pressure device
inserted within the cranial cavity has permitted approximate correlations to be
made between clinical signs and the levels of ICP. However, it should be kept in
mind that the main neurologic signs of a large intracranial mass (pupillary
dilatation, abducens palsies, drowsiness, and the Cushing response, as discussed
in Chap. 17) are due to displacement of brain tissue and therefore do not bear a
strict relationship to ICP. As a rule, patients with normal BP retain normal mental
alertness with ICP of 25 to 40 mmHg unless there is concurrent shift of brain
tissue. Stated another way, coma generally cannot be attributed to elevated ICP
alone. Only when ICP exceeds 40 to 50 mmHg do cerebral perfusion pressure
(CPP) and cerebral blood flow diminish to a degree that results in loss of
consciousness. Any further elevations are followed imminently by global
ischemia and brain death. Nonetheless, high levels of ICP that are often found
under conditions of brain distortion, as discussed in Chaps. 17 and 35, in the
context of head injury.
From our own observations, it appears that the brain shift and herniation that
causes the pupil to dilate on the side of a mass lesion generally corresponds to an
ICP of 28 to 34 mmHg. (Again, this is an association, not a direct effect of the
elevated ICP). However, there are many exceptions, as, for example, when the
mass in the medial temporal lobe is contiguous to the third nerve, and with slowly
growing lesions, which may raise the ICP with few clinical signs. Likewise,
unilateral or bilateral abducens palsies do not bear a strict relationship to the
degree of elevation of ICP. This sign is more frequent when raised ICP is due to
diffusely distributed brain swelling, hydrocephalus, meningitic processes, or
pseudotumor states.
The consequences of increased intracranial pressure differ in infants and small
children, whose cranial sutures have not closed. Then the clinical problem
involves differentiation from other types of enlargement of the head with or
without hydrocephalus, such as constitutional macrocrania or an enlarged brain
(megalencephaly; or hereditary metabolic diseases such as Krabbe disease,
Alexander disease, Tay-Sachs disease, Canavan spongy degeneration of the
brain), and from subdural hematoma or hygroma, neonatal ventricular
hemorrhage, and various cysts and tumors.
Monitoring of ICP
There is considerable evidence that the outcome in patients with intracranial mass
lesions is favorably influenced by maintaining the intracranial pressure at levels
well below those which compromise cerebral perfusions. An ICP below 20 mmHg
is given as a target, since the compliance curve becomes steep beyond this level
and small increments in cerebral volume may cause large elevations in pressure.
Unfortunately, the direct measurement of ICP and aggressive measures to
counteract high pressures have not yielded uniformly beneficial results,
and—after several decades of popularity—the routine use of such devices
remains controversial. The problem may be partly a matter of the time at which
monitoring is instituted and the proper selection of patients for aggressive
treatment of raised ICP. Only if the ICP measurements are to be used as a guide to
medical and surgical therapy is their use justified. Also figuring in the decision to
institute monitoring are the prospects of ameliorating the underlying lesion, the
patient's age, and the associated medical disease(s). Our practice has been to
measure ICP with an indwelling fiberoptic monitor or intraventricular drain in
otherwise salvagable patients who are stuporous or comatose and in whom a
traumatic or other intracranial mass has caused either a shift of intracranial
structures or severe generalized brain swelling. The monitor is generally placed on
the same side as a mass lesion.
The emergency management of raised ICP is considered in greater detail in
Chaps. 34 and 35, where it is discussed in relation to stroke and cerebral trauma.
A comprehensive discussion can also be found in the monograph on intensive care
(Ropper) listed in the references.