Vol.18, No.
6 June 1996 V Small Animal Neurology
Continuing Education Article
FOCAL POINT
★ Increases in intracranial
pressure are a potentially lethal
complication of intracranial
disease.
KEY FACTS
■ Once the compensatory
mechanisms are exhausted,
small increases in the volume of
an intracranial component can
cause dramatic increases in
intracranial pressure.
■ Clinical signs reflecting increases
in intracranial pressure are often
nonspecific.
■ Unilateral mydriasis should evoke
immediate and aggressive
therapy to reduce intracranial
pressure.
■ Intracranial pressure may
rebound if dehydration follows
mannitol therapy.
Intracranial Pressure
in Dogs and Cats
Washington State University
Rodney S. Bagley, DVM
T he brain resides in a unique physiologic environment. Protected by, but
also confined within, the bony limits of the cranium, the brain exists in
equilibrium with the cerebrospinal fluid and blood. Disease of the
brain parenchyma or other intracranial structures often alters this physiologic
equilibrium.
Pathophysiologic sequelae associated with diseases of the brain include ven-
tricular obstruction, alterations in cerebral blood flow, hemorrhage, and ede-
ma.1 Many intracranial diseases increase the relative volume within the in-
tracranial cavity, ultimately increasing the intracranial pressure. Clinical
abnormalities resulting from changes in intracranial pressure occur primarily
through decreases in cerebral blood flow. Compartmentalized increases in in-
tracranial pressure often cause lethal brain herniation.2
Increases in intracranial pressure have major clinical ramifications. An under-
standing of what intracranial pressure is and how it is altered by intracranial
disease is therefore important for appropriate management of animals with var-
ious intracranial diseases.
NORMAL INTRACRANIAL PHYSIOLOGY
Intracranial pressure is the pressure exerted between the skull and the in-
tracranial tissue. Because the skull is inelastic as compared with intracranial tis-
sue, intracranial pressure is determined primarily by changes in intracranial tis-
sue volume and the compensatory ability of these tissues to accommodate
volume changes.3–6
Intracranial Compliance
The major components contributing to intracranial volume are brain tissue
(intracranial cellular elements), cerebrospinal fluid, and blood.3 Intracranial
disease often increases the volume of one of these components. A brain tumor,
for example, increases the volume of the tissue component. For intracranial
pressure to remain normal, one or both of the other components must decrease
in volume in compensation (Figure 1). This compensation is called intracra-
nial compliance.
Although compliance initially helps stabilize intracranial pressure, it has lim-
its. When compliance is exhausted, intracranial pressure increases4–6 (Figure 2).
Small Animal The Compendium June 1996

The degree of compensation, with hypoventilation. The ampli-

however, may vary between indi- tude of the third component (the
viduals and may be influenced by dicrotic wave [P3]) may be altered
the extent and location of an in- by changes in venous pressure,
tracranial mass as well as cerebral possibly because of the changes in
blood flow characteristics.4,5 As in- intrathoracic pressure during
tracranial pressure increases, the breathing.7
pressure within the intracranial Periodic elevations in intracra-
space decreases cerebral blood nial pressure (plateau waves) with
flow. When cerebral perfusion de- ensuing return of intracranial
creases to a critical level, neuronal pressure to normal levels can oc-
ischemia, hypoxia, dysfunction, Figure 1—Relationship among the three major
cur in humans with intracranial
8
and death ultimately result. tissue components in the cranium (left). When disease. The basis of these period-
Intracranial pressure normally the volume of one of these components in- ic elevations is unknown; howev-
varies within a finite range. Peri- creases, the volumes of the other two must de- er, they may result from associated
odic fluctuations may result from crease for intracranial pressure to remain nor- changes in respiratory and blood
such normal body functions as mal (right). When the brain component flow patterns with subsequent al-
coughing or abdominal straining increases because of a space-occupying mass, terations in PaCO2.8 In this situa-
as increases in intrathoracic pres- the cerebrospinal fluid and blood components tion, single-time measurements of
sure and venous pressure impair must be reduced to compensate. intracranial pressure may miss
venous return from the intracra- episodic elevations; critical peri-
nial space. With intracranial dis- ods of raised intracranial pressure
ease, intracranial pressure may in- might therefore be overlooked.
crease persistently or episodically, Intracranial pressure may also
thus resulting in persistent or affect the configuration of the in-
episodic clinical abnormalities, re- tracranial pulse pressure wave.
spectively. With increasing intracranial pres-
sure, the amplitude of the P2
Intracranial Pulse component progressively increases
Pressure Wave while the amplitude of P1 changes
Cerebral blood flow and cere- minimally. 6,7 Consequently, the
brospinal fluid are in constant normal sawtooth-shaped wave be-
flux. Consequently, intracranial comes more rounded (Figure 4).
pressure is dynamic and pulsatile: Figure 2—Intracranial pressure (ICP) compli- This change may precede clinical-
a small pressure wave occurs al- ance curve. As the volume of an intracranial ly significant increases of absolute
most simultaneously with each component increases, compensatory mecha- intracranial pressure and suggests
heartbeat6,7 (Figure 3). This wave nisms prevent dramatic increases in intracra- decreasing compliance within the
is called the intracranial pulse nial pressure and no clinical signs are noted intracranial space.6
pressure wave. This wave is best (A). After the volume increase exceeds the ca- No apparent clinical abnormali-
seen when intracranial pressure is pacity of the compensatory mechanisms, small ties are associated with decreased
measured with a pressure trans- increases in the volume of an intracranial intracranial pressure; however,
ducer placed within a lateral ven- component result in dramatic increases in in- acute reduction in intracranial
tracranial pressure. Clinical signs become ap-
tricle; the wave has three separate parent (B). Severe clinical signs (C). volumes, such as may occur with
peaks or spikes.6,7 The first spike ventriculoperitoneal shunting,
(the percussion wave [P1]) is be- may result in damage to intracra-
lieved to originate from the pulsa- nial vessels and subsequent in-
tion of blood vessels within the choroid plexus; a pulsa- tracranial hemorrhage.9 More commonly, clinical ab-
tion is associated with each heart contraction.7 normalities result from increased intracranial pressure.
The origins of the second and third components of
the wave are not definitively established. However, ven- Cerebral Perfusion
tilation status affects the amplitude of the second com- The major intracranial effect of increasing intracra-
ponent (the tidal wave [P2]). The amplitude of the nial pressure is the alteration of cerebral perfusion pres-
tidal wave decreases with hyperventilation and increases sure.4,5,10 Cerebral perfusion depends on systemic blood

PERCUSSION WAVE ■ TIDAL WAVE ■ DICROTIC WAVE

The Compendium June 1996 Small Animal

flow and intracranial pressure as follows: creases and cerebral perfusion pressure subsequently
drops dangerously low, a large catecholamine release oc-
CPP = MABP – ICP curs.10 This catecholamine release may result in myocar-
dial ischemia (brain–heart syndrome).10,12,13 Clinically,
where CPP is cerebral perfusion pressure, MABP is ventricular arrhythmia is noted. Focal myocardial is-
mean arterial blood pressure, and ICP is intracranial chemia is evident, and focal white streaks are visible in
pressure.4,6 For cerebral perfusion pressure to remain the myocardium.12 Myocardial degeneration is a com-
constant, increases in systemic mon histologic finding. Brain–heart
blood pressure must accompany syndrome has been associated with
increases in intracranial pressure. various intracranial and spinal
Cerebral perfusion pressure is pathologic lesions and in several
not the only determinant of cere- species, including dogs, sheep, cat-
bral blood flow; but as cerebral tle, horses, pigs, goats, and hu-
perfusion pressure decreases, mans.10,12
cerebral blood flow usually de-
creases. MEASURING INTRACRANIAL
Blood flow to the brain is cou- PRESSURE
pled to the cerebral metabolic Cerebrospinal Fluid Pressure
rate. When cerebral blood flow Intracranial pressure can be mea-
decreases, the brain recognizes sured from various intracranial
the ischemia and evokes a spec- compartments. Cerebrospinal fluid
trum of physiologic alterations pressure, as a reflection of intracra-
known as the cerebral ischemic nial pressure, can be measured
response.11 These physiologic al- within the ventricles of the brain, at
terations are believed to emanate the cisterna magna, in the sub-
from vasomotor centers in the arachnoid space overlying the
lower brain stem. Failure of ade- brain, or in the lumbar area (the
quate blood flow to remove car- cistern in humans). In the past,
bon dioxide from receptors in measurements of cerebrospinal flu-
these centers increases local car- Figure 3—Intracranial pulse pressure wave as id pressure in animals have been
bon dioxide concentrations— measured by a fiberoptic intracranial pressure used to estimate intracranial pres-
thus, in turn, stimulating the monitoring system. The measured absolute in- sure. 14–19 Needle puncture and
sympathetic nervous system to tracranial pressure is 12 mm Hg. The intracra- manometer readings have been
increase systemic blood pressure. nial pulse pressure wave normally has a saw- used to provide this information.
Systemic hypertension results as tooth configuration. Use of a manometer to measure
an attempt to maintain cerebral cerebrospinal fluid pressure, howev-
blood flow. er, has several significant draw-
backs. First, it is poorly suited to
Systemic Effects long-term monitoring of intracra-
Baroreceptors within the sys- nial pressure. As mentioned, in-
temic vascular system recognize tracranial pressure is dynamic and it
the hypertension and send this is important to recognize and quan-
information to vagal centers also tify fluctuations in intracranial
found in the lower brain stem. pressure. Second, anesthesia is re-
The resultant increase in sys- quired for needle puncture in all
temic vagal tone reflexly causes but comatose animals.
bradycardia. The reflex brady- Third, if ventricular obstruction
cardia (Cushing’s reflex) associat- or herniation occurs, the cerebro-
ed with systemic hypertension Figure 4—Changes in the cerebrospinal fluid spinal fluid spaces may become
may explain why many dogs pulse pressure wave with increasing intracra- compartmentalized. Depending on
with intracranial disease have nial pressure. The wave form becomes more where cerebrospinal fluid pressure
rounded. The measured absolute intracranial
bradycardia.11 is measured, pressure measurements
pressure is 17 mm Hg.
As intracranial pressure in- may not accurately reflect global in-

SYSTEMIC HYPERTENSION ■ BRAIN–HEART SYNDROME ■ MANOMETER

Small Animal The Compendium June 1996

tracranial pressure. Evidence TABLE I sure through vasodilatory ef-

from humans with unilater- fects on cerebral vessels and
Cerebrospinal Fluid Pressure in
al structural brain lesions a subsequent increase in
Clinically Healthy Dogs
suggests that intracranial cerebral blood flow.33–37 Of
pressure is most accurately Pressure (mm Hg) a the commonly used inhalant
reflected in the cere- Mean Range Reference anesthetics, halothane causes
brospinal fluid pressure ipsi- the largest degree of cerebral
lateral to the lesion.20 5 — 14 vasodilatation.33–38 Increases
Intraventricular measure- 7 — 15 in cerebral blood flow can
ments of cerebrospinal fluid — 5–10 16 increase intracranial pressure
pressure provide the most 9 4–16 17 because of the associated in-
accurate reflection of the in- 6 4–10 18 crease in the blood compo-
tracranial pressure. Such nent of intracranial volume.
measurements, however, are aPressures converted from millimeters of cerebrospinal fluid The ultimate effect on in-
associated with a higher rate to millimeters of mercury and rounded to nearest whole num- tracranial pressure of the in-
of infection than are less in- ber. creased cerebral blood flow
vasive methods.21,22 Also, if depends on whether cerebral
ventricle collapse is associat- vascular autoregulation is in-
ed with the disease, cannu- tact (see the section on Hy-
lation of the ventricle may TABLE II perventilation). Body size
be difficult or impossible. may also influence measured
Brain Tissue Pressure in Clinically Healthy Dogsa
Epidural, subarachnoid, and intracranial pressure. Large
subdural screws were devel- Pressure (mm Hg)
dogs, for example, have slight-
oped to avoid entering the ly greater intracranial pres-
brain parenchyma during Mean Range Reference sures than do small dogs.19
monitoring of intracranial 9.8 8–13 32 With these considerations
pressure but have yielded in- 10 8–12 40 and limitations in mind, in-
consistent and often inaccu- 11 8–14 41
tracranial pressure values have
rate results in comparison been determined for healthy
9.6 8–12 42
with intraventricular mea- dogs.14–19 Most of these values
23–25
surements. a
Measurements were obtained with a fiberoptic monitoring represent measurements of
Measurement of brain tis- system from dogs under isoflurane anesthesia. the cerebrospinal fluid pres-
sue pressure is used in lieu sure at the cisterna magna.
of measurements of cere- Table I summarizes cere-
brospinal fluid pressure. It allows for accurate measure- brospinal fluid pressure and intracranial pressure values for
ments of intracranial pressure (in comparison with in- healthy dogs. Most of the cerebrospinal fluid pressure
traventricular measurements) but avoids ventricular readings fall between 5 and 12 mm Hg.14–19
26–32
catheterization.
Fiberoptic Intracranial Pressure Monitoring
Factors Influencing Intracranial Pressure To address the need for long-term recording of in-
Information on intracranial pressure in healthy, tracranial pressure, a fiberoptic intracranial pressure
awake dogs is scarce. Also, the effects of normal activi- monitoring system has been developed for use in hu-
ties (e.g., eating, drinking, coughing, and sneezing) on mans and adapted for use in dogs and cats. With this
intracranial pressure have not been established. Numer- system, pressures can be measured from the cere-
ous physiologic and nonphysiologic variables influence brospinal fluid or brain tissue. This system yields accu-
intracranial pressure measurements. These include rate measurements for long-term monitoring in hu-
anesthetic agents33–37 and body weight.19 The effects of mans and has gained acceptance in clinical practice.26,31
anesthetic agents on intracranial pressure are many and The same system has been used to monitor intracranial
varied. Anesthesia may be needed in order to measure pressure in dogs and cats.32,39–45
intracranial pressure, but anesthesia itself alters in- Table II shows brain tissue pressures as measured in
tracranial pressure. Specific effects of anesthetic agents healthy dogs by this fiberoptic system. These measure-
on intracranial pressure have been reviewed.33–37 ments tend to be slightly higher than the cerebrospinal
Most inhalant anesthetics increase intracranial pres- fluid pressure measurements (Table I). Measurements

INTRAVENTRICULAR MEASUREMENTS ■ ANESTHESIA ■ LONG-TERM MONITORING

The Compendium June 1996
of brain tissue pressure ob-
tained with this fiberoptic sys-
tem agree (±3 mm Hg) with
measurements of intraventricu-
lar pressure obtained by con-
ventional transducers in dogs.28
Similar degrees of change in in-
tracranial pressure were noted
regardless of the type of trans-
ducer used.28
Because the various monitor-
ing devices yield different abso- Figure 5— This fiberoptic intracranial pressure ment of the transducer cable,
lute measurements but reflect catheter broke because of excessive animal move- we have noted that in small
similar degrees of change, ment.
knowing the absolute value of
intracranial pressure may be
less important than documenting a trend (e.g., persis-
tent increase in intracranial pressure). The difference in vations in pressure readings, the bolt should be screwed
absolute values as measured by various devices may also
explain why the threshold of pathologically increased
intracranial pressure has not been established.46
Previous studies have reported the use of fiberoptic
monitoring of intracranial pressure in dogs. 32,39–45
Fiberoptic intracranial pressure monitoring has been
useful in establishing changes in intracranial pressure
under anesthesia and during intracranial surgery.32,39–45
In one study using isoflurane as a maintenance anesthet-
ic, mean intracranial pressure was found to be approxi-
mately 10 mm Hg (range 8 to 13 mm Hg).32 Other
studies have found a slightly higher mean intracranial
pressure but a similar range of pressures in dogs (Table
II).39–45 Again, the fiberoptic method of intracranial
pressure monitoring yields slightly higher readings
overall than the readings produced by a manometer
measuring cerebrospinal fluid pressure at a cere-
bromedullary puncture site.14–19
Transducer Positioning
Positioning of the fiberoptic transducer can influence
the absolute measurements of intracranial pressure. At
our hospital, the tip of the transducer is placed approxi- ment of intracranial pressure. As intracranial pressure
mately 3 to 5 millimeters into the brain parenchyma in
dogs and cats. This can be performed by roughly judg-
ing, before implantation, how far the transducer ex-
tends out of the retaining bolt. Marking black dots on
the transducer cable helps in this evaluation.
Before brain tissue is encountered, recorded measure-
ments usually remain below 5 mm Hg. When brain
parenchyma is entered, pressures increase sharply to
above 5 mm Hg. Ideally, at this time, the intracranial
pulse pressure wave is seen. Again, black dots on the
transducer cable allow for assessment of distance as the
cable is advanced. If the cable is advanced to the level
DOCUMENTING A TREND ■ SECURING BOLT ■ TRANSPORT OF ANIMAL
Small Animal
of the two closely opposed
black dots, the cable tip will
extend approximately 3 mil-
limeters past the end of the se-
curing bolt. If the transducer
cable is advanced too far into
the brain parenchyma, falsely
elevated measurements will be
obtained and increased brain
damage may occur.
In addition to proper place-
dogs and cats (<15 kg), screw-
ing the bolt into the skull too
far may also falsely elevate mea-
surements of intracranial pressure. To prevent false ele-
just far enough to secure it into the skull.
Obviously, measuring intracranial pressure with this
fiberoptic system is invasive and may cause brain dam-
age. When the transducer is properly placed, however,
associated brain damage is usually minimal.45 Besides
the mechanical damage produced by the cable, focal
hemorrhage and edema are seen in the cortex where the
cable is implanted.45
At Washington State University, we are beginning to
monitor intracranial pressure in nonanesthetized dogs
and cats after brain trauma or surgery. The fiberoptic
system seems well suited for this purpose, and few com-
plications have been encountered. If animals are violent,
propulsive, or uncoordinated in their movements, how-
ever, the cable or bolt might become dislodged. The
fiberoptic cable can be broken if it is bent; subsequently,
it malfunctions (Figure 5). The transducer cable can be
disconnected from the monitor, without apparent inac-
curacy in measurement, to facilitate transport of the ani-
mal from area to area within the hospital.
Noninvasive Doppler techniques for measurement of
cerebral blood flow may provide an indirect measure-
increases in humans, the transcranial Doppler ultra-
sonography wave forms showed that blood flow during
diastole starts out low, drops to zero, and is then re-
versed.47 The use of this technology for measuring cere-
bral blood flow in dogs is currently being evaluated.
INTRACRANIAL PRESSURE
IN PATHOLOGIC STATES
Increases in intracranial pressure are often responsible
for clinical decline in many animals with brain disease.1
Because of the confining nature of the skull, increases
in one of the compartments that make up intracranial
Small Animal The Compendium June 1996

volume elevate intracranial pressure once compensation ments of intracranial pressure in animals have not yet
is exhausted. With structural brain disease, the brain been compiled. Although some researchers have sug-
component usually enlarges because of infiltration by gested that the degree and persistence of the increase in
neoplastic cells, edema, or inflammation. As the vol- intracranial pressure is associated with outcome after
ume of the brain tissue compartment increases, the head injury,48,49 others have suggested that data ob-
cerebrospinal fluid and blood compartments must de- tained through monitoring of intracranial pressure do
crease or intracranial pressure will increase. Compensa- not improve prognosis.50
tion for increased brain tissue volume initially involves Intracranial pressures in dogs with intracranial abnor-
shifting of cerebrospinal fluid out of the skull; de- malities have been reported infrequently.19,39 However,
creased production of cerebrospinal fluid; and eventual- not all animals with space-occupying intracranial dis-
ly, decreased cerebral blood flow.6 eases have associated increases in intracranial pressure.
These compensatory mechanisms
prevent increases in intracranial
pressure for an undetermined peri-
od. In general, the more slowly the Types of Brain Herniation
compartment increases in volume,
the more readily this volume in- Tentorial • Downward displacement of the most
crease is compensated for. When medially placed cerebral structures
compensatory mechanisms are ex- through the tentorial notch, caused by a
hausted, relatively small increases in supratentorial mass. Pressure is exerted on
intracranial volume result in dra- underlying structures, including the brain
matic elevations of intracranial pres- stem. Also called caudal transtentorial,
sure. 1,3–6
Clinical signs become ap- transtentorial, or uncal herniation.
parent at this time.
Initial signs of increased intracra- Foramen Magnum • Protrusion of the caudal cerebellum
nial pressure may be nonspecific and through the foramen magnum, exerting
limited to alterations in mental sta- pressure on the medulla oblongata.
tus (i.e., progression to stupor and
coma), cranial nerve dysfunction, Subfacial • Herniation of the cingulate gyrus medially
and paresis. Clinical signs of signifi- and ventrally below the falx cerebri.
cantly increased intracranial pressure
often become obvious too late in the
disease to allow for effective therapy. At Washington State University, dogs and cats with in-
tracranial pressures greater than 15 to 20 mm Hg are
What Constitutes Increased treated and pressures are monitored. In dogs that have
Intracranial Pressure? recovered from brain injury, intracranial pressures have
The threshold at which intracranial pressure becomes decreased within the first 24 to 48 hours. This de-
pathologic has not been established.46 The uncertainty crease, however, does not always ensure functional
surrounding this threshold may result from the incon- recovery.
sistency between various types of monitoring equip-
ment as well as from the normal variation in baseline Lethal Effects—Brain Herniation
intracranial pressure. Most of the information from hu- As intracranial volume increases beyond the limits of
man studies suggests that intracranial pressure above 15 compensation, intracranial pressure can increase so pre-
to 20 mm Hg is pathologically increased.48,49 Cerebral cipitously that shifts of brain parenchyma (i.e., brain
blood flow, however, may not be significantly decreased herniation) result.2 Coma and severe neurologic impair-
until intracranial pressure reaches approximately 30 ment ensue. Brain herniation is usually lethal if brain
mm Hg.47 stem compression results.
Intracranial pressure has been raised to high levels The major types of brain herniation are tentorial,
(>100 mm Hg) before brain death occurred.10 We have foramen magnum, and subfacial (see the box). Hernia-
seen intracranial pressure as high as 30 to 40 mm Hg in tion can also occur through a craniotomy defect.2,51
dogs that subsequently recovered from brain injury. Clinical signs of tentorial herniation often result from
Clinical data that are needed in order to base treatment pressure distributed downward through the midbrain,
recommendations and prognosis on absolute measure- with subsequent compression of the oculomotor nerve.

PATHOLOGIC THRESHOLD ■ FUNCTIONAL RECOVERY ■ BRAIN STEM COMPRESSION

Small Animal The Compendium June 1996

If the herniation is unilateral, the ipsilateral pupil may well as blood pressure (pressure autoregulation). Cere-
be dilated and unresponsive to light. The pupils of ani- bral vessels change diameter through perivascular
mals at risk for tentorial herniation should therefore be changes in pH as a direct re-
monitored. Unilateral mydriasis in such a situation sult of Pa CO 2; a similar re- Treatments
should evoke immediate and aggressive attempts to de- sponse in the chemosensitive for Increased
crease intracranial pressure. area of the medulla oblonga- Intracranial Pressure
Foramen magnum herniation may occur quickly and ta stimulates respiration.
results in respiratory arrest because of associated pres- If autoregulation is intact,
sure on the respiratory centers in the caudal brain stem. hyperventilation to decrease ■ Head elevation (30˚)
Foramen magnum herniation is invariably fatal; surgi- Pa CO 2 will cause cerebral ■ Diuretics (mannitol or
cal attempts at decompression after this type of hernia- vasoconstriction, thus de- furosemide)
tion in dogs have not been helpful.52 creasing cerebral blood vol- ■ Hyperventilation
ume and consequently de- ■ Craniectomy and
Treatment of Increased Intracranial Pressure creasing the intracranial
durotomy
Treatments for elevated intracranial pressure (see the pressure. Cerebrovascular au-
box) include head elevation, hyperventilation, aspira- toregulatory capability, how-
tion of cerebrospinal fluid, administration of diuretics, ever, can be affected by various intracranial processes.
barbiturate therapy, hypothermia, and decompressive For example, local acidosis (which often results from
surgery. Obviously, definitive treatment of the primary hypoxia or ischemia) disrupts local autoregulatory
disease process is paramount. functions.55
If chemical autoregulation is absent in an area of dis-
Head Elevation eased brain, hyperventilation will not alter vascular di-
Head elevation to 30˚ above heart level decreases in- ameter in the affected area. Blood flow in that area de-
tracranial pressure primarily by facilitating venous pends on blood flow in the normal areas of the brain.
drainage.53 It has been suggested that head elevation As PaCO2 is decreased by hyperventilation, vessels in
may decrease cerebral perfusion and may therefore be normal areas of the brain constrict. Vessels in the dam-
detrimental to brain function. A recent study in hu- aged or abnormal area of the brain, however, are al-
mans, however, has shown that cerebral perfusion pres- ready maximally dilated and cannot constrict.
sure and cerebral blood flow are maintained and in- Hyperventilation-induced vasoconstriction increases
tracranial pressure is concurrently decreased when the vascular resistance in normal areas of the brain, thus
head is elevated 30˚. 53 In combination with other shunting blood into the abnormal area (this process is
methods of decreasing intracranial pressure, this simple called the inverse steal or Robin Hood phenomenon).55
treatment may be beneficial. This phenomenon has the upside of increasing cerebral
blood flow to abnormal and potentially hypoxic areas
Hyperventilation of the brain. The downside, however, is potentiation of
Hyperventilation can decrease intracranial pressure hemorrhage and cerebral edema in the abnormal area.
because of the effects of PaCO2 The opposite may occur as
on cerebral blood flow. 4,5,54 PaCO2 increases. Vessels in nor-
Cerebral vessels are directly re- mal brain tissue surrounding
sponsive to PaCO2, and cerebral the diseased area dilate, where-
blood flow is coupled to cere- as vessels in the abnormal area
bral metabolic rate. As PaCO2 are already maximally dilated
increases, cerebral vessels dilate because of loss of autoregula-
to increase blood flow to the tion. Vascular resistance de-
brain (Figure 6). The opposite creases in the normal areas of
effect is seen when PaCO2 de- the brain and blood is shunted
creases. away from abnormal areas,
This effect of Pa CO 2 is a thus potentially decreasing
component of the autoregula- hemorrhage and edema but re-
tion of cerebral blood flow. sulting in further hypoxia (the
Cerebral vessels can change di- Figure 6—Effect of changes in blood pressure and steal phenomenon).55
PaCO2 on the diameter of cerebral vasculature (cere-
ameter in response to Pa CO 2 Autoregulation of cerebral
brovascular autoregulation).
(chemical autoregulation) as blood flow can also occur sub-

RESPIRATORY ARREST ■ STEAL PHENOMENON ■ INVERSE STEAL

Small Animal The Compendium June 1996

sequent to changes in systemic cerebral blood flow does not

blood pressure, thus maintain-
ing stable cerebral blood flow.4
This regulatory response pre-
vents underperfusion and sub-
sequent ischemia during times
of hypertension and hemor-
rhage and edema at times of
hypertension. Usually, cerebral
blood flow remains constant
through systemic blood pres-
sure shifts of between 50 and
150 mm Hg.4 Above and be-
low these limits, however, cere- Figure 7— Dysfunctional pressure autoregulation ations of intracranial blood
bral blood flow is directly de- with intact chemical (PaCO2-responsive) autoregula- flow.
pendent on systemic blood tion. This phenomenon is often found in patients
with head trauma.
pressure.
Whether autoregulation re-
mains intact in a patient with
brain disease is difficult for the clinician to predict. Au- decrease PaCO2, cause vasoconstriction, decrease cere-
toregulation of global pressure has been found to be in-
tact in approximately 69% of human patients with
head trauma.56 Level of consciousness has been suggest-
ed as a crude, direct clinical indicator of autoregulatory
function.4 Local loss of autoregulation, however, is al-
most impossible to predict clinically without sophisti-
cated testing equipment that is practically unavailable.
At least in cases of head trauma, one form of autoreg-
ulation may remain intact while the other becomes im-
paired or ceases to function.56 In cases of head trauma,
pressure autoregulation is often abnormal whereas
PaCO2-responsive autoregulation remains intact (Figure
7). This dissociative vasoparalysis has important ramifi-
cations during treatment. As the cerebrovascular re-
sponse to blood pressure changes is abnormal, a more
intimate control of systemic blood pressure and central
venous pressure is required to prevent large shifts of
blood pressure and subsequent changes in cerebral
blood flow. Although correction of hypotension is often
necessary for animals with concurrent head trauma and
shock, hypervolemia should be avoided.57
Depending on whether pressure autoregulation is in-
tact, increases or decreases in systemic blood pressure
can increase intracranial pressure. If pressure autoregu-
lation is defective, significant increases in mean arterial to increases in hydrostatic pressure of the white matter.
blood pressure will increase cerebral blood flow and ul-
timately intracranial pressure.56 If pressure autoregula-
tion is intact, decreased blood pressure will cause cere-
brovascular vasodilatation, thus increasing cerebral blood
flow and ultimately increasing intracranial pressure.
Because of cerebral swelling, pressure autoregulation
may misleadingly seem intact (false autoregulation) in
patients with vasomotor paralysis.55 In this situation,
increase when systemic blood
pressure is increased, thus sug-
gesting intact pressure autoreg-
ulation. The cerebral swelling,
however, prevents further dila-
tion of cerebral vessels, thus
preventing an additional in-
crease in cerebral blood flow,
regardless of blood pressure. All
of the foregoing factors can af-
fect intracranial pressure by
contributing to myriad alter-
Because chemical autoregula-
tion often remains intact in pa-
tients with head injury, hyper-
ventilation may be useful to
bral blood flow, and subsequently decrease intracranial
pressure. Animals should be hyperventilated to main-
tain PaCO2 between 28 and 32 mm Hg (to prevent as-
sociated cerebral hypoxia from poor ventilation). Endo-
tracheal intubation and ventilator support can be
performed under the influence of barbiturate anesthesia
or neuromuscular blockade. Appropriate ventilator
management is imperative.
Diuretics
Many intracranial diseases are associated with brain
edema. In humans with head trauma, for example,
brain edema peaks between 24 and 48 hours after in-
jury.4 Brain edema is classified as cytotoxic, interstitial,
or vasogenic.51 Cytotoxic edema (intracellular edema)
results from failure of cellular energy, with resultant
failure to extrude sodium from within the cell. This
edema most often results from toxicity, ischemia, or
hypoxia.
Interstitial edema is increased water content of the
periventricular white matter because of movement of
cerebrospinal fluid across the ventricular walls in hy-
drocephalus. Periventricular white matter is reduced be-
cause of the disappearance of myelin lipids secondary
Although any or all of these types of edema may be
present in an animal with brain disease, vasogenic ede-
ma is the most common form associated with neoplasia
of the central nervous system. This type of edema re-
sults from vascular injury secondary to physical disrup-
tion of the vascular endothelium or functional alter-
ations in the tight junctions of endothelium.
Studies have shown that blood vessels within brain

DISSOCIATIVE VASOPARALYSIS ■ FALSE AUTOREGULATION ■ VENTRICULAR MANAGEMENT

The Compendium June 1996 Small Animal

tumors of rats are abnormal: the vessels have fenestra- tosis, however, seemed correlated with the presence of
tions, widened interendothelial junctions, increased edema.
pinocytic vesicles, infolding of luminal membranes, Mannitol. As cerebral edema contributes to intracra-
loosened and thickened basement membranes that are nial volume and subsequent increases in intracranial
partially lamellar or disrupted, and widened extracellu- pressure, treatments that decrease cerebral edema are
lar spaces.58 Similarly, endothelial fenestrations, en- often used to lower intracranial pressure. Mannitol is
dothelial gaps, lack of endothelium, and increased the diuretic most commonly used to decrease cerebral
pinocytic activity in the capillary endothelium are edema and intracranial pressure. In the past, mannitol
found in humans with brain tumor.59 was believed to decrease cerebral edema primarily
Differences in transmural pressure gradients result in through osmotic effects. However, other effects (e.g.,
extravasation of fluid from cerebral vessels to the extra- concurrent decrease in blood viscosity and free-radical
cellular fluid spaces of the brain.60 Areas of the brain scavenging) may, in fact, be more beneficial.62 Decreas-
where the extracellular fluid space is normally enlarged ing blood viscosity increases cerebral perfusion at the
provide a natural conduit for fluid movement. Increases same level of blood pressure (Figure 8). Vasoconstric-
in intravascular pressure due to loss of autoregulation, tion results, thus lowering cerebral blood volume and
vascular obstruction, or hypertension (Cushing’s re- concurrently lowering intracranial pressure.
sponse, cerebral ischemic response) may perpetuate Although mannitol may decrease peritumoral edema,
edema formation. it may be more effective at reducing the water content
Vasogenic edema migrates away from areas of vascu- in normal brain tissue than in diseased brain tissue. A
lar disruption via bulk flow.60 Fluid moves depending dose of 1 to 2 g/kg of mannitol is administered intra-
on the balance between the opposing forces of capillary venously to dogs and cats over 5 to 10 minutes. Benefi-
hydrostatic pressure and tissue resistance pressure. Vas- cial effects usually occur in 10 to 30 minutes. In hu-
ogenic edema usually spreads through the white matter, mans and dogs with normal intracranial pressure,
possibly because of the orderly arrangement of nerve mannitol infusion is associated with an initial short-
fibers found there. Also, the movement of this type of lived increase in intracranial pressure.62,63 Although in-
edema may be related to low capillary density and tracranial pressure may be increased initially, it decreas-
blood flow in normal white matter. Deep white matter es subsequently.64–67 Mannitol produces a precipitous
of the affected cerebral hemi- decline in intracranial pressure
sphere is preferentially affected. in dogs and humans with ele-
At Washington State Univer- vated intracranial pressure; the
sity, 31 dogs with brain tumor decrease in intracranial pres-
underwent magnetic resonance sure in normal dogs is less dra-
imaging to assess edema in matic.
brain tissue; 76% of the dogs Contraindications to manni-
with tumor had some degree of tol administration include
associated edema.1 Meningio- hypovolemia and ongoing in-
ma was the tumor type most tracranial hemorrhage. Manni-
often associated with cerebral tol has also been shown to in-
edema, although there were duce histamine release from
not enough cases for this result basophils, which may result in
to be statistically significant. In hypotension and a shocklike
one survey of cerebral edema in Figure 8—Mannitol decreases blood viscosity, there- state.68
humans with meningioma, no by increasing cerebral perfusion. When the cerebral Mannitol use has been asso-
relationship was found be- metabolic rate is decreased, as it often is in cases of ciated with a rebound effect;
tween histologic subtype of the head trauma, the decreased viscosity results in luxury after mannitol administration,
meningioma and edema—ex- perfusion. In response, the cerebral vessels constrict, intracranial pressure may re-
cept for the malignant tumors, thus decreasing intracranial blood volume and con- turn to or even exceed the orig-
which were commonly associ- sequently intracranial pressure (ICP). If dehydration inal level. 62 Several explana-
ated with edema.61 Location or follows mannitol administration, blood viscosity in- tions for this phenomenon
size of the tumor was not sig- creases, thus causing sludging and impeding cerebral have been proposed. Decreased
nificantly associated with ede- blood flow. The result is vasodilatation, increased fluid intake after mannitol ad-
ma. Increased tumor cellularity intracranial blood volume, and a rebound in in- ministration and subsequently
tracranial pressure.
and increased incidence of mi- increased vascular viscosity

MENINGIOMA ■ PERITUMORAL EDEMA ■ REBOUND EFFECT

Small Animal
may be responsible. Preventing dehydration after man-
nitol administration may decrease this potential sec-
ondary complication.62
Furosemide. Furosemide is a loop diuretic that may
help reduce intracranial pressure primarily or may po-
tentiate the effects of mannitol. When given as a preop-
erative diuretic to humans undergoing craniotomy,
furosemide (0.7 mg/kg intravenously) was comparable
with mannitol for lowering intracranial pressure.69 Un-
like mannitol, furosemide did not produce an initial in-
crease in intracranial pressure.
Other hypertonic solutions seem to be less effective
than mannitol or furosemide at lowering intracranial
pressure.70 These other solutions are more freely dif-
fusible across cell membranes and may therefore be un-
able to establish a significant osmotic gradient for fluid
movement.
Cerebrospinal Fluid Aspiration
Aspiration of cerebrospinal fluid was the first method
developed for decreasing intracranial pressure.5,54 In hu-
mans, aspiration of cerebrospinal fluid is most helpful if
the patient has a ventriculostomy and if intracranial
pressure does not exceed 30 mm Hg.5 Routine collec-
tion of cerebrospinal fluid for the purpose of reducing
intracranial pressure is not recommended if intracranial
pressure is suspected to exceed 30 mm Hg because of
the increased risk of precipitating brain herniation.71 A
recent study suggests that this caveat, however, may not
pertain for dogs and cats.72
Barbiturates
Barbiturates can be used to induce coma, thereby de-
creasing cerebral metabolism, cerebral blood flow, and
subsequently intracranial pressure.73 Barbiturates may
benefit cerebral blood flow by causing vasoconstriction
in normal tissue, thus shunting blood to ischemic areas.
Other suggested benefits include decreases in vasogenic
edema, decreased oxygen metabolism, decreases in in-
tracellular calcium, and free-radical scavenging.73 These
drugs are usually administered as a constant infusion in
order to achieve and maintain a burst-suppression pat-
tern on the electroencephalogram.73 Arterial blood pres-
sure should be monitored closely because barbiturates
can result in hypotension, which may decrease cerebral
blood flow and thus increase cerebral ischemia.74
Results of barbiturate coma for humans with elevated
intracranial pressure have been variable.73,74 As with
other treatments, assessment of success should be based
not only on the ability of the treatment to decrease in-
tracranial pressure but also on the ultimate degree of
functional recovery. In the treatment of humans with
traumatic brain disease, barbiturate therapy may be
BURST-SUPPRESSION PATTERN ■ BLOOD GLUCOSE ■ REWARMING
The Compendium June 1996
more beneficial for patients who have preserved cere-
brovascular reactivity to changes in Pa CO 2 than for
those who lack this reactivity.74
Corticosteroids
Corticosteroids are widely used in the treatment of
spinal trauma and have been recommended as a treat-
ment for elevated intracranial pressure.75,76 Although
corticosteroids reduce cerebral edema in patients with
brain tumor, they should be used cautiously for pa-
tients with brain injury. One study in rats has suggested
that corticosteroids may be advantageous in cases of
brain injury75; however, corticosteroids may not be effi-
cacious in cases of head trauma and are known to per-
petuate neuronal damage if ischemia is present.77,78
Corticosteroid administration may increase blood
glucose, a factor that may adversely influence outcome
after head injury.79 Also, the onset of beneficial effects
of decreasing cerebral edema may be delayed too long
to be helpful in acute elevations of intracranial pressure.
Whether corticosteroid administration is beneficial or
harmful for dogs or cats with head injury and elevated
intracranial pressure has not yet been documented.
Hypothermia
Hypothermia has been used experimentally in dogs
and clinically in humans to decrease intracranial pres-
sure when other treatments are insufficient.80–82 Cooling
of the body may prevent the ischemia-induced release
of excitatory neurotransmitters, such as glutamate.80
The decrease in extracellular levels of the excitatory
neurotransmitters may prevent the rapid influx of calci-
um into cells, thus leading to production of free radi-
cals and eventually killing the cells.
Conventional hypothermia, wherein the core body
temperature is lowered to below 30˚C, decreases cere-
bral metabolic rates and may reduce cerebral edema.80
Cooling to this level, however, has been associated with
unfavorable outcomes and cardiovascular instability.
Milder degrees of hypothermia (core body temperature
between 31˚C and 35˚C) are currently being used.82 Al-
though hypothermia does reduce intracranial pressure,
morbidity and mortality are persistent concerns, espe-
cially because brain herniation may occur during re-
warming.
Craniotomy
Intracranial contents are confined within the crani-
um. It would follow, therefore, that surgical removal of
part of the skull might relieve intracranial pressure.
Unilateral or bilateral craniectomy has been used as
a treatment for increased intracranial pressure that
cannot be relieved by any of the methods discussed
Small Animal
above.83–87 While removal of a portion of the skull may
be beneficial, subsequent incision of the dura seems to
be significantly more effective in lowering intracranial
pressure. This effect has been shown clinically in hu-
mans and experimentally in dogs and cats.43,45,85 Ulti-
mate recovery of function, however, remains dependent
on the primary brain damage caused by the initial dis-
ease process. How much the surgical procedure will re-
duce intracranial pressure is uncertain.
In dogs and humans, craniectomy has been shown to
reduce intracranial pressure by 15%; durotomy decreas-
es intracranial pressure by an additional 65%.43,45,85 In-
tracranial pressure in clinically healthy dogs approached
atmospheric pressure when a lateral rostrotentorial
craniectomy and durotomy were performed. A similar
procedure might be appropriate for animals with struc-
tural disease if the procedure led to similar intracranial
decompression. It is possible, however, that the benefits
of craniotomy are short-lived and may not persist in
the postoperative period.
SUMMARY
Increases in intracranial pressure are common causes
of clinical deterioration in dogs and cats with brain dis-
ease. Intracranial pressure is dynamic and unpredictable
and can reach life-threatening levels before producing
clinical signs. Elevations in intracranial pressure can be
expected to occur in any animal with structural brain
disease. Evaluation and treatment of these elevations in
intracranial pressure should ultimately improve the
prognosis for companion animals with various intracra-
nial diseases.
No clear consensus exists on how and when to treat
companion animals that are suspected to have increased
intracranial pressure. If a dog or cat’s clinical signs raise
the suspicion of increased intracranial pressure and if
clinical signs are mild and nonprogressive, the animal is
monitored by repeated neurologic assessments and in-
tracranial imaging (computed tomography or magnetic
resonance imaging) is performed as soon as possible.
Depending on the abnormalities seen, specific treat-
ment for the primary intracranial process or its sequelae
(e.g., edema) can be instituted.
If the animal is deteriorating neurologically, an imag-
ing study and objective intracranial pressure monitor-
ing should be performed in succession as soon as possi-
ble. If the animal is severely impaired or showing signs
of herniation and imaging or objective intracranial
monitoring cannot be performed, the animal’s head is
elevated and treatment with mannitol, furosemide, and
methylprednisolone is initiated. If the animal continues
to deteriorate and additional treatment is requested, en-
dotracheal intubation (under neuromuscular blockade
CRANIECTOMY ■ DUROTOMY ■ CLINICAL DETERIORATION
The Compendium June 1996
or light anesthesia) and hyperventilation should be per-
formed with blood-gas monitoring. Decompressive
craniectomy and durotomy can be used as a surgical
approach to controlling intracranial pressure.
Because the prognosis for animals with uncontrol-
lably increased intracranial pressure is poor, it is advis-
able to have a high index of suspicion for intracranial
pressure changes in dogs and cats with intracranial dis-
ease. Recognizing the subtle clinical changes that occur
with increasing intracranial pressure and treating in-
creased intracranial pressure early in the course of the
disease offer the best chance of recovery.
About the Author
Dr. Bagley is affiliated with the Department of Veterinary
Clinical Sciences, College of Veterinary Medicine, Wash-
ington State University, Pullman, Washington, and is a
Diplomate of the American College of Veterinary Internal
Medicine (Neurology and Internal Medicine).
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