Intracranial hypertension: Physiology,

pathophysiology and management

BARBARA SHWIRY, CRNA
JOSEPH P. GIFFIN, MD
JAMES E. COTTRELL, MD
Brooklyn, New York

The authors present a review of the

management of patients with intracranial
injury. The purpose of the article is to
provide the anesthetist with a working
knowledge of the physiology of intracranial
dynamics and pathophysiology of
intracranialinsult. Emergency techniques
and perioperative management are
discussed.

Physiology and pathophysiology

The management of a patient who has sustained
a severe cerebral insult requires an understanding
of the volume pressure relationship of the intracranial contents: cerebrospinal fluid (CSF), intravascular blood, and brain tissue.
Intracranial pressure (ICP) is the pressure
relative to atmospheric pressure within the ventriculo-subarachnoid space. Pressures are given in
millimeters mercury (mmHg) or centimeters
water (cmH 2 O). Lundberg has described a normal
ICP as 10 mmHg; slightly increased as 11-20
mmHg; moderately increased as 21-40 mmHg; and
severely increased above 40 mmHg. 1'6
Earlier concepts of intracranial pressure and
volume relationships were described by Monroe
and Kelli between 1783 and 1835. They proposed
that the intracranial contents were nearly incompressable. 2 It was not until 1846 that Burrows
described the contribution of CSF to intracranial
dynamics. 3 The modified Monroe-Kelli Doctrine

264

states that a change in volume of one of the intracranial constituents must be accompanied by a
reciprocal change in one or both of the other
constituents if pressure change is to be avoided.
Although CSF accounts for only 10% of the total
intracranial volume, CSF translocation is the
major means of buffering for expanding intracranial masses. 4 6 An understanding of CSF dynamics is therefore helpful in planning a regimen
for patients with intracranial hypertension.
Cerebrospinal fluid formation is accomplished
primarily by the choroid plexus located in the
lateral, third and fourth ventricles. Small amounts
of CSF are also produced in the perivascular space
and from structures in the central canal of the
spinal cord. The rate and direction of CSF flow is
dependent on the structure of the subarachnoid
space, pressure gradients secondary to arterial and
respiratory pulsations and sudden changes in position. Cerebrospinal fluid is primarily absorbed
through the arachnoid villi which protrude into
the dural venous sinuses. Small quantities are
absorbed along the perineural and perivascular
spaces.
The rate of CSF formation is constant, despite
an ICP of 150 mmHg (200 cmH 2 O). However,
the rate of CSF absorption increases with increased
ICP. Reabsorption is exclusively dependent on the
hydrostatic pressure difference between the subarachnoid space and the dural sinuses. 7-'" Changes
in volume of the intracranial content lead to predictable changes in the CSF pressure, which de-

Journal of the American Association of Nurse Anesthetists

pend not only on the magnitude of the volume

change but also on the craniospinal compliance.
(Compliance is the ratio of change in volume to
the corresponding change in pressure. Compliance
may also be understood as a measure of the stiffness or rigidity of the craniospinal compartment).
The craniospinal compartment becomes noncompliant or "tight," when an increase in the
volume of one of the intracranial constituents is
not accompanied by a reciprocal decrease in the
volume of another. A "slack" or compliant brain
is associated with reciprocal volume changes. 9-11
Intracranial volume-pressure relationships may be
described by the intracranial compliance curve.
(Figure 1.)
Initial compensatory mechanisms which modify increases in ICP include the shift of CSF into
spinal subarachnoid space, the expansion of which
is accommodated by displacement of epidural
venous blood; increased reabsorption of CSF
across the arachnoid villi; and reduction in intracranial blood volume due to the pressure exerted
by the CSF on the thin-walled cerebral veins. 5,12
A slowly increasing mass will displace CSF
from its intracranial compartment through the
foramen magnum into the distensible subarachnoid
space. As ICP begins to increase, CSF absorption
can increase, thus providing additional ICP bufFigure 1
Representation of intracranial volume pressure
relationship.
80
ICP

60

(torr) 4020-

INTRACRANIAL

VOLUME
Between points 1 and 2 initial spatial compensation
prevents an increase in ICP. At point 2 compliance is
reduced and volume additions progressively increase
ICP. At point 3 ICP is already high and even small
increases in volume will result in marked intracranial
hypertension-point 4.
(Shapiro HM: Neurological anesthesia. In: Miller RS, ed.
Anesthesia, pg. 1082, Churchill Livingstone Inc., New York,
Edinburgh, London and Melbourne, 1981. Reprinted by
permission of Churchill Livingstone.)

June/1984

fering; with time, the overall CSF content in the

cerebrospinal axis is reduced. A very important
factor is the time required for spatial compensation. As much as 1 ml CSF/min can be expressed
from the cranial space in the presence of increased pressure. If rapid displacement of CSF
were not possible, rapid expansion of even the
smallest mass would be incompatible with life. 5
When the ability of CSF to act as the ICP
buffer has been exhausted and further spatial
compensation cannot be achieved by reduction in
intracranial blood volume, brain stem compression occurs. Progressive enlargement of the intracranial mass distorts brain tissue and leads to
herniation through the foramen magnum, collapse
of the large CSF cistern and compression of the
arachnoid villi. 5

Cerebral blood flow and ICP

Intrinsic regulation of cerebrovascular resistance (CVR) is the most important determinant
of cerebral blood flow. Many factors influence
CVR by altering the pressure gradient across the
vessels or by changing resistance within them.
Resistance across the vessels refers to arterial and
venous pressure at brain level and ICP. Resistance
within the vessels refers to the degree of active
constriction or dilatation of cerebral vessels and the
viscosity of blood.
Cerebral blood volume (CBV) is equal to the
cerebral perfusion pressure (CPP) divided by the
cerebral blood flow (CBF) :
CPP
CBV --CBF
Factors affecting CVR and, therefore, regulating CBF, include chemical and external factors
such as arterial carbon dioxide tension (PaCO 2),
myogenic (autoregulation) and neurogenic.
Variations in PaCO 2 produce rapid and significant changes in CBF. Carbon dioxide (CO2)
diffuses through vascular walls so that changes in
PaCO 2 are eventually reflected in the PCO 2 of the
CSF. Arterial smooth muscle is extremely responsive to environment pH, which is determined by
a variety of factors including the concentration of
CO2 and bicarbonate ions in the CSF. Carbon
dioxide concentration is largely determined by
PaCO,; bicarbonate concentration is controlled by
cerebral metabolic processes because the bloodbrain barrier is permeable to CO 2 and essentially
impermeable to bicarbonate. Variations of PaCO 2
from 20-80 mmHg produce direct 2% changes in
CBF for every 1 mmHg change in PaCO 2. (Figure 2.) Hypercapnia dilates cerebral vessels and
increases CBF, CBV, and ICP. Hypocapnia con-

265

stricts cerebral vessels, thereby reducing CBF,

CBV, and ICP. Hyperventilation is therefore a
useful therapeutic maneuver in patients with intracranial hypertension.
Arterial oxygen tension is inversely related to
CBF. (Figure 2.) Marked hypoxia (PaO 2 < 50
mmHg) significantly increases CBF and ICP, and
is capable of overriding the effects of hypocarbia.
This appears to be a threshold phenomena, since
increased CBF is not seen until PaO 2 decreases to
a level below which hypoxia causes progressive
brain tissue lactic acidosis. 14
Cerebral blood flow remains relatively constant over a wide range of arterial pressures, provided systemic blood pressure changes relatively
slowly. This phenomena, called autoregulation, is
a mechanism by which arteries alter their diameter
in response to changes in transmural pressure so
that the pressure transmitted to the microcirculation is maintained at a relatively constant level.
In normotensive patients the lower limit of
autoregulation is a mean arterial pressure (MAP)
of 50 mmHg, below which CBF decreases. At a
MAP of 45-55 mmHg, symptoms of cerebral ischemia (nausea, syncope, dizziness, blurred vision,
and so forth) appear. The upper limit of autoregulation in a normotensive patient is 150 mmHg.
(Figure 2.) Above this pressure the constrictor
response is lost and the blood-brain barrier is disrupted, thereby increasing the formation of edema.
In chronic arterial hypertension the autoregulatory curve is displaced to the right. Cerebral
Figure 2
Representation of factors controlling CBF.

100 -

. --

--------

o --

Part

--

5-

\ PI

"y
oI
0

Paco,

50

//

100

150

'

500

Pressure
(torr]

"Part" shows limits of autoregulation, Plc represents

intracranial pressure.
(Samuels SI: Anesthesia for supratentorial tumor. In: Cottrell
JE and Turndorf H, eds., Anesthesia for Neurosurgery, pg.
153, C.V. Mosby Co., St. Louis, Toronto and London, 1980.
Reprinted with permission of C.V. Mosby, Co.)

266

vessels adapt to higher pressure levels, and upper

and lower limits of autoregulation are increased.
In awake patients with hypertension (MAP's between 125-180 mmHg), the lower limits of autoregulation are 90-125 mmHg. In these patients
clinical signs of cerebral ischemia occurred when
the MAP ranged between 35-80 mmHg.5 Chronic
hypertensives should not be subjected to pressures
as low as those tolerated by patients with normal
4,5, 9-1
blood pressure.
Cerebral perfusion pressure (CPP) is an estimate of the pressure gradient between the internal
carotid artery and the subarachnoid veins, that is,
the pressure gradient across the entire brain. Cerebral perfusion pressure is equal to the MAP
minus the ICP: CPP = MAP - ICP.
In functioning autoregulation, CPP ranges
from 85-95 mmHg. Cerebral perfusion pressure
may be narrowed by either a fall in MAP or an
4, 7 1
increase in ICP. Neurogenic influence on CBF is small. The
larger arteries and arterioles on the surface of and
within the brain are supplied with sympathetic
nerves from the superior cervical ganglion and
with parasympathetic nerves from the greater
petrosal branch of the facial nerve. Combined experimental studies indicate that maximal stimulation of sympathetic nerves reduces CBF 5-10%; a
similarly moderate vasodilator response has been
observed with parasympathetic stimulation. Perhaps the major contribution of neurogenic influence on CBF is seen during hemorrhagic hypotension where sympathetic stimulation enhances
the tone of the arterial vessels so that the autoregulatory response curve is shifted to the right.
Acute hypertension or hypotension is better tolerated if the sympathetic nerves are stimulated
10 11, 16
simultaneously. ,
If the injury to the brain is great enough, the
resultant responses include depressed neuronal
activity, acidosis, edema and disturbances of all
CBF regulatory mechanisms. Brain lactic acidosis
is characterized by cerebral vasomotor paralysis,
particularly abolished autoregulation. The formation of edema is related, in part, to vasomotor
paralysis which tends to increase capillary hydrostatic pressure, and damage to the blood-brain
barrier. The combination of hypercapnia, cerebral
acidosis, impaired autoregulation, and systemic
hypertension promote the formation and spread of
edema. Edema distorts brain tissue and further increases ICP, which induces even more tissue hy4,5,8 9,12
poxia and acidosis.

The signs and symptoms associated with increased ICP are related to traction on cerebral

Journal of the American Association of Nurse Anesthetists

vessels, distortion of the pain-sensitive dura mater,

impending herniation and intermittent vascular
compression, or midline shifts or axial distortion
of the brain stem. Headache, nausea, vomiting
and papilledema are symptoms of increased ICP.
Changes in vital signs have served as an accurate
index of the severity of intracranial hypertension.
The combination of systemic hypertension, bradycardia and respiratory irregularity (an occurrence
secondary to cerebral ischemia and medullary
compression), is known as the Gushing Response.
Third nerve dysfunction, decerebration, alterations in muscle tone and loss of consciousness also
0
5 ,9 1
occur with severe distortion of brain mass. '

Neurodiagnostics
Computerized axial tomography (CAT scan)
is used for diagnosis of increased ICP. Other diagnostic tests which are helpful include pneumoencephalography, ventriculography, cerebral angiogram and myelogram.
General anesthesia for neuroradiologic procedures may be required in pediatric patients and
with extremely apprehensive or uncooperative
adults. Choice of anesthetic agent should be based
on neuroanesthetic principles which will be discussed in detail. However, nitrous oxide (N 20)
is not recommended after air studies have been
done since up to seven days are required for air
injected into the ventricles to be absorbed. 17
Nitrous oxide will expand this air and may produce a further increase in ICP. Complete reabsorption of air can be confirmed by x-ray.
Management
The initial treatment of patients with acute
elevation of ICP is rapid reduction of the intracranial volume to decrease ICP, improving cerebral perfusion and energy supply and demand. In
addition, brain shifts and distortions and their
associated systemic effects may be corrected.
Endotracheal intubation and mechanical ventilation are used to maintain PaO 2 of normal
values and hypocarbia. Most traumatic head-injured
patients spontaneously hyperventilate as a result
of severe intracerebral metabolic acidosis caused
by the brain injury. Controlled hyperventilation
must be guided by arterial blood gases. It is recommended that PaCO 2 be 25-30 mmHg. There is
evidence that a PaCO 2 of less than 20 mmHg
reduces CBF to near minimal values, causing tissue
hypoxia. Although cerebral vascular CO 2 reactivity
is impaired in areas of injury, CO 2 reactivity may
remain in the surrounding tissue. Hyperventilation will stimulate an attempt at restoration of

June/1984

normal cerebral pH and, therefore, the preservation of viable brain tissue. Hyperventilation may
also allow corticosteroids to begin reducing cerebral edema. 9,11
Sedatives and muscle relaxants may be necessary to facilitate intubation and to maintain controlled ventilation without increasing MAP or
edema. If the blood brain barrier is intact, osmotic
diuretics reduce ICP by increasing plasma osmolality greater than brain osmolality with subsequent renal excretion of brain extracellular water.
Cerebrospinal fluid formation is also decreased.
Mannitol is often used and is administered intravenously in a dose of .25-0.5 g/kg given within 15
minutes. Mannitol begins to reduce ICP within
10-15 minutes. The effect of the initial dose lasts
at least 2 hours.
Some of the disadvantages of mannitol inherent in all osmotic dehydrating agents include:
transient increases in circulating and cerebral
blood volumes and ICP, changes in blood coagulation and viscosity, increased serum osmolality and
decreased serum electrolytes. These effects are attenuated or prevented when the smaller dose of
.25-0.5 g/kg is used instead of the standard recommended dose of 1.0 g/kg.
Recent studies have advocated the use of
furosemide (Lasix) s8 or ethacrynic acid (Edecrine) 19 for reduction of intracranial hypertension. Systemic diuretics reduce ICP by (1) reducing the volume of the intracranial contents in
proportion as the percentage amount of total body
water decreases, and (2) by decreasing CSF formation. Both furosemide and ethacrynic acid have
direct effects on brain cells; they decrease chloride
and water transport into astrocytes of damaged
brain tissue, thus preventing cytotoxic edema. As a
primary diuretic, in doses of 1.0 mg/kg, furosemide reduced ICP without significant osmolar or
electrolyte change. Furosemide may be used as an
adjuvant in doses of .15-.30 mg/kg. With any
diuretic, serum potassium is measured frequently
and replaced if decreases below 3.5 mEq/L occur.
Steroids are commonly used to decrease vasogenic edema associated with tumor, hematoma or
abscess. They may be less effective in edema associated with acute infarction or cytotoxic edema
from asphyxia, hypoxia or hypo-osmolality. The
mechanism by which steroids affect cerebral edema
is not known, however their effectiveness is thought
to be due to stabilization of the blood-brain barrier and enhancement of cerebral energy supply
and metabolism. Steroids will not rapidly reduce
ICP; however, within hours they may improve
the neurologic status of those patients in whom

267

vasogenic injury is complicated by edema. Dexamethasone, 10-20 mg initially followed by 16-64

mg/day, 10 or methylprednisolone, 100 mg followed
9 16
by 100 mg/day, has been used. '
Reversal of impending herniation has been
reported following aggressive management with
hyperventilation, dehydrating agents and sedatives.
These treatment modalities are utilized to some
extent for patients with non-acute neurologic
pathology as well as in the crisis situation.
When the acute situation has stabilized, further treatment modalities may be considered to
include barbiturates or sedatives, temperature
control, CSF diversion, and surgical decompres59o
sion. ' , ,
The use of barbiturates has been shown to be
effective in reducing ICP without a simultaneous
reduction in CPP. There is a dose-related depression in cerebral metabolism and a significant reduction in CMRO 2, theoretically affording the
brain some protection during periods of hypoxia. 5
Since in the doses required to lower ICP (1.0-8.0
mg/kg/hr of thiopenthal or pentobarbital), signs
of neurologic deterioration are masked, it is recommended that barbiturates be reserved for patients
in coma. Prolonged barbiturate-induced coma and
improvement in neurologic outcome with treatment of resistant intracranial hypertension has
been under intense investigation. Therapeutic effectiveness and improvement in neurologic outcome is under debate. Recent investigations suggest that barbiturate therapy may have no benefit
in cases of global ischemia. In addition, the complication rate, and amount of time and personnel
necessary to maintain a prolonged anesthetic state,
is extremely costly. 20

Induced hypothermia is seldom used although

it has been employed for a variety of clinical situations-most notably clip ligation of intracranial aneurysms. Hypothermia reduces CBF and CMRO 2.

For each degree decrease below 370 C, CMRO 2 is

decreased 7%. Among the complications of induced hypothermia are cardiac arrhythmias, and
shivering during cooling and rewarming which increases CMRO 2 by 50-200%. 21 Moderate hypothermia in combination with drugs that have an

anti-edema effect

(barbiturates, steroids)

may

prove to be a better alternative. 5

Cerebrospinal fluid diversion is indicated

when ventricular fluid outflow pathways are obstructed and/or intracranial CSF pathways are
obliterated. Cerebrospinal fluid diversion is accomplished with the insertion of ventriculoatrial
shunt, ventriculoperitoneal shunt or, though rarely,
ventriculolumbar shunt. The ventricular drainage

268

shunts reduce ICP by providing a low resistance

pathway for CSF drainage.
Surgical decompression, external and/or internal, may be done for uncontrollable brain swelling, especially in patients with severe craniocerebral trauma. External decompression involves removal of part of the skull, and is usually done for
evacuation of epidural or subdural hematomas.
Internal decompression involves removal of part
of the brain. The major effect of decompressive
surgery is the reduction in midline shift, brain
herniation and/or brain stem displacement. 10
Anesthetic management
Anesthetic management is based upon the
knowledge that the injured brain has regions of
tissue acidosis, loss of autoregulation, loss of metabolic control of tissue perfusion and loss of CO 2
reactivity. The choice of anesthetic techniques is,
therefore, determined by their effects on CBF,
CMRO 2 and ICP.
The preoperative anesthetic visit includes
evaluation of the state of intracranial tension and
general medical condition. Traumatic head-injured patients should be carefully assessed for possible internal injuries of the chest and abdomen.
Patients with decreased consciousness should be
assessed for possible aspiration pneumonitis. Chest
x-ray and arterial blood gases will help in the
clinical assessment. Intravascular volume and electrolyte balance must be evaluated, especially in
those patients treated with diuretics. 21
The presence of intracranial hypertension determines the use of premedicants. Lethargic, obviously obtunded patients should receive no premedication. In patients with no or minimal symptoms
of increased ICP, small doses of anti-emetic sedatives or diazepam may be given. Diazepam has
minimal cardiorespiratory effects, reduces CBF,
31 ,3 5
Hyand has amnesic and anti-seizure activity.
droxyzine (Vistaril) has sedative and anti-emetic
effects and little effect on ICP.31,35 Atropine or
glycopyrrolate may be used to prevent excessive
secretions and vagal reflexes. However, atropine is
not recommended in patients presenting with cerebral aneurysms because of the increased heart rate
(HR) and MAP. 21
Narcotics as premedicants are avoided because
of their potential respiratory depression, decreased
levels of consciousness, nausea, vomiting, and pupil
constriction. Likewise the butyrophenones (droperidol) are avoided because of their respiratory
depressant and hypotensive effects.

Monitoring
Management of the brain-injured patient is

Journal of the American Association of Nurse Anesthetists

most rationally approached by first obtaining a

measurement of ICP. This can be accomplished
by one of several methods: an intraventricular
catheter, a subdural bolt or an epidural cup-catheter. (Figure 3.) Measurement of ICP during the
perioperative period will alert the anesthetist to
dangerous increases in pressure and allow for rapid
treatment.
Direct blood pressure monitoring allows for
careful control of blood pressure and frequent
analysis of arterial blood gases. The radial, femoral, brachial, axillary and dorsalis pedis arteries
are suitable for short-term cannulation.
A peripheral nerve stimulator will help to
assess the extent of muscle paralysis. Muscle relaxation is necessary to prevent straining and coughing
on the endotracheal tube, and any movement during dissection of vital structures.
Measurement of urinary output via a Foley"
catheter provides assessment of volume status and,
during periods of hypotension, may indicate decreased renal perfusion.
An esophageal stethoscope provides continuous auscultation of heart and breath sounds. An
esophageal temperature probe provides continuous
observation of body temperature. Because hyperthermia increases CMRO 2 and CBF, it must be
promptly treated.
Figure 3
Illustration of commonly used techniques and sites
for intracranial pressure monitoring.
SUBURAL BOLT

FROM EPIDURAL
TRANSDUCER
I

TRANSDUCER

Air embolus
During operations when the patient is in the
sitting position, air entrainment is a major complication. Whenever the wound is 5 cm or more
higher than the level of the right heart, a negative
pressure is created in the venous system and air
entrainment can occur. A right atrial catheter,
placed through the subclavian, basilic, or internal
or external jugular veins, provides a route for
aspiration of air. Experimental evidence indicates
that maximum aspiration of air is accomplished
when the catheter tip is just below the junction of
the superior vena cava and the right atrium. A
multi-orificed catheter would withdraw more air
than a single-orifice catheter. In addition, a multiorificed catheter would eliminate the possibility
of suction adhesion to the chamber wall, and efficiency of the catheter would not be as severely
compromised by clot formation. 22 Exact location of
the catheter may be confirmed by chest x-ray.22
The right atrial catheter is also useful for infusion
of fluids and drugs as well as measurement of
cardiac filling pressures.
The Doppler TM is reportedly the most sensitive device for detection of air emboli. However,
recent investigations have found that the DopplerTM detected air which was of no clinical significance and valuable operative time was wasted
treating air emboli. Clinically significant air emboli can be detected by either the Swan-GanzTM
catheter or the end-tidal CO 2 monitor (FETCO2 )
(either one in conjunction with a precordial DopplerTM). Both monitoring devices were equally
rapid in (1) detecting the clinical significance of
air (the DopplerTM detected air no more than 30
seconds before pulmonary artery pressure (PAP)
or FETCO 2 changes developed), and (2) indicating the resolution of the embolus and the safe
continuation of surgery.23
Venous air embolism causes intense pulmonary vasoconstriction which results in markedly
increased pulmonary vascular resistance. Small
volumes of air in the pulmonary circuit are reflected by increased PAP and ventilation-perfusion
abnormalities which are reflected in a decreased
FETCO 2 and/or increased venous admixture. 23
End tidal CO 2 is inversely related to the PaCO z.

Induction of anesthesia

(Shapiro HM:

Neurological anesthesia.

In: Miller RS, ed.

Anesthesia, pg. 1093, Churchill Livingstone Inc., New York,

Edinburgh, London and Melbourne, 1981. Reprinted by
permission of Churchill Livingstone.)

June/1984

The anesthetic technique is determined by

the effects of drugs and maneuvers on CBF, CBV,
CMRO2 and ICP. Investigators have documented
intraoperative increases in ICP during laryngoscopy, intubation, application of head clamps, and
insertion of the Gigli saw guide. In those patients

269

who presented with increased ICP preoperatively,

the increase in pressure during perioperative maneuvers was significant. 25 Appropriate anesthetic
techniques will prevent or attenuate this response.
Sodium thiopental, a potent cerebral vasoconstrictor, increases CVR and decreases CBV and
ICP. In addition, CMRO 2 is significantly decreased and parallels the decrease in CBF. Althesin
is a steroid compound with short-lasting anesthetic
properties. Although not available in the United
States, it is a popular drug for induction and
maintenance of anesthesia in Great Britain. Althesin has much the same effect as barbiturates;
potent vasoconstriction with a decrease in CBF,
CMRO 2 and ICP. 11
Midazolam maleate is a water soluble benzodiazepine recently introduced for induction of
anesthesia. Recent investigations have found that
midazolam does not increase ICP when used as an
induction agent in patients with brain tumors. 26
Prevention of increased ICP during laryngoscopy and intubation is achieved by total muscle
relaxation in a well narcotized or sedated patient.
Pancuronium bromide, .06-0.1 mg/kg is the muscle
relaxant of choice for intubation and maintenance
since ICP changes are insignificant following its
use. The mild tachycardia that occurs with pancuronium has been reported to result from vagolysis.
For patients requiring rapid sequence induction,
0.20 mg/kg of pancuronium may be used since
onset is as rapid as with succinylcholine. 27 Gallamine has also been found to produce a mild tachycardia with no significant alteration in ICP. 28
Succinylcholine has been shown to moderately
increase ICP even when fasciculations have been
prevented. 24,25,30 Recent reports have noted suc-

cinylcholine-induced hyperkalemia in patients with

closed head injury and no evidence of peripheral
paralysis. 31 Although succinylcholine is not contraindicated in patients with intracranial pathology,

parallel reduction in CMRO 2. 46 Morphine and

meperidine decrease CMRO 2 and CBF during hypocapnia. During normocapnia these narcotics
33 46
have shown no significant effect on CBF. '
Administration of intravenous lidocaine 1.5
mg/kg one minute before laryngoscopy will prevent increases in ICP associated with endotracheal
stimulation.35 Additional doses of lidocaine may
be given prior to noxious stimuli to prevent increases in ICP without cardiovascular depression.
Equipotent doses of pentothal are as effective to
control intracranial hypertension, however, arterial
pressure would also be significantly reduced. In
patients with intracranial hypertension and systemic hypotension, a further reduction in arterial
36 3 7
pressure may compromise cerebral perfusion. *
Droperidol (0.3 mg/kg) significantly decreases
CBF and, to a lesser extent, CMRO 2. Persistant
postoperative drowsiness may mask signs of intracranial events since central nervous system (CNS)
depression may persist for 6-24 hours.3 3 The benzodiazepines, notably diazepam, may also be used as
an adjuvant. Diazepam has been shown to cause a
34, 8
parallel reduction in CBF and CMRO 2.
Ketamine causes profound cerebral vasodilation and greatly increased CNS activity and is,
therefore, not recommended. 89
Nitrous oxide, when used with oxygen will

Figure 4
Measurement of CBF in volunteers receiving various
levels of MAC for halothane, enflurane and isoflurane.
Cerebral Blood Flow
(ml/min/loog)

Halothane
1

150

1/

pancuronium is considered to be a safe alternative.

In addition to the non-depolarizing property

of d-Tubocurarine, ganglionic blockade and histamine release occurs. Cerebral blood vessels may
dilate and increase CBV and ICP. 28 Metocurarine

(metubine iodide) is a non-depolarizing muscle

relaxant similar to d-Tubocurarine in onset time

and duration of action. Among the non-depolarizing muscle relaxants available in the United States

(metocurarine, pancuronium, gallamine and dTubocurarine), metocurarine produces the least

Enflurane

100

50

X SE
I

ne
2

MAC
The volunteers were paralyzed with d-Tubocurarine.
PaC02 and SAP were kept at normal levels.

cardiovascular change. The effect of metocurarine

on intracranial dynamics is presently being investigated.

Fentanyl (.006 mg/kg) reduces CBF with a

270

(From Eger, El II, Isoflurane: A compendium and reference,

1981. Reprinted with permission by Ohio Medical Anesthetics, Division of Airco.)

Journal of the American Association of Nurse Anesthetists

cause cerebral vasodilation and thereby increase

CBV and ICP. However, the cerebral vasoconstrictive effects of hyperventilation, barbiturates
and narcotics will counteract this response when
used concomitantly. 40
The volatile anesthetics, halothane, enflurane,
and isoflurane are potent cerebral vasodilators, and
cause dose-dependent increases in CBF and ICP.
(Figure 4.) Impairment of autoregulation is directly proportional to the dose (1.1-1.6 MAC).
The concomitant decrease in MAP and increase in
ICP can severely compromise CPP.48'49 Although
hyperventilation prior to the introduction of inhalational anesthetics should attenuate the increase
in ICP, reports of ICP elevation, despite hypocarbia, do exist.43 Hyperventilation may fail to
prevent a rise in ICP because vascular response to
changes in CO2 is impaired in areas of injury.
Halothane concentrations greater than 0.5
MAC reduce CPP and CVR. Furthermore, halothane has been found to alter brain water and
electrolyte distribution and permeability of the

June/1984

blood-brain barrier, thus contributing to the for43 44

mation of cerebral edema. .
Convulsant activity, as noted by the electroencephalogram, occurred with enflurane administration, especially during the period of deep anesthesia combined with hypocarbia. 4 5-47 As with
halothane and enflurane, hyperventilation prior to
the introduction of isoflurane may prevent an
increase in ICP. During normocapnia, isoflurane
produced a 25% increase in ICP, while halothane
and enflurane produced pressure increases of
100%. 5 Animal studies indicate that the effect of
isoflurane on brain water and electrolyte distribution after cryogenic injury is comparable to that
seen with halothane. 51 Comparison studies in animals indicate that an increase in ICP and edema
were greatest with the volatile anesthetics and least
with barbiturates or neurolept anesthetics. 51 (Table
I reviews the effects of anesthetic agents on intracranial dynamics in patients with head injury.)
Fluid management

These patients may have a depleted intra-

271

vascular volume due to aggressive diuretic therapy,

poor oral intake and restriction of intravenous
fluids. An adequate circulating blood volume is
necessary to prevent severe hypotension on induction and with position change.
Content of intraoperative fluids and the rate
of fluid administration depend on the preoperative
fluid deficit, maintenance fluid requirements, urine
output and blood loss. Fluid loss and input should
remain relatively equal. Blood replacement depends on intraoperative losses and preoperative
hematocrit. It is best to replace blood loss with
blood and not with crystalloids. Colloids should be
avoided as they may easily pass through a disrupted
blood-brain barrier and increase cerebral edema.
Lactated Ringer's is the solution of choice. Administration of dextrose should be less than 100
gms/24 hours, as dextrose acts as a diuretic and its
resultant water of oxidation will increase edema
formation. Urine output, serum and urine osmolality and electrolytes, and hematocrit should
be frequently monitored throughout the perioperative period. 52
Blood pressure control
Acute, traumatic brain injured patients frequently present with systemic hypertension. This
is a necessary mechanism to maintain cerebral
perfusion; hypertension at this time should not be
aggressively treated. If hypertension persists after
decreasing ICP to less than 20 mmHg, steps should
be taken to restore normal cardiovascular hemodynamics and prevent rebleeding and increased
ICP.
Systemic hypertension can occur intraoperatively as a result of light anesthesia or surgical
manipulation and retraction of the brain stem or
cranial nerves. If deepening of anesthesia or discontinuing surgical stimulation does not resolve
the hypertension, then antihypertensives are indicated. Sodium nitroprusside, trimethaphan, hydralazine or nitroglycerine may be used. It is not
within the scope of this article to elaborate on
methods of antihypertensive therapy. The authors
to the references at the end of the
refer the reader
2 55 58
article. 1, Emergence and immediate postoperative care
Emergence from anesthesia must be smooth;
the patient must not cough or strain on the endotracheal tube as this will increase systemic blood
pressure and ICP and threaten hemostasis. Lidocaine intravenously may be helpful in preventing
coughing and straining while the head dressing is
being applied. Emergence from anesthesia and re-

272

versal of muscle relaxants depends upon the patient's preoperative status, area of surgical manipulation, and intraoperative problems.
Patients who were unconscious preoperatively,
not responsive postoperatively or who had lesions
in the area of the respiratory center (surgical
stimulation can cause significant postoperative
edema and respiratory depression can ensue, requiring reintubation) are kept asleep and paralyzed.
Stable, responsive patients may be reversed
with neostigmine or edrophonium and atropine or
pyridostigmine and glycopyrrolate. Those patients
who are asleep but breathing adequately and
tolerating the endotracheal tube should remain
intubated to prevent regurgitation and aspiration.
Controlled ventilation and hypocarbia should be
maintained during the postoperative period until
the patient demonstrates an ability to maintain
adequate ventilation and protective reflexes have
returned. Patients who have regained protective
reflexes may be extubated in the operating room
following established criteria. Persistent respiratory depression after reversal of muscle relaxation
and reaccumulation of CO 2 may be treated with
minimal doses of naloxone (0.1-0.4 mg). Narcotic
reversal is rarely necessary and should be avoided
53 54
if increased MAP is undesirable.
Heart rate and rhythm and blood pressure
are monitored during the patient's transport from
the operating room to the recovery room. Continuous cardiovascular and ICP monitoring is resumed in the recovery room. Laboratory tests including ABG's, serum and urine osmolality and
electrolytes, glucose and chest x-ray are done frequently throughout the postoperative period.
Steroids, diuretic therapy and fluid restriction are
16 21,24,25
continued to minimize cerebral edema.5 '

Summary:
Patients presenting with neurologic injury
represent one of the most challenging situations in
clinical anesthetic practice. Most investigators and
clinicians have obtained optimal results with a
balanced narcotic anesthetic coupled with intensive management of cardiovascular, pulmonary and
intracranial dynamics.
An understanding of intracranial dynamics
and the effects of therapeutic and anesthetic intervention can make a significant difference in the
prognosis of the brain injured patient.
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AUTHORS
Barbara Shwiry, CRNA, graduated from Kings County
Hospital School of Nursing in 1975. She received her anesthesia
education from the Medical College of Pennsylvania in Philadelphia. She is presently on Staff at Kings County Hospital,
Department of Anesthesiology and is a Clinical and Didactic
Instructor in Neuroanesthesia at the Kings County Hospital
Center School for Nurse Anesthetists. Ms. Shwiry is involved in
several research projects concerning neuroanesthesia and is
Clinical Research Coordinator for the School of Nurse Anesthesia.
Joseph P. Giffin, MD, is Assistant Professor, Department of
Anesthesiology, State University Hospital, Downstate Medical
Center, Brooklyn, New York.
James E. Cottrell, MD, is Professor and Chairman, Department of Anesthesiology, State University Hospital, Downstate
Medical Center, Brooklyn, New York.

Journal of the American Association of Nurse Anesthetists