Otolaryngol Clin N Am

40 (2007) 455–462

Intracranial Pressure Concerns in Lateral

Skull Base Surgery
Rebekah Clemena, Douglas D. Backous, MD, FACSb,*
a
Seattle Pacific University, P.O. Box 900, X10-0N, Seattle, WA 98111-0900, USA
b
Otology, Neurotology and Skull Base Surgery, Section of Otolaryngology-Head
and Neck Surgery, Virginia Mason Medical Center, 1100 Ninth Avenue,
X10-0N, Seattle, WA 98101, USA

Cerebrospinal fluid (CSF) leaks occur in 2% to 30% of lateral skull base

procedures [1]. Less appreciated are transient or intermittent increases in in-
tracranial pressure (ICP), which can manifest as delayed arousal from anes-
thesia or persistently poor mental status after a prolonged procedure.
Because of anatomic proximity to and manipulation of critical vascular
structures in the neck and skull base, patients are at risk for ICP fluctuations
with potentially severe sequelae. Understanding the basic principles of CSF
formation and resorption, the connection of venous pressure to ICP, and ar-
terial autoregulation is critical in designing safe surgical approaches in the
lateral skull base.
This article serves as a concise review of CSF metabolism and ICP regu-
lation for otolaryngologists and lateral skull base surgeons. It examines the
methodologies for preventing and treating acute elevations of ICP encoun-
tered during lateral skull base surgery.

Cerebrospinal fluid metabolism and intracranial pressure regulation

In adults, the average CSF volume ranges from 90 to 150 cm3, with 40 cm3
in the lateral ventricles. CSF is produced in the choroid plexus, a highly con-
voluted region of pia mater located throughout the intracranial ventricular
system. CSF circulates by way of the foramen of Monroe into the third ven-
tricle and continues through the sylvan aqueduct into the fourth ventricle.
Flow continues through the subarachnoid space into the spinal canal via

This work was supported by the Listen for Life Foundation at the Virginia Mason
Medical Center.
* Corresponding author.
E-mail address: otoddb@vmmc.org (D.D. Backous).

0030-6665/07/$ - see front matter Ó 2007 Elsevier Inc. All rights reserved.
doi:10.1016/j.otc.2007.03.012 oto.theclinics.com
456 CLEMEN & BACKOUS

the foramina of Luschka (laterally) and Magendie (midline) into the spinal
canal. CSF is absorbed into the cerebral venous system through arachnoid
villi, which are located mainly in the sagittal sinus (Fig. 1) [2].
CSF has four main functions. It provides physical support and buoyancy
for the brain. This ‘‘water jacket’’ is protective because CSF volume fluctuates
reciprocally with changes in intracranial blood volume to contribute to a safe
ICP. Because the brain is devoid of a lymphatic system, byproducts of metab-
olism are principally removed by the capillary circulation or directly by trans-
fer through the CSF. The direct CSF route is particularly important when
increased amounts of lactic acid are produced in the brain. Finally, CSF main-
tains a safe chemical environment for brain tissues [3].
Because of the phenomenon of autoregulation, the brain is able to regu-
late arterial blood flow in accord with metabolic demand. Intracranial

Fig. 1. Schematic diagram of CSF production and absorption pathways. The circulation of the
CSF to the subarachnoid space and its absorption into the venous systems via the arachnoid
villi are shown.
 LATERAL SKULL BASE SURGERY 457

arterial blood flow is maintained constantly over a range of perfusion pres-

sures from 60 to 150 mm Hg. Loss of autoregulation results in cerebral
blood flow and blood volume passively fluctuating with changes in systolic
pressure, which is most commonly seen in end-stage intracranial hyperten-
sion. Unlike the arterial system, the central venous system does not autore-
gulate. Acute fluctuations in venous pressure directly impact CSF pressure.
Normal limits of ICP range from 5 to 15 mm Hg or 65 to 195 mm H2O in
the prone position. ICP varies with circulatory cycle and respiratory phase,
age, and position. Factors that control ICP can be summarized as:

ICP ¼ If  Rout þ Pss

where If is CSF formation rate, Rout is resistance to outflow of CSF, and Pss
is sagittal sinus pressure.
A large increase in the rate of CSF formation, as in the rare instance of
a choroid plexus papilloma, would be required to create an impact CSF
pressure. Outflow resistance can be altered by increased protein concentra-
tion in the CSF, inflammatory changes in the dura caused by meningitis, or
blood in the subarachnoid space causing resistance to outflow by impairing
CSF absorption at the arachnoid villi [4]. Superior vena cava syndrome, jug-
ular venous occlusion, surgical removal of a dominant jugular vein, and
acute thrombosis of the sagittal sinus elevate sinus pressure and impair
flow from the subarachnoid space.
Central venous anatomic variations may predispose patients to transient
ICP changes intraoperatively. Approximately 41.3% of people are right
dominant, 37.6% have equal drainage, and 18.5% are left dominant in re-
gard to drainage through the sigmoid sinus and jugular bulb. Two percent
have only right-sided venous outflow, and 0.53% have left-only drainage
through the skull base into the neck (Fig. 2) [5].
Positioning the neck in a flexed position on a shoulder roll, a common
technique in head and neck surgery, can compromise venous drainage in
a dominant jugular vein and result in elevated ICP. Compounding this prob-
lem is the placement of central venous catheters in the jugular system during
surgery, sacrifice of an internal jugular vein during neck dissection, or cases
that require sacrifice of a jugular bulb to remove a neoplasm. When evalu-
ating CT or MRI scans during preoperative planning, surgeons should
determine the side of dominance for jugular venous outflow to prevent po-
tential complications.
The Monro-Kellie hypothesis states that the skull is a rigid sphere occu-
pied by noncompressible, liquid/gel tissues [6,7]. Blood (75 mL), CSF (150
mL), and brain matter (1400 mL) are the principal tissues in the cranial
vault. Acute changes in ICP result in shifting or compression of the fixed
brain liquid/gel mass within the intracranial cavity. Compression of brain
against the falx cerebri or tentorium cerebelli, herniation through the fora-
men magnum, or leakage of CSF from sites in the skull or spinal canal can
458 CLEMEN & BACKOUS

Fig. 2. Axial T1-weighted MRI with gadolinium of the posterior fossa shows right-sided
venous outflow dominance (A). Non-dominent sigmoid sinus (B).

occur in situations in which ICP remains high or when there has been spon-
taneous, traumatic, or iatrogenic violation of the dura.

Localization of dural defects

Identification of dural defects and CSF leaks at the time of surgical dis-
ruption is essential to prevent the progression of avoidable complications. If
a defect is not identified or a CSF leak develops postoperatively, localization
of dural violation is crucial to the management of CSF leakage. Recent ad-
vances in CT and MR technology have allowed detailed imaging of the skull
base with greater diagnostic accuracy.
High-resolution CT remains the primary imaging modality for localiza-
tion of cranial vault defects. Although limited to identifying bony defects,
high-resolution CT scans are often the only modality needed for diagnosis
(Fig. 3A, B) [8]. The addition of intrathecal fluorescein increases the diag-
nostic accuracy of a CT but does carry the risk of brain irritation resulting
in seizures [9]. Partial volume averaging can introduce false-positive findings
in up to 9.5% of cases with inactive CSF leaks [10].
CT cisternography may be used in conjunction with high-resolution CT
imaging. This modality serves as a complementary test in cases of false-pos-
itive and false-negative results. CT cisternography demonstrates movement
of contrast through the defect with a sensitivity of 85% and is particularly
useful when the frontal and sphenoid sinuses act as reservoirs [11,12]. A
weakness of high-resolution CT and CT cisternography is the inability to
detect inactive leaks at the time of study. Such procedures are also invasive
and cumbersome and increase patient exposure to radiation.
MRI and MR cisternography provide noninvasive alternatives to intrathe-
cal contrast-enhanced high-resolution CT. These techniques can distinguish
 LATERAL SKULL BASE SURGERY 459

Fig. 3. (A) Intraoperative view of right tegmen dehiscence (B) High-resolution coronal CT scan
of the right temporal bone. The white arrow indicates a tegmen defect.

inflammatory tissue from meningoencephaloceles but do not define bony de-

tails, as with CT scanning. A fast spin echo sequence with fat suppression and
image reversal on MR cisternography highlights the fistula because CSF
sharply contrasts with the faded surrounding tissues [13]. As with CT, there
must be an active leakage at the time of the study; however, serial MR studies
can be performed efficiently and without extensive radiation exposure (Fig. 4).

Acute management of elevated intracranial pressure

Early identification of elevated ICP facilitates appropriate acute manage-
ment. In patients without ICP monitoring, symptoms such as delayed or

Fig. 4. Sagittal T1 MRI shows diffuse dural enhancement (arrow) in a case of low CSF pressure
and CSF leak.
460 CLEMEN & BACKOUS

failed ability to arouse after anesthesia, relapsing loss of consciousness in the

postoperative period, visual changes, severe headache, or persistent CSF
leakage necessitate an emergent head CT or MRI to assess for effacement
of the cerebral hemispheres or ventricular enlargement. Acute medical man-
agement of CSF leaks begins with intubation and hyperventilation, osmotic
diuresis, or placement of a lumbar drain.

Hyperventilation and osmotic diuresis

Hyperventilation reduces brain engorgement by immediately decreasing
ICP and cerebral blood flow by using the vasoconstrictor effects of respira-
tory alkalosis [14]. For patients who have acute brain swelling intraopera-
tively or who are already on assisted ventilation, dropping the end-tidal
PaCO2 to 25 to 27 mm Hg has a rapid effect of lowering ICP until a source
for the pressure increase can be determined. If postoperative patients relapse
into unconsciousness, intubation for airway protection and hyperventilation
should be considered.
Mannitol is also a rapid and effective method for reducing ICP [15]. Its
use results in an osmotic diuresis; the altered osmolar gradient facilitates
fluid shifts and reduces cerebral edema. Given intravenously at a dose of
1 g/kg body weight over a period of 10 to 15 minutes, mannitol causes
a rise in serum osmolality of approximately 20 to 30 mOsm/L, with return
to control levels in approximately 3 hours. A dose of 1.5 to 2 g/kg body
weight lowers CSF pressure significantly for 3 to 8 hours, but repeat use
risks a rebound effect with increased ICP [14]. Urine output should be
matched with crystalloid replacement to maintain intravascular volume be-
cause osmotic diuretics can cause hypovolemia, which further compromises
venous outflow from the brain.
ICP monitoring facilitates immediate assessment of prescribed interven-
tions. Inclusion of a neurosurgeon or critical care specialist and placement
of the patient in an intensive care unit setting until stability is achieved
are mandatory.

Lumbar puncture
External lumbar drainage is a common modality used postoperatively for
prevention or treatment of CSF fistulae. It serves as a helpful control of ICP
through the removal of designated amounts of CSF based on daily produc-
tion of CSF. Overdrainage may create a negative ICP and result in
pneumocephalus.

Lumbar drain
External lumbar drainage is commonly used as an intraoperative or post-
operative adjunct for preventing or treating CSF fistulae. Extreme caution
must be exercised regarding the amount of CSF drained; overdrainage
 LATERAL SKULL BASE SURGERY 461

can result in headaches or violation of dural bridging veins and result in sub-
dural bleeding. External lumbar drainage is an effective modality; however,
the duration should be restricted because the risk of complications increases
with the duration of drain maintenance [16].

Chronic management
Lumboperitoneal shunts
Lumboperitoneal shunts are valuable therapy for CSF decompression in
the setting of communicating hydrocephalus but are ill advised in cases of
noncommunicating hydrocephalus because of risk of tonsillar herniation
[17]. The lumboperitoneal shunt has a single-chamber reservoir and two dis-
tal slit valves. Similar to external lumbar drainage, the perforated end of the
catheter is introduced into the subarachnoid space. The end of the catheter
with the slit valves is tunneled subcutaneously to the abdominal region and
inserted into the peritoneum. Prevention of catheter misplacement is greatly
increased through meticulous dissection and identification of various tissue
layers.
Complications associated with lumboperitoneal shunts include bowel in-
jury, wound infection, obstruction, spinal epidural hematoma, and over-
drainage headaches. No reservoir or flush chamber is available for CSF
withdrawal or fluid injection with the umboperitoneal shunt. If overdrain-
age headaches result, the lumboperitoneal shunt is either ligated or removed.
Such patients may require the placement of a ventriculoperitoneal shunt
with a programmable valve that allows for drainage volume adjustments [3].

Ventriculoperitoneal shunts
Ventriculoperitoneal shunting is used to relieve chronically elevated ICP
caused by hydrocephalus through the redirection of CSF from the ventricles
of brain into the abdominal cavity. Ventriculoperitoneal shunt systems in-
volve three components: a ventricular catheter, a valve reservoir, and a peri-
toneal catheter. The ventricular catheter is inserted into the lateral ventricle
via an occipital trajectory. Complications with ventriculoperitoneal shunts
include incorrect insertion, obstruction, wound infection, and poorly regu-
lated CSF drainage. Insertion of the ventricular catheter also carries a small
significant risk of intracerebral bleeding. Symptoms of shunt malfunctions
include headache, fever, drowsiness, and convulsions.

Summary
To prevent unanticipated acute shifts in ICP in patients who are under-
going lateral skull base surgery, a basic understanding of CSF metabolism
and ICP homeostasis is essential for skull base surgeons. Although
462 CLEMEN & BACKOUS

autoregulation protects the intracranial arterial blood flow with little impact
on ICP, acute fluctuations in central venous outflow translate directly to el-
evations of ICP. Central line placement in the neck should be avoided, and
critical planning for patient positioning to avoid compromise to the jugular
venous system can avoid ICP shifts. The internal jugular vein should be sac-
rificed only when absolutely necessary. Early identification of patients with
elevated ICP can reduce the risk of damage to critical brain structures. In-
clusion of a neurosurgeon and possibly a critical care specialist is essential to
maximize patient performance as pharmacotherapy and external drainage
procedures are implemented.

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