Intracranial Pressure Concerns In Lateral

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 intracranial pressure (ICP), which can manifest as delayed arousal from anesthesia 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 arterial 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 regulation for otolaryngologists and lateral skull base surgeons. It examines the methodologies for preventing and treating acute elevations of ICP encountered 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 convoluted region of pia mater located throughout the intracranial ventricular system. CSF circulates by way of the foramen of Monroe into the third ventricle 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: [email protected] (D.D. Backous). 0030-6665/07/$ - see front matter Ó 2007 Elsevier Inc. All rights reserved. doi:10.1016/j.otc.2007.03.012

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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 metabolism are principally removed by the capillary circulation or directly by transfer through the CSF. The direct CSF route is particularly important when increased amounts of lactic acid are produced in the brain. Finally, CSF maintains a safe chemical environment for brain tissues [3]. Because of the phenomenon of autoregulation, the brain is able to regulate 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.

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arterial blood flow is maintained constantly over a range of perfusion pressures 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 hypertension. Unlike the arterial system, the central venous system does not autoregulate. 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 concentration 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, jugular 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 regard 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 problem 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 evaluating CT or MRI scans during preoperative planning, surgeons should determine the side of dominance for jugular venous outflow to prevent potential complications. The Monro-Kellie hypothesis states that the skull is a rigid sphere occupied 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 foramen magnum, or leakage of CSF from sites in the skull or spinal canal can

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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 spontaneous, traumatic, or iatrogenic violation of the dura.

Localization of dural defects Identification of dural defects and CSF leaks at the time of surgical disruption 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 advances 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 localization 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 diagnostic 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-positive 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 intrathecal contrast-enhanced high-resolution CT. These techniques can distinguish

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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 details, 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 management. 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.

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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 management 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 respiratory alkalosis [14]. For patients who have acute brain swelling intraoperatively 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 because osmotic diuretics can cause hypovolemia, which further compromises venous outflow from the brain. ICP monitoring facilitates immediate assessment of prescribed interventions. 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 production of CSF. Overdrainage may create a negative ICP and result in pneumocephalus. Lumbar drain External lumbar drainage is commonly used as an intraoperative or postoperative adjunct for preventing or treating CSF fistulae. Extreme caution must be exercised regarding the amount of CSF drained; overdrainage

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can result in headaches or violation of dural bridging veins and result in subdural 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 distal 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 injury, wound infection, obstruction, spinal epidural hematoma, and overdrainage headaches. No reservoir or flush chamber is available for CSF withdrawal or fluid injection with the umboperitoneal shunt. If overdrainage 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 involve three components: a ventricular catheter, a valve reservoir, and a peritoneal 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 regulated 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 undergoing lateral skull base surgery, a basic understanding of CSF metabolism and ICP homeostasis is essential for skull base surgeons. Although

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autoregulation protects the intracranial arterial blood flow with little impact on ICP, acute fluctuations in central venous outflow translate directly to elevations 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 sacrificed only when absolutely necessary. Early identification of patients with elevated ICP can reduce the risk of damage to critical brain structures. Inclusion of a neurosurgeon and possibly a critical care specialist is essential to maximize patient performance as pharmacotherapy and external drainage procedures are implemented. References [1] Fishman AJ, Marrinan MS, Golfinos JG, et al. Prevention and management of cerebrospinal fluid leak following vestibular schwannoma surgery. Laryngoscope 2004;144(3):501–5. [2] Kapil M, McMenomey SO, Delashaw JB. Indications for cerebrospinal fluid drainage and avoidance of complications. Otolaryngol Clin North Am 2005;38:577–82. [3] Milhorat TH. The third circulation revisited. J Neurosurg 1975;42:628–45. [4] Marmarou A, Shulman K, Rosende RM. A nonlinear analysis of the cerebrospinal fluid system and intracranial pressure dynamics. J Neurosurg 1978;48:332–44. [5] Durgun B, Ilglt ET, Cizmel MO, et al. Evaluation by angiography of the lateral dominance of the drainage of the dural venous sinuses. Surg Radiol Anat 1993;15:125–30. [6] Davson H, Welch K, Segal MB. The physiology and pathology of the cerebrospinal fluid. New York: Churchill Livingstone; 1987. p. 1013. [7] Carrau RL, Snyderman CH, Kassam AB. The management of cerebrospinal fluid leaks in patients at risk for high-pressure hydrocephalus. Laryngoscope 2005;115(2):205–12. [8] Kerr JT, Chu F, Bayles S. Cerebrospinal fluid rhinorrhea: diagnosis and management. Otolaryngol Clin North Am 2005;28:597–611. [9] Bateman N, Jones NS. Rhinorrhea feigning cerebrospinal fluid leak: nine illustrative cases. J Laryngol Otol 2000;114:462–4. [10] ElGammal T, Brooks BS. MR cisternography: initial experience in 41 cases. AJNR Am J Neuroradiol 1994;15:1647–56. [11] Chow JM, Goodman D, Mafee MF. Evaluations of CSF rhinorrhea by computerized tomography with metrizamide. Otolaryngol Head Neck Surg 1989;100:99–105. [12] Manelfe C, Cellerier P, Sobel D, et al. Cerebrospinal fluid rhinorrhea: evaluation with metrizamide cisternography. AJR Am J Roentgenol 1982;138:471–6. [13] Zweig JL, Carrau RI, Celin SE, et al. Endoscopic repair of CSF leaks to the sinonasal tract: predictors of success. Otolaryngol Head Neck Surg 2000;123:195–201. [14] Fishman RA. Cerebrospinal fluid in diseases of the nervous system. Philadelphia: WB Saunders Company; 1992. p. 129. [15] Donato T, Shapira Y, Artru A, et al. Effect of mannitol on cerebrospinal fluid dynamics and brain tissue edema. Anesth Analg 1994;78:58–66. [16] Van Aken MO, Feelders RA, de Marie S, et al. Cerebrospinal fluid leakage during transsphenoidal surgery: postoperative external lumbar drainage reduces the risk for meningitis. Pituitary 2004;7(2):89–93. [17] Lollis SS, Weider DJ, Phillips JM, et al. Ventriculoperitoneal shunt insertion for the treatment of refractory perilymphatic fistula. J Neurosurg 2006;105(1):1–5.