Brain Tumor and Craniotomy
June M. Chan
Kane O. Pryor
A 47-year-old woman who was previously healthy presents with a 4-month history of headache, with intermittent diplopia and gait disturbance developing over the last month. She is admitted after her family witnesses an acute episode of profound lethargy, altered cognition, and vomiting. Neurologic examination is remarkable for abnormal right-sided cranial nerve V, VII, and VIII function, nystagmus, and ataxic gait. Magnetic resonance imaging (MRI) shows a large, right posterior fossa mass that is only slightly hyperintense on T2-weighted images but is clearly demarcated after the intravenous injection of gadolinium contrast. The impression is of a petroclival meningioma, with mass effect on the pons and fourth ventricle. Magnetic resonance angiogram shows a highly vascular tumor drawing principal blood supply from the ascending pharyngeal branch of the ipsilateral external carotid artery. The patient improves clinically following the administration of dexamethasone and mannitol, and the infusion of 2% sodium chloride and is monitored in the neurosurgical intensive care unit (ICU). The day after admission, the patient undergoes uneventful cerebral angiography and partial embolization of the tumor under general anesthesia. She is now scheduled for posterior fossa craniotomy and resection of the tumor.
A. Medical Disease and Differential Diagnosis
What is the pathology of intracranial tumors?
What is intracranial pressure (ICP), and what are its determinants?
How does the presence of a mass alter the ICP in this patient, and what are the clinical manifestations of these alterations?
What is cerebral blood flow (CBF), and what are its determinants?
What are the cerebral steal syndromes?
Are there any issues specific to posterior cranial fossa pathology?
What is the role of preoperative embolization therapy?
B. Preoperative Evaluation and Preparation
What are the special considerations in preoperative evaluation of the patient scheduled for posterior fossa craniotomy?
In a patient who presents with intracranial hypertension, what management might have already been initiated preoperatively, and what are the implications for anesthetic management?
What are the types of intraoperative neurophysiologic monitoring (IOM) that would likely be used for this procedure, and how will they affect the anesthetic management plan?
What are the options for patient positioning during posterior fossa surgery?
What are the principal disadvantages associated with the common posterior fossa craniotomy positions?
How does the sitting position affect your preoperative assessment and planning?
How should the patient position ultimately be determined?
Should this patient receive premedication?
C. Intraoperative Management
What are the anesthetic goals for craniotomy?
What monitors should be used during craniotomy?
Would you monitor for venous air embolism (VAE)? What are the monitoring options?
What specific risks are associated with induction of anesthesia?
How would you induce anesthesia?
What are the effects of anesthetics on cerebral metabolic rate of oxygen (CMRO2), CBF, and ICP? With this in mind, how would you maintain anesthesia?
How would you manage ventilation and maintain arterial carbon dioxide?
How would you approach diuretic therapy?
How would you manage serum glucose?
How would you approach fluid management?
Once the bone plate is removed and the dura retracted, the surgeon reports that the brain is still “tight.” What would be your response?
If deliberate hypotension is indicated, how will you achieve it?
While the surgeon is resecting tumor from near the brainstem, the patient’s heart rate suddenly drops to 20 beats per minute. What is your assessment and management?
Are there any measures you can take to prevent VAE?
During the procedure, the precordial Doppler becomes loud and turbulent. The endtidal CO2 (ETCO2) drops from 31 mm Hg to 13 mm Hg, and the systemic pressure from 121/63 mm Hg to 64/32 mm Hg. What is your assessment and management plan?
What is your approach to emergence? What if the patient does not wake up?
D. Postoperative Management
What postoperative complications are of greatest concern? What level of monitoring is required?
What is your approach to postoperative pain control?
In the ICU, the patient’s neurologic status deteriorates and ICP monitoring is instituted. What are the different methods of monitoring ICP, and what are their limitations?
A. Medical Disease and Differential Diagnosis
A.1. What is the pathology of intracranial tumors?
Intracranial tumors may be primary neoplasms or secondary to metastases, infection, inflammation, or vascular disruption. Primary cancers can be classified according to their cell origin, or according to their anatomic location (see Table 17.1). In the United States between 2006 and 2010, meningiomas were the most common (35.8%), followed by gliomas (28%) and pituitary tumors (15.8%). Secondary metastases are far more common than primary intracranial tumors, although the exact incidence is unknown, and most likely originate from lung cancer, breast cancer, and melanoma.
TABLE 17.1 Classification of Intracranial Tumors | |||||||||
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Although the cause of primary intracranial neoplasms remains unclear, there are genetic conditions that predispose to tumor development. There is, for instance, a clear association between meningiomas and neurofibromatosis type 2. Other conditions linked with the development of brain tumors include neurofibromatosis type 1 and 2, von Hippel-Lindau syndrome, tuberous sclerosis, Li-Fraumeni syndrome, and Turcot syndrome. These conditions are associated with extra-tumor manifestations that should be carefully considered during preoperative evaluation (see Table 17.2).
Kufe DW, Pollock RE, Weichselbaum RR, et al, eds. Holland-Frei Cancer Medicine. 6th ed. Hamilton, Canada: BC Decker; 2003. http://www.ncbi.nlm.nih.gov/books/NBK13658/. Accessed January 30, 2015.
Nayak L, Lee EQ, Wen PY. Epidemiology of brain metastases. Curr Oncol Rep. 2012;14(1):48-54.
Ostrom QT, Gittleman H, Farah P, et al. CBTRUS statistical report: primary brain and central nervous system tumors diagnosed in the United States in 2006-2010. Neuro Oncol. 2013;15(suppl 2):ii1-ii56.
A.2. What is intracranial pressure (ICP), and what are its determinants?
Normal ICP is 5 to 15 mm Hg (6 to 20 cm H2O). This pressure results from the physiologic interactions of intracranial structures within the rigid skull. Anatomically, these structures are enclosed within a cranial vault that is divided by tough dural partitions, the falx and tentorium cerebelli. Functionally, intracranial structures can be conceptualized as three compartments within a minimally compliant space:
Parenchyma, consisting of cellular, extracellular, and intracellular fluid components, occupying 80% to 85% of total intracranial volume (˜1,400 mL in the average adult)
Cerebrospinal fluid (CSF), occupying 10% of total intracranial volume (˜75 mL in the cisterns, 50 mL in the subarachnoid space, and 25 mL in the ventricles)
Intracranial blood volume, consisting of both arterial and venous blood, which occupies 5% to 10% total intracranial volume (averaging 150 mL in the adult)
Without compensation, alterations in any one of these compartments will lead to increases in ICP. Monro (1783) and Kellie (1824) first hypothesized that an increase in the
volume of one compartment results a compensatory decrease in the other compartments, thereby preserving normal ICP. Initially, CSF can drain to the spinal CSF reservoir and venous blood to the extracranial veins. This minimizes the change in ICP during the early phases of intracranial volume expansion. However, this compensation is limited, especially if the expansion is rapid. At a critical point, these compensatory mechanisms are exhausted, and even small increases in intracranial volumes will result in significant increases in ICP.
volume of one compartment results a compensatory decrease in the other compartments, thereby preserving normal ICP. Initially, CSF can drain to the spinal CSF reservoir and venous blood to the extracranial veins. This minimizes the change in ICP during the early phases of intracranial volume expansion. However, this compensation is limited, especially if the expansion is rapid. At a critical point, these compensatory mechanisms are exhausted, and even small increases in intracranial volumes will result in significant increases in ICP.
TABLE 17.2 Genetic Conditions Associated with Intracranial Tumors | |||||||||||||||||||||||||||||||||||||||
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Early signs of increased ICP include morning—classically occipital—headache, vomiting, minor behavioral changes, sedation, and cognitive slowing. Papilledema on funduscopy is an important sign that is often missed on examination. Further increases in ICP can eventually lead to compressive cranial neuropathies (typically CN VI, causing unilateral mydriasis) and herniation of brain tissue through a noncompliant partition—rapidly resulting in irreversible regional and global neuronal injury.
Kellie G. An account of the appearances observed in the dissection of two of three individuals presumed to have perished in the storm of the 3rd, and whose bodies were discovered in the vicinity of Leith on the morning of the 4th November 1821 with some reflection son the pathology of the brain. Trans Med Chir Sci Edinburgh. 1824;1:84-169. https://archive.org/details/transactionsmed00unkngoog. Accessed January 30, 2015.
Kurishima C, Tsuda M, Shiima Y, et al. Coupling of central venous pressure and intracranial pressure in a 6-year-old patient with Fontan circulation and intracranial hemorrhage. Ann Thorac Surg. 2011;91(5):1611-1613.
Miller RD, Cohen NH, Eriksson LI, et al, eds. Miller’s Anesthesia. 8th ed. Philadelphia, PA: Elsevier Saunders; 2015:2158-2199.
Monro A. Observations on the Structure and Functions of the Nervous System: Illustrated with Tables. Edinburgh, Scotland: Creech and Johnson; 1783. http://digi.ub.uni-heidelberg.de/diglit/monro1783. Accessed January 30, 2015.
Ursino M, Lodi CA. A simple mathematical model of the interaction between intracranial pressure and cerebral hemodynamics. J Appl Physiol. 1997;82:1256-1269.
A.3. How does the presence of a mass alter the ICP in this patient, and what are the clinical manifestations of these alterations?
Within the constraints of the intracranial compliance model outlined earlier, there are certain characteristics of an intracranial mass that influence the degree of ICP alteration:
Size: An intracranial mass exerts effects through its own intrinsic volume and any surrounding edema. Any space-occupying lesion within a relatively fixed intracranial compartment is compensated for through decreases in volume of other intracranial contents.
Rate of growth: A rapidly expanding mass outpaces the rate in which compensatory volume shifts can occur, which leads to an increase in ICP.
Anatomic location: The infratentorial space is notable for being highly susceptible to massrelated alterations in ICP. The area bound by the tentorium cerebelli and occiput is much lower in volume and compliance when compared with the supratentorial space. It also contains vital structures involved in CSF bulk flow between different compartments: the fourth ventricle, which communicates with the supratentorial ventricles and subarachnoid cisterns, and the foramen magnum, which communicates with the spinal column. Any volume shift within the infratentorial space may therefore precipitate a noncommunicating hydrocephalus, which further compromises compensatory mechanisms for intracranial hypertension.
Local tissue dysfunction: The presence of an intracranial tumor causes local effects on surrounding tissue through invasive destruction, induction of neoangiogenesis through the release of oncogenic factors, or compression with ischemic cellular disruption. This results in an inflammatory response that causes further tissue edema and increases in ICP.
Taken together, these considerations account for the differences in the clinical presentation of intracranial masses. A slow-growing mass, particularly in the peripheral supratentorial space, can become sizable with minimal symptoms due to compensatory volume remodeling, whereas a small infratentorial lesion can obstruct the fourth ventricle and rapidly cause significant intracranial hypertension.
In this patient, a slow-growing meningioma has been able to attain a large size before becoming symptomatic. The patient’s earliest signs and symptoms were most likely due to a localized mass effect. Nevertheless, the acute decompensation, with rapidly developing signs and symptoms of elevated ICP, probably represent the added component of CSF outflow obstruction at the fourth ventricle. Even with the clinical improvement provided by steroid therapy and osmotic diuresis, this patient certainly has very little volume reserve and intracranial compliance even small further increases in volume—such as an increase in cerebral blood volume (CBV) precipitated by a minimum alveolar concentration (MAC) of volatile anesthetic—have the potential to cause a precipitous spike in ICP.
Miller RD, Cohen NH, Eriksson LI, et al, eds. Miller’s Anesthesia. 8th ed. Philadelphia, PA: Elsevier Saunders; 2015:2158-2199.
Ropper AH. Lateral displacement of the brain and level of consciousness in patients with an acute hemispheral mass. N Engl J Med. 1986;314:953-958.
Schaller B, Graf R. Different compartments of intracranial pressure and its relationship to cerebral blood flow. J Trauma. 2005;59:1521-1531.
A.4. What is cerebral blood flow (CBF), and what are its determinants?
The brain is only 2% of total adult body weight, yet receives 15% of the resting cardiac output via the carotid and vertebral arteries. This disproportionately high blood flow is due to the brain’s metabolic requirement of oxygen (MRO2), which consumes approximately 3.5 mL O2/min/100 g brain tissue, or 20% of total body MRO2. CBF is approximately 750 mL per minute in the adult, or 50 mL/min/100 g averaged across gray and white matter. Gray matter, which contains neuronal nuclei, is metabolically more active than white matter and consumes 75 versus 45 mL/min/100 g brain tissue.
CBF is determined by cerebral perfusion pressure (CPP), which describes the pressure gradient for blood flow across the cerebral vascular bed, and cerebral vascular resistance (CVR):
CBF = CPP / CVR
On a global level, CPP is the difference between the inflow and outflow pressures of the brain’s blood supply. However, the cerebral circulation behaves as a Starling resistor: Its enclosure within the rigid cranial vault allows extravascular pressure (ICP) to compress and compromise venous outflow. Hence, CBF can be expressed as:
CBF = (mean arterial pressure [MAP] − outflow pressure) / CVR
where outflow pressure = CVP or ICP, whichever is higher.
CBF is highly regulated to ensure substrate delivery matches the metabolic demands of neural tissue and to prevent excess blood flow causing cerebral hyperemia. This is termed flow-metabolism coupling and is achieved through alterations in CVR via four overlapping mechanisms occurring on a regional and global cerebral level:
Vascular myogenic autoregulation
CBF is maintained constant across MAPs of approximately 50 to 150 mm Hg. Based on recent studies in humans, the extremes of this range should be approached with caution, especially the lower boundary; CBF can decrease at MAPs of 60 or even 70 mm Hg. Chronic hypertension causes a rightward shift in the CBF-MAP relationship. Hypocapnia has been demonstrated to broaden the autoregulatory range, whereas hypercapnia and elevated ICP decreases the responsiveness of pressure autoregulation.
Metabolic autoregulation
Carbon dioxide (CO2): CO2 is a potent cerebral vasodilator. It exerts its effects on the cerebral vasculature primarily by altering CSF pH, although there is evidence that CSF PCO2 also has a direct effect on cerebral vascular smooth muscle. At normotensive ranges, CBF has a linear relationship with acute changes in PaCO2 between 20 and 80 mm Hg, with CBF changing by 2% to 4% for every mm Hg change in PaCO2. Beyond this range, further changes are limited by extremes in vascular diameter. This response is blunted by systemic hypotension and volatile anesthesia. It is important to note that prolonged hypocarbia or hypercarbia (beyond 6 to 8 hours) will ultimately have little effect on CVR, as CSF pH normalizes with active transport of bicarbonate over the blood-brain barrier. Further, subsequent correction of PaCO2 would likely result in rebound cerebral hyper- or hypoperfusion.
Oxygen (O2): Although variations in PaO2 within the physiologic range do not affect CVR, acute hypoxemia below 50 mm Hg causes cerebral vasodilation, rapidly reaching maximal response at approximately 30 mm Hg. The exact mechanism of how this occurs is unclear, but it likely involves the direct effects of by-products from anaerobic metabolism and cellular ischemia, such as lactic acid and adenosine. This mechanism is also impaired in the presence of volatile anesthesia.
Neurogenic autoregulation
Compared with myogenic and metabolic mechanisms, the autonomic nervous system plays a minor role in cerebral autoregulation. Both sympathetic innervation of cerebral arterioles and circulating sympathomimetics attenuate increases in CBF during severe hypertension, hypoxia, and hypercapnia.
As stated earlier, the presence of an intracranial mass induces dysfunction in surrounding neural tissue via several mechanisms, resulting in ischemia and inflammation. This acidic microenvironment promotes local vasodilatation and vasoplegia with subsequent narrowing of the pressure autoregulatory range. Regional CBF becomes dependent on MAP and ICP, with little ability to compensate for changes in systemic blood pressure. Mass effect alone can increase ICP enough to critically compromise CPP with apparently normal MAP.
A conservative approach to the management of CPP would suggest that it should not be allowed to fall below 70 mm Hg for any extended period in the baseline normotensive patient. Although a more moderate approach targeting CPPs in the 60- to 70-mm Hg range is commonly used, most neuroanesthesiologists agree that sustained CPP values under 60 mm Hg place the brain at risk, despite the possible neuroprotection afforded by the presence of a GABAergic anesthetic agent.
Giulioni M, Ursino M. Impact of cerebral perfusion pressure and autoregulation on intracranial dynamics: a modeling study. Neurosurgery. 1996;39:1005-1014.
Miller RD, Cohen NH, Eriksson LI, et al, eds. Miller’s Anesthesia. 8th ed. Philadelphia, PA: Elsevier Saunders; 2015:2158-2199.
Sharma D, Bithal PK, Dash HH, et al. Cerebral autoregulation and CO2 reactivity before and after elective supratentorial tumor resection. J Neurosurg Anesthesiol. 2010;22:132-137.
ter Laan M, van Dijk JM, Elting JW, et al. Sympathetic regulation of cerebral blood flow in humans: a review. Br J Anaesth. 2013;111(3):361-367.
Yoon S, Zuccarello M, Rapoport RM. pCO(2) and pH regulation of cerebral blood flow. Front Physiol. 2012;3:365.
A.5. What are the cerebral steal syndromes?
Any intracranial pathology, including marginal ischemia and inflammation surrounding a mass lesion, can cause localized dysfunction of normal cerebral autoregulation and an impaired response to vasoactive agents. The microvasculature in the pathologic region can have an essentially fixed resistance. In this case, if vasodilation occurs in other normal regions of the brain, the decreased vascular resistance in the normal tissue can theoretically shunt blood flow away from the pathologic regions, which are already most vulnerable. This phenomenon is known as cerebral steal.
In anesthesia management, cerebral steal is most relevant in the context of hypercapnia and the use of volatile anesthetics. Both of these cause vasodilation of normal vasculature and potentially cause decreased regional CBF in pathologic areas. For volatile anesthesia, cerebral vasodilatation is usually considered to be significant when given in doses of 1 MAC or greater, but as a dose-dependent effect, it may be clinically apparent at 0.5 MAC. During hypocapnia, when there is vasoconstriction in normal tissue, the opposite may occur. In this case, blood flow to pathologic regions can actually increase. This phenomenon is known as inverse steal or the Robin Hood effect. While both steal effects have been well reported in human literature, the clinical relevance of steal and inverse steal phenomena is unclear. Nonetheless, it is prudent to consider it in anesthetic management.
Alexandrov AV, Sharma VK, Lao AY, et al. Reversed Robin Hood syndrome in acute ischemic stroke patients. Stroke. 2007;38(11):3045-3048.
Darby JM, Yonas H, Marion DW, et al. Local “inverse steal” induced by hyperventilation in head injury. Neurosurgery. 1988;23:84-88.
McCulloch TJ, Thompson CL, Turner MJ. A randomized crossover comparison of the effects of propofol and sevoflurane on cerebral hemodynamics during carotid endarterectomy. Anesthesiology. 2007;106(1):56-64.
Miller RD, Cohen NH, Eriksson LI, et al, eds. Miller’s Anesthesia. 8th ed. Philadelphia, PA: Elsevier Saunders; 2015:2158-2199.
A.6. Are there any issues specific to posterior cranial fossa pathology?
Surgery for tumors in the posterior fossa presents several challenges not seen with supratentorial surgery (Table 17.3). The posterior fossa is a tightly enclosed space in which tumors are often in direct contact with critical brainstem structures, including the cranial nerves and brainstem nuclei. The margin for error when operating near these structures is extremely
small, as can be the spatial reserve for postoperative inflammation. The patient with a posterior fossa tumor, especially one close to the brainstem, can worsen neurologically in the hours following surgery as a result of postsurgical inflammation causing edema.
small, as can be the spatial reserve for postoperative inflammation. The patient with a posterior fossa tumor, especially one close to the brainstem, can worsen neurologically in the hours following surgery as a result of postsurgical inflammation causing edema.
TABLE 17.3 Specific Anesthetic Considerations in Posterior Fossa Craniotomy | ||||||||||||||||||||||||
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In addition to the risk of neuronal damage, surgery in proximity to brainstem nuclei can trigger significant intraoperative autonomic and collateral hemodynamic instability, which can be extremely challenging to manage. The most common autonomic event is an acute increase in vagal tone, which in some instances can lead to a prolonged period of asystole, and can be immediately followed by a reflexive surge in sympathetic tone. Further, the risk to cranial nerves and other structures often demands IOM—such as somatosensory evoked potentials (SSEPs), brainstem auditory evoked potentials, or electromyography (EMG)—all of which can substantially restrict and dictate anesthetic management.
Finally, the posterior fossa cannot be accessed with the patient in the conventional supine position. In the past, the sitting position was highly favored by neurosurgeons and presented marked anesthetic challenges because of the increased risk of VAE. Although still common in some centers, the sitting position has fallen out of favor; nonetheless, all of the positions that permit access to the posterior fossa pose management difficulties that must be considered. The risk of VAE, although reduced, often still exists. Other considerations include loss of jugular outflow, deterioration of pulmonary compliance, strain on the cervical spine and brachial plexus, and a lack of access to central venous lines and the airway. In patients who are critically ill or otherwise at risk for life-threatening intraoperative events, it must be remembered that cardiopulmonary resuscitation will always require that the patient be rapidly returned to the supine position.
Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of posterior fossa mass lesions. Neurosurgery. 2006;58:S47-S55.
Gurol ME, St Louis EK. Treatment of cerebellar masses. Curr Treat Options Neurol. 2008;10:138-150.
Kan P, Couldwell WT. Posterior fossa brain tumors and arterial hypertension. Neurosurg Rev. 2006;29:265-269.
Miller RD, Cohen NH, Eriksson LI, et al, eds. Miller’s Anesthesia. 8th ed. Philadelphia, PA: Elsevier Saunders; 2015:2158-2199.
A.7. What is the role of preoperative embolization therapy?
Highly vascular tumors, especially those that are anatomically difficult to access, present a high risk for substantial intraoperative bleeding. In addition to the systemic risks associated with gross blood loss, peritumor bleeding can severely compromise surgical exposure and exacerbate neuronal and neurovascular inflammation.
To reduce this risk, patients often undergo embolization of the vessels feeding the tumor in the days immediately before surgery. An arterial catheter is inserted, usually in the femoral artery, and guided under fluoroscopy until it rests in any of the vessels that have evolved to supply only the tumor and not normal brain. Low-dose systemic heparinization to achieve activated clotting times of 200 to 300 seconds is required to prevent the formation of microthrombi. At this point, an embolic agent is slowly delivered to occlude the vessel, reducing its vascular supply and thus the degree of bleeding during the operative resection. Currently, the embolic agents available can be considered as two groups: particulate (using a variety of substances such as coils, gelatin sponges, fibrin glue, and polyvinyl alcohol) and liquid (ethylene vinyl alcohol, hyperosmolar mannitol). The choice of agent is determined by angiographic anatomy, tumor vascularity, and tumor histology. Because of collateralization and reestablishment of blood supply, embolization is effective for only a short period and is usually performed within 48 hours of the intracranial resection.
Tumor embolization comes with its own risks and challenges: Vascular anatomy might not always permit embolization, and the embolization itself can precipitate peri-tumor edema and hyperemic changes in blood flow dynamics. These changes are particularly relevant in this patient with a posterior fossa tumor proximate to the brainstem. Deposition of embolic agent into vessels supplying normal brain amounts to an embolic stroke and can have catastrophic consequences. Catheter-related complications including vessel dissection and rupture, and access site hematomas are well described. Further, embolizations
often require general anesthesia and thus assume all of the associated general and neurospecific risks. Current literature reports embolization-related complication rates for meningiomas at between 2.9% and 4.6% but with significant decreases in intraoperative blood loss.
often require general anesthesia and thus assume all of the associated general and neurospecific risks. Current literature reports embolization-related complication rates for meningiomas at between 2.9% and 4.6% but with significant decreases in intraoperative blood loss.
Ashour R, Aziz-Sultan A. Preoperative tumor embolization. Neurosurg Clin N Am. 2014;25(3):607-617.
Carli DF, Sluzewski M, Beute GN, et al. Complications of particle embolization of meningiomas: frequency, risk factors, and outcome. AJNR Am J Neuroradiol. 2010;31:152-154.
Raper DM, Starke RM, Henderson F Jr, et al. Preoperative embolization of intracranial meningiomas: efficacy, technical considerations, and complications. Am J Neuroradiol. 2014;35(9):1798-1804.
Young WL. Anesthesia for endovascular neurosurgery and interventional neuroradiology. Anesthesiol Clin. 2007;25:391-412.
B. Preoperative Evaluation and Preparation
B.1. What are the special considerations in preoperative evaluation of the patient scheduled for posterior fossa craniotomy?
In addition to the routine thorough preoperative evaluation, the evaluation of the patient for craniotomy should answer several questions that critically influence anesthesia management:
What is the ICP? If ICP is still in the normal range, how much intracranial compliance reserve is likely to exist?
How is autoregulation likely to be affected by the pathology and chronic changes in blood pressure? What range of arterial pressures will be required to preserve adequate CPP and CBF?
Does the patient have any of the electrolyte and endocrine abnormalities associated with intracranial pathology or treatment, such as neurogenic diabetes insipidus, or hypernatremia resulting from hypertonic saline therapy?
Is the lesion highly vascular, difficult to access, or situated proximate to one of the large draining veins—all of which increase the probability of significant bleeding?
What is the likely positioning, and does it incur a risk of VAE, obstruction of jugular venous outflow, or neck hyperextension? Are there preoperative patient conditions that would significantly increase the risk of, or preclude certain positions, such as patent foramen ovale and right to left intracardiac shunts?
Is the tumor located in a position close to the brainstem such that severe autonomic dynamics are likely?
Will the baseline neurologic status affect the ability to extubate or to establish an early neurologic assessment after general anesthesia?
Will the anesthetic technique need to accommodate specific monitoring requirements, such as electroencephalography (EEG), electrocorticography, brainstem auditory evoked responses (BAERs), or SSEPs?
Fischer SP. Preoperative evaluation of the adult neurosurgical patient. Int Anesthesiol Clin. 1996;34:21-32.
Jellish WS, Murdoch J, Leonetti JP. Perioperative management of complex skull base surgery: the anesthesiologist’s point of view. Neurosurg Focus. 2002;12:E5.
Lieb K, Selim M. Preoperative evaluation of patients with neurological disease. Semin Neurol. 2008;28:603-610.
Miller RD, Cohen NH, Eriksson LI, et al, eds. Miller’s Anesthesia. 8th ed. Philadelphia, PA: Elsevier Saunders; 2015:2158-2199.
B.2. In a patient who presents with intracranial hypertension, what management might have already been initiated preoperatively, and what are the implications for anesthetic management?
A patient with evidence of intracranial hypertension will be aggressively monitored and treated preoperatively; it is likely that the preoperative assessment will occur in an intensive care setting. The anesthesiologist must be familiar with the management of intracranial hypertension. These therapies will likely need to be initiated or continued in the operating room. Further,
the anesthesiologist must be mindful of potential sequelae that can arise from various perioperative therapies and interventions such as:
the anesthesiologist must be mindful of potential sequelae that can arise from various perioperative therapies and interventions such as:
Corticosteroids. Treatment can lead to hyperglycemia, which should be aggressively treated to maintain plasma glucose less than 150 to 180 mg per dL while taking care to avoid hypoglycemia.
Head elevation. Care should be taken to maintain 30-degree head elevation, where possible, and to avoid rapidly lowering the head during transport.
Diuretics (mannitol, furosemide). These can result in electrolyte or acid-base abnormalities. Decreased preload can increase the risk of hypotension in the peri-induction period.
Isotonic or hypertonic saline therapy. This can result in hypernatremia or a hyperchloremic, non-anion gap metabolic acidosis.
Intubation and institution of hyperventilation. If prolonged, the CBF response to CO2 can become diminished or absent, with a risk for dangerous increases in CBF and ICP if hyperventilation is rapidly ceased. It can also lead to a compensatory loss of bicarbonate and other basic metabolic buffers leading to the development of acidosis if ventilation was normalized. Care should be taken to avoid hypoventilation during transport.
Ventriculostomy. This is usually clamped during transport to or from the ICU, as the level of the drain relative to the head is critical, and accidental changes in position can result in excessive draining of CSF. It should be attended to on arrival to the operating room because even relatively short periods of clamping can result in elevations of ICP.
Manipulation of systemic pressures to optimize CPP. Care should be taken to ensure drug infusions are maintained during transport to avoid rebound hypertension or hypotension.
Drug-induced cerebral vasoconstriction and coma. Propofol infusion and pentobarbital are the typical agents currently used in the United States, following the decline in the availability of thiopental. This signifies a critical neurologic status. The therapy is often continued as the primary anesthetic.
Deliberate hypothermia. This signifies a critical neurologic status and requires discussion of intraoperative temperature management goals with the neurosurgeon and neurointensivist because the neuroprotective benefits may be countered by hypothermia-induced coagulopathy.
Li LM, Timofeev I, Czosnyka M, et al. Review article: the surgical approach to the management of increased intracranial pressure after traumatic brain injury. Anesth Analg. 2010;111:736-748.
Perez-Barcena J, Llompart-Pou JA, O’Phelan KH. Intracranial pressure monitoring and management of intracranial hypertension. Crit Care Clin. 2014;30(4):735-750.
Stevens RD, Bhardwaj A. Evolving paradigms in the management of severe traumatic brain injury. Crit Care Med. 2005;33:2415-2417.
Vincent JL, Berré J. Primer on medical management of severe brain injury. Crit Care Med. 2005;33:1392-1399.
B.3. What are the types of intraoperative neurophysiologic monitoring (IOM) that would likely be used for this procedure, and how will they affect the anesthetic management plan?
IOM uses a combination of stimulators and sensing electrodes to detect the functional integrity of sensory, motor, and cranial nerves and their associated nerve tracts and/or muscles. The primary monitoring modalities are EMG, evoked potentials (EPs), and EEG. EEG is rarely used for craniotomies for tumor resection and will not be considered in detail in this chapter.
EMG records the electrical activity within muscle in response to the stimulation of its innervating cranial or peripheral nerve. The most common EMG monitoring during posterior fossa surgery is for cranial nerve VII, although monitoring of V, IX, X, and XI is frequently encountered. Usually, the surgeon will deliver a very low current to a structure he or she believes could be the cranial nerve of interest, and muscular activity is monitored in the distribution of the nerve. Mechanical manipulation of a nerve will often also cause muscular activity, which may herald potential inadvertent injury. EMG is relatively unaffected by volatile and intravenous anesthetic agents but requires intact functioning of the neuromuscular
junction. Therefore, neuromuscular blockers cannot be used for EMG monitoring beyond anesthetic induction. Some anesthesiologists advocate the use of succinylcholine for intubation; nevertheless, a low intubating dose of a medium-duration nondepolarizing agent such as rocuronium, vecuronium, or cisatracurium typically allows adequate return of muscular function by the time monitoring is relevant and avoids the potential problems associated with succinylcholine.
junction. Therefore, neuromuscular blockers cannot be used for EMG monitoring beyond anesthetic induction. Some anesthesiologists advocate the use of succinylcholine for intubation; nevertheless, a low intubating dose of a medium-duration nondepolarizing agent such as rocuronium, vecuronium, or cisatracurium typically allows adequate return of muscular function by the time monitoring is relevant and avoids the potential problems associated with succinylcholine.
EPs measure electrical activity generated within the nervous system in response to a stimulus. The most common EP monitoring encountered during resection of posterior fossa tumors is the BAER, which monitors cranial nerve VIII and auditory pathway function (including portions of the brainstem, midbrain, and the primary auditory cortex) in response to sounds generated in the auditory canal. SSEPs can also be used to monitor dorsal column-medial lemniscus tract integrity, which is useful for posterior fossa surgery given the superficial location of the medial lemniscus in the brainstem and pons. These are elicited via electrical stimulation of peripheral sensory nerves (most commonly median and posterior tibial nerves) and recorded via scalp needle electrodes directed over the somatosensory cortex. Similarly, motor evoked potentials (MEPs) are obtained through transcranial stimulation of cortical pyramidal cells and recorded distally along the spinal cord, motor nerves, and muscle.
EPs are recorded as positive and negative deflections from baseline. The time delay from stimulus to first recorded deflection is termed the latency, and the maximal deflection from baseline is the amplitude. A significant increase in latency or decrease in amplitude of EPs can reflect injury along the nerve tract, or dysfunction due to physiologic or pharmacologic factors. Anesthetic agents can dramatically alter EPs in the absence of other abnormalities (Table 17.4). Although BAERs are reasonably robust, MEPs (and SSEPs to a lesser but still significant degree) are exquisitely sensitive to volatile anesthetics, which cause decreases in amplitude and increases in latency in a dose-dependent manner. Further, neuromuscular blockers cannot be used if MEPs are proposed. Volatile agents should be kept at less than 0.5 MAC, and nitrous oxide should not be used. The anesthetic plan will often rely heavily on opioids; propofol and dexmedetomidine infusions are also often incorporated, the latter of which may also offer improvements in overall hemodynamic stability. Perhaps more important than the specific anesthetic regimen is that a maintenance equilibrium is established for the baseline neurophysiology measurements and is then kept constant throughout the procedure. Pseudo-equilibrated steady-state continuous infusions are key to this strategy.
TABLE 17.4 Anesthetic Effects on Intraoperative Neuromonitoring | ||||||||||||||||||
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