CLEVELAND CLINIC CLEVELAND, OHIO and Irene Osborn, MD
CLINICAL PROFESSOR OF ANESTHESIOLOGY
DIRECTOR OF NEUROANESTHESIA DIVISION
ALBERT EINSTEIN COLLEGE OF MEDICINE BRONX, NEW YORK
1
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For Christine, Andrew and Lauren In loving memory of my father DET
To my teachers, my trainees and my patients who have taught me so much
Irene Osborn
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1. Supratentorial Tumors 3
David E. Traul and Rachel Diehl
2. Anesthesia for Posterior Fossa Mass 9
Valerie L. Howell, Margaret M. Collins and Lauryn R. Rochlen
3. Awake Craniotomy 17
Shobana Rajan and Vibha Mahendra
4. Transsphenoidal/Pituitary Surgery 29
Vaia T. Abatzis and Edward C. Nemergut
SECTION 2 VASCULAR PROCEDURES
5. Cerebral Aneurysm Clipping 41
Irene Osborn and Jocelin Jones Molina
6. Arteriovenous Malformation 49 Allison Spinelli and Liang Huang
7. Carotid Endarterectomy/Stenting 55
Hui Yang
8. Interventional Neuroradiology 65 Irene P. Osborn and Liang Huang
9. Endovascular Thrombectomy in Acute Ischemic Stroke 71 A. Elisabeth Abramowicz
10. Extracranial-Intracranial Bypass 79
Wael Saasouh and David E. Traul SECTION 3 SPINE
11. Anesthesia for Anterior/Posterior Spine Surgery 87
Thomas N. Pajewski
12. Unstable Cervical Spine and Airway Management 99
Michael R. Moore and Ehab Farag
13. Metastatic Spine Disease 105
Juan P. Cata
SECTION 4 PEDIATRIC PROCEDURES
14. Chiari Malformations 113
Marco Maurtua, Mathew Lyons, and Nicholas DaPrano
15. Craniosynostosis and Anesthetic Management for Cranial Vault Remodeling 121
Hannah Hsieh, Lauren Thornton, and Glenn Mann
16. Pediatric Spine Surgery
Abigail E. Meigh, Ingrid A. Fitz-James Antoine, and Veronica Carullo
17. Myelomeningocele 139
Joanne Spaliaras
SECTION 5 FUNCTIONAL PROCEDURES
18. The Patient for Epilepsy Surgery 147 Haitham Ibrahim and Irene Osborn
19. Deep Brain Stimulation/Stereotaxic Surgery 153 Sandra Machado
SECTION 6 OTHER PROCEDURES
20. Traumatic Brain Injury and C-Spine Management 161 Matthew Wecksell and Kenneth Fomberstein
21. Cerebrospinal Fluid Shunts 167 Jinu Kim and Aleka Scoco
22. Neurosurgery in Pregnancy 175 David Berman and Ben Touré
SECTION 7 NEUROANESTHESIA COMPLICATIONS
23. Elevated ICP 185 Sergey Pisklakov, Haitham Ibrahim, and Ingrid Fitz-James Antoine
24. Subarachnoid Hemorrhage 191 K. H. Kevin Luk and Deepak Sharma
25. Venous Air Embolism 201
Julia I. Metzner and Deepak Sharma
26. Postoperative Visual Loss in Spine Surgery 209
David E. Traul
SECTION 8 NEUROANESTHESIA CONCEPTS
27. Neurophysiology/Neuroprotection 217 Hossam El Beheiry
28. Neurophysiologic Monitoring 229 Antoun Koht and Tod B. Sloan
29. Neuromuscular Disorders and Anesthesia 237 Mariel Manlapaz and Perin Kothari
CONTRIBUTORS
Vaia T. Abatzis, MD
Assistant Professor of Anesthesiology University of Virginia School of Medicine Charlottesville, Virginia
A. Elisabeth Abramowicz, MD Associate Professor of Anesthesiology New York Medical College Valhalla, New York
Hossam El Beheiry, MBBCh, PhD, FRCPC Trillium Health Partners, Mississauga Associate Professor of Anesthesia University of Toronto Toronto, Ontario, Canada
Frederic A. Berry, PhD Professor of Anesthesiology Professor of Neurosurgery University of Virginia Health System Charlottesville, Virginia
Veronica Carullo, MD Associate Professor Departments of Anesthesiology and Pediatrics Albert Einstein College of Medicine Bronx, NY
Juan P. Cata, MD
Department of Anesthesiology and Perioperative Medicine MD Anderson Cancer Center The University of Texas Houston, Texas
Nicholas DaPrano, MD Department of General Anesthesia Cleveland Clinic Cleveland, Ohio
Rachel Diehl, MD Department of General Anesthesia Cleveland Clinic Cleveland, Ohio
Ehab Farag, MD, FRCA Professor of Anesthesiology Cleveland Clinic Lerner College of Medicine Cleveland, Ohio
Ingrid A. Fitz-James Antoine, MD Assistant Professor Departments of Anesthesiology and Pediatrics Albert Einstein College of Medicine Bronx, NY
Kenneth Fomberstein Lennox Hill Hospital New York, New York
Valerie L. Howell, DO Fellow in Neuroanesthesia University of Michigan Health System Ann Arbor, MI
Liang Huang, MD Fellow in Neuroanesthesia Montefiore Medical Center Bronx, New York
Antoun Koht, MD Professor of Anesthesiology, Neurological Surgery, and Neurology
Northwestern University Feinberg School of Medicine Chicago, Illinois
Perin Kothari, DO Anesthesiology Institute Cleveland Clinic Cleveland, Ohio
Mathew Lyons, MD Department of General Anesthesia Cleveland Clinic Cleveland, Ohio
Sandra Machado, MD Department of General Anesthesia Cleveland Clinic Cleveland, OH
Vibha Mahendra, MD Baylor College of Medicine, Department of Anesthesiology Houston, Texas
Mariel Manlapaz, MD Department of General Anesthesia Cleveland Clinic Lerner College of Medicine Cleveland, OH
Marco Maurtua, MD, CHSE
Department of General Anesthesia Cleveland Clinic Cleveland, Ohio
Abigail E. Meigh, DO
Anesthesiologist
St. Joseph’s Regional Medical Center Paterson, NJ
Margaret M. Mora, MD Fellow in Neuroanesthesia
University of Michigan Health System Ann Arbor, MI
Jocelin Jones Molina, MD
Resident in Anesthesiology
Albert Einstein College of Medicine Montefiore Medical Center Bronx, New York
Michael R. Moore, MD
Department of General Anesthesia Cleveland Clinic Cleveland, Ohio
Edward C. Nemergut, MD
Professor of Anesthesiology and Neurological Surgery
University of Virginia School of Medicine Charlottesville, VA
Irene Osborn, MD
Clinical Professor of Anesthesiology
Albert Einstein College of Medicine Director, Division of Neuroanesthesia Montefiore Medical Center Bronx, New York
Thomas N. Pajewski, PhD, MD
Associate Professor of Anesthesiology and Neurological Surgery
Director of Neuroanesthesiology University of Virginia Health System Charlottesville, Virginia
Shobana Rajan, MD
Staff Anesthesiologist
Cleveland Clinic Lerner College of Medicine Cleveland, Ohio
Lauryn R. Rochlen, MD
Staff Anesthesiologist Neuroanesthesia Fellowship Director University of Michigan Health System Ann Arbor, MI
Wael Saasouh, MD
Clinical Fellow in Neuroanesthesiology Cleveland Clinic Cleveland, Ohio
Aleka Scoco, MD
Department of Neurosurgery
Albert Einstein College of Medicine Montefiore Medical Center Bronx, NY
Tod B. Sloan, MD, MBA, PhD Professor Emeritus University of Colorado School of Medicine Aurora, Colorado
Joanne Spaliaras, MD
Assistant Professor of Anesthesiology
Albert Einstein College of Medicine Bronx, NY
Allison Spinelli, DO
Assistant Professor of Anesthesiology
Albert Einstein College of Medicine Montefiore Medical Center Bronx, NY
David E. Traul, MD, PhD
Department of General Anesthesia Section Head of Neuroanesthesia Cleveland Clinic Cleveland, Ohio
Hui Yang, MD, PhD
General Anesthesiology Cleveland Clinic Cleveland, Ohio
Matthew Wecksell, MD
Chief, General Anesthesiology
Department of Anesthesiology
Associate Professor of Anesthesiology and Neurosurgery Westchester Medical Center
Advanced Physician Services Member of the Westchester Medical Center Health Network Valhalla, New York
SECTION 1
ONCOLOGIC PROCEDURES
1. SUPRATENTORIAL TUMORS
David E. Traul and Rachel Diehl
STEM CASE AND KEY QUESTIONS
A 69-year-old woman presents with a 1-year history of memory loss and apathy. Her husband states that he has noticed personality changes over this period of time. Her past medical history is significant for hypertension and dyslipidemia. She denies any history of headaches, numbness/weakness, changes in vision, or trauma. She has never smoked. She takes atorvastatin, and her blood pressure (BP) is well-controlled with losartan-hydrochlorothiazide. Vitals signs are BP 140/80, pulse 72 bpm, and SaO2 99% on room air. On exam, she is alert and fully oriented.
Labwork reveals normal complete metabolic panel and complete blood count. The patient undergoes a magnetic resonance imaging (MRI) examination which reveals a large skull-based supratentorial tumor (see Figure 1.1).
The patient is started on corticosteroids and scheduled to undergo biopsy and surgical resection of the tumor through a bifrontal craniotomy.
WHAT ARE THE MOST COMMON HISTOLOGICAL TYPES OF SUPRATENTORIAL TUMORS IN ADULTS? WHAT PREOPERATIVE TESTS WOULD BE IMPORTANT TO YOU?
The patient arrives in the OR and states she is very nervous. She denies any complications with anesthesia in the past. She has an 18 g antecubital IV line.
WHAT MONITORS ARE APPROPRIATE IN THIS PATIENT FOR HER SURGERY? SHOULD YOU PREMEDICATE THE PATIENT FOR HER NERVOUSNESS? WHAT ARE THE GOALS FOR INDUCTION AND MAINTENANCE OF ANESTHESIA FOR CRANIOTOMIES?
The patient is anesthetized and positioned for surgery. Her head is placed in Mayfield pins and the incision is made. The surgeon requests mannitol be administered.
WHEN IS THE BEST TIME TO GIVE MANNITOL, AND HOW DOES IT LOWER INTRACRANIAL PRESSURE (ICP)? WHAT MAINTENANCE FLUIDS WOULD YOU USE AND WHY?
After the bifrontal craniotomy is performed and the orbital bar removed, the surgeon states that the brain is still
“tight” and asks if there is anything you can do to help relax the brain.
WHAT ARE THE MAIN CONSTITUENTS OF THE CRANIUM, AND HOW MUCH OF EACH DO WE HAVE? HOW DOES THE BRAIN COMPENSATE FOR ELEVATED ICP? WHAT ARE SOME WAYS THAT THE ANESTHESIOLOGIST CAN DECREASE ICP? WHAT IS THE EFFECT OF PCO 2 , PAO 2 , CMRO 2 , AND POSITIVE ENDEXPIRATORY PRESSURE (PEEP) ON ICP? DESCRIBE THE EFFECT OF VOLATILE AND IV ANESTHETICS ON BLOOD FLOW AND ICP. WHAT IS CRITICAL BLOOD FLOW, AND HOW CAN YOU CHANGE CRITICAL FLOW? HOW CAN YOU CALCULATE CEREBRAL PERFUSION PRESSURE (CPP)?
The procedure has gone well, and the surgeon states that the incision is now being closed.
WHAT IS YOUR PLAN FOR EMERGENCE FROM ANESTHESIA?
The patient is removed from the Mayfield pins and a head dressing is applied. After 15 minutes, the patient is still not responsive, and the surgery team is getting concerned.
WHAT IS THE DIFFERENTIAL DIAGNOSIS FOR DELAYED EMERGENCE FROM CRANIOTOMY?
The patient is now fully awake and alert and is transferred to the neurological intensive care unit for further monitoring.
DISCUSSION
INCIDENCE AND PRESENTATION
The Central Brain Tumor Registry of the United States (CBTRUS) reported 379,848 cases of primary brain and other central nervous system (CNS) tumors from 2010 to 2014.1 The overall incidence rate for all primary brain and CNS tumors was 22.64 per 100,000 population, with the highest incidence rate (40.82) reported in persons older than 40 years of age.
>50ml/min/100g
Dysfunction of Neurons
<18ml/min/100g
<10ml/min/100g
<6ml/min/100g
Figure 1.1. Changes in cerebral blood flow (CBF) and corresponding electroencephalogram (EEG) findings. Normal CBF is >50 mL/min per 100 g of tissue. EEG changes may be detected when CBF <18 mL/min per 100 g of tissue, with cell death occurring at a CBF rate <10mL/min per 100 g.
Most of these tumors were nonmalignant (68.5%), and the median age at diagnosis was 59 years. Overall, meningioma was the most common reported histology at 36.8%, followed by pituitary (16.2%) and glioblastoma (14.9%). The majority of all tumors (>70%) were supratentorial.
Although the exact incidence of brain metastases is unknown, intracranial metastases from systemic malignancies comprise the majority of brain tumors, with up to one-third of all cancer patients affected.2 The most common systemic cancers with intracranial metastases are melanoma, lung cancer, and renal cancer.3
Patients with supratentorial tumors may present with a wide variety of signs and symptoms depending on the location of the tumor and its histological type. Neurological symptoms from high-grade gliomas and brain metastases tend to manifest over a shorter time course than symptoms from lower grade tumors. Generalized symptoms may include headache, nausea/vomiting, and neurocognitive dysfunction, and the patient may have signs of increased ICP. Focal deficits may also be present, such as weakness, sensory loss, and aphasia. Seizures, either focal or generalized, are often the presenting symptom and are more common in low-grade tumors.4
PREOPERATIVE ANESTHESIA CONSIDERATIONS
History and physical
Patients with supratentorial tumors quite often present for urgent, if not emergent, surgical resection. Therefore, a complete preoperative assessment is not always feasible. When possible, the patient should be optimized as much as possible. History and physical examination should include a full neurologic evaluation that includes mental status, cranial nerve function, motor and sensory testing, reflexes, and coordination testing that is documented prior to surgery in order to properly assess any postoperative deviations. Signs of increased ICP including altered mental status, papilledema, and hypertensive bradycardia should be assessed. If present, symptoms of
increased ICP may be temporarily alleviated by interventions such as raising the patient’s head, administration of IV hypertonic fluids, or placement of an intraventricular drain. Any comorbidity such as cardiovascular disease, respiratory disease, or renal disease should be adequately evaluated with further testing completed as warranted by the specific patient requirements. Previous surgeries and anesthetic experiences are important data prior to proceeding with surgery. Since the patient may develop significant bleeding during the procedure, a complete blood count should be obtained. Other labwork should include a basic chemistry panel and coagulation studies. Patients with primary brain tumors or metastatic disease are at a higher risk of thrombotic events, and the use of anticoagulation therapy must be known prior to surgery. Antiplatelet medications should be discontinued 7–10 days prior to surgery. Warfarin should also be discontinued prior to surgery, but anticoagulation may be bridged with low-molecular-weight heparin. Neuroimaging with computerized tomography (CT) and MRI should be reviewed to assist in developing a differential diagnosis and to formulate the anesthetic plan.
Vascular access and monitoring
Adequate vascular access should be obtained with at least two large-bore peripheral IV lines. Central venous access may be justified if there is a potential for significant blood loss, in patients with extensive cardiac or pulmonary comorbidities, when the risk of venous air embolism is high, or in patients without satisfactory peripheral access. An arterial catheter for continuous BP monitoring should be placed in addition to standard monitors. Placement of the arterial catheter prior to induction may be warranted in patients with large tumors and in situations where there is a large mass effect or increased ICP. A urinary catheter should also be placed.
Anxiolytics should be used with caution preoperatively in patients with supratentorial tumors. Sedation from anxiolytics (such as midazolam) puts the patient at risk for hypercapnia, hypoxemia, and airway obstruction that may lead to increases in PaCO2, cerebral blood flow (CBF), and ICP. However, patients presenting for tumor resection may have very high anxiety levels and associated hypertension that increases CBF and worsens an otherwise compensated elevated ICP. Therefore, use of preoperative anxiolytics should be used on a case-by-case basis and only in a monitored setting. Preoperative corticosteroids used for mass effect and anticonvulsant therapies should be continued the day of surgery,
PERIOPERATIVE ANESTHESIA CONSIDERATIONS
Induction of anesthesia
The goals of anesthesia induction for patients undergoing resection of supratentorial tumors are to maintain adequate ventilatory control (avoiding hypoxemia and hypercapnia), suppress sympathetic output and hypertension, and minimize cerebral venous outflow obstruction. This can be achieved by
adequately pre-oxygenating the patient followed by administration of propofol (1–2 mg/kg) combined with fentanyl (1–2 µg/kg) or remifentanil (1 µg/kg). Etomidate (0.2–0.4 mg/kg) may be substituted for propofol in patients with co-existing cardiac dysfunction or hemodynamic instability.
Nondepolarizing muscle relaxants (NDMRs) have minimal direct effect on cerebral metabolic rate, ICP, or CBF. Typically, middle- to short-acting NMDRs such as rocuronium, vecuronium, or cisatracurium are used for induction and maintenance of muscle relaxation during intracranial procedures. Pancuronium is usually avoided due to its long-term effect combined with its vagolytic activity that may increase cardiac output, thereby increasing CBF and ICP. Succinylcholine may be used in the setting of rapid intubations or potential difficult airways, but has several disadvantages for routine use. First, succinylcholine’s depolarization of acetylcholine receptors results in an efflux of potassium, which, in the setting of profound muscle weakness or immobility, may produce life-threatening hyperkalemia. Additionally, succinylcholine can cause transient increases in ICP; however if coadministered with an IV agent (i.e., propofol) this is usually not clinically significant. Consideration should be given to reports that the duration of N-Methyl-D-aspartate (NMDA) muscle blockade is shortened by long-term use of anticonvulsant agents such as phenytoin and carbamazepine.5,6
Patient positioning should be evaluated prior to incision to optimize jugular venous drainage and to avoid excessive hyperflexion or extreme lateral extension of the head. Pinning of the head in a holder device can produce a profound nociceptive stimulus and should only be performed when the patient has received adequate analgesia by local anesthetic infiltration or bolus administration of remifentanil or fentanyl. If a sympathetic response does occur with head pinning, hemodynamic control can be regained with IV bolus of propofol or an antihypertensive agent such as esmolol.
Maintenance of anesthesia
The primary goals of anesthesia maintenance during resection of supratentorial tumors are to control cerebral homeostasis via control of CBF and cerebral metabolic rate (CMR) and to provide a neuroprotective environment by decreasing cerebral energy demands and minimizing areas of ischemia and edema. The optimal anesthetic maintenance regimen required to achieve these goals is a subject of much debate, with the greatest controversy centered on the use of volatile agents versus IV agents as maintenance anesthesia for intracranial procedures. To date, there has been no prospective trial that definitively favors the clinical outcomes of one technique over the other in elective intracranial procedures.7–12 The advantages of volatile agents consist in their predictability, their titratability, and their ability for rapid emergence. The drawback of using volatile agents for intracranial procedures is their ability to increase CBF and ICP13,14; however, this effect can be minimized by using lower mean alveolar concentrations (MAC) and mild hyperventilation.14–16 IV anesthetics are an attractive option for intracranial surgery since they decrease in both CBF and CMR, thereby lowering ICP without increasing the risk
of cerebral ischemia.8,13 However, unlike volatile anesthetics, awakening times with IV agents are often more difficult to predict.
Opioid infusions (fentanyl, remifentanil, alfentanil) during intracranial surgery are particularly useful as they decrease the amount of volatile agent required to provide adequate anesthesia and therefore minimize the effects on CBF and ICP. Opioids also help blunt the hemodynamic response to head pinning. Remifentanil has become a very popular opioid to use in intracranial surgery due to its short context-sensitive half-life and minimal effects on CBF and ICP.17 Additionally, the use of remifentanil is associated with a more rapid emergence when compared to fentanyl.18,19
Typically, at our institution, patients undergoing elective intracranial procedures are maintained with 0.5 MAC volatile anesthetics with an opioid infusion (remifentanil or fentanyl) and muscle paralysis. Total IV anesthesia (TIVA) with propofol/remifentanil infusions is considered when difficulties with elevated ICP are anticipated.
Management of increased ICP
The cranial vault is a rigid, enclosed space with the volume of the brain (85%), cerebrospinal fluid (10%), and blood (5%) determining the ICP. Normally, the ICP is 8–12 mm Hg. Since CPP depends on ICP, increased ICP puts the cerebral tissue at risk for ischemia. Increases in volume of any one of the three components will result in increased ICP unless the volume of another component is decreased. Therefore, normal ICP can be maintained in the presence of a supratentorial tumor via decreasing CSF volume (displacement or absorption) and/or decreasing cerebral blood volume. However, at some point, elastance (ΔP/ΔV) in the system is maximized, and further increases in the size of the tumor (or edema) will cause the ICP to rise precipitously.
The anesthesiologist has several techniques at her disposal to reduce ICP and promote adequate blood flow and surgical conditions. When possible, avoidance of elevated ICP is best done by raising the head of the bed and removing any compression on the jugular veins. Administration of IV steroids (dexamethasone 4 mg every 6 hours) can also help prevent increased ICP by reducing tumor-associated edema.20 Other intraoperative interventions, such as avoiding high PEEP (which may limit venous return) and ensuring adequate muscle relaxation will also help prevent rises in ICP. When increased ICP is already present, administration of osmotic agents can reduce brain size by decreasing interstitial water. Mannitol is an osmotic diuretic that reduces interstitial water by increasing plasma oncotic pressure. Mannitol should be given as a bolus (1 g/kg body weight) around the time of incision and can lower the ICP in 1–5 minutes with peak effect seen between 20 and 60 minutes.20 The effects of mannitol last 2–3 hours, and repeat administration may actually worsen cerebral edema in an increase in ICP.21 Hypertonic saline and furosemide are also effective in reducing ICP and facilitating surgical exposure.
The CMR is another important determination of CBF, and therefore ICP. Due to flow–metabolism coupling,
Table 1.1. EFFECTS OF COMMON INHALATIONAL AGENT ON CEREBRAL BLOOD FLOW (CBF), CEREBRAL METABOLIC RATE (CMR), AND INTRACRANIAL PRESSURE (ICP)
VOLATILE AGENT CBF CMR ICP
Halothane
Isoflurane
Sevoflurane
Desflurane
Nitrous oxide
Changes in CBF (and therefore ICP) with isoflurane, sevoflurane, and desflurane depend on concentrations administered, with higher concentrations causing a vasodilatory effect and therefore increasing CBF. Some of the vasodilatory effects on ICP may be attenuated with hyperventilation.
reductions in CMR will cause a parallel reduction in CBF, and this relationship can be of benefit to the anesthesiologist. Hypothermia, for instance, decreases CMR by approximately 6% for every 1°C decrease in temperature. However, due to the risks of even mild hypothermia in the surgical setting (increased infection rate, coagulation disorders), this technique is seldom used in intracranial surgery. Both inhalational and IV anesthetics can decrease CMR and lower ICP (Table 1.1). Since all inhalational agents are also vasodilators, the relationship between reduction in CMR and MAC concentrations is not linear. Reduction in CBF by volatile agents is more pronounced at lower MAC (<0.5) concentrations, where flow–metabolism coupling predominates. At higher MAC concentrations, the vasodilatory property of volatile agents predominates and balances out the reduction in CBF. IV agents, on the other hand, reduce CMR and are vasoconstrictors (Table 1.2). The notable exception is ketamine, which increases CMR, CBF, and ICP.
Table 1.2. EFFECTS OF COMMON INTRAVENOUS AGENTS ON CEREBRAL BLOOD FLOW (CBF), CEREBRAL METABOLIC RATE (CMR), AND INTRACRANIAL PRESSURE (ICP)
INTRAVENOUS AGENT
Barbiturates
Benzodiazepines
Opioids
Most intravenous agents cause a reduction in CBF and CMR, with the notable exception of ketamine. Opioids produce very little effect on CBF and CMR except with high doses.
Blood flow and CPP
Normal neuronal function in the healthy adult requires a CBF of 50 mL/min per 100 g of tissue (Figure 1.1). CBF is regulated at the level of the cerebral arteriole and is dependent on forward pressure gradient and PaCO2. The pressure gradient is the result of CPP, which is determined by the equation CPP = MAP – ICP. Cerebral autoregulation keeps CBF relatively constant throughout a range of CPP of 50–150 mm Hg via alterations in vasomotor tone. When CPP is inadequate, neuronal dysfunction occurs at CBF of less than 18 mL/min per 100 g of tissue and delayed cell death is seen when CBF is less than 10 mL/min per 100 g of tissue.
Fluid therapy
Another area of debate in neurosurgery procedures is the choice fluid replacement therapy for intracranial surgery. As the integrity of the blood–brain barrier is often compromised in patients undergoing surgical resection of supratentorial tumors, administration of large volumes of IV fluids is thought to contribute to cerebral edema. However, maintaining normovolemia and avoiding hypotension are important goals for successful surgical outcome. Dextrose-containing solutions are typically avoided in intracranial procedures as hyperglycemia has been shown to worsen outcomes of cerebral ischemia.22–24 Hypotonic solutions, such as lactated Ringer’s (273 mOsm/L), are often avoided since they are thought to exacerbate cerebral edema. Normal (0.9%) saline is slightly hypertonic (308 mOsm/L), which may improve cerebral edema and is typically the fluid of choice for intracranial procedures. Colloids are also suitable alternatives for fluid replacement since their ability to increase plasma oncotic pressure could potentially decrease brain edema.
EMERGENCE FROM ANESTHESIA
The anesthetic goals at the end of intracranial surgery are a rapid emergence and extubation in the setting of controlled hemodynamic and respiratory parameters. Prior to extubation, the PaCO2 should be allowed to gradually rise to normal levels, adequate reversal from neuromuscular blockade should be determined, and the patient should be normothermic. Coughing or “bucking” on the endotracheal tube can elevate ICP and may be prevented with the continuation of remifentanil infusion or with the administration of IV lidocaine (0.5–1 mg/ kg). Hypertension should be promptly treated with esmolol or other IV agents, and persistent hypertension may necessitate calcium channel blocker infusion (nicardipine). Postoperative pain may be significant, especially if remifentanil was utilized during the procedure, and should be treated with short-acting opioids or IV acetaminophen.
In cases of delayed awakening following intracranial procedures, the differential diagnosis includes three main categories: (1) neurological causes such as ongoing seizure, hemorrhage, or stroke; (2) physiological cause, such metabolite or electrolyte disturbances, hypothermia, or hyperglycemia; and (3) pharmacological cause such as continued
neuromuscular block, opioid overdose, and persistent anesthesia. In such instance, an emergent head CT scan is warranted.
REVIEW QUESTIONS
1. A patient is undergoing craniotomy for a frontal tumor resection with general anesthesia using sevoflurane and remifentanil as maintenance. The patient has the following vital signs: BP 135/85, pulse 60 bpm, ETCO2 38 mm Hg, SpO2 99%. The surgeon asks you to facilitate more brain relaxation. What is the most appropriate intervention?
a) Increase PEEP
b) Lower the head of the bed
c) Increase sevoflurane
d) Increase minute ventilation
Correct Answer: d. Increasing the minute ventilation will result in hypocapnia, which in turn produces cerebral vasoconstriction. Assuming intact autoregulation, this will result in a reduction of brain volume and improve the surgical conditions in this case.
2. What is the expected effect on cerebral metabolic rate of oxygen consumption, CBF, and ICP when utilizing ketamine for induction of general anesthesia in a patient with a known supratentorial mass?
a) Decreased CBF, decreased CMR, decreased ICP
b) Increased CBF, increased CMR, increased ICP
c) Increased CBF, increased CMR, decreased ICP
d) Decreased CBF, increased CMR, decreased ICP
Correct Answer: b. Ketamine increases CBF, CMR, and ICP, although the increase in CMR is minimal. This contrasts with volatile anesthetics which decrease CBF, CMR, and ICP at 1 MAC.
3. Which of the following is the most appropriate choice for maintenance IV fluids in an otherwise healthy adult patient undergoing resection of a supratentorial mass?
a) D5 normal saline
b) 3% saline
c) 0.9% saline
d) Lactated Ringer’s
Correct Answer: c. Maintaining euvolemia is critical for successful outcomes in neuroanesthesia. Normal saline is an ideal choice since it is slightly hypertonic and may therefore improve cerebral edema; 3% saline may be utilized to decrease ICP. However, it would not be the first choice for maintenance fluids. Fluids containing glucose should be avoided as hyperglycemia has a negative impact on cerebral ischemia outcomes. Hypotonic solutions, including lactated Ringer’s, should also be avoided as they may increase cerebral edema.
4. All of the following are benefits of remifentanil except:
a) Improved postoperative pain control
b) Decreased requirement for volatile agents
c) Minimal effects on CBF and ICP
d) Rapid emergence compared to fentanyl
Correct Answer: a. Remifentanil is frequently utilized in neuroanesthesia to supplement volatile anesthetics, and its effect on CBF and ICP is minimal. Emergence from remifentanil is reliable due to its short context-sensitive half-life. However, remifentanil will not improve postoperative pain, so pain control may be necessary with a bolus of short-acting opioids including fentanyl on emergence.
5. All of the following are true regarding neuromuscular blockade in a patient with supratentorial mass EXCEPT:
a) Succinylcholine may result in life-threatening hyperkalemia.
b) Pancuronium is the preferred NDMR in cases of increased ICP.
c) Nondepolarizing muscle relaxants have minimal effect on ICP.
d) Depolarizing muscle relaxants may cause transient increases in ICP
Correct Answer: b. Pancuronium is not an ideal muscle relaxant for most neuroanesthesia procedures due to its long duration of action and its vagolytic effect, which may lead to increased CBF and ICP.
6. Which of the following is an appropriate goal for emergence?
a) Normocapnia
b) Avoiding reversal of neuromuscular blockade
c) Hypothermia
d) Permissive hypertension
Correct Answer: a. The goals for emergence from intracranial surgery include a normal physiologic PaCO2, normothermia, and complete reversal of neuromuscular blockade. In addition, tight control of BP is necessary during emergence and can be managed with esmolol.
7. Regarding CBF in an otherwise healthy adult, all of the following are true EXCEPT:
a) Normal CBF is 100 mL/min per 100 g of tissue.
b) Cerebral autoregulation maintains CBF throughout a CPP range of 50–150 mm Hg.
c) Neuronal dysfunction occurs at CBF of less than 18 mL/min per 100 g of tissue.
d) Delayed cell death is seen when CBF is less than 10 mL/min per 100 g of tissue.
Correct Answer: a. CBF in a healthy adult is 50 mL/min per 100 g of tissue.
8. Which of the following will produce the greatest decrease in ICP:
a) Hyperventilation to decrease PaCO2 from 60 to 30.
b) Increase volatile anesthesia agent to 2 MAC
c) Increase PaO2 from 80 to 100
d) Increase temperature by 1°C
Correct Answer: a. There is a linear relationship between CBF and PaCO2 for PaCO2 of 20–70 mm Hg. Therefore, reduction in PaCO2 from 60 to 30 mm Hg will result in a significant decrease in CBF and ICP. PaO2 of less than 50 mm Hg can increase CBF and ICP. However, a change in PaO2
within physiologic range will not cause a significant change. Hypothermia, not hyperthermia, will decrease CMR by approximately 6% for every 1°C decrease in temperature.
9. All of the following are true regarding the actions of mannitol EXCEPT:
a) Peak effect of mannitol is between 20–60 minutes after administration.
b) Repeated doses of mannitol may cause a paradoxical increase in ICP.
c) Mannitol works as an osmotic diuretic by decreasing plasma oncotic pressure.
d) Mannitol duration of action is 2–3 hours.
Correct Answer: c. Mannitol is an osmotic diuretic that decreases brain size by decreasing interstitial water via an increase in plasma oncotic pressure.
10. Which of the following statements about propofol is TRUE:
a) Increases CMR and decreases CBF
b) Increases CMR with induction doses only
c) Maintains cerebral autoregulation
d) Uncouples CBF and CMR
Correct Answer: c. Propofol, as well as opioids, barbiturates, and sedative-hypnotics, does not cause uncoupling of CBF and CMR. While most IV agents maintain cerebral autoregulation, volatile agents at high MAC levels may impair cerebral autoregulation.
QUESTIONS AND ANSWERS
This chapter has accompanying questions and answers which are available to subscribers as part of the Oxford eLearning platform. To access the questions, go to http:// oxfordmedicine.com/neuroanesthesiaPBL
REFERENCES
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7. Todd MM, Warner DS, Sokoll MD, et al. A prospective, comparative trial of three anesthetics for elective supratentorial craniotomy.
Propofol/fentanyl, isoflurane/nitrous oxide, and fentanyl/nitrous oxide. Anesthesiology. 1993;78(6):1005–1020.
8. Petersen KD, Landsfeldt U, Cold GE, et al. Intracranial pressure and cerebral hemodynamic in patients with cerebral tumors: a randomized prospective study of patients subjected to craniotomy in propofol-fentanyl, isoflurane-fentanyl, or sevoflurane-fentanyl anesthesia. Anesthesiology. 2003;98(2):329–336.
9. Fraga M, Rama-Maceiras P, Rodiño S, Aymerich H, Pose P, Belda J. The effects of isoflurane and desflurane on intracranial pressure, cerebral perfusion pressure, and cerebral arteriovenous oxygen content difference in normocapnic patients with supratentorial brain tumors. Anesthesiology. 2003;98(5):1085–1090.
10. Chui J, Mariappan R, Mehta J, Manninen P, Venkatraghavan L. Comparison of propofol and volatile agents for maintenance of anesthesia during elective craniotomy procedures: systematic review and meta-analysis. Can J Anaesth. 2014;61(4):347–356.
11. Sneyd JR, Andrews CJ, Tsubokawa T. Comparison of propofol/ remifentanil and sevoflurane/remifentanil for maintenance of anaesthesia for elective intracranial surgery. Br J Anaesth. 2005;94(6):778–783.
12. Citerio G, Pesenti A, Latini R, et al. A multicentre, randomised, openlabel, controlled trial evaluating equivalence of inhalational and intravenous anaesthesia during elective craniotomy. Eur J Anaesthesiol. 2012;29(8):371–379.
13. Kaisti KK, Metsähonkala L, Teräs M, et al. Effects of surgical levels of propofol and sevoflurane anesthesia on cerebral blood flow in healthy subjects studied with positron emission tomography. Anesthesiology. 2002;96(6):1358–1370.
14. Kaisti KK, Långsjö JW, Aalto S, et al. Effects of sevoflurane, propofol, and adjunct nitrous oxide on regional cerebral blood flow, oxygen consumption, and blood volume in humans. Anesthesiology. 2003;99(3):603–613.
15. Bundgaard H, von Oettingen G, Larsen KM, et al. Effects of sevoflurane on intracranial pressure, cerebral blood flow and cerebral metabolism. A dose-response study in patients subjected to craniotomy for cerebral tumours. Acta Anaesthesiol Scand. 1998;42(6):621–627.
16. Holmström A, Akeson J. Desflurane increases intracranial pressure more and sevoflurane less than isoflurane in pigs subjected to intracranial hypertension. J Neurosurg Anesthesiol. 2004;16(2):136– 143.
17. Warner DS, Hindman BJ, Todd MM, et al. Intracranial pressure and hemodynamic effects of remifentanil versus alfentanil in patients undergoing supratentorial craniotomy. Anesth Analg. 1996;83(2):348–353.
18. Guy J, Hindman BJ, Baker KZ, et al. Comparison of remifentanil and fentanyl in patients undergoing craniotomy for supratentorial spaceoccupying lesions. Anesthesiology. 1997;86(3):514–524.
19. Balakrishnan G, Raudzens P, Samra SK, et al. A comparison of remifentanil and fentanyl in patients undergoing surgery for intracranial mass lesions. Anesth Analg. 2000;91(1):163–169.
21. Kaufmann AM, Cardoso ER. Aggravation of vasogenic cerebral edema by multiple- dose mannitol. J Neurosurg. 1992;77(4): 584–589.
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23. Kimura K, Iguchi Y, Inoue T, et al. Hyperglycemia independently increases the risk of early death in acute spontaneous intracerebral hemorrhage. J Neurol Sci. 2007;255(1–2):90–94.
24. McGirt MJ, Woodworth GF, Brooke BS, et al. Hyperglycemia independently increases the risk of perioperative stroke, myocardial infarction, and death after carotid endarterectomy. Neurosurgery. 2006;58(6):1066–1073; discussion 1066–1073.
ANESTHESIA FOR POSTERIOR FOSSA MASS
Valerie L. Howell, Margaret M. Collins and Lauryn R. Rochlen
STEM CASE AND KEY QUESTIONS
A 56-year- old female patient with no known medical history presented to her primary care physician with a chief complaint of bilateral headache, dizziness, and right-sided hearing loss that began 1 month ago. Physical exam revealed end- gaze nystagmus and ataxic gait. Initial workup included retinal exam, which revealed no abnormalities and no papilledema. Additional evaluation included a magnetic resonance imaging (MRI) scan of the brain which revealed a lobulated, heterogeneously enhancing right cerebellopontine angle cistern mass measuring 5.4 cm × 5.4 cm × 5.0 cm posterior to the internal auditory canal (Figure 2.1). Audiology report confirmed severe sensorineural hearing loss. Following interpretation of the MRI, the patient is admitted to the hospital for observation of neurologic status and initiated on acetazolamide and dexamethasone therapy. After further discussion with the neurosurgical team, she consented to undergo a posterior fossa craniotomy for resection of the tumor.
WHAT ARE THE BOUNDARIES OF THE POSTERIOR FOSSA?
It is bounded anteriorly and medially by the dorsum sellae of the sphenoid bone, anteriorly and laterally by the superior border of the petrous part of the temporal bone, posteriorly by the internal surface of the squamous part of the occipital bone and superiorly bound by the tentorium cerebelli. The floor of the posterior fossa is made up of the sphenoid, occipital, temporal, and mastoid angles of the parietal bones. The posterior and inferior limit is the foramen magnum.
WHAT ARE COMMON PRESENTING COMPLAINTS
OF A PATIENT WITH A POSTERIOR FOSSA MASS?
Symptoms typical of posterior fossa masses include cerebellar dysfunction (ataxia, nystagmus, dysarthria), brainstem compression (cranial nerve palsy, altered consciousness, abnormal respiration), or elevated intracranial pressure
(ICP) due to obstructive hydrocephalus (headache, nausea, papilledema).
WHAT ARE SPECIFIC PREOPERATIVE CONSIDERATIONS FOR A PATIENT WITH A POSTERIOR FOSSA MASS?
The patient with mass lesion of the posterior fossa is at risk of obstructive hydrocephalus due to obstruction of cerebrospinal fluid (CSF) flow through the fourth ventricle or the cerebral aqueduct of Sylvius. Such obstruction may be present even with small lesions. Careful history and evaluation of available imaging studies may be useful in determining the presence of increased ICP. Medication review should focus on use of corticosteroids, diuretics, and carbonic anhydrase inhibitors. Corticosteroids should be administered up to and including the day of surgery. Laboratory data should be evaluated for corticosteroid-induced hyperglycemia and electrolyte disturbances due to diuretic use. Preoperative anxiolytics, such as benzodiazepines and opioids, should be used with caution in patients with posterior fossa lesions as their use may lead to hypoventilation resulting in acute clinical decompensation from increases in ICP. Use of anxiolytics should be individualized to each patient and only administered when uninterrupted care can be provided by a qualified anesthesia professional.
WHAT POSITIONS ARE COMMONLY UTILIZED FOR POSTERIOR FOSSA SURGERY? WHAT ARE THE ADVANTAGES AND DISADVANTAGES OF EACH POSITION?
Resection of a posterior fossa mass may be approached from a semi-lateral, prone, supine with head turned, or sitting position. Selection of the patient position depends on location of the tumor, patient risk factors, and surgeon preference. Historically, the sitting position was favored by surgeons since it improved surgical exposure, maintained anatomical orientation, promoted venous drainage, improved hemostasis, and facilitated gravitational drainage of CSF and blood from the field. Some anesthesiologists preferred the position as it allowed improved access to the endotracheal
Figure 2.1. Magnetic resonance imaging (MRI) T2 image of a right cerebellopontine angle cistern mass; the mass extends from the level of the tentorium caudally to the foramen magnum abutting and displacing the facial and vestibular nerves with significant compression of adjacent cerebellum, pons and medulla.
tube, chest wall, and upper extremities, as well as allowed for free diaphragmatic movement. Risks associated with the sitting position include peripheral nerve injury, midcervical spinal cord injury and quadriplegia, swelling of the upper airway and hemodynamic alterations related to postural hypotension, and the potential for lethal venous air embolism. Non-sitting positions are associated with less risk of venous air embolism but increase the possibility of positioning-related peripheral nerve injury and the obstruction of cranial venous blood drainage related to excessive head rotation. Many injuries related to positioning can be prevented by careful attention to padding of pressure points, avoidance of stretch or compression at plexuses, and avoidance of excessive neck rotation or flexion.
THE SURGEON INSISTS ON OPERATING WITH THE PATIENT IN THE SITTING POSITION. WHAT CONCERNS SPECIFIC TO THE SITTING POSITION WILL YOU DISCUSS WITH THE SURGEON?
When considering the sitting position for posterior fossa mass resection, one must evaluate if the patient has any preexisting conditions that would preclude such a position. Absolute contraindications to craniotomy in the sitting position include right-to-left intracardiac or intrapulmonary shunt. Relative contraindications include severe carotid stenosis and severe cervical spinal stenosis. Further concern includes the risk of reduced cerebral perfusion pressure (CPP) due to postural hypotension secondary to reduced venous return and resultant decreased cardiac output.
WHAT MONITORS SHOULD BE USED FOR THE CASE? WHAT ARE YOUR HEMODYNAMIC GOALS DURING INDUCTION OF GENERAL ANESTHESIA?
Preoperatively, a transthoracic echocardiogram (TTE) or transesophageal echocardiogram (TEE) is needed to assess the presence of a patent foramen ovale (PFO). Standard American Society of Anesthesiologists (ASA) monitors will be utilized as well as a temperature monitor, urinary catheter, intraarterial catheter, and multiorifice central venous catheter with the tip placed at the junction of the superior vena cava and right atrium. Invasive lines may be placed preor postinduction depending on the clinical scenario. TEE monitoring can also be placed after positioning to assess for air in the right heart during the procedure. Additionally, a precordial Doppler can be used to assess for vascular air embolism (VAE) in which the characteristic windmill murmur would be heard. Assuming a reassuring airway, induction of anesthesia can be obtained with care taken to minimize increases in ICP (hypoxia and hypercarbia), avoid the extremes of blood pressure (BP) variance, and maintain cerebral oxygenation.
IS THERE A ROLE FOR INTRAOPERATIVE NEUROPHYSIOLOGIC MONITORING? WHAT TYPES? HOW WOULD THIS INFLUENCE YOUR ANESTHETIC PLAN?
The posterior fossa is densely packed with important neural structures that, if damaged, may lead to devastating complications. Intraoperative neurophysiologic monitoring, such as brainstem auditory evoked potentials or somatosensory evoked potentials (SSEPs), monitor 20% of brainstem function during surgery but do not relate perfect real-time monitoring or detection of injury to all tracts. Continuous electromyography (EMG) of the cranial nerves VI and VII during microvascular decompression, surgery for fourth-ventricle tumors, and acoustic neuroma surgery enhance operative safety. In this case, brainstem auditory evoked potentials and somatosensory evoked potentials would be useful. To facilitate intraoperative monitoring, the inhalational anesthetic should be limited to 0.5 mean alveolar concentrations (MAC), and a propofol infusion should be used to supplement sedation. Opiates may be administered in bolus or infusion form. Muscle relaxants may be used during tracheal intubation and patient positioning, but their continued use should be avoided to allowing for EMG monitoring.
WHAT ARE THE MONITORING OPTIONS FOR VENOUS AIR EMBOLISM? WHICH WILL YOU CHOOSE?
Monitoring for VAE relies on detection of air in the right heart via ultrasound visualization, auscultation via Doppler, or through interpretation of standard monitors with high index of suspicion. TEE is the most sensitive monitor for detection of air embolism, and precordial Doppler is the most sensitive noninvasive mode of
detection. The Doppler probe should be placed at the second intercostal space on either side of the sternum or between the right scapula and the spine. Pulmonary air embolisms can be detected with the appearance of nitrogen in expired air, drop in PaCO2, a rise in pulmonary artery pressures, appearance of air in the right heart on TEE, or by auscultation of a windmill murmur by precordial Doppler. A pulmonary artery catheter can detect increases in right heart pressures but is less sensitive in detecting VAE than precordial Doppler.
WHAT ARE THE INTRAOPERATIVE SIGNS OF VENOUS AIR EMBOLISM?
Signs of VAE depend on the rate and volume of air entrained. In adults, a lethal dose may be 200–300 mL (3–5mL/kg). Decreased end tidal carbon dioxide is seen due to an increase in pulmonary vascular resistance causing right heart strain and increased alveolar dead space. If the embolism is large (~5 mL/kg), a gas airlock may result in cardiac arrest. The most common signs of VAE are tachypnea, tachyarrhythmias, hypoxemia, hypotension, wheezing on auscultation, and decreased EtCO2. Unexplained hypotension or decrease in EtCO 2 should immediately raise suspicion for VAE.
WHAT ARE MANAGEMENT STRATEGIES FOR VAE?
1. Prevention of further air entry: Alert the surgeon and “flood the field” with sterile saline and soaked gauze, as well as eliminating other sites of air entry. Reposition the patient into a head-down, left lateral tilt to sequester the air in the apex of the right ventricle. Transient jugular compression has been advocated by some sources as a means of decreasing the pressure gradient for air entry.
2. Reduction in the volume of entrained air: Nitrous oxide should be immediately discontinued and 100% oxygen instituted. Aspiration of air through a properly positioned multiorifice central venous catheter should be attempted.
3. Hemodynamic support: Ventilate using 100% oxygen, assist with positive inotropes such as epinephrine, norepinephrine, or dobutamine as indicated, and rapidly initiate chest compressions when necessary.
WHAT POSTOPERATIVE COMPLICATIONS ARE OF GREATEST CONCERN FOLLOWING POSTERIOR FOSSA SURGERY?
Ischemic complications following posterior fossa surgery may be present due to VAE, global hypotension, or prolonged surgical retraction. Pneumocephalus or tension pneumocephalus may occur after air enters the brain or spaces around the brain following dural incision. Tension pneumocephalus is an emergency and may cause brain herniation. Macroglossia and airway swelling may occur after excessive neck flexion, causing obstruction of
venous drainage. Damage or edema of vital centers of the brainstem may cause cardiac arrhythmias or postoperative respiratory depression. Diminished gag reflex or cough reflex causing aspiration may occur after damage to cranial nerves. Stretch, compression or ischemia of peripheral nerves most commonly present in the common peroneal and recurrent laryngeal nerves. Spinal cord injury may be caused by extreme neck flexion decreasing cord blood supply during the sitting position.
DISCUSSION
ANATOMY OF THE POSTERIOR FOSSA
The posterior cranial fossa is the inferior most of the three cranial fossae and is densely packed with vital structures (Figure 2.2).1 It is bounded anteriorly and medially by the dorsum sellae of the sphenoid bone, anteriorly and laterally by the superior border of the petrous part of the temporal bone, posteriorly by the internal surface of the squamous part of the occipital bone, and superiorly bound by the tentorium cerebelli. The floor of the posterior fossa is made up of the sphenoid, occipital, temporal, and mastoid angles of the parietal bones. The posterior and inferior limit is the foramen magnum. The contents of the posterior cranial fossa are listed in Table 2.1.
PATHOLOGY OF THE POSTERIOR FOSSA
Posterior fossa tumors are more common in children than in adults; 54–70% of childhood brain tumors occur in the posterior fossa as opposed to 15–20% occurrence in adult brain tumor populations.2– 4 Common tumors for resection or procedures within the posterior fossa include those listed in Table 2.2.2– 4
Figure 2.2. The margins of the posterior cranial fossa; tentorium cerebelli superiorly, clivus anteriorly, and occiput posteriorly.
Table 2.1. CONTENTS OF THE POSTERIOR CRANIAL FOSSA
BRAIN STRUCTURES NERVES VESSELS CSF
Medulla
Pons
Midbrain
Cerebellum
Facial nerve
Vestibulocochlear nerve
Glossopharyngeal nerve
Vagus nerve
Spinal accessory nerve
Hypoglossal nerve
PRESENTATION AND DIAGNOSTIC
EVALUATION OF POSTERIOR FOSSA MASSES
Patients with mass lesion of the posterior fossa seek medical attention due to symptom manifestation related directly to tumor position. With lesions within the cerebellum, patients present with ataxia, nystagmus, and dysarthria. When lesions cause focal compression of the brainstem, cranial nerve palsies involving the third, fourth, or sixth cranial nerves are most common, resulting in ocular palsies, diplopia, and altered
Table 2.2. COMMON LESIONS FOR RESECTION AND PROCEDURES WITHIN THE POSTERIOR FOSSA
LESIONS CEREBELLOPONTINE ANGLE LESIONS
Cerebellar lesions
Petroclival lesions
Ependymoma/ Ependymoblastoma
Pineal lesions
Brainstem glioma
Choroid plexus papilloma/ carcinoma
Dermoid tumors
Aneurysm/arteriovenous malformation
Procedures Microvascular decompression
Chiari I decompression
Vertebral arteries
Dural veins
Anterior spinal artery
Posterior spinal arteries
Internal jugular vein
Inferior petrosal sinus
Sigmoid sinus
Meningeal branches of the ascending pharyngeal and occipital arteries
Labyrinthine artery
Cerebral aqueduct
Fourth ventricle
ACOUSTIC SCHWANNOMA MENINGIOMA EPIDERMOIDS
Astrocytoma
Arachnoid cyst
Cerebellar convexity meningioma
Cerebellar metastasis
Hemangioblastoma
Cerebellar arteriovenous malformation
Medulloblastoma
Metastasis
Chordoma
Meningioma
Trigeminal neuralgia
Hemifacial spasm
consciousness. Even the smallest of lesions may obstruct flow of CSF through the fourth ventricle or cerebral aqueduct resulting in elevated ICP secondary to obstructive hydrocephalus with symptoms of headache, nausea, frequent vomiting, strabismus, and papilledema.5
For diagnostic evaluation, MRI is preferred for visualization of tumor location and character, which assists in presumptive diagnosis and surgical planning. Cerebral angiography may be used to assess the vascular supply of the tumor and determine potential for embolization to reduce intraoperative blood loss.5
TREATMENT OPTIONS FOR POSTERIOR FOSSA MASSES
Patients are commonly treated with medical management while surgical planning is undertaken.
Corticosteroids and diuretics are initiated to reduce edema that may be exacerbating symptoms. Additionally, CSF volume may be manipulated by pharmacologic suppression of CSF formation or diversion via internal or external shunting.5
The goals of surgical resection within the posterior cranial fossa are to establish a diagnosis through biopsy, decrease pressure on the brainstem, and relieve intracranial hypertension to avoid herniation.
SURGICAL COMPLICATIONS
Common complications following posterior fossa mass surgeries include CSF leak, meningitis, wound infection, CN palsy, cerebellar edema, hydrocephalus, pneumocephalus, cerebellar hematoma, cerebellar mutism, and death.6 These complications are important for anesthesiologists to consider as they influence decisions regarding patient positioning, use of monitoring, anesthetic requirements, extubation, and postoperative disposition.
POTENTIAL COMPLICATIONS RELATED TO POSITIONING
Resection of a posterior fossa mass may be approached from a semi-lateral, prone, supine with head turned, or sitting position depending on location of the tumor, patient risk factors, and surgeon preference. Historically, the sitting position was favored by surgeons since it improved surgical exposure,
maintained anatomical orientation, promoted venous drainage improved hemostasis, and facilitated gravitational drainage of CSF and blood from the field.7,8 Some anesthesiologists preferred the position as it allowed improved access to the endotracheal tube, chest wall, and upper extremities, as well as allowed for free diaphragmatic movement.8 Risks associated with the sitting position include peripheral nerve injury, midcervical spinal cord injury and quadriplegia, swelling of the upper airway, hemodynamic alterations related to postural hypotension, and the potential for lethal venous air embolism.8 As surgical techniques have evolved and risks revealed, the sitting position is used less frequently.
While non-sitting positions are associated with less risk of VAE, the risk is not completely ameliorated.9 In the prone position there is decreased pulmonary compliance and increased ventilation–perfusion mismatch, atelectasis, and facial/airway edema. Furthermore, the face, airway, and torso of the patient become inaccessible, compromising the ability of the care team to respond to pulmonary or cardiovascular events. While the supine, lateral, and semi-lateral positions eliminate many of these concerns, they maintain a risk of positioning-related peripheral nerve injury and excessive head rotation associated cranial venous drainage obstruction. Blood loss/blood transfusion, brainstem retraction injury resulting in lower cranial nerve dysfunction, and duration of surgery have been reported to be greater in these horizontal positions compared to sitting.9 Many injuries related to positioning can be prevented by careful attention to padding of pressure points, avoidance of stretch or compression at plexuses, and avoidance of excessive neck rotation and flexion.
Resection of posterior fossa masses performed in the sitting position can be performed safely under the conscientious care of the surgeon and anesthesiologist.9 Preparation and safe placement into the sitting position is quite challenging (Figure 2.3). It is therefore important to determine if the patient can tolerate this position prior to proceeding. There are absolute contraindications to performing craniotomy in the sitting position: intracardiac right-to-left shunt via a PFO and right-toleft intrapulmonary shunt via pulmonary arteriovenous (AV) fistula. In the presence of these pathologies, devastating cerebral or coronary occlusion may result if air is entrained into the circulatory system. Relative contraindications include severe carotid stenosis, severe cervical spinal stenosis, or severe hypovolemia or cachexia; special care should be taken for those patients with abnormal baroreceptor function, prior stroke, or known cerebrovascular disease as the occurrence of hypotension while anesthetized in the sitting position may be exaggerated and more harmful.10
One must consider the potential for VAE, particularly for patients in the sitting position.11 Air is entrained into the systemic vasculature due to a gravitational pressure gradient that exists between the elevated surgical site and the right atrium. The major site of entrainment is through noncollapsible cerebral venous sinuses due to their dural attachments, although air may enter through any vein.7 Outcomes of VAE are dependent on the rate of air entrainment and the volume of air entrained.12 A symptomatic dose, approximately 50 mL, causes injury to the pulmonary capillary network, which stimulates
Figure 2.3. Positioning and monitors utilized in a sitting craniotomy. The arrow denotes the location of the subclavian multiorifice central line. The star denotes the position of the precordial Doppler, which is located beneath a clear drape.
release of inflammatory mediators resulting in pulmonary edema, pulmonary vasoconstriction, bronchoconstriction, and, ultimately, hypoxemia. Lethal doses of approximately 300 mL (3–5 mL/kg) produces a “gas airlock”/complete right ventricular outflow obstruction and quickly causes a dramatic decrease in cardiac output, spiraling into cardiovascular collapse, myocardial ischemia, and death should intervention not ensue.12 The incidence of VAE while in the sitting position has been reported in 7–76% of cases depending on the sensitivity of the method of detection.7 The majority of events, however, do not result in hemodynamic compromise. Intraoperative signs of VAE include decreases in end tidal carbon dioxide, oxygen saturation on pulse oximetry, arterial oxygen tension, systemic BP or increases in central venous pressure, arterial carbon dioxide tension, and airway pressures; and ST-T segment changes on electrocardiogram (EKG) and tachyarrhythmias.12
The most sensitive monitor for VAE is TEE, which may detect as little as 0.02 mL/kg of venous air within the right ventricle. Precordial Doppler ultrasound has a similar sensitivity of 0.05 mL/kg. Other devices for monitoring (in order or decreasing sensitivity) include: pulmonary artery (PA) catheter, transcranial Doppler, end tidal nitrogen, end tidal carbon dioxide (0.5 mL/kg), oxygen saturation, esophageal stethoscope, and electrocardiogram.8,12 The invasiveness of the monitor is justified by the level of risk of VAE, but for most cases use of precordial Doppler along with common and standard monitors (EKG, EtCO2, SpO2, and arterial BP) is sufficient for detection of clinically relevant volumes of air.9 TEE requires special expertise and has not been demonstrated to provide additional clinical benefit.12 Preventative measures include choosing an alternative position, careful surgical technique, optimization of volume status, use of positive pressure ventilation, and avoidance of hyperventilation, nitrous oxides, and agents that increase venous capacitance (nitroglycerin).12
Management of VAE centers around three tenets, simultaneously executed.12
1. Prevention of further air entry: Alert the surgeon and “flood the field” with sterile saline and soaked gauze. Eliminate other air entry sites. Reposition the patient into a head-down, left lateral tilt to sequester the air in the apex of the right ventricle. Transient jugular compression has been advocated by some sources as a means of decreasing the pressure gradient for air entry.
2. Reduction in the volume of air entrained: Nitrous oxide should be immediately discontinued and 100% oxygen instituted; aspiration of air through a properly positioned multiorifice central venous catheter should be attempted.
3. Hemodynamic support: Ventilate using 100% oxygen; assist with positive inotropes such as epinephrine, norepinephrine, or dobutamine as indicated; and rapidly initiate chest compressions when necessary.
ANESTHETIC CONSIDERATIONS
FOR POSTERIOR FOSSA PROCEDURES
Symptomatic patients can deteriorate quickly, necessitating close attention to neurological status in the preoperative period. 10 Specifically, frequent assessment of changes in level of consciousness, cardiorespiratory dysfunction, signs of intracranial hypertension, cranial nerve dysfunction, ability to clear secretions, and maintenance of airway patency is required. Medical management or external CSF draining strategies should be continued until and including the day of surgery. Anxiolytics and analgesics as premedications should be individualized and titrated carefully while in total attendance of the patient as they are often very sensitive to the sedating effects; resultant hypoventilation leading to increased ICP can have significant clinical effects. In addition to standard monitors, an invasive arterial BP monitor should be placed for all posterior fossa procedures. Hemodynamic lability frequently occurs related either to positioning (venous pooling associated with sitting positions) or due to acute increases in vagal tone (severe, symptomatic bradycardia or asystole) related to manipulation of the brainstem. The arterial catheter should be zeroed at the level of the external auditory meatus to best correlate with CPP. This is particularly important in the sitting patient when otherwise mean arterial pressures may measure well below CPP, placing the patient at risk of cerebral ischemia. Preinduction versus postinduction placement will be patient-specific depending on existing comorbidities and fragility of cerebral autoregulation. The need for central venous access will be determined by many patient factors including ease of suitable peripheral access, anticipated blood loss, and need for vasopressors or hypertonic therapy as well existing comorbidities.
Intraoperative neurophysiologic monitoring is commonly used for tumors of the posterior fossa, Electromyography monitoring of cranial nerves V, VII, IX, X, and XII allows the surgeon to identify and avoid injury during dissection and resection. Neuromuscular blocking drugs should be avoided after induction and intubation, or reversed for EMG monitoring. Cranial nerve VIII is most frequently monitored during posterior fossa surgery via brainstem auditory evoked response (BAER) monitoring. Somatosensory evoked potentials (SSEP) are often used to monitor cortical integrity and assist in monitoring for position-related peripheral nerve injuries. Unlike BAERs, the most resistant of all neurophysiologic monitoring types, SSEPs may mimic neuronal injury by increasing latency and decreasing the amplitude of evoked responses with commonly used anesthetic agents, most notably volatile agents. The anesthetic plan then must accommodate by maintaining a MAC of less than 0.5.
All patients who have undergone posterior fossa surgery should be monitored in an intensive care setting with frequent exams of neurologic status. Prior to immediate postoperative extubation, the anesthesiologist must consider the patient’s risk of complications. Determinants to consider include difficulty of resection, degree of retraction of neural tissue, extensive brainstem manipulation that may result in brainstem
edema, length of surgery, and preexisting conditions. An anesthetic plan which results in quick emergence allows for rapid assessment of neurologic status and intervention. Due to the proximity of the neural components responsible for consciousness within the posterior fossa, postoperative edema can lead to a worsened clinical exam immediately postoperatively, with improvement over the following days.6 Such an event would necessitate maintenance of tracheal intubation and mechanical ventilation. Beyond those neural structures of consciousness, injury to cranial nerves or cranial nerve nuclei can render patients unable to protect their airway due to poor cough and inability to swallow or handle secretions. Such dysfunction may develop in the hours following emergence and extubation. Should one experience a prolonged wake-up after pharmacologic and metabolic derangements have been excluded, a neurologic cause must be considered. Since many neurologic causes of delayed emergence require quick intervention to avoid disability, time taken to arrive at a diagnosis influences outcome. A computed tomography (CT) scan performed directly from the operating room can offer quick information necessary for diagnosis.
CONCLUSION
Surgery in the posterior fossa is challenging for both the anesthesiologist and the surgeon. Many complications are possible, several which are unique to posterior fossa surgery. Vigilant planning, care, and monitoring throughout the perioperative period are necessary to limit risks and complications. Anesthetic care is focused on prevention of common complications, maintenance of hemodynamic stability, facilitation of intraoperative neurophysiologic monitoring, and early postoperative neurologic evaluation through timely emergence.
REVIEW QUESTIONS
1. All of these cranial nerves are located within the posterior fossa EXCEPT:
a) Trigeminal nerve
b) Vagus nerve
c) Hypoglossal nerve
d) Glossopharyngeal nerve
e) Vestibulocochlear nerve
Correct Answer: a. The trigeminal nerve is only cranial nerve listed that is not in the posterior cranial fossa. It is present in the middle cranial fossa and exits through three separate foramen (the superior orbital fissure, the foramen rotundum, and the foramen ovale).
2. Which of the following statements concerning brainstem auditory evoked responses is true?
a) They monitor cortical function.
b) They are affected by changes in PaCo2.
c) They are affected by mild hypothermia.
d) They are more resistant to anesthetic effects than somatosensory evoked responses.
e) They are abolished coincident with flattening of the EEG.
Correct Answer: d. Brainstem auditory evoked potentials (BAEPs) are considered the easiest of the somatosensory evoked potentials to monitor and are least sensitive to changes in preoperative variables.
3. Presenting symptoms of posterior fossa masses related to brainstem compression include all of the following EXCEPT :
a) Cranial nerve palsy
b) Nystagmus
c) Altered consciousness
d) Abnormal respiration
e) Abnormal hemodynamics
Correct Answer: b. Nystagmus represents a symptom related to cerebellar dysfunction, not due to brainstem compression.
4. The most sensitive monitor to detect a VAE is:
a) Precordial Doppler
b) End-tidal CO2
c) End-tidal nitrogen
d) TEE
e) PA pressure
Correct Answer: d. TEE is the most sensitive monitor to detect a VAE. It can detect as little as 0.02 mL/kg of venous air within the right ventricle.
5. Relative contraindications to performing a craniotomy in the sitting position include all of the following EXCEPT:
a) Severe carotid stenosis
b) Patent foramen ovale
c) Severe cervical spinal stenosis
d) Severe hypovolemia
e) Cachexia
Correct Answer: b. Presence of a PFO is considered an absolute contraindication to performing surgery in the sitting position.
ADVANCED EXAM QUESTIONS
6. A 55-year-old man has quadriplegia after undergoing suboccipital craniotomy in the sitting position for the treatment of acoustic neuroma. Which of the following is the most likely cause?
a) Air embolism with the presence of probe patent foramen ovale
b) Compression of the cervical cord related to neck flexion
