7 Anesthesia in Endoscopic Skull Base and Brain Surgery

Nelson Mizumoto

Tips and Pearls

• The choice of the anesthesia technique is determined by the tumoral pathologic characteristics, such as tumor vascularization, surrounding edema, or production of hormones by the tumor.

• The correlation between tumor localization and the adjacent structures at the skull base indicates the complications likely to occur.

• Preexisting diseases of the cardiovascular, respiratory, renal, or locomotor systems interfere with the anesthesia of the central nervous system (CNS).

• Good monitoring of hemodynamics and pulmonary ventilation is essential to both prevention and treatment of intraoperative complications.

• The anesthesiologist must be familiar with the CNS physiopathologic mechanisms and their interactions with anesthetics, to synchronize his or her actions with those of the surgical team.

• Hormone-secreting tumors or large tumors compressing the hypothalamic-pituitary neural axis may induce changes in the neuroendocrine baseline and cause a panhypopituitarism event that will affect the cardiovascular, pulmonary, osteomuscular, and hydroelectrolytic functions.

• Cardiac arrhythmias can be triggered by the surgical manipulation of structures of the CNS.¹^,²

• When the surgical field is located on a higher level than the right cardiac atrium, the presence of lesions in venous vessels at the surgical site may lead to a venous air embolism (VAE).³

• Whereas patient immobility is essential for surgery, the necessary dose of muscle relaxants does not always correlate with the body weight of the patient.

• The association of short- and medium-acting anesthetics provides better results than the administration of a short- or medium- duration anesthetic alone.

• If there is a risk of liquid fistula, cough must be prevented during the removal of the endotracheal tube and recovery of consciousness, because the intrathoracic pressure increases the intracranial pressure (ICP), augmenting the risk of liquor infiltration into the dura mater through the puncture sealed by the blood clot (or the grafted patch).

Introduction

Advances in neuroimage scanning techniques and the improvement of surgical equipment and of intraoperative and postoperative monitoring resources have made possible the surgical resection of tumors located at the skull base through the transnasal endoscopy approach, with lower morbidity. Nevertheless, due to the close localization of large vessels at the skull base and the intimate correlations with the hypothalamic- pituitary neural axis, the cranial nerves, the pons, and the medulla oblongata, surgical manipulation in this area can cause cardiac arrhythmias, arterial brady/tachycardia, hypo/hypertension,⁴ depression of consciousness level, depression of the respiratory centers, and hydroelectrolytic alterations. Additionally, it can induce vascular lesions of difficult hemostasis and the risk of venous air embolism.

Tumor Features that Should Determine Anesthesia Selection

Pituitary tumors can cause specific alterations, which are associated with the implicated neurohormone as follows.

Cushing’s Disease

Microadenoma in the anterior pituitary secretes abnormal high levels of adrenocorticotropic hormone (ACTH) and increases plasmatic cortisol, which causes several body changes. The vascular fragility makes difficult the venous and arterial access. Arterial hypertension and tachycardia interfere with the evaluation of the depth of anesthesia.⁵ The use of betablockers to treat arterial hypertension and tachycardia is helpful, as they reduce the need for great amounts of anesthesia. In the assessment of depth of anesthesia, electrocardiogram (ECG) and invasive arterial pressure monitoring is complemented by the bispectral index (BIS),⁶ which monitors the electroencephalographic activity. Cortisol-induced bone resorption leads to osteoporosis, requiring the careful handling of the patient to prevent bone fractures. The hyperaldosteronism and the hypokalemic alkalosis can cause cardiac arrhythmias, making difficult the diagnosis of cardiac arrhythmias caused by surgical procedures in areas close to the hypothalamus.⁷ The conversion of muscle proteins into glucose reduces the muscular mass as well as the amount of curare necessary to ensure immobility. The hyperglycemia must be treated to prevent hyperglycemic coma, which could complicate the recovering of consciousness.

Acromegaly

Acromegaly is often associated with pituitary adenoma and is caused by the tumor’s high secretion of growth hormone (GH). The resulting enlargement of the lower jaw, oral cavity, and tongue interferes with the laryngoscope during tracheal intubation. The increase of muscular mass requires a higher dose of curare for muscle relaxation, because the internal organs are also enlarged. The enlarged lungs require higher volume flow during assisted ventilation. The size of the heart also increases, but leads to interstitial fibrosis and infiltrating lymphomononuclear myocarditis, posing a risk of cardiac ischemia and making the proper procedures more difficult. A higher cardiac output is needed to perfuse the enlarged organs and muscular mass. However, despite the heart’s hypertrophy, its contractility is compromised and may result in cardiac arrest.8 The associated hyperglycemia is mediated by the excess of GH that induces resistance against insulin activity. Acromegalic patients must be fully awaken before tracheal extubation is done because the decreased ventilation caused by the partial encephalic depression, due to the residual action of anesthetics, is aggravated by the enlarged tongue that obstructs the respiratory pathways, compromising breathing.

Prolactinoma

Patients with prolactin-producing pituitary tumors who are treated with dopamine agonist drugs (e.g., bromocriptine) may present dopamine-like cardiovascular effects such as arterial hypotension and cardiac arrhythmia in a hypertensive patient.⁹

Pituitary Tumors or Tumors in the Sella Turcica Area

Whether or not these are hormone-producing tumors, they eventually compress the hypothalamic-pituitary neural axis as their volume increases, thus causing panhypopituitarism.¹⁰ The reduction of synthesis of ACTH, GH, and thyroid-stimulating hormone (TSH) renders the patient more sensitive to anesthesia and cardiovascular depressant drugs, making it difficult to evaluate the depth of anesthesia. Again, the BIS monitor can be useful. Surgical ablation of the pituitary stalk causes sudden arterial hypotension in the immediate postsurgical period, due to adrenal insufficiency associated with decreased ACTH secretion. Lesions of the hypothalamicpituitary neural axis can cause diabetes insipidus (DI),¹¹^,¹² leading to free water loss through the kidney and increase of sodium in the plasma, which results in hypernatremia. Diuresis may reach an output of 15 to 20 mL/kg/hour, rendering the patient hypovolemic and susceptible to arterial hypotension. Plasmatic sodium increases to 155 to 160 mEq/L and elevates plasma osmolarity to 310 to 315 mEq/L. Vasopressin must be promptly administered to prevent seizures as soon as the DI hypothesis is confirmed. Edema around the tumor indicates loss of integrity of the blood–brain barrier in that area and possible reduction of vascular-arterial reactivity, suggesting the use of anesthetics that reduce the metabolic rate and induce cerebral vasoconstriction. Intravenous anesthetics, except ketamine, reduce neuron metabolism and induce vasoconstriction.

Meningioma and Angioma

In vascularized tumors, such as meningiomas and angiomas, the discrete to moderate arterial hypotension reduces surgical bleeding, also preserving the cerebral blood flow (CBF) in the absence of intracranial hypertension (ICH). Arterial hypertension significantly increases bleeding inside the tumor and its surroundings, because there is no vasoconstrictor response to the increased arterial pressure in these areas, as a result of reduced arterial self-regulation.

Characteristics of Structures Adjacent to the Tumor

Invasive blood pressure (IBP) shows sudden variations in extensive arterial hemorrhage due to lesions in arteries of the skull base involved by the tumor. Immediate arterial hypotension must be induced through higher doses of anesthetics or the use of arterial vasodilators. However, the reduction of blood flow may cause brain ischemia. Some drugs that induce arterial hypotension through systemic vasodilation (e.g., sodium nitroprusside and halogenated anesthetics) also lead to cerebral vasodilation, thus increasing both intracranial blood and intracranial pressure. If necessary, the carotids must be compressed. Blood components must be available for transfusion because the hemorrhage can be difficult to control.

Venous Air Embolism

The proximity of the field of tumor access to the venous sinus may cause venous injury and a venous air embolism (VAE). Air bubbles in the superior cava vein increase the central venous pressure (CVP), and once they reach the cardiac chambers they augment the pressure in the right atrium and hinder blood output through the right ventricle. Air bubbles passing through capillary vessels in lung alveoli also hinder the blood flux. Therefore, hypotension and tachycardia ensue. Pulmonary perfusion reduces and compromises gaseous exchanges in the alveoli, with the consequent fall of exhaled CO₂ [endtidal carbon dioxide concentration (E_T-CO₂)] and O₂ saturation in arterial blood. Cardiac Doppler detects air bubbles inside the cardiac chambers. The prophylaxis against VAE consists of volume adjustment to prevent the negative balance in the volume replacement and the use of 6 to 8 cm of peak endexpiratory pressure (PEEP) H₂O. Treatment consists of warning the surgeon, reducing the proclivity and aspiration of air bubbles through the inserted catheter, with the orifices positioned in the superior cava vein and in the right atrium, and, if needed, administering a rapid infusion of volume and compression of jugular veins (if possible). In cases of hypotension, administer vasopressor medication.

Arrhythmias and Blood Pressure Changes Associated with Surgical Procedures

Arrhythmias and changes in arterial pressure, emerging from surgical manipulation of the hypothalamus or of the brainstem, require the immediate warning of the surgeon to reduce harmful stimulation of the CNS, because the stronger the stimulus, the worse the cardiovascular alterations will be. The increase of the depth of anesthesia reduces both arrhythmias and blood pressure changes. Nevertheless, the stimulus continues, and a more serious lesion of the CNS may occur despite the reduced impact on the cardiovascular tract. Intense changes in arterial pressure, as a consequence of surgical manipulation of the brainstem and of the bulb, may signal changes in the patient’s respiratory pattern during awakening because of the vicinity of the respiratory centers to the bulbar cardiovascular centers. The intensive manipulation of the bulb may compromise the recovery of consciousness because the ascending reticular activating system (ARAS), responsible for wakefulness, is situated in this area.

When a tumor is compressing cranial nerves, tracheal intubation must be maintained to avoid pulmonary infection, because the glossopharyngeal (IX) and the hypoglossal (II) nerves are responsible for the sensitivity of the larynx, pharynx, and trachea as well as for bronchial motility. Dysfunction of these nerves reduces sensitivity to any substance in the oropharyngeal tract and causes difficulty in swallowing, thus facilitating the aspiration of substances into the trachea and bronchi.

The excessive manipulation of the oculomotor nerve (III) induces pupillary dilation that interferes with the neurologic assessment. In such cases, early awakening is necessary to allow the assessment of consciousness degree and motor activity as well.

Patient’s Monitoring

Electrocardiography identifies the source of cardiac arrhythmias, whereas the invasive arterial pressure promptly shows either hypo- or hypertension states. Central venous pressure helps in volume replacement and in the diagnosis and treatment of venous air embolism. Capnography and oxygen saturation indicate changes in pulmonary ventilation and variations in the ventilation/perfusion ratio. Intrathoracic pressure guides adjustments in ventilation and curare dosing. Doppler, BIS, and curare-action monitoring are supporting tools during anesthesia.

Patient’s Positioning for Transnasal Approach

The positions that favor venous drainage from the brain and reduce intracranial pressure are as follows:

1. The head must be above the cardiac atrium to favor venous drainage by gravity, because the encephalic segment of the venous system does not have valves.

2. The optimum positioning for the transnasal approach is dorsal decubitus with an approximately 20-degree inclination of the bench, and an extended neck.

3. Flexion or rotation of the neck must be avoided to prevent compression of the internal jugular vein.

4. It is important to carefully check and remove any form of external compression of the neck.

5. Excessive volume of intravascular infusion and the rise of intrathoracic pressure must be avoided to prevent increasing the central venous pressure.

6. The surgical field is better exposed with the head-above-the-heart position that also reduces local hemorrhage. However, because the surgical field is higher than the heart, the opening of any venous system may lead to VAE. Note that for each 13 cm of head elevation above the heart, there is a correspondent 10 mm Hg reduction in the cerebral perfusion pressure. Therefore, the distance between the surgical field and the heart must be considered when arterial hypotension is induced to diminish arterial hemorrhage. Moreover, the invasive arterial pressure transducer must be positioned at the median point of the head.

7. When a graft is needed to seal a liquoric fistula, the positioning of flexed legs and internal rotation of the right thigh must be carefully done, especially with patients suffering from Cushing disease and osteoporosis, to prevent pathologic fractures.

Action of Anesthetics

The selected anesthetics must not contribute to the increase of intracranial pressure if it is already high. Anesthetics reduce the neuronal metabolic rate, but the necessary concentrations to provide encephalic protection may be too high, causing cardiovascular depression and systemic arterial hypotension, which reduces cerebral perfusion. In such cases, arterial hypotension is curbed with volume infusion and, if necessary, the association of a vasopressor drug. The depth of anesthesia should not be decreased because the metabolic rate would increase and elevate ICP.

Intravenous Anesthetics (Droperidol, Barbiturates, Propofol, Remifentanil)

These drugs depress the cardiovascular system without causing vasodilation. Some undesirable effects in the CNS, however, may occur. High doses of fentanyl (200 mg/kg) may increase the metabolic rate and activate the limbic system, inducing electroencephalogram (EEG) hyperactivity similar to a convulsive seizure.12 Etomidate in subclinical doses may stimulate EEG activity in patients with a history of convulsive crises.¹³^,¹⁴ Ketamine increases cerebral blood flow and therefore strongly elevates neuronal metabolic rates, which may lead to convulsive crises.¹⁵

Inhalation Anesthetics

Besides reducing the metabolic rate, halogenated anesthetics cause a certain degree of cerebral vasodilation by interfering with the intrinsic mechanism of cerebral arteries that regulates neuronal metabolic reduction and vasoconstriction. Therefore, although halogenated anesthetics reduce neuron metabolism, they also induce cerebral vasodilation due to their action upon the arterial muscular fibers. As the cerebral vasodilation increases the volume of encephalic blood, the intracranial pressure is also increased. In the presence of deep hypocapnia, enflurane may evoke EEG activity similar to convulsive crises.¹⁶

Anesthetics that depress functional neuron activity also reduce their metabolic rate and therefore do not damage nerve cells, because they also decrease cellular oxygen intake. However, the neuronal metabolic rate may already be reduced by an existing low oxygen delivery associated with hypoxia or deep hypocapnia or due to an accentuated state of poor encephalic perfusion or deep anemia.

When PaO₂ is lower than 60 mm Hg, cerebral arterial dilation takes place in response to hypoxia, as an attempt to maintain oxygen delivery through the increased blood flow to the brain. In the process, as PaO₂ reduces to 30 mm Hg, this cerebral reflex action is unable to sustain the delivery of oxygen to the neurons.

The induction of hypocapnia to reduce cerebral blood volume and intracranial pressure may lead to ischemia when PaCO₂ reaches values below 25 mm Hg, as a consequence of intensive vasoconstriction in areas of the brain in which the vascular reactivity is preserved. Cerebral perfusion pressure (CPP) results from the difference between the mean arterial pressure (MAP) and the intracranial pressure (ICP). The increase of ICP or the reduction of MAP that results in CPP levels lower than 40 mm Hg is extremely damaging to the brain. Sharp and acute lowering of the hematocrit count may compromise cerebral vascular reactivity.

Perioperative Management of Endoscopic Transnasal Sellar Surgery

Before anesthesia induction, it is important to check for possible preexisting oculomotor lesions. The eyes must be protected with cream or gel that does not contain atropine in the formulation, to avoid mydriasis, which would later interfere with the neurologic assessment.

• The tracheal intubation probe should be properly positioned and well fixed to prevent accidental extubation during the surgical manipulation of the transnasal access or during intraoperative procedures such as single-lung intubation through the endotracheal passage. Ventilation must be checked through auscultation, and the oral cavity must be filled with a small tampon to prevent blood or serum access to the oropharyngeal area and consequent aspiration into the trachea and bronchi.

• Soft tissues at the site of the surgical access are infiltrated with adrenaline to reduce intraoperative bleeding, but excess adrenaline leads to hypertension, tachycardia, and extrasystole. To counter these cardiovascular alterations, the infusion of short-acting anesthetics should be increased and, if needed, beta-blockers and arterial hypotensors should be added.

• For skull base surgeries, the immobility of the patient is of utmost importance, due to the complexity of the brain structures that may either be involved in the surgical field or be next to it. Therefore, the depth of anesthesia and the dosage of muscle relaxant must be properly considered according to the patient’s physical and clinical characteristics.

Postoperative Care

• To help the graft’s sealing a cerebrospinal fluid (CSF) leak, the introduction of a drainage catheter in the lumbar subarachnoid space may be required for continuous liquid drainage in the postoperative phase. The anesthesiologist is the best-prepared professional to perform the lumbar puncture and to insert the catheter, due to his familiarity with these procedures. Furthermore, the drainage of liquor through the fistula during the intraoperative phase may have caused liquoric hypotension, thus making it more difficult to localize the subarachnoid space during the lumbar puncture.

• The prevention of coughing during extubation is essential and must be done as soon as the patient recovers consciousness, because the intrathoracic pressure increases the risk of CSF leak if the dura mater has been injured.