Patients having transsphenoidal surgery offer many unique challenges to the anesthesiologist. Because of the prominent role of the pituitary gland in the endocrine system, patients require meticulous preoperative assessment, intraoperative management, and postoperative care. The successful anesthetic management of patients undergoing transsphenoidal surgery requires a working understanding of the relevant pathophysiology and the possible implications of anesthesia and surgery.
Pituitary adenomas are normally found in adults with a peak incidence during the fourth to the sixth decade of life. Patients with tumors of the pituitary gland may be commonly encountered and represent approximately 10% of diagnosed brain neoplasms. Approximately 75% of pituitary tumors are “functioning” and produce a single, predominant hormone. Although the overall incidence of pituitary tumors remains relatively low, autopsy series suggest that as many as 20% of people may have a pituitary tumor on postmortem examination. Consequently, it appears that the overwhelming majority of pituitary tumors are asymptomatic. Pituitary adenomas are often classified based upon their size at the time of discovery. Tumors larger than 10 mm in any dimension are classified as macroadenomas , whereas tumors smaller than 10 mm are classified as microadenomas .
In general, pituitary tumors can present in three discrete ways: (1) hormonal hypersecretion; (2) local mass effects; or (3) tumors may be discovered incidentally during cranial imaging for an unrelated condition. Functioning tumors are usually composed of a single cell type and produce a single, predominant hormone. Patients having functioning tumors and the signs and symptoms of hormone excess will be discussed in detail later.
Local mass effect upon adjacent structures by the expanding intrasellar mass may be encountered in any type of pituitary tumor. Indeed, the most common complaints of patients with a sellar mass are headache and, in patients with a macroadenoma, visual loss. Visual loss results from compression of the optic chiasm and is classically temporal or bitemporal hemianopsia. Intrasellar growth can cause anterior pituitary compression and dysfunction, resulting in hypopituitarism. Hypopituitarism results from the compression of normal gland by the expanding intrasellar mass. As patients with “nonfunctioning” tumors do not, by definition, have hormone excess, their presenting symptoms are all related to local mass effects.
General Preoperative Concerns
As in the case of any expanding intracranial mass, patients can experience raised intracranial pressure (ICP). Pituitary tumors may increase ICP in two different ways: (1) directly, by mass expansion in the sella with subsequent edema; or (2) indirectly, by obstruction of the third ventricle. Despite the fact that most patients will have a headache, elevated ICP is quite rare. Should ICP be increased, it is critical to avoid any maneuver that might further increase ICP and result in brainstem herniation or impairment of cerebral perfusion. The preoperative use of mannitol to decrease ICP should be considered.
All patients require thorough preoperative laboratory evaluation before surgery. Evaluation should include a complete blood count to assess the presence of anemia or other hematologic abnormalities. Men having pituitary tumors and low testosterone have an increased incidence of preoperative anemia. Coagulation studies including prothrombin time (PT) are not mandatory unless the patient has history of, or risk factors for, bleeding. A blood urea nitrogen (BUN) and creatinine are useful as indicators of renal function; however, they may not be necessary in otherwise healthy individuals. A metabolic panel to evaluate possible hyponatremia, hypercalcemia, hyperglycemia, and other metabolic abnormalities is indicated. Hypernatremia may indicate posterior pituitary dysfunction and the presence of diabetes insipidus (DI). Patients with Cushing’s disease may have a hypokalemic alkalosis. The endocrine evaluation of each patient should include a thyroid panel (thyroxine, thyroid stimulating hormone [TSH]), and serum levels of cortisol. Many patients will have hypothyroidism or low cortisol secondary to hypopituitarism and mass effect of the tumor. Overtly hypothyroid patients should have thyroid function normalized before surgery. Patients with adrenal suppression and low cortisol will require supplementation. Many patients will have a defective stress response to surgery and require perioperative “stress dose” steroids. If patients are not surgical candidates or require further evaluation before definitive tumor resection, medical therapy is available to abrogate some of the systemic effects of functional adenomas. Additionally, medical therapy may represent the first line treatment in some instances (e.g., prolactinomas).
Review of preoperative computed tomography (CT), magnetic resonance imaging (MRI), and occasionally cerebral angiograms are particularly valuable when a patient’s clinical presentation includes facial pain, facial numbness, visual field disturbances, or other cranial nerve palsies. Often, these symptoms can suggest lateral extension of the tumor into the cavernous sinus. If such is the case, the possibility of hemorrhage from damage to the cavernous sinus or the internal carotid should be anticipated. Large bore intravenous access should be secured and blood products should be readily available before surgical incision.
Preoperative Concerns Related to Endocrine Disease
Optimal anesthetic management necessitates a thorough understanding of the pathophysiology associated with neuroendocrine disease. Advances in laboratory evaluation and radio imaging have allowed for earlier diagnosis and visualization of tumors; however, it is important to note that most tumors have an insidious, nonspecific onset. Patients may not seek medical care for years, often not until they have developed severe, multiorgan disease. Special attention in this discussion will be given to acromegaly and Cushing’s disease because they present a number of unique challenges to the anesthesiologist ( Table 3-1 ).
|Respiratory||Obstructive sleep apnea|
|Renal||Chronic volume expansion||Nephrolithiasis|
|Gastrointestinal||Colon polyps||Increased appetite|
The unregulated hypersecretion of growth hormone by the anterior pituitary leads to the increased production of somatomedins, namely insulin-like growth factor-I (IGF-I), by the liver. Children, in whom the epiphyses have not closed, experience gigantism. Adults, in contrast, develop acromegaly. Approximately 98% of all acromegaly results from a pituitary adenoma. Growth hormone hypersecretion affects all tissues and organ systems in the body, including the heart, lungs, liver, and kidneys.
Cardiac disease is the most important cause of morbidity and mortality in acromegalic patients. Indeed, the most frequent cause of death in untreated acromegaly is cardiovascular, with 50% of patients dying before the age of 50. Older reviews suggest that as many of 80% of patients died from cardiovascular complications before the age of 60. A recent series suggested that as many as 10% of newly diagnosed patients may have overt heart failure upon initial diagnosis. The most prominent feature of acromegalic cardiac disease is myocardial hypertrophy. Left ventricular hypertrophy (LVH) can occur in the presence of systemic hypertension, but also occurs in at least 50% of normotensive acromegalic patients. Overall, two thirds of patients will have LVH at the time of diagnosis. The prevalence of LVH increases with patient age and is greater than 90% in elderly patients with a long disease duration. One study revealed that the prevalence of LVH is greater when left ventricular mass is indexed for height rather than for body surface area (BSA) in patients with active acromegaly.
Echocardiography reveals increases in left ventricular mass, stroke volume, cardiac output, and isovolumic relaxation time. These changes occur independently from systemic hypertension. The combination of normal or increased systolic function and a high incidence of heart failure implies that, at least on initial presentation, many patients appear to be in high-output heart failure. Diastolic dysfunction is clearly an early sign of acromegalic cardiomyopathy. A poorly compliant left ventricle and its accompanying need for high filling pressures may be considered the hallmark of acromegalic cardiomyopathy. Many patients will report decreases in exercise tolerance. Increases in heart rate during exercise decrease diastolic filling time, which leads to decreased stroke volume and cardiac output. Diastolic dysfunction may exist even in the absence of clinically appreciable left ventricular hypertrophy. Although hypertrophy of the left ventricle may be prominent, evidence of right ventricular enlargement also exists. Long disease duration may be associated with decreases in systolic function and cardiac output. Left ventricular size may return to normal after medical or surgical therapy; however, this is more common in young patients with a shorter disease duration. Nevertheless, return of normal diastolic function may not occur and may reflect the persistence of interstitial myocardial fibrosis.
Valvular disease has become recognized as an important cause of ventricular dysfunction and heart failure in acromegaly. In one autopsy series, 19% of patients had mitral or aortic valve abnormalities. Recently, Pereira et al found aortic regurgitation (> trace) in 30% and mitral regurgitation (> moderate) in 5% of acromegalic patients. The prevalence of valvular disease was closely related to disease duration and the presence of LVH. In addition, Colao et al found mitral or aortic valve disease (including leaflet fibrosis and annular calcification) in 86% of patients with active, untreated acromegaly. It is interesting to note that among patients with biochemical evidence of a “cure” for at least 1 year, the prevalence of such structural valve abnormalities remains high at 73%. Valvular disease is closely related to the presence of LVH; however, it is unclear why the incidence of valvular disease remains high despite a reduction in the prevalence of LVH. Regardless, changes in valvular architecture and function are more likely with a long disease duration and seem less likely to improve with medical or surgical therapy.
Although the larger, more proximal coronary arteries are rarely stenotic in acromegaly, coronary artery disease of the smaller vessels has been described. Indeed, defects in myocardial perfusion have been described using single photon emission computed tomography (SPECT). As such, the presence of angina should alert the physician to the possibility of myocardial ischemia, regardless of the patient’s age.
Classically, it had been thought that the incidence of supraventricular and ventricular ectopy was not increased in resting acromegalics ; however, given the poor exercise tolerance of acromegalic patients and a lower threshold to what may be considered “exercise,” cardiac arrhythmias are frequently observed. In a recent case report, Holter monitoring of one newly diagnosed acromegalic patient revealed 17,249 premature ventricular complexes in a single day. It is noteworthy that this number was decreased almost sixfold with 2 months of octreotide treatment. In addition to supraventricular and ventricular ectopy, disorders of the conduction system, such as bundle branch blocks, can also occur. EKG changes such as S-T segment depression, T-wave abnormalities, and increased QRS voltage are typical of LVH and are frequently observed.
After cardiovascular disease, respiratory disease is the most common cause of death in untreated acromegaly. Sleep apnea secondary to upper airway obstruction (obstructive sleep apnea or OSA) can affect up to 70% of acromegalic patients. It is interesting to note that airway obstruction is threefold more common among male acromegalics than female acromegalics. Nocturnal airway obstruction is not always reversed after surgical cure. In addition to OSA, central respiratory depression of unknown etiology may also be noted. Pneumomegaly is observed in 50% of acromegalic patients and ventilation-perfusion mismatching may also be increased.
Hypertrophy of the facial bones, especially the mandible, and coarsening of facial features lead to significant changes in patient appearance. Soft tissues of the nose, mouth, tongue, and lips become thicker and help give acromegalic patients their characteristic facade. In addition to the easily observed external changes, there is thickening of the laryngeal and pharyngeal soft tissues. Hypertrophy of the periepiglottic folds, calcinosis of the larynx, and recurrent laryngeal nerve injury can all contribute to airway obstruction and respiratory disease. Indeed, hypertrophy can cause significant reduction in the size of glottic opening. Laryngeal stenosis and abnormal vocal cord function may be present and patients may report hoarseness or changes in vocal tone, quality, or strength. It is interesting to note that vocal cord function is quickly reversed and may return to normal within 10 days of surgery.
A high risk of perioperative airway compromise has been well documented in acromegalics with OSA. As such, narcotics and benzodiazepines should be administered with caution to any acromegalic carrying the diagnosis of OSA. Given the high percentage of acromegalic patients with OSA and the fact that OSA is underdiagnosed in most patient populations, the prudent physician should attempt to elicit a history of OSA in all acromegalic patients. Any history of excessive daytime somnolence, snoring, or frank sleep apnea (often noted by the patient’s spouse) should alert the physician to the possibility of OSA, especially among male patients.
Among children with gigantism, approximately 20% to 25% of patients have McCune-Albright syndrome (polyostotic fibrous dysplasia). In contrast to pituitary gigantism or acromegaly, growth hormone excess in McCune-Albright syndrome normally results from somatotroph hyperplasia; however, a pituitary adenoma may be present. This rare hypersecretory syndrome consists of polyostotic fibrous dysplasia, café au lait spots, sexual precocity, hyperthyroidism, hyperparathyroidism, and hyperprolactinemia. The anesthetic management of this rare disorder has been previously reviewed. Patients may require a larger than expected endotracheal tube. Indeed, it may be more appropriate to select endotracheal tube size based upon patient height rather than patient age. Skeletal involvement, with associated fractures, bony deformities, and weakness, can be severe. Many patients may report orthopedic procedures. Patients with McCune-Albright syndrome may also exhibit signs and symptoms of Cushing’s disease secondary to ACTH-independent hypercortisolism.
Cushing’s disease specifically results from the unregulated hypersecretion of adrenocorticotropic hormone (ACTH) by a pituitary adenoma and consequent hypercortisolism. Cushing’s syndrome is more frequently encountered in clinical practice and may result from any number of conditions that result in hypercortisolism. Indeed, the most common cause of Cushing’s syndrome is iatrogenic. In Cushing’s disease, long-term exposure to excessive circulating glucocorticoids results in significant pathophysiology.
Systemic hypertension is among the most common manifestations of Cushing’s disease. Indeed, as many as 80% of patients with Cushing’s disease have systemic hypertension and 50% of untreated patients have severe hypertension with a diastolic blood pressure greater than 100 mm Hg. Increased endogenous corticosteroids have been shown to cause systemic hypertension by a variety of mechanisms.
Hydrocortisone has been shown to increase cardiac output. Increases in cardiac output may occur secondary to enhanced responses to endogenous catecholamines. Patients with Cushing’s disease have an increased expression of the angiotensinogen II (type I) receptor and potentiation of inositol triphosphate production in vascular smooth muscle cells. This leads to increased sensitivity to endogenous vasoconstrictors such as angiotensin II, epinephrine, and norepinephrine. Indeed, an enhanced chronotropic effect with isoproterenol infusion has been observed in patients with Cushing’s disease. In addition, patients exhibit an increased pressor response to norepinephine.
There is evidence that hypercortisolism leads to an increase in the hepatic production of angiotensinogen. The increase in angiotensinogen activates the renin-angiotensin system, which leads to angiotensin-mediated vasoconstriction as well as to an increase in plasma volume. In addition, the mineralocorticoid effects of cortisol and hydrocortisone lead directly to sodium and water retention. The classic presentation of a hypokalemic alkalosis is actually more common in Cushing’s syndrome, especially with ectopic ACTH production. Nitric oxide synthesis may be suppressed. Supplementation with l -arginine can prevent hypertension in rats given ACTH, further suggesting that alterations in nitric oxide synthesis may be an important etiologic factor. Alterations in diurnal blood pressure variation and attenuation in nighttime decreases in blood pressure have also been observed in patients with Cushing’s disease.
With hypertension ubiquitous among patients with Cushing’s disease, it is not surprising that LVH is also very common. Indeed, a high prevalence of LVH and concentric remodeling has been reported in Cushing’s disease. Using echocardiography, reduced midwall systolic performance and diastolic dysfunction can be observed in at least 40% of patients and disproportionate hypertrophy of the intraventricular septum has been reported. Nevertheless, it should be noted that relative wall thickness (RWT) is not related to blood pressure levels. As such, it seems likely that excess plasma cortisol may be at least a second causal factor. EKG abnormalities are common in patients with Cushing’s disease. High voltage QRS complexes and inverted T waves suggesting left ventricular hypertrophy and left ventricular strain have been described. Despite resolution of many cardiovascular symptoms of disease upon successful resection of the adenoma, it is important to note that increases in cardiovascular morbidity and mortality persist for at least 5 years.
As in acromegaly, OSA is also common among patients with Cushing’s disease. Polysomnographic studies indicate that as many as 33% of patients with Cushing’s disease have mild sleep apnea and 18% of patients have severe sleep apnea. Complaints of daytime sleepiness are very common. Weight gain and centripetal obesity are commonly observed in Cushing’s disease. As obese patients are more likely to have OSA than nonobese patients, it seems that obesity may play a role in high prevalence of OSA observed among patients with Cushing’s disease. In addition, patients develop fat depots over the cheeks and temporal regions, giving rise to the rounded “moon-facies” characteristic of the disease. Whether these changes in the head and upper airway affect the incidence of OSA has not been investigated. The airway management of patients with a history of OSA may be challenging. Tracheal intubation may be more difficult and these patients may be significantly more sensitive to sedative medications, including benzodiazepines and narcotic analgesics. As in acromegaly, narcotics and benzodiazepines should be used with great care and always during continuous monitoring by qualified personnel. It should be noted that a link between OSA and hypertension has been well described.
Glucose intolerance occurs in at least 60% of patients with Cushing’s disease, with overt diabetes mellitus present in up to one third of all patients. Indeed, there is evidence that a high prevalence of occult Cushing’s disease may exist among patients with diabetes mellitus, type II. Patients taking oral hypoglycemic agents should be instructed not to take any such agent the morning of surgery because they will not be allowed to eat before the procedure. A significant portion of patients with Cushing’s disease, especially those with long-standing disease, may require insulin for glucose control. In such patients, avoidance of morning insulin the day of surgery may put the patient at risk for significant perioperative hyperglycemia. At the same time, the patient’s normal dose of insulin may put the fasting patient at risk for significant perioperative hypoglycemia. A reasonable compromise may include a lower dose of “long-acting” insulin preparations with preoperative blood sugar measurements guiding regular (or “fast-acting”) insulin therapy. Regardless, all patients with diabetes should have at least one blood glucose tested before surgery and at least one tested in the immediate postoperative period. It has been clearly established that hyperglycemia can aggravate ischemic injury in the brain and spinal cord. Although no randomized studies exist that demonstrate a “safe” level of hyperglycemia, current practice suggests that any blood glucose greater than 180 mg/dL (10.1 mmol/L) should be treated with insulin. One must always weigh the benefits of “tight” intraoperative glucose control against the risk of severe, unintentional hypoglycemia in an unconscious patient.
Diffuse osteoporosis may occur in up to 50% of patients having Cushing’s disease. Almost 20% of patients may have pathologic fractures and many patients with long-standing Cushing’s syndrome have lost height because of osteoporotic vertebral collapse. In addition, aseptic necrosis of the femoral and humeral heads can occur in Cushing’s syndrome. Particular care should be taken when positioning patients during surgery.
Many patients with Cushing’s disease report generalized weakness, and a myopathy of the proximal muscles of the lower limb and the shoulder girdle have been described. The respiratory muscles can also be affected and patients can present in respiratory failure secondary to respiratory muscle weakness. It is possible that muscle weakness may play a role in the prevalence of OSA among patients with Cushing’s disease (see earlier). Nevertheless, there are no data to suggest a change in the susceptibility to succinylcholine or nondepolarizing neuromuscular blockers.
Nephrolithiasis is common in Cushing’s disease and approximately 50% of active, untreated patients have detectable stones. It is noteworthy that 27% of patients that had been surgically cured also had detectable stones. Systemic arterial hypertension and excessive urinary uric acid excretion seem to play a pivotal role. Infections are more common in patients with Cushing’s disease ; however, an empiric change in usual perioperative antibiotics is unnecessary.
Hypercortisolism also results in skin thinning. Patients may appear to have senile purpura with many small bruises and a loss of subcutaneous fat. Cannulation of superficial veins for intravenous access can be extremely difficult and minimal trauma may result in bruising.
The function of both the pituitary-thyroid axis and the pituitary-gonadal axis is suppressed in patients with Cushing’s syndrome because of a direct effect of cortisol on TSH and gonadotrophin secretion. Patients may therefore have signs and symptoms of thyroid or gonadal insufficiency. Exophthalmos secondary to increased retro-orbital fat deposition may be present in up to one third of patients with Cushing’s disease. The anesthesiologist should be cognizant of the presence of exophthalmos; a corneal abrasion can be a painful complication of an otherwise successful surgery.
Prolactinomas are the most frequently observed type of hyperfunctioning pituitary adenoma and represent 20% to 30% of all clinically recognized tumors and half of all functioning tumors. In women, hyperprolactinemia causes amenorrhea, galactorrhea, loss of libido, and infertility. Osteopenia may also be noted. Hyperprolactinemia is frequently observed in polycystic ovarian syndrome (POS). Obviously, it is important to differentiate POS from a prolactinoma.
In men, symptoms of hyperprolactinemia are relatively nonspecific and include decreased libido, impotence, premature ejaculation, erectile dysfunction, and oligospermia. Prolactin levels tend to be higher in men, regardless of whether macroadenoma or a microadenoma is present. Owing to an earlier diagnosis in women, more than 90% of prolactin-secreting microadenomas are diagnosed in females. Macroadenomas are equally common in men and women. More than 90% of patients respond to medical therapy with a dopamine agonist such as bromocriptine or cabergoline ; however, normalization of prolactin levels occurs more quickly in patients with microadenomas. Nevertheless, few patients with a prolactinoma will come in for surgical excision. There are few anesthesia-specific ramifications of hyperprolactinemia and it will not be discussed further.
Thyrotropic (TSH-producing) Adenomas
Thyrotropic adenomas are rare and represent no more than 2.8% of all pituitary tumors. The unregulated hypersecretion of TSH by a pituitary adenoma results in elevated thyroxine and clinical hyperthyroidism. Signs and symptoms of hyperthyroidism include palpitations, tachycardia, tremor, weight loss, difficulty sleeping, and heat intolerance. A goiter is commonly observed. As thyrotropic adenomas are extremely rare, most patients are often first treated for other causes of hyperthyroidism such as Graves disease. As such, these tumors are often allowed to grow and can be quite large upon diagnosis. The diagnosis is made by elevated serum thyroxine accompanied by inappropriately high TSH level in the presence of a pituitary adenoma.
Given the delay in diagnosis of these tumors and their large size, many patients often have symptoms related to the local mass effect of the tumor. In addition, more than 60% of thyrotrophic adenomas are locally invasive at the time of surgery. The review of preoperative radiographic studies is critical to assess tumor size and invasiveness and to assess for the risk of blood loss. Hyperthyroidism should be controlled before a patient undergoes surgical resection. Antithyroid medication such as propylthiouracil may reduce thyroid hormone production, and somatostatin analogs such as octreotide can suppress TSH-production and may reduce tumor size. The effects of hyperthyroidism on anesthesia have been discussed elsewhere.
Tumors producing sufficient follicle-stimulating hormone (FSH), luteinizing hormone (LH), or α-subunit are rarely associated with any specific symptoms. Most gonadotrophic tumors are clinically nonfunctioning and will be discovered incidentally or secondary to local mass effects as described previously. High serum FSH may cause chronic ovarian hyperstimulation and chronic pelvic pain in young women and men may have high serum testosterone.
Nonfunctioning Tumors: Nonfunctioning Adenomas, Rathke Cleft Cyst, Craniopharyngioma
Nonfunctioning (null cell) adenomas are the second most common type of pituitary tumors, accounting for 20% to 25% of pituitary adenomas. Craniopharyngiomas and Rathke cleft cysts are less common. As each of these tumors is not associated with the hypersecretion of a hormone, they almost always have symptoms related to local mass effects (see previous discussion). Patients must be evaluated for hypopituitarism, and associated hypothyroidism and adrenal insufficiency must be evaluated before surgery. Many patients will have mild hyperprolactinemia secondary to the so-called “stalk effect.” This results from disinhibition of prolactin secretion secondary to a decrease in dopamine-mediated tonic inhibition of prolactin release. Treatment with dopamine analogs, such as bromocriptine or cabergoline, may result in symptomatic relief (at least from symptoms related to hyperprolactinemia). Posterior pituitary dysfunction and diabetes insipidus (DI) can also occur but is much less common.
Plans for the intraoperative anesthetic management of patients undergoing transsphenoidal surgery should be based upon the assessment of each patient’s individual disease process. Successful intraoperative management includes an understanding of techniques for successful airway management and placement of appropriate monitors. Selection of anesthetic agents should be tailored to facilitate surgical exposure, preserve cerebral perfusion and oxygenation, and provide for rapid emergence and neurological assessment.
The placement of invasive monitoring should always be based on each patient’s preoperative assessment. Given that cardiovascular disease often occurs with both Cushing’s disease and acromegaly, an arterial catheter may be indicated. In addition, transsphenoidal surgery can be associated with significant intraoperative hemodynamic changes (see later discussion). Indeed, an arterial line may allow for earlier diagnosis and treatment of both hypotension and hypertension. Nevertheless, reserve an arterial catheter for patients with poor exercise tolerance, patients with signs and symptoms of congestive heart failure, or patients with documented cardiomyopathy. Indeed, there is no evidence that excessive hemodynamic instability accompanies acromegaly in the absence of specific cardiovascular disease.
It should be noted that secondary to soft tissue overgrowth, blood flow through the ulnar artery may be compromised in up to 50% of acromegalic patients. Thus blood flow to the hand can be entirely dependent on collateral radial flow. The presence or history of carpal tunnel syndrome (median thenar neuropathy) makes this more likely. In such patients, placement of a radial artery catheter may be unnecessarily risky. The consideration of alternative sites (e.g., femoral) for intra-arterial monitoring should be considered.
Generally speaking, central venous pressure (CVP) or pulmonary artery pressure (PAP) monitoring is not necessary in transsphenoidal surgery. In any patient with cardiovascular disease significant enough to necessitate CVP or PAP monitoring, medical therapy to abrogate cardiovascular disease should be initiated until the patient is a better candidate for elective surgery. Should the patient require surgery emergently (for increased ICP, pituitary apoplexy, etc.), it should be noted that in patients with a cardiomyopathy that a pulmonary artery catheter (PAC) may be a better monitor of left ventricular preload; however, this correlation has been challenged. Central venous access may be necessary in some patients, particularly those with Cushing’s disease where cannulation of peripheral veins can be difficult.
As noted above, acromegaly induces significant changes in airway anatomy. Indeed, successful endotracheal intubation and management of the acromegalic airway can be extremely difficult. As might be expected, difficult laryngoscopy and poor laryngeal view has been associated with Mallampati class 3 and 4 airway examinations; however, 20% of acromegalic patients assessed as Mallampati class 1 and 2 have been noted to be difficult to intubate. As such, the Mallampati classification has poor “negative predictive value,” and difficult endotracheal intubation may be unpredictable in acromegalic patients. Indeed, routine tracheostomy had been historically advocated for management of the acromegalic airway; however, this is rarely necessary. The anesthesiologist should approach any acromegalic airway, regardless of anticipated difficulty, with extreme caution. Flexible fiberoptic laryngoscopy can be more difficult. A large variety of alternative airway management tools should be readily available ( Figures 3-1, 3-2, 3-3, and 3-4 ). The Parker Flex-Tip ( Figure 3-5 ) endotracheal tube is associated with higher success rates during fiberoptic tracheal intubation compared with standard endotracheal tubes and may be particularly useful in acromegalic patients with laryngeal stenosis. The intubating Laryngeal Mask Airway (Fast-Trach LMA, Figures 3-1 and 3-2 ), has been associated with a low (52.6%) first-attempt success rate in unparalyzed acromegalic patients. As always, awake techniques offer the greatest margin of safety.