Adenohypophysis

The adenohypophysis secretes an array of hormones under the regulation of the hypothalamus. Releasing and inhibiting factors are secreted into a capillary network within the hypothalamus (Table 135-1). Via portal vessels, these compounds then enter a second capillary network within the adenohypophysis, where they either enhance or inhibit secretion of adenohypophyseal hormones (Figure 135-2). Further secretion of hormones by the anterior pituitary is then regulated via feedback control of hypothalamic and adenohypophyseal secretion in response to concentrations of hormones secreted by target glands. Given the complex interactions among the hypothalamus, anterior pituitary, target endocrine glands, and end organs, disease or dysregulation at any point within these pathways can cause dysfunction of one or more hormone axes.

Cushing disease

Adrenocorticotropic hormone (ACTH) acts upon the adrenal cortex to increase cortisol production. In patients with Cushing disease, excessive production of ACTH, usually by an ACTH-producing adenoma, results in hypercortisolemia. Cortisol has a broad range of physiologic effects, including increased gluconeogenesis, reduced systemic glucose utilization, protein catabolism, increased lipolysis, increased gastric acid production, bone reabsorption, and immune suppression. Clinical manifestations include hyperglycemia, skeletal muscle weakness, “moon facies,” “buffalo hump,” osteoporosis, poor wound healing, and increased infection rate. Perioperative concerns include possible difficulty with airway management, aberrant serum electrolyte or glucose concentrations, muscle weakness, and difficulty positioning due to osteoporosis or body habitus.

Acromegaly

Acromegaly results from excessive secretion of growth hormone by the adenohypophysis. Growth hormone exerts its effect either directly on target cells or via stimulating hepatic secretion of insulin-like growth factor (also known as somatomedin C). Together, excessive growth hormone and somatomedin C production result in inappropriately increased protein synthesis, gluconeogenesis, lipolysis, chondrocyte proliferation, and bone mineralization, as well as muscle sarcomeric hyperplasia. This results in organomegaly and overgrowth of bones, muscles, and connective tissues.

The impact of these changes on the respiratory and cardiac systems are of primary concern during the perioperative period. Specifically, hypertrophy of facial bones, tongue, airway soft tissues, and glottic structures render the patient susceptible to developing obstructive sleep apnea. Additionally, difficulties with mask fit, bag-mask ventilation, and direct laryngoscopy have been reported. Mandibular hypertrophy increases the distance between the lips and vocal cord. Vocal cord dysfunction, secondary to stretching of the recurrent laryngeal nerve, and impaired mobility of the cricoarytenoid joints can further impact airway management. Indirect videolaryngoscopic (e.g., McGrath Series 5 video laryngoscope or GlideScope Ranger) or awake fiberoptic intubations are prudent options when managing the airway of these individuals. Intubation may be performed after the induction of anesthesia, but difficulty with mask ventilation and laryngoscopy, by any means, should be anticipated, and backup equipment should be readily available. Costal cartilage hypertrophy can lead to restrictive pulmonary physiology.

Cardiovascular manifestations of acromegaly include hypertension, cardiac hypertrophy, left ventricular diastolic dysfunction (generally with preserved systolic function at rest until late in the course of the disease), and arrhythmias. Coronary artery insufficiency can occur and is related to increased O₂ demand from a hypertrophic heart and reduced coronary blood flow due to increased cardiac filling pressures that occur with diastolic dysfunction. Despite beliefs to the contrary, hypertrophy of the transverse carpal ligament does not increase the risk of ischemic complications of the hand with cannulation of the radial artery.

Hyperprolactinemia

Signs and symptoms of increased prolactin production are more concrete in women (i.e., galactorrhea, amenorrhea, infertility) than in men (e.g., decreased libido, erectile dysfunction). As such, prolactin-secreting tumors tend to be larger, and possibly more invasive, in men at the time of surgery because of delayed diagnosis. Although the manifestations of hyperprolactinemia cause no overt concerns for anesthesia, medications used to pharmacologically manage increased serum prolactin concentration (e.g., bromocriptine or cabergoline) can be associated with nausea, orthostatic hypotension, and cardiac valvular dysfunction.

Pituitary hyperthyroidism

Pituitary hyperthyroidism results from excessive production of thyroid-stimulating hormone by a pituitary adenoma that, in turn, causes increased triiodothyronine (T₃) and thyroxine (T₄) production (both are important metabolic regulators). These tumors are rare, and thus, many patients undergo treatment for other causes of hyperthyroidism (e.g., Graves disease) prior to detection of the pituitary disease, thereby delaying the diagnosis. Such interventions include radioactive thyroid ablation or thyroidectomy, leading to decreased thyroid hormone production and loss of negative feedback on secretion of thyroid-stimulating hormone, which, in turn, can enhance tumor growth. Delayed diagnosis and tumor growth increase the likelihood of neoplastic encroachment on surrounding structures (e.g., the cavernous sinus), which places the patient at increased risk for developing intraoperative bleeding and iatrogenic central nervous system injury during the resection. Patients may also be hyperthyroid, hypothyroid, or euthyroid at the time of surgery. Unless visual loss is acutely threatened, patients should be rendered physiologically euthyroid, using medical treatment, prior to surgery.

Hypopituitarism

Hypopituitarism, or pituitary failure, most commonly results from compression of normal gland by pituitary tumors. However, other causes are possible, such as infection, inflammation, and trauma. Signs and symptoms are often nonspecific and depend on the extent of hormone deficiency. In acute pituitary failure (i.e., apoplexy or acute pituitary infarction), decreases in serum corticotropin and cortisol levels occur quickly due to their short half-lives. As such, signs and symptoms of acute apoplexy include acute hyponatremia, profound hypotension, and shock. In this context, treatment with corticosteroids can be lifesaving. In those with chronic hypopituitarism, growth hormone deficiency is most common; deficiencies of thyroid-stimulating hormone, prolactin, and hormones produced by the neurohypophysis (i.e., oxytocin and vasopressin) are quite rare. Patients with chronic hypopituitarism will likely require perioperative corticosteroid supplementation.

Neurohypophysis

Unlike the adenohypophysis, which contains hormone-secreting cells, the neurohypophysis contains distal axons of peptidergic neurons with cell bodies located in the supraoptic and paraventricular nuclei of the hypothalamus. These neurons synthesize and secrete either oxytocin or vasopressin (i.e., antidiuretic hormone), which are released into the systemic circulation via capillaries located in the neurohypophysis (see Figure 135-2).

Oxytocin is best known for modulating labor and delivery and release of breast milk. Vasopressin is one of the principal hormones regulating water balance. Normally, the strongest stimulus for vasopressin secretion is increased serum osmolality, mediated via hypothalamic osmoreceptors. Vasopressin increases water reabsorption by the kidney and causes systemic arteriolar constriction.

The most common manifestation of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) is hyponatremia. SIADH is usually asymptomatic if the syndrome is mild; however, seizures and coma can occur if the serum sodium concentration acutely decreases below 120 mEq/L. In the setting of chronic SIADH, adaptive mechanisms minimize symptoms despite very low serum sodium concentrations. Treatment usually involves fluid restriction for mild cases and, otherwise, slow (<1-2 mEq·L⁻¹·h⁻¹) correction of hyponatremia with hypertonic saline, as rapid correction can potentially cause central pontine myelinolysis.

Diabetes insipidus (DI) refers to inappropriate production of hypotonic urine due to either inadequate production of vasopressin (i.e., central DI) or renal unresponsiveness to vasopressin (i.e., nephrogenic DI). Initial treatment should focus on replenishing intravascular volume, which may require the use of 0.9% saline in patients with severe hypovolemia, despite hypernatremia, and correcting hypernatremia. Additionally, for central DI, vasopressin or a synthetic analog (i.e., 1-desamino-8-D-arginine vasopressin [DDAVP]) may be administered. No specific treatment exists for nephrogenic DI.

Management of patients having pituitary operations

The most common indication for pituitary surgery is tumor resection. Tumors derived from secretory cells are typically smaller at the time of diagnosis than nonsecreting tumors. As cited earlier, delayed diagnosis of pituitary neoplasia may result in tumor growth manifesting clinically as headache or visual field deficit (due to optic chiasm compression).

The pituitary gland is most commonly approached transnasally via the sphenoid sinus, whereas craniotomy is usually reserved for patients with large and invasive tumors. The preoperative evaluation should focus on the physiologic and anesthetic implications of any endocrinopathy; any preexisting neurologic deficits should be noted, and the risk of intraoperative bleeding or surgical disruption of adjacent structures (i.e., cavernous sinus, optic chiasm) should be stratified.

For transnasal operations, the hypopharynx is packed with moistened gauze following orotracheal intubation to minimize gastric accumulation of blood. The surgeon may request placement of a lumbar cerebrospinal fluid (CSF) drain. This will allow injection of air into the CSF, slightly increasing CSF volume and, thus, displacing a tumor inferiorly, or withdrawal of CSF, displacing a tumor superiorly within the sella turcica. N₂O should be used with care in patients in whom air was injected into the lumbar CSF drain. Local anesthetic agents containing epinephrine may be injected into the nasal mucosa, with or without application of topical cocaine, to reduce bleeding. This intervention may induce transient, but significant, hypertension.

Common complications following surgery include nausea and vomiting, CSF leak, and transient hypopituitarism with or without DI. Other complications include infection or injury to neural (i.e., optic chiasm, cranial nerves contained within the cavernous sinus) or vascular (i.e., carotid artery) structures.