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The anterior pituitary gland consists of five identifiable types of secretory cells (and the hormones that they secrete): somatotrophs (GH), corticotrophs (ACTH), lactotrophs (prolactin), gonadotrophs (luteinizing hormone [LH] and follicle-stimulating hormone [FSH]), and thyrotrophs (TSH). Secretion of these pituitary hormones is largely regulated by a negative-feedback loop by hypothalamic regulatory hormones and by signals that originate from the target site of pituitary action. Six hypothalamic hormones have been characterized: dopamine, the prolactin-inhibiting hormone; somatostatin, the GH release-inhibiting hormone; GH-releasing hormone (GHRH); corticotropin-releasing hormone (CRH); gonadotropin-releasing hormone (GnRH or LHRH); and TRH. Most pituitary tumors (>60%) are hypersecretory and are classified according to the excess production of a specific anterior pituitary hormone.
The three most common disorders of pituitary hypersecretion are those related to excesses of prolactin (amenorrhea, galactorrhea, and infertility), ACTH (Cushing's syndrome), or GH (acromegaly). In addition to knowing the pathophysiologic processes of the disease involved, the anesthesiologist must determine whether the patient recently underwent air pneumoencephalography. If so, nitrous oxide should not be used; this practice lessens the risk of intracranial hypertension from gas collection. CT or MRI of the sella has largely replaced neuroencephalography, but the latter is still performed.
Acromegaly is a syndrome that consists of characteristic facies, weakness, enlargement of the hands (often to the point of rendering the usual oximeter probes difficult to use) and feet, thickening of the tongue (often to the point of making endotracheal intubation difficult), and enlargement of the nose and mandible with spreading of the teeth (often to the point of requiring larger than normal laryngoscopic blades).[274] [275] The patient may even appear myxedematous. Other findings include abnormal glucose tolerance and osteoporosis. The most specific test for acromegaly is measurement of GH before and after glucose administration. The typical acromegalic has very elevated fasting levels of GH (usually above 10 g/mL), and the levels do not change appreciably after the oral administration of glucose. In the normal state, glucose markedly suppresses the GH level. A few patients with active acromegaly have normal levels of fasting GH, and GH levels are not suppressed by glucose. In addition, elevated plasma insulin-like growth factor type I (IGF-I), also known as somatomedin C, is pathognomonic of GH excess. The drug L-dopa, which normally causes an elevation of GH in normal subjects, either has no effect or lowers GH levels in acromegalics. More than 99% of cases of acromegaly are attributable to pituitary adenoma. Thus, the primary treatment of acromegaly is transsphenoidal surgery. If the pituitary tumor is not totally removed, patients are often offered external pituitary irradiation. In the case of suprasellar extension, conventional transfrontal hypophysectomy is often performed. The dopaminergic agonist bromocriptine can lower GH levels, but the long-term follow-up with this drug is not favorable. Octreotide, a long-acting analog of somatostatin, now given in depot form about once a month, produces effective palliation in 50% of patients.
The effects of excessive GH stem from both direct actions of the hormone on tissue and stimulation of the
Prolactin has been one of the most interesting markers to identify patients with pituitary tumors. Elevated prolactin levels are often, but not invariably associated with galactorrhea. Females commonly present with amenorrhea, and males present with impotence. Optimal therapy for prolactin-secreting tumors is now believed to be the dopamine agonist bromocriptine or cabergoline. These drugs, which are extremely effective in controlling the prolactin level and restoring gonadotropin function, are used when fertility is desired. When normal menses, contraception, and skeletal integrity are desired, birth control pills are the treatment.[278] Side effects of bromocriptine include orthostatic hypotension, gastroparesis (possible increased risk of aspiration), constipation, and nasal congestion (possible need for oral intubation).[278] With large prolactin-secreting tumors (macroadenomas), loss of other pituitary function is common, and evaluation of thyroid and adrenocortical status is indicated. Preoperative and preprocedure preparation of patients with Cushing's syndrome is discussed in the section on ACTH excess.
Anterior pituitary hypofunction results in deficiency of one or more of the following hormones: GH, TSH, ACTH, prolactin, or gonadotropin. Preoperative and preprocedure preparation of patients who are chronically deficient in ACTH and TSH is discussed earlier. No special preoperative and preprocedure preparation is required for a patient deficient in prolactin or gonadotropin; deficiency in GH, however, can result in atrophy of cardiac muscle, a condition that may necessitate preoperative and preprocedure cardiac evaluation. Nonetheless, anesthetic problems have not been documented in patients with isolated GH deficiency. Acute deficiencies are another matter.
Acute pituitary deficiency is often caused by bleeding into a pituitary tumor. In surgical specimens of resected adenomas, as many as 25% show evidence of hemorrhage. These patients often present with acute headache, visual loss, nausea or vomiting, ocular palsy, disturbances of consciousness, fever, vertigo, or hemiparesis. In such patients, rapid transsphenoidal decompression should be accompanied by consideration of replacement therapy, including glucocorticoids and treatment of increased intracranial pressure.
Obstetric anesthesiologists are often aware of these pituitary failure problems: Sheehan's syndrome is the clinical manifestation of pituitary infarction associated with hypotension after or during obstetric hemorrhage. Conditions that strongly suggest this diagnosis are failure to start postpartum lactation, increasing fatigue, cold intolerance, and especially hypotension unresponsive to volume replacement and pressors.
Secretion of vasopressin, or antidiuretic hormone (ADH), is enhanced by increased serum osmolality or the presence of hypotension. Inappropriate secretion of vasopressin, without relation to serum osmolality, results in hyponatremia and fluid retention. This inappropriate secretion can result from a variety of CNS lesions; from drugs such as nicotine, narcotics, chlorpropamide, clofibrate, vincristine, vinblastine, and cyclophosphamide; and from pulmonary infections, hypothyroidism, adrenal insufficiency, and ectopic production from tumors. Preoperative and preprocedure management of a surgical patient with inappropriate secretion of vasopressin includes appropriate treatment of the causative disorders and restriction of water. Occasionally, drugs that inhibit the renal response to ADH (e.g., lithium or demeclocycline) should be administered preoperatively to restore normal intravascular volume and electrolyte status.
Most of the clinical features associated with the syndrome of inappropriate antidiuretic hormone (SIADH) secretion are related to hyponatremia and the resulting brain edema; these features include weight gain, weakness, lethargy, mental confusion, obtundation, and disordered reflexes and may culminate in convulsions and coma. This form of edema rarely leads to hypertension.
SIADH should be suspected in any patient with hyponatremia who excretes urine that is hypertonic relative to plasma. The following laboratory findings further support the diagnosis:
Noting the response to water loading is a useful way of evaluating patients with hyponatremia. Patients with SIADH are unable to excrete dilute urine even after water loading. Assay of ADH in blood can confirm the diagnosis. Too vigorous treatment of chronic hyponatremia can result in disabling demyelination. [279] [280] The increase in serum sodium should not be greater than 1 mEq/L/hr[279] [280] (see the discussion of hyponatremia in the later section "Electrolyte Disorders").
Patients with mild to moderate symptoms of water intoxication can be treated with restriction of fluid intake
Treatment should be directed at the underlying problem. If SIADH is drug induced, use of the drug should be withdrawn. Inflammation should be treated with appropriate measures, and neoplasms should be managed with surgical resection, irradiation, or chemotherapy, whichever is indicated.
No drugs are available that can suppress release of ADH from the neurohypophysis or from a tumor. Dilantin and narcotic antagonists such as naloxone and butorphanol have some inhibiting effect on physiologic ADH release but are clinically ineffective in patients with SIADH. Drugs that block the effect of ADH on renal tubules include lithium, which is rarely used because its toxicity often outweighs its benefits, and demethylchlortetracycline in doses of 900 to 1200 mg/day. The latter drug interferes with the ability of the renal tubules to concentrate urine, thereby causing excretion of isotonic or hypotonic urine and lessening the hyponatremia. Demethylchloretracycline can be used in ambulatory patients with SIADH when it is difficult to restrict fluids.
When a patient with SIADH comes to the operating room for any surgical procedure, fluids are managed by measuring central volume status by CVP, pulmonary artery lines, or the cross-sectional left ventricular area at end-diastole on transesophageal echocardiography and by frequent assays of urine osmolarity, plasma osmolarity, and serum sodium, including the period immediately after surgery. Despite the common impression that SIADH is frequently seen in elderly patients in the postoperative period, studies have shown that the patient's age and the type of anesthetic used have no bearing on the postoperative development of SIADH. It is not unusual to see many patients in the neurosurgical ICU suffering from this syndrome. The diagnosis is usually one of exclusion. Patients with SIADH generally require only fluid restriction; very rarely is hypertonic saline needed.
Lack of ADH, which results in diabetes insipidus, is caused by pituitary disease, brain tumors, infiltrative diseases such as sarcoidosis, head trauma (including trauma after neurosurgery), or lack of a renal response to ADH. The last can occur as a result of such diverse causes as hypokalemia, hypercalcemia, sickle cell anemia, obstructive uropathy, and renal insufficiency. Preoperative or preprocedure treatment of diabetes insipidus consists of restoring normal intravascular volume by replacing urinary losses, administering desmopressin nasally, and giving daily fluid requirements intravenously.
Perioperative management of patients with diabetes insipidus is based on the extent of the ADH deficiency. Management of a patient with complete diabetes insipidus and a total lack of ADH does not usually present any major problem as long as the side effects of the drug are avoided and the presence of the condition is known before surgery. Just before surgery, the patient is given the usual dose of DDAVP (desmopressin acetate) intranasally or an intravenous bolus of 100 mU of aqueous vasopressin, followed by constant infusion of 100 to 200 mU/hr.[281] The dose is usually adjusted to permit the daily break-through polyuria that avoids the iatrogenic syndrome of SIADH. We have found it useful to continue that dosing regimen perioperatively in all ambulatory patients who can take fluid orally in the postoperative period. All the intravenous fluids given intraoperatively should be isotonic to reduce the risk of water depletion and hypernatremia. Plasma osmolality should be measured every hour, both intraoperatively and immediately after surgery. If plasma osmolality rises well above 290 mOsm/L, hypotonic fluids can be administered; the rate of the intraoperative vasopressin infusion can be increased to more than 200 mU/hr.
For patients who have a partial deficiency of ADH, it is not necessary to use aqueous vasopressin perioperatively unless plasma osmolality rises above 290 mOsm/L. Nonosmotic stimuli (e.g., volume depletion) and the stress of surgery usually cause the release of large quantities of ADH perioperatively. Consequently, these patients require only frequent monitoring of plasma osmolality during this period.
Because of side effects, the dose of vasopressin should be limited to that necessary for control of diuresis.[282] The oxytoxic and coronary artery-constricting properties of vasopressin make this limit especially applicable to patients who are pregnant or have coronary artery disease.[282]
Another problem for anesthesiologists is the care of patients who come to the operating room with a vasopressin drip for the treatment of bleeding from esophageal varices. This treatment is less common since the advent of laser therapy for varices. However, when vasopressin is given, the vasoconstrictive effect of vasopressin on the splanchnic vasculature is used to decrease bleeding. Such patients are often volume depleted and may have concomitant coronary artery disease. Because vasopressin has been shown to markedly decrease oxygen availability, primarily as a result of decreased stroke volume and heart rate, monitoring of tissue oxygen delivery may be useful. In 1982, Nikolic and Singh[283] described a patient with a history of angina pectoris who received a combination of cimetidine and vasopressin for esophageal varices. Bradyarrhythmias and AV block occurred and necessitated placement of a pacemaker. On two occasions, discontinuation of either of these drugs alleviated the symptoms. This effect indicates that the combination of cimetidine and vasopressin could be deleterious to the heart because of the combined negative inotropic and arrhythmogenic effects of the two drugs.
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