Disorders of the adrenal gland
Adrenal insufficiency
Disease that results in insufficient adrenal hormone production (i.e., hypoadrenocorticism or Addison’s disease) may adversely affect the condition of the patient and overall anesthetic risk. The main risks are associated with electrolyte abnormalities and impaired stress response-associated compensatory mechanisms.
The primary function of the mineralocorticoid aldosterone is to stimulate absorption of sodium ions in the distal renal tubules and to promote potassium excretion. Aldosterone deficiency may thereby result in hyponatremia and hyperkalemia. Hyponatremia with concurrent water loss can produce lethargy, nausea, decreased cardiac output, hypovolemia, hypotension, and/or impaired renal perfusion. Hyperkalemia may result in muscle weakness, decreased cardiac conduction, and excitability and bradycardia. Hyperkalemia greater than 5.5 mEq/L should be addressed prior to anesthesia whenever possible. Dextrose administration, alkalinization of plasma (to drive potassium back into the cells), and/or insulin administration may be effective for treatment of hyperkalemia. For severe hyperkalemia affecting cardiac conduction, calcium gluconate (0.3mL/kg) may be administered intravenously (IV) slowly using a 10% solution (which provides 9.3 mg Ca2+/mL or 0.47mEq/mL) to provide immediate relief from the electrical conduction abnormalities associated with hyperkalemia. Calcium therapy is effective in this instance by raising the threshold potential for depolarization to compensate for the raised resting potential associated with hyperkalemia.
A patient with hypoadrenocorticism should be stabilized prior to anesthesia. The treatment objectives are: (1) to correct the dehydration and treat hypovolemic shock if present, (2) to support renal function, (3) to correct electrolyte imbalances, and (4) to supply glucocorticoids. In an Addisonian crisis, priorities are to correct the patient’s pH, hypotension, hyponatremia, hyperkalemia, hypoglycemia, and electrocardiographic dysrhythmias.1
Cortisol depletion impairs renal excretion of water and energy metabolism, decreases stress tolerance, and can cause anorexia, vomiting, and/or diarrhea. Addisonian patients have decreased stress tolerance, thus their anesthetic management involves glucocorticoid supplementation and IV fluid volume replacement. Use of the anesthetic etomidate is associated with a 2–3-hour depletion of glucocorticoids following a single injection, and should be avoided in Addisonian patients. A balanced electrolyte solution should be administered intraoperatively at a rate of 10–20mL/kg/h.
Hyperadrenocorticism
Hyperadrenocorticism (Cushing’s disease) is a common endocrine disease and presents fewer challenges for successful anesthetic care than does hypoadrenocorticism. Patients with hyperadrenocorticism will be predisposed to infection and poor wound healing. There is increased risk of pulmonary thrombosis in the perianesthetic period. Due to the aforementioned reduction in endogenous corticosteroid release associated with etomidate injection, this anesthetic may be suitable for the patient with Cushing’s disease.2 Propofol is another option for induction of anesthesia due to its potent vasodilating effect on peripheral vasculature.
Blood pressure monitoring and support are important for patients with hyperadrenocorticism because they are prone to hypertension. Preanesthetic evaluation should include baseline arterial blood pressure measurement. Chronic preexisting hypertension may predispose the anesthetized patient to greater risk during periods of anesthetic-related hypotension due to downregulation of vascular control.3
Many patients with hyperadrenocorticism have a large pendulous abdomen, which can impair ventilation during anesthesia. Monitoring ventilation with end-tidal carbon dioxide, pulse oximetry, and/or arterial blood gas analysis is warranted.
Pheochromocytoma
Animals with a functional tumor of the adrenal gland producing excessive catecholamines represent a high-risk group for anesthesia. Pheochromocytoma may be suspected in middle-aged dogs with a history of acute collapse, panting, tachycardia, and restlessness. Hypertension and tachycardia are of primary concern and should be evaluated prior to administration of anesthetic premedications. Premedication with acepromazine (0.05mg/kg, up to a maximum of 1 or 2mg per dog) may be helpful for lowering arterial blood pressure, as is the use of other alpha antagonist medications such as phenoxybenzamine (0.25 mg/kg) or phentolamine (loading dose 0.05–0.1 mg/kg followed by infusion at 10 mcg/kg/min). Blood pressure should be monitored during anesthesia. Nitroprusside infusion (1–5 mcg/kg/min) or magnesium sulfate (40 mg/kg IV bolus followed by infusion at 15mg/kg/h) may be effective for treatment of surgical-induced periods of extreme hypertension.4 Following surgical removal of a pheochromocytoma, exogenous catecholamine support for blood pressure should be available (e.g., dobutamine or dopamine infusion) as blood pressure and cardiac output can fall precipitously.
Diabetes mellitus
Insulin is essential for normal cellular metabolism and function. The effects of insulin on normal cellular function include: (1) inhibition of glycogenolysis, (2) inhibition of gluconeogenesis, (3) inhibition of lipolysis, (4) stimulation of glucose uptake into cells, (5) stimulation of potassium transport into cells, and (6) suppression of ketogenesis. Lipolysis is inhibited with a resultant accumulation of ketone bodies, causing osmotic diuresis and metabolic acidosis. Prolonged hyperglycemia and ketonemia can lead to: (1) metabolic acidosis, (2) dehydration, (3) circulatory collapse, (4) renal failure, and/or (5) coma and death.
Diabetes mellitus should be suspected in any patient with the following clinical signs: (1) a recent history of polyuria, polydipsia, weight loss, or rapid onset of cataracts; (2) dehydration, weakness, collapse, mental dullness, hepatomegaly, and/or muscle wasting; and/or (3) increased rate and depth of respiration and breath with a sweet acetone odor.5 Severe metabolic acidosis (a pH of less than 7.1) should be treated with sodium bicarbonate to return pH to at least 7.2.
A patient with diabetes mellitus should be stabilized and regulated prior to anesthesia. Anesthesia should be delayed in patients with serum glucose concentration >300mg/dL when practical to do so. Ideal anesthetic management of a diabetic involves proper patient preparation and use of antagonizable or short-acting agents such that recovery time can be minimized. Drugs that can be antagonized (opioids and benzodiazepine tranquilizers) or are readily eliminated from the patient (propofol, etomidate, and inhalant anesthetics) should be considered. In normal animals, alpha2 adrenoceptor agonists (xylazine, dexmedetomidine) decrease pancreatic release of insulin, resulting in hyperglycemia. The impact of alpha2 adrenoceptor agonists in patients with diabetes mellitus has not been determined in a clinical setting. Therefore, most clinicians avoid the use of these agents in diabetic patients. The clinician should attempt to get the patient awake as soon as possible so the animal can resume its normal feeding schedule. The procedure should be scheduled early in the morning after the administration of one-half the patient’s normal dose of insulin. Preoperative and serial intraoperative and postoperative blood glucose levels should be determined. Ideally, the blood glucose should be maintained between 150 and 250 mg/dL. During the procedure, 2.5–5% dextrose in a balanced electrolyte solution should be administered to prevent hypoglycemia when blood glucose trends downward.
Diabetes insipidus
While not a disorder of the pancreas, diabetes insipidus does mimic the clinical sign of polyuria seen with diabetes mellitus. Polyuria resulting from vasopressin deficiency is characterized by dilute urine in spite of a strong stimulus for vasopressin secretion. There is an absence of renal disease and a rise in urine osmolality can be documented following administration of vasopressin. When presented for anesthesia, the patient with diabetes insipidus is predisposed to water and electrolyte abnormalities. Thus, the serum sodium, chloride, and potassium concentrations should be determined. Hypernatremia is likely to occur in this condition and should be corrected slowly in cases with chronic elevation. This may be accomplished by judicious free water administration using 5% dextrose in water. Desmopressin has been used to treat diabetes insipidus and may prevent hypernatremia. Cases of surgical hypophysectomy given desmopressin have been reported to become hypernatremic despite prophylaxis.6 It is theorized that fluid administration and water intake in the postoperative period may have resulted in insufficient compensation for hypercortisolism-induced vasopressin resistance.
Insulinoma
Malignant proliferation of beta-cells in the pancreas leads to excessive insulin secretion and hypoglycemia. Animals with insulinoma may receive medical therapies or ultimately, surgical excision of the tumor. Medical therapy may be directed toward destruction of the beta cells using streptozocin. Administration of corticosteroids, diazoxide, somatostatin analogues (e.g., octreotide), and dietary management are used to mitigate the hypoglycemia. During anesthesia of the patient with insulinoma, serum glucose should be monitored and glucose-containing fluids should be administered IV as needed. Dextrose solutions (2.5% or 5%) may be used for IV bolus or continuous infusion. Following surgical excision of an insulinoma, the animal should be monitored closely for signs of pancreatitis. Approximately 10% of dogs will develop diabetes mellitus following surgical excision of an insulinoma.
Hyperparathyroidism occurs with much greater frequency than hypoparathyroidism. Middle-aged dogs that present with polyuria/polydipsia and have hypercalcemia may be hyperparathyroid, a condition that appears overrepresented by the Keeshond breed. Three other commonly diagnosed conditions that should also be considered on the differential list are lymphosarcoma, hypoadrenocorticism, and chronic renal failure. Preanesthetic considerations for these patients should focus on assessment and correction of significant electrolyte abnormalities and hydration status. During surgical excision of parathyroid tumors, aggressive treatment of hypercalcemia is not warranted and efforts should be directed toward the management of fluid therapy to correct dehydration using physiological saline solution. Potassium supplementation may be required as well. Following adequate hydration of the patient, diuretic therapy with furosemide (2–4mg/kg IV) for enhancing calciuresis may be initiated. When possible, at least one normal parathyroid gland will be left in situ during tumor excision and this will prevent permanent hypoparathyroidism. A transient hypocalcemia may develop following tumor excision if the normal glands have suffered atrophy due to chronic parathyroid hormone suppression. This scenario is more likely when the presurgical serum calcium concentration is greater than 15mg/dL.7 Postoperative administration of vitamin D may help to avoid hypocalcemic-induced tetany.
Hypoparathyroidism occurs with less specificity in signalment compared to hyperparathyroidism. Hypocalcemic animals with abrupt onset of neurological or neuromuscular abnormalities that seem to become worse with exercise may be hypoparathyroid. Differential diagnosis of hypocalcemia includes hypoparathyroidism, renal failure, ethylene glycol toxicosis, acute pancreatitis, eclampsia, anticonvulsant therapy, and hypoalbuminemia. In dogs with naturally occurring hypoparathyroidism, 80% were observed to have grand mal convulsions. Thus, perianesthetic management of the hypoparathyroid patient may include administration of diazepam. Treatment of hypocalcemia with 10% calcium gluconate (1 mL/kg, slowly, IV) is preferred over calcium chloride due to the potential for the latter to cause extravascular tissue sloughing.
Hypothyroidism is a common disorder among dogs and very rare in cats. Decreased secretion of thyroxine (T4) and triiodothyronine (T3) may result from dysfunction within the thyroid, lack of thyrotropin-releasing hormone by the hypothalamus, or lack of thyroid-stimulating hormone (TSH) from the pituitary (secondary hypothyroidism). Canine thyroiditis is generally thought to be an autoimmune disorder of middle-aged dogs, but can occur at any age. Clinical presentation is fairly nonspecific and includes low metabolic rate, lethargy, mental dullness, weight gain, and cold intolerance. Slow recovery from general anesthesia can often be related to hypothyroidism. Laryngeal paralysis, megaesophagus, and, rarely, seizure activity may be associated with hypothyroidism. Sinus bradycardia, low QRS amplitude, inverted T waves, and decreased left ventricular function have been observed in hypothyroid dogs.8 While there is no specific anesthetic protocol directed to animals with hypothyroidism, use of drugs that are readily antagonizable or that normally undergo rapid metabolism and elimination are logical choices. Cardiovascular support to maintain normal blood pressure during anesthesia is also warranted. Since obesity may be associated with hypothyroidism, close attention should be given to ventilatory function during anesthesia. Mechanical ventilation may be required to maintain normocapnia. Hypothyroid patients may be prone to developing hypothermia while anesthetized and therefore core body temperature should also be monitored.
Hyperthyroidism is commonly diagnosed in both dogs and cats. Clinical findings include weight loss, increased appetite, polyuria/polydipsia, hyperactivity, and tachycardia. Presence of a cardiac murmur may also be noted. Congestive heart failure and hypertrophic cardiomyopathy are sometimes associated with hyperthyroidism in cats.9 One or more liver enzymes (alanine transaminase, alkaline phosphatase, lactate dehydrogenase, and aspartate transaminase) are frequently elevated in cats with hyperthyroidism, although this finding is usually of minor consequence in terms of anesthetic management. The primary goal during anesthetic management of the hyperthyroid patient is to avoid exacerbation of the tachycardia associated with this hypermetabolic state, especially in the face of cardiac dysfunction. Alpha2 adrenoceptor agonists and anticholinergic agents are avoided while opioids are often included as premedications in these patients. Induction of anesthesia is accomplished using propofol or, when congestive heart failure or cardiomyopathy is suspected, etomidate. Ketamine (including the combination of diazepam and ketamine) and Telazol® (tiletamine and zolazepam; Pfizer Animal Health, New York) are usually avoided in order to minimize drug-related increases in heart rate. The electrocardiograph and arterial blood pressure should be monitored during anesthesia. Hypercapnia (as a consequence of hypoventilation) should be prevented by supporting ventilation as guided by end-tidal or arterial carbon dioxide tensions determined using capnography or blood gas analysis, respectively. Tachycardia may be treated during anesthesia using propranolol (0.05mg/kg IV), esmolol (100–200mcg/kg IV), or lidocaine (0.25–0.5mg/kg IV).
Revised from “Endocrine Disease” by Ralph C. Harvey and Michael Schaer in Lumb and Jones’ Veterinary Anesthesia and Analgesia, Fourth Edition.
1. Harvey R.C., Schaer M. Anesthesia for the patient with endocrine disease. In: Lumb andJones’ Veterinary Anesthesia, 4th ed. W.J. Tranquilli, J.C. Thurmon, and K.A. Grimm, eds. Ames, IA: Blackwell, 2007, pp 933–936.
2. Smith J.A. Endocrine disease. In: Veterinary Anesthesia and Pain Management Secrets. S.A. Greene, ed. Philadelphia, PA: Hanley and Belfus, 2002, pp 197–200.
3. Melian C., Perez-Alenz M.D., Peterson M.E. Hyperadrenocorticism in dogs. In: Textbook of Veterinary Internal Medicine, 7th ed. S.J. Ettinger and E.C. Feldman, eds. St. Louis, MO: Elsevier, 2010, pp 1816–1847.
4. Herrera M., Nelson R.W. Pheochromocytoma. In: Textbook of Veterinary Internal Medicine, 7th ed. S.J. Ettinger and E.C. Feldman, eds. St. Louis, MO: Elsevier, 2010, pp 1865–1871.
5. Nelson R.W. Canine diabetes mellitus. In: Textbook ofVeterinary Internal Medicine, 7th ed. S.J. Ettinger and E.C. Feldman, eds. St. Louis, MO: Elsevier, 2010, pp 1782–1796.
6. Rijnberk A. Diabetes insipidus. In: Textbook of Veterinary Internal Medicine, 7th ed. S.J. Ettinger and E.C. Feldman, eds. St. Louis, MO: Elsevier, 2010, pp 1716–1722.
7. Feldman E.C. Disorders of the parathyroid glands. In: Textbook of Veterinary Internal Medicine, 7th ed. S.J. Ettinger and E.C. Feldman, eds. St. Louis, MO: Elsevier, 2010, pp 1722–1751.
8. Scott-Moncrieff J.C.R. Hypothyroidism. In: Textbook of Veterinary Internal Medicine, 7th ed. S.J. Ettinger and E.C. Feldman, eds. St. Louis, MO: Elsevier, 2010, pp 1751–1761.
9. Mooney C.T. Hyperthyroidism. In: Textbook of Veterinary Internal Medicine, 7th ed. S.J. Ettinger and E.C. Feldman, eds. St. Louis, MO: Elsevier, 2010, pp 1761–1779.
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