The adrenal gland is composed of adrenal cortex and medulla. The active principles of adrenal medulla are the catecholamines secretion which include adrenaline 80% and noradrenaline 20%. Tyrosine is derived from dietary sources and converted to adrenaline and noradrenaline. The conversion is catalysed by enzyme and its metabolism is excreted in urine.
The catecholamines exerts their effects on target organs by binding to receptors sites. Epinephrine has both alpha and beta effects. Norepinephrine has mainly alpha effect. Adrenal medulla is the only endocrine gland which is under nervous control. When the peripheral end of the splanchnic nerve is stimulated adrenaline and noradrenaline are liberated.
The adrenal cortex secretes three types of hormones: glucocorticoids, mineralocorticoids and sex hormones. The adrenal cortex is essential to life. It participates in responses to stress and through its chief hormones influences the metabolism of carbohydrates, proteins, fat, electrolytes and water. Adrenocorticotrophic hormone (ACTH) stimulates the synthesis of cortisol and 17-ketosteroids by adrenal cortex. Three factors are of major importance in regulating ACTH, first is homeostatic cortisol, second is plasma circadian rhythm with high level in the early morning and low level late in the evening. Third factor is stress, thus plasma ACTH levels are increased during fever, trauma or surgery resulting in increased secretion of cortisol.
The synthesis and secretion of adrenal mineralocorticoids are dependent primarily upon the renin angiotensin system.
The main disorders of adrenal gland include either :
(1) Pheochromocytoma : catechol secreting tumour derived from chromaffin tissue usually the adrenal medulla. It is a life-thretening tumour, manifested commonly with palpitation, headaches, and diaphoresis. Diagnosis by measurement of urinary and plasma catecholamine. With preoperative alpha, beta blockers and restoration of blood volume. The primary goals of anaesthesia and surgery is to avoid massive sympathetic outflow. Postoperative replacement is usually required as sympathetic tone continue to decrease.
(2) Excess secretion of corticosteroid (cushing syndrome). The patient presents mainly with centripetal obesity, hypertension, osteoporosis and glucose intolerance. The aim of perioperative steroid therapy is to prevent acute adrenal insufficiency and crisis. The most accurate method for confirming increased glucocorticoid secretion is to measure the cortisol production rate by an isotope dilution technique.
Anaesthetic of choice include thiopentone followed by suxamethonium, nitrous oxid, halothane because these agents do not cause significant stimulation of adrenocortical function.
(3) Adrenocortical insufficiency : a patient with primary adrenal insufficiency presenting as (Addison’s disease) usually exhibits hypoaldosteronism present mainly with hypovolaemia and hyperkalamia, if patient is not stressed usually have no perioperative problems, avoid narcotics because they are very sensitive to barbiturates. Induction of anaesthesia by very slow thiopentone. Addison’s crisis may occur postoperative which treated immediately by I.V. hydrocortisone succinate.
(4) Excess mineralocorticoid : sodium retention, potassium depletion, hypertension, hypokalamic alkalosis, these symptoms constitute primary hyperaldosteronism or (Conn’s syndrome) most often the result of a unilateral adenoma. Successful treatment is spironolactone with restoring potassium equilibrium.
(5) Mineralocorticoid deficiency : hypoaldosteronism, a much less common either congenital or following unilateral adrenalectomy. Most of patients have low blood pressure, most symptoms due to hyperkalemic acidosis. Treatment with mineralocorticoids (9 fluorocortisone preoperatively) with monitoring.