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Adrenal disorders

Adrenal Gland

Adrenal Gland

TESTS OF ADRENAL FUNCTION

Plasma Cortisol Description This is direct measure of the primary secretory product of the adrenal cortex by radioimmunoassay technique. Serum concentration varies with circadian cycle so normal values vary with time of day and stress level of patient (8 a.m. levels typically double that of 8 p.m. levels). Useful as an initial step to assess adrenal dysfunction, but further workup is usually necessary.

Nursing and Patient Care Considerations A fasting sample is preferred. Blood specimens should coincide with circadian rhythm with draw time indicated on laboratory slip.

Interpretation of test results:


Decreased values seen in: adrenal hyperplasia, Addison's disease, anterior pituitary hyposecretion, secondary hypothyroidism, hepatitis, and cirrhosis. Increased values seen in: hyperthyroidism, stress (eg, trauma, surgery), carcinoma, Cushing's syndrome, hypersecretion of corticotropin by tumors (oat cell cancer), adrenal adenoma, and obesity.

24-Hour Urinary Free Cortisol Test Description Test measures cortisol production during a 24-hour period. Useful to establish diagnosis of hypercortisolism. Less influenced by diurnal variations in cortisol.

Nursing and Patient Care Considerations Instruct patient in appropriate collection technique. Collection jug should be kept on ice and sent to laboratory promptly when collection completed. Interfering factors:

Elevated values pregnancy, oral contraceptives, spironolactone, stress. Recent radioisotope scans can interfere with test results.

Dexamethasone Suppression Test Description The dexamethasone suppression test (DST) is a valuable method to evaluate adrenal hyperfunction. Adrenal production and secretion of cortisol is stimulated by adrenocorticotropic hormone (ACTH, corticotropin) from the pituitary gland.

Dexamethasone is a synthetic steroid effective in suppressing corticotropin secretion. In a healthy patient, the administration of dexamethasone will inhibit corticotropin secretion and will cause cortisol levels to fall below normal.

Nursing and Patient Care Considerations Explain the procedure to the patient.

Overnight 1 mg DST (used primarily to identify those without Cushing's syndrome). Administer dexamethasone 1 mg orally at 11 p.m. Draw cortisol level at 8 a.m. before patient rises. Expect suppressed cortisol levels (less than 5 mcg/dL).

High-dose overnight DST (helpful to distinguish Cushing's disease from other forms of Cushing's syndrome). Give patient dexamethasone 8 mg orally at 11 p.m. Draw cortisol level at 8 a.m. before patient rises. Suppressed cortisol levels (less than 50% of baseline value) indicative of patient with corticotropin-secreting pituitary adenoma (Cushing's disease). Unsuppressed cortisol levels are associated with ectopic corticotropin secretion (malignancy) or adrenal tumors.

Adrenocorticotropic Stimulation Test Description ACTH stimulates the production and secretion of cortisol by the adrenal cortex. Demonstrates the ability of the adrenal cortex to respond appropriately to ACTH. This is an important test to evaluate adrenal insufficiency, but may not distinguish primary insufficiency from secondary insufficiency.

Nursing and Patient Care Considerations Obtain baseline cortisol level. Administer 0.25 mg ACTH (cosyntropin [Cortrosyn] I.V. or I.M.). Collect cortisol levels at times ordered (usually at 30 and 60 minutes). Interpretation of test results:

Range of normal responses may vary; however, typically a rise in cortisol of double baseline value is considered normal.

Diminished response adrenal insufficiency with low cortisol values, adrenal tumor with high cortisol values, prolonged glucocorticoid therapy. Exaggerated response adrenal hyperplasia with high cortisol values.

Corticotropin Releasing Hormone Stimulation Test Description Test measures responsiveness of pituitary gland to corticotropin-releasing hormone (CRH), a hypothalamic hormone that regulates pituitary secretion of ACTH. Useful to differentiate the cause of excess cortisol secretion when ectopic source of ACTH is suspected. In general, CRH will stimulate ACTH secretion in the pituitary, but not in nonpituitary corticotropin-secreting tissues.

Nursing and Patient Care Considerations Describe procedure to patient.

Patient is given CRH (1 mcg/kg or 100 mcg) I.V. Catheters are advanced through the femoral veins to areas near the adrenal glands, so sampling can take place near ACTH secretion. Blood samples for ACTH test are collected at 2, 5, 10, and 15 minutes.

Normal response is a rise in ACTH to at least double the baseline value.

Interpretation of test results:


Brisk rise in ACTH double baseline value Cushing's disease. No response in ACTH corticotropinindependent Cushing's syndrome (adrenal tumor) or ectopic source of corticotropin secretion (ectopic tumor). Test can produce false-negative response.

Cushing syndrome

Definition

Cushing syndrome is a spectrum of clinical abnormalities caused by an excess of corticosteroids, particularly glucocorticoids.

Classification
ACTH

Dependent

Pituitary dependent bilateral adrenal hyperplasia Ectopic ACTH syndrome (bronchial carcinoid, small cell lung carcinoma) Iatrogenic (ACTH therapy)

Non ACTH dependent


Iatrogenic (chronic glucocorticoid therapy) Adrenal adenoma Adrenal carcinoma

Pseudo-Cushing syndrome is cortisol excess as a part of another illness. Alcohol excess Major depressive illness Primary obesity

Etiology
Adrenal hyperplasia Secondary to pituitary ACTH over production Pituitary hypothalamic dysfunction Pituitary ACTH or CRH producing micro and macro adenoma

Secondary to ACTH or CRH producing endocrine tumors (bronchiogenic carcinoma, carcinoid of the thymus, pancreatic carcinoma, bronchial adenoma) Adrenal macro nodular hyperplasia Adrenal micro nodular hyperplasia Sporadic Familial Primary adrenal neoplasms such as adrenal adenoma and carcinoma and

primary cortical hyperplasia Exogenous and iatrogenic causes Prolonged use of glucocorticoids Prolonged use of ACTH

Pathophysiology
Due to etiological factors Normal feedback mechanism of mechanisms that control the function of adrenal cortex is disturbed

Overproduction of endogenous corticosteroids Signs and symptoms of Cushing syndrome

CLINICAL MANIFESTATIONS
Insidious in onset. Muscle weakness and fatigability due to mobilization of peripheral supportive tissue. Hypertension and weight gain due to sodium and water retention. centripetal distribution of adipose tissue with truncal obesity moon face accumulation of fat in the posterior neck and back.

Selective atrophy of fast twitch myofibres with resultant decreased muscle mass. Glucocorticoid induce gluconeogenesis with resultant hyperglycemia and polydipsia mimicking diabetes mellitus. Skin is thin fragile and easily bruised, cutaneous strior in the abdomen due to catabolic effect of protien causing loss of collagen Bone resorption result in development of fracture.

Increased risk for infection. Hirsutism and mineralized abnormalities like oligomenorrhea or amenorrhea due to increased adrenal androgens. Emotional changes may be profound, ranging from irritability to severe depression confusion or even frank psychosis. thinning of scalp hair. Posterior sub capsular cataract.

Extra adrenal Cushing syndrome caused by pituitary or ectopic ACTH secretion.

Symptoms of Excess Cortisol


Truncal obesity Moon face Fat deposits supraclavicular fossa and posterior neck- buffalo hump HTN Hirsutism Amenorrhea or impotence Depression Thin skin Easy bruising Purplish abdominal striae Proximal muscle weakness Osteoporosis Diabetes Mellitus Avascular necrosis Wound healing impaired Pysch symptoms Hyperpigmentation Hypokalemic alkalosis

DIAGNOSTIC EVALUATION Urine cortisol. Overnight Dexamethasone test. Diurnal rhythm of plasma cortisol. Insulin tolerance test. High dose dexamethasone suppression test. Corticotropin releasing harmone test

Screening Test
Overnight dexamethasone suppression test (1 mg at 11 pm, cortisol measured at 8 am) normal <2 micrograms/dL Or 24 hour urine free cortisol (>140 nmol/day)

Confirmatory Test
Low dose dexamethasone suppression test Dexamethasone 0.5 mg q 6 x 48 hours Measure urine cortisol during the last 24 hours (urine free cortisol >20 micrograms/dL or urine 17-hydroxycorticosteroid >4.5 mg/d) Or plasma cortisol (failure to fall to <5 micrograms/dL)

Confirmatory Test
Low dose dexamethasone suppression test Dexamethasone 0.5 mg q 6 x 48 hours Measure urine cortisol during the last 24 hours (urine free cortisol >20 micrograms/dL or urine 17-hydroxycorticosteroid >4.5 mg/d) Or plasma cortisol (failure to fall to <5 micrograms/dL)

Treatment
Cushings Disease: Transphenoidal resection of pituitary adenoma Adrenal neoplasms: resection Ectopic ACTH: resection if possible Bilateral adrenal hyperplasia: may need adrenalectomies (lifelong glucocorticoid and mineralcorticoid replacement)

Medical Adrenalectomy
Medications that inhibit steroidogenesis Ketoconazole (600 to 1200 mg/day) metyrapone (exacerbates female virilization) (23 g/day) Mitotane(2-3 G/day)- slow onset Aminoglutethinide (1g/day) Ocreotide can work in 1/3 of patients. Major side affect is adrenal insufficiency, therefore start at lowest dose and titrate

Drug Name:Metyrapone (Metopirone) Description:Inhibitor of endogenous adrenal corticosteroid synthesis. Inhibits 11-B-hydroxylation reaction in the adrenal cortex .Adult Dose:1 g/d PO divided qid; increase gradually, not to exceed 4.5 g/d

Drug Name:Ketoconazole (Nizoral) Description:Imidazole broad-spectrum antifungal agent that acts on several of the P450 enzymes, including the first step in cortisol synthesis, cholesterol side-chain cleavage, and conversion of 11deoxycortisol to cortisol. Adult Dose200-400 mg PO bid/tid

Drug Name;Aminoglutethimide (Cytadren) Description:Inhibits conversion of cholesterol to delta-5-pregnenolone, which, in turn, reduces the production of adrenal glucocorticoids, mineralocorticoids, aldosterone, estrogens, and androgens. Adult Dose:250 mg PO bid initially; increase to 2 g qid

Prognosis

Benign adrenal adenoma- 95% 5 year survival, 90% 10 year Cushings disease (pituitary adenoma) same survival, but 10-20% transphenoidal resection failure rate over 10 years. Ectopic ACTH survival depends on malignancy Unknown cause of elevated ACTH- 65% 5 year survival, 55% 10 year survival Adrenal carcinoma- median survival 7 months

Complications of Cushing's if Untreated


Diabetes HTN Osteoporotic fractures and avascular necrosis Infections Nephrolithiasis Psychosis

Hyperaldosteronism

Definition

Aldosteronism is a condition associated with hyper secretion of mineral corticoid aldosterone.

Classification
Primary aldosteronism Cause lie within the adrenal gland May be due to a adrenal leision which is benign It produce hypokalemia, hypernatremia and secondary hypertension.

Secondary Aldosteronism Stimulus is extra adrenal Condition include sodium wasting renal disease, excessive laxative and diuretic use, dehydration , cirrhosis with ascities, heart failure.

Primary aldosteronism
Definition Primary aldosteronism indicate a primary autonomous overproduction of aldosterone with resultant suppression of renin angiotensin system and decreased plasma renin activity

Incidence and prevalence


primary aldosteronism accounts for 0.052% of cases of hypertension in the general population Twice common in women as in men Usually occur in ages between 30 and 50.

Etiology
aldosterone producing adrenal adenoma. Bilateral cortical nodular hyperplasia Rarely adenocarcinoma

Pathophysiology
Due to hypersecretion of aldosterone Increased renal tubular exchange of intratubular sodium for secreted potassium and hydrogen ions

Hypernatremia hypokalemia hypovolemia Hypertension muscle weakness hypertension Cerebral infarct, renal damage

Clinical manifestation
Usually asymptomatic But findings include Hypernatremia hypokalemia and hypertension. Large urinary output leads to polydipsia Hypokalemia leads to metabolic alkalosis metabolic alkalosis causes adecrease in ionized calcium levels which can result in tetany and respiratory suppression.

Diagnostic evaluation
Serum potassium decreased Urine PH- NEUTRAL TO ALKALINE Serum sodium increased Metabolic alkalosis Test for mineralocorticoid suppressibility Radionuclide scanning technique to visualize tumors.

Management
Adrenalectomy Dietary sodium restriction Aldosterone antagonist

Secondary Aldosteronism
Definition Secondary aldosteronism refers to an appropriately increased production of aldosterone in response to activationof renin angiotensin system.

Etiology
Occurs in association with accelerated phase of hypertension or on the basis of an underlying edema disorder like cirrhosis or nephrotic syndrome. Narrowing of major renal arteries by atherosclerosis Profound renal vasoconstriction. Renin producing tumors

Pathophysiology

Due to etiological factors Narrowing of renal arteries Decrease in renal blood flow

Overproduction of renin
Hypokalemia, alkalosis, hypertension, increased aldosterone.

Hypofunction of adrenal cortex

Primary adrenocortical deficiency (addisons disease)


Definition Addison's disease is an uncommon disorder resulting from progressive destruction of the adrenal cortex by an autoimmune process or other disease.

Incidence

Usually rare , but may occur at any age and affect both sexes equally.

Etiology and risk factors


Result from progressive destruction of adrenals Anatomic destruction of adrenal gland Idiopathic atropy:autoimmune,adreno leukodystropy Surgical removal:bilateral adrenelectomy infection

Tuberculosis Fungal-histoplasma capsulatum Viral Haemorrhage Invasion:metastasis from the lung,breast,Gi tract Metabolic failure in hormone production Congenital adrenal hyperplasia Enzyme inhibitirs(metyrapone,ketoconazole) Cytotoxic agent ACTH blocking antibiotics

Mutation in ACTH receptor gene Adrenal hypoplasia congenita RISK FACTORS a history of other endocrine disorders Taking glucocorticoid for more than 3 weeks withsudden cessation Taking glucocorticoid more than once every other day

Pathophysiology

Adrenal antibiotics(cytotoxic T lymphocytes) Autoimmune destruction of specific adrenal antigens

Blocks the binding of ACTH to its receptors

Inability of the adrenal cortex to produce hormones Adrenal insufficiency

Clinical features

Insidious onset of fatigability,weakness,pigmentation of skin,weight loss,anorexia,nausea,vomiting,hypotension ,pigmentation of mucus membrane,abdominal pain,salt craving,diarrhea,constipation,syncope and occassional hypoglycemia

Asthenia is a cardinal symptom.early it may be sporadic -More evident at the time of stress -As adrenal function become more impaiired the patient is continuously fatigued Hyperpigmentation appears as diffuse brown or bronze darkening of elbows,creases of the hand

-Bluish black patches may appear on mucus membrane -Tanning following sun exposure -Arterial hypotension 80/50 or less Abnormalities of gi function Mild anorexia with weight loss to fulminating nausea,vomitting,diarrhea and abdominal pain

Excessive irritability and restlessness Axillary's and pubic hair decreased in women due to loss of adrenal adrogens

Diagnostic tests

Serum sodium,chloride, and bicarbonate decreased Serum pottasium level elevated Low cortisol level Low aldosterone level ACTH stimulation test :plasma ACTH will be more Blood count to assess anemia Blood glucose X ray,CT,MRI

Management
Medical: -all patients should receive specific hormone replacement -Glucocorticoid-hydrocortisone(cortiso) is the mainstay treatment 20-30mg/day -To stimulate normal diurnal rhythm 2/3rd is taken in morning and 1/3rd evening

Side effects -Insomnia,irritability,mental excitement Minerelocorticoid-fludeocortisone 0.050.1mg/day orally -Maintain ample intake of Na -Measure blood pressure or serum electrolyte Androgen:DHEA 25-50mg/day orally

Secondary adrenocortical insufficiency


ACTH deficiency causes secondary adrenocortical insufficiency ETIOLOGY -prolonged administration of excess glucocorticoids -deficiencies of multiple pituitary hormones

pathophysiology

Due to etiological factors Loss of adrenalresponsiveness to ACTH and failure of pituitary ACTH release Adrenal atropy and prolonged pituitary adrenal insufficiency

Adrenal insufficiency characterized by low blood cortisol and ACTH levels

Clinical features
Weakness,fatigability Severe dehydration Hyponatremia Hyperkalemia GI disturbances include anorexia,nausea vomitting,weight loss,diarrhea

Diagnostic test

ACTH test:metyrapone and insulin induced hypoglcemia

treatment

Glucocorticoid therapy

Acute adrenocortical insufficiency


Also called ADDISONIAN CRISIS OR ADRENAL CRISIS it may be a rapid and overwhelming intensification of chronic adrenal insufficiency of chronic adrenal insufficiency usually precipiated by sepsis or surgical stress

causes

Sepsis Surgical stress Acute haemorrhagic destruction of both glands Septicemia with pseudomonas and meningococcemia Congenital adrenalhyperplasia Drugs which inhibits steroids synthesis(ketoconazole )

Clinical features
Manifestations are related to degree of hormones deficiency and electrolyte imbalance and include Suddenpenetrating pain at back ,abdomen and legs Depressed or changed mentation Volume depletion

Hypotension Loss of consciousness Shock Nausea and vomiting Fever hypoglycemia

management
Replace steroids -hydrocortisone at 100mg iv bolus followed by 100mg every 8hrs for 24hrs Replacement of Na and water deficits-an isotonic solution usually correct the volume depletion,salt depletion and hypotension

Vasoconstrictive agent dopamine as adjuant to volume depletion Sodium polysterene sulfonate orally or as enema in combination with sorbital.it is a resin that releases Na ions in exchange of K ions Hypoglycemia corrected with 5% dextrose

Adrenal steroids glucocorticoids Evaluating patient prior to initiating steroid therapy 1. Chronic infection-if TB is present steroid therapy should be given in conjunction in antitubercular drug 2. Diabetes mellitus 3. Prolonged therapy may aggravate DM

Osteoporosis with vertebral fracture or comcompression is a high risk complication Peptic ulcer,gastric hypersecretion,esophagitis Hypertension or cardiovascular diseases Psychological difficulties-sleeplessness is common

hypoaldosteronism

Isolated aldosterone deficiency accompanied by normal cortisol production occurs in association with hyporeninism as an inherited biosynthetic defect postoperatively following removal of aldosterone secreting adenoma,during protracted heparin or heparinoid administration

features
Unexplained hyperkalemia Severe cases,urine sodium wastage occurs at a normal salt intake.In milder forms,excessive loss of urine sodium occurs only with salt restriction

pathophysiology

Due to renal disease,autonomic neuropathy extracellular fluid volume expansion Plasma renin fail to rise following Na restriction and K changes Failure of aldosterone level to rise

Diagnostic test
Serum K level ACTH stimulation test Renin and aldosterone levels

management

Replace mineralocorticoid 0.05-0.15mg fludrocortisones daily orally Patients with hyporeninic hypoaldosteronism may require higher doses Potential risk in patient with hypertension,mild renal insufficiency and CCF Reduce salt intake and administer frusemide

pheochromocytoma
Definition Pheochromocytoma is a catecholamine secreting tumor of the chromaffin cells of the sympathetic nervous system that is usually found in the adrenal medulla

Incidence and prevalence


Are rare In autopsy series the incidence is 0.1^% in client with diastolic hypertension Equal in men and women Rare after 60yrs

Etiology and risk factors


Unknown cause Familial bases-10% appear to have familial syndromes-MEN 2A and 2B syndromes,neurofibromatosis

pathophysiology

The pathophysiology of the pheochromocytoma is best appreciated with an understanding of catecholamine biochemistry. The following is an abbreviated version of the important steps in the biosynthesis and metabolism of catecholamines.

Tyrosine
Dihydroxyphenylalanine (DOPA) Dopamine (DA) Norepinephrine + Epinephrine

Homovanillic acid (HVA) + Vanillylmandelic acid (VMA)

an alteration in the regulation of the catecholamine biosynthesis possibly suggests an alteration in the feedback inhibition of tyrosine hydroxylase, the key enzyme in the production of catecholamines.

Location and morphology


In adult 80% are unilateral,10% are bilateral.,10% are extra adrenal Size ranges from 100gm to 3 kg Tumors are highly vascular and made up of large polyhedral ,pleomorphic chromaffin cells Less than 10% are malignant

Extraadrenal tumors
Weigh 20-40gm and are less than 5cm diameter Located in abdomen,urinary bladder(10%) less than 3% seen in neck within the sympathetic ganglia

Clinical features
Hypertension - common manifestation -40% B>P elevation occur during attack -often severe and not treated with antihypertensives Paroxysm/crisis: -Occur in half of patients -May be frequent or sporadic

Sudden onset Last from a few mnts to several hours or longer Headache,profuse sweating,palpitations Apprehensions are common Pain in chest and abdomen Nausea and vomiting pallor

B.P elevated with tachycardia Paroxyms may be precipitated by any activity that displaces abdominal content.smoking,micturation may stimulate paroxysms Activities that displaces abdominal content include bending,exercising,straining,vigorous palpations of abdomen in pregnancy

Cardiac manifestations-sinus bradycardia,arrythmias,angina,MI,cardiom yopathy Carbohydrate intolerence Hypercalcemia Fever Polyuria Urinary bladder pheochromocytomasproduce typical paroxysms in relation to micturation,hematuria

diagnosis
History and p/E Lab test -elevated haematocrit due to diminished plasma volume -increased ESR due to production of interleukin Assay of urinary catecholamines

Assay of urinary VMA levels -performed on 24hr urine specimen -advice client to avoid tea,coffee,chocolate,vannilla for atleast 2 days before the test -normal less than 7mg in 24 hrs

Direct assay of catecholamines -normal epinephrine-0.02-0.2mg/L norepinephrine-0.1-0.5mg/L X-ray imaging,CT,MRI Pheochromocytomas of urinary bladdercystoscopy

complications
Cardiomyopathy Multisystem organ failure Acute pancreatitis Renal failure

management

Alpha-adrenergic blocking agents


At low doses, alpha-adrenergic receptor blockers may be used as monotherapy in the treatment of hypertension. At higher doses, the agents may cause sodium and fluid to accumulate. As a result, concurrent diuretic therapy may be required to maintain the hypotensive effects of the alpha-receptor blockers.

Drug Name :Phenoxybenzamine (Dibenzyline) Adult Dose:10 mg PO bid initially; increase dose by 10-mg increments every other day until an optimal dosage is obtained; usual dosage range is 20-40 mg PO bid/tid

Drug Name: Phentolamine (Regitine)

Adult Dose:Prevention or control of hypertension in pheochromocytomas: 5 mg IV/IM 1-2 h before surgery; repeat prn; administer 5 mg IV during surgery as indicated to control paroxysms of hypertension, tachycardia, respiratory depression, or seizures

Drug Name:Prazosin (Minipress)

Adult Dose: 1 mg PO bid/tid initially; increase prn; not to exceed 20 mg/d PO divided bid/tid

Drug Category: Beta-adrenergic

blocking agents

These agents are used as adjunctive therapy for cardiac effects. The agents inhibit chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation.

Drug Name:Propranolol (Inderal)

Adult Dose: Hypertension: 40 mg/dose PO bid; may increase 10-20 mg/dose q35d; not to exceed 640 mg/d Pheochromocytoma preoperatively: 60 mg/d PO for 3 d in divided doses; inoperable tumor, 30 mg/d PO in divided doses

Drug Name:Labetalol (Normodyne, Trandate)

Adult Dose: Incremental doses starting at 20-40 mg IV; a response should be obtained within 5 min and a maximum effect at 10 min; IV dose can be doubled q30-60min until target BP is achieved; not to exceed 300 mg total dose

Drug Category: Nitrates These agents provide peripheral and coronary vasodilation. Drug Name: Sodium nitroprusside (Nipride, Nitropress) Adult Dose0.3-0.5 mcg/kg/min IV continuous IV infusion initially, titrate upward by 0.5 mcg/kg/min increments to effect; usual dose is 3-4 mcg/kg/min; infusion rates >10 mcg/kg/min may lead to cyanide toxicity

Drug Category: Antiarrhythmic

agents

These agents alter the electrophysiologic mechanisms responsible for arrhythmia. Drug Name: Amiodarone (Cordarone) Adult DoseRapid loading: 5 mg/kg IV; not to exceed 450 mg; mixed in D5W infused over 10-30 min; not to exceed 50 mg/kg

Drug Name:Lidocaine (Xylocaine) Adult Dose0.7-1.4 mg/kg IV push, repeat in 5 min; not to exceed 300 mg/h; follow with an infusion of 2-4 mg/kg/min

Surgical management
Adrenalectomy It is the surgical removal of one or both adrenal glands depending on tumors whether it is unilateral or bilateral Techniques Standard transabdominal Thoraco abdominal Retroperitoneal laproscopic

CARE OF THE PATIENT UNDERGOING ADRENALECTOMY Adrenalectomy may be unilateral or bilateral to treat adrenal tumors, Cushing's syndrome, or hyperaldosteronism. It is accomplished through abdominal or flank incision. Careful manipulation of the gland is necessary if surgery is for pheochromocytoma to prevent excessive release of epinephrine causing hypertensive crisis

Preoperative Management BP and fluid volume are optimized. Surgery and nursing care are explained to patient. Patient is shown where adrenal glands lie on top of kidneys and where incision may be on abdomen or loin area. BP will be checked frequently before and after surgery and glucocorticoids will be given to cover period of stress (surgery) because at least one adrenal gland will be removed. Patient is prepared as for major abdominal surgery

Postoperative Management Usual postoperative care for abdominal surgery includes frequent check of vital signs; assessment for hemorrhage; turning, coughing, and deep breathing; early ambulation; slow progression of diet when bowel sounds return; and control of pain with scheduled opioid administration or patient-controlled analgesia I.V. hydrocortisone (Solu-Cortef) is given as directed to prevent adrenal crisis

Nonstressful environment is maintained, rest is promoted, and meticulous care is given to protect the patient from infection and from other complications that could cause adrenal crisis. Serum sodium, potassium, and glucose are monitored for abnormality.

Sodium and potassium may normalize, or potassium may become elevated (because of transient adrenal insufficiency after surgery). Electrolyte imbalances may persist for 4 to 18 months after surgery.

Hypertension may persist for 3 to 6 months after surgery

Hydrocortisone treatment causes glucose to rise and worsens control in patients with diabetes; may require additional treatment Complications Hemorrhage, adrenal crisis

Providing Patient Education Teach patient with bilateral adrenalectomy that glucocorticoid and mineralocorticoid replacement is necessary for rest of life. Administer additional doses I.M. in times of stress. Administer oral glucocorticoids after unilateral adrenalectomy and teach patient that this treatment will be needed for 6 months to 2 years after surgery until remaining adrenal gland can compensate.

Encourage wearing or carrying this information at all times, so that proper treatment can be instituted if patient becomes unconscious. Encourage follow-up to monitor for signs of adrenal insufficiency