Patient A, a man 50 years of age, is admitted for diagnosis and initial management of suspected adrenal hypofunction with acute adrenal insufficiency. For the past five years, Patient A has been under considerable stress managing his failing contracting business. Initially, he dismissed his complaints of fatigue and weakness as job-related. Lately, the symptoms have been difficult to ignore and associated with anorexia, nausea, and vomiting. He has lost 30 pounds over the past three months without dieting. He complains of frequently feeling cold and has had two syncopal attacks in the month prior to admission. He reports that although he has spent essentially all this time indoors at the office, his skin has become as dark as his employees who work outdoors.

On the morning of admission, he did not wake at his usual early hour and told his wife that he felt gravely ill. His wife called the family physician, who instructed her to take Patient A to the emergency department. After evaluation in the emergency department, Patient A is admitted to the critical care unit (CCU).

A medical history is obtained from Patient A's wife. She states that the patient has no allergies to medications but was very allergic to ragweed when they were first married. During the first 10 years of their marriage, Patient A had frequent asthma attacks requiring treatment with epinephrine injections. The asthma attacks diminished in frequency during his middle years, and his wife cannot remember when he last had an attack.

Patient A also has a history of coccidioidomycosis, which was active for several years late in adolescence and in early adulthood. Mrs. A has no recollection of being told of changes in the patient's routine chest x-rays for some time. Ten years previously, Patient A was diagnosed with hypertension, but his blood pressure has been well-controlled with daily exercise and dietary changes.

Patient A has been married to his wife for 35 years and has three grown children who live out of state. His contracting business had been successful until five years ago, when a decrease in housing starts resulted in a decline in business and increased financial stress.

Upon admittance to the CCU, a full physical exam is conducted (Table 2). A chest x-ray is done and shows normal lung fields and a smaller than expected heart. Several laboratory tests are ordered, with the following results:

Based on the results of the assessment, Patient A is diagnosed with possible acute adrenal insufficiency and possible Addison disease.

Shortly after arriving in the CCU, Patient A vomits a large amount of bile-colored gastric contents and then develops coma and shock. His blood pressure is 60/10 mm Hg, his heart rate is 50 beats per minute, and his respiratory rate is 8 breaths per minute and gasping. He is quickly resuscitated with rapid IV infusion of normal saline, hydrocortisone sodium succinate (100 mg IV), tracheal intubation, and artificial ventilation. A double lumen nasogastric tube is inserted and connected to low constant suction. An indwelling urinary catheter is inserted and connected to a urine meter. Patient A's condition stabilizes as he becomes alert and orientated, has adequate spontaneous ventilation, and maintains adequate cardiac output and blood pressure. Efforts are made to confirm the diagnosis of Addison disease.

The physician orders diagnostic tests of adrenal, thyroid, and pituitary function. Results of the 24-hour urine collection assessed for 17-ketosteroids and 17-hydroxycorticosteroids indicates that adrenal secretion of cortisol, corticosterone, cortisone, and 11-hydroxycorticosternone is inadequate. The result of the plasma cortisol response to ACTH test confirms the diagnosis of Addison disease. The latest results of tests of thyroid and pituitary function are within normal limits.

Patient A is prescribed fludrocortisone acetate (0.1 mg daily) and hydrocortisone (20 mg daily) as replacement therapy. He responds well and is transferred out of the CCU four days after admission.

Consider the information that has been presented in this course regarding adrenal insufficiency and Addison disease.

Patient B, a man 26 years of age, is in the hospital recovering from surgical clipping of an aneurysm on the anterior communicating artery. Three days after surgery, he begins voiding large quantiles of very pale urine. His IV intake is 80 mL/hour, and his oral intake is minimal. The specific gravity of the urine is 1.002, and the patient's calculated urine output is more than 200 mL/hour for four consecutive hours. The nurse observes that during the past two hours Patient B's blood pressure has declined from 120/80 mm Hg to 110/70 mm Hg and that his heart rate has increased from 68 beats per minute to 110 beats per minute. The nurse notifies the neurosurgeon of the large unconcentrated urinary output and the changes in vital signs.

Patient B has suffered chronic severe headaches, and the diagnosis of cerebral aneurysm led to the cerebrovascular procedure. The surgical procedure went well, and Patient B was recovering as expected.

Upon the onset of diuresis, a full physical exam is conducted (Table 3). Laboratory findings are:

Based on the findings of the assessment, Patient B is diagnosed with diabetes insipidus secondary to manipulation of the pituitary.

The neurosurgeon orders 2.5 units of aqueous vasopressin to be administered immediately intramuscularly. Following administration, urine output is reduced to 60 mL/hr in 30 minutes. The urine osmolality level two hours later is 760 mOsm/L. Patient B continues to be monitored to determine if the pituitary damage is permanent and if he requires long-term desmopressin therapy.

Consider the information that has been presented in this course regarding diabetes insipidus.

Patient C is a Hispanic man, 60 years of age. He is brought to the emergency department by his family because of acute mental confusion and combativeness. His wife and son report that he has been complaining of anorexia, a nonproductive cough, and unusual fatigue and weakness for the past seven months. During this time, he lost 40 pounds. In the past two weeks, Patient C has been unusually irritable and occasionally irrational. The day before admission, the patient's confusion and disorientation became so severe that he tried to hit his wife. Because she could not manage him alone, the patient's wife asked their son to come and stay with them.

The morning of the admission, Patient C has a seizure (with signs consistent with a tonic-clonic seizure), and the family transports the patient to the emergency department for evaluation.

Patient C's wife reports that her husband drinks six 12-ounce beers daily and has smoked two to three packs of cigarettes per day for the 35 years of their marriage. She has no knowledge of Patient C's family medical history. In addition, Patient C has only rarely seen a physician for illnesses and has never had a routine physical examination.

Upon presentation to the emergency department, a full physical exam is conducted (Table 4). An electrocardiogram (ECG) is normal with nonspecific ST-T wave changes. Skull imaging is normal, but a chest x-ray visualizes a mass in the lower right lobe. Laboratory studies find:

Based on the findings of the assessment, Patient C is diagnosed with severe hyponatremia secondary to water intoxication. A lack of history for excessive water intake suggests SIADH.

The physician suspects that Patient C has SIADH, and further diagnostic studies are planned and carried out. The supraclavicular lymph node is biopsied. The pathology report identifies the node as small-cell lung cancer.

Patient C's serum cortisol is 10 mcg/dL in the morning. A 24-hour urine collection is completed, and 17-ketosteroids excretion is 9 mg per day and sodium excretion is 150 mEq per day. Patient C's fluid intake is restricted, furosemide is administered, and hypertonic saline is carefully infused. As the patient undergoes diuresis, his serum sodium gradually returns to normal and his sensorium improves. His wife is relieved at the return of her normally gentle husband.

Extended management includes assessment of the underlying cause of the SIADH, assumed to be metastatic small-cell lung cancer. The patient is referred to an oncologist for further testing and treatment.

Consider the information that has been presented in this course regarding SIADH.