A 60-year-old woman comes to the emergency room in a coma. The patient’s temperature is 32.2°C (90°F). She is bradycardic. Her thyroid gland is enlarged. There is diffuse hyporeflexia. BP is 100/60. Which of the following is the best next step in management?
The clinical picture strongly suggests myxedema coma. Unprovoked hypothermia is a particularly important sign. Myxedema coma constitutes a medical emergency; treatment should be started immediately. Should laboratory results fail to support the diagnosis, treatment can be stopped. An intravenous bolus of levothyroxine is given (500 μg loading dose), followed by daily intravenous doses (50-100 μg). Impaired adrenal reserve may accompany myxedema coma, so parenteral hydrocortisone is given concomitantly. Intravenous fluids are also needed but are less important than thyroxine and glucocorticoids; rewarming should be accomplished slowly, so as not to precipitate cardiac arrhythmias. If alveolar ventilation is compromised, then intubation may also be necessary. Hyponatremia and an elevated PCO2 are laboratory markers of severe myxedema. CT of the head would not be the first choice, since a structural brain lesion would not explain the hypothermia, diffuse goiter, or hyporeflexia seen in this case.
A 19-year-old man with insulin-dependent diabetes mellitus is taking 30 units of NPH insulin each morning and 15 units at night. Because of persistent morning glycosuria with some ketonuria, the evening dose is increased to 20 units. This worsens the morning glycosuria, and now moderate ketones are noted in urine. The patient complains of sweats and headaches at night. Which of the following is the most appropriate next step in management?
Episodic hypoglycemia at night is followed by rebound hyperglycemia. This condition, called the Somogyi effect, develops in response to excessive insulin administration. An adrenergic response to hypoglycemia results in increased glycogenolysis, gluconeogenesis, and diminished glucose uptake by peripheral tissues; hence the prebreakfast blood sugars are often elevated. Checking the blood sugars at 2 and 5 AM will demonstrate the hypoglycemia and allow the proper treatment changes—less long-acting insulin at bedtime, not more—to be made. Nocturnal hypoglycemia is a common problem with intermediate-acting insulin such as NPH. The nearly peakless long-acting insulins glargine and detemir rarely lead to the Somogyi effect. If early morning hypoglycemia is documented, discontinuing the NPH and converting the patient to a basal-bolus regimen would be indicated.
A 25-year-old woman is admitted for hypertensive crisis. The patient’s urine drug screen is negative. In the hospital, blood pressure is labile and responds poorly to antihypertensive therapy. The patient complains of palpitations and apprehension. Her past medical history shows that she developed hypertension during an operation for appendicitis at age 23.
Which of the following is the most likely diagnosis?
Hypertensive crisis in this young woman suggests a secondary cause of hypertension. In the setting of palpitations, apprehension, and hyperglycemia, pheochromocytoma should be considered. Pheochromocytomas are derived from the adrenal medulla. They are capable of producing and secreting catecholamines. Unexplained hypertension associated with surgery or trauma may also suggest the disease. Clinical symptoms are the result of catecholamine secretion. For example, the patient’s hyperglycemia is a result of a catecholamine effect of insulin suppression and stimulation of hepatic glucose output. Hypercalcemia has been attributed to ectopic secretion of parathormone-related protein. Renal artery stenosis can cause severe hypertension but would not explain the systemic symptoms or laboratory abnormalities in this case. An anxiety attack can produce palpitations, apprehension, and mild to moderate elevation in blood pressure but would not produce hypercalcemia nor elevated blood pressure poorly responsive to treatment. Essential hypertension can occur in a 25-year-old but again would not account for the laboratory changes. Diabetes mellitus does not cause hypertension unless renal insufficiency has already developed; her hyperglycemia will likely resolve when the pheochromocytoma is removed. Once pheochromocytoma is suspected, a urine or plasma specimen for metanephrines or fractionated catecholamines is the commonly used diagnostic study. If a plasma sample is used, it is drawn from an indwelling IV catheter so that the pain of phlebotomy does not raise the catecholamine levels. After biochemical evidence of catecholamine overproduction is found, imaging studies (CT scan, radionuclide imaging) will localize the problem for curative surgery.
A 23 year old man complains of persistent headache. He has noticed gradual increase in his ring size and his shoe size over the years. On physical examination, he has a peculiar deep, hollow-sounding voice and a prognathic jaw. Bedside visual field testing suggests bitemporal hemianopsia.
What initial studies are indicated?
The patient has excessive growth of soft tissue that has resulted in coarsening of facial features, prognathism, and frontal bossing—all characteristic of acromegaly. This growth hormone–secreting pituitary tumor will result in bitemporal hemianopsia when the tumor impinges on the optic chiasm, which lies just above the sella turcica. Growth hormone–secreting tumors are the second commonest functioning pituitary tumors (second to prolactinomas). Serum IGF-1 (insulin-like growth factor-1) level will be elevated and is usually the first diagnostic test. Since 40% of GH-producing tumors also produce prolactin, a prolactin level should be obtained as well. Growth hormone secretion is pulsatile and a single GH level is often equivocal; the GH level must be suppressed (usually with glucose) to diagnose autonomous overproduction. Dexamethasone suppression is used in the evaluation of Cushing syndrome, with partial suppressibility suggesting a pituitary cause, but this patient’s presentation strongly suggests acromegaly, not Cushing syndrome. Once GH overproduction is documented, an MRI scan of the pituitary will show the size and extent of the tumor (most are macroadenomas > 1 cm). The lateral skull film is insufficiently sensitive for this purpose. Growth hormone stimulation tests (insulin-induced hypoglycemia, arginine plus GHRH) may be used to diagnose growth hormone deficiency, but would not be useful to diagnose GH overproduction, where a suppression test should be used.
A patient with small cell carcinoma of the lung develops increasing fatigue but is otherwise alert and oriented. Serum electrolytes show a serum sodium of 118 mg/L. There is no evidence of edema, orthostatic hypotension, or dehydration. Urine is concentrated with an osmolality of 550 mmol/L. Serum BUN, creatinine, and glucose are within normal range. Which of the following is the next appropriate step?
The patient described has hyponatremia, normovolemia, and concentrated urine. These features are sufficient to make a diagnosis of inappropriate antidiuretic hormone secretion. If ADH were responding normally to the patient’s hypotonic state, the urine would be dilute and the excess water load would be excreted. Treatment necessitates restriction of fluid (free-water) intake. Insensible and urinary water loss results in a rise in serum Na + and serum osmolality and symptom improvement. If the patient has CNS symptoms such as confusion, obtundation, or seizures, hypertonic saline is cautiously administered to raise the serum sodium out of the danger zone (usually a rise of 4-8 mEq/L). Normal saline would treat volume depletion, but this patient is euvolemic. Isotonic saline would not address the freewater excess. Loop diuretics lead to modest free-water loss in the urine but would be less important than fluid restriction. The tetracycline derivative demeclocycline decreases renal response to ADH and can be used in cases where the hyponatremia does not respond to fluid restriction. SIADH can occur as a side effect of many drugs or from carcinoma (especially small cell carcinoma of the lung), CNS disorders (head trauma, CNS infection) or benign lung diseases (especially lung abscesses or other chronic infections).
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