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Diagnosing Secondary Hypertension EDWARD ONUSKO, M.D., Clinton Memorial Hospital, Wilmington, Ohio

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Diagnosing Secondary Hypertension EDWARD ONUSKO, M.D., Clinton Memorial Hospital, Wilmington, Ohio COVER ARTICLE PROBLEM-ORIENTED DIAGNOSIS Diagnosing Secondary Hypertension EDWARD ONUSKO, M.D., Clinton Memorial Hospital, Wilmington, Ohio Secondary hypertension is elevated blood pressure that results from an underlying, iden- tifiable, often correctable cause. Only about 5 to 10 percent of hypertension cases are thought to result from secondary causes. The ABCDE mnemonic can be used to help deter- mine a secondary cause of hypertension: Accuracy of diagnosis, obstructive sleep Apnea, Aldosteronism, presence of renal artery Bruits (suggesting renal artery stenosis), renal parenchymal disease (Bad kidneys), excess Catecholamines, Coarctation of the aorta, Cushing’s syndrome, Drugs, Diet, excess Erythropoietin, and Endocrine disorders. An algorithm showing the general strategy to help screen for factors involved in secondary hypertension is presented. Routine urinalysis, complete blood cell count, blood chemistry profile (potassium, sodium, creatinine, fasting glucose, fasting lipid levels), and a 12-lead electrocardiogram are recommended for all patients with hypertension. (Am Fam Physi- cian 2003;67:67-74. Copyright© 2003 American Academy of Family Physicians) atients with hypertension other risk factors for cardiovascular dis- have some underlying mech- orders (e.g., diabetes mellitus, hyperlipi- anism that elevates their demia); and detection of secondary blood pressure. Conceptu- causes of hypertension. Physicians can ally, it is useful to think of use the mnemonic ABCDE to help deter- Ppatients with hypertension as having mine secondary causes in the patient either essential hypertension (systemic with elevated blood pressure (Table 1). hypertension of unknown cause) or sec- ondary hypertension (hypertension that Diagnosis: ABCDE results from an underlying, identifiable, A: ACCURACY, APNEA, ALDOSTERONISM often correctable cause).1 Although only Accuracy. The first, most practical step about 5 to 10 percent of hypertension in evaluating an elevated blood pressure cases are thought to result from sec- reading is to investigate its accuracy. A Members of various family practice depart- ondary causes, hypertension is so com- blood pressure cuff that is too small, tight- ments develop articles mon that secondary hypertension proba- fitting sleeves that are not removed, or a for “Problem-Oriented bly will be encountered frequently by the brachial artery that is noncompressible Diagnosis.” This is one primary care practitioner.2-4 because of calcification (sometimes seen in a series from the The sixth report of the Joint National in the elderly) can cause falsely elevated Department of Family Practice at the Univer- Committee on Prevention, Detection, readings. White-coat hypertension (blood sity of Cincinnati Col- Evaluation, and Treatment of High Blood pressure that is elevated in the physician’s lege of Medicine. Pressure (JNC-VI)5 defines four goals for office but normal at other times) accounts Guest coordinator of the evaluation of the patient with ele- for about 20 percent of patients with ele- the series is Susan vated blood pressure: detection and con- vated readings.3 JNC-VI recommends Montauk, M.D. firmation of hypertension; detection of confirming high blood pressure readings target organ disease (e.g., renal damage, outside of the office setting. congestive heart failure); identification of Apnea. Obstructive sleep apnea (OSA), a repetitive mechanical obstruction of the upper airway during sleep, is an indepen- 6 The first, most practical step in evaluating an elevated blood dent risk factor for hypertension. At least one half of patients with OSA have pressure reading is to investigate its accuracy. hypertension.7 Treatment of OSA with surgery or nasal continuous positive air- JANUARY 1, 2003 / VOLUME 67, NUMBER 1 www.aafp.org/afp AMERICAN FAMILY PHYSICIAN 67 TABLE 1 Findings That Suggest Secondary Hypertension Findings Disorder suspected Further diagnostic studies Snoring, daytime somnolence, obesity Obstructive sleep apnea Sleep study Hypernatremia, hypokalemia Aldosteronism Ratio of plasma aldosterone to plasma renin activity, CT scan of adrenal glands Renal insufficiency, atherosclerotic Renal parenchymal Creatinine clearance, renal cardiovascular disease, edema, disease ultrasonography elevated blood urea nitrogen and creatinine levels, proteinuria Systolic/diastolic abdominal bruit Renovascular disease Magnetic resonance angiography, captopril (Capoten)-augmented radioisotopic renography, renal arteriography Use of sympathomimetics, perioperative Excess catecholamines Confirm patient is normotensive setting, acute stress, tachycardia in absence of high catecholamines. Decreased or delayed femoral pulses, Coarctation of aorta Doppler or CT imaging of aorta abnormal chest radiograph Weight gain, fatigue, weakness, Cushing’s syndrome Dexamethasone-suppression test hirsutism, amenorrhea, moon facies, dorsal hump, purple striae, truncal obesity, hypokalemia Use of drug in Table 2 Drug side effect Trial off drug, if possible High salt intake, excessive alcohol Diet side effects Trial of dietary modification intake, obesity Erythropoietin use in renal disease, Erythropoietin side Trial off drug, if possible polycythemia in COPD effect Paroxysmal hypertension, headaches, Pheochromocytoma Urinary catecholamine metabolites diaphoresis, palpitations, tachycardia (vanillylmandelic acid, metanephrines, normetanephrines) Plasma free metanephrines Fatigue, weight loss, hair loss, diastolic Hypothyroidism TSH levels hypertension, muscle weakness Heat intolerance, weight loss, Hyperthyroidism TSH levels palpitations, systolic hypertension, exophthalmos tremor, tachycardia Kidney stones, osteoporosis, depression, Hyperparathyroidism Serum calcium, parathyroid lethargy, muscle weakness hormone levels Headaches, fatigue, visual problems, Acromegaly Growth hormone level enlargement of hands, feet, tongue CT = computed tomography; COPD = chronic obstructive pulmonary disease; TSH = thyroid-stimulating hormone. 68 AMERICAN FAMILY PHYSICIAN www.aafp.org/afp VOLUME 67, NUMBER 1 / JANUARY 1, 2003 Secondary Hypertension way pressure reduces hypertension in these patients.8 Daytime somnolence, obesity, snor- Increased urinary excretion of potassium signals hyperal- ing, lower-extremity edema (secondary to the dosteronism, which should be suspected in all hypertensive right-sided congestive heart failure that occurs patients with unprovoked hypokalemia. after repetitive anoxic insults to the myo- cardium during sleep), morning headaches, and nocturia suggest OSA.9 There is a high incidence of OSA in patients with chronic tions of hypertensive persons, the incidence of obstructive pulmonary disease (COPD). A renovascular hypertension is less than 1 per- formal sleep study usually is needed for diag- cent.14 However, identification of this rela- nosis of OSA and determination of corrective tively small population can be important interventions. because surgery or angioplasty can reverse the Aldosteronism. Primary hyperaldosteronism hypertension, especially if performed early is defined as overproduction of aldosterone enough to prevent permanent renal damage. independent of its usual regulator, the renin- Magnetic resonance angiography (MRA) is angiotensin system.10 The resulting retention of a noninvasive imaging modality with a sensi- excess salt and water suppresses renin levels (as tivity of 100 percent and a specificity of 70 to opposed to elevating renin levels, which causes 90 percent compared with renal arteriography secondary hyperaldosteronism). Increased uri- for detection of renal artery stenosis.2,15 MRA nary excretion of potassium signals hyperal- best delineates the proximal renal vasculature dosteronism, which should be suspected in all and is therefore useful as an initial diagnostic hypertensive patients with unprovoked (i.e., tool for patients suspected of having athero- not diuretic-induced) hypokalemia.11 The next sclerotic renal artery stenosis, which usually diagnostic test should be demonstration of an involves the proximal renal artery.16 Patients elevated ratio of plasma aldosterone levels to suspected of having FMD, which tends to plasma renin activity.12 involve the distal renal artery, should undergo conventional angiography or computed B: BRUITS, BAD KIDNEYS tomographic angiography.16 (RENAL PARENCHYMAL DISEASE) Another initial diagnostic test is the captopril Bruits. Renovascular hypertension is (Capoten)-augmented radioisotopic reno- defined as hypertension resulting from com- gram.17 This test is based on the fact that a kid- promised arterial supply to the kidneys. About ney that is receiving an inadequate blood sup- 65 percent of renovascular disease is sec- ply will activate the renin-angiotensin system. ondary to atherosclerosis in the renal arteries, Therefore, a single dose of the angiotensin-con- usually seen after age 50 in patients at risk for verting enzyme (ACE) inhibitor captopril will arterial compromise (e.g., smokers, patients abruptly reduce renal function in the ischemic with diabetes, patients with known athero- kidney. A scan is considered positive if there is sclerotic disease).13 The remainder of patients delayed or decreased uptake of the radioisotope will demonstrate fibromuscular dysplasia in the stenotic kidney compared with the non- (FMD) and will tend to be younger (25 to 50 stenotic one, so this test is not as useful if steno- years of age) at the time of diagnosis.13 sis is present bilaterally.2 About one half of patients with renovascu- Duplex ultrasound scanning is
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