Quem investigar, Hipertensão primária ou secundária?

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Quem investigar, Hipertensão primária ou secundária?

Mensagem  Convidad em Ter Jul 16, 2013 1:54 am

GENERAL CLINICAL CLUES — There are a number of general clinical clues that are suggestive of secondary hypertension (table 1):

Severe or resistant hypertension. Resistant hypertension is defined as the persistence of hypertension despite concurrent use of adequate doses of three antihypertensive agents from different classes, including a diuretic. (See "Definition, risk factors, and evaluation of resistant hypertension", section on 'Definitions'.)
An acute rise in blood pressure developing in a patient with previously stable values.
Age less than 30 years in non-obese, non-black patients with a negative family history of and no other risk factors (eg, obesity) for hypertension.
Malignant or accelerated hypertension (eg, patients with severe hypertension and signs of end-organ damage such as retinal hemorrhages or papilledema, heart failure, neurologic disturbance, or acute kidney injury). (See "Malignant hypertension and hypertensive encephalopathy in adults".)
Proven age of onset before puberty.
In addition to these clues, there are other findings that specifically suggest renovascular or other forms of secondary hypertension as described in the following sections.

CLINICAL CLUES FOR RENOVASCULAR HYPERTENSION — Renovascular hypertension is the most common potentially correctable cause of secondary hypertension. The incidence varies with the clinical setting. It probably occurs in less than 1 percent of patients with mild hypertension [2]. By comparison, between 10 and 45 percent of white patients with severe or malignant hypertension have renal artery stenosis. Renal artery stenosis can be detected in many individuals with other manifestations of atherosclerosis, such as coronary artery disease (10 to 14 percent) and peripheral arterial and aortic disease (24 to 35 percent) [3].

For reasons that are not well understood, renovascular disease is less commonly identified in black patients [4,5]. As an example, the prevalence of renal artery stenosis in high-risk patients with severe or refractory hypertension was 27 to 45 percent in whites, compared with 8 to 19 percent in blacks [4]. A more extreme disparity was found in a retrospective review of all patients diagnosed with renal artery stenosis at a single center, 95 percent of whom were white [5]. However, two studies that prospectively screened individuals with or without clinical clues for renovascular hypertension found similar rates of renal artery stenosis in blacks and whites [6,7]. Referral bias is a possible explanation for this discrepancy, given that blacks diagnosed with renal artery stenosis were more likely than whites to have severe or refractory hypertension and a history of stroke or myocardial infarction [5].

There is a variety of findings associated with a higher likelihood of hypertension being secondary to renovascular disease. The 2005 American College of Cardiology/American Heart Association (ACC/AHA) guidelines on Peripheral Artery Disease propose that diagnostic testing for renal artery stenosis is indicated in the following settings, assuming that a corrective procedure would be considered if renovascular disease were detected [8]. As with other vascular diseases, long-term management of these patients can be affected by the potential for progressive vascular occlusion.

The general clinical clues for any cause of secondary hypertension as cited in the preceding section. (See 'General clinical clues' above.)
Onset of severe hypertension (blood pressure ≥180 mmHg systolic and/or 120 mmHg diastolic) after the age of 55 years.
Unexplained deterioration of kidney function during antihypertensive therapy, especially an acute and sustained elevation in the serum creatinine concentration by more than 50 percent that occurs within one week of instituting therapy with an angiotensin converting enzyme (ACE) inhibitor or angiotensin II receptor blocker (ARB). (See "Renal effects of ACE inhibitors in hypertension".)
Severe hypertension in patients with diffuse atherosclerosis, particularly those over age 50. The relationship between atherosclerotic renal artery stenosis and atherosclerosis at other sites (eg, coronary, peripheral arterial) is discussed separately. (See "Chronic kidney disease associated with atherosclerotic renovascular disease", section on 'Association with systemic atherosclerosis'.)
Severe hypertension in a patient with an unexplained atrophic kidney or asymmetry in renal sizes of >1.5 cm. A unilateral small kidney (≤9 cm) has a 75 percent association with the presence of large vessel occlusive disease.
Severe hypertension in patients with recurrent episodes of acute (flash) pulmonary edema or refractory heart failure with impaired renal function [9]. In a series of 55 patients with renovascular hypertension, for example, 23 percent had recurrent episodes of pulmonary edema requiring hospitalization. Flash pulmonary edema was more common in patients with bilateral compared with unilateral renal artery stenosis. The factors that contribute to acute decompensation include a hypertension-induced increase in afterload, inability of a hypertrophied left ventricle to relax in diastole (ie, diastolic with or without systolic dysfunction), sodium retention due to activation of the renin-angiotensin-aldosterone system, and associated renal dysfunction [10,11]. (See "Evaluation of acute decompensated heart failure".)
A systolic-diastolic abdominal bruit that lateralizes to one side. This finding has a sensitivity of approximately 40 percent (and is therefore absent in many patients) but has a specificity as high as 99 percent [12]. Systolic bruits alone are more sensitive but less specific [12]. The patient should be supine, moderate pressure should be placed on the diaphragm of the stethoscope, and auscultation should be performed in the epigastrium and all four abdominal quadrants.
In summary, radiologic testing to confirm the presence of renal artery stenosis may be indicated in patients for whom the history is suggestive (based upon a general assessment of clinical risk factors) and in whom a corrective procedure will be performed if renovascular disease is detected. There is little value and potential harm from radiologic testing if the patient is not a candidate for a corrective procedure. Imaging methods for renovascular hypertension, and how one makes the choice between medical and interventional therapy in such patients, are discussed elsewhere. (See "Establishing the diagnosis of renovascular hypertension" and "Treatment of unilateral atherosclerotic renal artery stenosis" and "Treatment of bilateral atherosclerotic renal artery stenosis or stenosis to a solitary functioning kidney" and "Treatment of fibromuscular dysplasia of the renal arteries".)

CLINICAL CLUES FOR OTHER FORMS OF SECONDARY HYPERTENSION — Other causes of secondary hypertension also must be excluded in the appropriate settings (table 1).

Primary kidney disease — The presence of primary kidney disease is suggested by an elevated serum creatinine concentration and/or an abnormal urinalysis. (See "Overview of hypertension in acute and chronic kidney disease".)

Primary aldosteronism — The main clinical clue suggestive of primary aldosteronism is otherwise unexplained or easily provoked hypokalemia due to urinary potassium wasting. However, more than one-half of patients have a normal serum potassium concentration. Primary aldosteronism should also be suspected in the presence of slight hypernatremia, drug-resistant hypertension, and/or hypertension with an adrenal incidentaloma. Measurement of the ratio of the plasma aldosterone concentration to plasma renin activity can help identify such patients [13], although inappropriate elevation of aldosterone is also a common feature in obese patients [14]. (See "Approach to the patient with hypertension and hypokalemia" and "The adrenal incidentaloma", section on 'Aldosteronomas'.)

Oral contraceptives — Oral contraceptives often raise the blood pressure within the normal range but can induce overt hypertension. (See "Effect of oral contraceptives and postmenopausal hormone therapy on blood pressure".)

Pheochromocytoma — Pheochromocytoma should be suspected if there are paroxysmal elevations in blood pressure (which may be superimposed upon stable chronic hypertension), particularly if associated with the triad of headache (usually pounding), palpitations, and sweating. In addition, patients with drug-resistant hypertension and those with an adrenal incidentaloma should be evaluated for pheochromocytoma. Patients identified with pheochromocytoma are rarely asymptomatic. (See "Clinical presentation and diagnosis of pheochromocytoma" and "The adrenal incidentaloma", section on 'Pheochromocytoma'.)

Cushing's syndrome — Cushing's syndrome (including that due to glucocorticoid administration) is usually suggested by the classic physical findings of cushingoid facies, central obesity, proximal muscle weakness, and ecchymoses. However, Cushing's or subclinical Cushing's syndrome should also be suspected in patients with drug-resistant hypertension and in those with an adrenal incidentaloma. (See "Epidemiology and clinical manifestations of Cushing's syndrome" and "The adrenal incidentaloma", section on 'Subclinical Cushing's syndrome'.)

Sleep apnea syndrome — The sleep apnea syndrome is most commonly identified in obese men who snore loudly while asleep. These patients have repeated apneic episodes at night due to passive collapse of the pharyngeal muscles during inspiration, such that the airway becomes occluded from the apposition of the tongue and soft palate against the posterior oropharynx. A variety of other symptoms may be seen including headache, daytime somnolence and fatigue, morning confusion with difficulty in concentration, personality changes, depression, persistent systemic hypertension, and potentially life-threatening cardiac arrhythmias. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults".)

Patients with obstructive sleep apnea often retain sodium and fail to respond optimally to antihypertensive drug therapy [15]. Correction of the sleep apnea may improve blood pressure control [16]. (See "Cardiovascular effects of obstructive sleep apnea", section on 'Systemic hypertension'.)

Coarctation of the aorta — Coarctation of the aorta is one of the major causes of secondary hypertension in young children but may first be detected in adulthood (image 1A-B). The classic findings are hypertension in the upper extremities, diminished or delayed femoral pulses ("brachial-femoral delay"), and low or unobtainable arterial blood pressure in the lower extremities. In addition, a prominent "to-and-fro machinery murmur" from the aorta may be heard over the posterior chest.

Patient age, the site of origin of the left subclavian artery, and the severity of the coarctation affect the pattern of blood pressure findings. As an example, the origin of the left subclavian artery is just distal to the coarctation in some patients; in this setting, the left brachial pulse is diminished compared to the right and equal to the femoral pulse. (See "Clinical manifestations and diagnosis of coarctation of the aorta".)

Based upon the 2003 JNC 7 report on hypertension and the 2008 American College of Cardiology/American Heart Association (ACC/AHA) guidelines for adults with congenital heart disease, patients with hypertension should be evaluated for possible coarctation of the aorta [17,18]. This involves palpating the brachial and femoral pulses simultaneously to assess amplitude and timing, looking for diminished arterial pulses and brachial-femoral delay. In addition, the ACC/AHA guidelines recommended measurement of supine bilateral arm (brachial artery) blood pressures and prone right or left supine leg (popliteal artery) blood pressures to search for differential pressures. (See "Examination of the arterial pulse", section on 'Unequal or delayed pulses'.)

Other endocrine disorders — Hypertension may be associated with both hypothyroidism, which may be suspected because of suggestive symptoms or an elevated serum thyroid stimulating hormone level, and primary hyperparathyroidism. The latter is most often suspected because of otherwise unexplained hypercalcemia, which may affect vascular reactivity, day-night blood pressure regulation, and renal function [19-21]. (See "Diagnosis of and screening for hypothyroidism" and "Diagnosis and differential diagnosis of primary hyperparathyroidism" and "Clinical manifestations of hypercalcemia".)

Fonte: Stephen Textor, MD; et al. Who should be evaluated for renovascular or other causes of secondary hypertension? Uptodate, Set 10, 2012.


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