-This patient likely has secondary hypertension.
-History and physical exam
–The Causes of Secondary Hypertension, reviewed.
-BPs have been repeated for accuracy.
-Diet and drug-related causes reviewed.
–2017 AAFP Algorithm reviewed.
Diagnostic studies:
–TSH, ECG, UA and Urine Creatine, CBC (Hct), CMP (Cr, eGFR, gluc.), Fasting lipid panel.
-Renin and aldosterone levels to calculate the aldosterone-to-renin ratio–get for nearly all patients — to r/o primary hyperaldosteronism.
-Doppler U/S of renal arteries to r/o RAS
–If OSA suspected, get polysomnography.
–If coarctation suspected, get TTE (for children) or CTA / MRA (for adults).
–If a pheochromocytoma is suspected, get 24-hour urinary fractionated metanephrines and normetanephrines (catecholamines). Plasma free metanephrines if HA present.
–If Cushing’s or hypercortisolism suspected, get either a 24-hr urinary free cortisol (UFC) or 1 mg Dexamethasone Suppression Test (DST), or 11 p.m. salivary cortisol.
–If hyperparathyroidism is suspected, get serum calcium (to look for hypercalcemia).
-If renal bruit, get CTA / MRA (for adults)
Treatment per cause.
Key Points
- Pheochromocytoma is suggested by the triad of episodic headaches (usually pounding), sweating, and tachycardia (w/ palpitations).
- “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, and, therefore, nearly all patients with suspected secondary hypertension should be evaluated for primary aldosteronism.” Stephen Textor, MD, from uptodate.com
- “Primary hyperaldosteronism is a relatively common cause of resistant hypertension. Because there are effective treatments, it is reasonable to consider testing for hyperaldosteronism in patients with resistant hypertension. This is true even for patients with a normal potassium level. The preferred initial test is a morning renin to aldosterone ratio. A ratio <20 (when plasma aldosterone is reported in ng/dL and plasma renin activity is in ng/mL/hr) effectively rules out primary hyperaldosteronism. A ratio >=20 with a serum aldosterone level >15 ng/dL suggests aldosteronism, but a salt suppression test must be done for confirmation. Although abdominal MRI may detect an adrenal mass, it is not recommended as a test for hyperaldosteronism. Urinary potassium levels do not play a role in the diagnosis of primary hyperaldosteronism.” AAFP Test question answer
- Diagnostic studies explained: ECG to eval heart; CBC (HCT); CMP (fasting blood glucose, Electrolytes, creatinine and GFR, calcium); UA and Urine Creatinine to work up causes of parenchymal kidney disease.
- ECG, UA, CBC, CMP, Fasting lipid panel to eval of HTN and other CV risk factors. Also to r/o renal parenchymal disease, thyroid disorder, etc.
What is the most common cause of resistant HTN?
Answer: Obstructive sleep apnea.
“OSA is found in 30-40% of hypertensive patients and 60-70% of patients with resistant hypertension, whereas primary aldosteronism is present in only 7-20% of patients with resistant HTN. RAS is seen in 2-24% of cases of resistant HTN in various studies, renal parenchymal disease in 2-4%, and thyroid disease in less than 1%” From uptodate.com
GENERAL CLINICAL CLUES FOR SECONDARY HYPERTENSION
There are a number of general clinical clues that, in isolation or in combination, are suggestive of secondary hypertension:
- 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.
- 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 hypertension 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).
- 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.
KTA: Secondary HTN is a problem with the Adrenal glands (3 causes), Kidneys, Plumbing system (Coarctation of aorta & Renal artery stenosis), the thyroid and parathyroid glands. Then there are drugs from the outside that we put into our system.
In essence, HTN is an issue with the plumbing system. The pipes are narrowed. The pipes can be:
1) Narrowed in one area (as in coarctation of the aorta and renal artery stenosis) or
2) Squeezed smaller circumferentially everywhere so that the diameter reduces 2/2 to vasopressor effects of endocrine hormones. ( e.g.catecholamines). It will only take a small decrease in the circumference of small pipes like the arterioles and capillaries to have things backed up. Add to that the reduction in size of all pipes, even the larger ones.
3) Filtration of exit way of the plumbing system is clogged so that water comes into the pipes but doesn’t go out and adds pressure inside the pipes. E.g. we drink water that goes into the pipes and urinating it removes it so that too much water doesn’t remain in the pipe. If the kidneys aren’t working, then too much water is left in the pipe.
If you hear a systolic bruit just to the right of his umbilicus of an elderly patient with a strong history of CAD, don’t jump to trying to get renal U/S or any other study to confirm renal artery stenosis. If their blood pressure is well controlled, especially after adding an ACE and ARB, the right approach is to simply monitor their serum creatinine.
“Renal artery stenosis may be present in as many as 5% of patients with hypertension. It is often seen in those who have coronary artery disease and/or peripheral vascular disease. Hypertension requiring four or five drugs to control, abdominal bruits, and development of hyperkalemia or renal insufficiency after initiating therapy with an ACE inhibitor can all point toward renal artery stenosis as a diagnosis. For patients with renal artery stenosis who have good control, no testing is necessary other than monitoring renal function, particularly if an ACE inhibitor or ARB is part of the regimen. Screening tests recommended by clinical guidelines include duplex ultrasonography, CT angiography, or MR cystography” ABFM.
Reference
Am Fam Physician. 2017 Oct 1;96(7):453-461.http://www.aafp.org/afp/2017/1001/p453.html
http://www.aafp.org/afp/2010/1215/p1471.html