Surgically Correctable Hypertension

Dr Arvind Kohli
Hypertension may be primary or idiopathic which may develop as a result of environmental or genetic causes, or secondary hypertension which is elevated blood pressure that results from an underlying, identifiable, often correctable cause, which has multiple etiologies, includng renal, vascular, and endocrine causes. Primary or essential hypertension accounts for 90-95% of adult cases, and secondary hypertension accounts for 2-10% of cases. Secondary hypertension is amenable to surgical correction.
Diagnosis of Secondary Hypertension
Accuracy
The first, most practical step in evaluating an elevated blood pressure reading is to investigate its accuracy. White-coat hypertension (blood pressure that is elevated in the physician’s office but normal at other times) accounts for about 20 percent of patients with elevated readings. Ambulatory blood pressure monitoring has become important diagnostic aid in identifying Secondary Hypertension.
Apnea  Obstructive sleep apnea (OSA), a repetitive mechanical obstruction of the  upper airway  during sleep, is an independent risk factor for Hypertension at least one half of patients with OSA have hypertension. Treatment of OSA with surgery or nasal continuous positive air way pressure reduces hypertension in these patients. A formal sleep study usually is needed for diagosis of OSA and determination of corrective interventions.
Bruits  Renovascular hypertension is defined as Hypertension resulting from compromised arterial supply to the kidneys. About 65 percent of renovascular disease is secondary to athersclerosis in the renal arteries, usuallly seen after age 50 in patients at risk of arterial compromise (e.g smokers, patients with diabetes, patients with known atherosclerotic disease). The remainder of patients will demonstrate fibromuscular dysplasia (FMD) and will tend to be younger (25 to 50 years of age) at the time of diagnosis.
About one half of patients with renovascular hypertension  will have an abdominal bruit identifiable on physical examination Bruits heard in both systole and diastole are more suggestive of renovascular hypertension than systolic bruits alone.
Bad Kidneys
Renal parenchymal disease can be a cause or consequence of hypertension. Progressive renal damage is caused by the mechanical and humoral effects of glomerular hypertension. The renal damage decreases the kidneys’ ability to excrete salt and excess fluid (resulting in a lwo renin state, as opposed to the high renin state found in enovascular hypertension), and the hypertension worsens. As renal damage progresses, hyperparathyroidism develops and erythropoietin production increases, exacerbating the hypertension. Thus, a vicious cycle of worsening renal function and hypertension begins.
Coarctation of the Aorta
Coarctation of the aorta is a congenital narrowing of the aortic lumen, most often occurring just distal to the origin of the left subclavian artery. Patients with less severe forms of the disorder may not be diagnosed until young adulthood but have a high incidence of premature death, Diagnostic clues include decreased lower-extremity (femoral) pulses with upper-extremity hypertension, dyspnea on exertion, and chest radiographic findings of notched ribs (from dilated collateral vessels) and dilation of the aorta above and below the constriction.
Erythropoietin
Elevated erythropoetin levels can be endogenous (as in response to the chronic hypoxia of COPD) or exogenous (administered to alleviate the anemia seen in chronic renal failure). High erythropoietin levels can elevate blood.
Endocrine Disorders
Hypothyroidism can cause decreased cardiac output with a compensatory increase in vascular tone, resulting in a more prominent rise in diastolic blood  pressure than in systolic blood pressure. Conversely, hyperthyroidism induces increased cardiac output and compensatory decreased vascular tone, causing a greater increase in systolic blood pressure.
Hyperparathyroidism (primary or secondary to chronic renal insufficiency) is a potentially reversible cause of  hypertension. Its incidence in hypertensive patients is about 1 percent, compared with a 0.1 percent incidence in the general population. However, only 30 to 40 percent of patients with hyperparathyroidism have hypertension, and parathyroidectomy does not reliably resolve hypertension in patiens with  this disorder.
Pregnancy-induced hypertension has an incompletely understood neurohumoral mechanism (possibly initiated by inadequate establishment of blood supply to the developing placenta) and occasionally can develop in the immediate postpartum period.
Primary hyperaldosteronism is defined as overproduction of aldosterone independent of its usual regulator, the renin-angiotensin system. The resulting retention of excess salt and water suppresses renin  levels (as opposed to elevating renin levels, which causes secondary hyperaldosteronism). Increased urinary excretion of potassium signals hyperal-dosteronism, which should be suspected in all hypertensive patients with unprovoked (i.e not diuretic-induced) hypokalemia.
Pheochromocytoma is another endocrine cause of hypertension. The classic-symptoms include headache, diaphoresis, palpitations, and praxoysmal hypertension. The syndrome can vary depending on the types of catecholamines being produced, the amount and frequency of their release into the circulation, and other factors. The usual screening test has been urinary measurement of catecholamine metabolites (vanillylmandelic acid, metanephrines, normetanephrines). Determination of plasma free metanephrines might be  the test of first choice for diagnosis of this tumor, although availability of this test at hospital and reference laboratories is limited. Pheochromocytoma is very rare, and routine screening in hypertensive patients is not recommended.
Cushing’s syndrome can cause hypertension via the mineralocorticoid effects of excess glucocorticoids and is best screened for with a dexamethasone-suppression test.
Surgical Treatment of Hypertension
Although some patients with adrenal tumors can be effectively treated with medications, most patients should have surgery. Excising hormonally active adrenal masses through a relatively low-risk, minimally invasive operation (laparoscopic adrenalectomy) can resolve hypertention and other health problems, including the obesity, diabetes, hypertension and osteoporosis associated with Cushing’s syndrome. Because the adrenal glands are situated in and around important blood vessels and other structure and because adrenalectromies are relatively rare procedures, patients are generally referred to a tertiary care specialist. Increasingly, patients who are on multiple medications for difficult-to-control hypertension are benefitting from this relatively simple laparoscopic operation.
Coarctation Of Aorta There are several surgical techniques to repair aortic coarctation. The options include:  Resection with end-to-end anastomosis. This method involves removing the narrowed segment of the aorta (resection) followed by connecting the two ends of the aorta together (anastomosis). Subclavian flap aortoplasty. A portion of the left subclavian artery, the blood vessel that delivers blood to your left arm, might be used to expand the narrowed area of the artery. Bypass graft repair. This technique involves bypassing the narrowed area by inserting a plastic tube called a graft between the portions of the aorta. Patch aortoplasty. Your doctor might treat your coarctation by cutting across the narrowed area of the aorta and then attaching a patch of synthetic material to widen the blood vessel. Patch aortoplasty is useful if the coaractation involves a long segment of the aorta.
Balloon angioplasty and stenting Balloon angioplasty is an option for initially treating aortic coarctation or for treating re-narrowing  (re-coarctation) that has occured after surgery.
Renal Artery Stenosis Angioplasty is effective for treating renovascular hypertension associated with atheromatous lesions Bypass procedures include aortorenal, hepatorenal, splenorenal, and ileorenal conduits constructed with autologous saphenous veins, autologous arteries, or prosthetic material.
(The author is Consultant Cardiotoracic & Vascular Surgeon SSH Jammu)

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