Dr Sanjay Gupta Professor Department of Surgery University College of Medical Sciences New Delhi

SURGICALLY CORRECTABLE HYPERTENSION

Surgically Correctable Hypertension

Blood Pressure continuous, normally

distributed variable Hypertension level of BP above which

Investigations are worthwhile Treatment does more good than harm

140/90 mm Hg BP measurement Use correct

Machine, cuff, position, technique Consider ambulatory BP monitoring

Surgically Correctable Hypertension

>95% of all hypertension is
Essential hypertension Renal Renovascular Endocrine Others

Primary (Essential) <5% is Secondary (identifiable cause)

Surgically Correctable Hypertension

Suspect a secondary cause when Poor response to therapy (resistant) Worsening of control Stage 3 hypertension (SBP>180 or DBP>110) Onset <20 or >50 years age Significant target organ damage Lack of family history Findings on history/ physical examination/ laboratory testing suggesting a secondary hypertension

Surgically Correctable Hypertension

Causes of secondary hypertension

Signs & Symptoms

Multiple vascular risk factors, abdominal bruit, unexplained renal insufficiency Protienuria, renal dysfunction, nocturia, peripheral edema Hypokalemia, nocturia, cramps Hematuria, flank masses, family history Daytime sleepiness, snoring, obesity Proximal weakness, diabetes, truncal obesity, striae, hypokalemia Renal artery stenosis Renal parenchymal disease Primary aldosteronism PKD Sleep apnea Cushings syndrome

Young age, reduced/ delayed femoral pulses

Headache, palpitation, sweating, pallor, tachycardia

Coarctation of aorta
Pheochromocytoma

Screening Investigations
Expensive Limitations of various tests In the presence of clinical/ lab features of

secondary hypertension Decision to screen depends upon

Risk of intervention (age, comorbidity) Response to medical treatment

Essential and secondary hypertension may coexist

Some Surgically Correctable Causes of Secondary Hypertension

Renal Parenchymal Disease

Causes
Unilateral reflux, tumor (Wilms, JGA), obstruction Bilateral glomerulonephritis, cystic kidney disease

HTN both cause and consequence Investigations

Protienuria, high creatinine Isotope renal scan, renin studies

Treatment
Correct underlying cause Dialysis, transplant Nephrectomy (Tumors, non-functioning kidney)

Renovascular Hypertension
Causes
Atherosclerosis (75-90%), Fibromusucular dysplasia

(10-25%), others (rare)

Clinical features
Onset <30 (FMD) or >50 Years (atherosclerosis)

Sudden uncontrolled/ accelerated/ malignant HTN

Episodes of pulmonary edema (normal LV function) Epigastric bruit

Azotemia induced by ACE inhibitors

Renovascular Hypertension Investigations

Investigation
Duplex u/s MR angiography

Sensitivity
90-95% 88-95%

Specificity
60-90% 95%

Remarks
Economical Operator dependent False positives Cost

Angiography

Gold standard
Low

Gold standard
Low

Invasive, nephrotoxic Does not predict BP response

Invasive May predict response to treatment

Renin levels Captopril renography

Renovascular Hypertension Treatment

Goal Control HTN, preserve renal functions Not all renal artery stenosis cause HTN
Medical ACEI, ARB treatment Prior to definitive treatment Long term management of unstable patients Surgical Percutaneous treatment angioplasty FMD success in 82-100%; Restenosis in 5-11%; HTN cure in 60% Atherosclerosis - success in 60-80%; restenosis in 10-47%, HTN cure in <30%; results better after stenting Used mainly for complex aorto-renal lesions

Renal artery bypass surgery

Angioplasty
Fibromuscular dysplasia Atherosclerosis

Primary Aldosteronism
Causes
Adenoma (40-70%); idiopathic/ bilateral

hyperplasia (30-60%)

Clinical features
Unprovoked hypokalemia (weakness/ paralysis,

cramps, polyuria) Severe target organ damage

Primary Aldosteronism
Lab Investigations
Serum aldosterone/ renin ratio >30:1 Non-suppression of aldosterone to sodium load

(measured in serum/ urine)

Imaging
High resolution CT/ MRI Detects lesions> 0.5 cm For suspected smaller lesions compare bilateral

aldosterone/ cortisol ratios (difference >4 significant)

Primary Aldosteronism Treatment

Medical
For idiopathic hyperaldosteronism Preoperatively in case of adenoma Aldosterone receptor antagonist (Spironolactone)

Surgical
For aldosterone secreting adenoma Surgical excision (preferably laparoscopic)

Pheochromocytoma
Causes
Adenoma of chromaffin cells Adrenal (Pheochromocytoma) Extra-adrenal (Paraganglioma) 10% are malignant

15% are bilateral

10% are familial May be associated with MEN, multiple

neurofibromatosis

Pheochromocytoma
Clinical features
HTN Paroxysmal (30-50%), sustained (50%) Triad of severe headache, palpitation, sweating often

precipitated by drugs (antidepressents, beta blockers) Uncommon presentations (shock, acidosis) Differential diagnosis
Cerebrovascular events Drugs (Ephidrine, cocaine) Panic attacks, hypoglycemia

Pheochromocytoma Investigations
Investigation Biochemical screening Test Plasma free metanephrines/ catecholamines Sensitivity Very high 99% Specificity Moderate 89% Very high 98%

Urinary fractionated Moderate metanephrines 90% Clonidine suppression test Radiological localization CT/ MRI MIBG/ PET scan

Failure to suppress plasma metanephrines/ catecholamines First line investigation If CT/ MRI do not localize

Pheochromocytoma - Treatment
Preoperative Alpha blockers 2-6 weeks till BP normal

Beta blockers (if For tachyarrythmia - should required) follow alpha blockers
Volume expansion Physiological Preoperative fluid infusion

Operative

Adrenalectomy Laparoscopic (good Transperitoneal localization) Retroperitoneal Open surgery Adrenalectomy Open surgery
Postoperative Chemotherapy I 131 tagged MIBG

Malignancy

Cushings Syndrome
Clinical features
Due to glucocorticoid excess Moon face, central obesity, striae, hirsuitism etc.

Causes
Pitutary ACTH excess (Cushings disease) (2%), Ectopic

ACTH (15%) Adrenal adenoma (8%), carcinoma (9%), hyperplasia (rare) Glucocorticoid therapy (commonest)

Differential diagnosis
Obese HTN, Polycystic Ovarian Disease

Cushings Syndrome
Investigations
High, non suppressible glucocorticoids Urinary cortisol, Dexamethasone suppression Serum ACTH levels Localization imaging, venous sampling

Treatment
Pitutary surgery Excision of adrenal adenoma, carcinoma

Bilateral adrenalectomy

Coarctation of Aorta
Clinical features
Dyspnea, headache, cold feet (> in children) Delayed pulses, difference in BP in extremities

Diagnosis
Echocardiography, CXR Surgical repair Aortoplasty, stenting

Prognosis
HTN recurs in 25-33%

Sleep Apnea
Symptoms
Restless sleep, daytime sleepiness, morning

headache, snoring

Diagnosis
Polysomnography, Berlin questionnaire

Treatment
Weight loss Laryngeal surgery CPAP

Novel Surgical Treatments

Baroreflex stimulation
Carotid nerve stimulation using implanted electrodes

Reduces sympathetic tone

Rheos System (Minnesota)

Renal nerve ablation

Reduced feedback to CNS
Reduced renin release Technique Surgical nephrectomy/ sympathectomy Percutaneous, trans-arterial RF ablation

Age Based Diagnostic Approach

Children and adolescents (birth 18 years)
Renal parenchymal disease Coarctation of aorta

Young adults (19-39 years)

Renal artery stenosis (FMD) Thyrotoxicosis

Middle aged (40-64 years)

Adrenal Aldosteronism, Cushings, Pheochromocytoma Obstructive sleep apnea

Older adults (>65 years)

Atherosclerotic RAS Renal failure

Frequency of Occurrence
Common
Renal parenchymal disease
Renovascular HTN

Uncommon
Pheochromocytoma
Cushings Coarctation of aorta

Aldosteronism
Sleep apnea

Hypo/ hyperthyroidism

Summary
<5% of all HTN patients have secondary cause It is often overlooked and underscreened Controversy exists over screening and treatment

in some cases Testing can be expensive and requires clinical suspicion and understanding of various tests However, when properly diagnosed and treated, the results are gratifying

Thank You!