Secondary hypertension work up

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Secondary hypertension work up

  1. 1. ‫الرحمن‬ ‫ا‬ ‫بسم‬ ‫الرحيم‬
  2. 2. Secondary Hypertension Work-up By Tamer Moustafa Abe Elghany MD, FESC
  3. 3. Overview  “ Secondary” HTN accounts for ~5-10% of other cases and represents potentially curable disease  Often overlooked and underscreened  Controversy over screening and treatment in some cases
  4. 4. Overview  Testing for 2ry HTN can be expensive and requires high index of clinical suspicion.  General principles:  New onset HTN if <30 or >50 years of age  HTN refractory to medical Rx (>3-4 meds)  Specific clinical/lab features typical for dz :
  5. 5. Routine Laboratory Tests 1. Urinalysis 2. Complete blood count 3. Blood chemistry (potassium, sodium and creatinine) 4. Fasting glucose 5. Fasting lipid profile 6. Standard 12-leads ECG Investigation of all patients with hypertension
  6. 6. Renal Parenchymal Disease  Common cause of secondary HTN (2- 5%)  HTN is both cause and consequence of renal disease  Assessment of creatinine clearance and GFR are diagnostic.
  7. 7. Renovascular HTN  Incidence 1-30%  Etiology  Atherosclerosis 75-90%  Fibromuscular dysplasia 10-25%  Other  Aortic/renal dissection  Takayasu’s arteritis  Thrombotic/cholesterol emboli  CVD  Post transplantation stenosis  Post radiation
  8. 8. Renovascular HTN - Clinical  History  Onset HTN age <30 or >55  Negative FH of HTN  Sudden onset uncontrolled HTN in previously well controlled pt  Accelerated/malignant HTN  Intermittent pulm edema with nl LV fxn  Clinical exam. /Lab. findings  Epigastric bruit, particulary systolic/diastolic  Advanced fundal changes, grade III/IV retinopathy  Azotemia induced by ACEI, ARBs or diuretics  Paradoxical worsening of HTN with diuretics  2ry aldosteronism : ↑ plasma renin & ↓ s. Na&K  Unilateral small kidney, difference >1.5cm, on sonography
  9. 9. Renovascular HTN - diagnosis  Physical findings (bruit)  Duplex U/S  Captopril renography  Magnetic Resonance Angiography  Renal Angiography
  10. 10. RAS screening/diagnostics Sens Spec Limitation/Etc Duplex U/S 90-95% 60-90% Operator dependent, 10-20% Captopril Renography 83-91% 87-93% Accuracy reduced in pt with renal insufficiency, lacks anatomical info; good predictor of BP response MRA 88-95% 95% False positive artifact resp, peristalsis, tortuous vessels; cost Bruit 39-65% 90-99% Insensitive, severe stenosis may be silent Angiography Gold std Gold std Invasive, nephrotoxicity, little value in predicting BP response
  11. 11. Screening Strategy (Index of suspicion & need intervention)
  12. 12. Fibromuscular dysplasia  10-25% of all RAS  Young female, age 15-40  Medial disease 90%, often involves distal RA
  13. 13. Atherosclerotic RAS  75-90% of RAS  Usually men, age>55, other atherosclerotic dz
  14. 14. Fibromuscular Dysplasia, before and after PTRA Atherosclerotic RAS before and after stent Safian & Textor. NEJM 344:6;
  15. 15. Primary Aldosteronism Primary Aldosteronism, previously felt to be an unlikely cause of 2ry HTP, now is more commonly observed depending on the severity of HTP : 8% Stage 2 13% of Stage 3) and 20% of those with resistant hypertension. (10th Annual SMA-ASH Carolinas Georgia Chapter Meeting, 2006)
  16. 16. Primary Aldosteronism  Prevalence .5- 2.0% (5-12% in referral centers)  Etiology  Adrenal adenoma  Bilat adrenal hyperplasia, glucocorticoid suppressible hyperaldo, adrenal carcinoma  Clinical:  May be asymptomatic.  Headache, weakness, paralysis, polyuria  Retinopathy, edema uncommon  Hypokalemia (K normal in 40%), metabolic alkalosis, high-nl Na
  17. 17. Screening for Hyperaldosteronism • Spontaneous hypokalemia (<3.5 mmol/L). • Profound diuretic-induced hypokalemia (<3.0 mmol/L). • Hypertension refractory to treatment with 3 or more drugs. • Incidental adrenal adenomas.
  18. 18. Pheochromocytoma  Catecholamine-producing neuroendocrine tumor that arises from chromaffin cells  Adrenal Medulla : 80-85% pheochromocytomas  Extra-adrenal paragangliomas  Often in head and neck (glomus jugulare) and rarely produce catecholamines.  Some can be dopamine producing.
  19. 19. Epidemiology  Incidence: 1 in 100,000 each year  Prevalence among pts with HTP In adults – 0.1-0.6% In children – 1%  Traditional rule of 10  10% bilateral, 10% familial, 10% extra-adrenal, and 10% malignant. Recent reports found 12-24% of sporadic pheochromocytoma with germline mutation.
  20. 20. Clinical Presentation  Paroxysmal attacks of Headache, palpitations, and sweating.  Adults more often have paroxysmal hypertension (50%) while  Children have sustained hypertension (70-90%)  20% of children will be normotensive at diagnosis.
  21. 21. Screening for Pheochromocytoma • Paroxysmal and/or severe sustained hypertension refractory to usual antihypertensive therapy; • Hypertension and symptoms suggestive of catecholamine excess (two or more of headaches, palpitations, sweating, etc); • Hypertension triggered by B-blockers, MAO inhibitors, clonidine, micturition, changes in abdominal pressure or tyramine containing foods. • Incidentally discovered adrenal mass. • Multiple endocrine neoplasia (MEN) 2A (medullary carcinomas of thyroid) or 2B (mucosal neuromas) ; von Recklinghausen’s neurofibromatosis, or von Hippel-Lindau disease.
  22. 22. Pheochromocytoma – Screening.  Best detected during or immediately after episodes Sensitivity Specificity Plasma free metanephrine >.66nmol/L 99% 89% 24hr urine metanephrine (>3.7nmol/d) 77% (95%) 93% (96%) 24 urine VMA 64% 95% Lenders, et al. JAMA 2002 Mar 20;287(11):1427-34
  23. 23. Pheochromocytoma - Diagnosis  Imaging for localization of tumor Sens Spec PPV NPV (MIBG) scintigraphy 78% 100% 100% 87% CT 98% 70% 69% 98% MRI 100% 67% 83% 100% Akpunonu, et al. Dis Month.October 1996, p688
  24. 24. Cushing’s syndrome/ hypercortisolism  Rare cause of secondary HTN (.1-.6%)  Etiology: pituitary microadenoma, iatrogenic (steroid use), ectopic ACTH, adrenal adenoma  Clinical  Sudden weight gain, truncal obesity, moon facies, abdominal striae, DM/glucose intolerance, HTN, prox muscle weakness, skin atrophy, hirsutism/acne
  25. 25. Cushings syndrome
  26. 26. Cushings syndrome - diagnosis  Screen:  24 Hr Urine free cortisol  >90ug/day is 100% sens and 98% spec  false + in Polycystic Ovarian Syndrome, depression  Confirm  Low dose dexamethasone suppression test  1mg dexameth. midnight, measure am plasma cortisol (>100nmol is +)  Other tests include dexa/CRH suppresion test  Imaging  CT/MRI head (pit) chest (ectopic ACTH tumor)
  27. 27. Coarctation of Aorta  Congenital defect, male>female  Clinical  Differential systolic BP arms vs legs (=DBP)  May have differential BP in arms if defect is prox to L subclavian art  Diminished/absent femoral art pulse  Often asymptomatic  Echo-Doppler, CT angiography, aortography.
  28. 28. Coarctation of Aorta Brickner, et al. NEJM 2000;342:256-263
  29. 29. Hyperthyroidism  33% of thyrotoxic pt develop HTN  Usually obvious signs of thyrotoxicosis  Dx: TSH, Free T4/3, thyroid RAIU
  30. 30. Hypothyroidism  25% hypothyroid pt develop HTN  Mechanism mediated by local control, as basal metabolism falls so does accumulation of local metabolites; relative vasoconstriction ensues
  31. 31. Summary  Screening for 2ry HTN can be expensive and requires clinical suspicion and knowledge of limitations of different tests  General principles:  New onset HTN if <30 or >50 years of age  HTN refractory to medical Rx (>3-4 meds)  Specific clinical/lab features typical for dz : @ Hypokalemia in the absence of diuretic therapy may indicate a state of mineralocorticoid excess @ Excess aldosterone production (Conn’s) @Excess glucocorticoid production (Cushing’s) @Excess T3&T4 (hyperthyroidism) @ Epigastric bruits, differential BP in arms, episodic HTN/flushing/palp.
  32. 32. Summary
  33. 33. Tamer MD, FESC

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