‫الرحمن‬ ‫ا‬ ‫بسم‬
‫الرحيم‬
Secondary
Hypertension
Work-up
By
Tamer Moustafa Abe Elghany
MD, FESC
Overview
 “ Secondary” HTN accounts for ~5-10%
of other cases and represents potentially
curable disease
 Often overlook...
Overview
 Testing for 2ry HTN can be expensive and requires high index of
clinical suspicion.
 General principles:
 New...
Routine Laboratory Tests
1. Urinalysis
2. Complete blood count
3. Blood chemistry (potassium, sodium and
creatinine)
4. Fa...
Renal Parenchymal Disease
 Common cause of secondary HTN (2-
5%)
 HTN is both cause and consequence of
renal disease
 A...
Renovascular HTN
 Incidence 1-30%
 Etiology
 Atherosclerosis 75-90%
 Fibromuscular dysplasia 10-25%
 Other
 Aortic/r...
Renovascular HTN - Clinical
 History
 Onset HTN age <30 or >55
 Negative FH of HTN
 Sudden onset uncontrolled HTN in p...
Renovascular HTN - diagnosis
 Physical findings (bruit)
 Duplex U/S
 Captopril renography
 Magnetic Resonance Angiogra...
RAS screening/diagnostics
Sens Spec Limitation/Etc
Duplex U/S 90-95% 60-90%
Operator dependent, 10-20%
Captopril
Renograph...
Screening Strategy (Index of suspicion & need intervention)
Fibromuscular dysplasia
 10-25% of all RAS
 Young female, age 15-40
 Medial disease 90%, often involves
distal RA
Atherosclerotic RAS
 75-90% of RAS
 Usually men, age>55, other atherosclerotic dz
Fibromuscular Dysplasia, before
and after PTRA
Atherosclerotic RAS before and after stent
Safian & Textor. NEJM 344:6;
Primary Aldosteronism
Primary Aldosteronism, previously felt to be an
unlikely cause of 2ry HTP, now is more
commonly obs...
Primary Aldosteronism
 Prevalence .5- 2.0% (5-12% in referral centers)
 Etiology
 Adrenal adenoma
 Bilat adrenal hyper...
Screening for Hyperaldosteronism
• Spontaneous hypokalemia (<3.5 mmol/L).
• Profound diuretic-induced hypokalemia (<3.0
mm...
Pheochromocytoma
 Catecholamine-producing neuroendocrine
tumor that arises from chromaffin cells
 Adrenal Medulla : 80-8...
Epidemiology
 Incidence: 1 in 100,000 each year
 Prevalence among pts with HTP
In adults – 0.1-0.6%
In children – 1%
...
Clinical Presentation
 Paroxysmal attacks of Headache, palpitations,
and sweating.
 Adults more often have paroxysmal hy...
Screening for Pheochromocytoma
• Paroxysmal and/or severe sustained hypertension refractory to usual
antihypertensive ther...
Pheochromocytoma – Screening.
 Best detected during or immediately after
episodes
Sensitivity Specificity
Plasma free
met...
Pheochromocytoma - Diagnosis
 Imaging for localization of tumor
Sens Spec PPV NPV
(MIBG) scintigraphy 78% 100% 100% 87%
C...
Cushing’s syndrome/
hypercortisolism
 Rare cause of secondary HTN (.1-.6%)
 Etiology:
pituitary microadenoma,
iatrogenic...
Cushings syndrome
Cushings syndrome - diagnosis
 Screen:
 24 Hr Urine free cortisol
 >90ug/day is 100% sens and 98% spec
 false + in Pol...
Coarctation of Aorta
 Congenital defect, male>female
 Clinical
 Differential systolic BP arms vs legs
(=DBP)
 May have...
Coarctation of Aorta
Brickner, et al. NEJM 2000;342:256-263
Hyperthyroidism
 33% of thyrotoxic pt develop HTN
 Usually obvious signs of thyrotoxicosis
 Dx: TSH, Free T4/3, thyroid...
Hypothyroidism
 25% hypothyroid pt develop HTN
 Mechanism mediated by local control, as
basal metabolism falls so does
a...
Summary
 Screening for 2ry HTN can be expensive and requires clinical
suspicion and knowledge of limitations of different...
Summary
Tamer
MD, FESC
Secondary hypertension work up
Secondary hypertension work up
Secondary hypertension work up
Secondary hypertension work up
Secondary hypertension work up
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  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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