Secondary hypertension work up
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Transcript of Secondary hypertension work up
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الرحمن ا بسمالرحيم
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Secondary Hypertension Work-up
By
Tamer Moustafa Abe Elghany
MD, FESC
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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
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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 :
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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
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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.
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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
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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
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Renovascular HTN - diagnosis
Physical findings (bruit) Duplex U/S Captopril renography Magnetic Resonance Angiography Renal Angiography
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RAS screening/diagnosticsSens 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
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Screening Strategy (Index of suspicion & need intervention)
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Fibromuscular dysplasia
10-25% of all RAS Young female, age 15-40 Medial disease 90%, often involves
distal RA
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Atherosclerotic RAS
75-90% of RAS Usually men, age>55, other atherosclerotic dz
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Fibromuscular Dysplasia, beforeand after PTRA
Atherosclerotic RAS before and after stentSafian & Textor. NEJM 344:6;
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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)
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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
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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.
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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.
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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.
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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.
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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.
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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
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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
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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
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Cushings syndrome
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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)
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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.
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Coarctation of Aorta
Brickner, et al. NEJM 2000;342:256-263
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Hyperthyroidism
33% of thyrotoxic pt develop HTN Usually obvious signs of thyrotoxicosis Dx: TSH, Free T4/3, thyroid RAIU
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Hypothyroidism
25% hypothyroid pt develop HTN Mechanism mediated by local control, as
basal metabolism falls so does accumulation of local metabolites; relative vasoconstriction ensues
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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.
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Summary
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Tamer MD, FESC