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الرحمن ا بسمالرحيم
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 overlooked and underscreened Controversy over screening and
treatment in some cases
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 :
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
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.
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
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
Renovascular HTN - diagnosis
Physical findings (bruit) Duplex U/S Captopril renography Magnetic Resonance Angiography Renal Angiography
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
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, beforeand after PTRA
Atherosclerotic RAS before and after stentSafian & Textor. NEJM 344:6;
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)
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
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.
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.
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.
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.
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.
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
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
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
Cushings syndrome
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)
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.
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 RAIU
Hypothyroidism
25% hypothyroid pt develop HTN Mechanism mediated by local control, as
basal metabolism falls so does accumulation of local metabolites; relative vasoconstriction ensues
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.
Summary
Tamer MD, FESC
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