secondary hypertension

1. SECONDARY HYPERTENSION
CAUSES AND DIAGNOSTIC APPROACH
WITH
MANAGEMENT OF HYPERTENSIVE EMERGENCY
BY : DR. RAJ KISHOR SINGH
JR-2, DEPT OF MEDICINE

2. HYPERTENSION
Current clinical criteria for defining hypertension generally are based on the
average of two or more seated blood pressure reading during each of
two or more out patient visits.
• A recent classification a/c to-AHA/2O17ACC recommend blood pressure
criteria for defining-
• Normal bp
• Elevated bp
• Stage 1 and stage 2 hypertension
*this classification slightly different from JNC7

4. • PRIMARY ESSENTIAL HPERTENSION;
TYPES
• SECONDARY HYPERTENSION
• It accounts for only 5-20% of hypertensive patients
• A specific underlying disorder causing the elevation of blood
pressure.
Essential hypertension is the term applied to the 80-95%of hypertensive
patients in which elevated blood pressure results from complex interaction
between multiple genetic and environmental factors

6. Causes of secondary hypertension
• Renal( most common cause)
• Renovascular
• Aortic coarctation
• Obstructive sleep apnea
• Preeclampsia/eclampsia
• Neurogenic-
psycogenic,polyneurits,acute increased intracranial
hypertension, acute spinal cord section
• Endocrine – Hypothyroidism,Hyperthyroidism,Hypercalcemia,Acromegaly
• Drugs/toxin-
High- dose estrogen,
Adrenal steroids,
cyclosporine,TCA,MAOi,Erythropoitin,NSAIDs

7. When to suspect secondary hypertension clinically?
•Absence of family history of hypertension
•Severe hypertension > 180/110 mm Hg with onset at age < 20 years or > 50 years
•Difficult-to-treat or resistant hypertension with significant end-organ damage feature
• Combination of pain (headache), palpitation, pallor and perspiration (phaeochromocytoma)
•Polyuria, nocturia, proteinuria or hematuria – indicative of renal disease
• Absence of peripheral pulses, brachiofemoral delay and abdominal or peripheral vessel bruits
•History of polycystic renal disease or palpable enlarged kidney
•Cushingoid features, multiple neurofibromatosis
•Significant elevation of serum creatinine with use of ACE inhibitors
•Hypertension in children
•History of snoring, daytime somnolence, obesity, short and thick neck – Obstructive Sleep Apnea

8. 1. Renal parenchymal diseases
 Renal diseases is the most common causes of secondary hypertension.
 Secondary HTN is more severe in glomerular diseases than in interstitial diseases.
 Proteinuria >1000mg/day and an active urine sediments are indicator of PRIMARY
RENAL DISEASE
 CAUSES-
1. Glomerulonephritis
2. Pyelonephritis
3. Neprocalcinosis
4. Polycystic kidney disease
5. Neoplasm
6. Analgesic nephropathy
7. Gout with renal failure
8. Obstructive nephropathy
.

9. 2. Renovascular hypertension
Renal artery stenosis is also a common cause of secondary hypertension with 2%
prevalence
The most common cause of renovascular hypertension in India is Takayasu’ disease –a
progressive aortoarteritis.
Takayasu’s disease is a non-specific pan arteritis affecting MOSTLY young women.
Hypertension is mainly due to renal artery stenosis which can be unilateral or bilateral
• The most common cause of renovascular disease in Western population are
atherosclerotic disease in 60% of elderly population and fibromuscular dysplasia in
35% of young
• Fibromuscular dysplasia sometimes produce total occlusion and can be associated
with renal artery aneurysm.
• Atherosclerotic disease cause the proximal segment renal artery stenosis and
fibromuscular dysplasia involves the distal segment of renal artery.

10. Takayasu arteritis of renal artery

11. Renal artery stenosis is more likely if-
• Hypertension is severe, of recent onset or difficult
to control
• Kidneys are asymmetrical in size
• Pulmonary edema occurs repeatedly
• Unexplained deterioration of renal function or detrition of
renal function on ACE inhibitor/ARB.
Diagnostic approach to renovascular hypertension

12. • A paraumbilical bruit is heard in 50-60% of patients with renovascular hypertension and 10%
cases of essential hypertension. A diastolic renal bruit is more specific than systolic bruit.
• Wherever there is a high degree of suspicion, direct selective renal arteriography is
recommended.
• Colour Doppler Ultrasound (CDUS), CT angiography and Gadolinium contrast-MRI angiography
are other good and non-invasive modalities. MRI angiography has higher sensitivity (90%) and
specificity (92%).
• 99Tc – DTPA and I-131 – orthoiodohippurate scan are useful non-invasive investigations.
• CONTRAST ARTERIOGRAPHY remains the gold standard for evaluation and identification of
renal artery lesion . Intra-arterial injection with digital subtraction angiography (DSA) may be
used.

13. 3.Primary Aldosteronism
• Definition:Primary aldosteronism is due to excess aldosterone secretion by the
adrenal cortex ,secreted generally by adenomas and occasionally due to bilateral
adrenocortical hyperplasia.
• The prevalence varies from <2%- 15% of hypertensive individual. This is potentially
curable form of hypertension.
• In these pt. increased aldosterone production is independent of renin-angiotensin
system and the consequences are;
1) Sodium retention
2) Hypertension
3) Hypokalemia
4) Low Plasma renin activity(PRA)

14. • Generally diagnosed at age of 30 -50 years.
• Mostly asymptomatic ; however infrequently, headache, muscle
cramp,polyuria,polydipsia,paresthesias or muscle weakness may be present as
consequences of hypokalemic alkalosis. Hypertension usually mild-moderate but
occasionally may be severe.
• suspected in a case of hypertension showing persistent hypokalemic metabolic
alkalosis in the absence of diuretic therapy.
 Screening Test
a) Plasma Aldosterone to Plasma Renin Activity (PA/PRA) ratio >30:1 (normal < 10) is 90%
sensitive and 91% specific for Primary Hyper Aldosteronism.
b) Unprovoked hypokalemia(<3.1mmol/L)
.

15. Diagnosis
• Confirmed by –demonstrating failure to suppress plasma aldosterone to
<227pmol/L(<10ng/dl) after IV infusion of 2Lof isotonic saline over 4 hour.
• Alternatively confirmed by failure to suppress aldosterone in response to oral
NaCl load,fludrocortisone,or captopril.
 It is usually diagnosed by imaging techniques.
a) CT /HRCT if CT is not diagnostic, then we do
b) Adrenal scintigraphy with 6β-[I131] iodomethyl-19-norcholesterol after
dexamethasone suppression(0.5mg every 6hr for 7 days)

16. 4. CUSHING’S SYNDROME
• Hypertension occurs in 75-80% of patients with Cushing syndrome.
• The mechanism may be related to stimulation of mineralocorticoid receptor by
cortisol and increased secretion of other adrenal steroids.
• This syndrome is related to excess cortisol production due to either ACTH
secretion (from pituitary tumor or an ectopic tumor) or
ACTH independent adrenal production of cortisol as well as
administration of exogenous glucocorticoid.

17. Cushing syndrome

18. Cushing syndrome : Diagnosis
Screening test;
• 24 hr. urine free cortisol :>90ug/day is 100%sensitive and 98% specific.
• Recent evidences suggests that late night salivary cortisol(>5nmol/L) is also
a sensitive and convenient screening test
Confirmatory test-
• Low dose dexamethasone suppression test – Give 1mg dexamethasone at
11 p.m. and draw a sample of blood at 8 a.m. for cortisol measurement
{>50nmol is +ve.}
• CT /MRI SCAN of head (pituitary) and chest (ectopic ACTH TUMOR)

19. 5. PHEOCHROMOCYTOMA
• This is uncommon found in approximately 2 individuals per million
population.
• Pheochromocytoma is catecholamine secreting tumor of adrenal medulla
• Hypertension is primary related to increased circulating catecholamine
(norepinephrine,neuropeptide y) and other vasoactive substance but in few
cases epinephrine is main catecholamine which produce hypotension rather
than hypertension.

20. Pheochromocytoma
Essential of dignosis
• Attack of headache, profuse sweating, episode of palpitation (constitute classical
triad) sustained or paroxysmal hypertension ,anxiety and feeling of impending
doom
• Laboratory testing consists of measuring catecholamine in either using
a) 24 hr. urinary metanephrine excretion
b) Fractionated plasma free metanephrines.
• CT and MRI are both in similar sensitivity of imaging adrenal tumor
• while T2 weighted MRI with gadolinium contrast is better than CT in extra adrenal
tumor.
• MIBG labelled with I-131 is the most specific way of diagnosing adrenal and extra
adrenal pheochromocytomas and PET scan using 18-F flurodeoxyglucose(FDG) is
also useful.

21. 6.Coarctation of aorta
• most common congenital cardiovascular cause of hypertension
• 35% of children is associated with Turner syndrome.
• Coarctaion of aorta consists of localized narrowing of aortic arch just distal to the
origin of the left subclavian artery.
Clinical presentation-
• differential systolic BP in arms and leg
• diminished/absent femoral artery pulse
• May be differential BP in arms if defect is proximal to left subclavian artery.
Diagnosis- may be confirmed by chest x-ray and trans esophageal
echocardiography.
Therapeutic options include surgical repair and balloon angioplasty.

22. Coarctation of aorta
Reason of differential BP Inferior rib notching

23. Miscellaneous cause of Secondary hypertension
Obstructive sleep apnea
The severity of hypertension correlates severity of sleep apnea. Diagnosis can be
confirmed by polysomnography.
Weight loss and administration of continuous positive airway pressure (CPAP) or bi-level
positive airway pressure(BiPAP) during sleep is an effective therapy.
Hypertension during pregnancy is usually caused by PreEclampsia Eclampsia , and gestational
hypertension.
OCP/ESTROGEN:A small increased in BP occurs in most women taking Estrogen or oral contraceptive.
This is caused by volume expansion due to increased angiotensinogen and consequent
activation of RAAS .
Thyroid disease- mild diastolic hypertension in hypothyroidism, where as hyperthyroidism causes
systolic hypertension.
Acute stressful situations cause intense sympathetic discharge and may temporarily induce
hypertension.
Common conditions include Hypoglycemia, exposure to cold, burns, perioperative period and post
head injury
Drugs: NSAID, sympathomimetic amines, glucocorticoids, cocaine and amphetamines can all cause
significant hypertension.

24. MANAGEMENT OF HYPERTENSIVE
EMERGENCY

25. What is hypertensive emergency?
• Hypertensive emergencies are abrupt, severe elevations in blood pressure,
in a patient with underlying hypertension or related to sudden onset
hypertension in previously normotensive individual.
• systolic blood pressure [SBP] greater than 180 mm Hg and/or
• diastolic blood pressure [DBP] greater than 120 mm Hg) associated with the
presence of target-organ dysfunction
Emergency includes ;
• Hypertensive encephalopathy(headache ,confusion, alter mental status)
• Hypertensive nephropathy(hematuria, proteinuria, and acute kidney injury)
• Progressive retinopathy

26. How Hypertensive emergency is different from urgency?
Hypertensive emergency
• Symptomatic severe hypertension
• Presence of acute end organ
damage
• BP reduced within minutes to
hour.
Hypertensive urgency
• Asymptomatic severe hypertension
• Absence of acute end organ damage
• BP reduced within a few hr.

27. Goal of therapy
Goal time BP Target
• First hour Reduce MAP(mean arterial pressure) by no more than 25%
• 2–24 hour maintain SBP 160 mm Hg and/or DBP 110 mm Hg
• 24–48 hour Outpatient BP goals according to the 2017 JNC
Guidelines for Management of High Blood Pressure.
Initially in Patients without encephalopathy or any catastrophic event, it is preferable to
reduce BP OVER an hour or longer with frequent dosing of short acting oral agent
such as
captopril, clonidine and Labetalol.
Excessive reduction of BP may precipitate Renal , coronary, cerebral ischemia.

28. A few hypertensive emergencies with preferred I.V DRUGS.
A)Hypertensive encephalopathy;
• I.V nitroprusside : short acting vasodilator with a rapid onset of action that allows for minute
to minute control of blood pressure.
• I.V Labetalol and Nicardipine are also effective agent.
B)Stroke- recommended drugs are – I.V NICARDIPINE, LABETALOL, NITROPRUSSIDE
a)Acute ischemic stroke :
In such cases antihypertensive should only be used if
SBP >220 mmhg or DBP >130 mmhg
If thrombolytic are to be given BP should be maintained at <185/110.
b) Hemorrhagic stroke : antihypertensive should be started if systolic
BP>180 mmhg ,or diastolic BP >130 mmhg.
c) subarachnoid hemorrhage - antihypertension management is controversial.

29. C)myocardial infarction /unstable angina –recommended iv drugs are – Nitroglycerin
Labetalol
Esmolol
D)acute left ventricular failure -drugs are- Nitroglycerin,
Enalprilate
Loop diuretics
E)Aortic dissection - Nitroprusside
Esmolol
Labetalol
f)Adrenergic crisis- PHENTOLAMINE,
Nitroprusside
g)Preeclampsia/eclampsia - Hydralazine ,
Labetalol

30. Usual intravenous dose of antihypertensive agent.
Labetalol
• 20 mg iv over 2 minute then 40-80 mg at every 10 min interval up to 300 mg total till
target BP is achieved.
• Total dose should not exceed 300 mg.
• 1-2 mg /min infusion till bp is achieved.
Nitroprusside
• Initial 0.3 µgm/kg/min to 10 µgm/kg/min. for every 10 min.
Nitroglycerin
• 5-20 µgm/min. in infusion ,then titrated by 5 µgm/min. at every 3-5 min. interval.