Hypertension

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Hypertension
In
Children
October, 2003
What are we doing here?
1. The Whys and Whats of hypertension.
Importance, epidemiology, definition.
2. The Hows of testing.
Technique, cuff size.
3. The Evaluation.
Coexisting disease, sustained, organ damage,
curable, benefit from tx, acute vs chronic?
4. The Treatment.
Meds, lifestyle
The Whys and Whats
Effects of Hypertension
Sustained elevated blood pressures associated with LVH, and
chronic macro and micro-vascular injury – kidneys, brain,
heart, peripheral vasculature.
Acute elevations associated with encephalopathy,
renal dysfunction/failure, CHF, stroke in otherwise
healthy organs.
Prevalence

1 - 3% of children have hypertension

increases in adolescents

9 - 30 % of adults (and maybe 90%
eventually?)
Blood Pressure Standards
1996 Update on the 1987 task force report
on high blood pressure in children and
adolescents
Standard tables based on age, sex, and height
Pediatrics 88(4):649-658, 1996
Interpretation of Blood
Pressure
Normal < 90 %tile
High Normal 90 - 95 %tile
Hypertension > 95 %tile
Classification of Hypertension
 Significant
95 - 99 %tile
–no acute target organ injury
 Severe
> 99 %tile
Blood Pressure Guestimates – 95th percentile Blood
Pressures for a 50th percentile Child
Systolic BP at 1 to 17 years = 100 + (age in years x 2)
Diastolic BP at 1 to 10 years = 60 + (age in years x 2)
Diastolic BP at 11 to 17 years = 70 + (age in years)
Somu et al Arch Dis Child 2003; 88:302
Severe Hypertension (99th percentile) – add 8
With two caveats:
Is it chronic or acute?
Is there acute or chronic end organ damage?
As always, you treat the patient and not the number.
The Hows of Testing
The Right Cuff

Bladder width 40% of
arm circumference
measured midway
between olecranon
and acromion

Cuff should cover 80-
100% of upper arm
circumference
Standard Position
 Patient
seated
 3-5 minutes rest
 Right arm supported
 Brachial artery at heart
level
Thigh BP
 Supine
 Cuff
arm
guidelines as for
Korotkoff Sounds
 K4
muffling
 K5
disappearance
 Age
limitations
Evaluation
Sustained, coexisting disease, organ damage,
curable, benefit from tx, acute or chronic?
Sustained?
 take your time to evaluate if hx and physical
do not suggest an acute, escalating problem
 repeated bp checks with appropriate cuff in
office or at home
 consider abpm
Patient ROS





abdominal pain, dysuria, frequency, nocturia,
enuresis, cola colored urine, polyuria (intrinsic
renal)
joint pain or swelling, fatigue, rash, Raynaud’s
(autoimmune)
headaches, dizziness, epistaxis, visual problems
weight loss, sweating, pallor, fever, palpitations
(catecholamine secreting tumor, thyroid)
muscle cramps, weakness, constipation
(hyperaldosteronism with hypokalemia)
PMH/Social Hx




Umbilical artery catheter
Substance abuse - steroids, cocaine
Medications - steroids, amphetamines,
sympathomimetics, oral contraceptives, calcineurin
inhibitors, NSAIDS
Herbals – ma huang/ephedra
Family History

hypertension

myocardial infarction

cerebrovascular disease

diabetes mellitus

hyperlipidemia

pheochromocytoma

polycystic kidney disease
Physical Examination





general pallor and edema (renal disease)
low leg pressures & high arm pressures (coarctation
of the aorta)
bruits (renovascular disease or arteritis)
café-au-lait spots or neurofibromas
(neurofibromatosis)
moon facies, buffalo hump (Cushing syndrome)
Physical Examination - 2

Bell palsy, neurologic deficits

fundi with a-v nicking, arteriolar narrowing, flame
lesions

features of Turner syndrome

features of Williams syndrome
Etiology: Newborn

Renal artery thrombosis

Renal artery stenosis

Renal vein thrombosis

Congenital renal abnormalities

Coarctation of the aorta

Bronchopulmonary dysplasia
Etiology: 1 to 6 years

Renal parenchymal diseases

Coarctation of the aorta

Renal artery stenosis
Etiology: 6 to 10 years

Renal artery stenosis

Renal parenchymal disease

Essential hypertension
Etiology: Adolescence

Essential hypertension

Obesity

Renal parenchymal disease

Renal artery stenosis
Renal Causes of Secondary HTN
in Children

Nephropathy

Renovascular

Renal Malformation

Wilms’ Tumor

Obstructive
Nephropathy

Trauma

Metabolic
(cystinosis,
oxalosis)

Pyelonephritis

Segmental
hypoplasia
CV Causes of Secondary HTN in
Children

Aortic Coarctation

Patent Ductus Arteriosus

Renal Artery Stenosis

Arteriovenous Fistula

Aortic Insufficiency

Polycythemia

Takayasu’s Arteritis
Endocrine Causes of Secondary
HTN in Children

Obesity

Pheochromocytoma

Hyperthyroidism

Congenital Adrenal Hyperplasia

17-hydroxylase Deficiency

Primary Hyperaldosteronism

Cushing’s Syndrome
Causes of Secondary HTN in
Children
Neurogenic Tumors
 Neurofibromatosis
 Neuroblastoma
Central Nervous System
 Increased Intracranial Pressure
 Dysautonomia
Causes of Secondary HTN in
Children








Drug Exposure
Sympathomimetic agents
Glucocorticoids
Fracture immobilization
Scoliosis repair
Burns
Heavy metal exposure (lead, cadmium)
Scorpion bites
Tailor Evaluation
History and Physical Examination
Age of patient
Severity of disease
Evaluation: High Normal

Family History

Social History
– tobacco use
– drugs

Examination
– weight
– target organ injury
Evaluation: Phase I

Serum electrolytes

BUN and creatinine

Urinalysis and culture

Echocardiography

+ Hematocrit, plasma lipids

+ Renal ultrasound with doppler
Evaluation: Phase II

plasma renin/aldo

catecholamines
– 24 hour urine
– plasma
Evaluation: Phase III
Directed by history, physical and prior
studies

VCUG, DMSA

Renal biopsy for nephropathy

CT or MRI for tumor
Evaluation: Phase III
continued

steroid suppression/stimulation

adrenal scintigraphy/MIBG

renal angiography for renal artery
stenosis
Reasons to consider arteriogram
Severe resistant hypertension without other
etiology
Increased PRA with normal noninvasive tests
Bruit
Solitary kidney with severe hypertension
Renal Arteriography
Trachtman et al, P. Neph 14:816-819
Abnormal
(N=12)
Age
11.8
Sex (M:F)
6:6
Race (W:B:O)
5:5:2
Duration (mo)
12.1
Peak BP
182/113
Creatinine
1.1
Prior Rx
4
Abnormal imaging studies
Renal US
5/9
Renal scan
2/3
Normal
(N=16)
11.5
6:10
9:6:1
9.8
175/102
1.0
5
1/9
2/3
Chronic Therapy
Non-pharmacologic
Primary hypertension
– weight control
– exercise
– stress reduction
– dietary (salt and calories)
– elimination of contributory medications
– smoking cessation
Chronic Therapy
Pharmacologic

Diuretics

Beta-adrenergic blockers

Angiotensin converting enzyme inhibitors

ARB’s

Calcium channel blockers

Vasodilators

Alpha-1-adrenergic blockers

Alpha-2-agonists

Selective aldosterone antagonists (Eplerenone)

Dopamine-1 agonist (Fenoldopam)
Diuretics






Concerns
– Lipid disorders
Contraindications
– salt wasting nephropathy
– athletes in hot weather
Reserve for those with Renal Disease
Thiazide - GFR 50 - 100 %
Furosemide - GFR < 50%
Aldactone - Hyperaldosterone states
– Nephrotic syndrome, CHF, Liver failure
Beta-blockers



Concerns
– Hyperlipidemia
– Asthma
– Cardiovascular effects
Cardioselective
– Atenolol
– Metoprolol
Non-selective
– Propranolol
Angiotensin Converting
Enzyme Inhibitors

Cautions
– Renal Artery Stenosis
– Solitary Kidney
– Renal Failure
– Infants
– Hyperkalemia
– Cough
– Angioedema
Calcium Channel Blockers

Short acting v. Long acting

Action: dilate peripheral arterioles by
blocking calcium transit

Nifedipine

Amlodipine

Felodipine

(Verapamil, Diltiazem)
Vasodilators

Side effects
– Tachycardia
– Water retention

Hydralazine

Minoxidil

Diazoxide

Sodium Nitroprusside
Alpha-1-Adrenergic Blockers

Side effect first dose hypotension

Modest potency

Prazosin/doxazocin

Phenoxybenzamine/phentolamine
pheochromocytoma
Central Alpha-2-Agonists

Side effects
– Somnolence
– Rebound hypertension

Indications
– Attention Deficit Disorder

Clonidine

Methyldopa

Guanabenz
Combination action
Labetalol – alpha (weak) and beta (non selective)
po or iv
lipids unchanged
Antihypertensives in Newborns
Diazoxide
iv
Initial: 1-2 mg/kg/dose
Max: 5 mg/kg/dose q 2-6 hrs prn
Nitroprusside iv
Initial: 0.25-0.5 mch/kg/min,
double q 15-30 min
Hydralazine iv, po Initial: 0.1-0.5 mg/kg/dose q 3-6 hrs
Max: 2 mg/kg/dose q 6 h (po 2x iv dose)
Propranolol iv,po Initial: po 0.25 mg/kg/dose q 6-8 hrs
Max: po 1-4 mg/kg/dose q 6-8 hrs
Initial: iv 0.01-0.15 mg/kg/dose q 6 hrs
Max: iv 4 mg/kg/dose q 6 hrs
Captopril
po
Initial: 0.01 mg/kg/dose q 6 hrs
Max: 0.1-1.0 mg/kg/dose q 6 hrs
Hypertensive Emergencies
Nicardipine 1-3 mcg/kg/min iv
Labetalol
1-3 mg/kg/hr iv
Esmolol
Load 500 mcg/kg, then 50-250 mcg/kg/min
Nitroprusside 0.5-0.8 mcg/kg/min iv
Enalapril
5-10 mcg/kg/dose iv q 6-12 hrs
Diazoxide
1-2 mg/kg/dose iv q 10-15 min
Phentolamine 0.1-0.2 mg/kg/iv (pheo)
Nifedipine
0.25-0.5 mg/kg po (max dose 20 mg)
Hydralazine 0.1-0.5 mg/kg iv ( max dose 25 mg)
Propranolol 0.01-0.05 mg/kg iv over 1 hr (max 10 mg)
Lasix
1-4 mg/kg iv
Fenoldopam 0.1 – 0.8 mcg/kg/min
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