Hypertension in children Pediatric hypertension This ppt is made by me using textbook of pediatrics,Nelson 20th edition.

1. HYPERTENSION
IN
CHILDREN
By:Dr.Chirag Patel
Nirmal Hospital,
Surat

2.  Primary (essential) hypertension occurs
commonly in adults and, if untreated, is a major risk
factor for myocardial infarction, stroke, and renal
failure.
 In adults with hypertension, 5 mm Hg  DBP--
coronary artery disease risk 20% , stroke risk
35%.
 hypertension is implicated in the etiology of nearly 50% of adults with
end-stage renal disease. The prevalence of adult hypertension
increases with age, ranging from 15% in young adults to 60% in
individuals older than 65 yr.

3.  Hypertensive children, although usually asymptomatic,
already manifest evidence of target organ damage.
 Up to 40% of hypertensive children have left ventricular
hypertrophy and hypertensive children have increased
carotid intima—media thickness, a marker of early
atherosclerosis.
 Primary hypertension during childhood often tracks into
adulthood.
 Children with BP >90th percentile ---2.4-fold greater risk
of hypertension as adults.
 nearly half of hypertensive adults had BP >90th
percentile as children.
 association between childhood hypertension and early
atherosclerosis in young adulthood.

4. PREVALENCE OF HYPERTENSION
IN CHILDREN
 In infants and young children, systemic hypertension is
uncommon, with a prevalence of <1%, when present, it
is often indicative of an underlying disease process
>90% cases(secondary hypertension).
 Severe and symptomatic hypertension in children is
usually caused by secondary hypertension.
 In contrast, the prevalence of primary essential
hypertension, mostly in older school-age children and
adolescents, has increased in prevalence in parallel with
the obesity epidemic.
 School screening studies show that approximately 10% of U.S. youth overall
have prehy-pertension and 2.5% have hypertension. The influence of obesity
on elevated BP is evident in children as young as 2-5 yr old. Approximately
20% of American youth are obese, and up to 10% of obese youth have
hypertension.

5. DEFINITION OF HYPERTENSION
 Hypertension:
systolic blood pressure (SBP) and/or diastolic BP
that is more than 95th percentile for age, sex, and
height specific on at least three occasions 1-3
weeks apart.
 Prehypertension:
SBP/DBP between 90th to 95th percentile persistently.
 In adolescents beginning at age 12 yr,
prehypertension is defined as BP between 120/80
mm Hg and the 95th percentile.

6.  white coat hypertension :
BP levels 95th percentile in a medical setting but
normal BP outside of the hospital.
 Stage 1 hypertension:
SBP/DBP >95th percentile but <5 mm Hg above the
99th percentile
 Stage 2 hypertension:
SBP/DBP > 99th percentile plus 5 mm Hg

7.  Stage 1 hypertension, if asymptomatic and without
target organ damage: allows time (1-2 week) for
evaluation before starting treatment
 Stage 2 hypertension calls for more prompt
evaluation and pharmacologic therapy
(Fig. 445-1).

9. MEASUREMENT OF BP IN CHILDREN
 children 3 yr or older BP checked during every
healthcare episode (the AHA recommends annual
BP checks).
 Selected children <3 yr old should also have their
BP checked, including those with a history of
prematurity, congenital heart disease, renal
disease, solid-organ transplant, cancer, treatment
with drugs known to raise BP, other illnesses
associated with hypertension (neurofibromatosis,
tuberous sclerosis, others), or evidence of
increased intracranial pressure.

10.  preferred method:auscultation and a BP cuff appropriate for
the size of the child's arm should be used.
 Elevated readings should be confirmed on repeat visits before
determining that a child is hypertensive.
 measured with child in sitting position after a period of quiet
for at least 5 min.
 Careful attention to cuff size to avoid over diagnosis,
 Cuff too short or narrow artificially increases BP readings.
 wide variety of bladder sizes should be available in any medical office where
children are routinely seen.
 An appropriate sized cuff has an inflatable bladder that is at
least 40% of the arm circumference at a point midway along
the upper arm.
 The inflatable bladder should cover at least two thirds of the
upper arm length and 80-100% of its circumference.

11.  Systolic pressure is indicated by appearance of the
1st Korotkoff sound.
 Diastolic pressure has been defined by consensus
as the 5th Korotkoff sound.
 Palpation is useful for rapid assessment of SBP,
although the palpated pressure is generally about
10 mm Hg less than that obtained via auscultation.
 Oscillometric techniques are used frequently in
infants and young children, but they are susceptible
to artifacts and are best for measuring mean BP.

12. AMBULATORY BLOOD PRESSURE MONITORING
(ABPM
 Ambulatory blood pressure monitoring (ABPM) is a procedure
where the child wears a device that records BP frequently,
usually every 20-30 min, throughout a 24 hr period while the child
goes about usual daily activities, including sleep.
 This allows calculation of the mean daytime BP, sleep BP, and
mean BP over 24 hr.
 It determine proportion of BP measurements that are in the
hypertensive range (BP load) and whether there is an
appropriate decrease in BP during sleep (nocturnal dip).
 ABPM particularly useful in the evaluation for white coat
hypertension and determining risk of hypertensive target organ
damage, evaluating resistance to pharmacologic therapy, and
evaluating patients with hypotensive episodes on
antihypertensive medication.
 ABPM is also useful for certain special populations, such as
children with chronic kidney disease, kidney transplant, and
diabetes mellitus and provide important information on
cardiovascular risk that cannot be determined as well by office
measurements.

13. ETIOLOGY AND PATHOPHYSIOLOGY
 BP product of cardiac output and peripheral vascular
resistance
 increase in either cardiac output or peripheral resistance
results in an increase in BP
 if 1 of these factors increases while the other decreases, BP
may not increase.
 secondary hypertension : result of another disease process
 primary (essential) hypertension:When no identifiable cause
 Many factors, including heredity, diet, stress, and obesity
 Secondary hypertension most common in infants and
younger children
 younger the child, the higher the BP and the presence of
symptoms related to hypertension, the more likely underlying
secondary cause of hypertension.

14.  Many childhood diseases can be responsible for
chronic hypertension (Table 445-1) or acute/
intermittent hypertension (Table 445-2).
 Hypertension in the premature infant:umbilical
artery catheterization and renal artery thrombosis.
 Hypertension during early childhood:by renal
disease,coarctation of the aorta, endocrine
disorders, or medications.
 In older school-age children and adolescents,
primary hypertension becomes increasingly
common

19.  Secondary hypertension in children : MC caused by renal
abnormalities; cardiovascular disease or endocrinopathies are
additional etiologies.
 Renal (chronic glomerulonephritis, reflux or obstructive nephropathy,
hemolytic uremic syndrome, polycystic or dysplastic renal diseases), or
renovascular hypertension, account for approximately 90 %of
children with secondary hypertension.
 Renal parenchymal disease and renal artery stenosis lead to
water and sodium retention thought to be, in part, secondary
to increased renin secretion.
 Coarctation of aorta should always be considered.
 Several endocrinopathies associated with hypertension:
involving the thyroid, parathyroid, and adrenal glands.
 Systolic hypertension and tachycardia ommon in
hyperthyroidism.
diastolic pressure is not usually elevated.

20.  Hypercalcemia, whether secondary to
hyperparathy-roidism or other causes, often results
in mild elevation in BP because of an increase in
vascular tone.
 Adrenocortical disorders (aldosterone- secreting
tumors, sodium retaining congenital adrenal
hyperplasia, Cushing syndrome) may produce
hypertension in patients with increased
mineralocorticoid secretion.
 conditions associated with real or apparent
mineralocorticoid excess (Table 445-3) and thus a
suppressed renin level form of secondary
hypertension.

22.  Pheochromocytomas: catecholamine-secreting tumors
give rise to hypertension
because cardiac and peripheral vascular effects of
epinephrine and norepinephrine.
 Children with pheochromocytoma usually have
sustained rather than intermittent or exercise-induced
hypertension.
 Pheochromocytoma develops in approximately 5% of
patients with neurofibromatosis.
 Rarely, secondary hypertension can caused by
pseudohyperaldosteronism,which leads to elevated BP
in the face of a suppressed renin level.
 Such disorders include Liddle syndrome, apparent
mineralocorticoid excess, and dexamethasone
suppressible aldosteronism.

23.  Altered sympathetic tone can be responsible for
acute or intermittent elevation of BP in children with
Guillain-Barré syndrome, poliomyelitis, burns, and
Stevens-Johnson syndrome.
 Sympathetic outflow from the central nervous
system affected by intracranial lesions.
 Drugs abuse, therapeutic agents, and toxins
 Cocaine provoke rapid increase in BP, can result in
seizures or intracranial hemorrhage.
 Phencyclidine:transient hypertension that may
become persistent in chronic abusers.
 Tobacco

24.  Sympathomimetic agents used as nasal
decongestants, appetite suppressants, and
stimulants for attention deficit disorder produce
peripheral vasoconstriction and varying degrees of
cardiac stimulation.
 Oral contraceptives to be suspected as a cause of
hypertension in adolescent girls, incidence is lower
with use of low-estrogen preparations.
 Immunosuppressant agents such as cyclosporine
and tacrolimus cause hypertension in organ
transplant recipients, and the effect is exacerbated
by the co-administration of steroids.
 heavy metal poisoning

25.  Children and adolescents with primary (essential) hypertension
commonly overweight, often strong family history of hypertension,usually
BP values at or only slightly above the 95th percentile for age.
 Primary hypertension MC form of hypertension in adults, recognized
more often in adolescents than in young children.
 cause of primary hypertension multifactorial:
obesity,
genetic alterations in calcium and sodium transport,
vascular smooth muscle reactivity,
renin—angiotensin system,
sympathetic nervous system overactivity,
insulin resistance
 lowering of uric acid levels results in lower BP in overweight youth with
hypertension or prehypertension.
 Some children and adolescents demonstrate salt-sensitive hypertension,
a factor which ameliorated with weight loss and sodium restriction.

26.  Normotensive children of hypertensive parents may
show abnormal physiologic responses that are similar to
those of their parents.
 When subjected to stress or competitive tasks, the
offspring of hypertensive adults, as a group, respond
with greater increases in heart rate and BP than do
children of normotensive parents.
 some children of hypertensive parents may excrete
higher levels of urinary catecholamine metabolites or
may respond to sodium loading with greater weight gain
and increases in BP than do those without a family
history of hypertension.
 The abnormal responses in children with affected
parents black population > white individuals.

27. CLINICAL MANIFESTATIONS
 primary hypertension:
 usually asymptomatic;
 BP elevation mild and detected during routine
examination or evaluation before athletic
participation.
 children may be obese.

28.  secondary hypertension:
o BP elevations ranging from mild to severe.
 usually not produce symptoms till pressure sustained or
rising rapidly
 clinical manifestations may show
 underlying disease process e.g.growth failure in
children with chronic kidney disease
 With substantial hypertension,
 headache,
 dizziness,
 epistaxis,
 anorexia,
 visual changes,
 seizures may occur

29.  Hypertensive encephalopathy (generalized or
posterior reversible encephalopathy syndrome)
 headache,
 vomiting,
 temperature elevation,
 visual disturbances,
 ataxia,
 depressed level of consciousness,
 CT abnormalities,
 seizures (Fig. 445-2).

31.  Cardiac failure, pulmonary edema, and renal
dysfunction (malignant hypertension) may occur in
marked hypertension.
 Bell palsy may be seen in asymptomatic or symptomatic
patients.
 Hypertensive crisis:
 decreased vision (retinal hemorrhages of hypertensive
retinopathy)
 papilledema,
 encephalopathy (headache, seizures, depressed level of
consciousness),
 heart failure,
 accelerated deterioration of renal function.

32.  Subclinical hypertensive target-organ injury is a
common clinical manifestation in children with essential
hypertension.
 left ventricular hypertrophy detected in up to 40% of
hypertensive children by echocardiography .
 Other markers of target organ damage in hypertensive
children:
 increased carotid intima—media thickness, hypertensive
retinopathy,
 microalbuminuria.
o Children with pre-hypertension also have evidence of
target organ damage, often at a magnitude intermediate
between that of normotensive and hypertensive children.

33. DIAGNOSIS
 evaluation of the child with chronic hypertension
should be to uncover underlying causes
 evaluating for comorbidities
 screening for evidence of target organ damage
 extent of evaluation for underlying causes depends
on suspected type of hypertension
 When secondary hypertension is a strong
consideration, as in younger children with severe
and symptomatic hypertension, an extensive
evaluation may be necessary (Fig. 445-3).
 Alternatively, overweight adolescents with a family
history who have mild elevations of BP may need
only a limited number of tests.

35.  careful history and physical examination in all cases
 family history for early cardiovascular events should be
obtained.
 Growth parameters to detect evidence of chronic
disease.
 BP in all 4 extremities to detect coarctation (thoracic or
abdominal) of the aorta.
 Unless the history and physical examination suggest
another cause, children with confirmed hypertension
should have an evaluation to detect renal disease,
including urinalysis, electrolytes, blood urea nitrogen,
creatinine, complete blood count, urine culture, and
renal ultrasound.
 Table 445-4 identifies other features of the physical
examination that may provide evidence of an underlying
cause of hypertension.

38.  Table 445-5 provides a more complete list of tests
to consider in the clinical evaluation of a child with
confirmed hypertension.
 serum potassium essential because hypokalemia
may be present in Liddle syndrome, glucocorti-coid
remedial aldosteronism, and apparent
mineralcorticoid excess syndrome
 Hyperkalemia may be seen in Gordon syndrome.

41.  Renovascular hypertension is often associated with other
diseases (Table 445-6) but may be isolated.

42.  Magnetic resonance or CT
angiography can reveal
renal artery stenosis, but
fluoroscopic angiography
may be needed, especially
to detect intrarenal arterial
stenosis (Fig. 445-4).

43.  Primary hypertension often clusters with other risk
factors.
 All hypertensive children should be screened for
comorbidities that may increase cardiovascular risk
fasting lipid panel for hyperlipidemia and
fasting glucose level for glucose intolerance
 sleep history in children with confirmed
hypertension to screen for sleep disordered
breathing, that is associated with high BP,
particularly in overweight children.

44.  What is most common manifestation of target-organ
damage in hypertensive children ?
 Left ventricular hypertrophy (LVH)
 All children with confirmed hypertension should
have echocardiography to evaluate for the
presence of LVH.
 Left ventricular mass measurements should be
indexed to height (m2) to account for effect of body
size.
 The presence of LVH is an indication to treat the
hypertension with pharmacologic therapy.

45. PREVENTION
 Prevention of high BP as part of the prevention of
cardiovascular disease and stroke,
 Other risk factors for cardiovascular disease
• Obesity
• elevated serum cholesterol levels
• high dietary sodium intake
• sedentary lifestyle
• alcohol and tobacco use
o increase in arterial wall rigidity and blood viscosity is
associated with exposure to the components of tobacco
may exacerbate hypertension.
o Population approaches to prevention of primary
hypertension include a reduction in obesity, reduced
sodium intake, and an increase in physical activity
through school- and community-based programs.

46. TREATMENT
 The Fourth Report recommended a management
algorithm for children with confirmed hypertension
according to whether the child has prehypertension,
stage 1 hypertension, or stage 2 hypertension (see
Figs. 445-1 and 445-5).

48.  mainstay of therapy for children with asymptomatic mild
hypertension without evidence of target-organ damage
is therapeutic lifestyle modification with dietary changes
and regular exercise.
 Weight loss is primary therapy in obesity-related
hypertension.
 It is recommended that all hypertensive children have
diet increased in fresh fruits, fresh vegetables, fiber, and
nonfat dairy, and reduced in sodium. ,
regular aerobic physical activity for at least 30-60 min on
most days
reduction of sedentary activities to less than 2 hr per
day

49.  Indications for pharmacologic therapy :
 symptomatic hypertension,
 secondary hypertension,
 hypertensive target organ damage,
 diabetes (types 1 and 2),
 persistent hypertension despite nonpharmacologic
measures
(Table 445-7).

52.  When indicated, antihypertensive medication should be
initiated as a single agent at low dose (see Fig. 445-5).
 The dose can then be increased until the goal BP is achieved.
 When to add second drug?
 Once the highest recommended dose is reached or if the child
develops side effects, then a second drug from a different
class can be added.
 Acceptable drug classes for use in children include
angiotensin-converting enzyme inhibitors, angiotensin
receptor blockers, n-blockers, calcium channel blockers, and
diuretics.
 Details on recommended doses of different classes of antihypertensive
medications for children can be found in the Fourth Report available free
online at www.nhlbi.nih.gov/health/ prof/heart/hbp/hbp_ped.pdf.

53.  The goal of therapy for hypertension should be to
reduce BP below the 95th percentile
except in the presence of chronic kidney disease,
diabetes, or target-organ damage, when the goal
should be to reduce BP to less than the 90th
percentile.
 Angiotensin-converting enzyme inhibitors or
angiotensin receptor blockers should be used for
children with diabetes and microalbuminuria or
proteinuric renal disease.
 P-Blockers or calcium channel blockers should be
considered for hypertensive children with migraine
headaches

54. SEVERE, SYMPTOMATIC HYPERTENSION
 Severe, symptomatic hypertension is a
hypertensive emergency that is often accompanied
by cardiac failure, retinopathy, renal failure,
encephalopathy,and seizures.
 IV is preferred so that the fall in BP can be carefully
titrated (Table 445-8).

56. SEVERE, SYMPTOMATIC HYPERTENSION
 Drug choices include labetalol, nicardipine, and
sodium nitroprusside.
 Why stepwise reduction in pressure should be
planned?
Because too rapid a reduction in BP may interfere
with adequate organ perfusion
 In general, the pressure should be reduced by 10%
in the 1st hr, and 15% more in the next 3-12 hr, but
not to normal during the acute phase of treatment.

57.  Hypertensive urgencies, usually accompanied by
few serious symptoms such as severe headache or
vomiting, can be treated either orally or
intravenously.
 The Fourth Report also includes detailed information on
antihypertensive drugs used for the management of severe
hypertension in children.

58.  Treatment of secondary hypertension must also focus
on the underlying disease such as chronic renal
disease, hyperthyroidism, adrenal—genital syndrome,
pheochromocytoma, coarctation of the aorta, or
renovascular hypertension.
 The treatment of renovascular stenosis includes
antihypertensive medications, angioplasty, or surgery
(Fig. 445-6).
 If bilateral renovascular hypertension or renovascular
disease in a solitary kidney is suspected, drugs acting
on the renin-angiotensin axis are usually contraindicated
because they may reduce glomerular filtration rates and
produce renal failure.

60.  SBP
90+[2*Age (yrs)]
 SBP 5thcentile Lowerlimit
70+[2*Age (yrs)]
 DBP 50+[2*Age (yrs)]
 DBP 60 60+Age(yrs)
 PP SBP-DBP(N:30-60 mmHG)
 MAP DP+1/3PP