Hi Per Tension en La Infancia y Adolescencia

8/8/2019 Hi Per Tension en La Infancia y Adolescencia

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Hypertension in Children and Adolescents

Mark M. Mitsnefes, MD, MS

Division of Nephrology and Hypertension, Cincinnati Childrens Hospital Medical Center andUniversity of Cincinnati College of Medicine, MLC 7022, 3333 Burnet Avenue, Cincinnati,

OH 45229-3039, USA

Hypertension is one of the most common health problems in the United States

and a powerful independent risk factor for cardiovascular and renal disease.

According to the National Health and Nutrition Examination Survey, at least

65 million American adults, or nearly one third of the adult population, havehypertension, which is defined as blood pressure (BP) !140/90 mm Hg. Another

one quarter of the US adult population have prehypertension, which is defined as

systolic blood pressure (SBP) between 120 and 139 mm Hg or diastolic blood

pressure (DBP) between 80 and 89 mm Hg.

Until recently, the incidence of persistent hypertension in children has been

low, with a range of 1% to 3% [1]. Recent data indicate that over the last decade,

however, average BP levels have risen substantially among American children

[2,3]. Obesity and other lifestyle factors, such as physical inactivity and increased

intake of high-calorie, high-salt foods, are thought to be responsible for this trend.As a result, the frequency of hypertension may be increasing, as evident in a

recent study of 5102 children in Houston schools in whom the prevalence of

hypertension was 4.5% [4]. Despite this relatively low frequency of hypertension

in children, it is currently recognized as an important health issue. First, there

is increasing evidence that hypertension has its antecedents during childhood,

because adult BP often correlates with childhood BP [5]. Second, hypertension in

children is viewed as a significant risk factor for the development of cardio-

vascular disease in adulthood [6,7].

0031-3955/06/$ see front matterD 2006 Elsevier Inc. All rights reserved.

doi:10.1016/j.pcl.2006.02.008 pediatric.theclinics.com

E-mail address: [email protected]

Pediatr Clin N Am 53 (2006) 493512
http://dx.doi.org/10.1016/j.pcl.2006.02.008http://pediatric.theclinics.com/mailto:[email protected]:[email protected]://pediatric.theclinics.com/http://dx.doi.org/10.1016/j.pcl.2006.02.008http://-/?-http://-/?-http://-/?-http://-/?-http://-/?-


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Definition

Unlike in adults, in whom the definition and classification of hypertension are based on health risks attributed to increased BP, in children, the definition of

hypertension is based on normative data. The Fourth Report on High Blood

Pressure in Children and Adolescents provided updated normative data for BP

for healthy children aged 1 to 17 years according to age, gender, and height for

fiftieth, ninetieth, and ninety-fifth and ninety-ninth percentiles [8]. The report

defined normal BP as systolic and diastolic values less than the ninetieth

percentile. Prehypertension is defined as an average SBP or DBP between the

ninetieth and ninety-fifth percentiles or if BP exceeds 120/80 mm Hg, even if

below the ninetieth percentile. Hypertension is defined as average SBP or DBPthat is ! ninety-fifth percentile on three or more occasions. The report also

defined the stages of hypertension in children. Stage 1 hypertension is defined as

an average systolic or diastolic BP between the ninety-fifth and ninety-ninth

percentile + 5 mm Hg; stage 2 hypertension is defined as a persistent BP above

the ninety-ninth percentile + 5 mm Hg. For example, in a 12-year-old boy with

height in the fiftieth percentile (Table 1), SBP of 123 to 136 mm Hg and DBP of

81 to 94 mm Hg represent stage 1 hypertension; BP N136/94 mm Hg represents

stage 2 hypertension. White-coat hypertension is defined as a persistently

elevated average office SBP or DBP more than the ninety-fifth percentile andaverage awake ambulatory reading outside the physician office less than the

ninety-fifth percentile. Masked hypertension or isolated ambulatory hypertension

recently emerged as a new entity and is defined as a condition in which patients

have normal office readings but elevated BP elsewhere [9]. Recent pediatric

studies have shown that masked hypertension is associated with left ventricular

hypertrophy (LVH), an independent predictor of cardiovascular morbidity and

mortality in adults [10,11].

Table 1

Blood pressure status in 12-year-old boy by age and height percentile

BP %

SBP DBP

Height percentile Height percentile

5th 10th 25th 50th 75th 90th 95th 5th 10th 25th 50th 75th 90th 95th

50th 101 102 104 106 108 109 110 59 60 61 62 63 63 64

90th 115 116 118 120 121 123 123 74 75 75 76 77 78 79

95th 119 120 122 123 125 127 127 78 79 80 81 82 82 8399th 126 127 129 131 133 134 135 87 87 88 89 90 90 91

Normal BP (b90th percentile): BP b120/76.

Prehypertension (BP between 90th and 95th percentile or b120/80): SBP of 120122 and DBP of

7680.

Stage 1 hypertension (BP between the 95th and 99thpercentile + 5 mm Hg): SBP of 123136 and DBP

of 8194.

Stage 2 hypertension (BP above the 99th percentile + 5 mm Hg): BP N136/94.

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Measurement of blood pressure in children

The accurate measurement of BP in children requires careful attention touse of standard procedure and equipment in an appropriate environment. The

National High Blood Pressure Education Program Working Group on High

Blood Pressure in Children and Adolescents recommended that children aged

3 years and older have their BP checked during routine visits and emergency

visits. BP should be measured in children b3 years old with a history of prema-

turity, low birth weight, congenital heart disease, kidney diseases, or a family

history of congenital kidney disease and solid-organ and bone marrow transplant.

Young children with systemic illnesses associated with hypertension (eg, neuro-

fibromatosis, tuberous sclerosis) or children who take drugs known to raise BPshould have their BP checked [8].

BP should be measured at least twice on each occasion in a childs right arm

after at least 3 to 5 minutes of rest in the seated position, which allows BP

comparison with the reference tables. Use of a mercury sphygmomanometer is

the gold standard for measurement of BP in a child. Because of its environmental

toxicity, however, mercury has been increasingly removed from use. Ane-

roid manometers that are semiannually calibrated can be used instead of mer-

cury sphygmomanometers.

SBP is determined by the onset of the first Korotkoff sound, whereas thefifth Korotkoff sound (disappearance of Korotkoff sounds) is used to define

DBP. The choice of appropriate cuff size is important. Too small a cuff for

the arm leads to falsely high BP. The appropriate cuff should have a bladder

width that is approximately 40% of a childs arm circumference, which

usually covers 80% to 100% of the arm circumference. A cuff size of 4 8 cm

is recommended for newborn-premature infants, 6 12 cm for infants, and

9 18 cm for older children. Many older children and adolescents require

the use of a standard or large adult cuff. If physician has a choice between

two cuffs, the larger cuff should be selected. The cuff should be inflated toat least 20 to 30 mm Hg above expected SBP (disappearance of the radial

pulse) and deflated at a rate of 2 to 3 mm Hg per second, which allows the

accurate determination of Korotkoff sounds. Overinflation should be avoided

because of possible discomfort, which could lead to inaccurate BP measure-

ment [8].

Automated BP devices have been used increasingly over the last decade. Most

of the machines use an oscillometric method to measure SBP and calculate the

DBP. The advantages of these devices are their ease of use, which allows

measurements in infants and critically ill patients in intensive care units, and lackof observer bias. These devices have problems with calibration, however. More

importantly, it should be remembered that published normative BP data are based

on the auscultation method, and it might be inappropriate to use those standards

when BP is obtained with an automated device. As recommended, measurements

obtained by oscillometric devices that exceed the ninetieth percentile should be

repeated by auscultation.

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Recently, ambulatory BP monitoring has emerged as a technology that

overcomes some limitations of casual BP measurement. Multiple measurements

of BP during a 24-hour period may reflect the continuous nature of BP. It offersthe assessment of BP in a patients normal environment during both awake and

sleep periods. Ambulatory BP monitoring might better identify patients who have

white-coat hypertension, which occurs when the BP is falsely high in an office

setting because of stress or anxiety. After completing ambulatory BP monitoring,

mean 24-hour BP and mean daytime and nighttime SBP and DBP data can be

compared against gender- and height-specific ninety-fifth percentiles derived

from normative pediatric ambulatory BP monitoring data [12]. Another ambu-

latory BP monitoring parameter is a calculation of BP load, a term for the per-

centage of BP readings that exceed the ninety-fifth percentile of normal for theindividual patient. Finally, ambulatory BP monitoring can determine the percent

decline in BP during sleep. Normally, BP decreases at least 10%, which is

referred to as dipping, during night hours; if BP declines less than 10%, this

pattern is called nondipping. In adults, nondipping has been associated with

hypertensive end-organ injury.

Factors that affect blood pressure in children

BP increases with age throughout childhood and adolescence; however, the

levels of BP percentiles tend to track over time, which means that children

maintain relatively the same BP percentile ranks as they grow with the same trend

during adolescent years. Body size is the major determinant for BP in children. A

direct relationship between weight and BP is well documented, particularly in the

second decade of life. Height, independent of age, predicts BP in children, which

led to the inclusion of height in normative BP tables.

Contrary to adult studies, in which hypertension is more prevalent in African

Americans compared with whites, the effect of race on BP in children is not clear.The Bogalusa Heart Study showed significantly higher BP in African American

compared with white children and adolescents [13]. In contrast, a much larger

survey found no significant difference in the prevalence of hypertension ac-

cording to race in children [14].

High intake of dietary sodium has been linked to increase in BP. The effect of

sodium intake is different among individuals with increased susceptibility to salt

among African Americans, however [13]. Potassium intake also influences BP.

Low potassium intake and high urinary sodium:potassium ratio are associated

with higher BP in adolescent girls [15].The presence of genetic influence on the development of hypertension is well

documented. Approximately 60% to 70% of hypertension in families can be

attributed to genetic factors [16]. Low birth weight recently was found to be a

possible risk factor for the development of hypertension [17]. Finally, uric acid

has been resurrected as a causal risk factor in essential hypertension. Data from

the Bogalusa Heart Study determined that childhood uric acid predicts adult BP

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pressure, which suggests that early elevation in serum uric acid levels may play a

key role in the development of human hypertension [18].

Causes and mechanisms of blood pressure elevation in children

The causes of elevated BP in children are multiple. Generally, hypertension

can be classified as primary (essential with no identified cause) and secondary

(an organic cause can be identified). The cause of hypertension in children is age

dependent. It is well known that the prevalence of secondary hypertension is

inversely related to age. Infants and preschool-aged children are almost never

diagnosed with essential hypertension and are most likely to have secondaryforms of hypertension.

Renal disorders and coarctation of the aorta are the most common causes of

hypertension in children up to age 6 years. In children aged 6 to 10 years, renal

parenchymal disease remains the most frequent cause of increased BP. With age,

the prevalence of essential hypertension increases, and after age 10 it becomes the

leading cause of elevated BP. Essential hypertension is usually mild or moderate.

Although the pathophysiology of essential hypertension is not well understood,

it likely involves genetic, environmental, and lifestyle influences. Obesity cur-

rently is emerging as the most common comorbidity of essential hypertension inpediatric patients, often manifesting during early childhood. Flynn and Alderman

[19] recently conducted a cross-sectional study of 70 children with primary

hypertension referred to a specialized pediatric hypertension clinic. The authors

showed that isolated systolic hypertension was present in 62.9% of subjects,

family history of hypertension was present in 86.2%, and 52.9% of hypertensive

patients were obese. The major concern is increasing prevalence of metabolic

syndrome (insulin-resistant syndrome), defined by the Adult Treatment Panel III

of the National Cholesterol Education Program as a cluster of traits that include

hyperinsulinemia, obesity, hypertension, and hyperlipidemia [20]. Researchersestimate that 1 million US adolescents meet the Adult Treatment Panel III criteria

for the metabolic syndrome. The prevalence of the metabolic syndrome in

adolescents is 4% overall but 30% to 50% in overweight children [21,22].

In children with chronic kidney disease, the prevalence of hypertension

increases with the severity of the disease. The North American Renal Transplant

Cooperative study report demonstrated that 49% of children who had chronic

renal insufficiency and 75% of children who underwent dialysis had uncontrolled

hypertension at time of entry to the database [23,24]. The prevalence of hyper-

tension remains high (74%) even after successful renal transplantation [25]. The pathophysiologic causes of elevated BP in patients who have chronic kidney

disease are multifactorial but can be classified into categories in which there is

an increase of cardiac output, total peripheral resistance, or both. Decreased

glomerular filtration rate, sodium retention, increased extracellular fluid, and in-

creased myocardial performance contribute to increased cardiac output. Increased

vascular resistance in chronic kidney disease may be secondary to either in-

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creased vasoconstriction or impaired vasodilatation. Increased activity of the sym-

pathetic and the renin-angiotensin systems and elevated levels of endothelin-1

and thromboxane mediate vasoconstriction, whereas decreased prostacyclin andnitric oxide activity is responsible for decreased vasodilatation [26]. In children

who have renal insufficiency, increased renin-angiotensin system activity most

likely is the major contributor of elevated BP, whereas fluid overload plays a

major role in the development of hypertension in children who undergo dialysis.

In children with renal transplant, immunosuppression therapy with cortico-

steroids and calcineurin inhibitors, chronic allograft dysfunction, and recurrence

of primary kidney disease are the major causes of elevated BP.

Other causes of hypertension in children are relatively rare and include sys-

temic arteritis (eg, Takayasu arteritis, Henoch-Schfnlein purpura) and oncologic(eg, pheochromocytoma, neuroblastoma, Wilms tumor, adrenal adenocarci-

noma), endocrinologic (eg, hyperthyroidism, Cushing syndrome and disease,

congenital adrenal hyperplasia, primary aldosteronism, Liddle and Gordon syn-

dromes, glucocorticoid-remediable aldosteronism, apparent mineralocorticoid

excess), and neurologic (eg, Guillian-Barre syndrome, increased intracranial

pressure, familial dysautonomia) disorders. Drug-induced hypertension always

needs to be considered (ie, steroids, sympathomimetics [decongestants], oral con-

traceptives, calcineurin inhibitors [cyclosporine and tacrolimus], cocaine).

Clinical evaluation

History and physical examination

A careful history and physical examination can provide clues to detect sec-

ondary causes of hypertension or make a diagnosis of essential hypertension.

Family history should address carefully a history of essential hypertension,cardiovascular, endocrine, and renal diseases, and stroke. The history of inher-

ited conditions, such as polycystic kidney disease and neurofibromatosis, also

should be determined. Medical history should focus on birth history and neonatal

course (ie, prematurity, bronchopulmonary dysplasia, and the use of umbilical

catheters), history of urinary tract infections (reflux nephropathy), hospitaliza-

tions, and other medical problems. All medications, including home remedies and

nonprescription pills, should be listed. In adolescents, a history of smoking or

using oral contraceptives, alcohol, or street drugs should be explored. Because of

an association of sleep apnea with obesity and high BP, a sleep history shouldbe obtained.

Pediatricians must recognize hypertensive emergencies that present as encepha-

lopathy that manifests as severe headache, vomiting, seizures, ataxia, stupor, and

visual disturbances. In infants, severe hypertension can present with symptoms

of congestive heart failure, such as irritability, respiratory distress, and failure

to thrive.

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Laboratory and diagnostic evaluation

Children with persistent BP of ninety-fifth percentile or more should undergo basic studies, including urinalysis and measurements of serum creatinine and

electrolytes. If one of these study results is abnormal, a urine culture and renal

ultrasound should be performed. In overweight patients with BP at the ninetieth

to ninety-fourth percentile and in all patients with BP of ninety-fifth percentile or

more, a fasting lipid profile should be performed to identify dyslipidemia. Fast-

ing glucose and insulin should be measured in overweight patients to identify

metabolic syndrome. In infants and young children younger than 10 years or in

patients in whom the history and physical examination raise suspicion for sec-

ondary hypertension, advanced laboratory and imaging investigation should beperformed. Plasma renin and aldosterone, plasma sampling, and 24-hour urine

collection for catecholamines or steroid (aldosterone and cortisol) levels might be

determined if there is a suspicion for hormone-mediated hypertension. Thyroid

function tests are performed to rule out hyperthyroidism. Radiographic imaging is

indicated to identify renovascular disease, with renal artery angiography

remaining the gold standard for diagnosing renal artery stenosis in children. A

summary of diagnostic clues and procedures for some specific causes of hyper-

tension is presented in Table 2.

Target-organ damage in children with hypertension

Primary hypertension in children usually is not associated with immediate risk

of adverse effects unless a patient develops a hypertensive crisis. It is currently

accepted, however, that primary hypertension can affect heart, kidney, retinal

vasculature, and other target organs.

Children who have hypertension are at risk for future cardiovascular disease.The evidence comes from autopsy studies that indicated a significant relationship

between hypertension and atherosclerotic lesions in adolescents and young adults

[27,28]. Recent studies also indicated that elevated BP during childhood is as-

sociated with increased carotid artery intima-media thickness in young adults

[29,30]. Sorof and colleagues [31] showed that children who have hypertension

have significantly higher carotid artery intima-media thickness than children who

do not have hypertension.

In adults who have hypertension, LVH is one of the strongest predictors of

cardiovascular morbidity and mortality. LVH is highly prevalent in children, asindicated in a study in which 55% of children who had hypertension had a left

ventricular mass (LVM) index above the ninetieth percentile and 14% had an

LVM index above 51 g/m2.7, a value associated with a fourfold greater risk of

adverse cardiovascular outcomes in adults [32]. The same authors showed that

LVH is often associated with left atrium enlargement, which may result from

volume overload and diastolic dysfunction [33]. The Task Force recommended

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Table2

Clinicalevaluationforcommoncausesofelevatedblood

pressureinchildren

Cause

History

Physicalexamination

Diagnosticprocedures

PrimaryHTN/metabolicsyndrome

Familyhistoryo

fhypertension,

cardiovasculard

isease,diabetes,

stroke,stress

Overweight,obese,acanthosis

nigricans

Urinanalysis,serumglucose

,

creatinine,electrolytes;urine

microalbuminuriaandserum

insulin,

ifmetabolicsyndromeissu

spected;

AbPM

toruleoutwhite-coat

hypertension

Sleepdisorders

SameasprimaryHTN;historyof

snoring

Same

asprimaryHTN;adenotonsillar

hypertrophy

SameasprimaryHTN;

polysomnography

Renaldiseases

Familyhistoryo

fkidneydisease;past

historyofUTI;

grosshematuria,

polyuria,dysuria,fatigue,edema,

flankpain,enuresis,hearingloss;

neonatalhistory

Grow

thretardation,pallor,rickets

(chro

nickidneydisease),edema,

rash,

arthritis(nephroticsyndrome,

glom

erulonephritis),abdominalmass/

palpa

blekidneysinnewborn

(obstructiveuropathy,polycystic

kidne

ys)

SameasprimaryHTN;CBC,urine

culture,renalultrasound(ad

ditional

proceduressuchasVCUG,

renal

scan,complementprofileofother

serologymightbeperforme

dbased

ontheinitialfindings)

Renovascular

Historyofsever

e,persistent,difficult-

to-controlhyper

tension,neonatal

historyofumbilicalarterycatheters,

historyofneuro

fibromatosis

Epigastric/flankbruit,cafe-au-lait

spots

(neurofibromatosis)

Renalarteryangiography(g

old

standard),orscintigraphyw

ithand

withoutACEinhibition),or

magnetic

resonanceangiography),or

3-dimensionalreconstructiveCT,

orspiralCTwithcontrast

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Coarcationofaorta

AssociationwithTurnersyndrome,

Williamssyndrome

Heartmurmur;weakpulsesinlower

extremities,BPinupperextremities

N10mmHghigherthaninlower

extremities

Echocardiography

Hyperthyroidism

Historyofweightloss,palpitation,

tremor

Tachycardia,thyromegaly,proptosis

Thyroidfunctiontest

Catecholamineexcess

(pheochromocytoma,

paraganglioma,neuroblastoma

Headache,sweating,nauseaand

vomiting,abdom

inalpain,

polydipsia,polyuria;associationwith

neurofibromatos

is,vonHippel-

Lindaudisease,

andmultiple

endocrineneoplasiasyndromes

Abdo

minalmass,pallor,flushing,

tachy

cardia,visualdisturbances,

acroc

yanosis

131Ior123Imeta-iodo-benzy

l-

guanidinescan;24-hoururine

cathecholamines(epinephrin

e,

norepinephrine)andtheirm

etabolites

(metanephrines)

Corticosteroidexcess(low-renin

hypertension)

Familyhistory(

Liddlesyndrome),

historyofrapid

weightgain

(Cushings),steroiduse

Moonfacies,truncalobesity,acne,

hirsutism,striae(Cushings),

ambiguousgenitalia(congenital

adren

alhyperplasia),muscle

weak

ness(Liddlesyndrome)

Serumelectrolytes,plasmarenin

activity,aldosterone;24-hou

rurine

cortisol,aldosterone;adrena

lgland

imagingwhenindicated

Abbreviations:ABPM,ambulatoryBPmonitoring;ACE,angiotensin-convertingenzyme;CBC,completebloodcount;HTN,hyp

ertension;VCUG,voidingcystoure

throgram.



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including echocardiography as a diagnostic procedure to diagnose LVH in chil-

dren with persistent BP at the ninety-fifth percentile or higher.

In addition to cardiovascular abnormalities, retinal abnormalities have beenreported in infants with hypertension [34]. The authors noted that patients whose

hypertension resolved had a normal retinal examination. Kidneys also should be

considered as a target organ for elevated BP. The North American Renal Trans-

plant Cooperative study data demonstrated a strong independent relationship be-

tween high BP and accelerated progression of renal failure in children who have

chronic kidney disease [23].

Treatment of hypertension in children

The goal of treatment is to reduce BP to a level below the ninetieth percentile

and prevent development of target-organ damage. Specific recommendations for

treatment of elevated BP depend on a patients clinical situation. The initial

therapy of mild elevations of BP seen with essential hypertension without target-

organ damage consists of nonpharmacologic intervention in the form of life-

style modification, including weight reduction for obesity-related hypertension,

regular physical activity, and dietary modification with low caloric intake andsalt restriction. Weight loss in overweight adolescents lowers BP and amelio-

rates cardiovascular risk factors, such as dyslipidemia and insulin resistance.

The American Heart Association recommends five guiding principles for the

treatment of overweight: (1) establish individual treatment goals and approaches

based on a childs age, degree of overweight, and presence of comorbidities,

(2) involve the family or major caregivers in the treatment, (3) provide assessment

and monitoring frequently, (4) consider behavioral, psychological, and social cor-

relates of weight gain in the treatment plan, and (5) provide recommendations

for dietary changes and increases in physical activity that can be implementedwithin the family environment and that foster optimal health, growth, and devel-

opment [35].

Family-based intervention is vital in achieving BP control in overweight

children. Sedentary activities, including watching TV and playing video and

computer games, should comprise no more than 2 hours per day. Children should

spend at least 30 to 60 min/d in physical activities. The recommended daily

sodium intake should approximate 1.2 g/d for 4- to 8-year-old children and 1.5 g/d

for older children. This amount is significantly lower than the current usual

sodium intake in the typical American family. Data from the Dietary Approachesto Stop Hypertension study in adults demonstrated that a high intake of vege-

tables, fruits, fibers, and low-fat dairy products leads to improvement in BP

even in the absence of weight reduction [36]. A similar study in children and

adolescents is currently being conducted. Nutritionist consultation can provide

guidelines and specific recommendations for individualizing a dietary plan. The

combination of weight loss, dietary modification, decreased sedentary activity,

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and improved physical fitness has been shown to reduce BP significantly in

children who have essential hypertension. Surgical approaches to treat severe

adolescent obesity are being undertaken by several centers [37]. Indicationsinclude a body mass index N40 kg/m2 and severe associated comorbidities, such

as obstructive sleep apnea, type 2 diabetes mellitus, and pseudotumor cerebri.

More severe elevation of body mass index (N50 kg/m2) may be an indication for

surgical treatment in the presence of less severe comorbidities, such as hyper-

tension and dyslipidemia, particularly if the degree of overweight hinders per-

forming the activities of daily living [35].

Children who have symptomatic essential hypertension, secondary hyper-

tension, diabetes-associated hypertension, evidence of target-organ damage

(LVH), or failed nonpharmacologic intervention require pharmacologic therapy.Most important in choosing a drug is its safety and efficacy. The 1997 US Food

and Drug Administration Modernization Act and the 2002 Best Pharmaceuticals

for Children Act led to a significant increase in the number of antihypertensive

drugs studied in children. The classification, preparations, and dosages of most

commonly used antihypertensive drugs are summarized in Table 3. The initial

drug choice is based on the mechanism and severity of the hypertension, patient

demographics, compliance issues, history of previous side effects, presence of

other medical problems, and concomitant drug therapy. In adults, JNC-7 (Joint

National Committee on BP) recommended thiazide diuretics as the first line oftherapy based on their efficacy, good tolerability, and low cost. In children, no

clinical trials have compared the effect of different classes of antihypertensive

drugs based on clinical endpoints. Most of the studies have focused only on the

ability to lower BP. Because all classes of antihypertensive drugs have been

shown to lower BP in children, the choice of drug therapy frequently is based on

preferences and experience of physicians. Angiotensin-converting enzyme in-

hibitors and calcium-channel blockers are the most common antihypertensive

medications prescribed currently across all pediatric ages. The wide use of these

medications is based on their effectiveness and relatively low rate of side effects.Angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers are

preferable in children who have diabetes, microalbuminuria, or chronic kidney

disease because of their renoprotective effect. A recent survey of pediatric ne-

phrologists showed that whereas angiotensin-converting enzyme inhibitors and

calcium-channel blockers were chosen by similar proportions of respondents

as initial agents for treatment of primary hypertension, most (84%) chose

angiotensin-converting enzyme inhibitors as their initial agent for hypertension in

children who had renal disease [38]. Calcium-channel blockers orb-blockers are

frequently used in children with migraine headaches. Drug therapy usually startswith a low dose of a single agent. The dose is titrated until BP goals are achieved.

If adequate BP control is not achieved with a single agent, a second agent should

be added.

In the case of hypertensive emergencies, attempts to lower BP rapidly to avoid

target-organ damage must be balanced against excessively lowering the BP,

which also can lead to target-organ damage, with cerebral ischemia being the



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Table3

Antihypertensivedrugs

foroutpatientmanagementofhy

pertensioninchildren1to17yearsold

Class

Drug

Dosea

Dosing

interval

Evidence

b

FDA

labelingc

Com

mentsd

ACEinhibitor

Benazepril

Initial:0.2mg/kgperdupto

10mg/d

qd

RCT

Yes

1.A

llACEinhibitorsarecontraindicatedin

pregnancy;femalesofchildbearing

age

sh

ouldusereliablecontraception

Maximum:0.6

mg/kgperdup

to40mg/d

2.C

heckserumpotassiumandcreatin

ine

periodicallytomonitorforhyperka

lemia

andazotemia

Captopril

Initial:0.30.5

mg/kg/dose

tid

RCT,CS

No

3.C

oughandangiodemaarereported

lyless

commonwithnewermembersofthisclass

th

anwithcaptopril

Maximum:6m

g/kgperd

4.B

enazepril,enalapril,andlisinoprillabels

containinformationonthepreparationofa

su

spension;captoprilmayalsobe

compoundedintoasuspension

Enalapril

Initial:0.08mg

/kgperdupto

5mg/d

qd-bid

RCT

Yes

5.FDAaprrovalforACEinhibitorsw

ith

pediatriclabelingislimitedtochildren

!

6yearsofageandtochildrenwith

creatinineclearance!

30ml/minper1.73m2

Maximum:0.6

mg/kgperdup

to40mg/d

Fosinopril

Children>50k

g:

qd

RCT

Yes

Initial:510m

g/d

Maximum:40mg/d

Lisinopril

Initial:0.07mg

/kgperdupto

5mg/d

qd

RCT

Yes

Maximum:0.6

mg/kgperdup

to40mg/d

Quinapril

Initial:510mg/d

qd

RCT,EO

No

Maximum:80mg/d

Angiotensin-

receptor

blocker

Irbesartan

612years:75150mg/d

qd

CS

Yes

1.A

llARBsarecontraindicatedinpr

egnancy;

fe

malesofchildbearingageshould

use

re

liablecontraception

!

13years150

300mg/d

2.C

heckserumpotassium,creatinine

periodicallytomonitorforhyperka

lemia

andazotemia

3.L

osartanlabelcontainsinformation

onthe

preparationofasuspension

Losartan

Initial:0.7mg/kgperdupto

50mg/d

qd

RCT

Yes

Maximum:1.4

mg/kgperdup

to100mg/d

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(continuedonn

extpage)

a-and

b-Blocker

Labetalol

Initial:13mg

/kgperd

bid

CS,EO

No

4.FDAapprovalforARBsislimited

to

children!

6yearsofageandtoch

ildren

w

ithcreatinineclearance!

30ml/m

inper

1.73m2

1.A

sthmaandovertheartfailureare

contraindications

Maximum:10

12mg/kgperd

upto1200mg/d

2.H

eartrateisdose-limiting

3.M

ayimpairathleticperformance

4.Shouldnotbeusedininsulin-depe

ndent

diabetics

b-Blocker

Atenolol

Initial:0.51m

g/kgperd

qd-bid

CS

No

1.N

oncardioselectiveagents(propran

olol)are

contraindicatedinasthmaandheartfailure

Maximum:2m

g/kgperdup

to100mg/d

2.H

eartrateisdose-limiting

Biso

prolol/HCTZ

Initial:2.5/6.25

mg/d

qd

RCT

No

3.M

ayimpairathleticperformance

Maximum:10/6.25mg/d

4.Shouldnotbeusedininsulin-depe

ndent

diabetics

Metoprolol

Initial:12mg/kgperd

bid

CS

No

5.A

sustained-releaseformulationof

propranololisavailablethatisdosed

once-daily

Maximum:6m

g/kgperdup

to200mg/d

Prop

ranolol

Initial:12mg/kgperd

bid-tid

RCT,EO

Yes

Maximum:4m

g/kgperdup

to640mg/d

Calcium

channel

blocker

Amlodipine

Children617

years:2.55mg

oncedaily

qd

RCT

Yes

1.A

mlodipineandisradipinecanbe

compoundedintostableextempora

neous

suspensions

Felo

dipine

Initial:2.5mg/d

qd

RCT,EO

No

2.Felodipineandextended-releasenifedipine

ta

bletsmustbeswallowedwhole

Maximum:10mg/d

3.Is

radipineisavailableinbothimm

ediate-

re

leaseandsustained-releaseformu

lations;

sustained-releaseformisdosedqd

orbid

Isradipine

Initial:0.150.2mg/kgperd

tid-qid

CS,EO

No

4.M

aycausetachycardia

Maximum:0.8

mg/kgperdup

to20mg/d

Exte

nded-release

nifedipine

Initial:0.250.5mg/kgperd

qd-bid

CS,EO

No

Maximum:3m

g/kgperdup

to120mg/d



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Class

Drug

Dosea

Dosing

interval

Evidence

b

FDA

labelingc

Com

mentsd

Central

a-agonist

Clonidine

Children!

2years:

bid

EO

Yes

1.M

aycausedrymouthand/orsedation

Initial:0.2mg/d

2.Transdermalpreparationalsoavailable

Maximum:2.4

mg/d

3.Suddencessationoftherapycanlead

to

severereboundhypertension

Diuretic

HCT

Z

Initial:1mg/kg

/d

qd

EO

Yes

1.A

llpatientstreatedwithdiureticss

hould

haveelectrolytesmonitoredshortly

after

in

itiatingtherapyandperiodicallythereafter

Maximum:3m

g/kg/dupto

50mg/d

2.U

sefulasadd-ontherapyinpatientsbeing

treatedwithdrugsfromotherdrug

classes

Chlorthalidone

Initial:0.3mg/kg/d

qd

EO

No

3.Potassium-sparingdiuretics(spironolactone,

triamtereneamiloride)maycauses

evere

hyperkalemia,especiallyifgivenw

ithACE

in

hibitororARB

Maximum:2m

g/kg/dupto

50mg/d

4.Furosemideislabeledonlyfortrea

tmentof

edemabutmaybeusefulasadd-ontherapy

in

childrenwithresistanthypertens

ion,

particularlyinchildrenwithrenald

isease

Furo

semide

Initial:0.52.0

mg/kgperdose

qd-bid

EO

No

5.C

hlorthalidonemayprecipitateazotemiain

patientswithrenaldiseasesandshouldbe

usedwithcautioninthosewithsev

ere

re

nalimpairment

Maximum:6m

g/kg/d

Spironolactone

Initial:1mg/kg

/d

qd-bid

EO

No

Maximum:3.3

mg/kg/dupto

100mg/d

Triamterene

Initial:12mg/kg/d

bid

EO

No

Maximum:34

mg/kg/dupto

300mg/d

Amiloride

Initial:0.40.625mg/kg/d

qd

EO

No

Maximum:20mg/d

Table3

(continued)

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Peripheral

a-agonist

Dox

azosin

Initial:1mg/d

qd

EO

No

May

causehypotensionandsyncope,

espe

ciallyafterfirstdose

Maximum:4m

g/d

Praz

osin

Initial:0.050.1mg/kg/d

tid

EO

No

Maximum:0.5

mg/kg/d

Tera

zosin

Initial:1mg/d

qd

EO

No

Maximum:20mg/d

Vasodilator

Hyd

ralazine

Initial:0.75mg

/kg/d

qid

EO

Yes

1.Tachycardiaandfluidretentionare

commonsideeffects

Maximum:7.5

mg/kg/dupto

200mg/d

2.H

ydralazinecancausealupus-like

sy

ndromeinslowacetylators

Minoxidil

Childrenb12y

ears:

qd-tid

CS,EO

Yes

3.Prolongedusedofminoxidilcancause

hypertrichosis

Initial:0.02mg

/kg/d

4.M

inoxidilisusuallyreservedforpatients

w

ithhypertensionresistanttomultipledrugs

Maximum:50mg/d

Children!12y

ears:

Initial:5mg/d

Maximum:100

mg/d

Includesdrugswithpriorpediatricexperienceorrecentlycompletedclinicaltrials.

Abbreviations:ARB,angiotensin-receptorblocker;bid,t

wicedaily;FDA,FoodandDrug

Administration;HCTZ,hydrochlorothiazide;qd,oncedaily;qid,fourtimes

daily;tid,threetimesd

aily.

a

Themaximumrecommendedadultusedshouldnotbeexceededinroutineclinicalpractice.

b

Levelofevidenceuponwhichdosingrecommenda

tionsarebased.CSindicatescaseseries;EO,expertopinion;RCT

,randomizedcontrolledtrial.

c

FDA-approvedpediatriclabelinginformationisavailable.RecommendeddosesforagentswithFDA-approvedpediatriclabelsarethedosescontain

edinthe

approvedlabels.Evenwhenpediatriclabelinginformatio

nisnotavailable,theFDA-approvedlabelshouldbeconsultedfo

radditionalsafetyinformation.

d

Commentsapply

toallmembersofeachdrugclassexceptwhereotherwisestated.

From

NationalHighBloodPressureEducationProgramW

orkingGrouponHighBloodPressuresinChildrenandAdolescents.Thefourthreportondiagnosis,e

valuation,

andtreatmentofhighb

loodpressureinchildrenandado

lescents.Pediatrics2004;114:569

;withpermission.



16/20

greatest risk. The safest way to treat a hypertensive crisis initially is to lower BP

using an antihypertensive medication that is administered by continuous

intravenous infusion in an intensive care unit, where the patient can be monitoredappropriately. Treating hypertensive crisis by continuous infusion is associated

with fewer complications than using intravenous bolus agents. Recently pub-

lished national guidelines on hypertension in children stated that a hypertensive

emergency should be treated with an intravenous antihypertensive agent to lower

the BP by up to 25% over the first 8 hours, followed by a further gradual

reduction in BP over the next 26 to 48 hours [8].

Table 4 demonstrates medications available to treat hypertensive emergencies.

Nicardipine, a dihydropyridine calcium-channel blocker, is primarily an arteriolar

vasodilator that has been used increasingly over the last 10 years and has beenshown to be safe and effective in treating hypertensive crisis and hypertensive

urgency in children. It is usually effective at 1 to 3 mg/kg/min and has a slightly

longer onset of action and half-life compared with nitroprusside. Unlike nitro-

prusside, nicardipine does not pose the risk for cyanide/thiocyanate toxicity

and can be used for a longer period of time. Disadvantages include the risk of

thrombophlebitis when given through a peripheral line and the potential to in-

crease intracranial pressure.

When a patient presents with hypertensive crisis, volume status should be

assessed. Many patients in hypertensive crisis are volume depleted because ofa combination of decreased oral intake during the insidious onset of hyperten-

sive crisis and pressure natriuresis. Volume depletion may lead to a further up-

regulation of the renin-angiotensin system that can potentiate the vasoconstrictive

effects of severely elevated BP on the endothelium. Volume repletion may lower

renin levels, help restore tissue perfusion, and prevent a precipitous fall in BP that

may occur with antihypertensive therapy.

Children who have been diagnosed with hypertension need careful monitor-

ing. In general, a primary physician is able to manage children with mild essential

hypertension: The emphasis should be directed at nonpharmacologic interven-tion. If in 6 months BP control is not yet achieved, drug therapy should be

offered. After initiation of pharmacologic treatment a patient must be seen by a

pediatrician within a 2-week period. The dose of medication should be adjusted

every 2 weeks until BP control is adequate. Once good BP control has been

achieved, twice-a-year follow-up is sufficient. After 6 months of normal BP and

if lifestyle and body weight have improved, the physician should decide whether

the dose of medication should be tapered down over a 1- to 6-month period of

follow-up until off therapy. The patient must be followed carefully for another

6 months and annually to ensure that the BP remains normal. In case of noresponse to a 1-month trial of antihypertensive therapy, referral to a specialist

is recommended.

Recommendations for athletic participation depend on the severity of hy-

pertension. The American Academy of Pediatrics published guidelines for sports

participation based on findings of the 26th Bethesda Conference on heart dis-

ease and athletic participation and of the second Task Force on Blood Pressure

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Table4

Antihypertensivedrugs

formanagementofseverehypertensioninchildren1to17yearsold

Drug

Class

Dosea

Route

Comments

Mostusefulb

Esmolol

b-blocker

100500mg/kg/min

IVinfusion

Veryshort-acting;constantinfusionpreffered;may

causepro

foundbradycardia;producedmodest

reduction

sinBPinapediatricclinicaltria

l

Hydralazine

Vasolidator

0.20.6mg/kg/dose

IV,IM

Shouldbegivenevery4hwhengivenIV

bolus;

recommendeddoseislowerthanFDAlabel

Labetalol

a-andb-blocker

Bolus:0.21.0mg/kg/doseupto

40mg/dose

IVbolusor

infusion

Asthmaa

ndovertheartfailurearerelative

contraind

ications

Infusion:0.253.0mg/kg/h

Nicardipine

Calcium-channelblocker

13mg/kg/min

IVinfusion

Maycausereflextachycardia

Sodium

nitroprusside

Vasolidator

0.5310mg/kg/min

IVinfusion

Monitorcyanidelevelswithprolonged(N7

2h)use

orinrenalfailure;orcoadministerwithso

dium

thiosulfate

Occasionallyusefulc

Clonidine

Centrala-agonist

0.050.1mg/dose,maybe

repeatedupto0.8mgtotaldose

po

Sideeffectsincludedrymouthandsedatio

n

Enalaprilat

ACEinhibitor

0.050.1mg/kg/doseupto

1.25mg/dose

IVbolus

Maycauseprolongedhypotensionandacu

terenal

failure,especiallyinneonates

Fenoldopam

Dopaminereceptoragonist

0.20.8mg/kg/min

IVinfusion

Produced

modestreductionsinBPinapediatric

clinicaltrialinpatientsupto12years

Isradipine

Calcium-channelblocker

0.050.1mg/kg/dose

po

Stablesuspensioncanbecompounded

Minoxidil

Vasolidator

0.10.2mg/kg/dose

po

Mostpotentoralvasolidator,long-acting

Abbreviations:IM,intramuscular;IV,intravenous;po,oral.

a

Alldosingrecommendationsarebasedonexperto

pinionorcaseseriesdataexcept

asotherwisenoted.

b

Usefulforhypertensiveemergenciesandsomehyp

ertensiveurgencies.

c

Usefulforhypertensiveurgenciesandsomehypertensiveemergencies.

From

NationalHighBloodPressureEducationProgramW

orkingGrouponHighBloodPressuresinChildrenandAdolescents.Thefourthreportondiagnosis,e

valuation,

andtreatmentofhighb

loodpressureinchildrenandado

lescents.Pediatrics2004;114:570

;withpermission.



18/20

Control in Children [39]. Children with hypertension less than the ninety-ninth

percentile and without target-organ damage have no limitations for competitive

sport activity. Children with significant hypertension (Nninety-ninth percentile)are restricted from competitive sports and high static activity until BP is under

control. High static activities include field events (throwing), gymnastics, karate/

judo, water skiing, weight lifting, bodybuilding, downhill skiing, wrestling, cy-

cling, decathlon, rowing, and speed skating. Participation of children with target-

organ damage should be determined on an individual basis according to the

severity of target-organ damage and hypertension.

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