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Hypertension
Last Updated: January 7, 2002
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AUTHOR INFORMATION

Section 1 of 11

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up

Miscellaneous Pictures Bibliography
Author: Adrian Spitzer, MD, Professor, Department of Pediatrics, Albert Einstein College of
Medicine; Director of NIH Training Program, Children's Hospital at Montefiore Medical Center
Adrian Spitzer, MD, is a member of the following medical societies: American Academy of
Pediatrics, American Federation for Medical Research, American Pediatric Society, American
Society of Nephrology, American Society of Pediatric Nephrology, International Society of
Nephrology, and Society for Pediatric Research
Editor(s): Ira H Gessner, MD, Professor, Department of Pediatrics, University of Florida College of
Medicine; Robert Konop, PharmD, Clinical Assistant Professor, Department of Pharmacy, Section
of Clinical Pharmacology, University of Minnesota; John W Moore, MD, MPH, Director of the Heart
Center for Children, St Christopher's Hospital for Children; Professor, Department of Pediatrics,
MCP Hahnemann School of Medicine; Gilbert Herzberg, MD, Assistant Professor, Department of
Pediatrics, Section of Pediatric Cardiology, New York Medical College; and Steven Neish, MD,
Director of Pediatric Cardiac Catheterization Services, Head of Pediatric Cardiology Division,
Associate Professor, Department of Pediatrics, University of Wisconsin and Children's Hospital
INTRODUCTION

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Author Inform
Introduction
Clinical
Differentials
Workup
Treatment
Medication
Follow-up
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Bibliography

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Section 2 of 11

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up

Miscellaneous Pictures Bibliography
Background: Hypertension is a major cause of morbidity and mortality in the US and many other
countries. The prevalence of hypertension in the adult population of the United States, defined by a
single measurement of 140/90 mm Hg or more obtained under nonstandardized conditions, is
estimated to be 15-20%. This compares with a prevalence of 1.5-2.0% among children aged 4-15
years in whom hypertension was defined as a blood pressure persistently greater than the 95th
percentile for age. This figure, however, fails to convey the observation that children with blood
pressures within the upper percentiles of normal range are at risk of becoming hypertensive later on in
life.
Blood pressure standards
For children in the US, extensive normative blood pressure data are not available. Standards have
been developed by a Task Force on Blood Pressure Control in Children commissioned by the Heart,
Blood, and Lung Institute of the National Institutes of Health, using the results of 9 surveys of 70,000
infants and children. Approximately equal numbers of boys and girls were surveyed. The percentile
curves describing the age-specific distributions of systolic and diastolic blood pressures in infants and
children, with corrections for height and weight, were published in 1987 and have been reproduced
extensively in other publications. Further details regarding the diagnosis and treatment of hypertension

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in infants and children are provided in the third report of the task force, published in 1996.
In accordance with the recommendations of the task force, a blood pressure is considered normal
when the systolic and diastolic values are less than the 90th percentile. Average systolic and/or
diastolic values, corrected for body size, at or greater than this percentile level but not exceeding the
95th percentile are considered high normal. Hypertension is defined as average systolic and/or
diastolic blood pressures greater than the 95th percentile. These definitions allow construction of a
table that can serve as a guide to the practicing physician (see Table 1).
Table 1. The 95th Percentile of Blood Pressures (mm Hg) in Children and Adolescents*

Girls

Girls

Boys

Boys

Age, years

50th percentile
for height

75th percentile
for height

50th percentile
for height

75th percentile
for height

104/58

105/59

102/57

104/58

111/73

112/73

114/74

115/75

12

123/80

124/81

123/81

125/82

17

129/84

130/85

136/87

138/88

*Adapted from "Update on the 1987 Task Force Report on High Blood Pressure in Children and
Adolescents: a working group report from the National High Blood Pressure Education Program"
Pathophysiology: The level of blood pressure is determined by the balance between cardiac output
and vascular resistance. A rise in either of these variables, in the absence of a compensatory decrease
in the other, increases mean blood pressure, which is the actual driving pressure. Multiple factors
regulate cardiac output and vascular resistance (see Table 2). In addition, some of these factors are
affected by changes in electrolyte homeostasis, particularly changes in sodium, calcium, and
potassium. Under normal conditions, the amount of sodium excreted in the urine matches the amount
ingested, resulting in near constancy of extracellular volume. Retention of sodium results in increased
extracellular volume, which is associated with an elevation of blood pressure. Through a variety of
physical and hormonal mechanisms, this triggers changes in both glomerular filtration rate and tubular
reabsorption of sodium, resulting in excretion of excess sodium and restoration of sodium balance.
A rise in intracellular concentration of calcium, brought about by changes in plasma calcium
concentration, increases vessel contractility. In addition, calcium stimulates the release of renin, the
synthesis of epinephrine, and the activity of the sympathetic nervous system. On the other hand,
increased potassium intake suppresses production and release of renin and induces natriuresis, thus
decreasing blood pressure. The complexity of the system explains the difficulties encountered in
identifying the mechanism that accounts for hypertension in a particular patient. This explains why, in a

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large number of patients, treatment is designed to affect regulatory factors rather than the cause of the
disease.
Table 2. Factors Affecting Blood Pressure*

Cardiac Output
Baroreceptors
Extracellular volume
Effective circulating volume
Atrial natriuretic
hormones
Mineralocorticoids
Angiotensin
Catecholamines
Sympathetic nervous system

Vascular Resistance
Pressors
Angiotensin II
Calcium (intracellular)
Catecholamines
Sympathetic nervous
system
Vasopressin
Depressors
Atrial natriuretic hormones
Endothelial relaxing factors
Kinins
Prostaglandin E2
Prostaglandin I2

*Modified from Gruskin AB et al

Frequency:

In the US: True incidence of hypertension in the pediatric population is not known. This stems,
in part, from the rather arbitrary definition of hypertension. In adults, hypertension was defined
on the basis of extensive studies that allowed correlation of the level of blood pressure with
detrimental outcomes, such as heart failure or stroke. Such studies have not been performed in
children, although reports on small sample populations of children provide compelling evidence
of a relationship between hypertension and both ventricular hypertrophy and atherosclerosis.
The figure quoted above (ie, 1.5-2.5% of children having hypertension) is based on a
compilation of studies. How many of these children qualify as hypertensive and develop
complications during adulthood remains unknown.

Internationally: Because of differences in genetic and environmental factors, incidence varies

from country to country and even from region to region within the same country.

Race: The task force noted no differences in blood pressure between black and white children.
However, black children of any age appear to demonstrate higher peripheral vascular resistance and a
greater sensitivity of their blood pressure to salt intake than white children.
Sex: No significant differences in blood pressure exist between girls and boys younger than 6 years.
From that age until puberty, blood pressure is slightly higher in girls than in boys. At puberty and
beyond, males have a slightly higher blood pressure than females.
Age: Blood pressure is affected by height and weight. However, these relationships do not become
evident until children are school-aged. The normative data published by the task force in 1987 consider
these factors. Numerous investigators have noted a correlation between the blood pressure of parents
and that of their offspring. The familial aggregation of blood pressure is detectable early in life.
CLINICAL

Section 3 of 11

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up

Miscellaneous Pictures Bibliography
History:
A well-taken history provides clues about the cause of hypertension and guides the nature and
sequence of the ensuing investigations. Relevant pieces of information include the following:
o
o
o
o
o

Prematurity
Bronchopulmonary dysplasia
History of umbilical artery catheterization
Failure to thrive
History of head or abdominal trauma

o
o

Family history of heritable diseases (eg, neurofibromatosis, hypertension)

Medications (eg, amphetamines, pressor substances, steroids, tricyclic antidepressants,
excessive ingestion of licorice, substance abuse)
Episodes of pyelonephritis (suggested perhaps by unexplained bouts of fever) possibly
resulting in renal scarring

Presenting symptoms and signs are not specific in neonates and are absent in most older
children unless the hypertension is severe. The signs and symptoms that should alert the
physician to the possibility of hypertension are depicted in Table 3.
Table 3. Presenting Signs in Neonates and Children
Neonates

Children (Additional)

Failure to thrive

Headaches

Seizure

Fatigue

Irritability or lethargy

Blurred vision

Respiratory distress

Epistaxis

Congestive heart failure

Bell palsy

Physical:
Measurement and recording of blood pressure
o

Blood pressure must be measured once a year in every child, preferably using a
mercury gravity manometer. Doppler and oscillometric techniques can be used in
children in whom auscultatory blood pressure measurements are difficult to obtain.

Repeated measurements over time are required to obtain meaningful information.

Proper cuff size is essential for accurate blood pressure measurement. The rubber
blade inside the cloth cover should be long enough to encircle the arm and wide enough
to cover approximately three fourths of the distance from shoulder to elbow.

The child should be relaxed and in a comfortable sitting or supine (infants) position with
the right arm resting on a supportive surface at the level of the heart.

The cuff should be inflated at a pressure approximately 20 mm greater than that at

which the radial pulse disappears and then allowed to deflate at a rate of 2-3 mm Hg/s.

The first Korotkoff sound (ie, appearance of a clear tapping sound) defines the systolic
pressure, while the fifth Korotkoff sound (ie, disappearance of all sounds) defines the
diastolic pressure. The fourth (low-pitched, muffled) sound and the fifth sound frequently
occur simultaneously, and the fifth sound may not occur at all. The sound on which the
diastolic blood pressure is based must be recorded.

Systolic blood pressure in the lower extremities must be measured when the elevation
of the systolic blood pressure in the upper extremities is first noted and when the
examiner finds amplitude of the arterial pulse in the legs to be lower than that in the
arms. A discrepancy between these values is indicative of coarctation of the aorta. With
the patient in the supine position, place a cuff on the calf. The cuff should be wide
enough to cover at least two thirds of the distance from knee to ankle. Doppler
ultrasound can be used to detect onset of blood flow, reflecting systolic blood pressure,
in either the posterior tibial or dorsalis pedis artery. The value should be compared with
similarly obtained Doppler systolic blood pressure in the arm.

Remember that the artifact of distal pulse amplification causes the value of systolic
blood pressure at the brachial artery to be less than that at the posterior tibial or dorsalis
pedis artery. This difference may be only a few millimeters in the infant but can rise to
10-20 mm Hg in the older child or adult. At no time should the systolic pressure in the
arm exceed that in the foot. If systolic pressure in the arm exceeds that in the foot, the
pressures in both arms and legs should be measured. Consistent recording of a
difference indicates presence of aortic coarctation.

Interpretation of blood pressure measurements

o

Hypertension is defined as average systolic and/or diastolic blood pressures greater

than the 95th percentile (see Table 1). Any child with a blood pressure exceeding the
90th percentile requires scrutiny. Except for patients with severe hypertension and target
organ damage, who call for immediate attention, several measurements of blood
pressure should be made at weekly intervals to determine whether the elevation is
sustained.

The average of these multiple measurements should be plotted on the appropriate

percentile chart. If the average measurement, corrected for body size, is between the
90th and 95th percentiles, the child's blood pressure should be monitored at 6-month
intervals. If the average blood pressure places the child at or greater than the 95th
percentile, the child should be evaluated further and considered for therapy.

A primary objective of the physical examination is identification of signs indicative of secondary

hypertension, including the following:
o

Caf au lait spots (pheochromocytoma)

Abdominal mass (Wilms tumor)

Abdominal bruit (coarctation of the aorta, renal vascular abnormalities)

Blood pressure difference between upper and lower extremities (coarctation of the
aorta)

Thyromegaly (hyperthyroidism)

Virilization (adrenal hyperplasia)

Stigmata of Bardet-Biedl, von Hippel-Landau, Williams, or Turner syndromes

Causes: Hypertension can be primary (ie, essential) or secondary.

In general, the younger the child and the higher the blood pressure, the greater the chance that
the hypertension is secondary to a potentially identifiable cause.

A review of literature revealed that 78% of 563 young patients with secondary hypertension had
a renal parenchymal abnormality. In the remaining 22%, the cause of hypertension, in order of
frequency, was renal artery stenosis, coarctation of the aorta, pheochromocytoma, and a variety
of other conditions.

The most common causes of hypertension in order of their relative frequency at various ages
are listed in Table 4.
Table 4. Common Causes of Hypertension by Age

Infants

Aged 1-6 years

Aged 7-12 years

Adolescents

Renal artery or vein

thrombosis

Renal artery
stenosis

Renal parenchymal
disease

Essential
hypertension

Congenital renal
anomalies

Renal parenchymal
disease

Renovascular
abnormalities

Renal parenchymal
disease

Coarctation of the
aorta

Wilms tumor

Endocrine causes

Endocrine causes

Bronchopulmonary
dysplasia

Neuroblastoma

Essential
hypertension

Prematurity (?)

Coarctation of the
aorta

Prematurity (?)

DIFFERENTIALS

Section 4 of 11

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up

Miscellaneous Pictures Bibliography
Other Problems to be Considered:
A step-wise approach to the differential diagnosis of hypertension in a child is depicted in Picture 1.

WORKUP

Section 5 of 11

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures
Bibliography

Lab Studies:
Proceed from simple tests that can be performed in an ambulatory setting to complex noninvasive tests and fina
invasive tests. The approximate order of the tests is as follows:
o

Urine dip-stick: This test is indicative of renal disease if positive for blood and/or protein.

Blood chemistry: An increased serum creatinine concentration is indicative of renal disease. Hypokalemi
suggests hyperaldosteronism.

Blood hormones: High plasma renin activity indicates renal vascular hypertension, including coarctation
aorta. A very low plasma renin activity is indicative of glucocorticoid remediable aldosteronism, Liddle sy
or apparent mineralocorticoid excess. High plasma aldosterone concentration is diagnostic of
hyperaldosteronism. High catecholamines (epinephrine, norepinephrine, dopamine) are diagnostic of
pheochromocytoma or neuroblastoma.

Urine hormones: High excretion of catecholamines and catecholamine metabolites (metanephrine) indic
pheochromocytoma or neuroblastoma.

Imaging Studies:
Echocardiography

Left ventricular hypertrophy results from chronic hypertension.

The hypertrophy is symmetric, consisting of equivalent increases in thickness of both the left ventricular
the ventricular septum and the left ventricular posterior wall.

Also assess left ventricular function.

Abdominal ultrasonography
o

This test may reveal structural anomalies of the kidneys, renal vasculature, or the presence of tumors.

Renal scarring is suggestive of excessive renin release.

Renal size asymmetry is suggestive of renal dysplasia or renal artery stenosis.

Renal or extrarenal masses are suggestive of Wilms tumor or neuroblastoma, respectively.

Radionuclide imaging (without or with captopril): Asymmetry is suggestive of renal artery stenosis.

Doppler studies: Asymmetry in renal artery blood flow is suggestive of renal artery stenosis.

Digital subtraction arteriography: Asymmetry between the 2 renal arteries is indicative of renal artery stenosis.

Angiography
o

This test may reveal differences in the structure (diameter) of the renal vessels.

Sampling of blood from renal arteries, renal veins, and aorta may reveal differences in renin secretion be

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