Background
Pediatric hypertension is now commonly observed. Hypertension is known to be a major cause of morbidity and mortality in the United States and in many other countries, and the long-term health risks to children with hypertension may be substantial. In the United States, extensive normative data on blood pressure (BP) in children are available.
The Task Force on Blood Pressure Control in Children, commissioned by the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health (NIH), developed standards for BP by using the results of 11 surveys of more than 83,000 person-visits of infants and children (including approximately equal numbers of boys and girls). The percentile curves were first published in 1987 and describe age-specific distributions of systolic and diastolic BP in infants and children, with corrections for height and weight.[1]
The Third Report of the Task Force, published in 1996, provided further details regarding the diagnosis and treatment of hypertension in infants and children.[2] In 2004, the Fourth Report added normative data and adapted the data to growth charts from the Centers for Disease Control and Prevention (CDC) for 2000.[3] In accordance with the recommendations of the Task Force, BP is considered normal when the systolic and diastolic values are less than the 90th percentile for the child’s age, sex, and height.
The Fourth Report introduced a new category, prehypertension, which is diagnosed when a child’s average BP is above the 90th percentile but below the 95th. Any adolescent whose BP is greater than 120/80 mm Hg is also given this diagnosis, even if the BP is below the 90th percentile. This classification was created to align the categories for children with the categories for adults from the recommendations of the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.
Stage I hypertension is diagnosed if a child’s BP is greater than the 95th percentile but less than or equal to the 99th percentile plus 5 mm Hg. Stage II hypertension is diagnosed if a child’s BP is greater than the 99th percentile plus 5 mm Hg.
If the systolic and diastolic pressures give rise to a discrepancy with respect to classification, the child’s condition should be categorized by using the higher value. Table 1 (see below) serves as a guide to the practicing physician. Full blood pressure tables for children and adolescents are available from the NHLBI.
Table 1. Ninety-Fifth Blood Pressure Percentiles for 50th and 75th Height Percentiles in Children and Adolescents[3] (Open Table in a new window)
| Age, y | 95th BP Percentile for Girls, mm Hg | 95th BP Percentile for Boys, mm Hg | ||
| 50th Height Percentile | 75th Height Percentile | 50th Height Percentile | 75th Height Percentile | |
| 1 | 104/58 | 105/59 | 103/56 | 104/58 |
| 6 | 111/74 | 113/74 | 114/74 | 115/75 |
| 12 | 123/80 | 124/81 | 123/81 | 125/82 |
| 17 | 129/84 | 130/85 | 136/87 | 138/87 |
Pathophysiology
BP 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 BP, which is the driving pressure.
Factors that affect cardiac output include the following[4] :
- Baroreceptors
- Extracellular volume
- Effective circulating volume - Atrial natriuretic hormones, mineralocorticoids, angiotensin
- Sympathetic nervous syndrome
- Factors that affect vascular resistance include the following[4] :
- Pressors - Angiotensin II, calcium (intracellular), catecholamines, sympathetic nervous system, vasopressin
- Depressors - Atrial natriuretic hormones, endothelial relaxing factors, kinins, prostaglandin E2, prostaglandin I2
Changes in electrolyte homeostasis, particularly changes in sodium, calcium, and potassium concentrations, affect some of these factors.
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 BP. By means of various physical and hormonal mechanisms, this elevation triggers changes in both the glomerular filtration rate (GFR) and the tubular reabsorption of sodium, resulting in excretion of excess sodium and restoration of sodium balance.
A rise in the intracellular calcium concentration, due to changes in plasma calcium concentration, increases vascular contractility. In addition, calcium stimulates release of renin, synthesis of epinephrine, and sympathetic nervous system activity. Increased potassium intake suppresses production and release of renin and induces natriuresis, decreasing BP.
The complexity of the system explains the difficulties often encountered in identifying the mechanism that accounts for hypertension in a particular patient. These difficulties are the main reason why treatment is often designed to affect regulatory factors rather than the cause of the disease.
In a child who is obese, hyperinsulinemia may elevate BP by increasing sodium reabsorption and sympathetic tone.
Etiology
Hypertension can be primary (ie, essential) or secondary. In general, the younger the child and the higher the BP, the greater the likelihood that hypertension is secondary to an identifiable cause (see Table 2 below). A secondary cause of hypertension is most likely to be found before puberty; after puberty, hypertension is likely to be essential.
Table 2. Common Causes of Hypertension by Age (Open Table in a new window)
| Infants | Children | Adolescents | |
| 1-6 y | 7-12 y | ||
| Thrombosis of renal artery or vein Congenital renal anomalies Coarctation of aorta Bronchopulmonary dysplasia | Renal artery stenosis Renal parenchymal disease Wilms tumor Neuroblastoma Coarctation of aorta | Renal parenchymal disease Renovascular abnormalities Endocrine causes Essential hypertension | Essential hypertension Renal parenchymal disease Endocrine causes |
A review of the literature revealed that most of the young patients with secondary hypertension had a renal parenchymal abnormality; in the remaining patients, the causes of hypertension (in order of frequency) were renal artery stenosis, coarctation of the aorta, pheochromocytoma, and a variety of other conditions.[5, 6]
Epidemiology
United States statistics
The true incidence of hypertension in the pediatric population is not known. This vagueness partly stems from the somewhat arbitrary definition of hypertension.
In adults, hypertension is defined on the basis of data from extensive studies that allowed correlation of BP with adverse events, such as heart failure or stroke. Similar studies have not been performed in children, although reports from small populations of children provided compelling evidence of a relation between hypertension and both ventricular hypertrophy and atherosclerosis.
In children, the definition of hypertension is based exclusively on frequency-distribution curves for BP. As a consequence, estimates of the prevalence of pediatric hypertension lack a scientific basis. The number of children who might be defined as having hypertension and the frequency with which they develop complications during adulthood remain unknown.
International statistics
Because of differences in genetic and environmental factors, incidences vary from country to country and even from region to region in the same country.
Age-related demographics
Height and weight affect BP. However, these relations do not become evident until children reach school age. The Task Force on Blood Pressure Control in Children considered these factors when they published their normative data in 1987.[1]
Numerous investigators have noted a correlation between the BP of parents and that of their offspring. Familial aggregation of BP is detectable early in life. Some data relate this association to concomitant obesity in both parent and child.
Sex-related demographics
There are no significant differences in BP between girls and boys younger than 6 years. From that age until puberty, BP is slightly higher in girls than in boys. At puberty and beyond, BP is slightly higher in male adolescents and men than in comparably aged female adolescents and women.
Race-related demographics
The Task Force on Blood Pressure Control in Children noted no differences in BP between African American and white children. However, both peripheral vascular resistance and sensitivity of BP to salt intake appear to be greater in African American children than in white children, at any age.
Prognosis
High blood pressure is a precursor of heart attacks and strokes, as has been well established in the adult literature.
Obese children have approximately a 3-fold higher risk for hypertension than nonobese children. As many as 41% of children with high BP have left ventricular hypertrophy (LVH).[7] Almost 60% of children with persistent elevated BP have relative weights greater than 120% of the median for their sex, height, and age. As in adults, in whom abdominal girth correlates to elevated blood pressure, studies show that this measurement is also to be considered in the assessment of a teenager with suspected BP elevation at an early age.[8]
Patient Education
Parents, caregivers, and children themselves must be properly advised about restriction of exercise, when appropriate. They must also be informed about the potential adverse effects of medication. Finally, it is vital to educate parents, caregivers, and children about the potential complications of persistent hypertension.
For patient education resources, see the Diabetes Center, as well as High Blood Pressure
[Guideline] Task Force. Report of the Second Task Force on Blood Pressure Control in Children--1987. Task Force on Blood Pressure Control in Children. National Heart, Lung, and Blood Institute, Bethesda, Maryland. Pediatrics. Jan 1987;79(1):1-25. [Medline].
[Guideline] Task Force. 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. National High Blood Pressure Education Program Working Group on Hypertension Control. Pediatrics. Oct 1996;98(4 Pt 1):649-58. [Medline].
[Guideline] NHLBI. National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents. The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. Pediatrics. Aug 2004;114(2 Suppl 4th Report):555-76. [Medline]. [Full Text].
Gruskin AB. Factors affecting blood pressure. In: Drukker A, Gruskin AB, eds. Pediatric Nephrology: Pediatric and Adolescent Medicine. 3rd ed. Basel, Switzerland: Karger; 1995:1097.
Gavrilovici C, Boiculese LV, Brumariu O, Dimitriu AG. [Etiology and blood pressure patterns in secondary hypertension in children]. Rev Med Chir Soc Med Nat Iasi. Jan-Mar 2007;111(1):70-81. [Medline].
Kapur G, Ahmed M, Pan C, Mitsnefes M, Chiang M, Mattoo TK. Secondary hypertension in overweight and stage 1 hypertensive children: a Midwest Pediatric Nephrology Consortium report. J Clin Hypertens (Greenwich). Jan 2010;12(1):34-9. [Medline].
Hanevold C, Waller J, Daniels S, Portman R, Sorof J. The effects of obesity, gender, and ethnic group on left ventricular hypertrophy and geometry in hypertensive children: a collaborative study of the International Pediatric Hypertension Association. Pediatrics. Feb 2004;113(2):328-33. [Medline].
Leung LC, Sung RY, So HK, et al. Prevalence and risk factors for hypertension in Hong Kong Chinese adolescents: waist circumference predicts hypertension, exercise decreases risk. Arch Dis Child. Sep 2011;96(9):804-9. [Medline].
[Guideline] University of Michigan Health System. Essential hypertension. Ann Arbor (MI): University of Michigan Health System; 2009 Feb. [Full Text].
Meyers RS, Siu A. Pharmacotherapy Review of Chronic Pediatric Hypertension. Clin Ther. Oct 7 2011;[Medline].
Schaefer F, Litwin M, Zachwieja J, Zurowska A, Turi S, Grosso A, et al. Efficacy and safety of valsartan compared to enalapril in hypertensive children: a 12-week, randomized, double-blind, parallel-group study. J Hypertens. Oct 21 2011;[Medline].
Aeberli I, Spinas GA, Lehmann R, l'Allemand D, Molinari L, Zimmermann MB. Diet determines features of the metabolic syndrome in 6- to 14-year-old children. Int J Vitam Nutr Res. Jan 2009;79(1):14-23. [Medline].
Gonzalez-Juanatey JR, Paz FL, Eiras S, Teijeira-Fernandez E. [Adipokines as novel cardiovascular disease markers. Pathological and clinical considerations]. Rev Esp Cardiol. Jun 2009;62 Suppl 2:9-16. [Medline].
Kshatriya S, Reams GP, Spear RM, Freeman RH, Dietz JR, Villarreal D. Obesity hypertension: the emerging role of leptin in renal and cardiovascular dyshomeostasis. Curr Opin Nephrol Hypertens. Oct 21 2009;[Medline].
Nakamura Y, Ueshima H, Okuda N, et al. Relation of serum leptin to blood pressure of Japanese in Japan and Japanese-Americans in Hawaii. Hypertension. Dec 2009;54(6):1416-22. [Medline].
| Age, y | 95th BP Percentile for Girls, mm Hg | 95th BP Percentile for Boys, mm Hg | ||
| 50th Height Percentile | 75th Height Percentile | 50th Height Percentile | 75th Height Percentile | |
| 1 | 104/58 | 105/59 | 103/56 | 104/58 |
| 6 | 111/74 | 113/74 | 114/74 | 115/75 |
| 12 | 123/80 | 124/81 | 123/81 | 125/82 |
| 17 | 129/84 | 130/85 | 136/87 | 138/87 |
| Infants | Children | Adolescents | |
| 1-6 y | 7-12 y | ||
| Thrombosis of renal artery or vein Congenital renal anomalies Coarctation of aorta Bronchopulmonary dysplasia | Renal artery stenosis Renal parenchymal disease Wilms tumor Neuroblastoma Coarctation of aorta | Renal parenchymal disease Renovascular abnormalities Endocrine causes Essential hypertension | Essential hypertension Renal parenchymal disease Endocrine causes |

