AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• DIFFERENTIALS
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• DIFFERENTIALS
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Hypertension is a major cause of morbidity and mortality in the United States and in many other countries. The prevalence of hypertension in the United States for people aged 60-69 years is more than 50%. This prevalence increases to approximately 75% among those aged 75 years. Hypertension is now commonly discovered in children. The long-term health risks to these children with hypertension may be substantial.

For children in the United States, extensive normative data for blood pressure (BP) 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 developed standards for BP by using the results of 11 surveys of more than 83,000 person visits of infants and children. Approximately equal numbers of boys and girls were surveyed. The percentile curves were first published in 1987 and describe age-specific distributions of systolic and diastolic BPs in infants and children with corrections for height and weight.¹

The Third Report of the Task Force, published in 1996, provides 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 See 2000 CDC Growth Charts: United States.

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 called prehypertension. The condition is diagnosed when a child's average BP exceeds the 90th percentile but is less than the 95th percentile. Any adolescent whose BP is greater than 120/80 mm Hg is also given this diagnosis, even if their reading is less than the 90th percentile. This classification was created to align the categories for children with the categories for adults from the 2003 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. A child is classified as having stage II hypertension if their BP is greater than the 99th percentile plus 5 mm Hg.

If the systolic and diastolic classifications cause a discrepancy, the child's condition should be categorized by using the higher value. Table 1 serves as a guide to the practicing physician. Full tables from the NHLBI may be found at Blood Pressure Tables for Children and Adolescents.

Table 1. The 95th Percentiles of Blood Pressure in Children and Adolescents³

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. Several factors regulate cardiac output and vascular resistance.

Factors that affect BP include the following:⁴

• Cardiac output
• • Baroreceptors
  • Extracellular volume
  • Effective circulating volume
  • • Atrial natriuretic hormones
    • Mineral corticoids
    • Angiotensin
  • Sympathetic nervous syndrome
• Vascular resistance
• • 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 the factors shown above. 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 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 the release of renin, synthesis of epinephrine, and activity of the sympathetic nervous system. 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. This difficulty explains 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.

Frequency

United States

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 for 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 relationship 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, estimations 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 remains unknown.

International

Because of differences in genetic and environmental factors, incidences vary from country to country and even from region to region in the same country.

Mortality/Morbidity

High blood pressure is a precursor of heart attacks and strokes; well established in the adult literature. Children who are obese have approximately a 3-fold higher risk for hypertension than children who are not obese. In studies, as many as 41% of children with high BP have left ventricular hypertrophy.⁵ Almost 60% of children with persistent elevated BP had relative weights greater than 120% of the median for their sex, height, and age.

Race

The Task Force on Blood Pressure Control in Children noted no differences in BP between African American and Caucasian children. However, peripheral vascular resistance and sensitivity of BP to salt intake appear greater in African American children than in Caucasian children, at any age.

Sex

No significant differences are observed 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.

Age

Height and weight affect BP. However, these relationships do not become evident until children are school aged. 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.

CLINICAL

Section 3 of 11  

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History

A well-taken history provides clues about the cause of hypertension and guides the nature and sequence of ensuing investigations.

• Relevant information includes the following:
• • Prematurity
  • Bronchopulmonary dysplasia
  • History of umbilical artery catheterization
  • Failure to thrive
  • History of head or abdominal trauma
  • Family history of heritable diseases (eg, neurofibromatosis, hypertension)
  • Medications (eg, pressor substances, steroids, tricyclic antidepressants, cold remedies, medications for attention deficit hyperactivity disorder [ADHD])
  • Episodes of pyelonephritis (perhaps suggested by unexplained fevers) that may result in renal scarring
  • Dietary history, including caffeine, licorice, and salt consumption
  • Sleep history, especially snoring history
  • Habits, such as smoking, drinking alcohol, and ingesting illicit substances
• Presenting symptoms and signs are not specific in neonates and absent in most older children unless their hypertension is severe.
• Signs and symptoms that should alert the physician to the possibility of hypertension include the following:
• • Neonates
  • • Failure to thrive
    • Seizure
    • Irritability or lethargy
    • Respiratory distress
    • Congestive heart failure
  • Children (Findings in addition to those observed in neonates)
  • • Headache
    • Fatigue
    • Blurred vision
    • Epistaxis
    • Bell palsy 

Physical

• Measurement and recording of blood pressure (BP)
• • Best medical care includes yearly measurement of BP in every child older than 3 years, preferably by means of auscultation with a mercury gravity manometer. Doppler and oscillometric techniques can be used in children in whom auscultatory BP measurements are difficult to obtain. Measurements obtained by using oscillometric devices that exceed the 90th percentile should be repeated with auscultation.
  • Measurements repeated over time are required to obtain meaningful information.
  • Proper cuff size is essential for accurate measurement of BP. The width of the rubber bladder inside the cloth cover should cover at least 40% of the patient's arm circumference at a point midway between the olecranon and the acromion. The length of the bladder in the cuff should cover 80-100% of the circumference of the arm. If a cuff is too small, the next larger cuff size should be used, even if it appears too large.
  • The child should be relaxed and in a comfortable, preferably sitting, position with the child's feet on the floor and the back supported. The patient's right arm should be resting on a supportive surface at the level of the heart. Infants can be examined while supine.
  • 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, whereas 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, or the fifth sound may not occur at all. Diastolic BP must be recorded. When Korotkoff sounds can be heard down to 0 mm Hg, the BP measurement should be repeated with less pressure applied to the head of the stethoscope than was applied before.
  • Systolic BP in the lower extremities must be measured when elevated systolic BP in the upper extremities is first noted regardless of whether amplitude of the arterial pulse seems lower in the legs to be lower than that in the arms. Increased systolic pressure in the arm suggests coarctation of the aorta. If found, systolic pressure must also be measured in the left arm and leg. 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 sonography can be used to detect onset of blood flow, which reflects systolic BP, in the posterior tibial or dorsalis pedis artery. The value should be compared with a similarly obtained Doppler systolic BP in the arm, again with the patient supine.
  • Remember that the artifact of distal pulse amplification causes the measured systolic BP 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. Magnitude of this artifact is directly proportional to the pulse pressure. In a patient with chronic aortic regurgitation, for example, the difference in measured systolic pressure may exceed 40 mm Hg. At no time should the systolic pressure in the arm exceed that in the foot. If it does, pressures in both arms and legs should be measured. Consistent recording of high arm systolic pressure indicates aortic coarctation. High pressure in only the right arm suggests that an obstruction is present proximal to origin of the left subclavian artery.
• Interpretation of BPs
• • Hypertension is defined as average systolic or diastolic BPs greater than those at the 95th percentile (see Table 1). Any child with a BP exceeding the 90th percentile requires scrutiny.
  • Patients with severe hypertension and target-organ damage require immediate attention. For other patients, several measurements of BP should be made at weekly intervals to determine if the elevation is sustained.
  • The average of multiple measurements should be plotted on an appropriate percentile chart. If the average measurement is between the 90th and 95th percentiles (ie, prehypertensive) the child's BP should be monitored at 6-month intervals. If the average BP is greater than the 95th percentile, the child should be evaluated further and therapy considered.
  • Patients with stage I hypertension should be seen again in 1-2 weeks. Those with stage II hypertension should be reevaluated in 1 week or sooner if the patient is symptomatic.
  • White-coat hypertension is diagnosed in a patient who has a BP above the 95th percentile when measured in the physician's office but who is normotensive outside the clinical setting. Ambulatory monitoring of BP usually is required to diagnose white-coat hypertension.
• Objective of physical examination: A primary objective of the physical examination is to identify signs of secondary hypertension, including the following:
• • Body mass index to assess for metabolic syndrome
  • Tachycardia to assess for hyperthyroidism, pheochromocytoma, and neuroblastoma
  • Growth retardation to assess for chronic renal failure
• • Café au lait spots to assess for neurofibromatosis
  • Abdominal mass to assess for Wilms tumor and polycystic kidney disease
  • Epigastric and/or abdominal bruit to assess for coarctation of the abdominal aorta or renal artery stenosis
  • BP difference between upper and lower extremities to assess for coarctation of the thoracic aorta
  • Thyromegaly to assess for hyperthyroidism
  • Virilization or ambiguity to assess for adrenal hyperplasia
  • Stigmata of Bardet-Biedl, von Hippel-Landau, Williams, or Turner syndromes
  • Acanthosis nigricans to assess for metabolic syndrome

Causes

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. A secondary cause of hypertension is most likely to found before puberty. After puberty, hypertension is likely to be essential.
• 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.
• Table 2. Common Causes of Hypertension by Age
  
  

  Infants	Children		Adolescents
  	1-6 y	7-12 y
  Thrombosis of renal artery or vein Congenital renal anomalies Coarctation of the aorta Bronchopulmonary dysplasia	Renal artery stenosis Renal parenchymal disease Wilms tumor Neuroblastoma Coarctation of the aorta	Renal parenchymal disease Renovascular abnormalities Endocrine causes Essential hypertension	Essential hypertension Renal parenchymal disease Endocrine causes

DIFFERENTIALS

Section 4 of 11  

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Other Problems to Be Considered

Pheochromocytoma

WORKUP

Section 5 of 11  

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Lab Studies

• In patients with hypertension, proceed from simple tests that can be performed in an ambulatory setting to complex noninvasive tests and finally to invasive tests.
• Findings from the patient's history and physical examination dictate the appropriate order of tests.
• • On urine dipstick testing, a positive result for blood and/or protein indicates renal disease.
  • Urine cultures are used to evaluate the patient for chronic pyelonephritis.
  • The CBC count may indicate anemia due to chronic renal disease.
  • Blood chemistry may be helpful. An increased serum creatinine concentration indicates renal disease. Hypokalemia suggests hyperaldosteronism.
  • Blood hormone levels may be measured. High plasma renin activity indicates renal vascular hypertension, including coarctation of the aorta, whereas low activity indicates glucocorticoid remediable aldosteronism, Liddle syndrome, or apparent mineralocorticoid excess. A high plasma aldosterone concentration is diagnostic of hyperaldosteronism. High values of catecholamine (epinephrine, norepinephrine, dopamine) are diagnostic of pheochromocytoma or neuroblastoma.
  • High urinary excretion of catecholamines and catecholamine metabolites (metanephrine) indicates pheochromocytoma or neuroblastoma.
  • Fasting lipid panels and oral (PO) glucose-tolerance tests are performed to evaluate metabolic syndrome in obese children.
  • Drug screening is performed to identify substances that might cause hypertension.
  • Urine sodium levels reflect dietary sodium intake and may be used as a marker to follow up a patient after dietary changes are attempted.

Imaging Studies

• Echocardiography
• • Left ventricular hypertrophy results from chronic hypertension. This finding confirms the chronicity of the hypertension and is an absolute indication for starting or intensifying treatment.
  • Left ventricular hypertrophy is symmetric, consisting of equivalent increases in thickness of both the left ventricular portion of the ventricular septum and the left ventricular posterior wall.
  • Also assess left ventricular function.
  • Echocardiography is essential in the evaluation of suspected aortic coarctation. Precise anatomic detail of the aortic arch and its branches must be obtained.
• Abdominal ultrasonography
• • This test may reveal tumors or structural anomalies of the kidneys or renal vasculature.
  • Renal scarring suggests excessive renin release.
  • Asymmetry in renal size suggests renal dysplasia or renal artery stenosis.
  • Renal or extrarenal masses suggest a Wilms tumor or neuroblastoma, respectively.
• Radionuclide imaging (without or with captopril): Asymmetry suggests renal artery stenosis.
• Doppler studies: Asymmetry in renal artery blood flow suggests renal artery stenosis.
• Digital subtraction arteriography: Asymmetry between the 2 renal arteries indicates renal artery stenosis.
• Angiography
• • 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 between the kidneys.
  • A renin activity ratio of 3:1 between the kidneys is considered diagnostic of renal vascular hypertension.
• Other tests
• • Cardiac catheterization is not necessary in the evaluation of aortic coarctation.
  • CT and MRI with angiography can provide further anatomic definition of an aortic coarctation, but neither study is necessary for diagnosis.

Other Tests

• Monitoring of blood pressure (BP) on a 24-hour basis may help in diagnosing white-coat hypertension and provides information about the risk of target end-organ damage.
• • White-coat hypertension is common because most children are uncomfortable at the physicians' office because of invasive examinations, vaccinations, blood draws, and other factors.
  • Use of the 24-hour monitor should be considered first in most uncomplicated cases of pediatric stage I hypertension.
• Polysomnography helps in identifying sleep disorders associated with hypertension. This test should be considered in obese children with a history of snoring, daytime sleepiness, or any sleep difficulties.
• Retinal examination may reveal retinal vascular changes.

TREATMENT

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Medical Care

To the extent possible, treatment of hypertension should address the cause and correct it. Reserve the therapeutic modalities described below for those children who have irremediable causes of hypertension or essential hypertension.

• Nonpharmacologic measures
• • Nonpharmacologic measures are important in the treatment of all patients with hypertension, regardless of its etiology or severity. In children with mild or moderate hypertension, this approach may suffice to lower blood pressure (BP) to within normal limits. A nonpharmacologic approach avoids the need for drugs that have adverse effects and that require a degree of compliance difficult to achieve in children.
• • Weight reduction should be a goal in overweight children with hypertension regardless of its etiology. Obesity and hypertension are closely correlated, particularly in adolescents.
  • Aerobic and isotonic exercises have a direct beneficial effect on BP. They help in reducing excess weight or maintaining appropriate body weight. Encourage participation in sports. Only patients with severe uncontrolled hypertension or cardiac abnormalities that require exercise restriction are exempt from aerobic and isotonic exercises.
  • Salt restriction probably benefits only a subgroup of patients with hypertension, particularly African American patients, who may have a defect in the cellular handling of sodium. However, given the excessive amount of salt in the typical American diet, reduced salt intake should be recommended to all patients with hypertension.
  • The Task Force recommends the Dietary Approaches to Stop Hypertension (DASH) eating plan (see Your Guide To Lowering Your Blood Pressure With DASH from the NHLBI).
  • Potassium supplementation can decrease BP and reduce ventricular hypertrophy in adults. How potassium supplementation affects children with hypertension remains to be tested. However, avoiding potassium depletion (eg, from diuretic therapy) and prescribing a potassium-rich diet in patients without renal insufficiency appear reasonable.
  • Stress-reducing activities (eg, meditation, yoga, biofeedback) can reduce BP when performed on a regular basis. However, this effect is lost when the activity is discontinued.
  • When sleep-disordered breathing is discovered, weight loss, tonsillectomy and adenoidectomy, and/or use of continuous positive airway pressure may improve the patient's sleep and secondarily improve BP.
• Pharmacologic measures
• • Some drugs currently used to treat hypertension in adults have been formally tested in children. Indications for pharmacologic treatment include symptomatic hypertension, secondary hypertension, hypertensive target-organ damage, diabetes, and hypertension that persists despite nonpharmacologic measures.
  • The Fourth Report recommends starting with a class of antihypertensive medication appropriate for each specific patient. Pediatric clinical trials have focused on the ability of each drug to lower BP, but the effects of these drugs on clinical endpoints have not been compared. Therefore, the choice of drug is the clinician's.
  • The Task Force recommends the use of ACE inhibitors or angiotensin II receptor blockers (ARBs) only for children with diabetes and microalbuminuria or proteinuric renal disease and recommends beta-blockers or calcium-channel blockers for children with hypertension and migraine headaches. A low dose of one drug should be started first. If unsuccessful, the dose should be uptitrated. BP is considered controlled when it is less than the 95th percentile in children with uncomplicated primary hypertension. When patients have chronic renal disease, diabetes, or hypertensive target-organ damage, the goal should be less than the 90th percentile. If BP is not controlled, a drug from another class should be added. If control is not achieved with 2 drugs, reconsider the possibility of secondary hypertension before adding a third drug.
  • In general, the treatment of chronic hypertension requires expertise that is seldom available in the general pediatrician. Therefore, referring patients to physicians who specialize in treatment of children with high BP is advisable. The American Society of Hypertension, Inc. (ASH) identifies physicians with expert skills and knowledge in the management of clinical hypertension and related disorders. It also grants such physicians the title Specialist in Clinical Hypertension. ASH provides a list of available specialists by city, state, and country (see the ASH Specialist Directory).
  • After BP is stabilized, the patient can return to the general pediatrician for follow-up care. The pediatrician should work in close collaboration with the specialist.
• Management of hypertensive crisis
• • Hypertensive crises occur as a result of an acute illness, such as postinfectious glomerulonephritis or acute renal failure, the excessive ingestion of drugs or psychogenic substances, or exacerbated moderate hypertension.
• • The clinical manifestations may be those of cerebral edema, seizures, heart failure, pulmonary edema, or renal failure. Remember that accurately assessing BP in every patient presenting with a seizure is essential, particularly when no seizure disorder has been established in that patient.
  • Anticonvulsant drugs are usually ineffective in treatment of a seizure due to a hypertensive crisis. However, seizures due to severe hypertension must be treated with a fast-acting antihypertensive drug.
  • Drugs currently used to treat hypertensive emergencies include nicardipine, labetalol, and sodium nitroprusside.
  • The goal of therapy is to decrease BP to normal. Clinicians should be familiar with the effect and adverse effects of these drugs. Patients must be supervised closely to avoid an excessively rapid decrease in BP, which may result in underperfusion of vital organs.
• Transcatheter therapy
• • Interventional cardiac catheterization procedures can be used to treat coarctation of the aorta. Balloon dilation of a previously untreated coarctation remains controversial. Some pediatric cardiologists recommend this approach and may also place a stent at the coarctation site. The appropriateness of this approach remains to be determined in studies of long-term outcome.
  • Balloon dilation, with or without stent placement, has gained widening acceptance for treatment of recurrent coarctation. Recurrence is most likely to arise when young infants must undergo surgical repair because of the severity of the lesion.
  • Interventional catheterization with balloon dilation can also successfully relieve many instances of discrete renal artery stenosis.

Surgical Care

Surgery may be required for children with severe renal vascular hypertension, renal segmental hypoplasia, coarctation of the aorta, Wilms tumor, or pheochromocytoma.

Consultations

A pediatric endocrinologist should be consulted when pheochromocytoma is suspected. If the diagnosis is confirmed, a qualified surgeon must remove the tumor. A pediatric endocrinologist should also be consulted when metabolic syndrome is diagnosed. A nutritionist can review the DASH eating plan with the patient's family and make further suggestions for weight loss and sodium reduction.

The Fourth Report provides a management algorithm (see Media file 1).

MEDICATION

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The following drugs currently are used in the treatment of hypertensive emergencies: labetalol 0.2-1 mg/kg/dose up to 40 mg/dose as an intravenous (IV) bolus or 0.25-3 mg/kg/h IV infusion, nicardipine 1-3 mcg/kg/min IV infusion, and sodium nitroprusside 0.53-10 mcg/kg/min IV infusion to start. Sublingual nifedipine is no longer recommended for the treatment of acute hypertension because of reports of death from hypotension in the adult population. Additional drug recommendations for patients aged 1-17 years may be found in The Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents.³ For neonatal doses, see the eMedicine article Neonatal Hypertension.

Many antihypertensive drugs are available for the treatment of chronic hypertension. The choice of drug is usually based on the mode of action and the potential for adverse effects. From a pharmacologic point of view, antihypertensive drugs are classified in the following categories: diuretics, which block sodium reabsorption at various levels of the renal tubules; adrenergic blockers, which act by competitively inhibiting the catecholamines; direct vasodilators, which act by means of a variety of mechanisms; ACE inhibitors, which block the conversion of angiotensin I to angiotensin II; angiotensin II receptor blockers (ARBs), which interfere with the binding of angiotensin II to angiotensin I receptors; and calcium-channel blockers, which block the entry of calcium into the cells, producing vasodilation.

Drug Category: ACE inhibitors –- These drugs prevent conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, and lower aldosterone secretion. ACE inhibitors are effective and well-tolerated drugs with no adverse effects on plasma lipid levels or glucose tolerance. They prevent the progression of diabetic nephropathy and other forms of glomerulopathies but appear to be less effective in African American patients than in Caucasian patients.

Patients with high plasma renin activity may have an excessive hypotensive response to ACE inhibitors. Patients with bilateral renal vascular disease or with single kidneys, whose renal perfusion is maintained by high levels of angiotensin II, may develop irreversible acute renal failure when treated with ACE inhibitors. ACE inhibitors may cause hyperkalemia; therefore, monitor serum potassium levels. ACE inhibitors are contraindicated in pregnancy. Cough and angioedema are less common with newer members of this class than with captopril. Serum potassium and serum creatinine concentrations should be monitored for the development of hyperkalemia and azotemia. Examples of agents from this class include captopril, lisinopril, and enalapril.

FOLLOW-UP

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• Follow-up
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• References

Further Outpatient Care

• Closely monitor patients with hypertension, particularly during the initial phase of therapy. A chemistry panel should be checked after therapy with an ACE inhibitor or an angiotensin II receptor blockers (ARBs) is started or increased.
• The frequency of visits is dictated by various factors, including the following:
• • Degree of control
  • Extent of understanding of the disease and its treatment by both the parents and/or caregivers and the patient
  • Adherence to nonpharmacologic and pharmacologic treatments
  • Ability to properly monitor blood pressure (BP) at home
  • Likelihood of drug adverse effects
  • Need to monitor for complications of hypertension
  • Need to monitor for weight loss
• After surgical or catheter treatment of coarctation of the aorta, patients must be monitored yearly with accurate measurement of systolic and diastolic pressures in the right arm. For these measurements, the patient should be properly positioned. Systolic pressures in both the right arm and leg should be obtained with the patient supine. Remember that systolic pressure in the lower leg should exceed that in the arm.

Patient Education

• For excellent patient education resources, see eMedicine's Diabetes Center. Also, visit eMedicine's patient education article, High Blood Pressure.

MISCELLANEOUS

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Medical/Legal Pitfalls

• Failure to recognize remediable causes of hypertension, especially coarctation of the aorta in a symptomatic infant
• Failure to properly advise the parents and/or caregivers and child about restriction of exercise, when appropriate
• Failure to inform parents and/or caregivers and child about the potential adverse effects of medication
• Failure to inform parents and/or caregivers and child about the potential complications of persistent hypertension

MULTIMEDIA

Section 10 of 11  

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• DIFFERENTIALS
• Workup
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• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Management algorithm. AMC = Apparent mineralocorticoid excess; GRA = Glucocorticoid remedial aldosteronism; VMA = Vanillylmandelic acid.
	View Full Size Image
Media type:  Graph

REFERENCES

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1. 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].
2. 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].
3. 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].
4. Gruskin AB. Factors affecting blood pressure. In: Drukker A, Gruskin AB, eds. Pediatric Nephrology: Pediatric and Adolescent Medicine. 3^rd ed. Basel, Switzerland: Karger; 1995:1097.
5. 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].
6. Bartosh SM, Aronson AJ. Childhood hypertension. An update on etiology, diagnosis, and treatment. Pediatr Clin North Am. Apr 1999;46(2):235-52. [Medline].
7. Falkner B, Gidding SS, Portman R, Rosner B. Blood pressure variability and classification of prehypertension and hypertension in adolescence. Pediatrics. Aug 2008;122(2):238-42. [Medline].
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Article Last Updated: Nov 7, 2008