Hypertension in the pediatric population 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 (JNC-7).
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. It may be categorized as prehypertension if the BP is between 90th to 95th percentile.
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]
Blood pressure (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] :
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.
Hypertension can be primary (ie, essential) or secondary. In general, the younger the child and the higher the blood pressure (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
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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]
The prevalence of systemic hypertension in children appears to be increasing, especially in view of the growing population of children with obesity.[7] However, the true incidence of hypertension in the pediatric population is not known. This vagueness partly stems from the somewhat arbitrary definition of hypertension and is in part related to incomplete blood pressure (BP) screening during routine pediatric clinical visits. Evaluation of the frequency of hypertension screening revealed that only two thirds of routine pediatric visits had BP measurements and there was no BP screening in 20% of overweight or obese children during their routine visits.[8] Furthermore, 75% cases of hypertension and 90% cases of prehypertension were not further investigated.[9]
A study that evaluated targeted screening of hypertension in 5207 Swiss children (age 10-14 y) found a 2.2% overall prevalence of hypertension in this population, with 14% overweight/obese. The investigators indicated that targeted screening of hypertension to children with either overweight/obesity or those with hypertensive parents helps to reduce the proportion of children to screen to 30% as well as helps to identify up to 65% of all those with hypertension.[10]
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, and stroke has become increasingly recognized as a cause of pediatric morbidity/mortality.[11]
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. However, recent evidence indicates that hypertension in adults originates in childhood, because childhood blood pressure predicts BP in the adult.[12, 13]
In a more recent study that evaluated simplified pediatric prehypertension and hypertension criteria versus the 2004 Fourth Report criteria[3] in 1225 adults from the Bogalusa Heart Study (27.1-y follow-up since childhood), investigators found that both criteria equally predicted the risk of adult hypertension and subclinical cardiovascular disease (hazard ratio = 3.1 and 3.2, respectively).[14] Children with hypertension were also at higher risk of high pulse wave velocity (a measurement of arterial stiffness), high carotid intima-media thickness, and left ventricular hypertrophy. For children aged 6-11 years, the simplified definition for prehypertension was 110/70 mm Hg and that for hypertension was 120/80 mm Hg; for those aged 12-17 years, they were 120/80 mm Hg and 130/85 mm Hg, respectively.[14]
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-, sex-, and race-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.
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.
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.
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.[15] As many as 41% of children with high blood pressure (BP) have left ventricular hypertrophy (LVH).[16] 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.[17]
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
A well-taken history provides clues about the cause of hypertension and guides the selection and sequencing of ensuing investigations. Presenting symptoms and signs are not specific in neonates and are absent in most older children unless the hypertension is severe.
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)
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
Signs and symptoms that should alert the physician to the possibility of hypertension in neonates include the following:
Seizure
Irritability or lethargy
Respiratory distress
Congestive heart failure
Signs and symptoms that should alert the physician to the possibility of hypertension in older children include all of the above, as well as the following:
Best medical care includes yearly measurement of blood pressure (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 with oscillometry 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 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 and young children 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, 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 the amplitude of the arterial pulse seems lower in the legs than 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 of mercury in the infant but can rise to 10-20 mm Hg in the older child or adult. The 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 higher arm systolic pressure indicates aortic coarctation. High pressure in only the right arm suggests that an obstruction is present proximal to the origin of the left subclavian artery.
Interpretation of blood pressure values
Hypertension is defined as an average systolic or diastolic BP above the 95th percentile. 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, the patient is 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.
So-called 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.
Identification of signs of secondary hypertension
A primary objective of the physical examination is to identify signs of secondary hypertension. The following should be evaluated to assess for potential causes of the hypertension:
Body mass index may lead to an evaluation for metabolic syndrome
Tachycardia may indicate hyperthyroidism, pheochromocytoma, and neuroblastoma
Growth retardation may suggest chronic renal failure
Café au lait spots may point to neurofibromatosis
An abdominal mass may lead to an evaluation for Wilms tumor and polycystic kidney disease
Epigastric or abdominal bruit may lead to the diagnosis of coarctation of the abdominal aorta or renal artery stenosis
BP difference between the upper and lower extremities indicates coarctation of the thoracic aorta
Thyromegaly may suggest hyperthyroidism
Virilization or ambiguity may suggest adrenal hyperplasia
Stigmata of Bardet-Biedl, von Hippel-Lindau, Williams, or Turner syndromes
Acanthosis nigricans may indicate metabolic syndrome
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 choice of tests.
The complete blood cell (CBC) count may indicate anemia due to chronic renal disease. Blood chemistry studies may be helpful. An increased serum creatinine concentration indicates renal disease. Hypokalemia suggests hyperaldosteronism (see potassium).
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 catecholamines (eg, epinephrine, norepinephrine, or dopamine) are diagnostic of pheochromocytoma or neuroblastoma.
On urine dipstick testing (see urinalysis), a positive result for blood or protein indicates renal disease. Urine cultures are used to evaluate the patient for chronic pyelonephritis. High urinary excretion of catecholamines and catecholamine metabolites (metanephrine) indicates pheochromocytoma or neuroblastoma. Urine sodium levels reflect dietary sodium intake and may be used as a marker to follow a patient after dietary changes are attempted.
Fasting lipid panels and oral glucose-tolerance tests are performed to evaluate metabolic syndrome in obese children. Drug screening is performed to identify substances that might cause hypertension.
Left ventricular hypertrophy (LVH) results from chronic hypertension. The finding of LVH on echocardiography confirms the chronicity of the hypertension and is an absolute indication for starting or intensifying treatment. LVH is symmetric, consisting of equivalent increases in in thickness for both the left ventricular portion of the ventricular septum and the left ventricular posterior wall. Left ventricular function must also be assessed.
Echocardiography is essential in the evaluation of suspected aortic coarctation. The aortic arch and its branches must be examined in precise anatomic detail. Doppler sonographic interrogation of the aortic arch should include pulse Doppler sampling from various portions of the aortic arch and continuous wave Doppler of the descending aorta. These data are useful in quantitating the severity of aortic obstruction.[18]
Abdominal ultrasonography 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.
On Doppler studies, asymmetry in renal artery blood flow suggests renal artery stenosis.
Angiography 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.
On digital subtraction arteriography, asymmetry between the 2 renal arteries indicates renal artery stenosis.
Ambulatory blood pressure monitoring (ABPM) displays blood pressure (BP) changes associated with physiologic activity and environmental stimuli during sleep as well as while awake, and it may serve to better assess the BP. The mean 24-hour BP (systolic and diastolic) are compared with gender- and height-specific 99th percentiles based data. ABPM is useful in the initial evaluation of elevated BP, to recognize subjects at risk, and in evaluating response to treatment.[13]
Monitoring of BP on a 24-hour basis may help in diagnosing so-called 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, fearing invasive examinations, vaccinations, blood draws, and other factors. Use of 24-hour BP monitoring should be considered first in most uncomplicated cases of pediatric stage I hypertension.
Cardiac catheterization is not necessary in the evaluation of aortic coarctation. However, it is an integral part of transcatheter interventions such as balloon angioplasty or stent therapy.[19]
Computed tomography (CT) and magnetic resonance imaging (MRI) with angiography can provide further anatomic definition of an aortic coarctation, but neither study is necessary for diagnosis.
Radionuclide imaging may be considered, with or without captopril; asymmetry suggests renal artery stenosis.
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.
To the extent possible, treatment of hypertension (see the image below) should address the cause and correct it. It is essential to recognize remediable causes of hypertension, especially coarctation of the aorta in a symptomatic infant. Reserve the therapeutic modalities described below for those children who have irremediable causes of hypertension or essential hypertension.[20]
Nonpharmacologic measures are important in the treatment of all patients with hypertension, regardless of its etiology or severity. Pharmacologic treatment is indicated in some cases. Interventional cardiac catheterization procedures have been employed as well. Surgery may be required for children with severe renal vascular hypertension, renal segmental hypoplasia, coarctation of the aorta, Wilms tumor, or pheochromocytoma.
In children with mild or moderate hypertension, nonpharmacologic therapy may suffice to lower blood pressure (BP) to within normal limits. This 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 all overweight children with hypertension, regardless of etiology. Obesity and hypertension are closely correlated, particularly in adolescents.[15]
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.
Potassium supplementation can decrease BP and reduce ventricular hypertrophy in adults. How potassium supplementation affects children with hypertension remains to be determined. However, avoiding potassium depletion (eg, from diuretic therapy) and prescribing a potassium-rich diet in patients without renal insufficiency appear reasonable.
A low-fat diet is recommended for all patients with a high BP; a low-salt diet is also recommended for all such patients, though it may yield only a 4% reduction of the elevated pressure (see Dietary Measures). 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, or use of continuous positive airway pressure may improve the patient’s sleep and secondarily improve BP.
Many of the antihypertensive agents available for adult use may also be used to manage hypertensive children and adolescents, even though only limited data are available to support this practice. Angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), and calcium-channel blockers have the strongest data to support their use in pediatric patients. Nevertheless, there is a need for more trials in pediatric populations, especially comparative trials of different agents.[21, 22]
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.[3] Pediatric clinical trials have focused on the ability of each drug to lower blood pressure (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 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 1 drug should be started first. If this dose is unsuccessful, it should be titrated upward.
In children with uncomplicated primary hypertension, BP is considered controlled when it is below the 95th percentile. In children with chronic renal disease, diabetes, or hypertensive target-organ damage, the goal should be a BP below 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, treatment of chronic hypertension requires expertise that is seldom available in the general pediatrician. Therefore, it is advisable to refer patients to physicians who specialize in treatment of children with high BP. 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 ordered by city, state, and country.
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.
Hypertensive crises occur as a result of an acute illness (eg, postinfectious glomerulonephritis or acute renal failure), 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. Accurate assessment of blood pressure (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. Seizures due to severe hypertension must be treated with a fast-acting antihypertensive drug.
The following drugs are currently 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 µg/kg/min IV infusion
Sodium nitroprusside, 0.53-10 µg/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 Neonatal Hypertension.
The goal of therapy is to lower BP to normal. Clinicians should be familiar with the therapeutic effects 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.
Interventional cardiac catheterization procedures can be used to treat coarctation of the aorta. Balloon dilation of a previously untreated (native) coarctation remains controversial. Some pediatric cardiologists recommend this approach and may also place a stent across the coarctation site. The appropriateness of this approach remains to be determined in studies of long-term outcome. For detailed discussion of the role of transcatheter therapy (balloon angioplasty and stents), the reader is referred to the Medscape Drugs and Diseases topic Coarctation of the Aorta.[19] Most physicians seem to prefer surgical treatment for neonates and infants (<1 y). Children older than 1 year with discrete native coarctation may be adequately managed with balloon angioplasty. If the segment of aortic coarctation is long, surgical treatment in younger children and stents in adolescents and adults are appropriate treatment approaches.
A study by Sezer et al indicated that stent placement in pediatric patients with coarctation of the aorta can lower blood pressure but may not reduce it to normal levels. In the study, which involved 15 children with native or recurrent coarctation of the aorta who underwent stenting, as well as 30 healthy sex-and-age-matched control subjects, the investigators found that the patients’ mean arterial pressure prior to stenting, 134.4 mm Hg, had been reduced to 115.5 mm Hg by the sixth month postprocedure but was still not as low as that in the control group (107.3 mm Hg).[23]
In a multi-institutional study of 350 patients in which surgery, balloon angioplasty, and stent implantation were used in the treatment of native aortic coarctation, investigators showed improvement in all three groups both immediately after the procedure and at follow-up.[24] However, the stent group (1) had less complications when compared with the surgical and balloon angioplasty groups, (2) had shorter hospitalization duration when compared with surgical patients, and (3) had lower coarctation gradients at follow-up when compared with balloon angioplasty patients. Despite those findings, the stent group also had higher reintervention rates when compared with the surgical and balloon groups, although these were noted as “planned” reinterventions.[24]
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.
A pediatric endocrinologist should be consulted when pheochromocytoma is suspected. If the diagnosis is confirmed, surgical removal of the tumor is indicated. A pediatric endocrinologist should also be consulted when metabolic syndrome is diagnosed.
A pediatric and/or an interventional pediatric cardiologist should be consulted in the management of aortic coarctation.
A nutritionist can review the DASH eating plan with the patient’s family and make further suggestions for weight loss and sodium reduction.
A low-fat diet should be followed by all patients with elevated blood pressure (BP). Low levels of adipocytokine has been noted in patients with elevated percent fat content.[25, 26] An absence of this substance may cause an elevation of BP.[27, 28]
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).
Closely monitor patients with hypertension, particularly during the initial phase of therapy. A chemistry panel should be checked after therapy with an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin II receptor blocker (ARB) is started or increased.
The frequency of visits is dictated by various factors, including the following:
Degree of BP control
Extent of understanding of the disease and its treatment on the part of both the parents or caregivers and the patient
Adherence to nonpharmacologic and pharmacologic treatments
Ability to monitor BP properly 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.
Guidelines on screening for hypertension in children and adolescents have been issued by the following organizations:
US Preventive Services Task Force (USPSTF)
American Heart Association(AHA)
National Heart, Lung and Blood Institute (NHLBI)
European Society of Hypertension (ESH)
A comparison of the recommendations are provided in Table 3, below.
Table 3. Guidelines for Blood Pressure Screening in Children and Adolescents
Table 3.
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Specific recommendations (all of them graded as expert opinion) from the 2011 NHLBI Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents include the following lifestyle modifications for prevention and first-line intervention[31] :
The cardiovascular health integrated lifestyle diet (CHILD 1)
Increases in moderate to vigorous physical activity
Weight management
For children with stage 2 hypertension and stage 1 secondary hypertension or left ventricular hypertrophy, first-line therapy should also include antihypertensive medications
Antihypertensive medication is second-line therapy for children with stage 1 primary hypertension who show no improvement with lifestyle modifications
Insufficient evidence exists to recommend the use of specific antihypertensive agents for specific age groups
Losartan, amlodipine, felodipine, fosinopril, lisinopril, metoprolol, and valsartan are tolerated over short periods, and can reduce blood pressure in children from ages 6-17 years but predominantly are effective in adolescents
Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) should be limited to children aged 6 years or older with creatinine clearance of 30 mL/min/1.73 m2 or greater; in black children, higher doses of fosinopril may be needed for effective blood pressure control
Calcium channel blockers are contraindicated in children less than 1 year old
Beta-blockers are contraindicated in children with asthma or insulin-dependent diabetes
Diuretics are useful as add-on therapy in patients being treated with drugs from other classes; however, potassium-sparing diuretics (spironolactione, triamterene, amiloride) may cause severe hyperkalemia, especially if given with an ACE inhibitor or ARB; all patients treated with diuretics should have electrolyte levels monitored shortly after initiating therapy and periodically thereafter
Vasodilators: Tachycardia and fluid retention are common side effects; hydralazine can cause lupuslike syndrome; minoxidil is usually reserved for patients with hypertension resistant to multiple drugs and its prolonged use can cause hypertrichosis
The 2009 European Hypertension Society (EHS) guidelines for blood pressure management in children are in agreement with those of the NHLBI, however, they offer more specific guidance as to the clinical conditions for which specific antihypertensive drugs are recommended or contraindicated.[32] See Table 4, below.
Table 4. European Society of Hypertension Recommendations for Hypertensive Medications in Pediatric Patients
Drugs currently used to treat hypertensive emergencies include nicardipine, labetalol, and sodium nitroprusside.
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 may be 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 various mechanisms
Angiotensin-converting enzyme (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
Calcium-channel blockers, which block the entry of calcium into the cells, producing vasodilation
Clinical Context:
Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.
Rapidly absorbed, but bioavailability is significantly reduced with food intake. It achieves a peak concentration in an hour and has a short half-life. The drug is cleared by the kidney. Impaired renal function requires reduction of dosage. Absorbed well PO. Give at least 1 h before meals. If added to water, use within 15 min.
Can be started at low dose and titrated upward as needed and as patient tolerates.
Clinical Context:
Enalapril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion. It helps control blood pressure (BP) and proteinuria. It decreases the pulmonary-to-systemic flow ratio in the catheterization laboratory and increases systemic blood flow in patients with relatively low pulmonary vascular resistance.
Enalapril has a favorable clinical effect when administered over a long period. It helps prevent potassium loss in distal tubules. The body conserves potassium; thus, less oral potassium supplementation is needed.
Clinical Context:
Lisinopril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.
Lisinopril is now commercially available as a 1 mg/ml oral solution (Qbrelis)
Clinical Context:
Benazepril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.
When pediatric patients are unable to swallow tablets or the calculated dose does not correspond with tablet strength, an extemporaneous suspension can be compounded. Combine 300 mg (15 tablets of 20-mg strength) in 75 mL of Ora-Plus suspending vehicle, and shake well for at least 2 minutes. Let the tabs sit and dissolve for at least 1 hour, then shake again for 1 minute. Add 75 mL of Ora-Sweet. The final concentration is 2 mg/mL, with a total volume of 150 mL. The expiration time is 30 days with refrigeration.
Clinical Context:
Fosinopril is a competitive ACE inhibitor. It prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion. It decreases intraglomerular pressure and glomerular protein filtration by decreasing efferent arteriolar constriction.
ACE inhibitors prevent conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, and lower aldosterone secretion. They 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 black patients than in white 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 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.
Clinical Context:
Atenolol is used to treat hypertension. It selectively blocks beta1-receptors, with little or no effect on beta2 types. Beta-adrenergic blocking agents affect blood pressure via multiple mechanisms.
Actions include a negative chronotropic effect that decreases heart rate at rest and after exercise, a negative inotropic effect that decreases cardiac output, reduction of sympathetic outflow from the central nervous system (CNS), and suppression of renin release from the kidneys. Atenolol is used to improve and preserve hemodynamic status by acting on myocardial contractility, reducing congestion, and decreasing myocardial energy expenditure.
Beta-adrenergic blockers reduce the inotropic state of the left ventricle, decrease diastolic dysfunction, and increase left ventricular compliance, thereby reducing the pressure gradient across the left ventricular outflow tract. Atenolol decreases the heart rate, thus reducing myocardial oxygen consumption and reducing myocardial ischemia potential. During intravenous (IV) administration, carefully monitor BP, heart rate, and electrocardiography (ECG).
Clinical Context:
Metoprolol is a selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. During IV administration, carefully monitor BP, heart rate, and ECG.
Clinical Context:
Propranolol has membrane-stabilizing activity and decreases the automaticity of contractions. It is not suitable for emergency treatment of hypertension. Do not give it IV in hypertensive emergencies.
Clinical Context:
This combination of a beta-blocker and a diuretic includes a selective beta1-adrenergic receptor blocker that decreases the automaticity of contractions.
Beta-blockers are especially useful in the concurrent treatment of hypertension and migraine. Dosing is limited by the bradycardia adverse effect. Drugs of this class should not be prescribed to athletes, because their athletic performance may be compromised. This class should not be used in patients with insulin-dependent diabetes, because these drugs blunt the normal warning symptoms of hypoglycemia.
Noncardioselective agents (ie, agents that elicit beta1 and beta2 blockade, eg, propranolol) are contraindicated in asthma and heart failure, due to their ability to cause bradycardia and bronchospastic actions. Selective beta1 -adrenergic blockers include atenolol and metoprolol. Labetalol elicits a mixed alpha and beta blockade. Another agent from this class is propranolol.
Clinical Context:
Hydrochlorothiazide inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium and water as well as of potassium and hydrogen ions.
Clinical Context:
Chlorthalidone inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium and water as well as of potassium and hydrogen ions.
Thiazide diuretics inhibit the reabsorption of sodium in the distal tubules, increasing the excretion of sodium, water, and potassium and hydrogen ions. They have been effective in treating hypertension of various etiologies. Besides diminishing sodium reabsorption, they also appear to diminish the sensitivity of blood vessels to circulating vasopressor substances. In all patients treated with diuretics, electrolyte levels should be monitored. Examples of thiazide diuretics are hydrochlorothiazide and chlorthalidone.
Clinical Context:
Furosemide is a loop diuretic that increases the excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and the distal renal tubule. It increases renal blood flow without increasing the filtration rate. The onset of action is generally within 1 hour. Furosemide increases potassium, sodium, calcium, and magnesium excretion.
The dose must be individualized to the patient. Depending on the response, administer furosemide at increments of 20-40 mg, no sooner than 6-8 hours after the previous dose, until the desired diuresis occurs. When treating infants, titrate with 1 mg/kg/dose increments until a satisfactory effect is achieved.
Diuretics have major clinical uses in managing disorders involving abnormal fluid retention (edema) and in treating hypertension; their diuretic action causes decreased blood volume.
Clinical Context:
Bumetanide increases the excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium, potassium, and chloride reabsorption in the ascending loop of Henle. These effects increase the urinary excretion of sodium, chloride, and water, resulting in profound diuresis. Renal vasodilation occurs after administration, renal vascular resistance decreases, and renal blood flow is enhanced. In terms of effect, 1 mg of bumetanide is equivalent to approximately 40 mg of furosemide.
Loop diuretics inhibit the reabsorption of sodium chloride in the thick ascending limb of the loop of Henle. They can be used to treat hypertension in patients with renal insufficiency; they are less effective than thiazide diuretics in patients who are hypertensive with normal renal function. Examples of loop diuretics are furosemide and bumetanide.
Clinical Context:
Amiloride is a potassium-conserving (antikaliuretic) pyrazine-carbonyl-guanidine that is chemically unrelated to other known antikaliuretic or diuretic agents. It possesses weak (compared with thiazide diuretics) natriuretic, diuretic, and antihypertensive activity. In some clinical studies, its activity increased the effects of thiazide diuretics. Amiloride is not an aldosterone antagonist, and its effects are observed even in the absence of aldosterone.
Amiloride exerts its potassium-sparing effect through inhibition of sodium reabsorption at the distal convoluted tubule, the cortical collecting tubule, and the collecting duct. This decreases the net negative potential of the tubular lumen and reduces both potassium and hydrogen secretion and their subsequent excretion.
Amiloride usually begins to act within 2 hours after an oral dose. Its effect on electrolyte excretion reaches a peak between 6 and 10 hours and lasts about 24 hours. Peak plasma levels are obtained in 3-4 hours, and plasma half-life ranges from 6 to 9 hours.
Amiloride is not metabolized by the liver and is excreted unchanged by the kidneys. About 50% of a dose of amiloride is excreted in urine and 40% in stool within 72 hours. The drug has little effect on glomerular filtration rate (GFR) or renal blood flow. Because the liver does not metabolize amiloride, drug accumulation is not anticipated in patients with hepatic dysfunction; however, accumulation can occur if hepatorenal syndrome develops.
Amiloride should rarely be used alone. When used as single agents, potassium-sparing diuretics, including amiloride, result in an increased risk of hyperkalemia (approximately 10% with amiloride). This agent should be used alone only when persistent hypokalemia has been documented and only with careful titration of the dose and close monitoring of serum electrolytes.
Potassium-sparing diuretics are used alone or in combination with other diuretics to prevent or correct hypokalemia. However, these drugs can cause hyperkalemia, particularly when given to patients with renal insufficiency or administered in combination with ACE inhibitors and ARBs. Examples of potassium-sparing diuretics are spironolactone and amiloride.
Clinical Context:
Amlodipine is generally regarded as a dihydropyridine, although experimental evidence suggests that it also may bind to nondihydropyridine binding sites. It is appropriate for the prophylaxis of variant angina and has antianginal and antihypertensive effects. Amlodipine blocks the postexcitation release of calcium ions into cardiac and vascular smooth muscle, thereby inhibiting the action of adenosine triphosphatase (ATPase) on myofibril contraction.
The overall effect is reduced intracellular calcium levels in cardiac and smooth-muscle cells of the coronary and peripheral vasculature, resulting in dilatation of coronary and peripheral arteries. Amlodipine also increases myocardial oxygen delivery in patients with vasospastic angina, and it may potentiate ACE inhibitor effects.
During depolarization, amlodipine inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium. It benefits nonpregnant patients with systolic dysfunction, hypertension, or arrhythmias. It has a substantially longer half-life than nifedipine and diltiazem and is administered once daily.
Clinical Context:
Felodipine relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery. It benefits nonpregnant patients with systolic dysfunction, hypertension, or arrhythmias. It can be used during pregnancy if clinically indicated.
Calcium-channel blockers potentiate ACE inhibitor effects. Renal protection is not proven, but these agents reduce morbidity and mortality rates in congestive heart failure. Calcium-channel blockers are indicated in patients with diastolic dysfunction. They are effective as monotherapy in black patients and elderly patients.
Clinical Context:
Isradipine is a dihydropyridine calcium-channel blocker. It inhibits calcium from entering select voltage-sensitive areas of vascular smooth muscle and myocardium during depolarization. This causes relaxation of coronary vascular smooth muscle, which results in coronary vasodilation. Vasodilation reduces systemic resistance and blood pressure, with a small increase in resting heart rate. Isradipine also has negative inotropic effects.
Calcium-channel blockers affect BP by decreasing vascular peripheral resistance. With short-acting calcium-channel blockers, the cardiac response to this action is variable, resulting in tachycardia. Long-acting preparations may cause a decrease in the heart rate.
Calcium-channel blockers are classified by their structure, and they have different degrees of selectivity in their effects on vascular smooth muscle. The dihydropyridines do not exert electrophysiologic effects and are commonly used to manage hypertension. Facial flushing may occur. Examples of calcium-channel blockers are include amlodipine and isradipine.
Clinical Context:
Irbesartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II at the tissue receptor site. It may induce a more complete inhibition of renin-angiotensin system than ACE inhibitors do, does not affect the response to bradykinin, and is less likely to be associated with cough and angioedema.
Clinical Context:
Losartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II. It may induce a more complete inhibition of renin-angiotensin system than ACE inhibitors do, does not affect the response to bradykinin, and is less likely to be associated with cough and angioedema. It is suitable for patients unable to tolerate ACE inhibitors.
Clinical Context:
Olmesartan blocks the vasoconstrictor effects of angiotensin II by selectively blocking the binding of angiotensin II to angiotensin I receptors in vascular smooth muscle. Its action is independent of the pathways for angiotensin II synthesis.
Clinical Context:
Valsartan is a prodrug that produces direct antagonism of angiotensin II receptors. It displaces angiotensin II from angiotensin I receptors and may lower blood pressure by antagonizing angiotensin I-induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses.
Valsartan may induce a more complete inhibition of renin-angiotensin system than ACE inhibitors do, does not affect the response to bradykinin, and is less likely to be associated with cough and angioedema. It is suitable for patients unable to tolerate ACE inhibitors.
ARBs lower BP by blocking the final receptor (ie, angiotensin II) in the renin-angiotensin axis. Like ACE inhibitors, they are contraindicated in pregnancy. Serum electrolyte and creatinine levels should be monitored. Examples of ARBs are irbesartan and losartan.
Clinical Context:
Clonidine is a central alpha-adrenergic agonist that stimulates alpha2-adrenoreceptors in the brainstem and activates inhibitory neurons, causing decreases in vasomotor tone and heart rate.
Central alpha-agonists lower BP by stimulating alpha2 -adrenergic receptors in the brainstem and activate inhibitory neurons, causing decreased vasomotor tone and heart rate. This class of drugs may cause dry mouth or sedation. Caution is warranted in patients with cerebrovascular disease, coronary insufficiency, sinus-node dysfunction, or renal impairment. A transdermal patch is available.
Sudden discontinuance of central alpha-agonists may lead to severe rebound hypertension. These drugs have been used in the past for the treatment of children with attention deficit hyperactivity disorder (ADHD) and still may be used successfully in patients with ADHD who also have hypertension. An example of a central alpha-agonist is clonidine.
Clinical Context:
Hydralazine decreases systemic resistance through direct vasodilation of arterioles. It is used to treat hypertensive emergencies. The use of a vasodilator will reduce systemic vascular resistance, which, in turn, may allow forward flow, improving cardiac output.
These drugs act directly on the smooth muscle in the peripheral vasculature to cause vasodilation. Tachycardia and fluid retention are common side effects. Prolonged use of minoxidil can cause hypertrichosis. Hydralazine can cause a lupuslike syndrome in certain populations of slow acetylators. Examples of direct vasodilators are minoxidil and hydralazine.
Clinical Context:
Doxazosin, a quinazoline compound, is a selective alpha1-adrenergic antagonist. It inhibits postsynaptic alpha-adrenergic receptors, causing vasodilation of veins and arterioles and decreases total peripheral resistance and BP.
Clinical Context:
Prazosin treats prostatic hypertrophy. It improves urine flow rates through relaxation of smooth muscle, accomplished by blocking alpha1-adrenoceptors in the bladder neck and prostate. When increasing the dose, administer the first dose of each increment at bedtime to reduce syncopal episodes. Although doses higher than 20 mg/day usually do not increase efficacy, some patients may benefit from doses as high as 40 mg/day.
Peripheral alpha-antagonists inhibit postsynaptic alpha-adrenergic receptors, resulting in vasodilation of veins and arterioles and decreasing total peripheral resistance and BP. These drugs often cause marked hypotension after the first dose. High doses are likely to cause postural hypotension. Of the peripheral alpha-antagonists, doxazosin and terazosin are selective for alpha1 -receptors. Prazosin is nonselective and inhibits both alpha1 - and alpha2 -receptors.
Edwin Rodriguez-Cruz, MD, Director, Section of Cardiology, Department of Pediatrics, San Jorge Children’s Hospital, Puerto Rico; Private Practice in Interventional Pediatric Cardiology and Internal Medicine, Centro Pedíatrico y Cardiovascular
Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: St Jude's Medical Co.<br/>Received grant/research funds from NOVARTIS for investigator; Received consulting fee from St. Jude Medical Corp. for speaking and teaching.
Chief Editor
Syamasundar Rao Patnana, MD, Professor of Pediatrics and Medicine, Division of Cardiology, Emeritus Chief of Pediatric Cardiology, University of Texas Medical School at Houston and Children's Memorial Hermann Hospital
Disclosure: Nothing to disclose.
Acknowledgements
Leigh M Ettinger, MD, MS Clinical Assistant Professor, Division of Pediatric Nephrology, The Joseph M Sanzari Children's Hospital, Hackensack University Medical Center
Disclosure: Nothing to disclose.
Ira H Gessner, MD Professor Emeritus, Pediatric Cardiology, University of Florida College of Medicine
Ira H Gessner, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.
John W Moore, MD, MPH Professor of Clinical Pediatrics, Section of Pediatric Cardiology, Department of Pediatrics, University of California San Diego School of Medicine; Director of Cardiology, Rady Children's Hospital
John W Moore, MD, MPH is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.
Adrian Spitzer, MD Clinical Professor Emeritus, Department of Pediatrics, Albert Einstein College of Medicine
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
Disclosure: Nothing to disclose.
Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Rao PS, Seib PM. Coarctation of the aorta. Medscape Drugs & Diseases from WebMD. Available at http://emedicine.medscape.com/article/895502-overview. September 25, 2014; Accessed: July 17, 2015.
[Guideline] University of Michigan Health System. Essential hypertension. Ann Arbor (MI): University of Michigan Health System; 2009 Feb.
[Guideline] U.S. Preventive Services Task Force. Final Recommendation Statement: Blood Pressure in Children and Adolescents (Hypertension): Screening. U.S. Preventive Services Task Force. Available at http://www.uspreventiveservicestaskforce.org/Page/Document/RecommendationStatementFinal/blood-pressure-in-children-and-adolescents-hypertension-screening. October 2013; Accessed: May 14, 2016.
(Endorsed by American Academy of Family Physicians)
2013
Asymptomatic children and adolescents
Insufficient evidence to recommend for or against screening for primary prevention of hypertension
N/A
American Heart Association (AHA)[30]
2014
Ages 3 to 17 years
Office measurement of blood pressure; 24-hour ambulatory BP monitoring to confirm diagnosis
Annually at well-child visits
National Heart, Lung and Blood Institute (NHLBI)[31]
(Endorsed by American Academy of Pediatrics)
2011
Ages 3 to 17 years
Office measurement of BP
Annually at well-child visits
European Society of Hypertension (ESH)[32]
2009
Ages 3 to 17 years
Office measurement of blood pressure; 24-hour ambulatory BP monitoring to confirm diagnosis prior to starting drug treatment
When seen in a medical setting
National Heart, Lung and Blood Institute (NHLBI)[31]
(Endorsed by American Academy of Pediatrics)
2011
Age <3 years
Office measurement of BP
Under the following conditions:
Prematurity, very low birth weight, or other neonatal complication requiring intensive care; congenital heart disease (repaired or unrepaired); recurrent urinary tract infections, hematuria, or proteinuria; known renal disease or family history of congenital renal disease; organ transplant, malignancy or bone marrow transplant; treatment with drugs known to raise BP; other systemic illnesses associated with hypertension; or evidence of increased intracranial pressure
European Society of Hypertension (ESH)[32]
2009
Age <3 years
Office measurement of blood pressure; 24-hour ambulatory BP monitoring to confirm diagnosis prior to starting drug treatment
When seen in a medical setting
Under special circumstances (eg, conditions requiring intensive care, congenital heart disease, renal disease, treatment with drugs known to raise BP and evidence of elevated intracranial pressure)
Drug Class
Indications
Contraindications
Angiotensin-converting enzyme (ACE) inhibitors/angiotensin II receptor blockers (ARBs)
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