Pediatric Annals

Special Issue Article 

Pediatric Hypertension

Debora Matossian, MD, MS

Abstract

The prevalence of elevated blood pressure and hypertension in children and adolescents has increased over the past decade. This trend is most likely related to increases in primary hypertension associated with increasing obesity rates in children. Lifestyle as well as genetics play a significant role in the development of primary hypertension. Hypertension in children and adolescents is under-recognized and undertreated. The 2017 Revised Clinical Practice Guideline for Screening and Management of High Blood Pressure in Children and Adolescents aimed to create new normative blood pressure tables using data from healthy weight children, meaning between the 5th and 85th percentile per the Centers for Disease Control and Prevention. Another important objective was to simplify normative data to ease screening and detection of elevated blood pressures. The consequences of chronic hypertension are significant, with its major affect being in poor cardiovascular health outcomes both in childhood and early adulthood. Challenges to detection and adequate treatment should be overcome with continued education and awareness to prevent the long-term effects of uncontrolled hypertension that starts in childhood. [Pediatr Ann. 2018;47(12):e499–e503.]

Abstract

The prevalence of elevated blood pressure and hypertension in children and adolescents has increased over the past decade. This trend is most likely related to increases in primary hypertension associated with increasing obesity rates in children. Lifestyle as well as genetics play a significant role in the development of primary hypertension. Hypertension in children and adolescents is under-recognized and undertreated. The 2017 Revised Clinical Practice Guideline for Screening and Management of High Blood Pressure in Children and Adolescents aimed to create new normative blood pressure tables using data from healthy weight children, meaning between the 5th and 85th percentile per the Centers for Disease Control and Prevention. Another important objective was to simplify normative data to ease screening and detection of elevated blood pressures. The consequences of chronic hypertension are significant, with its major affect being in poor cardiovascular health outcomes both in childhood and early adulthood. Challenges to detection and adequate treatment should be overcome with continued education and awareness to prevent the long-term effects of uncontrolled hypertension that starts in childhood. [Pediatr Ann. 2018;47(12):e499–e503.]

The prevalence of abnormal blood pressures (BP) is increasing in children. It occurs at rates similar to that of other common conditions that pediatricians frequently manage independently, such as asthma. Data show that approximately 11% of children and adolescents in the United States have abnormal BP.1

Elevated BP is often unrecognized due to several factors including lack of acute symptomatology until it is significantly elevated, suboptimal BP measurement techniques, and previously complicated childhood normative BP data. Even in those diagnosed with hypertension, treatment rates are low,2 likely also related to the relatively silent symptomatology as well as the lack of understanding of the potential long-term outcomes associated with years of uncontrolled hypertension.

Definition

The definition of hypertension was updated with the August 2017 release of the Clinical Practice Guidelines (CPG) for Screening and Management of High Blood Pressure in Children and Adolescents.3

For children age 13 years or older, the blood pressure staging will replicate that of adults, which was recently proposed by the American Heart Association and the American College of Cardiology: normal BP, <120/80 mm Hg; elevated BP (previously termed “prehypertension”), 120–129/80 mm Hg; stage 1 hypertension, 130–138/80–89 mm Hg; and stage 2 hypertension, >140/90 mm Hg.4

For preadolescents, the definition and staging terms have also changed. There are new normative BP tables with data compiled from children with healthy weight. The tables reference the BP to measured height as well as height percentile: elevated BP is now defined as ≥90th percentile but <95th or 120 mm Hg/80 mm Hg; stage 1 hypertension is defined as ≥95th percentile but <95th plus 12 mm Hg or 130–138 mm Hg/80–89 mm Hg; and stage 2 hypertension is defined as ≥95th percentile plus 12 mm Hg or ≥140 mm Hg/90 mm Hg.3

Etiology

Previously, hypertension in children was primarily due to a secondary cause and less commonly due to primary hypertension. With the increasing prevalence of obesity, this dogma has changed, and now primary (essential) hypertension appears to be the most common cause for elevated BP in pediatrics.5 This trend is particularly true for older children with a positive family history of hypertension and/or who are overweight/obese.6,7

Secondary Hypertension

Kidney disorders are the most common cause of secondary hypertension, accounting for 34% to 79% of cases.8 There should be a high index of suspicion for kidney disease in children younger than age 6 years with hypertension.9 Renal conditions causing hypertension are described in Table 1.

Renal Causes of Secondary Hypertension

Table 1.

Renal Causes of Secondary Hypertension

Coarctation of the aorta is another known secondary cause of hypertension. Higher BP on the right upper extremity when compared to the lower extremity BP is the clinical hallmark, and an echocardiogram would be used for confirmation.10 Patients with coarctation of the aorta are at increased risk of hypertension before repair, immediately after repair, and later in life.11,12 Masked hypertension can also be present after repair, and an ambulatory BP monitor may aid in the diagnosis.

Hypertension related to endocrinopathies is rare, but some of the causes include mineralocorticoid excess, catecholamine excess, glucocorticoid excess, hyperparathyroidism, and hyperthyroidism.7,8

Other causes include heavy metal intoxications (mercury, lead, cadmium), prescription drugs (oral contraceptives, central nervous system stimulants used for treatments of attention-deficit disorders, corticosteroids), over-the-counter medications (decongestant medications), and recreational drugs (cocaine, amphetamines).3

Diagnosis

The diagnosis of hypertension requires multiple BP measurements that correlate with stage 1 hypertension or beyond in the patient who is asymptomatic rather than a single-elevated BP reading in the office. The average of BP measurements in the hypertensive range on three separate visits is required for the diagnosis of hypertension. Repeating elevated BP in the same visit is equally important. Failure to repeat an initial BP reading >95th percentile would lead to a false “hypertensive” visit result in 54% of children who require follow-up visits.13 After an initial visit indicating hypertension, hypertension stage 1 or stage 2 was sustained in 2.3% and 11.3% of youth during the next visits, respectively.13

Normative data are based on auscultated BP and, therefore, should be the standard methodology employed. The BP should be measured on an upper extremity, preferably in the right arm, with the patient being calm, sitting upright, feet on the ground, arm supported at heart level, not talking, or eating. Improper technique can affect BP. It is crucial that the correct cuff size be used to obtain an accurate BP reading. The cuff bladder should cover 80% of the patient's arm circumference and the width should cover 40% of the arm circumference.14

The new CPG suggests an increasing role for routine ambulatory BP monitors to be performed for the evaluation of hypertension.15 The information from such a study is unique in its ability to diagnose nocturnal hypertension, masked hypertension (hypertension not present in the office setting), and white coat hypertension. Nocturnal hypertension is present when the average awake BP are adequate, but either (1) asleep BP load/averages are above the thresholds or (2) there is a lack of nocturnal dip (failure to decrease the BP by 10% from those of the awake period). White coat hypertension is an entity in which BP are elevated in the office but normal with 24-hour BP monitoring. BP treatments are not indicated in this case, but continued surveillance is recommended. Masked hypertension is characterized by normal casual blood pressures in the office, but elevated BP by 24-hour ambulatory BP monitoring. Patients with chronic kidney disease (CKD), obese patients, and aortic arch abnormalities (either repaired or unrepaired) are at greater risk for masked hypertension.16

Evaluation

Once the diagnosis of hypertension has been confirmed, the evaluation should differentiate between primary and secondary hypertension as well as identify comorbidities.

The CPG3 recommends that children diagnosed with hypertension have tests for serum blood urea nitrogen, creatinine, routine electrolytes, and urinalysis performed. Additionally, the guidelines suggest that a renal ultrasound be obtained if patients are younger than age 6 years or presenting with an abnormality in one of the above parameters. Further assessment should be guided based on comorbidities. Evaluation for children and adolescents who are obese should include a fasting lipid profile, liver function tests, and hemoglobin A1c. Fasting serum glucose, thyroid-stimulating hormone, drug screen, and a sleep study can be considered based on history. If there is a higher suspicion for secondary causes of hypertension, more extensive testing should be performed tailored to the specific signs and symptoms or laboratory abnormalities of concern.

Management

Lifestyle modifications should always be a primary intervention to treat elevated blood pressure, which includes17 (1) dietary: primarily by reducing dietary sodium. The Dietary Approach to Stop Hypertension consists of large amounts of fruit and vegetables, low-fat milk products, whole grains, fish, poultry, nuts, lean red meats, and limited sugar intake; (2) physical activity: 40 minutes of moderate to vigorous aerobic physical activity, at least 3 to 5 days per week improved systolic BP by an average of 6.6 mm Hg;18 (3) weight loss if overweight; (4) correction/treatment of comorbidities (such as hyperlipidemia, obstructive sleep apnea); and (5) stress reduction.

Pharmacologic Treatment

Failure to improve BP despite lifestyle modifications in stage 1 hypertension or stage 2 hypertension, evidence of end-organ damage, and hypertension in the setting of diabetes or chronic kidney disease (CKD) are indications for treatment with pharmacologic agents.3 Lifestyle modifications should continue while pharmacologic treatments are started. Common first-line agents include angiotensin converting enzyme (ACE) inhibitors, long-acting calcium channel blockers, and angiotensin receptor blockers.19,20 In patients with diabetes, CKD, or left ventricular hypertrophy, ACE inhibitors/angiotensin receptor blockers would be the preferred choice. Adolescents of childbearing age should be informed of the teratogenic effects of ACE inhibitors and angiotensin receptor blockers, and other agents may be preferred for these patients.

Obesity and Hypertension

Various mechanisms may play a role in the increased prevalence of hypertension in the obese child or adolescent. Hyperinsulinemia is one of the proposed mechanisms that play a causal role in obesity-associated hypertension.21 Elevated BP and abnormal glucose tolerance are 2 of 5 criteria for the definition of metabolic syndrome.22 When insulin resistance develops, there is compensatory hyperinsulinemia to achieve glucose control. Insulin activates the sympathetic nervous system, thereby increasing blood pressure. Hyperinsulinemia has also been shown to upregulate renal tubular sodium transport (increased sodium reabsorption in the distal tubule). An epidemiologic study by Yang et al.23 showed that the population was twice as likely to develop hypertension with a higher sodium intake, but participants who were overweight/obese had even higher odds (odds ratio 3.5) of developing hypertension with higher salt intake.

Inflammation has also been linked to obesity-associated hypertension. Obesity is associated with elevation of proinflammatory cytokines such as C-reactive protein and interleulin-6.24 Proinflammatory cytokines may alter vascular function. C-reactive protein also decreases endothelial nitric oxide synthase with subsequent attenuation of vasodilation response.25 Lastly, perivascular adipose tissue can also increase vascular smooth muscle tone.26

Hypertension and Chronic Kidney Disease

CKD can lead to hypertension, and chronic hypertension can lead to CKD. In patients with known CKD, BP should be evaluated at all medical encounters. Parenchymal, structural, and vascular kidney diseases are among the most common causes of hypertension in children.7,8 Hypertension is a known risk factor of progression of CKD as is the presence of proteinuria. Treatments of either likely slows the progression of CKD.27,28

If proteinuria is present in children with hypertension and CKD, ACE inhibitors or angiotensin receptor blockers are first-line therapy. Hyperkalemia may be a limiting factor in advanced stage CKD. The ESCAPE (Effect of Strict Blood Pressure Control and ACE Inhibition on Progression of Chronic Renal Failure in Pediatric Patients Study) trial demonstrated that target BP of <50th percentile in patients with CKD showed fewer composite CKD outcomes, including significant improvements in glomerular filtration rates.27 Patients with hypertension have higher incidence of alterations of the circadian rhythm and masked hypertension; therefore, routine 24-hour ambulatory BP monitoring is recommended.29,30

Hypertensive Target Organ Damage

Cardiac Structure

Left ventricular hypertrophy is the most common target organ damage. Daniels et al.31 found that 38.5% of teens with BP >90th percentile had left ventricular mass >95th percentile.

Vascular Changes

Both hypertension and dyslipidemia, which are comorbid conditions, are associated with subclinical atherosclerosis. Carotid intimal-medial thickness (cIMT), which is a marker for atherosclerosis and vascular health, was compared in matched normotensive control children versus children with hypertension. cIMT was higher in the hypertensive group.32

Cognitive Impairment

Neurocognitive alterations, including increased prevalence of learning disabilities, were found to be worse in children who are hypertensive compared to normotensive controls. The postulated mechanism is impaired cerebrovascular reactivity.33

Conclusions

It is imperative that hypertension in children and adolescents be appropriately recognized and managed, since there are important implications for future cardiovascular health. Although there are challenges in the measurement, diagnosis, and management of hypertension in children, the new guidelines provide the practitioner with some practical ways to overcome them. With the expected increasing trend in obesity rates, the issue of hypertension will also increase. Ongoing awareness and education are necessary to best care for this population of patients.

References

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Renal Causes of Secondary Hypertension

Category Pathophysiology
Vascular Large vessels   Renal artery stenosis Small vessels   Hemolytic uremic syndrome   Henoch-Schonlein purpura
Genetic Polycystic kidney disease (autosomal recessive and autosomal dominant) Congenital anomalies of the kidneys and urinary tract Monogenic   Liddle's syndrome   Pseudohypoaldosteronism type 2   Glucocorticoid-remediable aldosteronism   Syndrome of apparent mineralocorticoid excess
Nephritis Pyelonephritis Acute and chronic glomerulonephritis Acute and chronic interstitial nephritis
Parenchymal Renal scarring Renal trauma
Malignancies Wilms' tumor
Authors

Debora Matossian, MD, MS, is an Attending Physician, Division of Kidney Diseases, Ann & Robert H. Lurie Children's Hospital of Chicago; and an Assistant Professor of Pediatrics, Northwestern University Feinberg School of Medicine.

Address correspondence to Debora Matossian, MD, MS, Division of Kidney Diseases, Ann & Robert H. Lurie Children's Hospital of Chicago, 225 E. Chicago Avenue, Box 37, Chicago IL, 60611; email: dmatossian@luriechildrens.org.

Disclosure: The author has no relevant financial relationships to disclose.

10.3928/19382359-20181119-01

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