Clinical Practice Guideline for Screening and Management of High Blood Pressure in Children and Adolescents

Interest in childhood hypertension (HTN) has increased since the 2004 publication of the “Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents” (Fourth Report).¹ Recognizing ongoing evidence gaps and the need for an updated, thorough review of the relevant literature, the American Academy of Pediatrics (AAP) and its Council on Quality Improvement and Patient Safety developed this practice guideline to provide an update on topics relevant to the diagnosis, evaluation, and management of pediatric HTN. It is primarily directed at clinicians caring for children and adolescents in the outpatient setting. This guideline is endorsed by the American Heart Association.

When it was not possible to identify sufficient evidence, recommendations are based on the consensus opinion of the expert members of the Screening and Management of High Blood Pressure in Children Clinical Practice Guideline Subcommittee (henceforth, “the subcommittee”). The subcommittee intends to regularly update this guideline as new evidence becomes available. Implementation tools for this guideline are available on the AAP Web site (https://www.aap.org/en-us/professional-resources/quality-improvement/quality-improvement-resources-and-tools/Pages/hypertension.aspx).

The subcommittee was co-chaired by a pediatric nephrologist and a general pediatrician and consisted of 17 members, including a parent representative. All subcommittee members were asked to disclose relevant financial or proprietary conflicts of interest for members or their family members at the start of and throughout the guideline preparation process. Potential conflicts of interest were addressed and resolved by the AAP. A detailed list of subcommittee members and affiliations can be found in the Consortium section at the end of this article. A listing of subcommittee members with conflicts of interest will be included in the forthcoming technical report.

The subcommittee epidemiologist created a detailed content outline, which was reviewed and approved by the subcommittee. The outline contained a list of primary and secondary topics generated to guide a thorough literature search and meet the goal of providing an up-to-date systemic review of the literature pertaining to the diagnosis, management, and treatment of pediatric HTN as well as the prevalence of pediatric HTN and its associated comorbidities.

Of the topics covered in the outline, ∼80% were researched by using a Patient, Intervention/Indicator, Comparison, Outcome, and Time (PICOT) format to address the following key questions:

1. How should systemic HTN (eg, primary HTN, renovascular HTN, white coat hypertension [WCH], and masked hypertension [MH]) in children be diagnosed, and what is the optimal approach to diagnosing HTN in children and adolescents?

2. What is the recommended workup for pediatric HTN? How do we best identify the underlying etiologies of secondary HTN in children?

3. What is the optimal goal systolic blood pressure (SBP) and/or diastolic blood pressure (DBP) for children and adolescents?

4. In children 0 to 18 years of age, how does treatment with lifestyle versus antihypertensive agents influence indirect measures of cardiovascular disease (CVD) risk, such as carotid intimamedia thickness (cIMT), flow-mediated dilation (FMD), left ventricular hypertrophy (LVH), and other markers of vascular dysfunction?

To address these key questions, a systematic search and review of literature was performed. The initial search included articles published between the publication of the Fourth Report (January 2004) and August 2015. The process used to conduct the systematic review was consistent with the recommendations of the Institute of Medicine for systematic reviews.² 

For the topics not researched by using the PICOT format, separate searches were conducted. Not all topics (eg, economic aspects of pediatric HTN) were appropriate for the PICOT format. A third and final search was conducted at the time the Key Action Statements (KASs) were generated to identify any additional relevant articles published between August 2015 and July 2016. (See Table 1 for a complete list of KASs.)

A detailed description of the methodology used to conduct the literature search and systematic review for this clinical practice guideline will be included in the forthcoming technical report. In brief, reference selection involved a multistep process. First, 2 subcommittee members reviewed the titles and abstracts of references identified for each key question. The epidemiologist provided a deciding vote when required. Next, 2 subcommittee members and the epidemiologist conducted full-text reviews of the selected articles. Although many subcommittee members have extensively published articles on topics covered in this guideline, articles were not preferentially selected on the basis of authorship.

Articles selected at this stage were mapped back to the relevant main topic in the outline. Subcommittee members were then assigned to writing teams that evaluated the evidence quality for selected topics and generated appropriate KASs in accordance with an AAP grading matrix (see Fig 1 and the detailed discussion in the forthcoming technical report).³ Special working groups were created to address 2 specific topics for which evidence was lacking and expert opinion was required to generate KASs, “Definition of HTN” and “Definition of LVH.” References for any topics not covered by the key questions were selected on the basis of additional literature searches and reviewed by the epidemiologist and subcommittee members assigned to the topic. When applicable, searches were conducted by using the PICOT format .

In addition to the 30 KASs listed above, this guideline also contains 27 additional recommendations that are based on the consensus expert opinion of the subcommittee members. These recommendations, along with their locations in the document, are listed in Table 2.

Information on the prevalence of high blood pressure (BP) in children is largely derived from data from the NHANES and typically is based on a single BP measurement session. These surveys, conducted since 1988, indicate that there has been an increase in the prevalence of childhood high BP, including both HTN and elevated BP.^4,5 High BP is consistently greater in boys (15%–19%) than in girls (7%–12%). The prevalence of high BP is higher among Hispanic and non-Hispanic African American children compared with non-Hispanic white children, with higher rates among adolescents than among younger children.⁶ 

However, in a clinical setting and with repeated BP measurements, the prevalence of confirmed HTN is lower in part because of inherent BP variability as well as an adjustment to the experience of having BP measured (also known as the accommodation effect). Therefore, the actual prevalence of clinical HTN in children and adolescents is ∼3.5%.^7,8 The prevalence of persistently elevated BP (formerly termed “prehypertension,” including BP values from the 90th to 94th percentiles or between 120/80 and 130/80 mm Hg in adolescents) is also ∼2.2% to 3.5%, with higher rates among children and adolescents who have overweight and obesity.^7,9 

Data on BP tracking from childhood to adulthood demonstrate that higher BP in childhood correlates with higher BP in adulthood and the onset of HTN in young adulthood. The strength of the tracking relationship is stronger in older children and adolescents.¹⁰ Trajectory data on BP (including repeat measurements from early childhood into midadulthood) confirm the association of elevated BP in adolescence with HTN in early adulthood¹¹ and that normal BP in childhood is associated with a lack of HTN in midadulthood.¹¹ 

Of the 32.6% of US adults who have HTN, almost half (17.2%) are not aware they have HTN; even among those who are aware of their condition, only approximately half (54.1%) have controlled BP.¹² Unfortunately, there are no large studies in which researchers have systematically studied BP awareness or control in youth, although an analysis of prescribing patterns from a nationwide prescription drug provider found an increase in the number of prescriptions written for high BP in youth from 2004 to 2007.¹³ 

The SEARCH for Diabetes in Youth study found that only 7.4% of youth with type 1 diabetes mellitus (T1DM) and 31.9% of youth with type 2 diabetes mellitus (T2DM) demonstrated knowledge of their BP status.¹⁴ Even after becoming aware of the diagnosis, only 57.1% of patients with T1DM and 40.6% of patients with T2DM achieved good BP control.¹⁴ The HEALTHY Primary Prevention Trial of Risk Factors for Type 2 Diabetes in Middle-School Youth, which examined a school-based intervention designed to reduce cardiovascular (CV) risk among middle school students, found the prevalence of stage 1 or 2 HTN to be ∼9.5%.¹⁵ There was no significant reduction in HTN in the control group after the intervention; the intervention group saw a reduction in the prevalence of HTN of ∼1%, leaving 8.5% with BP still above the ideal range.

Researchers in a number of small, single-center studies have evaluated BP control in children and adolescents with HTN. One study found that lifestyle change and medications produced adequate BP control in 46 of 65 youth (70%) with HTN.¹⁶ Another study in which researchers used ambulatory blood pressure monitoring (ABPM) to assess BP control among a group of 38 children (of whom 84% had chronic kidney disease [CKD]) found that only 13 children (34%) achieved adequate BP control even among those who received more than 1 drug.¹⁷ A similar study found that additional drugs did increase rates of BP control in children with CKD, however.¹⁸ 

It is well recognized that HTN rates are higher in children with certain chronic conditions, including children with obesity, sleep-disordered breathing (SDB), CKD, and those born preterm. These are described below.

HTN prevalence ranges from 3.8% to 24.8% in youth with overweight and obesity. Rates of HTN increase in a graded fashion with increasing adiposity.^19,–24 Similar relationships are seen between HTN and increasing waist circumference.^4,25,26 Systematic reviews of 63 studies on BMI²⁷ and 61 studies on various measures of abdominal adiposity²⁸ have shown associations between these conditions and HTN. Obesity is also associated with a lack of circadian variability of BP,^29,30 with up to 50% of children who have obesity not experiencing the expected nocturnal BP dip.^31,–33 

Studies have shown that childhood obesity is also related to the development of future HTN.²² Elevated BMI as early as infancy is associated with higher future BP.³⁴ This risk appears to increase with obesity severity; there is a fourfold increase in BP among those with severe obesity (BMI >99th percentile) versus a twofold increase in those with obesity (BMI 95th–98th percentiles) compared with normal-weight children and adolescents.³⁵ 

Collectively, the results of these cross-sectional and longitudinal studies firmly establish an increasing prevalence of HTN with increasing BMI percentile. The study results also underscore the importance of monitoring BP in all children with overweight and/or obesity at every clinical encounter.

Obesity in children with HTN may be accompanied by additional cardiometabolic risk factors (eg, dyslipidemia and disordered glucose metabolism)^36,37 that may have their own effects on BP or may represent comorbid conditions arising from the same adverse lifestyle behaviors.^25,38 Some argue that the presence of multiple risk factors, including obesity and HTN, leads to far greater increases in CV risk than is explained by the individual risk factors alone. Although this phenomenon has been hard to demonstrate definitively, the Strong Heart Study did show that American Indian adolescents with multiple cardiometabolic risk factors had a higher prevalence of LVH (43.2% vs 11.7%), left atrial dilation (63.1% vs 21.9%; P < .001), and reduced LV systolic and diastolic function compared with those without multiple cardiometabolic risk factors.³⁹ Notably, both obesity and HTN were drivers of these CV abnormalities, with obesity being a stronger determinant of cardiac abnormalities than HTN (odds ratio, 4.17 vs 1.03).

SDB occurs on a spectrum that includes (1) primary snoring, (2) sleep fragmentation, and (3) obstructive sleep apnea syndrome (OSAS). Researchers in numerous studies have identified an association between SDB and HTN in the pediatric population.^40,–42 Studies suggest that children who sleep 7 hours or less per night are at increased risk for HTN.⁴³ Small studies of youth with sleep disorders have found the prevalence of high BP to range between 3.6% and 14%.^40,41 The more severe the OSAS, the more likely a child is to have HTN.^45,46 Even inadequate duration of sleep and poor-quality sleep have been associated with elevated BP.⁴³ 

There are well-established pathophysiologic links between childhood HTN and CKD. Certain forms of CKD can lead to HTN, and untreated HTN can lead to CKD in adults, although evidence for the latter in pediatric patients is lacking. Among children and adolescents with CKD, ∼50% are known to be hypertensive.^46,–48 In children and adolescents with end-stage renal disease (either those on dialysis or after transplant), ∼48% to 79% are hypertensive, with 20% to 70% having uncontrolled HTN.^49,–53 Almost 20% of pediatric HTN may be attributable to CKD.⁵⁴ 

Abnormal birth history—including preterm birth and low birth weight—has been identified as a risk factor for HTN and other CVD in adults⁵⁵; only low birth weight has been associated with elevated BP in the pediatric age range.⁵⁶ One retrospective cohort study showed a prevalence of HTN of 7.3% among 3 year olds who were born preterm.⁵⁷ Researchers in another retrospective case series noted a high prevalence of HTN in older children with a history of preterm birth.⁵⁸ It also appears that preterm birth may result in abnormal circadian BP patterns in childhood.⁵⁹ These data are intriguing but limited. Further study is needed to determine how often preterm birth results in childhood HTN.

Numerous studies have shown that elevated BP in childhood increases the risk for adult HTN and metabolic syndrome.^10,60,–62 Youth with higher BP levels in childhood are also more likely to have persistent HTN as adults.^60,63 One recent study found that adolescents with elevated BP progressed to HTN at a rate of 7% per year, and elevated BMI predicted sustained BP elevations.⁶⁴ In addition, young patients with HTN are likely to experience accelerated vascular aging. Both autopsy⁶⁵ and imaging studies⁶⁶ have demonstrated BP-related CV damage in youth. These intermediate markers of CVD (eg, increased LV mass,⁶⁷ cIMT,⁶⁸ and pulse wave velocity [PWV]⁶⁹) are known to predict CV events in adults, making it crucial to diagnose and treat HTN early.

Eighty million US adults (1 in 3) have HTN, which is a major contributor to CVD.¹² Key contributors to CV health have been identified by the American Heart Association (AHA) as “Life’s Simple 7,” including 4 ideal health behaviors (not smoking, normal BMI, physical activity at goal levels, and a healthy diet) and 3 ideal health factors (untreated, normal total cholesterol; normal fasting blood glucose; and normal untreated BP, defined in childhood as ≤90th percentile or <120/80 mm Hg). Notably, elevated BP is the least common abnormal health factor in children and adolescents⁷⁰; 89% of youth (ages 12–19 years) are in the ideal BP category.⁶ 

Given the prevalence of known key contributors in youth (ie, tobacco exposure, obesity, inactivity, and nonideal diet^12,71), adult CVD likely has its origins in childhood. One-third of US adolescents report having tried a cigarette in the past 30 days.⁷² Almost half (40%–48%) of teenagers have elevated BMI, and the rates of severe obesity (BMI >99th percentile) continue to climb, particularly in girls and adolescents.^73,–75 Physical activity measured by accelerometry shows less than half of school-aged boys and only one-third of school-aged girls meet the goal for ideal physical activity levels.⁷² More than 80% of youth 12 to 19 years of age have a poor diet (as defined by AHA metrics for ideal CV health); only ∼10% eat adequate fruits and vegetables, and only ∼15% consume <1500 mg per day of sodium, both of which are key dietary determinants of HTN.⁷⁶ 

Finally, measuring BP at routine well-child visits enables the early detection of primary HTN as well as the detection of asymptomatic HTN secondary to another underlying disorder. Early detection of HTN is vital given the greater relative prevalence of secondary causes of HTN in children compared with adults.

Given the lack of outcome data, the current definition of HTN in children and adolescents is based on the normative distribution of BP in healthy children.¹ Because it is a major determinant of BP in growing children, height has been incorporated into the normative data since the publication of the 1996 Working Group Report.¹ BP levels should be interpreted on the basis of sex, age, and height to avoid misclassification of children who are either extremely tall or extremely short. It should be noted that the normative data were collected by using an auscultatory technique,¹ which may provide different values than measurement obtained by using oscillometric devices or from ABPM.

In the Fourth Report, “normal blood pressure” was defined as SBP and DBP values <90th percentile (on the basis of age, sex, and height percentiles). For the preadolescent, “prehypertension” was defined as SBP and/or DBP ≥90th percentile and <95th percentile (on the basis of age, sex, and height tables). For adolescents, “prehypertension” was defined as BP ≥120/80 mm Hg to <95th percentile, or ≥90th and <95th percentile, whichever was lower. HTN was defined as average clinic measured SBP and/or DBP ≥95th percentile (on the basis of age, sex, and height percentiles) and was further classified as stage 1 or stage 2 HTN.

There are still no data to identify a specific level of BP in childhood that leads to adverse CV outcomes in adulthood. Therefore, the subcommittee decided to maintain a statistical definition for childhood HTN. The staging criteria have been revised for stage 1 and stage 2 HTN for ease of implementation compared with the Fourth Report. For children ≥13 years of age, this staging scheme will seamlessly interface with the 2017 AHA and American College of Cardiology (ACC) adult HTN guideline.^* Additionally, the term “prehypertension” has been replaced by the term “elevated blood pressure,” to be consistent with the AHA and ACC guideline and convey the importance of lifestyle measures to prevent the development of HTN (see Table 3).

New normative BP tables based on normal-weight children are included with these guidelines (see Tables 4 and 5). Similar to the tables in the Fourth Report,¹ they include SBP and DBP values arranged by age, sex, and height (and height percentile). These values are based on auscultatory measurements obtained from ∼50 000 children and adolescents. A new feature in these tables is that the BP values are categorized according to the scheme presented in Table 3 as normal (50th percentile), elevated BP (>90th percentile), stage 1 HTN (≥95th percentile), and stage 2 HTN (≥95th percentile + 12 mm Hg). Additionally, actual heights in centimeters and inches are provided.