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All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2018. | This topic last updated: Feb 14, 2018.
INTRODUCTION — It has become clear that hypertension (HTN) begins in childhood and adolescence, and that it
contributes to the early development of cardiovascular disease (CVD).
The evaluation of children with HTN will be reviewed here. The epidemiology, etiology, diagnosis, and treatment of
childhood HTN are discussed separately. (See "Epidemiology, risk factors, and etiology of hypertension in children and
adolescents" and "Definition and diagnosis of hypertension in children and adolescents" and "Nonemergent treatment of
hypertension in children and adolescents".)
In addition, the evaluation for hypertensive emergency is presented elsewhere. (See "Approach to hypertensive
emergencies and urgencies in children".)
DEFINITION — For children in the United States, the 2017 American Academy of Pediatrics (AAP) guidelines for
screening and managing high blood pressure for children and adolescents definitions are used to categorize blood
pressure for two different age groups (table 1) [1]. BP percentiles are based upon gender, age, and height (table 2 and
table 3). The age- and height-specific blood pressure percentiles may be determined using calculators for boys
(calculator 1) or for girls (calculator 2). (See "Definition and diagnosis of hypertension in children and adolescents".)
Childhood HTN is also divided into two categories depending upon whether or not an underlying cause can be identified
(table 4):
OVERVIEW
Rationale — There is good evidence that identifying children with HTN and successfully treating their primary HTN has
an important impact on long-term outcomes of CVD. Pediatric data include clinical studies that demonstrate
cardiovascular (CV) structural and functional changes in children with HTN, and autopsy studies that have shown an
association of blood pressure (BP) with atherosclerotic changes in the aorta and heart of children and young adults.
Children with primary HTN are likely to continue to have elevated BP as adults, and multiple randomized trials in adults
have shown that reduction of BP by antihypertensive therapy reduces CV morbidity and mortality. The magnitude of the
benefit increases with the severity of the HTN. In patients with secondary HTN, clinical outcomes vary depending on the
underlying etiology and whether the underlying cause is amenable to treatment. (See "Nonemergent treatment of
hypertension in children and adolescents", section on 'Rationale for intervention' and "Definition and diagnosis of
hypertension in children and adolescents", section on 'Tracking'.)
Thus, one of the most important components of the successful management of childhood HTN is distinguishing between
primary and secondary HTN, and if the latter determining whether there is an underlying cause that is amenable to
treatment.
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Goals — The goals of the evaluation of the hypertensive child or adolescent are to:
● For children with secondary HTN, identify secondary HTN (ie, an underlying cause of hypertension), which may be
cured, thereby avoiding the need for prolonged drug therapy (table 5). (See "Epidemiology, risk factors, and etiology
of hypertension in children and adolescents", section on 'Etiology'.)
● Identify other comorbid risk factors (eg, obesity and dyslipidemia) for cardiovascular disease (CVD) or diseases
associated with an increased risk for CVD (eg, diabetes mellitus) (table 6). CVD risk factors often occur
concurrently, which further increases the likelihood of premature atherosclerosis and CVD. The presence of another
CVD risk factor or disease associated with a high risk of CVD impacts the timing and choice of intervention for high
BP. (See "Risk factors and development of atherosclerosis in childhood", section on 'Risk factors' and "Diseases
associated with atherosclerosis in childhood" and "Nonemergent treatment of hypertension in children and
adolescents", section on 'Who should be treated'.)
● Identify children who should be treated with antihypertensive drug therapy. Indications for pharmacologic therapy
are discussed separately. (See "Nonemergent treatment of hypertension in children and adolescents", section on
'Who should be treated'.)
Most hypertensive children, particularly those who are likely to have secondary HTN, should be referred to a pediatric
nephrologist or other clinician with experience in childhood HTN.
INITIAL EVALUATION — The initial evaluation of the child with HTN includes history, physical examination, laboratory
tests, and imaging procedures. It is, as discussed above, primarily focused upon the following [1]:
● Differentiate primary from secondary HTN by looking for signs and symptoms that are associated with specific
underlying etiologies for HTN (table 7 and table 8).
● Identify comorbid cardiovascular disease (CVD) risk factors or diseases associated with a risk of CVD.
● Identify patients with stage 2 HTN or with evidence of end-organ injury so that pharmacologic therapy can be
initiated (See 'Definition' above and "Nonemergent treatment of hypertension in children and adolescents", section
on 'Who should be treated'.)
Symptomatic hypertension — Symptoms consistent with hypertensive emergencies include headache, seizures,
changes in mental status, vomiting, focal neurologic complaints, visual disturbances, and cardiovascular (CV)
complaints indicative of heart failure (such as chest pain, palpitations, cough, or shortness of breath). Children with
hypertensive emergency require pharmacologic therapy without delay and hospitalization for evaluation and ongoing
care. (See "Approach to hypertensive emergencies and urgencies in children" and "Management of hypertensive
emergencies and urgencies in children".)
Secondary versus primary hypertension — Secondary HTN should be suspected in children with one or more of
the following findings [1] (see "Epidemiology, risk factors, and etiology of hypertension in children and adolescents",
section on 'Etiology') (table 4):
● A thin child with a negative family history for HTN. (See "Epidemiology, risk factors, and etiology of hypertension in
children and adolescents", section on 'Obesity' and "Epidemiology, risk factors, and etiology of hypertension in
children and adolescents", section on 'Family history'.)
● Specific ambulatory BP patterns, such as sustained diastolic HTN, nocturnal HTN, and/or blunted nocturnal dipping.
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● History of snoring, daytime sleepiness (in adolescents), or hyperactivity (in younger children) are associated with
obstructive sleep apnea. (See "Evaluation of suspected obstructive sleep apnea in children", section on 'Clinical
manifestations'.)
● Family history of chronic or congenital renal disease (such as polycystic kidney disease), or other genetic conditions
that are associated with HTN, such as neurofibromatosis or tuberous sclerosis. (See "Neurofibromatosis type 1
(NF1): Pathogenesis, clinical features, and diagnosis" and "Renal manifestations of tuberous sclerosis complex".)
● History of drugs known to increase BP including glucocorticoids, central nervous system stimulants, decongestants
with pseudoephedrine, or oral contraceptives. Recreational drugs, including anabolic steroids and stimulants (eg,
cocaine and amphetamine).
● Physical finding(s) suggestive of systemic disease or a specific secondary etiology of HTN include (table 8):
• Cutaneous findings associated with tuberous sclerosis (ash leaf spots or adenoma sebaceum) or
neurofibromatosis (café-au-lait spots and neurofibromas).
• Ambiguous genitalia may be suggestive of congenital adrenal hyperplasia with excess endogenous secretion
of androgens and mineralocorticoids. Children with mineralocorticoid excess may develop hypokalemia. (See
"Evaluation of the infant with atypical genitalia (disorder of sex development)".)
• Edema and hematuria may be indicative of renal parenchymal disease. (See 'Laboratory evaluation and renal
imaging' below.)
● Clinical findings of arthritis or rash may be suggestive of glomerulonephritis due to systemic disorders, such as
immunoglobulin A vasculitis (IgAV; Henoch-Schönlein purpura [HSP]) or systemic lupus erythematosus (SLE).
Abdominal pain may also be present in patients with IgAV (HSP). (See "IgA vasculitis (Henoch-Schönlein purpura):
Clinical manifestations and diagnosis" and "Systemic lupus erythematosus (SLE) in children: Clinical manifestations
and diagnosis".)
• The presence of an abdominal bruit raises the possibility of renovascular disease, but its absence does not
exclude the diagnosis.
• Coarctation of the aorta is suggested by findings of hypertension in the upper extremities and low or
unobtainable blood pressure in the lower extremities, significant difference between right and left arm BP, and
diminished or delayed femoral pulses. (See "Clinical manifestations and diagnosis of coarctation of the aorta".)
• Symptoms suggestive of catecholamine excess in addition to elevated BP include headache, sweating, and
tachycardia. Possible etiologies include pheochromocytoma, neuroblastoma, or use of sympathomimetic drugs
including phenylpropanolamine (over-the-counter decongestant), cocaine, amphetamines, phencyclidine,
epinephrine, phenylephrine, and terbutaline, and the combination of a monoamine oxidase (MAO) inhibitor plus
ingestion of tyramine-containing foods.
• Findings suggestive of hyperthyroidism include tachycardia, proptosis, or enlarged thyroid or goiter. Of note,
HTN, particularly diastolic HTN, is associated with hypothyroidism. Clinical symptoms of hypothyroidism in
children include weight gain, exercise intolerance, constipation, fatigue, and cold intolerance.
Risk factors for CVD and hypertension — The history and physical examination should assess for risk factors that
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contribute to high BP and other cardiovascular disease (CVD) risk factors or diseases associated with CVD [1] (table 6).
● Identify overweight and obese children by calculating body mass index (BMI) (table 9 and figure 1 and figure 2).
BMI is defined as the weight in kg divided by height in m2. BMI and BMI percentiles may be determined using
calculators for boys (calculator 3) or for girls (calculator 4). (See "Definition; epidemiology; and etiology of obesity in
children and adolescents".)
● History of type 1 or 2 diabetes mellitus, chronic kidney disease (CKD), organ transplantation, cardiac disease,
Kawasaki disease, autoimmune disease, familial hypercholesterolemia, and cancer. (See "Diseases associated
with atherosclerosis in childhood".)
● History of sleep disorders or symptoms related to obstructive sleep (loud snoring, daytime sleepiness, or history of
apnea) [1-5]. (See "Evaluation of suspected obstructive sleep apnea in children".)
● History of physical activity to identify sedentary children in whom increased physical activity will improve BP and
help in weight reduction in children who are overweight or obese (BMI >85th percentile). (See "Nonemergent
treatment of hypertension in children and adolescents", section on 'Exercise' and "Nonemergent treatment of
hypertension in children and adolescents", section on 'Weight reduction'.)
● Dietary history may identify dietary contributors to HTN (excess salt intake) and contributors to CVD (consumption
of high-fat foods) and identify interventions that may decrease BP. (See "Nonemergent treatment of hypertension in
children and adolescents", section on 'Diet'.)
Physical findings of end-organ damage — The physical examination should include a retinal examination to detect
any retinal vascular changes due to HTN (image 1) (see "Ocular effects of hypertension"). Cardiac heave or laterally
displaced point of maximal impulse (PMI) may indicate left ventricular hypertrophy (LVH).
Laboratory evaluation and renal imaging — Initial laboratory evaluation in all children with persistent HTN is directed
at determining the etiology of HTN and identifying other CVD risk factors, especially in obese children [1]. We concur
with the following initial evaluation for all children with HTN recommended by the 2017 American Academy of Pediatrics
(AAP) guidelines for high BP [1]:
● Measurement of serum blood urea nitrogen (BUN), creatinine, and electrolytes and urinalysis. These tests permit
quick assessment of renal function and abnormalities in potassium homeostasis or acid-base status (eg, CKD or
congenital adrenal hyperplasia, Liddle syndrome). An abnormal urinalysis (eg, hematuria or proteinuria) and/or an
elevation in serum creatinine are suggestive of underlying renal disease. Glycosuria may be an indication of
diabetes mellitus.
● Measurement of lipid profile to identify children with dyslipidemia, another CVD risk factor. (See "Dyslipidemia in
children: Definition, screening, and diagnosis", section on 'Choice of screening test'.)
● Renal ultrasound for children less than six years of age or those with abnormal urinalysis or renal function,
regardless of age. Of note, for children who are referred to our center for evaluation of HTN, an initial renal
ultrasound is performed. (See 'Renal imaging' below.)
The 2016 European Hypertension Society guidelines for the management of high blood pressure in children and
adolescents includes a more extensive initial evaluation [6].
Obese children — Additional tests are recommended for children who are obese [1]:
● Hemoglobin A1c (screen for diabetes mellitus). (See "Epidemiology, presentation, and diagnosis of type 2 diabetes
mellitus in children and adolescents", section on 'Screening'.)
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● Aspartate transaminase and alanine transaminase (screen for fatty liver). (See "Comorbidities and complications of
obesity in children and adolescents", section on 'Nonalcoholic fatty liver disease' and "Nonalcoholic fatty liver
disease in children and adolescents".)
● Fasting lipid profile (additional screen for dyslipidemia). (See "Dyslipidemia in children: Definition, screening, and
diagnosis".)
● In our practice, we also will obtain a fasting serum glucose, especially if the urinalysis detects glycosuria.
FURTHER EVALUATION — Further evaluation is performed to assess for end-organ damage, specifically left
ventricular hypertrophy (LVH), to establish whether the HTN is primary or secondary, and in patients with secondary
HTN, to identify a potentially reversible cause of secondary HTN (table 4).
LV hypertrophy and echocardiography — Left ventricular hypertrophy (LVH) is the most prominent manifestation
of end-organ damage from HTN. LVH is associated with adverse cardiovascular disease (CVD) outcomes, and a
significant number of children and adolescents with HTN have LVH [7-12].
Echocardiography is the recommended modality to detect LVH due to pediatric HTN. The 2017 American Association of
Pediatrics (AAP) high blood pressure (BP) guidelines recommends echocardiography to assess for target-organ cardiac
damage be performed at the time when pharmacologic therapy is being considered [1]. LVH is defined as LV mass >51
g/m for children and adolescents older than eight years or LV mass >115 g/body surface area (BSA) for boys, and LV
mass >95 g/BSA for girls.
The recommended interval for subsequent echocardiographic assessment is based on the results of the initial study [1]:
● For children without evidence of LV target organ damage, echocardiography to monitor for subsequent end-organ
damage is repeated in one year for patients with stage 2 HTN, secondary HTN, or in patients with stage 1 HTN
whose BP is not well controlled despite intervention with pharmacologic and nonpharmacologic therapy.
● For children with evidence of LV target organ damage, echocardiography is performed at six months to monitor for
improvement or progression of damage. The results of the study are used to determine the scheduling of future
studies.
Electrocardiography should not be performed to assess for end-organ cardiac damage, as the study is not sensitive
enough to reliably identify pediatric patients with LVH [1].
Unproven vascular assessment and CVD outcome — Although there are several studies that have shown that
elevated BP is associated with adverse changes in vascular structure and function in children and adolescents, these
changes have not been correlated with cardiovascular (CV) events in adulthood. In addition, there are not sufficient data
to determine clinically useful threshold values with any of the tools that evaluate vascular structure and function [1]. As a
result, we concur with the 2017 AAP high BP guidelines that routine assessment of vascular structure and function
cannot be recommended.
Primary hypertension — Hypertensive children who fit the primary HTN profile need no further laboratory evaluation
beyond the initial testing cited above (table 4) [1,6].
Data are insufficient to determine whether measurements of serum uric acid and microalbuminuria are useful in the
evaluation and management of pediatric primary HTN [1]. As a result, routine assessment of uric acid and
microalbuminuria is not recommended in the care of children with elevated BP.
Secondary hypertension — Further evaluation of patients with findings suggestive of secondary HTN is directed
towards identifying the underlying cause. (See 'Secondary versus primary hypertension' above and "Epidemiology, risk
factors, and etiology of hypertension in children and adolescents", section on 'Secondary hypertension'.)
The following diagnostic studies may be performed in hypertensive children with a high degree of suspicion that an
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Plasma renin and aldosterone activity — Evaluation of plasma renin and aldosterone activity (PRA) may be useful
in patients in the following uncommon conditions:
● Excess mineralocorticoids (eg, aldosterone) secretion – Patients with mineralocorticoid excess usually present with
hypokalemia and metabolic alkalosis and their PRA is low and often unmeasurable. (See "Pathophysiology and
clinical features of primary aldosteronism".)
• Congenital adrenal hyperplasia is a common cause of excess mineralocorticoid secretion in children. Affected
patients may present as a neonate with ambiguous genitalia due to the excess secretion of androgens. (See
"Causes and clinical manifestations of primary adrenal insufficiency in children", section on 'Congenital adrenal
hyperplasia' and "Evaluation of the infant with atypical genitalia (disorder of sex development)".)
• Primary hypersecretion of aldosterone may result from familial hyperaldosteronism, a group of rare genetic
disorders, including glucocorticoid-remediable hyperaldosteronism (GRA). GRA should be considered in a
hypertensive child with a family history of early HTN (before age 21 years) and evidence of metabolic alkalosis
even in the absence of hypokalemia. (See "Familial hyperaldosteronism".)
● Suppressed mineralocorticoids – Rare genetic disorders with low levels of aldosterone and renin, despite
presenting with symptoms suggestive of mineralocorticoid excess, include Liddle syndrome,
pseudohypoaldosteronism type 2 (also referred to as Gordon syndrome) and syndrome of apparent
mineralocorticoid excess. (See "Genetic disorders of the collecting tubule sodium channel: Liddle's syndrome and
pseudohypoaldosteronism type 1", section on 'Liddle's syndrome' and "Etiology, diagnosis, and treatment of
hypoaldosteronism (type 4 RTA)", section on 'Pseudohypoaldosteronism type 2 (Gordon's syndrome)' and
"Apparent mineralocorticoid excess syndromes (including chronic licorice ingestion)".)
● Renin-secreting tumor – Renin-secreting tumors are rare both in children and adults. Patients generally present with
severe HTN, hypokalemia, metabolic alkalosis, and markedly elevated renin levels [14].
● Renovascular disease – The plasma renin activity may be elevated in children with renovascular HTN, but, as is
true in adults, it is a relatively insensitive test. Approximately 15 percent of children with arteriographically evident
renal artery stenosis have normal plasma renin activity [15,16].
Plasma and urine catecholamines — Patients with HTN due to disorders with catecholamine excess such as
pheochromocytoma and neuroblastoma will have elevated levels of both plasma and urine catecholamines and
metabolites. In addition to HTN, affected patients may present with headache, sweating, and tachycardia. In patients
with symptoms of catecholamine excess and elevated plasma and urine catecholamines, further evaluation is required.
(See "Pheochromocytoma and paraganglioma in children" and "Clinical presentation, diagnosis, and staging evaluation
of neuroblastoma".)
Renal imaging — As discussed previously, the 2017 AAP high BP guidelines recommend a renal ultrasound initially
for children less than six years of age, or those (regardless of age) with abnormal urinalysis or renal function [1]. Renal
ultrasonography is useful to determine the presence of both kidneys, presence of any congenital anomaly, or disparate
renal size, which may suggest renal scarring. In our tertiary center, we obtain an ultrasound for all patients referred for
hypertension evaluation. (See 'Laboratory evaluation and renal imaging' above.)
In patients with a strong suspicion for renal scarring based on history (eg, recurrent febrile urinary tract infections) or
with a suggestive but indeterminant finding on renal ultrasound, a 99mTc–dimercaptosuccinic acid (DMSA) renal scan
can be performed, since it is a more sensitive study to detect renal cortical loss and scarring [17].
Renovascular imaging — In our practice, renovascular imaging is considered when infants and children have
known predisposing factors or findings associated with renal artery stenosis such as prior umbilical artery catheter
placements, family history or findings for neurofibromatosis, an abdominal bruit, or a significant size discrepancy on
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renal ultrasonography. In addition, we consider renovascular imaging in younger children with HTN, who are less likely
to have primary HTN, and in patients with stage 2 HTN when no other cause has been identified. (See "Epidemiology,
risk factors, and etiology of hypertension in children and adolescents", section on 'Renovascular disease'.)
Standard digital subtraction angiography (DSA), previously called renal angiography, is the current gold standard for
evaluating renovascular disease in children. Although noninvasive tests such as magnetic resonance angiography
(MRA) and computed tomographic angiography (CTA) can be used to screen for renovascular diseases, they are not as
reliable as DSA in detecting renovascular disease [18]. If renovascular evaluation is required, a radiological center with
pediatric experience in these screening techniques should be chosen. The selection of the screening modality is
dependent upon the expertise of the clinical staff and the availability of appropriate equipment and development of safe
and useful protocols [19]. (See "Establishing the diagnosis of renovascular hypertension".)
We do not recommend routine duplex Doppler ultrasonography for evaluation of renovascular hypertension in otherwise
healthy children because of its low sensitivity/specificity for diagnosis of renal artery stenosis [18].
For children, these procedures are not universally available or routinely performed. Considerations that must be taken
into account in the use of these modalities to screen for renovascular disease in children include:
● When performing MRA, the need for conscious sedation or general anesthesia for small children and infants.
● The need to modify computed tomographic (CT) dosing to minimize unnecessary radiation exposures.
● The poorer sensitivity of Doppler ultrasonography compared with other imaging modalities in detecting renal
vascular hypertension, especially in patients who have segmental artery lesions [20,21]. As a result, Doppler
ultrasound should not be used to diagnosis renal artery stenosis.
Sleep study evaluation — Evaluation of obstructive sleep apnea (OSA), including polysomnography is considered
for children with history of snoring, daytime sleepiness (in adolescents), or hyperactivity (in younger children), especially
if they are obese. (See "Evaluation of suspected obstructive sleep apnea in children", section on 'Evaluation'.)
Drug screening — If HTN is suspected due to cocaine or amphetamine use, drug testing should be initiated. (See
"Cocaine: Acute intoxication", section on 'Laboratory and radiographic evaluation' and "Methamphetamine: Acute
intoxication", section on 'Laboratory evaluation'.)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and
regions around the world are provided separately. (See "Society guideline links: Hypertension in children".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and
"Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading
level, and they answer the four or five key questions a patient might have about a given condition. These articles are
best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient
education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade
reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to
your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and
the keyword(s) of interest.)
● Basics topics (see "Patient education: High blood pressure in children (The Basics)")
● Beyond the Basics topics (see "Patient education: High blood pressure in children (Beyond the Basics)")
● Hypertension (HTN) in childhood and adolescence contributes to premature atherosclerosis and the early
development of cardiovascular disease (CVD). (See 'Rationale' above and "Risk factors and development of
atherosclerosis in childhood", section on 'Hypertension'.)
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● The goals of the evaluation of a child or adolescent with HTN include (see 'Goals' above):
• Determine whether the patient is more likely to have primary HTN (no identifiable cause is found) or secondary
HTN (an underlying cause is identified) (table 4).
• Identify the child with secondary HTN who may have a curable disease (table 5). Hypertensive children, who
are likely to have secondary HTN, should be referred to a pediatric nephrologist or other clinician with
experience in childhood HTN for evaluation and management. (See 'Secondary versus primary hypertension'
above and 'Secondary hypertension' above.)
• Identify other comorbid risk factors (eg, obesity and dyslipidemia) for cardiovascular disease (CVD) or diseases
associated with an increased risk for CVD (eg, diabetes mellitus). (See "Risk factors and development of
atherosclerosis in childhood".)
• Identify children who should be treated with antihypertensive drug therapy. (See "Nonemergent treatment of
hypertension in children and adolescents", section on 'Who should be treated'.)
● The initial evaluation for all children with HTN includes a history, physical examination, and laboratory testing
including measurement of serum BUN, creatinine, and electrolytes, urinalysis, and lipid profile. The 2017 American
Academy of Pediatrics (AAP) revised guidelines recommends initial imaging with renal ultrasound be reserved for
children with hypertension who are less than six years of age, or any child with evidence of renal disease (abnormal
urinalysis or renal function). However, we obtain an ultrasound for all patients referred to our tertiary center for
evaluation of HTN. (See 'Initial evaluation' above.)
● For obese children with HTN, additional initial studies include hemoglobin A1c, aspartate transaminase and alanine
transaminase levels, and a fasting lipid profile. (See 'Obese children' above.)
● Further evaluation is performed to detect end-organ target damage and identify any potentially reversible cause of
secondary HTN:
• Left ventricular hypertrophy (LVH) is the most prominent manifestation of end-organ damage from HTN.
Echocardiography is the recommended modality to detect LVH for children with HTN and should be obtained
when antihypertensive pharmacologic therapy is being considered. (See 'LV hypertrophy and
echocardiography' above.)
• Based upon the initial history, physical examination, and laboratory evaluation, the clinician should be able to
establish whether the HTN is primary or secondary (table 4).
- For patients with primary HTN, no further evaluation is typically needed. (See 'Primary hypertension'
above.)
- For patients with a potentially reversible cause of secondary HTN, further evaluation to determine the
underlying etiology may include renal imaging studies (eg, renal scans or arteriogram), measurement of
plasma renin and aldosterone and plasma and urine catecholamines, sleep study evaluation, or drug
screening based on the results of the initial evaluation. (See 'Secondary hypertension' above.)
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GRAPHICS
2017 American Academy of Pediatrics updated definitions for pediatric blood pressure
categories
Normal BP Systolic and diastolic BP <90 th percentile Systolic BP <120 and diastolic BP <80 mmHg
Elevated BP Systolic and diastolic BP ≥90 th percentile to Systolic BP 120 to 129 and diastolic BP <80
<95 th percentile, or 120/80 mmHg to <95 th mmHg
percentile (whichever is lower)
Stage 1 HTN Systolic and diastolic BP ≥95 th percentile to 130/80 to 139/89 mmHg
<95 th percentile + 12 mmHg, or
130/80 to 139/89 mmHg (whichever is lower)
Reproduced with permission from: Pediatrics, Vol. 140, doi: 10.1542/peds.2017-1904. Copyright © 2017 by the AAP.
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1 year
Height (in) 30.4 30.8 31.6 32.4 33.3 34.1 34.6 30.4 30.8 31.6 32.4 33.3 34.1 34.6
Height (cm) 77.2 78.3 80.2 82.4 84.6 86.7 87.9 77.2 78.3 80.2 82.4 84.6 86.7 87.9
50 th 85 85 86 86 87 88 88 40 40 40 41 41 42 42
2 years
Height (in) 33.9 34.4 35.3 36.3 37.3 38.2 38.8 33.9 34.4 35.3 36.3 37.3 38.2 38.8
Height (cm) 86.1 87.4 89.6 92.1 94.7 97.1 98.5 86.1 87.4 89.6 92.1 94.7 97.1 98.5
50 th 87 87 88 89 89 90 91 43 43 44 44 45 46 46
3 years
Height (in) 36.4 37.0 37.9 39.0 40.1 41.1 41.7 36.4 37.0 37.9 39.0 40.1 41.1 41.7
Height (cm) 92.5 93.9 96.3 99.0 101.8 104.3 105.8 92.5 93.9 96.3 99.0 101.8 104.3 105.8
50 th 88 89 89 90 91 92 92 45 46 46 47 48 49 49
4 years
Height (in) 38.8 39.4 40.5 41.7 42.9 43.9 44.5 38.8 39.4 40.5 41.7 42.9 43.9 44.5
Height (cm) 98.5 100.2 102.9 105.9 108.9 111.5 113.2 98.5 100.2 102.9 105.9 108.9 111.5 113.2
50 th 90 90 91 92 93 94 94 48 49 49 50 51 52 52
5 years
Height (in) 41.1 41.8 43.0 44.3 45.5 46.7 47.4 41.1 41.8 43.0 44.3 45.5 46.7 47.4
Height (cm) 104.4 106.2 109.1 112.4 115.7 118.6 120.3 104.4 106.2 109.1 112.4 115.7 118.6 120.3
50 th 91 92 93 94 95 96 96 51 51 52 53 54 55 55
6 years
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Height (in) 43.4 44.2 45.4 46.8 48.2 49.4 50.2 43.4 44.2 45.4 46.8 48.2 49.4 50.2
Height (cm) 110.3 112.2 115.3 118.9 122.4 125.6 127.5 110.3 112.2 115.3 118.9 122.4 125.6 127.5
50 th 93 93 94 95 96 97 98 54 54 55 56 57 57 58
7 years
Height (in) 45.7 46.5 47.8 49.3 50.8 52.1 52.9 45.7 46.5 47.8 49.3 50.8 52.1 52.9
Height (cm) 116.1 118.0 121.4 125.1 128.9 132.4 134.5 116.1 118.0 121.4 125.1 128.9 132.4 134.5
50 th 94 94 95 97 98 98 99 56 56 57 58 58 59 59
8 years
Height (in) 47.8 48.6 50.0 51.6 53.2 54.6 55.5 47.8 48.6 50.0 51.6 53.2 54.6 55.5
Height (cm) 121.4 123.5 127.0 131.0 135.1 138.8 141.0 121.4 123.5 127.0 131.0 135.1 138.8 141.0
50 th 95 96 97 98 99 99 100 57 57 58 59 59 60 60
9 years
Height (in) 49.6 50.5 52.0 53.7 55.4 56.9 57.9 49.6 50.5 52.0 53.7 55.4 56.9 57.9
Height (cm) 126.0 128.3 132.1 136.3 140.7 144.7 147.1 126.0 128.3 132.1 136.3 140.7 144.7 147.1
10 years
Height (in) 51.3 52.2 53.8 55.6 57.4 59.1 60.1 51.3 52.2 53.8 55.6 57.4 59.1 60.1
Height (cm) 130.2 132.7 136.7 141.3 145.9 150.1 152.7 130.2 132.7 136.7 141.3 145.9 150.1 152.7
11 years
Height (in) 53.0 54.0 55.7 57.6 59.6 61.3 62.4 53.0 54.0 55.7 57.6 59.6 61.3 62.4
Height (cm) 134.7 137.3 141.5 146.4 151.3 155.8 158.6 134.7 137.3 141.5 146.4 151.3 155.8 158.6
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12 years
Height (in) 55.2 56.3 58.1 60.1 62.2 64.0 65.2 55.2 56.3 58.1 60.1 62.2 64.0 65.2
Height (cm) 140.3 143.0 147.5 152.7 157.9 162.6 165.5 140.3 143.0 147.5 152.7 157.9 162.6 165.5
13 years
Height (in) 57.9 59.1 61.0 63.1 65.2 67.1 68.3 57.9 59.1 61.0 63.1 65.2 67.1 68.3
Height (cm) 147.0 150.0 154.9 160.3 165.7 170.5 173.4 147.0 150.0 154.9 160.3 165.7 170.5 173.4
14 years
Height (in) 60.6 61.8 63.8 65.9 68.0 69.8 70.9 60.6 61.8 63.8 65.9 68.0 69.8 70.9
Height (cm) 153.8 156.9 162.0 167.5 172.7 177.4 180.1 153.8 156.9 162.0 167.5 172.7 177.4 180.1
15 years
Height (in) 62.6 63.8 65.7 67.8 69.8 71.5 72.5 62.6 63.8 65.7 67.8 69.8 71.5 72.5
Height (cm) 159.0 162.0 166.9 172.2 177.2 181.6 184.2 159.0 162.0 166.9 172.2 177.2 181.6 184.2
16 years
Height (in) 63.8 64.9 66.8 68.8 70.7 72.4 73.4 63.8 64.9 66.8 68.8 70.7 72.4 73.4
Height (cm) 162.1 165.0 169.6 174.6 179.5 183.8 186.4 162.1 165.0 169.6 174.6 179.5 183.8 186.4
17 years
Height (in) 64.5 65.5 67.3 69.2 71.1 72.8 73.8 64.5 65.5 67.3 69.2 71.1 72.8 73.8
Height (cm) 163.8 166.5 170.9 175.8 180.7 184.9 187.5 163.8 166.5 170.9 175.8 180.7 184.9 187.5
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The 50 th, 90 th, and 95 th percentiles were derived by using quantile regression on the basis of normal-weight children (BMI
<85 th percentile). BP stages are defined as elevated BP ≥90 th percentile but <95 th percentile; stage 1 HTN: ≥95 th percentile
or 130/80 to 139/89 mmHg; and stage 2 HTN: ≥95 th percentile + 12 mmHg or >140/90 mmHg.
Reproduced with permission from: Pediatrics, Vol. 140, doi: 10.1542/peds.2017-1904. Copyright © 2017 by the AAP.
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1 year
Height (in) 29.7 30.2 30.9 31.8 32.7 33.4 33.9 29.7 30.2 30.9 31.8 32.7 33.4 33.9
Height (cm) 75.4 76.6 78.6 80.8 83.0 84.9 86.1 75.4 76.6 78.6 80.8 83.0 84.9 86.1
50 th 84 85 86 86 87 88 88 41 42 42 43 44 45 46
2 years
Height (in) 33.4 34.0 34.9 35.9 36.9 37.8 38.4 33.4 34.0 34.9 35.9 36.9 37.8 38.4
Height (cm) 84.9 86.3 88.6 91.1 93.7 96.0 97.4 84.9 86.3 88.6 91.1 93.7 96.0 97.4
50 th 87 87 88 89 90 91 91 45 46 47 48 49 50 51
3 years
Height (in) 35.8 36.4 37.3 38.4 39.6 40.6 41.2 35.8 36.4 37.3 38.4 39.6 40.6 41.2
Height (cm) 91.0 92.4 94.9 97.6 100.5 103.1 104.6 91.0 92.4 94.9 97.6 100.5 103.1 104.6
50 th 88 89 89 90 91 92 93 48 48 49 50 51 53 53
4 years
Height (in) 38.3 38.9 39.9 41.1 42.4 43.5 44.2 38.3 38.9 39.9 41.1 42.4 43.5 44.2
Height (cm) 97.2 98.8 101.4 104.5 107.6 110.5 112.2 97.2 98.8 101.4 104.5 107.6 110.5 112.2
50 th 89 90 91 92 93 94 94 50 51 51 53 54 55 55
5 years
Height (in) 40.8 41.5 42.6 43.9 45.2 46.5 47.3 40.8 41.5 42.6 43.9 45.2 46.5 47.3
Height (cm) 103.6 105.3 108.2 111.5 114.9 118.1 120.0 103.6 105.3 108.2 111.5 114.9 118.1 120.0
50 th 90 91 92 93 94 95 96 52 52 53 55 56 57 57
6 years
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Height (in) 43.3 44.0 45.2 46.6 48.1 49.4 50.3 43.3 44.0 45.2 46.6 48.1 49.4 50.3
Height (cm) 110.0 111.8 114.9 118.4 122.1 125.6 127.7 110.0 111.8 114.9 118.4 122.1 125.6 127.7
50 th 92 92 93 94 96 97 97 54 54 55 56 57 58 59
7 years
Height (in) 45.6 46.4 47.7 49.2 50.7 52.1 53.0 45.6 46.4 47.7 49.2 50.7 52.1 53.0
Height (cm) 115.9 117.8 121.1 124.9 128.8 132.5 134.7 115.9 117.8 121.1 124.9 128.8 132.5 134.7
50 th 92 93 94 95 97 98 99 55 55 56 57 58 59 60
8 years
Height (in) 47.6 48.4 49.8 51.4 53.0 54.5 55.5 47.6 48.4 49.8 51.4 53.0 54.5 55.5
Height (cm) 121.0 123.0 126.5 130.6 134.7 138.5 140.9 121.0 123.0 126.5 130.6 134.7 138.5 140.9
50 th 93 94 95 97 98 99 100 56 56 57 59 60 61 61
9 years
Height (in) 49.3 50.2 51.7 53.4 55.1 56.7 57.7 49.3 50.2 51.7 53.4 55.1 56.7 57.7
Height (cm) 125.3 127.6 131.3 135.6 140.1 144.1 146.6 125.3 127.6 131.3 135.6 140.1 144.1 146.6
50 th 95 95 97 98 99 100 101 57 58 59 60 60 61 61
10 years
Height (in) 51.1 52.0 53.7 55.5 57.4 59.1 60.2 51.1 52.0 53.7 55.5 57.4 59.1 60.2
Height (cm) 129.7 132.2 136.3 141.0 145.8 150.2 152.8 129.7 132.2 136.3 141.0 145.8 150.2 152.8
11 years
Height (in) 53.4 54.5 56.2 58.2 60.2 61.9 63.0 53.4 54.5 56.2 58.2 60.2 61.9 63.0
Height (cm) 135.6 138.3 142.8 147.8 152.8 157.3 160.0 135.6 138.3 142.8 147.8 152.8 157.3 160.0
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12 years
Height (in) 56.2 57.3 59.0 60.9 62.8 64.5 65.5 56.2 57.3 59.0 60.9 62.8 64.5 65.5
Height (cm) 142.8 145.5 149.9 154.8 159.6 163.8 166.4 142.8 145.5 149.9 154.8 159.6 163.8 166.4
13 years
Height (in) 58.3 59.3 60.9 62.7 64.5 66.1 67.0 58.3 59.3 60.9 62.7 64.5 66.1 67.0
Height (cm) 148.1 150.6 154.7 159.2 163.7 167.8 170.2 148.1 150.6 154.7 159.2 163.7 167.8 170.2
14 years
Height (in) 59.3 60.2 61.8 63.5 65.2 66.8 67.7 59.3 60.2 61.8 63.5 65.2 66.8 67.7
Height (cm) 150.6 153.0 156.9 161.3 165.7 169.7 172.1 150.6 153.0 156.9 161.3 165.7 169.7 172.1
15 years
Height (in) 59.7 60.6 62.2 63.9 65.6 67.2 68.1 59.7 60.6 62.2 63.9 65.6 67.2 68.1
Height (cm) 151.7 154.0 157.9 162.3 166.7 170.6 173.0 151.7 154.0 157.9 162.3 166.7 170.6 173.0
16 years
Height (in) 59.9 60.8 62.4 64.1 65.8 67.3 68.3 59.9 60.8 62.4 64.1 65.8 67.3 68.3
Height (cm) 152.1 154.5 158.4 162.8 167.1 171.1 173.4 152.1 154.5 158.4 162.8 167.1 171.1 173.4
17 years
Height (in) 60.0 60.9 62.5 64.2 65.9 67.4 68.4 60.0 60.9 62.5 64.2 65.9 67.4 68.4
Height (cm) 154.4 154.7 158.7 163.0 167.4 171.3 173.7 154.4 154.7 158.7 163.0 167.4 171.3 173.7
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The 50 th, 90 th, and 95 th percentiles were derived by using quantile regression on the basis of normal-weight children (BMI
<85 th percentile). BP stages are defined as elevated BP ≥90 th percentile but <95 th percentile; stage 1 HTN: ≥95 th percentile
or 130/80 to 139/89 mmHg; and stage 2 HTN: ≥95 th percentile + 12 mmHg or >140/90 mmHg.
Reproduced with permission from: Pediatrics, Vol. 140, doi: 10.1542/peds.2017-1904. Copyright © 2017 by the AAP.
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Age:
Family history of HTN Children with a positive family history of Family history may be positive in some
primary HTN are more likely to have cases of secondary HTN due to a
primary HTN. monogenic cause (eg, autosomal
dominant polycystic kidney disease).
Symptoms of underlying disorder Patients with primary HTN are typically Patients with secondary HTN often have
asymptomatic. other symptoms related to the
underlying cause (eg, headache,
sweating, and tachycardia due to
catecholamine excess in patients with
pheochromocytoma).
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Data from:
1. Tunnessen WW, Roberts KB. Hypertension. In: Signs and Symptoms in Pediatrics, 3rd ed, Lippincott, Williams & Wilkins,
Philadelphia 1999. p.413.
2. Pappadis SL, Somers MJ. Hypertension in adolescents: a review of diagnosis and management. Curr Opin Pediatr 2003; 15:370.
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Obesity
Hypertension
Dyslipidemia
Smoke exposure
Special-risk conditions
High-risk conditions:
Diabetes mellitus
Chronic kidney disease
Cardiac transplantation
Kawasaki disease with current coronary artery aneurysms
Moderate-risk conditions:
Chronic inflammatory diseases (eg, SLE)
HIV infection
Nephrotic syndrome
Kawasaki disease with regressed coronary artery aneurysms
Depressive and bipolar disorders ¶
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CNS: Head trauma, headache, visual disturbance, lethargy, Elevated intracranial pressure
seizures, tremors, morning vomiting
Lead poisoning
Thyroid dysfunction
Renal vasculitis
Growth history: Excessive weight gain or loss, change in Obesity, thyroid dysfunction
growth percentiles
Dietary history: Types and amount of food ingested; salt Obesity, essential hypertension
craving
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General
Vital signs
BP differences in extremities If upper extremity BP > lower extremity BP, coarctation of aorta
Eye
Skin
Chest
Abdomen
Extremities
Arthritis Henoch-Schönlein purpura (IgA vasculitis), collagen vascular disease (systemic lupus
erythematous)
Neurologic
Genitalia
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References:
1. Flynn JT. Evaluation and management of hypertension in childhood. Prog Pediatr Cardiol 2001; 12:177.
2. The Fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. National
Heart, Lung and Blood Institute. National Institutes of Health. May 2004.
3. Flynn JT, Kaelber DC, Baker-Smith CM, et al. Clinical Practice Guideline for Screening and Management of High Blood Pressure
in Children and Adolescents. Pediatrics 2017; 140:e20171904.
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Severe obesity BMI ≥35 (class II obesity) BMI ≥120 percent of the 95 th percentile,
or a BMI ≥35 (whichever is lower) *[4,5]
BMI ≥40 (class III obesity) BMI ≥140 percent of the 95 th percentile,
or a BMI ≥40 (whichever is lower) [5]
AAP: American Academy of Pediatrics; IOM: Institute of Medicine; ES: Endocrine society; CDC: Centers for Disease Control; IOTF:
International obesity task force; BMI: body mass index.
* In children, several definitions of severe obesity have been used. The most widely accepted is BMI ≥120 percent of the 95 th
percentile, or a BMI ≥35 (whichever is lower). [3] This corresponds to approximately the 99 th percentile, or BMI Z-score ≥2.33 (ie,
2.33 standard deviations above the mean).
References:
1. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults--The Evidence Report.
National Institutes of Health. Obes Res 1998; 6 Suppl 2:51S.
2. Barlow SE, Expert Committee. Expert committee recommendations regarding the prevention, assessment, and treatment of
child and adolescent overweight and obesity: summary report. Pediatrics 2007; 120 Suppl 4:S164.
3. Wang Y. Cross-national comparison of childhood obesity: the epidemic and the relationship between obesity and socioeconomic
status. Int J Epidemiol 2001; 30:1129.
4. Kelly AS, Barlow SE, Rao G, et al. Severe Obesity in Children and Adolescents: Identification, Associated Health Risks, and
Treatment Approaches: A Scientific Statement From the American Heart Association. Circulation 2013.
5. Skinner AC, Skelton JA. Prevalence and Trends in Obesity and Severe Obesity Among Children in the United States, 1999-2012.
JAMA Pediatr 2014.
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Severe obesity in pediatric patients is defined as a body mass index (BMI) that is either ≥120% of the 95 th percentile curve, or
BMI ≥35 kg/m 2 (whichever is lower). The area defining severe obesity is shaded in red in the figure above. A BMI of 40 kg/m 2
is typically used as a threshold for weight loss surgery in adults and adolescents without major comorbidities. Note that this
threshold is well above the curve representing 120% of the 95 th percentile at all ages.
The black curves (50 through 97) represent the standard BMI growth reference from the CDC, published in 2000. The blue
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curves (110% through 190%) are derived by multiplying the 95 th percentile values by 1.1 through 1.9, respectively.
Source: Kelly AS, Barlow SE, Rao G, Inge TH, et al. Severe obesity in children and adolescents: Identification, associated health risks,
and treatment approaches. A scientific statement from the American Heart Association. Circulation 2013; 128:1689.
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Severe obesity in pediatric patients is defined as a body mass index (BMI) that is either ≥120% of the 95 th percentile curve, or
BMI ≥35 kg/m 2 (whichever is lower). The area defining severe obesity is shaded in red in the figure above. A BMI of 40 kg/m 2 is
typically used as a threshold for weight loss surgery in adults and adolescents without major comorbidities. Note that this
threshold is well above the curve representing 120% of the 95 th percentile at all ages.
The black curves (50 through 97) represent the standard BMI growth reference from the CDC, published in 2000. The blue curves
(110% through 190%) are derived by multiplying the 95 th percentile values by 1.1 through 1.9, respectively.
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Source: Kelly AS, Barlow SE, Rao G, Inge TH, et al. Severe obesity in children and adolescents: Identification, associated health risks, and
treatment approaches. A scientific statement from the American Heart Association. Circulation 2013; 128:1689.
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Representative digital retinal fundus photographs of mild (A,B), moderate (C,D), and severe (E,F) hypertensive
retinopathy, as graded with the simplified classification:
(A) Mild hypertensive retinopathy is indicated by the presence of generalized arteriolar narrowing, arteriovenous (AV)
nicking, and opacification of the arteriolar wall ("copper wiring").
(B) Mild hypertensive retinopathy with focal arteriolar narrowing.
(C,D) Moderate hypertensive retinopathy with multiple retinal hemorrhages and cotton wool patches.
(E,F) Severe hypertensive retinopathy with swelling of the optic disk, retinal hemorrhages, hard exudates, and cotton
wool patches.
From: Downie LE, Hodgson LA, Dsylva C, et al. Hypertensive retinopathy: Comparing the Keith-Wagener-Barker to a simplified
classification. J Hypertens 2013; 31:960. DOI: 10.1097/HJH.0b013e32835efea3. Copyright © 2013. Reproduced with
permission from Wolters Kluwer Health. Unauthorized reproduction of this material is prohibited.
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