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The first step in the evaluation of a child for hypertension is to define whether the child is in fact hypertensive. For children under 13 years of age, the normative data for blood pressure are interpreted based on gender, age, and height because all these are variables that influence blood pressure norms. The current hypertension definition and staging lead to seamless interfacing with the 2017 American Heart Association (AHA) and American College of Cardiology (ACC) adult hypertension guidelines for children over 13 years of age ( Table 11.1 ).
For Children Aged 1 to <13 yr | For Children Aged ≥13 yr | |
---|---|---|
Normal BP | <90th percentile | <120/<80 mm Hg |
Elevated BP | ≥90th to <95th percentile or 120/80 mm Hg to <95th percentile (whichever is lower) | 120–129/<80 mm Hg |
Stage 1 Hypertension | ≥95th to <95th percentile + 12 mm Hg or 130–139/80–89 mm Hg (whichever is lower) | 130–139/80–89 mm Hg |
Stage 2 Hypertension | ≥95th percentile + 12 mm Hg or ≥140/90 mm Hg (whichever is lower) | ≥140/90 mm Hg |
Data on blood pressure tracking from childhood to adulthood demonstrate that higher blood pressure in childhood correlates with hypertension in young adulthood. Autopsy and imaging studies reveal that hypertension is associated with poorer markers of vascular aging, which are known to predict cardiovascular events in adults.
Hypertension can be silent or may present with symptoms related to high blood pressure or the primary disease producing the hypertension (e.g., pheochromocytoma, lupus). Chronic hypertension is silent in most cases, but acute hypertension is typically symptomatic. A detailed history and physical examination will help guide the assessment of etiology and urgency for management. Summaries are provided in Tables 11.2 and 11.3 . Eliciting symptoms related to acute hypertension that could indicate urgency is critical in the initial assessment and management. Presentations with severe headache, vision changes, chest pain, respiratory distress, abdominal pain, seizure, or acute neurologic changes with elevated blood pressure should be considered emergent in any age group and need immediate attention.
History |
|
Physical exam |
|
Physical Findings | Potential Relevance |
---|---|
General | |
Pale mucous membranes, edema, growth retardation | Chronic renal disease |
Elfin facies, poor growth, retardation | Williams syndrome |
Webbing of neck, low hairline, widespread nipples, wide carrying angle | Turner syndrome |
Moon face, buffalo hump, hirsutism, truncal obesity, striae, acne | Cushing syndrome |
Habitus | |
Thinness | Pheochromocytoma, renal disease, hyperthyroidism |
Virilization | Congenital adrenal hyperplasia |
Rickets | Chronic renal disease |
Skin | |
Café-au-lait spots, neurofibromas | Neurofibromatosis, pheochromocytoma |
Tubers, “ash-leaf” spots | Tuberous sclerosis |
Rashes | Systemic lupus erythematosus, vasculitis (Henoch-Schönlein purpura), impetigo with acute nephritis |
Pallor, evanescent flushing, sweating | Pheochromocytoma |
Needle tracks | Illicit drug use |
Bruises, striae | Cushing syndrome |
Acanthosis nigricans | Type 2 diabetes, insulin resistance |
Eyes | |
Extraocular muscle palsy | Nonspecific, chronic, severe |
Fundal changes | Nonspecific, chronic, severe |
Proptosis | Hyperthyroidism |
Head And Neck | |
Goiter | Thyroid disease |
Adenotonsillar hypertrophy | Sleep-disordered breathing |
Webbed neck | Turner syndrome |
Cardiovascular Signs | |
Absent of diminished femoral pulses, low leg pressure relative to arm pressure | Aortic coarctation |
Heart size, rate, rhythm; murmurs; respiratory difficulty, hepatomegaly | Aortic coarctation, congestive heart failure |
Bruits over great vessels | Arteritis or arteriopathy |
Rub | Pericardial effusion secondary to chronic renal disease |
Pulmonary Signs | |
Pulmonary edema | Congestive heart failure, acute nephritis |
Picture of bronchopulmonary dysplasia | Bronchopulmonary dysplasia–associated hypertension |
Abdomen | |
Epigastric bruit | Primary renovascular disease or in association with Williams syndrome, neurofibromatosis, fibromuscular dysplasia, or arteritis |
Abdominal masses | Wilms tumor, neuroblastoma, pheochromocytoma, polycystic kidneys, hydronephrosis, dysplastic kidneys |
Jaundice | Alagille arteriohepatic dysplasia |
Neurologic Signs | |
Neurologic deficits | Chronic or severe acute hypertension with stroke |
Muscle weakness | Hyperaldosteronism, Liddle syndrome (hypokalemic low renin hypertension) |
Genitalia | |
Ambiguous, virilized | Congenital adrenal hyperplasia (11β- or 17α-hydroxylase deficiencies) |
Skeletal | |
Short metacarpal (4th, 5th) bones, short stature | Autosomal dominant hypertension with brachydactyly (Bilginturan disease) |
In addition to symptoms secondary to the hypertension, those related to potential etiology should be sought, especially since most hypertension in children is not primary hypertension. Renal causes are high in the differential in all children but vary according to age. Potential causes for each age group ( Tables 11.4 and 11.5 ) help guide the symptoms to be elicited and focus the physical examination. Neonates may present with gross hematuria or an abdominal mass. In later infancy the presentation may be similar to that in neonates, but edema would suggest glomerular pathology. Infants may also present with nonspecific symptoms of poor growth, weight loss, and/or fussiness. Childhood and adolescent acute hypertension may present with symptoms of gross hematuria, edema, rash, joint complaints, respiratory symptoms, or diarrhea depending on the etiology. Urinary symptoms can be a presentation of hypertension in childhood that would suggest a urologic abnormality not previously discovered. In later childhood and adolescence, the risk of recreational drug use increases, so symptoms of lethargy, irritability, anorexia, and poor school performance are relevant. Sleep problems could be related to sleep apnea or illicit drug use. Episodic palpitation or flushing may be symptoms related to catecholamine-secreting tumors or hyperthyroidism. Some disorders produce transient or intermittent hypertension ( Table 11.6 ).
Neonatal
Later infancy
|
Common Causes
Less Common Causes
Rare causes
|
Renal
Drugs and Poisons
Central and Autonomic Nervous System
Miscellaneous
|
Accurate blood pressure measurement is fundamental in identification of hypertension. Manual, auscultatory blood pressure is the most accurate, and the normative data are based on this method of blood pressure measurement. An accurate reading depends on positioning and appropriate cuff size. Sitting relaxed with uncrossed feet on the floor with the back supported and using a cuff with a bladder that covers a minimum of 80% midarm circumference and 40% of arm length are optimal.
In infants and those in whom Korotkoff sounds are not well heard, Doppler can be used to measure blood pressure accurately, but only systolic readings are obtained by that method. An oscillatory method may not be accurate but is useful as a screening tool, if done with a device calibrated for pediatric use. In an emergency setting a manual blood pressure measurement may not be feasible initially. A well-calibrated oscillatory device can be used for initial screening and frequent monitoring, and then validated with auscultatory method at the earliest opportunity.
Blood pressure measurement should be done on the right arm, unless there is known atypical anatomy that can confound that assessment. If blood pressure is found there to be elevated, four extremity readings should be obtained to evaluate for vascular anomalies, in particular aortic coarctation, which might further be suggested by the presence of a heart murmur. Lower extremity blood pressure is typically equal or higher than upper extremity blood pressure. Finding right upper extremity blood pressure >10 mm Hg above that of lower extremity blood pressure is a strong indication of aortic coarctation.
If the initial blood pressure reading is in the elevated blood pressure or stage 1 hypertension range, additional readings should be obtained on different days over days to weeks to confirm the presence of true hypertension. If there is concern that anxiety with clinic visits is affecting blood pressure assessment, 24-hour ambulatory blood pressure monitoring (ABPM) can be used to separate those with sustained hypertension from those with “white coat hypertension.” ABPM provides frequent readings in the home setting with diurnal information. The standards used for these readings are different from the casual blood pressure reading guidelines mentioned earlier.
Other pertinent physical examination information is critical in determining the urgency of the situation as well as the etiology. Abnormal fundoscopic findings such as papilledema and retinal hemorrhages and focal neurologic or encephalopathic findings are indicative of acute hypertensive emergency and the need for immediate therapeutic intervention along with prompt evaluation to identify the etiology. The physical findings help lead to both the effects of hypertension and the potential etiology. The presence of a gallop rhythm and rales on auscultation of the heart and lungs, along with edema, indicates volume overload as the cause of severe symptomatic hypertension, possibly from underlying glomerulonephritis. Edema, rash, and arthritis would suggest hypertension secondary to renal involvement from potential autoimmune disease. Diminished lower extremity pulses with discrepancy between upper and lower extremity blood pressures, along with a heart murmur, point to coarctation of the aorta. Abdominal or flank bruit may be present with renal artery stenosis. Findings of body habitus suggestive of Cushing syndrome, ambiguous genitalia, or features of hyperthyroidism can direct evaluation to endocrine causes. Physical exam findings associated with genetic syndromes that can have hypertension caused by abnormal renal or vascular development include coloboma, lens dislocation, ear tags, brachial cysts, café-au-lait spots, or a webbed neck (see Table 11.3 ).
Hypertension in children is uncommon and when present is usually from an identifiable cause other than primary essential hypertension. The preponderance of hypertension in adulthood is either primary hypertension, formerly called “essential hypertension,” or hypertension secondary to diabetic nephropathy. While the prevalence of primary hypertension is rising in childhood, the cause of hypertension in children and adolescents usually is secondary to an identifiable cause, and is most often from renal disease. Disease processes that cause hypertension in childhood typically manifest at different ages, with the major differences being between infants and older children.
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