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Hypertension

Hypertension: Excerpt from The Diagnostic Approach to Symptoms and Signs in Pediatrics

Major riskfactor for cardiac, cerebral, and renal vascular disease.

For clinical purposes, hypertensioncan be defined as systolic or diastolic BP > ninety-fifth percentilefor age, gender, and height (Tables32.1 and 32.2).

Table 32.1. Blood Pressure Levels for the Ninety-Fifth Percentilesof Blood Pressure for Boys 1–17 Yrs of Age by Percentilesof Height

		Systolic and Diastolic BP by Percentile ofHeight (mm Hg)b
Age (Yr)	BP Percentilea	5%	10%	25%	50%	75%	90%	95%
1	95th	98/55	99/55	101/56	102/57	104/58	106/59	106/59
2	95th	101/59	102/59	104/60	106/61	108/62	109/63	110/63
3	95th	104/63	105/63	107/64	109/65	111/66	112/67	113/67
4	95th	106/66	107/67	109/67	111/68	113/69	114/70	115/71
5	95th	108/69	109/70	110/70	112/71	114/72	115/73	116/74
6	95th	109/72	110/72	112/73	114/74	115/75	117/76	117/76
7	95th	110/74	111/74	113/75	115/76	116/77	118/78	119/78
8	95th	111/75	112/76	114/76	116/77	118/78	119/79	120/80
9	95th	113/76	114/77	116/78	117/79	119/80	121/80	121/81
10	95th	114/77	115/78	117/79	119/80	121/80	122/81	122/82
11	95th	116/78	117/79	119/79	121/80	123/81	124/82	125/83
12	95th	119/79	120/79	121/80	123/81	125/82	126/83	127/83
13	95th	121/79	122/80	124/81	126/82	128/83	129/83	130/84
14	95th	124/80	125/81	127/81	128/82	130/83	132/84	132/85
15	95th	127/81	128/82	129/83	131/83	133/84	134/85	135/86
16	95th	129/83	130/83	132/84	134/85	136/86	137/87	138/87
17	95th	132/85	133/85	135/86	136/87	138/88	140/89	140/89

^aBP percentile was determinedby single measurement.

^bHeight percentile was determinedby standard growth curves.

Adapted in part from the National High Blood Pressure EducationProgram Working Group on Hypertension Control in Children and Adolescents.Update on the 1987 Task Force Report on High Blood Pressure in Childrenand Adolescents: A Working Group Report from the National High BloodPressure Education Program. Pediatrics 1996;98:653–654;with permission.

Table 32.2. Blood Pressure Levels for the Ninety-Fifth Percentilesof Blood Pressure for Girls 1–17 Yrs of Age by Percentilesof Height

		Systolic and Diastolic BP by Percentile ofHeight (mm Hg)b
Age (Yr)	BP Percentilea	5%	10%	25%	50%	75%	90%	95%
1	95th	101/57	102/57	103/57	104/58	105/59	107/60	107/60
2	95th	102/61	103/61	104/62	105/62	107/63	108/64	109/65
3	95th	104/65	104/65	105/65	107/66	108/67	109/67	110/68
4	95th	105/67	106/67	107/68	108/69	109/69	111/70	111/71
5	95th	107/69	107/70	108/70	110/71	111/72	112/72	113/73
6	95th	108/71	109/71	110/72	111/73	112/73	114/74	114/75
7	95th	110/73	110/73	112/73	113/74	114/75	115/76	116/76
8	95th	112/74	112/74	113/75	115/75	116/76	117/77	118/78
9	95th	114/75	114/76	115/76	117/77	118/78	119/78	120/79
10	95th	116/77	116/77	117/77	119/78	120/79	121/80	121/80
11	95th	118/78	118/78	119/79	121/79	122/80	123/81	124/81
12	95th	120/79	120/79	121/80	123/80	124/81	125/82	126/82
13	95th	121/80	122/80	123/81	125/82	126/82	127/83	128/84
14	95th	123/81	124/81	125/82	126/83	128/83	129/84	130/85
15	95th	124/82	125/82	126/83	128/83	129/84	130/85	131/86
16	95th	125/83	126/83	127/83	128/84	130/85	131/86	132/86
17	95th	126/83	126/83	127/83	129/84	130/85	131/86	132/86

^aBP percentile was determinedby single measurement.

^bHeight percentile was determinedby standard growth curves.

Adapted in part from the National High Blood Pressure EducationProgram Working Group on Hypertension Control in Children and Adolescents.Update on the 1987 Task Force Report on High Blood Pressure in Childrenand Adolescents: A Working Group Report from the National High BloodPressure Education Program. Pediatrics 1996;98:653–654;with permission.

Principal Causes of Hypertension

1. Transienthypertension
2. Sustained hypertension
   1. Birthto one year
      1. Mostcommon
         1. Renalartery thrombosis after umbilical artery catheterization
         2. Coarctation of the aorta
         3. Congenital renal disease
         4. Renal artery stenosis
      2. Less common
         1. Bronchopulmonary dysplasia
         2. Patent ductus arteriosus
         3. Intraventricular hemorrhage
   2. One to ten years
      1. Most common
         1. Renaldisease
         2. Coarctation of the aorta
      2. Less common
         1. Renal artery stenosis
         2. Glucocorticoid excess
         3. Sex hormones
         4. Catecholamine excess
         5. Neuroblastoma
         6. Pheochromocytoma
      3. Mineralocorticoid excess
         1. High aldosteronemineralocorticoid excess
            1. Primary aldosteronism
            2. Glucocorticoid-remediable aldosteronism
            3. Hyperreninemic hyperaldosteronism
         2. Low aldosterone mineralocorticoid excess
            1. 17-Alpha-hydroxylasedeficiency
            2. 11-Beta-hydroxylase deficiency
            3. Apparent mineralocorticoid excess
      4. Hyperthyroidism
      5. Hypercalcemia
      6. Renal tumors
      7. Nervous system disorders
      8. Drugs
      9. Primary or essential hypertension
   3. Eleven years through adolescence
      1. Most common
         1. Renaldisease
         2. Primary or essential hypertension
         3. Less common
            1. All diagnoses listed above

Clinical Features and Diagnosis

Transient Hypertension

Frequentcauses are stress related (e.g., anxiety, pain, and burns). BP becomesnormal with relief of stress.

Another cause is increase in intravascularvolume with excessive use of saline, blood, or plasma. When intravascularvolume normalizes, BP returns to normal.

Finally, immobilization with placementin traction may cause increased BP, which resolves when immobilizationis no longer necessary.

Sustained Hypertension

Birth–1 Yr

Renal Artery Thrombosis after Umbilical Artery Catheterization

BP shouldbe monitored in infants with umbilical artery catheter; they shouldcontinue to be monitored after catheter has been removed.

Unilateral or bilateral enlarged kidneysand hematuria are clues to this diagnosis, which is usually confirmedby abdominal U/S with Doppler methods.

If thrombosis involves aorta, femoralpulses may not be palpable and blood flow to lower extremities maybe compromised.

Coarctation of Aorta

Usuallyinvolves thoracic aorta, although it can involve abdominal aorta.

Increased BP occurs at least in rightupper arm with decreased BP and diminished or absent pulses in lowerextremities.

2-D echocardiography, MRI, or aorticangiography can confirm diagnosis.

After surgical repair, transient increasein BP may occur within 1–2 days. Sustained increase inBP may be observed during week after repair, and often a few weeksto a few months thereafter.

Mechanism for persistent hypertensionin some patients after successful repair of coarctation may be relatedto overactivity of renin-angiotensin-aldosterone system.

Congenital Renal Disease

Hypertension may occur with renal dysplasia,hydronephrosis, nephrotic syndrome, and polycystic kidney disease.See Chap. 1, Abdominal Masses; Chap. 28, Hematuria; and Chap. 50, Proteinuria.

Renal Artery Stenosis

Stenosisof main or segmental renal artery caused by intrinsic or extrinsicrenal disease may result in severe hypertension.

Causes of intrinsic disease includemedial fibromuscular dysplasia (neurofibromatosis, idiopathic),intimal fibroplasia (neurofibromatosis), arteritis (Kawasaki disease,Takayasu disease, moyamoya, radiation), trauma (blunt, surgical),atherosclerosis (familial dyslipoproteinemia), posttransplantation(surgical, immune), aneurysm, embolism, and specific syndromes (Williams,Turner).

Causes of extrinsic disease includetumor (Wilms, pheochromocytoma, neuroblastoma, lymphoma), fibrousbands (congenital, postsurgical), and perirenal hematoma (trauma).

Renal arteriography remains gold standardfor visualization of lesions. Other useful tests include abdominalU/S with Doppler methods, captopril renography, and CTfor detection of mass lesions.

Bronchopulmonary Dysplasia

Infants with bronchopulmonary dysplasia maydevelop hypertension, even after discharge from nursery. See Chap. 10, Cough; Chap. 56, Respiratory Distress and Apnea;and Chap. 75, Wheezing.

Patent Ductus Arteriosus

Common in neonates, especially in preterminfants. Diastolic pressure is typically low or normal, and pulsepressure is increased. Increase in systolic BP is presumably dueto larger LV stroke volume. See Chap.7, Cardiac Failure, and Chap. 27, Heart Murmurs (Asymptomatic).

Intraventricular Hemorrhage

Common occurrence in preterm infants, especiallythose <32 wks' gestation. The more severe the hemorrhage(grades III and IV), the more likely that increased intracranialpressure will occur with an associated increase in BP.

1–10 Yrs

Renal Disease

Hypertension may occur with glomerulonephritis,pyelonephritis, hydronephrosis, hemolytic-uremic syndrome, and refluxnephropathy. See Chap. 1, AbdominalMasses; Chap.15, Dysuria; Chap.28, Hematuria; and Chap.50, Proteinuria.

Coarctation of Aorta

See previous section Coarctation of Aorta.

Renal Artery Stenosis

See previous section Renal Artery Stenosis.

Glucocorticoid Excess

Most commoncause is use of corticosteroids or adrenocorticotropic hormone (ACTH)for underlying medical disorder.

Less common cause is Cushing syndrome,which is usually due to adrenal hyperplasia or adrenal tumor thatresults in excess production of glucocorticoids and androgens. Usualcause of Cushing disease is pituitary adenoma producing excessiveamount of ACTH.

Produces increased weight gain, hypertension,and slow linear growth. See Chap.44, Obesity.

Sex Hormones

Oral contraceptives may produce hypertension.So may anabolic steroids that contain testosterone.

Catecholamine Excess

Major catecholaminesare dopamine, norepinephrine, and epinephrine.

Tumors that secrete excess catecholaminesinclude neuroblastoma and pheochromocytoma.

Neuroblastoma

Malignanttumor that may arise from adrenal medulla or other sympathetic nervous tissue.

Abdominal mass is common finding. Thereis usually increase in 24-hr urinary excretion of catecholamines.

Abdominal U/S and CT can usuallylocate the tumor. See Chap. 1,Abdominal Masses.

Pheochromocytoma

Peak incidenceof pheochromocytoma is in older children and adolescents. It maybe associated with neurofibromatosis and multiple endocrine neoplasiasyndromes.

Clinical manifestations include paroxysmalhypertension, palpitations, headache, nausea, vomiting, and emotionallability.

Increased concentration of catecholaminesand their metabolites (vanillymandelic acid is major metaboliteof epinephrine and norepinephrine) may be found in blood or 24-hrurine collection

If suspected by biochemical tests,abdominal U/S, CT, or MRI can usually locate tumor in adrenalgland or along sympathetic chain. Another useful test is scintigraphywith metaiodobenzyl guanidine (MIBG) labeled with ¹²³I.This compound concentrates in tissues that actively synthesize catecholaminesand can locate small tumors that may be otherwise difficult to detect.

Mineralocorticoid Excess

Rare inchildhood.

Plasma aldosterone concentration isincreased in true aldosterone excess, whereas in apparent mineralocorticoidexcess, features of aldosterone excess occur without increase inplasma aldosterone concentration.

Causes of mineralocorticoid excessproducing hypertension are listed in Table32.3.

Table 32.3. Causes of Mineralocorticoid Excess Producing Hypertension

High aldosterone mineralocorticoid excess

Primary aldosteronism

Adrenal hyperplasia (bilateral)

Adrenal tumor (adenoma, carcinoma)

Glucocorticoid-remediable aldosteronism

Hyperreninemic hyperaldosteronism

Renal ischemia

Juxtaglomerular cell tumor (renal hemangiopericytoma)

Bilateral endocrine dysfunction of kidneys

Low aldosterone mineralocorticoid excess

Enzyme deficiencies (17-alpha-hydroxylase, 11-beta-hydroxylase)

Apparent mineralocorticoid excess

11-beta-hydroxysteroid dehydrogenase deficiency

Licorice ingestion (inhibition of 11-beta-hydroxsteroid dehydrogenase)

High Aldosterone Mineralocorticoid Excess

Primary Aldosteronism

Excessiveamount of aldosterone may be produced by bilateral hyperplasia ofadrenal cortex or adrenal tumor (adenoma, carcinoma).

Characteristic findings include hypertension,hypokalemia, low plasma renin activity, and elevated plasma aldosterone.

Tumor mass may be visible with abdominalU/S or CT.

Glucocorticoid-Remediable Aldosteronism

Autosomal-dominantdisorder (also termed dexamethasone-suppressible aldosteronism)that has similar clinical and biochemical features to aldosterone-secretingadenoma.

Urinary excretion of 18-hydroxycortisoland 18-oxycortisol is increased.

Can be distinguished from primary aldosteronismby dexamethasone suppression of aldosterone within 2 wks of treatment.

Genetic loci have been mapped to chromosome8.

Hyperreninemic Hyperaldosteronism

Juxtaglomerularcells in kidney may produce excess renin, which results in increased serumconcentration of aldosterone.

Most common cause is renal ischemia,usually from renal artery stenosis. Rare cause is benign tumor ofjuxtaglomerular cells called renal hemangiopericytoma. Another rarecause is self-limited disorder of unknown etiology called bilateralendocrine dysfunction of kidney in which source of increased reninis bilateral.

Because many of these tumors are toosmall to be detected by imaging, renal vein sampling that revealsunilateral hypersecretion of renin is diagnostic.

Low Aldosterone Mineralocorticoid Excess

17-Alpha-Hydroxylase Deficiency

This enzymecatalyzes conversion of progesterone to 17-hydroxyprogesterone and pregnenoloneto 17-hydroxypregnenolone.

Gene locus has been mapped to chromosome10q24.

Deficiency in enzyme activity resultsin decreased sex hormone production.

Affected boys have ambiguous externalgenitalia and in some cases female-appearing genitalia with failureof masculinization at puberty. Girls have normal external genitaliaat birth and usually present at puberty with primary amenorrheaand lack of development of secondary sexual characteristics.

Excessive production of deoxycorticosteroneand corticosterone produces hypertension.

11-Beta-Hydroxylase Deficiency

Deficiencyimpairs conversion of deoxycorticosterone to corticosterone and11-deoxycortisol to cortisol.

Gene locus has been mapped to chromosome8q21.

Compounds proximal to enzyme blockaccumulate and produce hypertension as well as increase in androgens.

Excess in fetal androgen produces masculinizationof female fetus and ambiguous external genitalia. Boys appear normalat birth but can develop gynecomastia prior to puberty.

Diagnosis is confirmed by pattern ofsteroid secretion—high serum concentrations of deoxycorticosteroneand 11-deoxycortisol and low serum concentrations of cortisosteroneand cortisol.

Apparent Mineralocorticoid Excess

Due to deficiencyof enzyme 11-beta-hydroxysteroid dehydrogenase, which catalyzesconversion of cortisol to cortisone. Gene locus has been mappedto chromosome 1. Cortisol activates mineralocorticoid receptor,which leads to sodium retention and hypertension.

Lab findings include hypokalemia, metabolicalkalosis, and low plasma renin and aldosterone levels.

Similar presentation occurs with ingestionof large amounts of licorice that contains glycyrrhizic acid andits metabolite, glycyrrhetinic acid, both of which inhibit activityof 11-beta-hydroxysteroid dehydrogenase.

Hyperthyroidism

Systolichypertension may occur with hyperthyroidism. Other clinical featuresinclude tachycardia, nervousness, heat intolerance, weight loss,and enlarged thyroid gland.

Usual cause is Graves disease. See Chap. 42, Neck Masses.

Hypercalcemia

May causeabdominal pain, anorexia, constipation, polyuria, behavioral changes,and hypertension.

Possible causes include primary hyperparathyroidism,vitamin D intoxication, Williams syndrome, and malignancy.

Renal Tumors

Hypertensionassociated with Wilms tumor may be due to compression of renal artery orexcessive production of renin by tumor itself. Combination of renalU/S and abdominal CT define extent of mass and whetherinferior vena cava is involved.

Juxtaglomerular cell tumors produceexcessive amount of renin that is responsible for hypertension.CT can usually identify these tumors.

Benign hamartomatous renal tumors canoccur in association with tuberous sclerosis. In infancy, hypertensionand renal enlargement may precede other manifestations of disease.Renal U/S and CT are useful in locating tumors and definingtheir extent.

Nervous System Disorders

Hypertension may occur with Guillain-Barré syndrome,familial dysautonomia, and any cause of increased intracranial pressure,including brain tumor, meningitis, and encephalitis.

Drugs

Chronic corticosteroid use, oral contraceptives,cyclosporine, sympathomimetic drugs (phenylpropanolamine, phenylephrine),cocaine, amphetamines, and phencyclidine may produce hypertension.

Primary or Essential Hypertension

See later section Primary or Essential Hypertension.

11 Yrs through Adolescence

Renal Disease

See previous section Renal Disease.

Primary or Essential Hypertension

By definition,primary or essential hypertension is absence of other known causesof hypertension.

There is often positive family historyof hypertension, and these children are frequently overweight.

Results of UA and renal U/Sare normal, as are serum creatinine and blood urea nitrogen levels.Clinical dilemma is to decide if other tests need to be performedto exclude other causes. This problem is addressed in the followingsection.

Diagnostic Approach

BP can bemeasured at any age, but it should be measured in any child ≥3yrs of age each year. Any infant or child with unexplained heartmurmur, cardiomegaly, decreased femoral pulses, abdominal mass,seizures, any suspicion of cardiovascular or renal disease, or anyacute severe illness should have BP measured.

Arm BP should be measured with childsitting or supine with the cubital fossa at heart level. Width ofbladder cuff should cover two-thirds of distance between shoulderand elbow. Phase 1 and 5 Korotkoff sounds should be recorded. Ithas now been determined that phase 5 Korotkoff sound (disappearanceof Korotkoff sound) is reliable measure of diastolic BP in childrenof all ages. In child suspected of having hypertension, BP shouldbe measured in both arms and in at least 1 leg initially.

Complete history and physical examshould be performed in any child with hypertension. Extent of evaluationdepends on child's age, clinical presentation and findings,family history, level of BP, and whether increase in BP is transientor sustained.

Age

At any age, stress in form of anxiety, pain,or trauma is common cause of transient hypertension.Common and uncommon causes of sustained hypertensionby age are listed previously.In pediatric population, renal parenchymaldisease and renal artery stenosis are most common causes of severehypertension.Generally, the younger the child and higherthe BP, the more likely it is that an identifiable cause will befound.

Clinical Presentation

Childrenwith mild increase in BP are usually asymptomatic.

Infants <1 yr of age withsevere hypertension may have feeding problems, vomiting, irritability,failure to thrive, respiratory distress, cardiac failure, and seizures.

Older children with severe hypertensionmay have severe headache, blurred vision, funduscopic changes, focalor generalized seizures, or cardiac failure.

Family History

Many children and adolescents with primaryhypertension often have positive family history of hypertension.Polycystic kidney disease and glucocorticoid-remediable aldosteronismare genetic diseases associated with hypertension.

Level of Blood Pressure

When singleBP measurement indicative of increased BP has been recorded in asymptomaticchild, several BP measurements should be made subsequently to determinewhether hypertension truly exists.

If BP is in ninety-fifth percentilefor age, gender, and height, and especially if family history ispositive for primary hypertension and child is overweight, diagnosisis most likely primary hypertension.

Several tests should be performed initially:CBC, UA, blood urea nitrogen, serum electrolytes and creatinine,and renal U/S.

If results of these tests are normal,recommendations for decreasing salt intake and weight, and increasingexercise, should be made.

If BP becomes normal, no other investigationsare necessary, but the BP should be measured periodically.

If primary hypertension seems unlikelybased on negative family history, lack of obesity, and young age,the same tests should be performed.

Cortical imaging may be useful in child withhistory of significant vesicoureteral reflux to look for focal scarring.

Urinary tract obstruction may needto be investigated by combination of studies, including voidingcystourethrography, intravenous urography, and diuretic renography.

If diagnosis remains uncertain, plasmarenin activity (PRA) should be measured because low PRA is usefulscreening test for mineralocorticoid excess. Plasma aldosteronealso should be measured. Finally, renal angiography should be considered.

Cardiac organ damage can be evaluatedby echocardiography.

In all individuals with severe hypertension,investigations should search for underlying cause.

Several testsshould be performed: CBC with differential and platelet counts,UA, urine culture, serum electrolytes and creatinine, blood ureanitrogen, abdominal U/S, chest radiography, and echocardiography.

Other useful tests include plasma reninactivity, plasma aldosterone, morning and evening serum cortisol,urine timed collection for catecholamines, measurement of specificplasma steroids to diagnose 17-alpha-hydroxylase and 11-beta-hydroxylasedeficiencies, and captopril renography.

Renal angiography also should be considered.

Transient vs Sustained Hypertension

In somecases, whether hypertension is transient or sustained can only bedetermined with passage of time. If hypertension is severe, whetherit is transient or sustained, immediate therapy for BP control isnecessary to prevent severe complications (e.g., cerebral hemorrhageand infarction). Investigations to determine underlying cause canbe performed once BP is under control.

With sustained hypertension, repeatBP measurements must be made to assess its severity. Presence ofcardiomegaly, facial nerve palsy, and funduscopic changes of arteriolarnarrowing and arteriovenous nicking indicate long-standing severehypertension. These children must be investigated to determine causeof hypertension.

References

1. Barratt TM, et al., eds. Pediatric nephrology,4th ed. Baltimore: Lippincott Williams & Wilkins, 1999.
2. Behrman RE, et al., eds. Nelson textbook of pediatrics,16th ed. Philadelphia: WB Saunders, 2000.
3. Daniels SR. The diagnosis of hypertension in children:an update. Pediatr Rev 1997;18:131–135.
4. Hackman AM, Bricker JT. Preventive cardiology, hypertension,and dyslipidemia. In: Garson A Jr, et al., eds. The science andpractice of pediatric cardiology, 2nd ed. Baltimore: Williams &Wilkins, 1998:2243–2259.
5. Mune T, et al. Human hypertension caused by mutationsin the kidney isoenzyme of 11 beta-hydroxysteroid dehydrogenase.Nat Genet 1995;10:394–399.
6. National High Blood Pressure Education Program WorkingGroup on Hypertension Control in Children and Adolescents. Updateon the 1987 task force report on high blood pressure in childrenand adolescents: a working group report from the national high bloodpressure education program. Pediatrics 1996;98:649–658.
7. Online Mendelian Inheritance in Man (OMIM). McKusick-NathansInstitute for Genetic Medicine, Johns Hopkins University (Baltimore,MD) and National Center for Biotechnology Information, NationalLibrary of Medicine (Bethesda, MD), 2000. World Wide Web URL: http://www.ncbi.nlm.nih.gov/omim.
8. Rudolph AM, ed. Rudolph's pediatrics, 20thed. Stamford, CT: Appleton & Lange, 1996.
9. Scriver CR, et al., eds. The metabolic and molecularbases of inherited disease, 8th ed. New York, McGraw-Hill, 2001.
10. Sinaiko AR. Hypertension in children. N Engl J Med1996;335:1968–1973.

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Book Source Details

• Book Title: The Diagnostic Approach to Symptoms and Signs in Pediatrics
• Author(s): Paul S. Bellet
• Year of Publication: 2006
• Copyright Details: The Diagnostic Approach to Symptoms and Signs in Pediatrics, Copyright © 2006 Lippincott Williams & Wilkins.

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