Hypertension In Children

Apollo Medicine 2011 December
Review Article
Volume 8, Number 4; pp. 248–260
© 2011, Indraprastha Medical Corporation Ltd
Hypertension in children
NilamThaker*
*Consultant Paediatric Nephrologist, 86/3, H Colony, Near Nehrunagar Circle, Ambawadi, Ahmedabad, Gujarat, India.
ABSTRACT
The prevalence of hypertension in children is reported to be 1–3%. In recent years, the prevalence of hypertension
in school-aged children appears to be increasing, perhaps as a result of the increased prevalence of obesity (Sorof JM,
Lai D, Turner J, Poffenbarger T, Portman PJ. Overweight, ethnicity and the prevalence of hypertension in school-aged
children. Pediatrics 2004;113:475–82.). The majority of these children have mild hypertension, most often primary.
However, secondary causes of hypertension such as renal parenchymal diseases and renovascular disorders still
remain the leading cause of paediatric hypertension, particularly in children <12 years of age. Regardless of its
cause, the significant elevation of blood pressure can lead to acute organ dysfunction, and hypertensive child almost
always warrants a diagnostic evaluation.
Keywords: Antihypertensive therapy, children, essential hypertension, hypertension, hypertensive crisis, secondary
hypertension
Correspondence: Dr. Nilam Thaker, E-mail: nilamht@yahoo.co.in
doi: 10.1016/S0976-0016(11)60001-X
DEFINITIONS AND STAGING OF
HYPERTENSION
• Pre-hypertension is defined as systolic or diastolic blood
pressure (BP) between 90th and 95th percentiles. Adoles-
cents having BP >120/80mmHg, but below the 95th per-
centile are also included in this category.
• Hypertension is defined as systolic or diastolic BP exceed-
ing the 95th percentile for age, gender, and height, on at
least 3 separate occasions, 1–3 weeks apart.
Since the severity of hypertension influences its man-
agement, it is staged as below:
• Stage 1 hypertension: Systolic or diastolic BP values
exceeding the 95th percentile and up to 5mmHg above
the 99th percentile.
• Stage 2 hypertension: Systolic or diastolic BP values
5mmHg or more above the 99th percentile.
Two facts regarding levels and distribution of BP in
children and adolescence are well accepted; BP increases
steadily during growth and maturation, and adolescence is
a fast growth period during which body mass and BP change
rapidly. For these reasons, reference BP values specific to
gender, age, and height have been introduced for children
and adolescents by the Task Force group which is sponsored
by the National Heart, Lung and Blood Institute.1
Assessment of both systolic and diastolic pressures are
important and interpreted in relation to age- and height-related
normative data derived from fourth task group report
(Tables 1 and 2).2
Normative data from the Second Report
of Task Force should be used for defining hypertension in
infancy (Figure 1).3
White Coat Hypertension and Masked
Hypertension
In patients with white coat hypertension (WCH), BP is
>95th percentile in clinic or hospital setting, while it is
below 90th percentile in familiar environments. Opposite
phenomenon is called masked hypertension (MH) where
BP is normal in hospital, but high at home.4
Both are easily
diagnosed by ambulatory BP monitoring. Children with
WCH and MH require regular follow-up as they are at risk
of sustained hypertension.
Screening for Hypertension
Blood pressure should be measured in all children >3 years old
presented to healthcare setting.5
Blood pressure should also

Hypertension in children Review Article 249
be measured in at-risk younger children with: (i) History of
prematurity, very low birth weight, or interventions in neo-
natal intensive care unit (NICU); (ii) congenital heart dis-
ease; (iii) recurrent urinary tract infections, known renal or
urological diseases, hematuria or proteinuria; (iv) family
history of congenital renal disorders; (v) malignancy; (vi)
postorgan transplant; and (vii) conditions associated with
hypertension, e.g., neurofibromatosis, tuberous sclerosis, and
ambiguous genitalia.
ETIOLOGY
Primary or Essential Hypertension
Patients are usually obese and postpubertal children. They
typically show stage 1 hypertension and have no evidence
of target organ damage.
Secondary Hypertension
Up to 60–70% of incidence occurs due to renal parenchymal
disease, 5–20% due to renovascular causes and remaining due
to other causes (Table 3).
CLINICAL FEATURES AND CONSEQUENCES
Most patients with pre-hypertension and hypertension are
asymptomatic or have nonspecific symptoms.6
Headache, nausea, vomiting, and weight loss may be
present. Severe hypertension may present with sensorial
impairment, visual disturbances, focal neurological deficits,
seizures, and heart failure.
Infants may show irritability, failure to thrive, vomiting,
feeding problems, seizures, or respiratory distress. In the
newborn period, hypertension manifest with features mim-
icking sepsis, intracranial hemorrhage, or cardiorespiratory
distress. Therefore, accurate BP recording must be carried
out in all sick neonates.
If sustained hypertension remains untreated, it may give
rise to damage to various organs (Table 4).
Although it is generally agreed that early essential hyper-
tension poses little immediate risk to most children, it carries
the potential for future end-organ damage. In children, the
accurate identification of hypertension at the earliest possi-
ble age would, therefore, give healthcare providers the
opportunity to initiate preventive measures, thereby reducing
the chance of developing end-organ damage and its concom-
itant morbidity and mortality.7
EVALUATION OF HYPERTENSION
Careful history and physical examination provide clues to
the underlying etiology (Tables 5 and 6).
INVESTIGATIONS
The extent to which investigations are required depends on
the persistence and severity of hypertension. However, all
patients with hypertension should undergo baseline investi-
gations (Table 7). Obese and adolescent children should be
screened for associated co-morbidity.
Based on clinical features and baseline investigations,
a cause for hypertension is suggested in most instances.
Confirmation of the diagnosis requires specific investiga-
tions tailored to specific needs (Table 8).
MANAGEMENT
It is useful to distinguish essential from secondary hyperten-
sion. While the initial management for patients with essential
hypertension comprises lifestyle modifications, most patients
with sustained secondary hypertension require treatment
with antihypertensive agents.2
Pre-hypertension
Patients are primarily managed by lifestyle modifications (see
below) and revaluated 6 months later. The parents of these
children are informed and advised regarding careful follow-up.
Medications are not required unless the patient has co-morbid
conditions (e.g., chronic kidney disease, diabetes mellitus,
or dyslipidemia) or evidence of target organ damage.
Essential Hypertension
Patients with essential hypertension are initially managed
with lifestyle modifications. Pharmacological therapy is
initiated if there is (i) a co-morbid condition (chronic kidney
disease, diabetes mellitus, or dyslipidemia), (ii) target organ

250 Apollo Medicine 2011 December; Vol. 8, No. 4 Thaker
Table1Bloodpressurelevelsforboysbyageandheightpercentile.5
Age
(yr)
BP
(percentile)
SystolicBP(mmHg)DiastolicBP(mmHg)
HeightpercentileHeightpercentile
5th10th25th50th75th90th95th5th10th25th50th75th90th95th
150th8081838587888934353637383939
90th9495979910010210349505152535354
95th989910110310410610654545556575858
99th10510610811011211311461626364656666
250th8485878890929239404142434444
90th979910010210410510654555657585859
95th10110210410610810911059596061626363
99th10911011111311511711766676869707171
350th8687899193949544444546474848
90th10010110310510710810959596061626363
95th10410510710911011211363636465666767
99th11111211411611811912071717273747575
450th8889919395969747484950515152
90th10210310510710911011162636465666667
95th10610710911111211411566676869707171
99th11311411611812012112274757677787879
550th9091939596989850515253545555
90th10410510610811011111265666768696970
95th10810911011211411511669707172737474
99th11511611812012112312377787980818182
650th91929496989910053535455565757
90th10510610811011111311368686970717272
95th10911011211411511711772727374757676
99th11611711912112312412580808182838484
750th929495979910010155555657585959
90th10610710911111311411570707172737474
95th11011111311511711811974747576777878
99th11711812012212412512682828384858686
850th9495979910010210256575859606061
90th10710911011211411511671727273747576
95th11111211411611811912075767778797980
99th11912012212312512712783848586878788

950th95969810010210310457585960616162
90th10911011211411511711872737475767677
95th11311411611811912112176777879808181
99th12012112312512712812984858687888889
1050th979810010210310510658596061616263
90th11111211411511710911973737475767778
95th11511611711912112212377787980818182
99th12212312512712813013085868688888990
1150th9910010210410510710759596061626363
90th11311411511711912012174747576777878
95th11711811912112312412578787980818282
99th12412512712913013213286868788899090
1250th10110210410610810911059606162636364
90th11511611812012112312374757576777879
95th11912012212312512712778798081828283
99th12612712913113313413586878889909091
1350th10410510610811011111260606162636464
90th11711812012212412512675757677787979
95th12112212412612812913079798081828383
99th12813013113313513613787878889909191
1450th10610710911111311411560616263646565
90th12012112312512612812875767778797980
95th12412512712813013213280808182838484
99th13113213413613813914087878990919292
1550th10911011211311511711761626364656666
90th12212412512712913013176777879808081
95th12612712913113313413581818283848585
99th13413513613814014214288899091929393
1650th11111211411611811912063636465666767
90th12512612813013113313478787980818282
95th12913013213413513713782838384858687
99th13613713914114314414590909192939494
1750th11411511611812012112265666667686970
90th12712813013213413513680808182838484
95th13113213413613813914084858687878889
99th13914014114314514614792939394959697
BP:bloodpressure.

Table2Bloodpressurelevelsforgirlsbyageandheightpercentile.5
Age
(yr)
BP
(percentile)
SystolicBP(mmHg)DiastolicBP(mmHg)
HeightpercentileHeightpercentile
5th10th25th50th75th90th95th5th10th25th50th75th90th95th
150th8384858688899038393940414142
90th97979810010110210352535354555556
95th10010110210410510610756575758595960
99th10810810911111211311464646565666767
250th8585878889919143444445464647
90th989910010110310410557585859606161
95th10210310410510710810961626263646565
99th10911011111211411511669697070717272
350th8687888991929347484849505051
90th10010010210310410610661626263646465
95th10410410510710810911065666667686869
99th11111111311411511611773737474757676
450th8888909192949450505152525354
90th10110210310410610710864646566676768
95th10510610710811011111268686970717172
99th11211311411511711811976767677787979
550th8990919394959652535354555556
90th10310310510610710910966676768696970
95th10710710811011111211370717172737374
99th11411411611711812012078787979808181
650th9192939496979854545556565758
90th10410510610810911011168686970707172
95th10810911011111311411572727374747576
99th11511611711912012112280808081828383
750th9393959697999955565657585859
90th10610710810911111211369707071727273
95th11011111211311511611673747475767677
99th11711811912012212312481818282838484
850th959596989910010157575758596060
90th10810911011111311411471717172737474
95th11211211411511611811875757576777878
99th11912012112212312512582828383848586

950th96979810010110210358585859606161
90th11011011211311411611672727273747575
95th11411411511711811912076767677787979
99th12112112312412512712783838484858687
1050th989910010210310410559595960616262
90th11211211411511611811873737374757676
95th11611611711912012112277777778798080
99th12312312512612712912984848586868788
1150th10010110210310510610760606061626363
90th11411411611711811912074747475767777
95th11811811912112212312478787879808181
99th12512512612812913013185858687878889
1250th10210310410510710810961616162636464
90th11611611711912012112275757576777878
95th11912012112312412512679797980818282
99th12712712813013113213386868788888990
1350th10410510610710911011062626263646565
90th11711811912112212312476767677787979
95th12112212312412612712880808081828383
99th12812913013213313413587878889899091
1450th10610610710911011111263636364656666
90th11912012112212412512577777778798080
95th12312312512612712912981818182838484
99th13013113213313513913688888990909192
1550th10710810911011111311364646465666767
90th12012112212312512612778787879808181
95th12412512612712913013182828283848585
99th13113213313413613713889899091919293
1650th10810811011111211411464646566666768
90th12112212312412612712878787980818182
95th12512612712813013113282828384858586
99th13213313413513713813990909091929393
1750th10810911011111311411564656566676768
90th12212212312512612712878797980818182
95th12512612712913013113282838384858586
99th13313313413613713813990909191929393
BP:bloodpressure.

Table 3 Etiology of hypertension.
Renal parenchymal Renovascular Endocrine Neurological Cardiovascular Drug-induced Monogenic (+ve F/H,
low K, low renin)
Acute and chronic GN
ARF/CRF
Reflux nephropathy
Obstructive uropathy
HUS
Polycystic kidney
Hereditary nephritis
(Alport’s)
Vasculitis (lupus, HSP,
polyarteritis)
Renal artery
stenosis
Renal vessel
thrombosis
Aorto-arteritis
Cushing syndrome
Pheochromocytoma
CAH
Hyperaldosteronism
Hyperthyroidism
Hyperparathyroidism
Increased ICT
Guillain–Barré
syndrome
Coarctation of
aorta
PDA
Corticosteroids
Cyclosporin
Tacrolimus
Erythropoietin
Glucocorticoid-
remediated
aldosteronism
Apparent
mineralocorticoid
excess
Liddle’s syndrome
Gordon’s syndrome
GN: glomerulonephritis; ARF: acute renal failure; CRF: chronic renal failure; HUS: hemolytic-uremic syndrome; HSP: Henoch Schönlein purpura; CAH:
congenital adrenal hyperplasia; ICT: intracranial tension; PDA: patent ductus arteriosus.
B
SystolicBP
115
110
105
100
95
90
85
80
75
70
65
0 1 2 3 4 5 6
Months
95th
80th
75th
70th
7 8 9 10 11 12
75
70
65
60
55
50
45
DiastolicBP
0 1 2 3 4 5 6
Months
95th
90th
75th
50th
7 8 9 10 11 12
75
70
65
60
55
50
45
DiastolicBP
0 1 2 3 4 5 6
Months
95th
90th
75th
50th
7 8 9 10 11 12
115
110
105
100
95
90
85
80
SystolicBP
75
70
65
0 1 2 3 4 5 6
Months
95th
90th
75th
50th
7 8 9 10 11 12
A
87
68
51
4
101
65
59
4
106
63
63
5
106
63
66
5
106
63
68
6
105
65
70
7
105
66
72
8
105
67
73
9
105
68
74
9
105
68
76
10
105
69
77
10
105
69
78
11
105
69
80
11
90th
percentile
Systolic BP (mmHg)
Diastolic BP (mmHg)
Height (cm)
Weight (Kg)
76
68
54
4
98
65
55
4
101
64
56
4
104
64
58
5
105
65
61
5
106
65
63
6
106
66
66
7
106
66
68
8
106
66
70
9
106
67
72
9
106
67
74
10
105
67
75
10
105
67
77
11
90th
percentile
Systolic BP (mmHg)
Diastolic BP (mmHg)
Height (cm)
Weight (Kg)
Figure 1 Age-specific percentiles for blood pressure in boys (A) and girls (B) from birth to 12 months of age. Reprinted from the
Second Report of Task Force on Blood Pressure Control in Children.3
BP: blood pressure.

Table 6 Physical examination.
General examination Systemic examination
Blood Pallor, edema, rashes, Palpable kidney, renal
pressure pigmentation joint bruit, hepatomegaly,
in all four swelling, rickets (bony signs of heart failure,
limbs, deformity), obesity, short neurologic deficit
peripheral stature, ambiguous
pulsation genitalia/virilization
Table 7 Baseline investigations.
Evaluation for cause Co-morbidity Target organ damage
CBC FBS Heart: ECG, ECHO
Urea/creatinine Lipid profile Brain: MRI
Electrolytes, blood gas Uric acid Eyes: Fundus
Urine routine, C/S Kidneys: Proteinuria
Renal USG
CBC: complete blood count; USG: ultrasonography; FBS: fasting blood
sugar; ECG: electrocardiogram; ECHO: echocardiography; MRI: mag-
netic resonance imaging; C/S: culture and sensitivity.
damage, or (iii) failure of BP to decline below the 95th per-
centile, despite lifestyle modifications for 6 months.
NonpharmacologicTreatment
This includes lifestyle modification in the form of:
• weight reduction in obese,
• increased physical activity.
At least 30–60 min or more of physical activity every day
that is developmentally appropriate, enjoyable and involv-
ing a variety of activities,8
• dietary changes in the form of salt restriction. Recom-
mendations for daily sodium intake in children range
between 1 and 1.5g.
PharmacologicTreatment
Drug therapy is indicated in patients with (i) acute or chronic
complications of hypertension, including evidence of target
organ damage, (ii) secondary hypertension, (iii) stage 2
hypertension, (iv) stage 1 hypertension that persists despite
6 months of lifestyle modifications, and (v) pre-hypertension
or stage 1 hypertension with co-morbid conditions (diabetes,
chronic kidney disease or dyslipidemia).
Aim ofTreatment
• Reduction of BP to levels <95th percentile.
• Blood pressure <90th percentile when co-morbid condi-
tions or target-organ damage is present.
Angiotensin Converting Enzyme Inhibitors
Angiotensin converting enzyme inhibitors (ACEi) (capto-
pril, enalapril, etc.) directly block the formation of angi-
otensin II (AT-II), and at the same time increase bradykinin
level. The net results are reduced vasoconstriction, reduced
sodium and water retention, and increased vasodilatation
(through bradykinin).
Table 4 Target organ damage due to hypertension.
Brain Heart Kidney Eyes
Hypertensive encephalopathy Left ventricular hypertrophy Albuminuria Papilloedema
Intracerebral bleed Left ventricular failure Chronic kidney disease Hypertensive retinopathy
Table 5 History.
Symptoms of HTN Symptoms of underlying cause F/H Neonatal history
Headache, vomiting, visual
disturbance convulsion,
altered sensorium
Renal: Polyuria, nocturnal eneuresis,
UTI, hematuria, edema
Endocrine: Muscle weakness, sweating,
flushing
Systemic: Joint pain, rash, fever,
weight loss
Drugs: Steroids, CNI, EPO
Hypertension, diabetes,
obesity, renal diseases
Umbilical catheterization, neonatal
asphyxia, episodes of severe
hypotension, history of oligohydraminos
Infants: Irritability, failure
to thrive
HTN: hypertension; UTI: urinary tract infection; CNI: calcineurin inhibitor; EPO: erythropoietin; F/H: family history.

Angiotensin Receptor Blockers
Angiotensin receptor blockers (ARBs) (losartan, irbesartan)
competitively inhibit AT-II receptor and thereby decrease
peripheral vascular resistance (PVR). They have no action
on bradykinin production or metabolism (Figure 2).
Antihypertensive Drugs and their Mechanism
of Action
Blood pressure is a product of the cardiac output (CO) and
PVR.
BP=CO×PVR, CO=Heart rate×Stroke volume.
where, BP: blood pressure; CO: cardiac output; PVR: peri-
pheral vascular resistance
Various antihypertensive drugs (Table 9) decrease the
BP by decreasing either of the CO or of the PVR or both:
• Angiotensin converting enzyme inhibitors, ACEi (captopril,
enalapril, etc.).
• Angiotensin receptor blocker (losartan, irbesartan).
• Calcium channel blocker (CCB) (nifedipine, amlodipine,
etc.).
They inhibit the influx of calcium into arterial smooth
muscle cells and cause dilatation of peripheral arterioles.
Thereby, they decrease BP by decreasing PVR.
• Sympathoplegic drugs:
– Centrally acting adrenergic drugs, e.g., clonidine.
Angiotensinogen
Renin Kallikrein
Kininogen
ACE (Kininase-II)
BradykininAngiotensin-I
↑ BP ↓ BP
Angiotension-II
Vasoconstriction Aldosterone
secretion
Inactive products
↑ PVR ↑ Na+ and H2
O
retension
Vasodilation
↓ PVR
↑ Prostaglandin
synthesis
Figure 2 Renin–angiotensin system.
ACE: angiotensin converting enzyme; PVR: peripheral vascular resistance; BP: blood pressure.
Table 8 Additional diagnostic tests.
Glomerulonephritis Reflux nephropathy Renovascular Endocrine Coarctation of aorta
Serum C3, C4, ASO, MCU, DMSA Doppler renal vessel Plasma and urine cortisol, ECHO, angiography
ANA, dsDNA, Captopril renography urine catecholamine
ANCA MR angiography Thyroid hormones, parathormone
Renal biopsy Digital subtraction Plasma renin activity,
angiography aldosterone level
CT/MR imaging, MIBG scan
ASO: antistreptolysin-O; MCU: micturating cysto-urethrogram; DMSA: dimercaptosuccinic acid; ANA: antinuclear antibody; dsDNA: double-stranded
deoxyribonucleic acid; ANCA: anti-neutrophil cytoplasmic antibody; CT: computerized tomography; MR: magnetic resonance; MIBG: metaiodobenzyl-
guanidine; ECHO: echocardiography.

Clonidine is a centrally acting (presynaptic) α2-agonist.
It prevents neurotransmitter release, decreases sympa-
thetic tone, and thereby decreases BP.
– Drugs acting on peripheral nervous system:
❍
β-blocker (propranolol, atenolol, etc.)
They decrease BP by decreasing the CO through action
on β1-receptor. Labetalol is both α- and β-blocker.
It decreases BP by decreasing both CO and PVR.
❍
α-blocker (prazosin, phentolamine, etc.).
Prazosin is α1-blocker while phentolamine is α1- and
α2-blocker.They decrease the BP by decreasing PVR.
• Vasodilators (hydralazine, sodium nitroprusside, diazox-
ide, minoxidil).
They relax the smooth muscle of arterioles (and/or veins),
decrease PVR and BP.
• Diuretics (loop diuretic, thiazide).
By causing natriuresis, they decrease total blood volume
and CO.
Table 9 Oral antihypertensive agent.7
Agents Dose; frequency Comments
Angiotensin converting enzyme inhibitors, angiotensin receptor blockers
Captopril 0.3–6mg/Kg/day; tid Use cautiously if GFR <30mL/min/1.73m2
; avoid in renal
artery stenosis
Use smaller doses in neonates
Monitor serum potassium, creatinine regularly
Side-effects: Hyperkalemia, impaired renal functions; anemia,
neutropenia, dry cough infrequent
Enalapril 0.1–0.6mg/Kg/day; qd
Lisinopril 0.06–0.6mg/Kg/day; qd
Ramipril 6mg/m2
; qd
Irbesartan 4–5mg/Kg/day
Losartan 0.7–1.4mg/Kg/day; qd
Calcium channel blockers
Amlodipine 0.05–0.5mg/Kg/day; qd–bid Extended release nifedipine must be swallowed whole
Side-effects: Headache, flushing, dizziness, tachycardia;
at higher doses: Lower extremity edema, erythema
Nifedipine (extended release) 0.25–3mg/Kg/day; qd–bid
Isradipine 0.15–0.8mg/Kg/day; tid
Beta-blockers
Atenolol 0.5–2mg/Kg/day; qd–bid Atenolol: Decrease dose by 50% at GFR <50mL/min/1.73m2
;
give on alternate days at GFR <10mL/min/1.73m2
Sleep disturbances with propranolol, metoprolol; hyperlipidemia
Avoid in asthma, heart failure; blunt symptoms of hypoglycemia
Metoprolol 1–6mg/Kg/day; bid
Propranolol 1–4mg/Kg/day; tid
Labetalol 1–4mg/Kg/day; bid–tid
Central α-agonist
Clonidine 5–25mg/Kg/day; tid–qid Abrupt cessation may cause rebound hypertension; sedation
Peripheral α-antagonist
Prazosin 0.05–0.5mg/Kg/day; bid–tid May cause ‘first-dose’ hypotension, syncope
Vasodilators
Hydralazine 1–8mg/Kg/day; qid For hypertension refractory to other drugs
Side-effects: Headache, palpitation, fluid retention, congestive
heart failure; pericardial effusions, hypertrichosis with
minoxidil
Minoxidil 0.1–1mg/Kg/day; qd–bid
Diuretics
Frusemide 0.5–6mg/Kg/day; qd–bid Monitor electrolytes, fluid status periodically
Thiazides: Dyslipidemia, hyperglycemia, hyperuricemia,
hypokalemia, hypomagnesemia
Loop diuretics: Metabolic alkalosis, hypokalemia,
hypercalciuria
*Spironolactone 1–3mg/Kg/day; qd–bid
Metolazone 0.2–0.4mg/Kg/day; qd
Hydrochlorothiazide 1–3mg/Kg/day; qd
*Amiloride 0.4–0.6mg/Kg/day; qd
*Use cautiously with ACEi, angiotensin receptor blockers
GFR: glomerular filtration rate; ACEi: angiotensin converting enzyme inhibitor; qd: once daily; bid: twice daily; tid: thrice daily; qid: four times daily.

Principles ofTreatment (Figure 3)
• Therapy is initiated with one agent.
• Dose is increased until desired BP achieved.
If highest dose is not effective or side-effects, drug from
different group added.
• Drug with longer duration of action is preferred for better
compliance.
Length ofTherapy
The appropriate duration of treatment for a child or adoles-
cent is unknown. Some patients require lifelong therapy;
others may experience improvement or even resolution of
hypertension. For these reasons, if BP is under excellent con-
trol and no organ system damage is present, medications can
be tapered and discontinued under careful observation if the
underlying cause is corrected (i.e., renovascular hypertension,
drug-induced hypertension, adrenal tumors).9
Blood pressure
should be monitored carefully on follow-up, since a signifi-
cant proportion of patients become hypertensive in the future.
Specific Recommendations
Acute Glomerulonephritis
Hypertension is of short duration and occurs due to sodium
and water retention. Therefore, loop diuretics are preferred
and CCB and ACEi can be added if required.
Chronic Glomerulonephritis
Chronic kidney disease stages I–III (glomerular filtration
rate [GFR]>30mL/min/1.73m2
) therapy should be initiated
with ACEi, since these agents also reduce proteinuria and
retard the progression of renal damage.10
Treatment with
ACEi should be avoided in patients with advanced chronic
kidney disease (stages IV–V; GFR <30mL/min/1.73m2
)
because of the risk of hyperkalemia. Therapy in these cases
is initiated with either a CCB or a β-blocker.
Renovascular Disease
Therapy should be initiated with a CCB and/or β-blocker.Addi-
tional agents include prazosin, labetalol, clonidine, hydrala-
zine, and/or minoxidil.Therapy withACEi orARB is avoided
in patients with suspected or confirmed bilateral renovascular
disease, because of the risk of precipitation of renal failure.
Hypertensive Crisis
Acute elevation of BP to level likely to cause end-organ damage:
• Hypertensive emergency: Severe hypertension with imme-
diate and ongoing target organ damage.
• Hypertensive urgency: No target organ damage.
Blood pressure homeostasis is governed by the interaction
of multiple forces involving the cardiovascular system and
kidney, and modulated by neural and humoral mechanisms.
Tissue perfusion in the kidney, brain, and heart is main-
tained over a wide spectrum of BP fluctuations by humoral
and myogenic mechanisms, resulting in the autoregulation
of blood flow in various organs. End-organ damage from
severe hypertension occurs when BP rises above the ranges
of autoregulation.11,12
Hypertensive crisis is predominantly
angiotensin-dependent with high vascular reactivity, elevated
levels of norepinephrine and vasopressin, and decreased
levels of vasodilating hormones such as kininogens, kinins,
and prostacyclins.
Severe hypertension induces changes in the renal arte-
rioles that lead to endothelial damage, platelet and fibrin
deposition, and thromboxane release. This cascades into
vasoconstriction, ischemia, myointimal proliferation, and
decompensation of autoregulatory mechanisms resulting in
hypoperfusion to the heart, kidney, and brain. A microangi-
opathic hemolytic anemia and intravascular coagulation
develop that mimic thrombotic thrombocytopenic purpura.13
This sequence of events leads to proliferative endarteritis
and fibrinoid necrosis of the arterial wall.
Hypertensive crisis can result in hypertensive encepha-
lopathy from the cerebral hyperperfusion, endothelial dys-
function, microvascular injury, and cerebral edema. This in
turn can be manifested as posterior reversible encephalopa-
thy (PRES) in imaging studies (Figure 4).14
Changes are
noted in the posterior cerebral cortex and can be considered
to occur from vasogenic edema.
Start with CCB or
ACEi or β-blocker
Combination therapy (either)
• ACEi + CCB
• ACEi + thiazide diuretic
• β-blocker + CCB
Combine ACEi + CCB + prazosin/β-blocker/thiazide
Additional agents
Clonidine, labetalol, hydralazine, minoxidil
Blood pressure >95th percentile
Blood pressure >95th percentile
Figure 3 Approach to treatment.
CCB: calcium channel blocker; ACEi: angiotensin converting
enzyme inhibitor.

Management of Hypertensive Emergency
Blood pressure reduction is done as follows:
• The difference between the observed and desired (95th
percentile) BP is estimated:
– 25–30% of the desired reduction in the first 3–4h.
– 25–30% in the next 24h.
– Desired level over the next 2 days.
• Agents of choice include short-acting, intravenous (i.v.)
preparations that are titrated to response (sodium nitro-
prusside, labetalol, and nicardipine) (Table 10). Therapy
with enteral antihypertensive drugs should be instituted
within 6–12h of parenteral therapy, and the latter gradu-
ally withdrawn over the next 12–24h.
Intravenous Nicardipine
• Dihydropyridine CCB.
• Reduces PVR.
• It does not have a negative inotropic effect and can be
used in the presence of bronchospasm and in patients with
hepatic and renal failure.
• Its half-life is 10–15min and the onset of action is within
15min.
• Side-effects: Tachycardia and flushing.
Sodium Nitroprusside
• Rapid onset of action and reduces pre-load and after-
load; consequently, it is beneficial in congestive heart
failure induced by hypertensive crisis.
• Initially infused at a rate of 0.3–0.8μg/Kg/min, the dose
may be increased in increments of 0.1–0.2mg/Kg/min,
every 15min, if the desired reduction is not achieved.
Blood pressure is measured at least every 15 min.
• Use of the drug for >24–48h can lead to an accumula-
tion of thiocyanate, especially in the presence of renal
and hepatic insufficiency. Thiocyanate poisoning can
Table 10 Drugs used for hypertensive emergency.
Drugs Class Route Dose Side-effects
Nicardipine Calcium channel blocker i.v. 1–3μg/Kg/min Headache, increased intracranial pressure
Sodium nitroprusside Vasodilator i.v. 0.5–8μg/Kg/min Nausea, muscle twitching, headache, cyanide
toxicity with decreased renal function
Labetalol α- and β-blocker i.v. infusion
Bolus
0.5–3mg/Kg/h
0.2–1mg/Kg/dose
Nausea, bradycardia. Avoid in asthma,
congestive heart failure, hyperkalemia
Hydralazine Vasodilator i.v. 0.1–0.5 mg/Kg/
dose every 4–6h
Tachycardia, palpitation, flushing, headache
Phentolamine α-blocker i.v. 0.1–0.2mg/Kg/dose Used in pheochromocytoma. May cause
orthostatic hypotension, tachycardia
i.v.: intravenous.
A B
Figure 4 Magnetic resonance imaging. (A) Fluid-attenuated inversion recovery and (B) T2-weighted images. Bilateral, relatively sym-
metrical high-intensity areas are depicted in the white and gray matter of the occipital region.

cause methemoglobinemia, metabolic acidosis, altered
mental status and seizures.
Labetalol
• α- and β-sympathetic reduces PVR.
• It has a relatively long half-life (3–5 h), and this should
be taken into account when titrating the dose of the drug.
• It should not be used in patients with bronchospastic dis-
ease or congestive cardiac failure as it has a negative ino-
tropic effect. It should also be used with caution in
children with diabetes.
• Labetalol has the potential to worsen hyperkalemia, and
this has to be considered in children with impaired kid-
ney function.
• This drug can be given as an i.v. bolus, which can be
advantageous when an infusion cannot be started quickly.
Management of Hypertensive Urgency
No target damage but are at risk of progression to hyperten-
sive emergencies if not treated.
Control BP with oral medication gradually over 2–3 days.
Effective oral medications are CCB, clonidine, labeta-
lol and minoxidil (Table 11).
Finally, education, anticipatory guidance, early detection,
accurate diagnosis, and effective therapy may help improve
the long-term outcomes of children and adolescents with
hypertension.
REFERENCES
1. Report of the Task Force on Blood Pressure Control in
Children. National Heart, Lung and Blood Institute.
Pediatrics 1977;59:797–820.
2. National High Blood Pressure Education Program Working
Group on High Blood Pressure in Children and Adolescents.
The fourth report on the diagnosis, evaluation, and treatment
of high blood pressure in children and adolescents. Pediatrics
2004;114(Suppl 2):1–22.
3. Report of the Second Task Force on Blood Pressure Control
in Children 1987. National Heart, Lung and Blood Institute,
Bethesda, Maryland. Pediatrics 1987;79:1–25.
4. Stabouli S, Kotsis V, Toumanidis S, Papamichael C,
Constantopoulos A, Zakopoulos N. White-coat and masked
hypertension in children: association with target-organ damage.
Pediatr Nephrol 2005;20:1151–5.
5. Srivastava RN, Gulati A. Hypertension. In: Pediatric
Nephrology 5th ed. Srivastava RN, Bagga A, eds. New Delhi:
Jaypee Brothers 2011:337–59.
6. Bagga A, Kanitkar M, Ali U, et al. Evaluation and manage-
ment of hypertension. Indian Pediatr 2007;44:103–21.
7. Lurbe E, Alcon JJ, Redon J. Epidemiology and consequences
of childhood hypertension. Comprehen Pediatr Nephrol
2008;41:637–42.
8. Council on Sports Medicine and Fitness and Council on
School Health. Active healthy living: prevention of childhood
obesity through increased physical activity. Pediatrics 2006;
117:1834–42.
9. Gulati S. Childhood hypertension. Ind Pediatr 2006;43:
326–33.
10. Hogg RJ, Furth S, Lemley KV, et al. National Kidney
Foundation’s Kidney Disease Outcomes Quality Initiative clin-
ical practice guidelines for chronic kidney disease in children
and adolescents: evaluation, classification and stratification.
Pediatrics 2003;111:1416–21.
11. Chandar J, Zilleruelo G. Hypertensive crisis in children.
Pediatr Nephrol 2011;26:597–603.
12. Roman RJ. Autoregulation of blood flow. In: Hypertension
Primer: The Essentials of High Blood Pressure 3rd ed.
Izzo JL, Black HR, eds. Council for High Blood Pressure
Research, American Heart Association/Lippincott-Williams &
Wilkins, Philadelphia 2003:114–7.
13. Zhang B, Xing C, Yu X, Sun B, Zhao X, Qian J. Renal
thrombotic microangiopathies induced by severe hypertension.
Hypertens Res 2008;31:479–83.
14. Kwon S, Koo J, Lee S. Clinical spectrum of reversible posterior
encephalopathy syndrome. Pediatr Neurol 2001;24:361–4.
Table 11 Drugs used for hypertensive urgency.
Drugs Class Route Dose Side-effects
Isradipine Calcium channel blocker Oral 0.05–0.1mg/Kg/dose, maximum 5mg/dose Tachycardia, headache
Clonidine Central α-agonist Oral 5–25μg/Kg/day tds Sedation, rebound hypertension
Minoxidil Vasodilator Oral 0.1–2mg/Kg/day bd Hypertricosis, pericardial effusion
Labetalol α- and β-blockers Oral 1–3mg/Kg/day bd Bradycardia

Apollohospitals:http://www.apollohospitals.com/
Twitter:https://twitter.com/HospitalsApollo
Youtube:http://www.youtube.com/apollohospitalsindia
Facebook:http://www.facebook.com/TheApolloHospitals
Slideshare:http://www.slideshare.net/Apollo_Hospitals
Linkedin:http://www.linkedin.com/company/apollo-hospitals
Blog:Blog:http://www.letstalkhealth.in/

Hypertension In Children

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Hypertension In Children

Similar to Hypertension In Children (20)

More from Apollo Hospitals

More from Apollo Hospitals (20)

Recently uploaded

Recently uploaded (20)

Hypertension In Children