Hypertension in Children
Lesson Objectives
By the end of this lesson, learners should be able to:
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Define paediatric hypertension and distinguish between primary and secondary types.
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Identify common causes of secondary hypertension in children.
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Recognize the signs and symptoms of mild, severe, and secondary hypertension.
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Outline the investigations required for diagnosis and evaluation.
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Describe non-pharmacological and pharmacological management.
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Recognize and manage hypertensive crises.
Description
Paediatric hypertension is defined as systolic and/or diastolic blood pressure above the 95th percentile for age and gender on at least three separate occasions. Severe hypertension is considered when blood pressure readings are ≥5 mmHg above the 99th percentile.
Pre-hypertension refers to systolic or diastolic pressures between the 90th and 95th percentile.
Primary (essential) hypertension is diagnosed when no specific cause is identified, while secondary hypertension has a clear underlying cause. More than 90% of secondary hypertension in children is due to chronic kidney disease, renovascular disease, or coarctation of the aorta.
Common Causes of Secondary Hypertension in Children
| Category | Examples / Pathology |
|---|---|
| Renal | Acute/chronic glomerulonephritis, pyelonephritis, congenital anomalies (polycystic or dysplastic kidneys), obstructive uropathies (hydronephrosis), HUS, nephrotoxic drugs, trauma, radiation |
| Renovascular | Renal artery stenosis, polyarteritis, thrombosis, renal vein thrombosis |
| Cardiovascular | Coarctation of the aorta, high stroke volume conditions (PDA, aortic insufficiency, AV fistula, complete heart block — only systolic hypertension) |
| Endocrine | Hyperthyroidism (systolic HTN), pheochromocytoma, neuroblastoma, adrenal dysfunction, Cushing’s syndrome, hyperaldosteronism |
| Neurogenic | Increased intracranial pressure |
| Drugs / Chemicals | Steroids, sympathomimetic drugs (cough medicines), heavy metal poisoning (mercury, lead), CNS stimulants (cocaine) |
Signs and Symptoms
| Severity | Clinical Features |
|---|---|
| Mild hypertension | Usually asymptomatic |
| Severe hypertension | Headache, dizziness, nausea, vomiting, irritability, personality changes, neurological manifestations |
| Secondary hypertension | Signs of primary disease: congestive heart failure, renal dysfunction, stroke |
Investigations
| Routine Laboratory Tests | Significance of Abnormal Results |
|---|---|
| Urinalysis, urine culture, urea, creatinine, uric acid | Renal parenchymal disease |
| Serum electrolytes (e.g., hypokalaemia) | Hyperaldosteronism, adrenogenital syndrome, renin-producing tumours |
| ECG, CXR, ECHO | Cardiac causes, e.g., coarctation of the aorta |
| Specialised Tests | Purpose / Significance |
|---|---|
| IVU, Kidney US, CT scan | Renal parenchymal disease, renovascular disease, tumours (neuroblastoma, Wilms) |
| Plasma renin activity | High-renin hypertension, renovascular disease, renin-producing tumours, some Cushing’s syndrome, some essential hypertension; low-renin hypertension indicates adrenogenital syndrome or primary hyperaldosteronism |
| 24-hour urine for 17-ketosteroids / 17-hydroxycorticosteroids | Cushing’s syndrome, adrenogenital syndrome |
| 24-hour urine for catecholamines / VMA | Pheochromocytoma, neuroblastoma |
| Aldosterone | Hyperaldosteronism, renovascular disease, renin-producing tumours |
| Renal vein plasma renin activity | Unilateral renal parenchymal disease, renovascular hypertension |
| Abdominal aortogram | Renovascular hypertension, abdominal coarctation of aorta, unilateral renal parenchymal disease, pheochromocytoma |
Treatment
Supportive Measures:
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Encourage weight reduction if overweight
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Low salt diet
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Avoid smoking
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Regular exercise and reduce sedentary lifestyle
Whom to Treat:
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Symptomatic or severe hypertension
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Prehypertension with comorbidities (CKD, diabetes)
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Hypertensive children with diabetes or CVD risk factors
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Evidence of target-organ damage (most often LVH)
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Essential hypertension unresponsive to 4–6 months of non-pharmacologic therapy
Pharmacological Therapy:
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Secondary hypertension: Treat underlying cause; drug choice follows cause
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Chronic kidney disease: ACE inhibitors first-line; ARBs if intolerant
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Primary hypertension in adolescents: Low-dose thiazide diuretics first-line
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Diabetic children: ACE inhibitors first-line; ARBs if intolerant
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Diuretics: Cornerstone in essential hypertension; avoid in renal failure
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ACE inhibitors: Contraindicated in obstructive lesions (bilateral renal artery stenosis, aortic stenosis, coarctation)
Stepped-Care Approach:
| Step | Action |
|---|---|
| Step 1 | Initiate small dose of a single antihypertensive (thiazide or adrenergic inhibitor), adjust upwards |
| Step 2 | If inadequate, add or substitute second drug; start small and titrate |
| Step 3 | If BP remains elevated, add third drug (vasodilator) and reconsider secondary causes |
Hypertensive Crisis / Emergency
Definition:
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Severe BP: >180/110 mmHg or rapidly rising BP
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Neurological signs: hypertensive encephalopathy, severe headache, vomiting, irritability, apathy, papilloedema, retinal haemorrhage or exudates
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Congestive heart failure or pulmonary oedema
Management:
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Admit to ICU
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Reduce systolic BP by no more than 25% in first 8 hours, normalize gradually over 24–48 hours
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Control fluid intake: limited to urine output + insensible loss
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Treat seizures if present with IV diazepam 0.2 mg/kg
| Drug | Dose | Comments |
|---|---|---|
| Nifedipine | 0.2–0.5 mg/kg every 4–6 hrs, 12–24 hrs if retard | If conscious |
| Hydralazine | 0.15 mg/kg IV over 20 min, repeat q4–6 hrs | Slow infusion |
| Nitroprusside | 1–3 µg/kg/min IV infusion | Continuous monitoring required |
| Labetalol | 0.2–2 mg/kg/hour IV infusion | Alpha and beta blockade |
| Diazoxide | 3–5 mg/kg IV bolus | Acute lowering of BP |
| Furosemide | 1 mg/kg IV bolus | Initiate diuresis |