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Hypertensive crisis in pediatrics

By Tesfay Haile

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OUTLINEDefinition Classification of hypertensionHypertensive CrisisEpidemiologyRisk factorsPathophysiologyEtiologyClinical presentationsDiagnostic approachTreatmentTreatment algorisms

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Hypertension Systolic or diastolic blood pressure (BP) > 95th

percentile for sex, age, and height

Risk increases with body mass index (BMI).

Full clinical manifestations represent potential life-threatening events.

Definition

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Normotensive

Average SBP and DBP <90th % for age, sex and height

Pre-hypertension

Average SBP or DBP >90th but <95th percentile (OR >120/80)

Hypertension

Average SBP and/or DBP >95th percentile for age, sex and height on 3 separate occasions

Stage 1: 95th-99th percentile + 5 mmHgStage 2: >99th percentile + 5 mm Hg

Classification of hypertension

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Stage 2 hypertension usually causes hypertensive crisis

Hypertensive crisis an acute elevation in BP that can cause rapid end-organ dam-

age.

may occur

• in individuals previously not known to have HTN or• in those with previously diagnosed HTN.

further separated into hypertensive urgency and hypertensive emergency.

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Hypertensive urgency

is a situation where the blood pressure is severely elevated but not associated with end organ damage.

Hypertensive emergency exists when blood pressure reaches levels that

are damaging organs. generally occurs at blood pressure levels

exceeding 99th percentile

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Approximately 30% of children with BMI exceeding the 95th percentile have hypertension.

Acute hypertensive emergencies are relatively infrequent in the pediatric population.

In general, secondary hypertension is more common in infancy and childhood and, as adolescence approaches, there is a higher incidence of primary or essential hypertension.

Epidemiology

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BMI that exceeds the 95th percentilePreexisting hypertensionless effective outpatient systolic blood

pressure control

Risk Factors

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Hypertensive crisis is predominantly associated with the vasoconstrictive action of angiotensin.

Angiotensin II facilitates nor-epinephrine release and inhibits

reuptake, and potentiates vascular responsiveness to nor-

epinephrine.VASOCONSTRICTIO

N

Pathophysiology

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Severe hypertension induces changes in the renal arterioles 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.

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Age group Etiology History

Newborn -Renal artery and venous thrombosis-Coarctation of the aorta-Congenital nephrotic syndrome-Mydriatics-Theophylline overdose-Caffeine overdose

-Umbilical artery catheterization-Prolonged ventilation-Family history of renal disease-Medications

Infancy to 12 years

-Renal parenchymal disease-Renovascular disease-Tumor-Coarctation of the aorta

-Poor feeding-History of UTI-History of low birth weight-Family history of renal disease-Medications

Adolescence

-Essential hypertension-Renal parenchymal disease-Substance abuse-Renovascular disease

-Excessive weight gain-History of UTI-Family history of hypertension and renal disease

Etiology The etiology of hypertensive crisis by age group

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Symptoms of a hypertensive emergency include:

Headache or blurred vision Increasing confusion or level of

consciousness Seizure Increasing chest pain Increasing shortness of breath Swelling or edema (fluid buildup in the

tissues)

Clinical presentations

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After BP has been taken several times, immediately perform a focused physical examination, checking for evidence of neurologic dysfunction and congestive heart failure.

Funduscopy should be performed to assess for hemorrhage, papilledema, or infarcts.

Any discrepancy in upper- and lower-extremity BP measurements should be noted.

Presence of abdominal bruit suggests a renovascular cause of hypertension.

Diagnostic Approaches

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Laboratory Findings•Initial laboratory studies should include:

Complete blood count Electrolytes Blood urea nitrogen Serum creatinine Serum calcium Urinalysis Chest radiography Electrocardiography

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Imaging tests for diagnosis of hypertensive crisis Chest radiography

Intravenous pyelography

Voiding cystourethrography

Cardiac catheterization

Renal ultrasonography

Renal scan

Renal arteriography

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General considerations of treatment

Symptomatic hypertensive emergencies should be treated without delay to avoid further damage to vital organs.

BP should be decreased by no more than 25% in the first 2 hrs

Patient should undergo cardiac and continuous BP monitoring.

Any serious complications must be managed before or as hypertension is being treated (e.g, anticonvulsants should be administered to a seizing patient along with hypertensive medications).

Treatment

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Medication choice for hypertensive emergencies depends on several factors.

Patient’s clinical condition Presumed cause Whether a change occurred in cardiac output or

total peripheral resistance Whether end-organ involvement is present

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Goal of treatment

o The goal is to lower BP promptly but gradually.

A sudden decrease can lead to neurologic complications (e.g, intracranial bleeding).

The aim should be to decrease pressure by ≤ 25% over the first 8 hours, then gradually normalize BP over 26–48 hours.

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Non pharmacologic therapy

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Pharmacologic TreatmentTreatment of hypertensive urgencyo Oral antihypertensive agents are generally sufficient, although

parenteral therapy is sometimes indicated.

o Theories suggest: One-third of total planned BP reduction during the first 6 hours

Another third during next 24–36 hours

Final third during next 24–96 hours or longer

o 4–6 hours of observation should follow administration of antihypertensive in the emergency department to identify untoward effects, such as orthostasis.

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Treatment for Hypertensive Emergency

o Treatment is urgent, because one-third of severely hypertensive children develop neurologic abnormalities.

o Such as Cortical blindness

Infarction of the optic nerve

Hemiplegias

oDrugs are chosen on the basis of: Rapidity of action Ease of use Special situations Convention

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Drugs used in hypertensive urgencyDrug Class Route Dose Adverse effects

Furosemide Diuretic IV/PO 1–2 mg/kg/dose

Electrolyte disturbances

Nifedipine Ca++ channel blocker

Sub-lingual /PO

0.1–0.25 mg/kg/dose

Precipitous drop in blood pressure; tachycardia;headache

Clonidine Central α agonist

PO 0.05–0.3 mg Rebound hypertension; sedation

Minoxidil Vasodilator PO 0.1–2 mg/kg/dose

Pericardial effusion

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Drugs used in hypertensive emergencyDrug Class Route Dose Adverse Effect

Nicardipine Ca++ channel blocker

IV 1–3 mcg/kg/min Headache; increased intracranial pressure

Labetalol α and β blocker

IV in infusion

0.25–1.5 mg/kg/hr 0.2–1 mg/kg/doseMaximum 20mg/dose

Use with caution in hyperkalemia and CHF

Esmolol β blocker IV Bolus 100–500 mcg over 1 min;25–100 mcg/kg/min; can increase to 500 mcg/kg/min

Can cause CHF, bradycardia and brochospasm;contraindicated in cocaine toxicity

Hydralazine Vasodilator IV 0.1–0.5 mg/kg/dose. every 4-6 h

Tachycardia, flushing, Lupus like syndrome

Sodiumnitroprusside

Vasodilator IV 0.5–0.8mcg/kg/min Thiocyanate toxicity with decreased renal function

Enalaprilat ACE inhibitor

IV 0.005–0.01 mg/kg/day

Acute renal failure and hyperkalemia

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Treatment algorisms for hypertensive crisis

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Avoid in neonates and renalfailure

Algorism for the treatment of hypertensive crisisIV drugs

Hypertensive crisis Oral drugs

Hypertensive urgency

Hypertensive emergency

Nicardipine

LabetalolSodium

Nitroprusside

Fenoldopam

Hydralazine

Enalaprilat

Clevidipine

Isradipine /

NifedipineClonidine

Minoxidil

Furosemide

Avoid in hyperkalemia and acuteheart failure

Monitor

thiocy

anate

toxicity

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