This document discusses hypertensive emergencies in children, including definitions, etiology, management, and the updated AAP guidelines. It defines hypertensive urgency as elevated blood pressure without end organ damage, while hypertensive emergency involves acute elevation with end organ damage. Common causes in children include kidney disease, endocrine disorders, and drugs. Management involves stabilizing vital signs, confirming hypertension and end organ damage, evaluating for the underlying cause, and lowering blood pressure gradually using drugs like labetalol, sodium nitroprusside, and nicardipine. The updated AAP guidelines revised blood pressure classifications, recommended ambulatory blood pressure monitoring, and suggested screening investigations based on risk factors.

1. Hypertensive Emergencies in
Children
Moderator: Presenter:
Dr. Hiremath Sagar Dr. Ashwini. B. S

2. Contents
• Definitions
• Etiology
• Management
• Evaluation
• AAP new updated guidelines

3. Definition
Classification Children aged 1-12 y Adolescents ≥13 y
Normotensive <90th centile <120/80mmHg
Elevated BP ≥90th centile to ≤95th
centile
120/<80 to
129/<80mmHg
Stage 1 HTN ≥95th centile < 95th
centile +12mmHg
130/ 80 to 139/
89mmHg
Stage 2 HTN ≥95th centile
+12mmHg
>140/90mmHg

4. Contd..
• Hypertensive Urgency: elevated blood pressure without the presence of end
organ damage, although these patients may still manifest symptoms such as
headache and nausea.
• Hypertensive Emergency: acute elevation of blood pressure with presence of
end organ damage
IJPP Vol.14 No.3 JUL-SEPT 2012

5. Etiology
Renal
PSGN
AKI
Lupus nephritis
Endocrine
Pheochromocytoma
Cushing's
CAH
Rheumatic
SLE
Systemic sclerosis
CVS
Co-arctation of Aorta
Acute aortic dissection
Drugs
cocaine
amphetamines
clonidine withdrawal
MAOI interactions
erythropoietin
cyclosporine
The most common cause of hypertension during childhood is kidney disease.
Renovascular
Renal artery thrombosis
Takayasu Arteritis
Renal artery stenosis

6. Pathophysiology of hypertensive emergencies. (Kitiyakara C, Guzman NJ. Malignant hypertension
and hypertensive emergencies. J Am Soc Nephrol 1998;9:135.)
CPP= MAP- ICP

7. Vitals
Tachycardia
Hypertension
Low SpO2 (Pulm edema)
RS
B/L Basal Crepts (Pulm edema)
CVS
Gallop
CCF
CNS
Altered sensorium  Coma
Seizures
Head ache/ dizziness
Nausea
Vomiting
+/- FND
Eye
Blurring of vision
Papilledema
Retinal hemorrhage
Renal
Cola colored urine
Reduced u/o
Puffiness of face, edema
Clinical Features
PA
Palpable mass
Hepatomegaly

8. Management
ABC- Care
Confirm Hypertension &
Brief history- etiological clue
End organ damage
Hypertensive Urgency Hypertensive Emergency
Drugs to lower BP
no more than 25% within the first 24
hours using conventional oral therapy
Drugs to lower BP
reduced by less than
25% over the first 2 to 8 hours and
gradually the blood pressure should be
normalized over the next 24 to 48 hours
Continuous BP monitoring- preferably arterial
Hemodynamic monitoring in PICU
NO YES
Primary problem
Raised ICP- Rx
Raised ICP

9. Evaluation
History:
• Head ache, vomiting, altered sensorium, seizures, facial palsy, FNDs
• Chest pain, exertional dyspnea, palpitations
• Reduced u/o, cola colored urine, edema
• Prolonged Fever, rash, oral ulcers
• Drug abuse/ Corticosteroids/ Anabolic steroids/ Abrupt clonidine
withdrawal/ erythropoietin/ Cyclosporine
• Past H/O- UAC. F/H/O HTN, Endocrinopathy.
Etiology?
End organ
damage?

10. Examination-GPE
• Vitals- including 4 limb pulse and BP
• Growth failure anemia- CKD, truncal obesity- Cushing
• Head to toe:
• Pallor, flushing, diaphoresis- Pheochromocytoma
• Dysmorphism- Turner, Marfan
• Café au-lait spots- Neurofibromatosis
• Adenoma sebaceum- Tuberous sclerosis
• Malar rash- SLE
• Acanthosis Nigricans- Metabolic syndrome

11. Systemic
• Fundus- Look for papilledema, retinal hemorrhages
• Full neurologic examination- Exaggerated reflexes, plantars, FNDs
• Look for gallop, hepatomegaly, basal crepts, Apical impulse, Apical
heave, Murmur (CCF/ Ventricular hypertrophy)
• Mass- Wilms tumor, Neuroblastoma,
• Palpable kidney- PCKD, Hydronephrosis
• Epigastric/ Flank Bruit- RAS
• Genetalia- Ambiguous (CAH)
• Joint tenderness/ swelling- SLE/ CTDs

12. Investigations- Guided by history and
examination
• Urinalysis (RBC casts, proteinuria)- PSGN, AKI
• Blood urea, Serum creatinine, 24hr urine protein, urine protein creatinine ratio
• CBC and PS (HUS, anemia in CKD)
• CXR and ECG- look for pulm edema and Ventricular hypertrophy
• ECHO: Ventricular hypertrophy, structural abnormalities
• Suspected SLE: C3, ANA profile
• Suspected renal: Renal doppler, USG KUB
• CT/MRI brain: Look for cerebral edema/ Stroke/ SOL
• Urine toxicology: Drug abuse
• Urine catecholamines: Pheochromocytoma

13. Drugs in hypertensive emergencies
Labetalol
1st line IV medication for
Hypertensive emergency
In our set-up
Group
α+β blocker
MOA Reduce both
systolic &Diastolic
BP, HR same or
slightly low
S/E Postural
hypotension
C/I Asthma and
overt CCF
Onset 2.5min,
peak 15min, ½ life
5.5hr
Dose
0.25–3.0mg/kg/hr

14. Sodium Nitroprusside
Group
Vasodilator
MOA
Direct arterial and
venous smooth
muscle dilator
S/E Cyanide toxicity-
monitor levels if >72hrs
or infused with
thiosulphate
Onset & ½ life
Rapid onset short
acting
C/I Renal and hepatic
dysfunction
Dose
0.53–10 mcg/kg/min

15. Hydralazine
Group
Vasodilator
MOA
Arterial vasodilator,
reduce SBP
S/E Lupus like
syndrome in slow
acetylators,Reflex
tachycardia,Na and
H2O
retention,Headache
Onset & ½ life
5-10mins, 4-12hrs
C/I Fluid overload
Dose
0.2–0.6 mg/kg/dose,
4th hourly bolus dose
IM/IV

16. Esmolol Group
Cardio selective β
blocker
MOA
Reduces HR
S/E Bronchospasm,
profound
bradycardia, CCF
Onset & ½ life
Rapid onset ultra
short acting
Well suited for
critically ill
Dose
100–500
mcg/kg/min

17. Nicardipine Group
Calcium Channel
Blocker
MOA reduces
peripheral vascular
resistance
S/E headache,
nausea,
tachycardia and
hypotension, ↑ICP
Onset & ½ life
15mins, 10-15mins
C/I Raised ICP
Dose
0.5 to 1 μg/kg/min
max- 3 μg/kg/min
Can be used in
bronchospasm and
renal dysfunction
Need to be diluted in large
volume

18. Trinitroglycerine
Group
Arterio and venodilator
MOA
Release NO which
causes vascular smooth
muscle relaxation
S/E
Headache,
hypotension,
Abd pain
Route
Oral/sublingual/transder
mal
IV
C/I Concurrent use of
PDE5inhib,
Raised ICP,
pericardial tamponade
Dose
1-5mcg/kg/min up to
10mcg/kg/min

19. Phenoxybenzamine
Group
α-blocker
MOA
Overall reduction in
symp effects
Prior to resection of
pheochromocytoma,
paroxysmal HTN
S/E
Orthostatic
hypotension, reflex
tachycardia
C/I
Hypesensitivity
Dose
0.2 to
0.25mg/kg/dose
OD/BD

21. AAP HTN UPDATE
• New blood pressure charts for boys and girls.
• Blood pressure classification revised-
• Elevated BP for pre hypertension – 90th to 95th centile  90th to 95th centile
• Stage 1 HTN: 95th to 99th +5mmHg  95th to 95th +12mmHg
• Stage 2 HTN: >99th centile +5mmHg  >95th centile +12mmHg
• Stepwise guide lines to manage BP
• Increased stress on ABPM for pediatric HTN diagnosis
• Children >6 y of age were recommended to not routinely require extensive
investigation for secondary causes of HTN if they have a positive family
history of HTN, are overweight or obese, and/or do not have history or
physical examination findings suggestive of a secondary cause of HTN.

22. Contd..
• Monogenic HTN should be suspected in patients with a family history of early-
onset HTN, hypokalemia, suppressed plasma renin, or an elevated Aldosterone
Renin Ratio (ARR).
• Renovascular HTN should be suspected in children with stage 2 HTN, significant
diastolic HTN, discrepant kidney sizes on ultrasound, hypokalemia on screening
investigations, or an epigastric and/or upper abdominal bruit on physical
examination
• Electrocardiogram not recommended for assessing left ventricular hypertrophy.
• Echocardiography strongly recommended to assess for target organ damage at
the time of consideration of pharmacologic treatment of HTN.

23. Contd..
• Doppler renal ultrasonography may be useful in evaluation of renal artery
stenosis in normal weight children and adolescents >8 years of age who will
cooperate with the procedure.
• Indication to initiate treatment
• In hypertensive children and adolescents who have failed lifestyle modifications.
• Those with target organ damage such as left ventricular hypertrophy.
• Symptomatic HTN, or stage 2 hypertension without a clearly modifiable factor (e.g., obesity).
• Target BP: Reduction in systolic BP and diastolic BP to <90th percentile
• Beta blocker should not be used as initial anti- hypertensive. Usual choice of anti-
hypertensive should include ACEi, ARB, long-acting calcium channel blocker, or
thiazide diuretic.

24. References
1. Clinical Practice Guideline for Screening and Management of High Blood Pressure in Children and
Adolescents- AAP 2017
2. Evaluation and management of Hypertension- IP statement 44__17, 2007 volume feb
3. Evaluation and management of pediatric hypertensive crises: hypertensive urgency and hypertensive
emergencies- Nirali H Patel et al. Dovepress journal, open access emergency medicine nov 2012.
4. IJPP article- Hypertensive crisis in children- Vol.14 No.3 JULY SEPT 2012
5. American Academy of Pediatrics Clinical Practice Guidelines for Screening and Management of High Blood
Pressure in Children and Adolescents: What is New?- IP Update VOLUME 56__APRIL 15, 2019