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Hypertensive Emergencies in
Children
Moderator: Presenter:
Dr. Hiremath Sagar Dr. Ashwini. B. S
Contents
• Definitions
• Etiology
• Management
• Evaluation
• AAP new updated guidelines
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
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
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
Pathophysiology of hypertensive emergencies. (Kitiyakara C, Guzman NJ. Malignant hypertension
and hypertensive emergencies. J Am Soc Nephrol 1998;9:135.)
CPP= MAP- ICP
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
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
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?
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
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
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
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
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
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
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
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
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
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
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.
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.
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.
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
Approach to hypertensive emergencies in children

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Approach to hypertensive emergencies in children

  • 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
  • 20.
  • 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