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Hypertension in children
Presented by Dr. Pooja (Jr2)
Moderated by Dr. Rajdeep
Rationale for identification and treatment
• Rationale for identification and treatment
• International Childhood Cardiovascular Cohort (130) Consortium was
initiated to link childhood cardiovascular risk factors to adults disease
• 1) Childhood BP, is strongly predictive of adult BP
• 2) LVH is independent risk factor for cardiovascular events
• 3) Microalbuminuria is a powerful predictor of both renal
insufficiency and cardiovascular morbidity and mortality in adults.
The prevalence of microalbuminuria among children diagnosed with
hypertension is estimated to be 20%.
Indian scenario
• Indian scenario
• The application of international reference to Indian children that
differ in various demographic factors, may not be valid
• Higher diastolic pressures for both sexes than international standard
across all age groups.
• Higher blood pressure values in Indian population are of considerable
public health significance.
• Prevalence:
• Various studies have found prevalence in range between 4.7 and
19.4%
• The combined prevalence increases by nearly five times, to around
30%, in adolescents who are obese
RAAS
Diagnosis
.
• Hypertensive crisis : subdivided into 2 : hypertensive urgency and
hypertensive emergency.
• Hypertensive urgency describes severe hypertension but without any
end organ damage but can be more gradually reduced within few
days to avoid serious sequelae.
• Hypertensive emergency describes severe hypertension with end
organ damage which has to be reduced within minutes to avoid life
threatening complications.
MEASUREMENT
• Quiet room for 3-5 min
• Appropriate bp cuff size
• Bell of stethoscope over the brachial artey
• Kortoff sounds
Done in : Secondary HTN , CKD or structural renal
abnormalities,T1DM and T2DM,Solid-organ
transplant , Obesity , OSAS ,Aortic coarctation
(repaired) , Genetic syndromes associated with
HTN (neurofibromatosis, Turner syndrome,
Williams syndrome, coarctation of the aorta)
Ambulatory BP Monitoring (ABPM)
Screening in a busy OPD
• Based on the 90th percentile BP for age and sex at the 5th percentile
of height.
• Which gives the values in the table a NPV of >99%.
Differentiating Primary and Secondary HT
Secondary HTN
• Prepubertal
• Usually stage 2
• Diastolic / nocturnal
• May be positive
• Symptoms of underlying
disorder
Primary HTN
• Adolescents
• Usually stage 1
• Overweight/obese
• Positive family history
• Usually asymptomatic
ETIOLOGY
• RENAL –
• Chronic glomerulonephritis, Polycystic Kidney Disease
• VUR, Recurrent pyelonephritis, Obstructive kidney disease
• SLE, Renal Tumor, Trauma
• VASCULAR- Coarctation of Thoracic or Abdominal aorta
• Renal Artery Lesion (Stenosis, Thrombosis, Aneurysm)
• Umbilical Artery Catherisation
• Renal vein thrombosis
• Vasculitis
• ENDOCRINE –
• Hyperthyroidism
• Hypercalcemia
• Adrenocorticical Disorders- Aldosterone Secreting Tumours,CAH
• Cushing syndrome
• Pheochromocytoma
• Central Nervous System-
• Intracranial mass, Hemmorrhage
• Drugs
Approach to hypertension
Those with severe htn have and evidence of end organ involvement and
very likely have an underlying etiology.
Evaluation of HTN in Children and Adolesc
• Must begin with:
• - Thorough history (including hx of sleep disorder)
• - Drugs
• - Family history of hypertension, CVD risks, renal and endocrine
disorders
• - Other risk factors like lack of physical activity, unhealthy diet,
smoking and alcohol use
• - Complete review of other systems like headache, vomiting, seizures,
altered mental status
Evaluation of HTN in Children and Adolescent
Physical examination:
• • Calculate BMI
• • BP in both arms and right leg
• • Look for presence of radiofemoral delay
• • Look for presence of abdominal bruit
• • Ambiguous genetalia
• Any symptoms of any end organ damage
• headache, weakness, fatigue, dizziness, stroke-to rule out
cerebrovascular disease
• Any history of blurred vision-rule out retinal disease
• Angina pectoris –coronary artery disease
• Dyspnea –to rule out congestive heart failure
• Any history of epistaxis
• Facial palsy
Symptoms of secondary hypertension
• Endocrine - flushing, sweating, fever, palpitations, pallor, muscle
cramps-indicates catecholamine excess
• Virilization,primary amenorrhoea
• Vascular -Cold extremities ,intermittent claudication
• Renal causes
Dysuria,/polyuria ,nocturia ,hematuria ,edema ,weight loss,failure to
thrive
Chronic renal failure –odema ,growth retardation,fatigue ,polyuria
,features of rickets
Increased BUN and creatinine
Signs to look in hypertension
• BMI - to rule out metabolic syndrome
• Tachycardia - to rule out pheochromocytoma Hyperthyroidism
Neuroblastoma
• R-F delay - coA
• Growth retardation - in chronic renal failure ,chronic kidney disease
• Thyromegaly - seen in hyperthyroid
• virilization ,ambiguous genitalia - to rule out congenital adrenal
hyperplasia
• Rashes - to rule out systemic lupus erythematosis ,vasculitis (Hsp)
Impetigo with acute nephritis
• any genetic conditions - neurofibromatosis ,VHL , Williams syndrome ,Turner syndrome
• on auscultation - bruits heard over great vessels - Arteritis / arteriopathy
• any rub - rule out pericardial effusion secondary to cardiac disease
• palpable kidneys - seen in poly cystic kidney disease ,hydronephrosis ,multicystic
dysplastic kidney
• abdominal mass - in Wilms Tumor ,neuroblastoma ,pheochromocytoma
• epigastric /abdominal bruit - seen in coarctation of abdominal aorta , renal artery
stenosis
• Hepatosplenomegaly - seen in Autosomal recessive poly cystic kidney disease
• evidence of any 7 nerve palsy - to rule out focal neurological deficit
ESSENTIAL HYPERTENSION
• More common in older school age children and adolesents
• Patient are often overweight with strong family history of
hypertension
• Risk factors-diet –salt intake ,sleep problems and
• Obesity, genetic alteration in calcium and sodium transport
RAAS and sympathetic system over activity
Obese children -3 fold risk for htn compared with non obese children
• Identify secondary hypertension
• • Identify target-organ damage (LVH, proteinuria, renal scarring, or
retinopathy)
• • Identify additional cardiovascular risks(obesity/dyslipidemia/DM
Laboratory evaluation of HTN
• Basic:
• Serum chemistries, BUN, Cr, PRA
• CBC
• Urinalysis and Urine culture
• Renal ultrasound with doppler
• Evaluation for comorbidity:
• Fasting Lipid profile
• Fasting glucose
• Drug screen (if hx of drug use)
• Polysomnography (if hx of sleep disorder)
• Evaluation for end-organ damage:
• Echocardiogram
• Retinal exam
Additional Evaluation
• • Renovascular imaging
• -Renal scan
• -Duplex Doppler flow studies
• -MRA, CTA
• -Arteriogram
• • Other labs
• -Plasma and urine metanephrines
• -Plasma and urine steroids
MANAGEMENT
• MANAGEMENT
• • Non pharmacological measures
• • Pharmacological measures
Non Pharmacologic Therapy
• Recommended for all pts with HT
• • Wt reduction in obese pts.
• • Regular exercise
• • Dietary modification
• • Stress reduction
• • Preventing dyslipidemia, avoiding smoking, alchohol, caffeine,
energy drinks
Pharmacologic therapy
• INDICATIONS :
• Symptomatic HTN
• •Stage 2 HTN.
• •Stage 1 HTN without any evidence of end-organ damage and that
persists despite a trial of four to six months of non-pharmacologic
therapy.
• Hypertensive end-organ damage
• •Any stage of HTN or high BP for patients with chronic kidney disease
(CKD).
• Any stage of HTN for patients with DM
Choice of initial drug
• • Underlying cause of HTN
• • Concurrent disorders
• • And the preference and experience of the responsible clinician
• Primary HTN
• • ACE inhibitor or ARB-except for sexually active females.
• • If the target BP goal is not met with the maximum allowable dose of the
initial medication (ACE inhibitor or ARB), add a thiazide diuretic to the drug
regimen.
• For sexually active females -CCB be used as the initial antihypertensive
agent
• Renovascular Disease-CCB be used as the initial antihypertensive agent
• CKD/DM-ACE inhibitors be used as the initial antihypertensive agent ARBs
are a reasonable alternative.
DRUGS
Drug Class Initial dose Max dose Dosing
interval
s
ADR/contraindications Monitoring
Captopril ,
Enalapril
ACE inhibitors Infants :
0.05m/k/dose
Children :
0.5m/k/dose
6mkd OD -QID Cough, C/I in B/L renal
artery stenosis
Olmesartan ARB <35kg : 10mg 20 mg OD Less cough than ACE-
headache,
dizziness,hyperkalemia
Potassium
levels,AKI fetal
toxicity
Chlorthiazide Thiazide
diuretics
10mkd 20mkd Od-BD Dizziness,
Hypokalaemia,cardiac
dysarrythmias,
cholestatic jaundice ,
pancreatitis
Potassium
levels,cardiac
dysarrythmias,
cholestatic
jaundice ,
pancreatitis
Drugs
DRUG Class Initial dose Max dose Dosing
interval
ADR/ c/i Monitoring
Hydrochlorthi
azide
Thiazide
diuretics
1mkd 2mkd OD-BD
Amlodipine CCB 1-5yrs: 0-1mkd
>6yrs: 2.5mkd
0.6mkd
10mg
OD Flushing,
Headache,
peripheral ankle
edema
Nifedepine CCB 0.2-0.5mkd 3mkd OD-BD Unpredicatble and
uncontrolled fall in
BP
Centrally acting drugs used in hypertensive
crisis
Clonidine :
Target BP-AAP 2017 guidelines
• • Below the 90th percentile or <120/80 in adolescents (13 years or
older)
• • CKD -goal of mean arterial BP <50th percentile based on 24-hour
ambulatory blood pressure monitoring (ABPM)
Conclusion
• • Hypertension and obesity in children are increasing in an upward
trend
• • It is imperative that pediatric hypertension is recognized and
treated
• • It is advisable to measure blood pressure at every visit with the
appropriate technique, use the gender, age, and height specific blood
pressure table
• • It is important to encourage healthy lifestyles in all children and
adolescents and help institute lifestyle changes for weight reduction
in overweight children
THANKYOU

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hypertension guidelines.pptx management in ;peadiatrics

  • 1. Hypertension in children Presented by Dr. Pooja (Jr2) Moderated by Dr. Rajdeep
  • 2. Rationale for identification and treatment • Rationale for identification and treatment • International Childhood Cardiovascular Cohort (130) Consortium was initiated to link childhood cardiovascular risk factors to adults disease • 1) Childhood BP, is strongly predictive of adult BP • 2) LVH is independent risk factor for cardiovascular events • 3) Microalbuminuria is a powerful predictor of both renal insufficiency and cardiovascular morbidity and mortality in adults. The prevalence of microalbuminuria among children diagnosed with hypertension is estimated to be 20%.
  • 3. Indian scenario • Indian scenario • The application of international reference to Indian children that differ in various demographic factors, may not be valid • Higher diastolic pressures for both sexes than international standard across all age groups. • Higher blood pressure values in Indian population are of considerable public health significance.
  • 4. • Prevalence: • Various studies have found prevalence in range between 4.7 and 19.4% • The combined prevalence increases by nearly five times, to around 30%, in adolescents who are obese
  • 7. • Hypertensive crisis : subdivided into 2 : hypertensive urgency and hypertensive emergency. • Hypertensive urgency describes severe hypertension but without any end organ damage but can be more gradually reduced within few days to avoid serious sequelae. • Hypertensive emergency describes severe hypertension with end organ damage which has to be reduced within minutes to avoid life threatening complications.
  • 8. MEASUREMENT • Quiet room for 3-5 min • Appropriate bp cuff size • Bell of stethoscope over the brachial artey • Kortoff sounds Done in : Secondary HTN , CKD or structural renal abnormalities,T1DM and T2DM,Solid-organ transplant , Obesity , OSAS ,Aortic coarctation (repaired) , Genetic syndromes associated with HTN (neurofibromatosis, Turner syndrome, Williams syndrome, coarctation of the aorta)
  • 10. Screening in a busy OPD • Based on the 90th percentile BP for age and sex at the 5th percentile of height. • Which gives the values in the table a NPV of >99%.
  • 11.
  • 12. Differentiating Primary and Secondary HT Secondary HTN • Prepubertal • Usually stage 2 • Diastolic / nocturnal • May be positive • Symptoms of underlying disorder Primary HTN • Adolescents • Usually stage 1 • Overweight/obese • Positive family history • Usually asymptomatic
  • 13. ETIOLOGY • RENAL – • Chronic glomerulonephritis, Polycystic Kidney Disease • VUR, Recurrent pyelonephritis, Obstructive kidney disease • SLE, Renal Tumor, Trauma • VASCULAR- Coarctation of Thoracic or Abdominal aorta • Renal Artery Lesion (Stenosis, Thrombosis, Aneurysm) • Umbilical Artery Catherisation • Renal vein thrombosis • Vasculitis
  • 14. • ENDOCRINE – • Hyperthyroidism • Hypercalcemia • Adrenocorticical Disorders- Aldosterone Secreting Tumours,CAH • Cushing syndrome • Pheochromocytoma • Central Nervous System- • Intracranial mass, Hemmorrhage • Drugs
  • 15. Approach to hypertension Those with severe htn have and evidence of end organ involvement and very likely have an underlying etiology.
  • 16. Evaluation of HTN in Children and Adolesc • Must begin with: • - Thorough history (including hx of sleep disorder) • - Drugs • - Family history of hypertension, CVD risks, renal and endocrine disorders • - Other risk factors like lack of physical activity, unhealthy diet, smoking and alcohol use • - Complete review of other systems like headache, vomiting, seizures, altered mental status
  • 17. Evaluation of HTN in Children and Adolescent Physical examination: • • Calculate BMI • • BP in both arms and right leg • • Look for presence of radiofemoral delay • • Look for presence of abdominal bruit • • Ambiguous genetalia
  • 18. • Any symptoms of any end organ damage • headache, weakness, fatigue, dizziness, stroke-to rule out cerebrovascular disease • Any history of blurred vision-rule out retinal disease • Angina pectoris –coronary artery disease • Dyspnea –to rule out congestive heart failure • Any history of epistaxis • Facial palsy
  • 19. Symptoms of secondary hypertension • Endocrine - flushing, sweating, fever, palpitations, pallor, muscle cramps-indicates catecholamine excess • Virilization,primary amenorrhoea • Vascular -Cold extremities ,intermittent claudication • Renal causes Dysuria,/polyuria ,nocturia ,hematuria ,edema ,weight loss,failure to thrive Chronic renal failure –odema ,growth retardation,fatigue ,polyuria ,features of rickets Increased BUN and creatinine
  • 20. Signs to look in hypertension • BMI - to rule out metabolic syndrome • Tachycardia - to rule out pheochromocytoma Hyperthyroidism Neuroblastoma • R-F delay - coA • Growth retardation - in chronic renal failure ,chronic kidney disease • Thyromegaly - seen in hyperthyroid • virilization ,ambiguous genitalia - to rule out congenital adrenal hyperplasia • Rashes - to rule out systemic lupus erythematosis ,vasculitis (Hsp) Impetigo with acute nephritis
  • 21. • any genetic conditions - neurofibromatosis ,VHL , Williams syndrome ,Turner syndrome • on auscultation - bruits heard over great vessels - Arteritis / arteriopathy • any rub - rule out pericardial effusion secondary to cardiac disease • palpable kidneys - seen in poly cystic kidney disease ,hydronephrosis ,multicystic dysplastic kidney • abdominal mass - in Wilms Tumor ,neuroblastoma ,pheochromocytoma • epigastric /abdominal bruit - seen in coarctation of abdominal aorta , renal artery stenosis • Hepatosplenomegaly - seen in Autosomal recessive poly cystic kidney disease • evidence of any 7 nerve palsy - to rule out focal neurological deficit
  • 22. ESSENTIAL HYPERTENSION • More common in older school age children and adolesents • Patient are often overweight with strong family history of hypertension • Risk factors-diet –salt intake ,sleep problems and • Obesity, genetic alteration in calcium and sodium transport RAAS and sympathetic system over activity Obese children -3 fold risk for htn compared with non obese children
  • 23. • Identify secondary hypertension • • Identify target-organ damage (LVH, proteinuria, renal scarring, or retinopathy) • • Identify additional cardiovascular risks(obesity/dyslipidemia/DM
  • 24. Laboratory evaluation of HTN • Basic: • Serum chemistries, BUN, Cr, PRA • CBC • Urinalysis and Urine culture • Renal ultrasound with doppler • Evaluation for comorbidity: • Fasting Lipid profile • Fasting glucose • Drug screen (if hx of drug use) • Polysomnography (if hx of sleep disorder) • Evaluation for end-organ damage: • Echocardiogram • Retinal exam
  • 25. Additional Evaluation • • Renovascular imaging • -Renal scan • -Duplex Doppler flow studies • -MRA, CTA • -Arteriogram • • Other labs • -Plasma and urine metanephrines • -Plasma and urine steroids
  • 26. MANAGEMENT • MANAGEMENT • • Non pharmacological measures • • Pharmacological measures
  • 27. Non Pharmacologic Therapy • Recommended for all pts with HT • • Wt reduction in obese pts. • • Regular exercise • • Dietary modification • • Stress reduction • • Preventing dyslipidemia, avoiding smoking, alchohol, caffeine, energy drinks
  • 28. Pharmacologic therapy • INDICATIONS : • Symptomatic HTN • •Stage 2 HTN. • •Stage 1 HTN without any evidence of end-organ damage and that persists despite a trial of four to six months of non-pharmacologic therapy. • Hypertensive end-organ damage • •Any stage of HTN or high BP for patients with chronic kidney disease (CKD). • Any stage of HTN for patients with DM
  • 29. Choice of initial drug • • Underlying cause of HTN • • Concurrent disorders • • And the preference and experience of the responsible clinician
  • 30. • Primary HTN • • ACE inhibitor or ARB-except for sexually active females. • • If the target BP goal is not met with the maximum allowable dose of the initial medication (ACE inhibitor or ARB), add a thiazide diuretic to the drug regimen. • For sexually active females -CCB be used as the initial antihypertensive agent • Renovascular Disease-CCB be used as the initial antihypertensive agent • CKD/DM-ACE inhibitors be used as the initial antihypertensive agent ARBs are a reasonable alternative.
  • 31. DRUGS Drug Class Initial dose Max dose Dosing interval s ADR/contraindications Monitoring Captopril , Enalapril ACE inhibitors Infants : 0.05m/k/dose Children : 0.5m/k/dose 6mkd OD -QID Cough, C/I in B/L renal artery stenosis Olmesartan ARB <35kg : 10mg 20 mg OD Less cough than ACE- headache, dizziness,hyperkalemia Potassium levels,AKI fetal toxicity Chlorthiazide Thiazide diuretics 10mkd 20mkd Od-BD Dizziness, Hypokalaemia,cardiac dysarrythmias, cholestatic jaundice , pancreatitis Potassium levels,cardiac dysarrythmias, cholestatic jaundice , pancreatitis
  • 32. Drugs DRUG Class Initial dose Max dose Dosing interval ADR/ c/i Monitoring Hydrochlorthi azide Thiazide diuretics 1mkd 2mkd OD-BD Amlodipine CCB 1-5yrs: 0-1mkd >6yrs: 2.5mkd 0.6mkd 10mg OD Flushing, Headache, peripheral ankle edema Nifedepine CCB 0.2-0.5mkd 3mkd OD-BD Unpredicatble and uncontrolled fall in BP
  • 33. Centrally acting drugs used in hypertensive crisis Clonidine :
  • 34.
  • 35. Target BP-AAP 2017 guidelines • • Below the 90th percentile or <120/80 in adolescents (13 years or older) • • CKD -goal of mean arterial BP <50th percentile based on 24-hour ambulatory blood pressure monitoring (ABPM)
  • 36. Conclusion • • Hypertension and obesity in children are increasing in an upward trend • • It is imperative that pediatric hypertension is recognized and treated • • It is advisable to measure blood pressure at every visit with the appropriate technique, use the gender, age, and height specific blood pressure table • • It is important to encourage healthy lifestyles in all children and adolescents and help institute lifestyle changes for weight reduction in overweight children