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Hypertensive Pediatric
Patient when to intervene
DR ALTAF AHMAD BHAT
ASSISTANT CONSULTANT
PEDIATRIC EMERGENCY
 CASES
 HYPERTENSIVE CRISIS DEFINITION
 BLOOD PRESSURE: SCREENING AND MEASUREMENT
 ETIOLOGY
 CLINICAL FEATURES
 EVALUATION
 MANAGEMENT
Case no1:-as Seizure
 4 year old presented to emergency
 Generalized tonic colonic seizure aborted with iv midazolam
 History easy fatigability , FTT, few episodes of UTI in past , circumcised
 On examination significant pallor
 weight for age less than 10 percentile
 Height for age 25 percentile
 Blood pressure 140/100mmhg
 Labs elevated urea creatinine
 MCU gross Hydronephrosis
 Chronic kidney disease
Case no2 :- headache and Altered
sensorium
 13 year old known case of Myo-moya disease
 Presented with headache and progressed to altered sensorium
 In emergency GCS 13/15, irregular breathing
 Blood pressure 160/110
 Intervention
 secured airway ,
 midazolam infusion fentanyl infusion
 CT showed large intra parenchymal cranial bleed
 Progressed over 24 hours
 Child succumbed to illness
Case no3:- Hypo activity and change in behavior
 12 year old presented in emergency with history of URTI/ amoxcillin
 Followed by change behavior as per mother and increased hypo activity
 Blood pressure more than 99centile for age sex and height
 Heart rate fluctuations in emergency
 Working diagnosis Meninigo-encephalitis
 CSF analysis normal CT brain normal
 Admitted by Genpeds/neurology
 EEG global encephalopathy
 For blood pressure started clonidine
 MRI brain ADEM
 Methyl prednisolone
Case no 4 :-rash pain abdomen hematuria
 5 year old presenting to emergency with rash and pain abdomen from Abha ,
relapse HSP
 Previously healthy
 Recent onset pain abdomen intermittent colicky and joint pain
 Sudden onset rash over lower limbs progressed to buttocks and back
 Child complaining of mild headache and poor appetite
 On examination systemic exam reassuring
 Blood pressure more than 95th centile for age and sex
 Labs
 Urine analysis showing hematuria
 Renal profile mild elevated urea creatinine
 Followed by nephrology
Case no5:-tachypnea cyanosis
 2 week old new born
 Presented with tachypnea,
 Episodes of cyanosis
 Preductable post ductal saturation difference of 10%
 Examination stable except soft systolic murmur at LPSA
 No visible differential cyanosis
 Femoral pulses comparatively low volume than radial pulses
 right limb pressure is elevated than lower limbs
 Working diagnosis co-arctation
Case 4 year old
 Following with nephrology
 Case of bilateral dysplastic kidney
 On multiple hypertensive medication
 Presenting with headache and nausea
 Blood pressure recorded in Er more than 99th centile for age sex and height
 Hydrazaline iv given
Hypertensive crisis
 Normal blood pressure AAP2004/2017
 Elevated blood pressure , stage 1 and stage 2
 An acute episode of severely elevated blood pressure with potential for end-
organ damage, often exceeding the limits known for stage II Hypertension
 Subcategorized as hypertensive urgency, in which there are no signs of end-
organ damage, and hypertensive emergency, in which signs of end-organ
damage are present.
 Potential for rapidly progressing end-organ damage,
 Hypertensive crisis should be promptly identified and concomitantly treated
Brief overview
 Prevalence of hypertensive crisis among those presenting with HTN to range from
16 to 54%
Clinical analysis of hypertension in children admitted to the emergency department.
Pediatr Neonatol. (2010)
 National Health and Nutrition Examination Survey (NHANES) in preadolescent and
adolescent patients, the morbidity of hypertensive crisis was found to be between 1
and 4%
High blood pressure trends in children and adolescents in national surveys,
Circulation. (2007)
 cross-sectional, single-center study performed in Houston, Texas, established the
prevalence of hypertensive crisis among children to be as low as 0.6%
Management of hypertensive emergencies.Arch Dis Childhood.
 Dionne et al compiled available data on neonatal BP and generated a summary
table of BP values, including values for the 95th and 99th percentiles for infants
from 26 to 44 weeks’ postmenstrual age.
ETIOLOGY
 70–85% of hypertension is due to an underlying secondary cause.
 Renal parenchymal diseases, coarctation of the aorta are the most frequent
etiologies
 Newborns renal artery thrombosis/stenosis, congenital renal malformations, and
coarctation of the aorta,
 6 years of age , renal parenchymal disease and renal artery stenosis as secondary
causes of hypertension
 Endocrine pathologies such as pheochromocytoma, paragangliomas, and monogenic
causes of hypertension
 Adolescents nonadherence to prescribed medications,
 Abrupt withdrawal of antihypertensive medications,
 Substance abuse with cocaine and amphetamines,
 Over-the-counter agents containing phenylpropanolamine, pseudoephedrine, and
non-steroidal antiinflammatory drugs
Clinical feature
 Hypertensive urgency, also known as acute severe hypertension :-
non-specific symptoms,
irritability, poor feeding in infants and headache,
Nausea, fatigue, and dizziness in children and adolescents
 Hypertensive emergencies:-
Distinct signs of acute neurological, visual, cardiac, and renal damage
Acute neurological signs are most common
Disruption of the blood–brain barrier,
Insufficient oxygen delivery, edema micro-hemorrhages
 A severe neurological complication of hypertensive crisis in children is posterior
reversible encephalopathy syndrome (PRES),
Clinical features
 Hypertensive emergencies :-
visual changes in the form of acute ischemic optic neuropathy, papilledema,
hemorrhages, and cortical blindness
cardiovascular remodeling in the form of left ventricular hypertrophy ,(CHF),
dyspnea, chest discomfort, and gallop rhythm on auscultation.
 Several case reports have shown that hypertensive crisis in infants and
neonates may paradoxically present with hypotension and cardiogenic shock
 Hypertensive damage to the kidneys
Hematuria, flank pain, and oliguria.
Patients with unilateral renal artery stenosis may develop hyponatremic
hypertensive syndrome (HHS),
Evaluation
 History of a patient:-
Symptoms, past medical history, and perinatal, nutritional, psychosocial, family,
and medication history.
 Measurement of vital signs, including BP
 BP measurements are conducted manually or by automatic means
 Initial evaluation of a patient should focus on assessment of end-organ damage
during hypertensive emergencies
 The systemic examination
Cardiovascular system apex impulse ,heart sound , murmur ,parasternal pulsation
Abdominal evaluation (any bruit indicative renal vascular abnormalities, signs of
congestive hepatomegaly.
Neurological evaluation should encompass the mental status exam, reflexes, vision, tone,
and sensory or motor disturbances.
Ophthalmoscopy
Evaluation :-
 Complete blood count (CBC), serum chemistry, and urinalysis,
 For cardiac examination, ECG, ECHO, CXR have low sensitivity of these tests to detect
cardiopulmonary damage, can detect LVH, CCF
 Investigating renal and adrenal causes includes obtaining serum cortisol, renin, and aldosterone
levels, as well as urine catecholamine levels and proteinuria
 Renal imaging using computed tomography angiography or magnetic resonance angiography
may be used as an investigative tool for evaluation of renal artery stenosis, but lacks sensitivity
for detection of intra-parenchymal stenotic changes
 computerized tomography /magnetic resonance imaging scan of the brain may be required to
evaluate the extent of neurologic involvement, including evaluation for intracranial bleeding and
PRES
 Finally, in cases with a high index of suspicion for drug abuse, urine toxicology should be
conducted.
Office practice
 BP reading is at the stage 1 HTN level and the patient is asymptomatic
provide lifestyle counseling and recheck the BP in 1 to 2 weeks by auscultation
 BP reading is still at the stage 1 level
upper and lower extremity BP should be checked and BP should be rechecked in 3 months .
Nutrition and/or weight management referral should be considered as appropriate
 BP continues to be at the stage 1 HTN level after 3 visits,
ABPM should be ordered (if available),
diagnostic evaluation should be conducted, and treatment should be initiated.
 Subspecialty referral should be considered
 Stage 2 HTN should be repeated within 1 week. Alternatively, the patient could be
referred to subspecialty care within 1 week
MANAGEMENT
 children and adolescents diagnosed with hypertensive crisis, the treatment goal with
non-pharmacologic and pharmacologic therapy should be a reduction in SBP and DBP
to <90th percentile and <130/80 mm Hg in adolescents ≥ 13 years of age
 The rate of BP reduction should be 25% over a period of 6–8 h, which is gradually
reduced to normal over 24–72 h since sudden, drastic reductions in blood pressure can
itself contribute to organ damage secondary to ischemia
 intra-arterial blood pressure monitoring
Drug therapy
 IV agents :-
labetalol, a combined alpha and beta blocker
Although it should be avoided in those with asthma and heart failure.
Esmolol is a rapid-acting beta-1 blocker that is ideal for critically ill patients with multiorgan
failure, hypertensive crisis accompanying repair of congenital heart disease
Nicardipine, another first-line IV agent, is a potent and rapid-acting calcium channel blocker
(CCB) that decreases blood pressure via decreasing peripheral vascular resistance. Given via central
access due to risk for thrombophlebitis with peripheral use
clevidipine is an ultrashort-acting IV CCB with a rapid onset, arteriolar vasodilation rapid
inactivation by tissue and blood esterase but is absolutely contraindicated in patients with egg and
soy allergies.
Drugs
 Sodium nitroprusside
direct arterial and venous smooth muscle relaxant actions
frequently used due to its ease of titration to prevent fluctuations in BP
its short half-life, and therefore, the rapid onset and termination of effects.
Methemoglobinemia as well as cyanide and thiocyanate toxicities.
C/I Head injury
 commonly used vasodilator is hydralazine,
an arterial dilator that is used due to its rapid onset while continuous infusion with IV agents is
prepared.
In hypertensive emergencies, hydralazine decreases systemic venous resistance
causes reflex tachycardia by activation of the RAAS pathway, which can negate its antihypertensive
effects.
Drug induced lupus
Drugs
 Fenoldopam dopamine 1 receptor agonist fenoldopam causes increases in renal
blood flow and urinary flow, in addition to natriuresis. Fenoldopam can be used safely
for hypertensive crisis in patients with concurrent renal dysfunction
develops tolerance after 48 hours
 Enalaprilat is used for high-renin hypertension and is the only angiotensin-converting
enzyme inhibitor available as an IV formulation.
 Alpha adrenergic blockers such as phenoxybenzamine and doxazosin are
specifically used in catecholamine-induced hypertension such as paragangliomas and
pheochromocytoma
 Furosemide is a loop diuretic that causes natriuresis and diuresis and is effective in
children with volume-dependent hypertension, such as with oliguric AKI,
glomerulonephritis, or CHF.
Oral therapy
 Hypertensive urgency post hypertensive emergency period
 Isradipine, the most used oral therapy, is a second-generation dihydropyridine CCB that
antagonizes L-type calcium channels causing vasodilatation
 clonidine is another orally used antihypertensive drug A
Activates alpha 2-adrenergic receptors and decreases central sympathetic tone vasodilation.
Rebound hypertension
 Nifedipine and minoxidil
Minoxidil causes predominant arteriolar dilatation. It has a very potent BP-lowering effect in all forms of
hypertension, even in those that are refractory to other antihypertensives including volume
hypertension in hyper hydrated dialyzed children
Protracted minoxidil use has been associated with hirsutism, severe hypotension, and possible
pericardial effusion due to salt and water retention effects, which often necessitates use of furosemide
diuretic
Common Underlying Conditions
 Aortic coarctation is among the most common secondary cause of hypertensive crisis in
the pediatric population., which includes the use of the beta-blocker esmolol as the drug
of choice for infants and children with aortic coarctation. it has been useful to counteract
paradoxical hypertension emerging after repair of aortic coarctation.
 Although such measures aid in controlling hypertension due to aortic coarctation, the
definitive treatment of coarctation of aorta often involves surgical intervention
 Even after repair can present with masked Htn
Renovascular Hypertension,
 Angiotensin-converting enzyme (ACE) inhibitors, beta blockers, and diuretics.
 Fuid overload from renal parenchymal diseases and AKI may contribute to secondary
hypertensive crisis. Therefore, loop diuretics such as furosemide are the mainstay of
management for both glomerulonephritis and AKI since they counteract the sodium and
water retention associated with progressive glomerular damage
 In furosemide refractory cases, dialysis may help with management of fluid overload.
 IV calcium channel blockers such as nicardipine and clevidipine are potential alternatives for
hypertension management in patients with AKI
 Surgical measures such as revascularization, auto-transplantation, or nephrectomy (especially
in small, poorly functioning kidneys causing hypertension) may be required for refractory
cases
Endocrinologic Neoplasms: Pheochromocytoma and paraganglioma
 Plasma or urine metanephrine assays followed by CT/MRI to identify tumor location.
 Treatment involves threestage process for management of pheochromocytoma and
paragangliomas, with the goal of BP reduction to <50th percentile for age and weight
 The preoperative stage begins 14 days prior to surgical intervention with the initiation of
αblockers, such as phenoxybenzamine or doxazosin at a dose of 0.2 mg/kg/day with addition
of 6–10 g of salt and maintenance fluid to prevent hypotension
 Beta blockers are used 3 days prior to counteracting the tachycardia originating from the
catecholamine surge during intraoperative handling of tumour
 Use of β-blockers without α-blockers can prime to unopposed α-adrenergic stimulation and
exacerbate rise in BP, and thus it is very important to have alpha-adrenergic blockade prior to
initiation of beta blockers
 Ludwig etal advised to add tyrosine hydroxlase inhibitor metyrosine
Liddle syndrome
 Aldosterone-dependent epithelial sodium channel (ENaC) in the collecting ducts.
 Excessive sodium absorption culminating to hypertension, hypokalemia, metabolic
alkalosis, and a low plasma renin and aldosterone.
 The diagnosis is verified by screening for mutations in the genes encoding the β and γ
subunits ENaC.
 The treatment revolves around direct ENaC inhibition with sodium channel blockers
such as amiloride or triamterene and a low sodium diet to counteract altered ENaC
physiology
Congenital Adrenal Hyperplasia
 11β-hydroxylase deficiency and 17-α-hydroxylase deficiency
 11-hydroxylase deficiency prevents hydroxylation of 11-deoxycortisol
surplus of 11-deoxycorticosterone, which causes hypertension and hypokalemia due to
mineralocorticoid effects, in addition to virilization in these infants
 17-α hydroxylase deficiency creates a diversion for flow of pregnenolone and progesterone
toward mineralocorticoid production, excess of which leads to hypertension and hypokalemia
 Supplement glucocorticoids which down regulate ACTH secretion and suppress steroid
synthesis.
 Spironolactone, amiloride, and calcium channel blockers may be added to counteract HTN
 Genital abnormalities in females may necessitate surgery
Thank you

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Hypertensive crisis in children copy copy.pptx

  • 1. Hypertensive Pediatric Patient when to intervene DR ALTAF AHMAD BHAT ASSISTANT CONSULTANT PEDIATRIC EMERGENCY
  • 2.  CASES  HYPERTENSIVE CRISIS DEFINITION  BLOOD PRESSURE: SCREENING AND MEASUREMENT  ETIOLOGY  CLINICAL FEATURES  EVALUATION  MANAGEMENT
  • 3. Case no1:-as Seizure  4 year old presented to emergency  Generalized tonic colonic seizure aborted with iv midazolam  History easy fatigability , FTT, few episodes of UTI in past , circumcised  On examination significant pallor  weight for age less than 10 percentile  Height for age 25 percentile  Blood pressure 140/100mmhg  Labs elevated urea creatinine  MCU gross Hydronephrosis  Chronic kidney disease
  • 4. Case no2 :- headache and Altered sensorium  13 year old known case of Myo-moya disease  Presented with headache and progressed to altered sensorium  In emergency GCS 13/15, irregular breathing  Blood pressure 160/110  Intervention  secured airway ,  midazolam infusion fentanyl infusion  CT showed large intra parenchymal cranial bleed  Progressed over 24 hours  Child succumbed to illness
  • 5. Case no3:- Hypo activity and change in behavior  12 year old presented in emergency with history of URTI/ amoxcillin  Followed by change behavior as per mother and increased hypo activity  Blood pressure more than 99centile for age sex and height  Heart rate fluctuations in emergency  Working diagnosis Meninigo-encephalitis  CSF analysis normal CT brain normal  Admitted by Genpeds/neurology  EEG global encephalopathy  For blood pressure started clonidine  MRI brain ADEM  Methyl prednisolone
  • 6. Case no 4 :-rash pain abdomen hematuria  5 year old presenting to emergency with rash and pain abdomen from Abha , relapse HSP  Previously healthy  Recent onset pain abdomen intermittent colicky and joint pain  Sudden onset rash over lower limbs progressed to buttocks and back  Child complaining of mild headache and poor appetite  On examination systemic exam reassuring  Blood pressure more than 95th centile for age and sex  Labs  Urine analysis showing hematuria  Renal profile mild elevated urea creatinine  Followed by nephrology
  • 7. Case no5:-tachypnea cyanosis  2 week old new born  Presented with tachypnea,  Episodes of cyanosis  Preductable post ductal saturation difference of 10%  Examination stable except soft systolic murmur at LPSA  No visible differential cyanosis  Femoral pulses comparatively low volume than radial pulses  right limb pressure is elevated than lower limbs  Working diagnosis co-arctation
  • 8. Case 4 year old  Following with nephrology  Case of bilateral dysplastic kidney  On multiple hypertensive medication  Presenting with headache and nausea  Blood pressure recorded in Er more than 99th centile for age sex and height  Hydrazaline iv given
  • 9. Hypertensive crisis  Normal blood pressure AAP2004/2017  Elevated blood pressure , stage 1 and stage 2  An acute episode of severely elevated blood pressure with potential for end- organ damage, often exceeding the limits known for stage II Hypertension  Subcategorized as hypertensive urgency, in which there are no signs of end- organ damage, and hypertensive emergency, in which signs of end-organ damage are present.  Potential for rapidly progressing end-organ damage,  Hypertensive crisis should be promptly identified and concomitantly treated
  • 10. Brief overview  Prevalence of hypertensive crisis among those presenting with HTN to range from 16 to 54% Clinical analysis of hypertension in children admitted to the emergency department. Pediatr Neonatol. (2010)  National Health and Nutrition Examination Survey (NHANES) in preadolescent and adolescent patients, the morbidity of hypertensive crisis was found to be between 1 and 4% High blood pressure trends in children and adolescents in national surveys, Circulation. (2007)  cross-sectional, single-center study performed in Houston, Texas, established the prevalence of hypertensive crisis among children to be as low as 0.6% Management of hypertensive emergencies.Arch Dis Childhood.  Dionne et al compiled available data on neonatal BP and generated a summary table of BP values, including values for the 95th and 99th percentiles for infants from 26 to 44 weeks’ postmenstrual age.
  • 11. ETIOLOGY  70–85% of hypertension is due to an underlying secondary cause.  Renal parenchymal diseases, coarctation of the aorta are the most frequent etiologies  Newborns renal artery thrombosis/stenosis, congenital renal malformations, and coarctation of the aorta,  6 years of age , renal parenchymal disease and renal artery stenosis as secondary causes of hypertension  Endocrine pathologies such as pheochromocytoma, paragangliomas, and monogenic causes of hypertension  Adolescents nonadherence to prescribed medications,  Abrupt withdrawal of antihypertensive medications,  Substance abuse with cocaine and amphetamines,  Over-the-counter agents containing phenylpropanolamine, pseudoephedrine, and non-steroidal antiinflammatory drugs
  • 12. Clinical feature  Hypertensive urgency, also known as acute severe hypertension :- non-specific symptoms, irritability, poor feeding in infants and headache, Nausea, fatigue, and dizziness in children and adolescents  Hypertensive emergencies:- Distinct signs of acute neurological, visual, cardiac, and renal damage Acute neurological signs are most common Disruption of the blood–brain barrier, Insufficient oxygen delivery, edema micro-hemorrhages  A severe neurological complication of hypertensive crisis in children is posterior reversible encephalopathy syndrome (PRES),
  • 13. Clinical features  Hypertensive emergencies :- visual changes in the form of acute ischemic optic neuropathy, papilledema, hemorrhages, and cortical blindness cardiovascular remodeling in the form of left ventricular hypertrophy ,(CHF), dyspnea, chest discomfort, and gallop rhythm on auscultation.  Several case reports have shown that hypertensive crisis in infants and neonates may paradoxically present with hypotension and cardiogenic shock  Hypertensive damage to the kidneys Hematuria, flank pain, and oliguria. Patients with unilateral renal artery stenosis may develop hyponatremic hypertensive syndrome (HHS),
  • 14. Evaluation  History of a patient:- Symptoms, past medical history, and perinatal, nutritional, psychosocial, family, and medication history.  Measurement of vital signs, including BP  BP measurements are conducted manually or by automatic means  Initial evaluation of a patient should focus on assessment of end-organ damage during hypertensive emergencies  The systemic examination Cardiovascular system apex impulse ,heart sound , murmur ,parasternal pulsation Abdominal evaluation (any bruit indicative renal vascular abnormalities, signs of congestive hepatomegaly. Neurological evaluation should encompass the mental status exam, reflexes, vision, tone, and sensory or motor disturbances. Ophthalmoscopy
  • 15. Evaluation :-  Complete blood count (CBC), serum chemistry, and urinalysis,  For cardiac examination, ECG, ECHO, CXR have low sensitivity of these tests to detect cardiopulmonary damage, can detect LVH, CCF  Investigating renal and adrenal causes includes obtaining serum cortisol, renin, and aldosterone levels, as well as urine catecholamine levels and proteinuria  Renal imaging using computed tomography angiography or magnetic resonance angiography may be used as an investigative tool for evaluation of renal artery stenosis, but lacks sensitivity for detection of intra-parenchymal stenotic changes  computerized tomography /magnetic resonance imaging scan of the brain may be required to evaluate the extent of neurologic involvement, including evaluation for intracranial bleeding and PRES  Finally, in cases with a high index of suspicion for drug abuse, urine toxicology should be conducted.
  • 16. Office practice  BP reading is at the stage 1 HTN level and the patient is asymptomatic provide lifestyle counseling and recheck the BP in 1 to 2 weeks by auscultation  BP reading is still at the stage 1 level upper and lower extremity BP should be checked and BP should be rechecked in 3 months . Nutrition and/or weight management referral should be considered as appropriate  BP continues to be at the stage 1 HTN level after 3 visits, ABPM should be ordered (if available), diagnostic evaluation should be conducted, and treatment should be initiated.  Subspecialty referral should be considered  Stage 2 HTN should be repeated within 1 week. Alternatively, the patient could be referred to subspecialty care within 1 week
  • 17. MANAGEMENT  children and adolescents diagnosed with hypertensive crisis, the treatment goal with non-pharmacologic and pharmacologic therapy should be a reduction in SBP and DBP to <90th percentile and <130/80 mm Hg in adolescents ≥ 13 years of age  The rate of BP reduction should be 25% over a period of 6–8 h, which is gradually reduced to normal over 24–72 h since sudden, drastic reductions in blood pressure can itself contribute to organ damage secondary to ischemia  intra-arterial blood pressure monitoring
  • 18. Drug therapy  IV agents :- labetalol, a combined alpha and beta blocker Although it should be avoided in those with asthma and heart failure. Esmolol is a rapid-acting beta-1 blocker that is ideal for critically ill patients with multiorgan failure, hypertensive crisis accompanying repair of congenital heart disease Nicardipine, another first-line IV agent, is a potent and rapid-acting calcium channel blocker (CCB) that decreases blood pressure via decreasing peripheral vascular resistance. Given via central access due to risk for thrombophlebitis with peripheral use clevidipine is an ultrashort-acting IV CCB with a rapid onset, arteriolar vasodilation rapid inactivation by tissue and blood esterase but is absolutely contraindicated in patients with egg and soy allergies.
  • 19. Drugs  Sodium nitroprusside direct arterial and venous smooth muscle relaxant actions frequently used due to its ease of titration to prevent fluctuations in BP its short half-life, and therefore, the rapid onset and termination of effects. Methemoglobinemia as well as cyanide and thiocyanate toxicities. C/I Head injury  commonly used vasodilator is hydralazine, an arterial dilator that is used due to its rapid onset while continuous infusion with IV agents is prepared. In hypertensive emergencies, hydralazine decreases systemic venous resistance causes reflex tachycardia by activation of the RAAS pathway, which can negate its antihypertensive effects. Drug induced lupus
  • 20. Drugs  Fenoldopam dopamine 1 receptor agonist fenoldopam causes increases in renal blood flow and urinary flow, in addition to natriuresis. Fenoldopam can be used safely for hypertensive crisis in patients with concurrent renal dysfunction develops tolerance after 48 hours  Enalaprilat is used for high-renin hypertension and is the only angiotensin-converting enzyme inhibitor available as an IV formulation.  Alpha adrenergic blockers such as phenoxybenzamine and doxazosin are specifically used in catecholamine-induced hypertension such as paragangliomas and pheochromocytoma  Furosemide is a loop diuretic that causes natriuresis and diuresis and is effective in children with volume-dependent hypertension, such as with oliguric AKI, glomerulonephritis, or CHF.
  • 21. Oral therapy  Hypertensive urgency post hypertensive emergency period  Isradipine, the most used oral therapy, is a second-generation dihydropyridine CCB that antagonizes L-type calcium channels causing vasodilatation  clonidine is another orally used antihypertensive drug A Activates alpha 2-adrenergic receptors and decreases central sympathetic tone vasodilation. Rebound hypertension  Nifedipine and minoxidil Minoxidil causes predominant arteriolar dilatation. It has a very potent BP-lowering effect in all forms of hypertension, even in those that are refractory to other antihypertensives including volume hypertension in hyper hydrated dialyzed children Protracted minoxidil use has been associated with hirsutism, severe hypotension, and possible pericardial effusion due to salt and water retention effects, which often necessitates use of furosemide diuretic
  • 22. Common Underlying Conditions  Aortic coarctation is among the most common secondary cause of hypertensive crisis in the pediatric population., which includes the use of the beta-blocker esmolol as the drug of choice for infants and children with aortic coarctation. it has been useful to counteract paradoxical hypertension emerging after repair of aortic coarctation.  Although such measures aid in controlling hypertension due to aortic coarctation, the definitive treatment of coarctation of aorta often involves surgical intervention  Even after repair can present with masked Htn
  • 23. Renovascular Hypertension,  Angiotensin-converting enzyme (ACE) inhibitors, beta blockers, and diuretics.  Fuid overload from renal parenchymal diseases and AKI may contribute to secondary hypertensive crisis. Therefore, loop diuretics such as furosemide are the mainstay of management for both glomerulonephritis and AKI since they counteract the sodium and water retention associated with progressive glomerular damage  In furosemide refractory cases, dialysis may help with management of fluid overload.  IV calcium channel blockers such as nicardipine and clevidipine are potential alternatives for hypertension management in patients with AKI  Surgical measures such as revascularization, auto-transplantation, or nephrectomy (especially in small, poorly functioning kidneys causing hypertension) may be required for refractory cases
  • 24. Endocrinologic Neoplasms: Pheochromocytoma and paraganglioma  Plasma or urine metanephrine assays followed by CT/MRI to identify tumor location.  Treatment involves threestage process for management of pheochromocytoma and paragangliomas, with the goal of BP reduction to <50th percentile for age and weight  The preoperative stage begins 14 days prior to surgical intervention with the initiation of αblockers, such as phenoxybenzamine or doxazosin at a dose of 0.2 mg/kg/day with addition of 6–10 g of salt and maintenance fluid to prevent hypotension  Beta blockers are used 3 days prior to counteracting the tachycardia originating from the catecholamine surge during intraoperative handling of tumour  Use of β-blockers without α-blockers can prime to unopposed α-adrenergic stimulation and exacerbate rise in BP, and thus it is very important to have alpha-adrenergic blockade prior to initiation of beta blockers  Ludwig etal advised to add tyrosine hydroxlase inhibitor metyrosine
  • 25. Liddle syndrome  Aldosterone-dependent epithelial sodium channel (ENaC) in the collecting ducts.  Excessive sodium absorption culminating to hypertension, hypokalemia, metabolic alkalosis, and a low plasma renin and aldosterone.  The diagnosis is verified by screening for mutations in the genes encoding the β and γ subunits ENaC.  The treatment revolves around direct ENaC inhibition with sodium channel blockers such as amiloride or triamterene and a low sodium diet to counteract altered ENaC physiology
  • 26. Congenital Adrenal Hyperplasia  11β-hydroxylase deficiency and 17-α-hydroxylase deficiency  11-hydroxylase deficiency prevents hydroxylation of 11-deoxycortisol surplus of 11-deoxycorticosterone, which causes hypertension and hypokalemia due to mineralocorticoid effects, in addition to virilization in these infants  17-α hydroxylase deficiency creates a diversion for flow of pregnenolone and progesterone toward mineralocorticoid production, excess of which leads to hypertension and hypokalemia  Supplement glucocorticoids which down regulate ACTH secretion and suppress steroid synthesis.  Spironolactone, amiloride, and calcium channel blockers may be added to counteract HTN  Genital abnormalities in females may necessitate surgery

Editor's Notes

  1. which principally involves damage to the occipito-parietal white matter and basal ganglia, cerebellum, and brainstem. PRES can have a wide variety of presentation, ranging from minor symptoms such as headache, nausea, to major symptoms, such as altered mentation, seizures, focal neurologic deficit, or blindness
  2. presenting with polyuria, polydipsia, and headaches as well as other neurological symptoms
  3. Contraindications of that drug