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HYPERTENSION IN CHILDREN. Maria E. de Ferris, MD, MPH, PhD Associate Professor UNC Medical School. HTN in Children. Task Force on Blood Pressure Control in Children 1977 1987 Revised in 1996 and 2004 Epidemiological-based data >70,000 children used to define standards

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    1. HYPERTENSIONIN CHILDREN Maria E. de Ferris, MD, MPH, PhD Associate Professor UNC Medical School

    2. HTN in Children • Task Force on Blood Pressure Control in Children • 1977 • 1987 • Revised in 1996 and 2004 • Epidemiological-based data • >70,000 children used to define standards • Categorized by Gender/Age/Height

    3. Definitions • Normal • <90th percentile • High-normal • 90-95th percentile • Hypertension • >95th percentile on three consecutive measurements • This presumes 5% prevalence of hypertension in pediatric population **Tables in Harriet Lane**

    4. BP Racial Differences • AA children have higher readings than other races but not clinically relevant (in girls their stage of maturation is different) • Not different when controlled for their height and skin folding • AA have  sympathetic tone, dopamine  Hydrolyase, glucose, renin & heart rate •  periph. resistance, insulin & Na intol Daniels J Peds 1996: 125:208; Harshfield AJH 2002 15:525

    5. Genetic/Environmental Factors • Familial prevalence • dietary Na, K, Ca • Unlike adults, children do not respond to dietary changes • Among adolescents, females respond better to  Na diet

    6. Weight and BP • A direct relationship has been found between weight and BP at as early as 5 years of age • This is more prominent at the second decade of life • Between 13-17% of adolescents are obese and in more recent studies up to 30% Mutner2004 JAMA 291(17):2007; Williams 1992 AJPH 82:358

    7. Prevalence of Hypertension • About 25% of the adult population in the US has HTN • In children 90% is secondary HTN • In adults 90% is essential HTN • Direct relationship exists between weight and BP

    8. Accurate Measurement • Use Right arm • Sphygmomanometer device • Oscillometric in < 3yo • Auscultative method with manual sphygmomanometer • Cuff size • Too small = falsely high • Too large = falsely low • Width of cuff = 2/3 shoulderelbow • Inflate cuff 20-30 mm Hg above the point at which the radial pulse disappears. • Korotkoff Sounds • Now use 5th phase for all aged infants/children

    9. CV Effects of HTN • It accelerates Coronary artery disease • Risk factor for CVA, heart and renal failure • Direct correlation of LV measurement and HTN

    10. Ambulatory Blood Pressure Measurement • 24 hr. ABPM is used in many centers for adults and now children BP monitoring • Better than a ‘snap shot’ or single measurement • Detects circadian rhythms • Different in Txp patients “non-dippers”

    11. Etiology of Pediatric HTN • Spurious- inappropriate cuff, apprehension • Renal- renal parenchymal dz, acute GN, renal artery stenosis, renal vein thrombosis, pyelonephritis, HSP, HUS, stones, polycystic kidney dz • Cardiovascular- coarctation of the aorta, PDA, AV fistula • Endocrine- Hyperthyroidism, CAH, Cushing syn, Pheochromocytoma, Conn syndrome

    12. Etiology of Pediatric HTN (2) • CNS- ICP, Guillain-Barre, • Drugs- Sympathomimetics, steroids, cocaine & licorice • Neoplasm- Wilms Tumor, neuroblastoma • Collagen vascular/autoimmune • Immobilization/Traction • Malignant Hyperthermia

    13. Diff Dx. Of HTN: Newborn • Renal Artery Stenosis or Thrombosis • Renal Vein Thrombosis • Congential Anomalies • Coarctation of the Aorta • BPD, PDA less common IVH

    14. Dif. Dx. of HTN: Infancy • Coarctation of the aorta • Renovascular disease • Renal parenchymal disease

    15. Dif. Dx. Of HTN: 1-6 years • Renal Parenchymal disease • Renovascular disease • Coarctation of the Aorta • Endocrine causes (less common) • Essential HTN (less common)

    16. Dif. Dx. of HTN: 6-12 years • Renal Parenchymal disease • Renovascular disease • Coarctation of the Aorta • Endocrine causes (less common) • Essential HTN (less common) • Iatrogenic (less common)

    17. Dif. Dx. of HTN: 12-18 years • Essential HTN • Iatrogenic • Renal Parenchymal disease • Renovascular disease (less common) • Coarctation of the Aorta (less common) • Endocrine causes (less common)

    18. Causes of Pediatric HTN • Neonates • Renal, renal, renal! • Renal artery thrombosis • Renal artery stenosis • Congenital renal malformations • Coarctation of the aorta • BPD • Infants to 10 y.o.a. • Renal, renal, renal! • Renal artery stenosis • Renal parenchymal disease • Coarctation • 11y.o.a to adolescence • Renal parenchymal disease • Primary (essential) hypertension (on the rise!)

    19. Hypertensive Crises • Hypertensive Emergency: • BP greater than 99th percentile with evidence of end organ damage • Encephalopathy, Infarction, Cerebral hemorrhage, Myocardial ischemia • Hypertensive Urgency: • BP greater than 99th percentile without evidence of end organ damage

    20. Evaluation of HTN: History • NB period (UAC, BPD), growth pattern, use of medications (cold, contraceptives) • Urological or renal disorders • Endocrine (sweat, wt. loss, palpitations, fevers, muscle cramps & weakness • Family Hx

    21. Evaluation of HTN: PE • Fundoscopy (papilledema, hemorrhage) • Thyroid exam • Evidence of heart failure (gallop, hepatomegaly, edema), check 4 extremity BP & Femoral pulses • Abdominal exam (masses, bruit) • GU exam (virilization) • Neurologic exam (including visual acuity)

    22. Evaluation of HTN: PE (2) • Neurofibromas, café-au-lait spots, tuberous sclerosis, moon fascies, buffalo hump, hirsutism, rashes • Enlarged kidneys, abdominal masses • Chromosomal abnormalities (Turner, Williams, Von Hippel-Lindau)

    23. Urinalysis (protein, blood) Electrolytes BUN/Cr CBC EKG Renal US Consider: TSH Head CT Echocardiogram Renin level Urine VMA, HVA Urine drug screen Diagnostic Evaluation

    24. Headache Vision changes Altered mental status (lethargy) Vomiting Epistaxis Papilledema Retinal hemorrhages Cranial nerve palsy Paralysis Left Vent. H Heart failure Evidence of End Organ Damage

    25. HTN Evaluation Phase 1 • CBC, UA, Urine C&S (PRN) • SMAC 12, lipid panel • Renal US • Heart Echocardiogram

    26. HTN Evaluation Phase 2 • Renal Scan (with ACE inhibitor?) • Urine cathecolamines • Plasma and urinary steroids

    27. HTN Evaluation Phase 3 • Renal Artery Imaging or renal vein sampling • Caval sampling for cathecolamines • Scan of adrenals

    28. Goals of BP control • Do NOT decrease BP to normal levels because of hypo-perfusion • Aim of treatment should be 25-30% reduction (may need to decrease further if still symptomatic) • The goal is to achieve BP levels bellow the 95th (at the 50th) percentile for age and to prevent long term effects • Lower BP slower in patients with chronic rather than acute hypertension (look at EKG/ECHO)

    29. Management • Rule out hypertension secondary to elevated intracranial pressure before lowering BP • Lowering BP too fast can cause hypotension, poor cerebral perfusion causing permanent neurologic damage including vision loss, myocardial ischemia, renal hypoperfusion and ATN • Non-pharmacological means: diet, exercise

    30. HTN Rx: Diuretics • HCTZ - Decreases morbi/mortality • They do not work well if GFR < 30 ml/min • Most effective in combination w/other agents even at low doses • Caution: DM2, gout & cardiac arrhythmias • Used more for adult care

    31. HTN Rx: -Blockers • Selective -Blockers (prazosin, terazosin) block post-synaptic  receptors, relax vascular smooth muscles and  vascular resistance • Better at bedtime • Side effects:  BP (syncope w/1st dose), exacerbates incontinence

    32. DM Lipid abnormalities Symptomatic benign prostate hypertrophy Non-selective HTN -Blockers (phentolamine and phenoxybenzamine) are used in pheochromocytoma -Blockers are used in:

    33. Direct-Acting Vasodilators • Hydralazine & Minoxidil produce direct arterial vasodilation • Reflex tachycardia & fluid retention • May induce lupus-like syndrome (+ANA) • Nitroprusside for emergencies but check thyocyanide levels in 3 days

    34. Hydralazine • Vasodilator, arteriole • Dose:0.1-0.5 mg/kg/dose IV, may be repeated two times if no response, otherwise q 4-6hrs • Onset:5-20 min • Half life:2-6 hrs • Disadvantages:SLE-like syndrome, reflex tachycardia, flushing, worsens angina • DIAZOXIDE is similar in profile

    35. Clonidine • Centrally acting α2 agonist • Reduces cardiac output and peripheral resistance • Dose: 1-2.5mcg/kg/dose PO q 6 hrs • Onset: rapid (minutes) • Half life: up to 12 hrs • Advantages: Emergency Rx, ease of administration (PO) and can transition to long term therapy • Disadvantages: side effects (sedation, dry mouth, dizziness, postural hypotension), rebound hypertension after abrupt withdrawal in chronic use

    36. Nitroprusside • Vasodilator, venous and arterial • Dose: 0.5-8 mcg/kg/min • Onset: instantaneous • Half life: 10 min, thiocyanate 3-7 days • Advantages: Instantaneous onset and able to be titrated quickly • Disadvantages: Decreases preload and afterload and causes reflex tachycardia, photo degradation (cover in foil), metabolized to cyanide then thiocyanate (renally excreted and can cause nausea, vomiting, hallucinations, metabolic acidosis)

    37. -Blockers • Decrease cardiac contractility, renin release and central sympathetic outflow • Good choice with CAHD, atrial fib, SVT, migraine, hyperthyroidism and pro-op HTN • Shown to  morbi/mortality • Depression, sleep disturbance, impotence and  exercise tolerance (less severe w/ -1 selective blockers

    38. Asthma COPD 2nd and 3rd. degree heart block Sick sinus syndrome Moderate LV dysfunction IDDM Peripheral Vascular Disease -Blockers Should be avoided in:

    39. Labetolol • Combined β and α blocker (approx 10-15% α) • Reduces cardiac output, some peripheral vasodilatation • Dose: 0.2-1mg/kg IV bolus or 0.25-3mg/kg/hr drip • Onset: 5-10 min • Half life: 5 hrs • Advantages: used in renal disease, can be given in frequent boluses, no adverse effect on ICP or hypoxic VQ mismatch. • Disadvantages: not as potent as nicardipine & nitroprusside, not well studied in children, contra-indicated in asthma and decreased left ventricular function.

    40. Ca-Channel Blockers • Inhibit the movement of Ca ions from plasma into the cell through voltage-dependent Ca Channels, leading to vasodilation and low BP • Verapamil and diltiazem  peripheral resistance w/significant inotropic effects, slowing AV conductionCHF in LVH

    41. Ca-Channel Blockers: • Short acting not used in Chronic Rx • Sublingual nifedipine may cause MI • Good choice for elderly, AA & angina pats • Avoid in WPW Syndrome

    42. Nicardipine • Calcium channel blocker • Dose:1-5 mcg/kg/min, bolus 0.03mg/kg • Onset:rapid (1-2 min) • Half life:40 min • Advantages:fairly even drop of BP, hypotension unusual, reversible with Ca++ • Disadvantages:may increase ICP

    43. Nifedipine • Class II Calcium Channel Blocker • Arguably the most studied drug for pediatric hypertension • 1995 moratorium placed on sublingual fast-acting use in adults • Hypotension-related myocardial ischemia • Not FDA approved for hypertension

    44. Nifedipine • Calcium Channel Blocker • Peripheral arteriolar dilation • Dose: 0.25-0.5mg/kg q 4-6 hrs po/SL • Onset: 5-10 min, peak 30-60 min • Half life: 3-4 hrs • Advantages: can improve GFR and renal plasma flow, ease of administration, rapid onset, very effective (even in long-standing or severe hypertension) • Disadvantages: unpredictable drop in blood pressure, reflex tachycardia & cardiac output, metabolized by cytochrome P450 system

    45. ACE-Inhibitors • Inhibit angiotensin converting enzyme (AI to AII does not take place) • Appropriate first line of Rx for DM, heart failure, low ejection Fx and post-MI • Diuretics can enhance action

    46. ACE-Inhibitors • NEVER USE IN PREGNANT WOMEN • Never used if bil. renal artery stenosis • Cough 5-20% (related to bradykinin level) • Caution with renal impairment • May be used in Txp patients

    47. Angiotensin-II Receptor Antagonists • Similar effects as an ACE inhibitor • Less cough as they do not  bradykinin • Some cases of angioneurotic edema reported

    48. HTN Complications • Retinal Involvement • I and II changes (arteriolar narrowing, A-V nicking & copper wiring) = Chronic HTN • III and IV (rupture of vessels. Hgs. And exudates, optic disk edema) = accelerated or malignant HTN. • May resolve w/BP control

    49. Coronary Artery Disease • HTN increases hemodynamics • Regression of LVH improves CHF • HTN leads to CAD due to LVH • Rx of HTN alone does not resolve it

    50. Renal Involvement • HTN is the cause of renal failure in 33% of patients • Renal involvement is more frequent in AA or the elderly