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This document discusses the management of hypertensive emergencies in children. It defines hypertension and hypertensive crises, and outlines the urgency vs emergency distinction. It describes the prevalence of hypertension in children, potential causes, pathophysiology, and complications involving end organ damage if left untreated. Initial diagnostic approach involves assessing for end organ injury and its severity, with the immediate goal of therapy being to decrease blood pressure quickly in emergency situations.
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- 1. Management of Hypertensive Emergencies ModeratorDr Sunil K Rao Speaker Dr Sunil K Singh
- 2. INTRODUCTION • Hypertension is a silent killer. It can be a primary disease (essential hypertension) or due to some underlying disease process (secondary hypertension) (more common in pediatric population)
- 3. DEFINITIONS Normotensive • Average SBP and DBP <90th % for age, sex and height Pre-hypertension • Average SBP or DBP >90th but <95th percentile (OR >120/80 but <95th percentile ) Hypertension • Average SBP and/or DBP >95th percentile for age, sex and height on 3 separate occasions ▫ Stage 1: 95th-99th percentile + 5 mmHg ▫ Stage 2: >99th percentile + 5 mm Hg
- 4. White-coat hypertension • A patient with BP levels above the 95th percentile in a physician’s office or clinic who is normotensive outside a clinical setting. (Ambulatory BP monitoring is usually required to make this diagnosis).
- 5. Urgency vs. Emergency • Urgency – severely elevated BP with no current evidence of secondary organ damage, although if left untreated, target organ injury may result imminently → Decrease BP Soon • Emergency – severely elevated BP with evidence of target organ injury → Decrease BP Immediately • Target organs – CNS, heart, kidney, eye Constantine and Linakis, Pediatric Emergency Care, 2005
- 6. Prevalence • Systemic hypertension is an important condition in childhood, with estimated population prevalence of 1-2% in the developed countries. • Data is lacking from India; small surveys in school children suggest a prevalence ranging from 2-5%.
- 7. PATHOPHYSIOLOGY • Hypertensive Emergency ▫ Failure of normal autoregulatory function ▫ Leads to a sharp increase in systemic vascular resistance ▫ Endovascular injury with arteriole necrosis ▫ Ischemia, platelet deposition and release of vasoactive substances ▫ Further loss of autoregulatory mechanism ▫ Exposes organs to increased pressure
- 8. MECHANISM OF HYPERTENSIVE CRISIS Sudden severe increase in blood pressure Endothelial injury/dysfunction Pressure natriuresis Increase vasoconstrictors and decrease in vasoldilators Activation of procoagulation cascade and inhibition of fibronolytic mechanism Release of inflammatory markers and reactive oxygen species Volume depletion and positive feedback to reninangiotensin system Fibroinoid necrosis and myo-proliferation Further increase in blood pressure
- 10. CAUSES OF PERSISTENT HYPERTENSION • Renal parenchymal disease: Chronic glomerulonephritis, reflux nephropathy, obstructive uropathy, polycystic kidney disease, renal dysplasia • Renovascular hypertension: Idiopathic aortoarteritis (Takayasu disease), renal artery stenosis, renal artery Thrombosis • Cardiovascular disease: Coarctation of aorta • Primary (essential) hypertension • Endocrine: Pheochromocytoma, Cushing syndrome, congenital adrenal hyperplasia, primary hyperaldosteronism, Liddle’s syndrome, syndrome of apparent mineralocorticoid excess, glucocorticoid remediable aldosteronism, neuroblastoma • Renal tumors: Wilms’ tumor, nephroblastoma
- 11. Transient hypertension • acute glomerulonephritis, • acute intermittent porphyria, • Guillain Barre syndrome, • raised intracranial pressure, • corticosteroid • anxiety • hyperthyroidism.
- 12. Immediate concern • Is it hypertension ? { definition } • Is it hypertensive crisis ? { classify } • End organ damage ? { asses the severity } • Immediate goal of the Rx ? { target of therapy } Investigations ? { underlying cause } APPROACH
- 13. 7/19/07 Blood Pressure Measurement • Stephen Hales 1733 • Hollow glass tube in neck artery of horse • Blood rose 9 feet in glass tube Medicine, an Illustrated History 1987
- 14. Children >3 years old who are seen in a medical setting should have their BP measured. • Conditions Under Which Children • <3 Years Old Should Have Blood • Pressure Measured • ■ History of prematurity, very low • birthweight, or other neonatal complication • requiring intensive care • ■ Congenital heart disease (repaired or • nonrepaired) • ■ Recurrent urinary tract infections, • hematuria, or proteinuria • ■ Known renal disease or urologic • malformations • ■ Family history of congenital renal disease • ■ Solid organ transplant • ■ Malignancy or bone marrow transplant • ■ Treatment with drugs known to raise BP • ■ Other systemic illnesses associated with • hypertension (neurofibromatosis, tuberous • sclerosis, etc.) • ■ Evidence of elevated intracranial pressure
- 15. Measuring accurate BP’s • Cuff too small → high reading • Cuff too big → OK reading or no reading (usually not falsely low) • Lower extremities - Normally, BP is 10 to 20 mmHg higher in the legs than the arms ▫ Prefer arm if at all possible ▫ Right arm for comparison with standards
- 16. Cuff Size • Bladder width > 40% of mid-arm circumference. • Bladder length 80-100% of arm circumference. A. Ideal arm circumference B. Range of acceptable arm circumferences C. Bladder length D. Midline of bladder E. Bladder width F. Cuff width
- 17. 7/19/07 Recommended Dimensions for BP Cuff Bladders Age range Width (cm) Length (cm) Max. AC (cm) Newborn 4 8 10 Infant 6 12 15 Child 9 18 22 Small adult 10 24 26 Adult 13 30 34 Large adult 16 38 44 Thigh 20 42 52
- 18. 7/19/07
- 19. Oscillometric Devices Measure Mean Arterial Pressure (MAP) and calculates SBP and DBP ▫ The algorithms used are proprietary and NOT standardized ▫ Results can vary widely and they do not always closely match BP values obtained by auscultation ▫ These machines must be calibrated regularly
- 20. Manual vs. Automatic • Manual is the gold standard • Oscillometric measurements preferred in infants and ICU settings ONLY • All high readings should be confirmed with a manual
- 21. Sphygmomanometry • Rested for 5-10 minutes. • Sitting or supine position, the latter preferred for younger children. • The right arm is used for consistency and for comparison with standard tables; the cubital fossa should be at heartlevel and the observer's eye at the level of the mercury column. • Correct cuff size is crucial since a small cuff might overestimate the readings and vice versa .
- 22. Sphygmomanometry (Contd…) • With the stethoscope on the brachial artery, the mercury column is lowered slowly (2 mm per second). Systolic blood pressure is the point whenKorotkoff sounds are first heard (K1) and disappearance of sounds (K5) is the diastolic pressure. • If Korotkoff sounds persist, the measurement is repeated with less pressure on the stethoscope head. If the sounds persist at low intensity, then K4 (muffling of sounds) is recorded as the diastolic pressure. Blood pressure recordings should be expressed to the nearest 2 mm Hg. A high reading should be confirmed after the child has rested for 5 minutes and the average of 2-3 readings is taken as the value for that occasion.
- 23. POINTS TO BE REMEMBERED • BP should be recorded in all 4 limbs. • Cuff should not be applied two tight (low BP recording) or too loose (high BP recording). • BP monitoring subsequently should be taken in the same limb and position. • Normally the BP is 10-20mm Hg higher in lower limbs compared to the upper limbs.
- 25. How to use the tables • Need: ▫ Age, gender, height percentile ▫ BP charts ▫ Patient age = 10yrs, height = 140cms, sex = male. ▫ Age = 10yrs, height = 140cms, sex = male. ▫ Height percentile = 50th ▫ Blood pressure = 140/95
- 29. Immediate Concern: End organ damage? { assess the severity • the presentation depends on ▫ underlying medical conditions ▫ baseline systemic BP ▫ rate of rise and degree of BP elevation ▫ effects on end organs • common Sequelae of End-Organ Damage ▫ Encephalopathy ▫ Acute left ventricular failure ▫ Myocardial infarction & Unstable angina ▫ Pulmonary edema ▫ Stroke & Head trauma ▫ Life-threatening bleeding ▫ Aortic dissection
- 30. Acute complications (hypertensive crises) • . The occurrence of these complications is related to the rate of rise and duration of hypertension, rather than absolute blood pressure values. • Hypertensive encephalopathy is characterized by lethargy, dullness, headache, seizures and visual disturbances including blindness. • Cerebral infarction, hemorrhage and facial nerve palsy may occur. Neuroimaging shows features of white matter degeneration in the parieto-occipital area (posterior leukoencephalopathy), which are reversible with treatment. • Acute left ventricular failure is another life-threatening complication of severe hypertension.
- 31. Chronic complications (target organ damage) • Sustained hypertension results in changes in eyes (hypertensive retinopathy) • heart (increased left ventricular mass, diastolic dysfunction), • kidneys (albuminuria) • brain and blood vessels (increased initimal and medial thickness). • There is evidence that these changes are common, even in patients with long standing stage 1 hypertension.
- 32. Grade 1 Generalised arteriolar constriction - seen as `silver wiring` and Vascular tortuosities. Grade 2 + irregularly located, tight constrictions - `AV nicking` or `AV Nipping` Grade 3 + with cotton wool spots and flame-haemorrhages Grade 4 + with swelling of the optic disk (papillodema) only 8.6% had evidence of retinopathy diagnosed with an ophthalmoscope
- 34. Posterior Leukoencephalopathy T1 weighted images – normal appearing T2 weighted images – occipital hyperintensity
- 35. Initial Diagnostic Algorithm in the Evaluation of Hypertension Documented hypertension Gradient between upper and lower blood pressures Coarctation or aorta Abnormal urinalysis NoYes Predominant red blood cellsPredominant white blood cells Essential hypertensionRenovascular lesionendocrine NoYes Reflux nephritis Recurrent urinary tract infections Renal anomaly (and infection) Postinfectious nephritis Lupus nephritis Henoch schonlein purpura Nephrocalcoinosis Nephrolithiasis Other nephritis Renal vein thrombosis Thromboembolism Tumor
- 36. APPROACH TO A PATIENT HISTORY • Present and Past History ▫ Neonatal - prematurity, BPD, umbilical artery catheterization . ▫ Cardiovascular- History of CoA or surgery for it, history of palpitation , Headache, excessive sweating (excessive catecholamine levels). ▫ Renal- History of obstructive uropathy, UTI, radiation, trauma or surgery to kidney area. ▫ Endocrine- weakness, fiushing, weight loss, muscle cramps (hyperaldosteronism). Constipation ▫ Medication/Drugs - Corticosteroids, amphetamines, cold medications, antiasthamatic drugs, OCP, cyclosporine/tacrolimus, cocaine.NSAIDs Stimulant medications (eg, dexedrine, methylphenidate) Beta-adrenergic agonists (eg, theophylline), Erythropoietin, Tricyclic antidepressants, Recent abrupt discontinuation of antihypertensives
- 37. ▫ Habits - Smoking/drinking/ illicit drugs (eg, tobacco, ethanol, amphetamines, cocaine, phencyclidine, ▫ Symptoms of obstructive sleep apnea (ie, difficulty falling asleep, • Multiple nighttime awakenings, snoring, daytime somnolence • Diet (caffeine, salt intake) • Family History ▫ Essential hypertension , atherosclerotic heart disease, stroke. ▫ Familial or hereditary renal disease (PKD etc.)
- 38. PHYSICAL EXAMINATION • Accurate measurement of BP in all limbs. • Complete physical examination. ▫ Delayed growth/short stature (renal disease) ▫ Bounding peripheral pulses (PDA, AR) ▫ Weak or absent femoral pulses or BP differential between arms and legs (CoA) ▫ Abdominal bruits (Renal Vascular Disease) ▫ Abdominal mass(Wilms tumor, neuroblastoma, pheochromocytoma) ▫ Palpable kidneys (Polycystic kidney disease, hydronephrosis, multicystic dysplastic kidney, mass)
- 39. ▫ Skin lesions (café au lait spots, neurofibromas, adenoma sebaceum, striae, hirsutism, butterfly rash, Acanthrosis nigricans palpable purpura) ▫ Tenderness over kidney (renal infection). ▫ Ambiguous genitalia (CAH). ▫ Moon facies, truncal obesity, buffalo hump ▫ Thyromegaly, Proptosis, hyperdynamic circulation (Hyperthyroidism ▫ Signs of meningeal irritation, CNS Infections. ▫ Widely spaced nipples, Webbed neck (turner’s)
- 41. Evaluation for cause • Hemogram • Blood urea, creatinine, electrolytes • Fasting lipids, glucose, uric acid • Urinalysis, culture • 24-hr urinary protein or spot protein to creatinine ratio • Chest X-ray • Renal ultrasonography
- 42. Screen for target organ damage • Retinal fundus examination • Urine: microalbumin, spot protein to creatinine ratio • Chest X-ray, ECG, echocardiography • CT/MRI brain
- 43. Additional Diagnostic Tests for Sustained Hypertension Condition Diagnostic investigations Glomerulonephritis Complement (C3), ANA, ANCA, anti-dsDNA, renal biopsy Reflux nephropathy Micturating cystourethrogram, DMSA scintigraphy Renovascular hypertension Doppler flow studies, captopril renography Angiography (MR, spiral CT, digital subtraction or conventional) Renal vein renin activity Coarctation of aorta Echocardiography, angiography Endocrine causes Thyroxine, thyroid stimulating hormone Plasma renin activity, aldosterone Plasma and urinary cortisol Plasma and urine catecholamines; MIBG scan, CT/MR imaging ANA antinuclear antibody, ANCA antineutrophil cytoplasmic antibody, anti-dsDNA, anti-double stranded DNA antibody, DMSA demercaptosuccinic acid, MIBG meta-iodobenzyl guanidine
- 45. Classification of Hypertension in Children and Adolescents: Therapy Recommendations All patients to receive Therapeutic Life-style Changes (TLC) Pharmacologic Therapy Normal None Prehypertension Do not initiate therapy unless there are compelling indications such as chronic kidney disease (CKD), diabetes mellitus, heart failure, left ventricular hypertrophy (LVH). Stage 1 hypertension Initiate therapy based on indications for antihypertensive drug therapy or if there are compelling indications as above. Stage 2 hypertension Initiate therapy.
- 46. Non pharmacologic interventions- Weight reduction. Low salt intake*. Regular aerobic exercise. Dietary Approaches- fresh vegetables, fruits, and low-fat dairy Avoidance of smoking. Can start with recommending “no added salt” with ultimate goal of achieving the current recommendation of 1.2 grams/day total for 4- to 8-year-olds and 1.5 grams/day for children 9 years and older
- 47. Indications for antihypertensive drug therapy • Symptomatic hypertension • Secondary hypertension • Hypertensive target organ damage • Diabetes( types 1 & 2) • Persistent hypertension despite nonpharmacologic measures
- 48. Goals of antihypertensive therapy • Reduction of BP to < 95th percentile without any concurrent conditions. • Reduction of BP to <90th percentile with concurrent conditions (eg.Hyperlipidemia ,End organ damage, Obesity, CKD Complications etc).
- 49. Principles of treatment • Medications with a longer duration of action (once, twice daily dosing) are preferred for better compliance and less side effects. • Dose adjustment of antihypertensive medications need not be made more frequently than every 2-3 days.
- 50. • Therapy is initiated with one agent, at an appropriate dose and the dose is increased until the desired blood pressure is achieved. If the highest dose is not effective or if there are side effects, a drug from a different class is added or substituted.
- 51. Start with CCB or ACEI or β- blocker Combination therapy (either) • ACEI + CCB • ACEI + thiazide diuretic • β-blocker + CCB Combine ACEI + CCB + prazosin / β-blocker/thiazide Additional agents Clonidind, labetalol, hydralazine, minoxidil Therapy is initiated with a calcium channel blocker (CCB), angiotensin converting enzyme inhibitor (ACEI) or β adrenergic blocker. If two drugs are required, the ACEI (or β-blocker) should be combined with a CCB. Unsatisfactory control of blood pressure requires the use of additional agents. Blood pressure >95th centile Blood pressure >95th centile
- 52. COMBINATIONS TO BE AVOIDED • a or b blocker + clonidine (antagonism) • b blocker + CCB (marked bradycardia/ AV block). • Any 2 drugs of same class.
- 53. SECONDARY HYPERTENSION • Treatment should be aimed at removing the cause of hypertension whenever possible. • Curable forms of Hypertension Renal Unilateral kidney disease (Nephritis, Pyelonephritis, hydronephrosis) Cardiovascular CoA, Renal artery stenosis, thrombosis. Adrenal Pheochromocytoma, Neuroblastoma, hyperaldosteronism Miscellaneous Drugs/ OCP etc.
- 54. Management Algorithm of Systemic Hypertension
- 55. Oral antihypertensive medications Table Contd…
- 57. How Much Just Enough Depends on Acute vs. Chronic
- 58. What to do 1st • Monitor, Monitor, Monitor • Need cardiopulmonary monitoring • Need continual BP monitoring (frequently cycling cuff vs. arterial line) • Decide oral vs. IV ▫ Oral OK if asymptomatic ▫ IV necessary if acute target organ damage is present or imminent
- 59. Oral vs. IV IV Medication • Rapid Action • Titratable • Easy to adjust the dose • Requires IV access PO Medication • Don’t need an IV • Harder to control effects • Absorption variable • Slower kinetics can make titrating more difficult
- 61. Principles of treatment in Hypertensive emergencies • Patients with stage 2 hypertension may present with acute, life threatening target organ damage involving • Central nervous system (encephalopathy, seizures), • Heart (pulmonary edema) or • Kidneys (acute renal failure). • These patients need hospitalization for monitoring and supportive care. Blood pressure levels are usually 5-15 mm above the 99th percentile, and should be reduced to safe levels.
- 62. Principles of treatment in Hypertensive emergencies (Contd…) • Rapid reduction of blood pressure might, however, compromise blood flow and result in ischemic complications in the brain, retina, spinal cord and kidneys. Blood pressure reduction, therefore, must be regulated in order to prevent end organ damage to these organs. • Difference between the observed and desired (95th percentile) blood pressure is estimated; decrease the pressure by 25 percent or less over the first 8 hours after presentation and then gradually normalizing the BP over 26–48 hours. • 1 The Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents 2005 2 Srivastava RN, Bagga A. Hypertension. In: Srivastava RN, Bagga A. Pediatric Nephrology, 6th • ed. New Delhi: Jaypee Brothers, 2016
- 63. • The pressure should be reduced by 10% in the 1st hr, and 15% more in the next 3-12 hr, but not to normal during the acute phase of treatment.(Nelson 20th edition)
- 64. • Agents of choice include short acting, intravenous (IV) preparations that are titrated to response (sodium nitroprusside, nitroglycerine, labetalol and nicardipine) . Therapy with enteral antihypertensive drugs should be instituted within 6-12 hr of parenteral therapy, and the latter gradually withdrawn over the next 12-24 hr
- 65. • Volume depletion is common in patients with severe hypertension and IV administration of loop diuretic together with a potent anti- hypertensive agent might lead to a precipitous drop in blood pressure • Diuretics should therefore be avoided unless specifically indicated for volume overload as occurs in glomerulonephritis coexisting pulmonary edema.
- 66. Specific recommendations • Essential hypertension: • choices are between CCB and ACEI. • Therapy with β-blockers is recommended in patients who cannot tolerate ACEI or CCB.
- 67. Acute glomerulonephritis • Hypertension is of short duration associated with salt and water retention. • Fluid and sodium restriction and judicious use of loop diuretics are useful in patients with circulatory congestion, hypertension and edema. • Severe hypertension with or without encephalopathy is an emergency and usually responds to treatment with CCB and furosemide. Occasionally treatment with β-blocker or ACEI may be necessary.
- 68. Chronic kidney disease: target blood pressure is <90th percentile. stage I-III (GFR >30 mL/min/1.73 m2) therapy should be initiated with ACEI, since these agents also reduce proteinuria and retard progression of renal damage • Monitoring of serum potassium and creatinine is necessary, initially at 7-14 days and then every 1-3 month The dose of ACEI (or angiotensin receptor blockers) is reduced if serum creatinine exceeds 30-35% from the baseline or there is hyperkalemia. • Treatment with ACEI should be avoided in (stage IV-V; GFR <30 mL/min/1.73 m2). Therapy in these cases is initiated with either a CCB or β-blocker.
- 69. • Sodium intake is restricted to between 1-1.5 g (45-65 mEq sodium, 2.6-3.8 g salt). Co-administration of diuretics helps in reducing sodium and volume overload. • Thiazides (hydrochlorothiazide, chlorthalidone) are satisfactory, but not effective at GFR <30 mL/min/1.73 m2. Additional medications include α-blockers (prazosin, labetalol), centrally acting agents (clonidine) or vasodilators (hydralazine, minoxidil). The dosage of some medications (e.g., atenolol) need modification in renal impairment
- 70. Renovascular disease: therapy should be initiated with a CCB or/and a β-blocker. Additional agents include prazosin, labetalol, clonidine, hydralazine and/or minoxidil. • therapy with ACEI or ARB is avoided in patients with suspected or confirmed bilateral renovascular disease, these agents might be used cautiously in those with unilateral renovascular hypertension • angioplasty, or surgery
- 71. Complications of hypertension • ACEI are the preferred initial agents in subjects with ventricular dysfunction. • Additional therapy may be given with loop or thiazide diuretics, β blockers and aldosterone antagonists. ACEI or ARB are recommended for patients with associated proteinuria.
- 72. Proposed algorithm for the management of hypertensive crisis
- 73. Management of Hypertensive Emergencies Sodium nitroprusside • IV infusion: 0.3-8 μg/kg/min (in 5% dextrose) • Protect infusate from light • Onset of action at 30 seconds; peaks 2 min; disappears within 3 min of stoppage Medication for >48 hr at dose of >3 μg/kg/minute might cause cyanide toxicity (dizziness, confusion, seizures, jaw stiffness and lactic acidosis), which is treated with amyl nitrate, sodium nitrate and hemodialysis • IV infusion of sodium thiosulfate (one-tenth dose of nitroprusside) or hydroxycobalamin prevents toxicity Nitroglycerine • IV infusion: 1-3 μg/kg/min, increase 1 μg/kg/min q 30 min • Onset of action at 2-5 min; duration 5-10 min after discontinuation • Alternative to nitroprusside (especially in adults with coronary artery disease) • Methemoglobinemia, headache, tachycardia may occur; tachyphylaxis on prolonged use
- 74. Management of Hypertensive Emergencies Labetalol • IV infusion: 0.25-3 mg/kg/hr; or bolus: 0.2-1 mg/kg/dose; may repeat q 5-10 min to maximum 40 mg • Onset of action within 5-10 min; duration 3-6 hr • Orthostatic hypotension, abdominal pain, diarrhea may occur Avoid in patients with asthma, heart failure or heart block Nifedipine • PO: 0.25 mg/kg Unpredictable and often uncontrolled fall of blood pressure; might be used if no access to parenteral agents
- 75. Management of Hypertensive Emergencies Nicardipine • IV infusion: 0.5-5 μg/kg/min; maximum 5 mg/hr • May cause reflex tachycardia, increase cyclosporine levels • Avoid in head trauma, intracranial hemorrhage Phentolamine • IV bolus: 0.1-0.2 mg/kg (maximum 5 mg); repeat 2-4 hr • Used for pheochromocytoma; administer 1-2 hr prior to surgery • May cause reflex tachycardia
- 76. Take home message • All children >3 years of age attending OPDs should have their BP recorded (Special circumstances in children < 3 years). • Thorough history and physical examination followed by relevant investigations can clinch the cause of hypertension. • Treatment of secondary hypertension must also focus on the underlying disease.
- 77. thank you