Hypertension is prevalent in 2-5% of pediatric population. Hypertensive emergencies account for acute elevation of blood pressure with target organ damage and require rapid treatment to lower BP and prevent further damage. The document discusses definitions of hypertensive emergency and urgency, common causes, clinical presentations, investigations, and management approaches including use of intravenous antihypertensives like sodium nitroprusside, labetalol, and esmolol to gradually reduce BP and prevent end organ damage.

1. APPROACH TO MANAGEMENT OF
HYPERTENSIVE CRISIS IN PICU
DR C ABHIRAM KUMAR
FELLOW IN PICU
ASTER CMI HOSPITAL

2.  INTRODUCTION
 BP HOMEOSTASIS
 HYPERTENSION DEFINITION
 ETIOLOGY
 CLINICAL PRESENTATION
 MANAGEMENT

3.  Hypertension is prevelant in 2-5% of pediatric
population
 Hypertensive emergencies account for 1% of
emergency visits
 Secondary hypertension is the most important cause
in children although primary hypertension is being
increasingly recognised now

4. BP = CO SVR
 Hypertension can result due to increased cardiac
output or increased SVR
 Results in endothelial damage, activates local
coagulation cascade, platelet clumping and fibrinoid
necrosis.
 Increased BP causes pressure diuresis and secondary
activation of RAAS

7. DEFINITIONS

8.  HYPERTENSIVE EMERGENCY:
 Acute elevation of blood pressure with target organ
damage
 Most common target organs involved are CNS,
Cardiovascular system, eye and kidney
 Rate of rise of BP is more important than the absolute
value

9.  HYPERTENSIVE URGENCY:
 Acute rise in BP without target organ damage
 Can progress to emergency if not addressed
immediately

10.  Secondary hypertension most commonly present as
emergencies or urgencies
 Essential / primary hypertension is more common in
adolescent age and now increasingly seen in pediatric
population
ETIOLOGY

11.  Renal Causes
Renal Parenchymal diseases (78%)
Renal vascular diseases (12%)
 Cardiovascular
CoA(2%)
Condition with large stroke volume (PDA, AV fistula)
 Endocrine
Hyperthyroidism
Excessive Catecholamine levels (Pheochromocytoma)
Adrenal dysfunction (CAH 11b, 17 a hydroxylase deficiency)
Hyperaldosteronism (Conn's Syndrome, Renin Producing Tumors)
Hyperparathyroidism
 Neurogenic
Raised ICT, Poliomyelitis, LGB (Gullian Barry Syndrome).
 Drugs and Chemical
Sympathomimetic drugs , Amphetamines, Steroids, OCP, Heavy matal poising (Hg, Lead), Cocaine,
Cyclosporine
 Miscellaneous
Hypercalcemia, After Coarctation repair, Pre eclampsia etc.

13.  CNS- Hypertensive encephalopathy
Stroke
Intracranial Bleed
 CARDIAC- Myocardial ischemia
Acute heart failure
Pulmonary edema
Aortic dissection
CLINICAL PRESENTATION

14.  OCULAR- Papilledema
Retinal hemorrhages
 RENAL- Acute Renal Failure
Hematuria/Proteinuria
Pyuria

15.  CNS- Headache, nausea and vomiting, blurring of vision,
paresis, seizures, altered sensorium
 CVS- Breathlesness, orthopnea, dyspnea, chest pain,
abdominal pain
 OCULAR- Blurring of vision, blindness
 RENAL- Hematuria, generalised edema
SYMPTOMS AND SIGNS

16.  Hypertensive Encephalopathy(PRES)-
 Most common presentation of hyperytensive
emergencies
 Cerebral autoregulation is lost
 Symptoms such as headache(occipital), vomiting ,
altered sensorium and seizures

17.  Investigations to identify target organ damage
 Investigation for etiology
 Investigations should not delay the treatment
INVESTIGATIONS

18.  Investigations to identify target organ damage:
 CBC and Peripheral smear(TMA)
 Urine analysis and renal function tests
 Chest Xray , ECG and Echo
 Ct scan Brain/Fundus examination
 Ultrasonogram abdomen

19.  Investigations to identify etiology:
 Ultrasonogram doppler abdomen
 Plasma renin and aldosterone levels
 Serum cortisol, Thyroid function tests
 Urine VMA levels
 Urine and blood toxicology

21.  Initial ABC must be assessed as in any other emergency
and stabilised first
 Measure four limb blood pressure
 Set up an Invasive arterial line for continuous and accurate
blood pressure monitoring
 Hypovolemia can be present due to pressure diuresis and
natriuresis
TREATMENT

22.  Optimise sedation and analgesia
 In emergencies BP should be gradually reduced to
prevent ischemic organ damage
 Reduction targets:(95th centile for emergencies and
90th centile for urgencies)
First 8hrs- 20-25% of target
Next 8-12 hrs-Next 25% of target
Next 24-48 hrs- Next 50% of target

23.  Medication choice for hypertensive crisis depends on several
factors
Type of end organ involved
Rapidity of onset of action and ease of titration of medicine
Patient’s clinical condition

25.  Sodium Nitroprusside-
 Non selsctive vasodilator
 Rapid onset of action-30 sec
 Peak onset-2minutes and duration lasts for 2-4
minutes after cessation
 Dose-0.3 mic to 5mic/kg/min

26.  Mechanism of action-
 Interacts with HB to form methemoglobin and
releases cyanide and nitric oxide
 Nitric oxide activates guanyl cyclase in vascular
smooth muscle which activates Cellular GMP and
causes relaxation of smooth muscle and vasodilation

28.  Side effects-
 Precipitous hypotension most common
 Reflex tachycardia(use beta blocker)
 Methemoglobenemia
 Thiocyanate toxicity
 Cyanide toxicity- rare but most fatal complication
 Tachycardia, almond smell on breath, seizures, lactic acidosis
 Discontinue SNP, administer 100% o2.
 3% Sodium nitrite4-6 mg/kg iv slowly
 Sodium thiosulfate 150-200mg/kg iv over 15minutes
 Hydroxycobalamin 70mg/kg iv
 Sodium bicarbonate-1-2 meq/kg to correct acidosis

29.  Labetalol-
 Competitive alpha-1 and Beta adrenergic receptor
antagonist
 Alpha-1 blockade causes vasodilation and beta
blockade prevents reflex sympathetic stimulation
 Intrinsic sympathomimetic activity on Beta-2
receptors further causing vasodilation

30.  Oral bioavailabilty-20-40%
 IV form- 1:7- alpha: beta blockade
 Onset-2-5 min, peak-5-15 minutes, effect-2-4 hrs
 Bolus of 0.25 mg/kg initially followed by 0.3-3mg/kg/hr
infusion
 Side effects include bradycardia, hypotension and
bronchospasm
 Contraindicated in asthmatics

31.  Esmolol-
 Ultrashort acting Beta-1 adrenergic antagonist
 No intrinsic sympathomimetic activity
 Onset-60s, Peak -8-10min, effect-15-30minutes
 Bolus dose-300-500mic/kg over1-3minutes
 Infusion-25-200 mic grams/kg/min
 Side effects include significant bradycardia,
hypotension and bronchoconstriction

33.  Hydralazine-
 Arteriolar dilator
 Can be given IV, IM or oral
 Onset-5-20min, Effect-2-6 hrs
 0.15mg/kg-Q4-6th hrly(IV), 0.25mg/kg(oral)
 Hypotension, tachycardia,nausea, flushing and
headache

34.  Drugs in CNS involvement-
Labetalol is drug of choice
Labetalol preffered over SNP
Avoid Ca channel blockers alone
 Drugs In renal failure-
Feneldopam/Nicardipine
Avoid SNP(thiocyanate toxicity)
Enalaprilat contraindicated in renal artery stenosis
Drug of choice

35.  Drugs in acute heart failure:
SNP especially when pulmonary edema present
Labetalol and Nitroglycerin can also be used
Avoid Ca channel blockers(reflex tachycardia)
 Coarctation Of Aorta-
Esmolol is the drug of choice
Enalaprilat also used

36.  Hypertension in pediatric population is being increasingly
recognised
 Rate of rise of Blood Pressure is more important than the
absolute value in target organ damage
 It is important to differentiate urgency from emergency
 Primary goal of treatment is to prevent end organ damage
and reduce BP gradually
 Investigations to find the etiology should not delay the
cause for treatment
CONCLUSION

37.  Iv antihypertensives are used in hypertensive
emergencies to lower the BP
 Oral antihypertensives are used in urgencies
 BP should be gradually reduced to prevent ischemic
organ damage
 Pain and anxiety are important reversible causes of
hypertension which needs to be addressed