Hypertensive Urgency/Emergencies

Contributing Author: Natalie Hecht, NP

Definition

• Hypertension: systolic BP and/or diastolic BP >95th percentile (based on gender, age and height) on at least 3 readings

• Hypertensive urgency: severe increase in BP without signs of organ damage; may present with mild symptoms, such as headaches and/or nausea

• Hypertensive emergency: severe increase in BP accompanied by life-threatening symptoms and/or acute organ damage

* Degree of hypertension is less important than signs of end organ damage

NIH Blood Pressure Tables for Children and Adolescents: http://www.nhlbi.nih.gov/health-pro/guidelines/current/hypertension-pediatric-jnc-4/blood-pressure-tables

Diagnosis

• Measurement

  • Arterial line BP is most accurate  

  • If noninvasive, blood pressure is most reliably measured in right upper extremity (ensure proper cuff size: cuff too small leads to falsely elevated BP)

• Signs of end organ damage

  • Brain: encephalopathy is most common manifestation of hypertensive emergency

    • Severe nausea/vomiting, headache, vision changes

    • Mental status changes: confusion, lethargy, coma

    • Cerebral edema

    • Seizures

    • Stroke

  • Eyes

    • Decrease in peripheral vision

    • Papilledema, retinal hemorrhage /retinopathy  

  • Kidneys

    • Acute renal failure

    • Elevated creatinine

    • Hematuria and proteinuria (though this is usually a manifestation of glomerulonephritis as the cause of HTN)

  • Heart

    • Left ventricular heart failure due to sudden increase in afterload

    • Pulmonary edema

    • Myocardial ischemia

    • Aortic dissection, especially in patients with predisposition (Marfan)  

    • On exam: diffuse fine crackles, S3 gallop

Etiology

• Renal: most common etiology of hypertension in pediatric patients

  • Renal artery stenosis

  • PSGN

  • HUS

• Neuro

  • Acute stroke (may be cause of HTN or reflex response to maintain CPP)

  • Pseudotumor cerebri

• Cardiac

  • Aortic dissection (accompanying sx include chest or abd pain)

  • Coarctation

• Endocrine

  • Thyroid crisis

  • Cushing syndrome

  • Pheochromocytoma

• Ingestions/drugs

  • PCP, cocaine, amphetamines

Immunosuppressive therapy (ie tacrolimus or cyclosporine) or erythropoietin use

Workup and Management

Work Up

• Electrolytes, CBC, UA

• EKG, CXR, ECHO

• 4 limb BPs

• Fundoscopic exam to assess papilledema, retinal hemorrhage

• Detailed neuro exam: meningeal irritation, visual fields

• Kidney US

• Drug screen

• History of Marfan syndrome

• Pregnancy test to rule out preeclampsia (positive pregnancy may also impact meds used)

Management

• Goal: decrease BP by 20-25% of overall goal (usually, goal is 95th-99th percentile of BP for age, gender and height). Gradually normalize BP over 24-48 hours. Dropping the BP rapidly may worsen end-organ damage.

• Medications: Generally safest to begin with continuous infusion, which can be titrated or held based on response

  • First line  

    • Clevidipine: Calcium Channel Blocker (dihydropyridine), smooth muscle relaxation and vasodilation       

      • 0.5-1 mcg/kg/min initially, titrated by increments of 0.5-1 mcg/kg/min (max 10 mcg/kg/min). (Tobias JD et al, 2011)  Adult dosing 1-2 mg/hr up to max of 21 mg/hr.

      • Comes in oil-in-water emulsion containing 200 mg/ml (2 kcal/mL) of lipid

      • Onset of action 2-4 minutes with duration 5 to 15 minutes. 

      • Metabolized by rapid hydrolysis in bloo and extravascular tissue by esterases. Half-life elimination 1 minutes (terminal 15 minutes) 

    • Nitroprusside: Breaks down to release NO, nonselective vasodilator, decreases both systemic and pulmonary resistance

      • 0.3-0.5mcg/kg/min initial dose to max of 5mcg/kg/min

      • Rapid onset with peak hypotensive effect within 2 minutes

      • Cyanide poisoning, leading to severe lactic acidosis can occur after hours to days of drip. Methemoglobinemia causing acidosis is another adverse effect.

    • Nicardipine: CCB, smooth muscle relaxation and vasodilation

      • Loading dose 5-10mcg/kg, followed by infusion of 0.5-1mcg/kg/min. May increase slowly every 15 minutes to max of 5mcg/kg/min

      • Onset of action 5-15 min, peak effect 30 min - 2 hrs

      • Reflex tachycardia may occur

    • Labetalol: alpha-1 & beta blocker

      • 0.2-1 mg/kg/dose up to 40mg/dose (start at lower range) as an initial bolus dose, then 0.25-3mg/kg/hr

      • Onset of action  2-5 min, peak effect 5-15 min

      • Contraindicated in asthmatics, patients with heart failure

• • Second line

    • Esmolol: beta-1 agonist

      • Loading dose of 300-500mcg/kg, then infusion of 25-200mcg/kg/min, which may be increased q5-15min to max of 1,000mcg/kg/min

      • Peak effect 6-10 min, ultra short acting

      • Associated with bradycardia

      • Contraindicated in heart block, cardiogenic shock, asthma / bronchoconstriction

  • For use in hypertensive urgency only, not emergency:

    • Isradipine: CCB

      • 0.05-0.1 mg/kg/dose

      • Onset 1 hour, peak effect 2-3 hours

    • Nifedipine: CCB

      • Oral or sublingual administration only  

      • 0.25-0.5mg/kg/dose (start low due to risk of precipitous hypotension)

      • Onset 15-30 min with half life 1.5 hr

      • May cause reflexive tachycardia

    • Hydralazine: vasodilator of arterial smooth muscle  

      • Slower onset and longer acting than labetalol & nicardipine

      • 0.2-0.6mg/kg/dose

      • Onset 30 min - 2 hr, duration 6-12 hr

      • May be given q4hr

      • IV or IM

      • Volume depletion is common in hypertensive crises; consider IV crystalloid if BP is dropping excessively to assist with organ perfusion

From Singh et al, International Journal of Nephrology, 2012

References

1) Helfaer & Nichols, Rogers’ Handbook of Pediatric Intensive Care. 4th Edition, 2009.

2) The Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents. Pediatrics

3) Flynn JT. Management of hypertensive emergencies and urgencies in children. UpToDate. 2015