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Hypertensive crisis in children

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Abstract

Hypertensive crisis is rare in children and is usually secondary to an underlying disease. There is strong evidence that the renin-angiotensin system plays an important role in the genesis of hypertensive crisis. An important principle in the management of children with hypertensive crisis is to determine if severe hypertension is chronic, acute, or acute-on-chronic. When it is associated with signs of end-organ damage such as encephalopathy, congestive cardiac failure or renal failure, there is an emergent need to lower blood pressures to 25-30% of the original value and then accomplish a gradual reduction in blood pressure. Precipitous drops in blood pressure can result in impairment of perfusion of vital organs. Medications commonly used to treat hypertensive crisis in children are nicardipine, labetalol and sodium nitroprusside. In this review, we discuss the pathophysiology, differential diagnosis and recent developments in management of hypertensive crisis in children.

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Correspondence to Gastón Zilleruelo.

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Answers:

A: 2

B: 3

C: 1

D: 1

Questions (answers appear following the references)

Questions (answers appear following the references)

  1. A.

    The pathogenesis of hypertension in hypertensive crisis is all of the following except:

    1. 1.

      Increased activity of the renin angiotensin system

    2. 2.

      Increased nitric oxide activity

    3. 3.

      Increased sympathetic activity

    4. 4.

      Endothelial dysfunction

    5. 5.

      Decreased kininogen activity

  2. B.

    A 45-day-old premature infant who weighed 700 g at birth is being weaned from oxygen to room air. An ophthalmologist performed an eye exam. The infant was noted to have an acute increase in blood pressure from a baseline of 70/40 mmHg to 130/70 mmHg with tachycardia. The most likely etiology is:

    1. 1.

      History of umbilical artery catheterization

    2. 2.

      Development of broncho-pulmonary dysplasia

    3. 3.

      Phenylephrine eye drops

    4. 4.

      Renal parenchymal disease

    5. 5.

      Coarctation of aorta

  3. C.

    A 5-year-old female had a living donor kidney transplant. Seven days after the transplant she had a seizure. Her blood pressure was 170/120 mmHg, and her serum creatinine was 0.8 mg/dl. Calcineurin inhibitors were started on the third post-transplant day, and she was also started on mycophenolate mofetil. She is polyuric. What would you most likely expect to find upon investigation.

    1. 1.

      Posterior reversible encephalopathy

    2. 2.

      Acute vascular rejection

    3. 3.

      Fluid overload

    4. 4.

      Increased intracranial pressure

    5. 5.

      High mycophenolate mofetil levels

  4. D.

    An 8-year-old male has ESRD and is on hemodialysis. He had severe hypertension which improved with aggressive fluid removal and re-adjustment of his dry weight. His hypertension was managed with β blockers, clonidine and a calcium channel blocker. Blood pressures are now generally 110/80 mmHg. Which of the following would you consider as the next step.

    1. 1.

      Wean clonidine

    2. 2.

      Stop calcium channel blocker

    3. 3.

      Increase β blocker

    4. 4.

      Increase dry weight

    5. 5.

      All of the above

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Chandar, J., Zilleruelo, G. Hypertensive crisis in children. Pediatr Nephrol 27, 741–751 (2012). https://doi.org/10.1007/s00467-011-1964-0

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