Brown Pediatrics

Brown's Pediatric Residency Blog

Month: March 2017

Too Much Pressure

Image Credit: Pixabay

 

 

Case: Andrew is a 16yo post-pubertal male without any past medical history who comes to clinic for his annual well-child check. His vitals at triage showed a blood pressure of 142/92. You note that he was seen in urgent care twice in the last 2 months with a similarly high blood pressures. His BMI is >95th percentile. How should you address his blood pressure today? Specifically, what further workup and/or treatment should be undertaken?

 

Diagnosis 

How is high blood pressure classified? (based on The Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents)

  • Hypertension is defined as an average systolic blood pressure (SBP) and/or diastolic BP (DBP) that is ≥95th percentile for gender, age, and height on 3 occasions.
    • These 3 occasions needs to be separated by days-weeks
    • Note: Measures obtained by oscillometric devices (aka automatic BP machines) that exceed the 90th percentile should be repeated by auscultation.
  • Prehypertension in children is defined as average SBP or DBP levels that are ≥90th percentile but <95th percentile.
    • As with adults, adolescents with BP levels >120/80 mmHg should be considered prehypertensive.
  • A patient with BP levels ≥95th percentile in a physician’s office or clinic, who is normotensive outside a clinical setting, has “white-coat hypertension.”
    • Ambulatory BP monitoring (ABPM) is usually required to make this diagnosis.

Image Credit: Pixabay

 

 

Epidemiology

  • The prevalence of primary and secondary hypertension is 4.5% and 13%, respectively (Gupta-Malhotra et al, 2015)
    • Given low screening rates, true prevalence may be higher
  • Children with essential (primary) hypertension tend to be older (>6), have a family history of hypertension (Gupta-Malhotra et al, 2015)
    • Conversely, infants and preschool-aged children with elevated blood pressure are more likely to have a secondary form of hypertension.

 

Etiology & Workup

  • While secondary causes of hypertension are more common in children than adults, children can also have primary hypertension (see Table below

 

<1yr old (%) 1-5 years (%) 6-12 years (%) 13-19years (%)
Respiratory (61) Respiratory (29) Essential (57) Essential (49)
Renal (13) Renal (27) Renal (27) Renal (20)
Medication Related (9) Essential (19) Neurological (7) Medication Related (11)

Table 1: Most common causes of hypertension by age (adapted from Gupta-Malhotra et al, 2015)

  • Workup for secondary causes should be individualized
    • Children with BPs ≥95th percentile (stage 1 hypertension) should have the following (NHBPEP, 2004; Ingelfinger JR, 2014):
      • Targeted History and Physical to elicit risk factors including: relevant past medical history, family history, medications and other exposures (e.g. stimulants, etc), and physical exam.
        • Retinal Exam also indicated for children with ≥Stage 1 HTN
      • Lab Studies: basic metabolic panel, complete blood count, urinalysis & culture
        • Other lab studies could include (if clinically indicated): fasting lipid panel and glucose, plasma renin, plasma and urine steroid levels, and/or plasma and urine catecholamines
      • Imaging: Renal ultrasound and echo

 

Treatment

  • For children with pre-hypertension and Stage 1 hypertension, lifestyle changes are recommended first line (Ingelfinger JR, 2014).
    • Examples include: dynamic exercise, DASH diet (Couch SC et al, 2008)

Image Credit: Pixabay

 

 

  • For children who continue to be hypertensive despite lifestyle interventions, evidence of end organ damage, or evidence of secondary etiologies pharmacologic intervention may be required
    • No consensus exists for “optimal” first line agent
      • Acceptable regimens include: ACE inhibitors, calcium channel blockers, or diuretics (Dhull RS et al, 2016).

 

Back to the Case: Upon seeing Andrew, you repeat his blood pressure manually, which is also high. He has no other “red flags” on history or exam. Given his age and comorbidities (obesity), Andrew most likely has essential hypertension (3 readings >140/90). Initial workup should include: basic labs (BMP, CBC, and UA) and imaging (renal ultrasound and ECHO). Provided these are all reassuring, he should first undergo lifestyle interventions, with medical management initiated if his BPs do not normalize.

 

References

  1. “The Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents.” Pediatrics Aug 2004, 114 (Supplement 2) 555-576
  2. Couch SC et al. “The Efficacy of a Clinic-based Behavioral Nutrition Intervention Emphasizing a DASH-type Diet for Adolescents with Elevated Blood Pressure.” J Pediatr. 2008;152(4)494-501
  3. Dhull RS et al. “Pharmacologic Treatment of Pediatric Hypertension.” Current Hypertension Reports. 2016;18:32
  4. Ingelfinger JR. “The Child or Adolescent with Elevated Blood Pressure.” NEJM. 2014;370:2316-2325
  5. Gupta-Malhotra M et al. “Essential Hypertension vs. Secondary Hypertension Among Children.” Am J Hypertens. 2015;28(1):73-80
  6. Sinaiko AR. “Hypertension in Children.” NEJM. 1996;335:1968-1973.
  7. Yang Q et al. “Trends in High Blood Pressure among United States Adolescents across Body Weight Category between 1988 and 2012.” JPeds. 2016;169:166-73.e3.

Pass the salt…

Post Created by: Dani Halpern, MD

Case: 5yo M comes into the ED with nausea, confusion, and headache. On exam, he is sleepy but noticeable uncomfortable. He has moist mucous membranes, pupils are reactive and he has no noticeable edema. Suddenly, he begins to have a generalized tonic-clonic seizures. Amid the chaos and his mother’s crying you check a BMP and lo and behold his Na comes back as 125!

 

Image credit: http://westeastonpa.com/wp-content/uploads/2015/03/no-salt.jpg

What is the pathophysiology of hyponatremia?

When there is an acute drop in sodium in the blood, water is pulled into the intracellular fluid so cells, especially brain cells, begin to swell. This causes meningeal irritation and the manifested symptoms of nausea, confusion, headache, vomiting and eventually, seizures.

Effects of Hyponatremia on the Brain and Adaptive Responses

Image from: Adrogue HJ et al, 2000

What is the workup of hyponatremia?

Choice of diagnostic algorithms:

  • Classic algorithm begins with an evaluation of patient’s fluid status.
    • Hypovolemic hyponatremia: ↓↓Na/↓H20 Euvolemic hyponatremia: ↔Na/↑H20   Hypervolemic hyponatremia: ↑ Na/↑↑H20
    • This is notoriously difficult to do accurately and clinicians have been shown to be very inaccurate in their assessment with sensitivities ranging from 0.5-0.8 and specificities 0.3-0.5 (Chung HM et al, 1987)
  • Alternative algorithm: (Milionis HJ et al, 2002).

Application of Alternative Algorithm

(Adapted from Milionis HJ et al, 2002)

Step 1: Verify this is an accurate level and is not spuriously low

Step 2: Obtain serum osmolality: (normal 275-290)

  • Low serum osmolality: True hyponatremia
  • Normal serum osmolality: Results from either large volumes of isotonic fluid lacking sodium (most common = mannitol), or in cases of hyperparaproteinemia or hyperlipidemia/triglyceridemia, that latter cases being referred to as “pseudohyponatremia” (see below for illustration). This is only seen in labs that use flame photometry; newer methods using ion-specific electrode have nearly eliminated this entity (Androgue HJ et al, 2000).

  • Increased osmolality: Osmotically active substances (most commonly glucose), draw water out of cells, effectively diluting serum sodium
    • Correction is approximately 2 mEq Na for every 100 glucose is >100

Step 3: Obtain urine Osm and Urine Sodium

  • <100 mOsm/kg = Appropriate water Excretion
    • Primary polydipsia/ psychogenic water drinking
      • Adult needs to drink about 18L for noticeable decrease in Na
    • Low solute intake (e.g. malnutrition, “beer potomania”)
  • >100 mOsm/kg = impaired water excretion. Can be due to problems in 3 different locations in process of diluting urine (this is where urine sodium comes in):
    • <20 mEq/L: hypovolemia (most common cause) and other states of decreased effective arterial blood volume (e.g. cirrhosis, congestive heart failure, nephrotic syndrome (rare in the absence of concurrent renal failure or volume depletion))
    • >40 mEq/L: SIADH vs renal salt wasting (e.g. renal dysplasia, post-obstructive diuresis, post-ATN diuresis), diuretics [mostly thiazide diuretics, uncommon with loop diuretics], adrenal insufficiency, metabolic alkalosis) THIS IS WHERE CLINICAL ASSESSMENT OF VOLUME STATUS ACTUALLY MATTERS (SIADH: restrict water.  Salt wasting: give salt or stop drugs)

In summary, a diagnosis of SIADH requires SOsm < 275, Uosm >100, UNa >30 (Because the fact that urine sodium is not low suggests that the patient is not volume depleted)

Treatment

Image Credit: pixabay.com

In general, treatment of hyponatremia must weigh the benefits of therapy against the risks of overcorrecting, namely, osmotic demyelination (Adrogue HJ et al, 2000).

General Principles

  1.  If the patient has severe symptoms (e.g. seizures, CNS depression), hypertonic saline (3-5cc/kg) should be administered (Brenkert TE et al, 2013)
  2. When correcting hyponatemia, the rate of correction should not exceed 8mmol/L on any day of treatment  (Adrogue HJ et al, 2000).
  3. Treat the underlying condition, as detailed above

 

And now a table for all the conditions that often get confused for one another: 

First test yourself:

SIADH Renal salt wasting Hypovolemia
Volume Status
Serum Na
Urine Na
Serum Osm
Urine Osm
Urine output
ADH

 

Answers: 

 

SIADH Renal salt wasting Hypovolemia
Volume Status Euvolemic Hypovolemic hypovolemic
Serum Na low low Low
Urine Na > 40 >>40 <20
Serum Osm low low low
Urine Osm > plasma Osm > plasma Osm >plasma Osm
Urine output Low high low
ADH high high high

Faculty Reviewer: R. Kremsdorf, MD


References

Adrogué HJ, Madias NE, and Madias NE. “Hyponatremia.” N Engl J Med. 2000;342:1581-1589

Brenkert TE et al. “Intravenous hypertonic saline use in the pediatric emergency department.” Pediatr Emerg Care. 2013 Jan;29(1):71-3.

Chung HM, Kluge R, Schrier RW, Anderson RJ. “Clinical assessment of extracellular fluid volume in hyponatremia.” Am J Med. 1987;83: 905-908

Milionis HJ, Liamis GL, Elisaf MS. “The hyponatremic patient: a systematic approach to laboratory diagnosis.” Canadian Medical Association Journal. 2002;166(8):1056-1062.

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