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Difficulty: EasyPediatric Gastrointestinal Disorders

A 4-week-old boy is brought to the emergency department by his parents due to a 3-day history of worsening vomiting. The parents report that he forcefully vomits a large amount of milk immediately after almost every feed. The vomitus does not contain bile. Despite the vomiting, the infant appears hungry and eagerly accepts feeds right after an episode. He has had only one wet diaper in the past 12 hours. Vital signs are temperature 37.0°C (98.6°F), heart rate 165/min, blood pressure 70/40 mm Hg, and respiratory rate 40/min. Physical examination reveals a sunken anterior fontanelle, dry mucous membranes, and markedly decreased skin turgor. Palpation of the abdomen reveals a firm, mobile, olive-shaped mass in the right upper quadrant. Laboratory studies are obtained and show the following:

Laboratory ParameterValue
Sodium132 mEq/L
Potassium2.8 mEq/L
Chloride86 mEq/L
Bicarbonate35 mEq/L
Blood urea nitrogen32 mg/dL
Creatinine0.6 mg/dL

Which of the following is the most appropriate next step in the management of this patient?

  1. Intravenous normal saline and potassium replacementAnswer
  2. B
    Immediate surgical pyloromyotomy
  3. C
    Measurement of arterial blood gases to calculate expected respiratory compensation
  4. D
    Empirical administration of intravenous ampicillin and gentamicin
  5. E
    Reassurance and transition to smaller, more frequent thickened feeds

Answer

Intravenous normal saline and potassium replacement
The correct answer is intravenous normal saline and potassium replacement. This infant presents with the classic triad of hypertrophic pyloric stenosis (HPS): projectile nonbilious vomiting, a palpable 'olive-shaped' mass in the right upper quadrant, and a hypochloremic, hypokalemic metabolic alkalosis. The persistent vomiting of gastric contents leads to profound volume depletion and loss of hydrochloric acid. In response to hypovolemia, the kidneys activate the renin-angiotensin-aldosterone system, leading to sodium reabsorption at the expense of potassium and hydrogen ion excretion (paradoxical aciduria), which further exacerbates the hypokalemia and metabolic alkalosis. While a Ramstedt pyloromyotomy is the definitive treatment for HPS, it is highly dangerous to induce anesthesia in an infant with a severe uncorrected metabolic alkalosis, as it significantly increases the risk of postoperative apnea. Therefore, the absolute first step in management is aggressive rehydration with intravenous normal saline and the addition of potassium chloride once urine output is established.

Step-by-Step Solution

1
Identify the clinical diagnosis based on the classic triad
The patient has a 3-day history of nonbilious projectile vomiting, an olive-shaped abdominal mass, and visible signs of severe dehydration, which is diagnostic for hypertrophic pyloric stenosis.
Recognizing the pathognomonic clinical signs establishes the primary diagnosis.
2
Analyze the laboratory findings
The labs reveal hyponatremia, hypokalemia, hypochloremia, and elevated bicarbonate, representing a hypochloremic, hypokalemic metabolic alkalosis with prerenal azotemia.
Persistent vomiting of gastric hydrochloric acid causes loss of fluid, hydrogen, and chloride. The kidneys attempt to conserve volume by retaining sodium at the expense of excreting potassium, worsening the hypokalemia.
3
Determine the priority of management
Before the definitive surgical treatment (pyloromyotomy) can be performed, the infant must receive aggressive intravenous fluid and electrolyte replacement.
Operating on an infant with severe metabolic alkalosis carries an unacceptably high risk of anesthesia-induced respiratory depression and postoperative apnea.

Key Concept

In hypertrophic pyloric stenosis, the immediate priority in management is medical optimization with intravenous fluid resuscitation and correction of the hypochloremic, hypokalemic metabolic alkalosis prior to surgical pyloromyotomy.
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Topics

Pediatric Gastrointestinal Disorders

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