**** A 28-year-old woman with severe anorexia is admitted for nutritional rehabilitation. Within 48 hours of initiating enteral feeding, she develops muscle weakness, cardiac arrhythmias, and respiratory distress. Which metabolic abnormality is most characteristically responsible?

1. A

   Hyponatremia

2. B

   Hypocalcemia

3. C

   Hypophosphatemia

4. D

   Hyperkalemia

Appeared in: AIIMS Rishikesh NO - 2019

Explanation

• The patient's presentation of acute muscle weakness, cardiac arrhythmias, and respiratory distress after starting nutritional support is a classic sign of refeeding syndrome.
• Refeeding syndrome is triggered by the reintroduction of nutrition (especially carbohydrates) in a chronically malnourished person, such as someone with severe anorexia.
• The resulting insulin surge causes a rapid shift of phosphate from the blood into the cells to produce energy (ATP).
• This leads to a severe drop in serum phosphate levels (hypophosphatemia), which is the hallmark of the syndrome.
• The lack of phosphate impairs energy production, causing dysfunction in high-energy-demand tissues like the heart, diaphragm, and skeletal muscles, explaining the patient's symptoms.

Why Other Options Were Wrong

• Option A: While fluid shifts in refeeding syndrome can cause dilutional hyponatremia (low sodium), it is not the primary cause of the severe cardiac and muscular symptoms described.
• Option B: Hypocalcemia can occur in refeeding syndrome, often related to hypomagnesemia (which impairs PTH secretion), but it is not the central or most characteristic abnormality driving the acute cardiorespiratory failure.
• Option D: This is the opposite of what occurs in refeeding syndrome. The insulin surge drives potassium INTO the cells, causing profound HYPOkalemia, not hyperkalemia.

Related Visual

Clinical Relevance

• Nursing practice connection: This is primarily an exam-oriented knowledge point with limited direct bedside application, so retain Refeeding Syndrome as background academic context rather than a clinical decision trigger.
• Nurses must identify patients at high risk for refeeding syndrome, including those with anorexia nervosa, chronic alcoholism, cancer cachexia, and prolonged starvation.
• The cornerstone of nursing management is prevention, following the principle of "start low and go slow" when reintroducing nutrition.
• Crucial nursing interventions include baseline and daily monitoring of electrolytes (phosphate, potassium, magnesium), cardiac monitoring, and assessing for signs of fluid overload or muscle weakness.

How to Approach the Question

• First, identify the key elements of the clinical scenario: a high-risk patient (severe anorexia), a specific trigger (initiation of enteral feeding), and a distinct set of acute symptoms (muscle weakness, arrhythmias, respiratory distress).
• Recognize that this combination of a malnourished patient rapidly deteriorating after feeding is the classic presentation of a specific complication.
• Connect the symptoms to their underlying physiology. Muscle weakness, especially of the diaphragm (respiratory distress), and cardiac instability point to a failure of cellular energy metabolism.
• Recall the pathophysiology of refeeding syndrome, where an insulin surge drives key electrolytes into cells.
• Identify the hallmark electrolyte disturbance of refeeding syndrome, which is responsible for the energy failure.
• Evaluate the options and select the one that matches this hallmark disturbance: hypophosphatemia.

Concept Tested & Keywords

• Concept Tested: Refeeding Syndrome
• Stem keywords: anorexia, nutritional rehabilitation, enteral feeding, muscle weakness, cardiac arrhythmias, respiratory distress
• Lead-in keywords: most characteristically responsible
• Clinical cues: Patient with severe anorexia identifies a high-risk individual for malnutrition.
• Clinical cues: Onset of symptoms within 48 hours of initiating feeding is a classic timeframe for refeeding syndrome.

Question ID

QGIeS6RmqkkIzezbZtZ3zV

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Reference Book

E6 Nelson Textbook of Pediatrics(2024) — Volume 1 pp. 552-554, 476-478