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Zorluk: OrtaSomatic Symptom and Eating Disorders

A 22-year-old woman is admitted to the inpatient psychiatric unit for the management of severe anorexia nervosa, restricting subtype. On admission, her body mass index (BMI) is 13.8 kg/m². Her vital signs show a blood pressure of 88/54 mm Hg, pulse of 44/min, and respiratory rate of 12/min. Physical examination reveals temporal wasting and fine, downy hair on her arms and back. Initial laboratory studies show normal serum electrolytes. A closely monitored nutritional rehabilitation program is initiated with enteral feedings. On the third day of hospitalization, the patient develops acute-onset profound muscle weakness, areflexia, and difficulty breathing. An electrocardiogram demonstrates premature ventricular complexes. Which of the following pathophysiologic mechanisms is the primary cause of this patient's acute clinical deterioration?

  1. Intracellular shift of phosphate driven by insulin secretionCevap
  2. B
    Renal wasting of potassium due to secondary hyperaldosteronism
  3. C
    High-output heart failure due to profound thiamine deficiency
  4. D
    Decreased calcium ionization secondary to metabolic alkalosis
  5. E
    Rebound hypoglycemia from an exaggerated pancreatic response

Cevap

The acute clinical deterioration is caused by an intracellular shift of phosphate driven by insulin secretion.
This patient is experiencing refeeding syndrome, a potentially fatal complication of nutritional rehabilitation in chronically malnourished individuals, such as those with severe anorexia nervosa. During starvation, the body shifts to catabolism, maintaining normal serum electrolyte levels despite profound total-body depletion. The reintroduction of carbohydrates triggers a massive release of insulin. This insulin surge drives the intracellular uptake of glucose, phosphate, potassium, and magnesium. The rapid intracellular shift of phosphate severely depletes serum phosphate levels. Because phosphate is essential for the production of adenosine triphosphate (ATP) and 2,3-bisphosphoglycerate (2,3-BPG), profound hypophosphatemia leads to cellular energy failure and tissue hypoxia. This manifests clinically as acute muscle weakness, areflexia, respiratory failure (due to diaphragmatic weakness), and cardiac arrhythmias, precisely matching the patient's presentation.

Adım Adım Çözüm

1
Identify the patient's baseline clinical state and recent intervention.
The patient has severe restricting anorexia nervosa with profound malnutrition (BMI 13.8) and is undergoing initial nutritional rehabilitation.
Establishing the context of chronic starvation followed by sudden feeding is crucial for recognizing the risk of refeeding syndrome.
2
Analyze the acute clinical presentation.
On hospital day 3, she develops acute muscle weakness, areflexia, respiratory difficulty, and cardiac arrhythmias.
These symptoms point to a severe intracellular energy deficit and an alteration in cellular membrane function.
3
Connect the intervention to the pathophysiologic response.
Enteral feeding causes a massive insulin surge, which drives glucose and electrolytes (particularly phosphate) into cells, resulting in severe serum hypophosphatemia.
Phosphate is required for ATP synthesis; its sudden depletion leads to generalized cellular dysfunction and the observed clinical deterioration.

Anahtar Kavram

Refeeding Syndrome Pathophysiology
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Konular

Somatic Symptom and Eating Disorders

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