A Fatal Case of Takotsubo Cardiomyopathy Secondary to Refractory Hypoglycemia in Severe Starvation: An Autopsy Case Report

Abstract

A 56-year-old, severely malnourished man presented with loss of consciousness due to hypoglycemia. Echocardiography revealed left ventricular apical ballooning, indicating takotsubo cardiomyopathy. Although his caloric intake was gradually increased to avoid refeeding syndrome, hypoglycemia was refractory, and repetitive glucose administration was required. On day 4 of admission, he developed severe refractory hypoglycemia with a progressive decrease in blood pressure. Consequently, pulseless ventricular tachycardia followed by pulseless electrical activity developed. Although venoarterial extracorporeal membrane oxygenation was introduced, the patient did not respond to the treatment and died. Autopsy revealed myocardial degeneration and contraction-band necrosis, indicative of takotsubo cardiomyopathy. No coronary stenosis was observed. The liver showed moderate hepatocyte atrophy and autophagosomes, consistent with starvation and not with refeeding syndrome. We speculated that refractory hypoglycemia induced extreme catecholamine secretion, which led to severe complications of takotsubo cardiomyopathy, such as fatal arrhythmia and extremely low cardiac output. Early recognition of these critically ill patients and timely therapeutic interventions, including strict glycemic control and adequate caloric intake, may improve patient outcomes.

Keywords: refeeding syndrome; refractory hypoglycemia; starvation; takotsubo cardiomyopathy; venoarterial extracorporeal membrane oxygenation (va-ecmo).

Figure 1. Electrocardiographic findings on admission (day 1) and day 2

ECG shows sinus bradycardia and no ST-segment changes on admission (A). On day 2, ECG shows negative T waves in I, aVL, and precordial leads from V2 to V5 (red arrows) (B). ECG, electrocardiogram.

Figure 2. Chest X-ray at admission

Initial chest X-ray demonstrated mild interstitial pulmonary edema (red arrows).

Figure 3. Two-dimensional echocardiogram at admission

Echocardiography revealed a severely decreased LV ejection fraction of 20%, with global hypokinesis and apical akinesia (red arrows). End-diastolic (A) and end-systolic (B) frames at admission showed dyskinesia of apex and middle segment of the LV. Ao, aorta; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

Figure 4. The patient’s clinical course and blood glucose trends

bpm, beats per minute; DBP, diastolic blood pressure; HR, heart rate; LVEF, left ventricular ejection fraction; SBP, systolic blood pressure; VA-ECMO, venoarterial extracorporeal membrane oxygenation.

Figure 5. Microscopic view of heart (A, B).

A low-power view of cardiac muscle showed diffuse myocardial atrophy and degeneration. (H&E staining) (A). Contraction band necrosis was observed (red arrows). (Phosphotungstic acid hematoxylin staining) (B). H&E, hematoxylin and eosin stain.

Figure 6. Microscopic view of the liver (A, B) and lung (C)

A low-power view of the liver showed diffuse hepatocyte atrophy. (H&E staining) (A). A view of hepatocytes observed by electron microscopy showed autophagosome (red arrows) and perinuclear space (B). A low-power view of lung showed blood accumulation in the alveolar spaces (red arrows). (H&E staining) (C). H&E, hematoxylin and eosin stain.