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Case Reports
. 2020 Jul 30;10(3):e2020185.
doi: 10.4322/acr.2020.185.

Sudden death caused by Clostridium perfringens sepsis presenting as massive intravascular hemolysis

Affiliations
Case Reports

Sudden death caused by Clostridium perfringens sepsis presenting as massive intravascular hemolysis

Katsuya Chinen. Autops Case Rep. .

Abstract

An 80-year-old Japanese woman with diabetes mellitus was admitted with gastrointestinal symptoms and pyrexia. At presentation, liver abscesses and severe hemolytic anemia were noted. Before detailed diagnostic evaluation and adequate treatment, she suddenly died 2.5 hours after admission. The autopsy and bacteriological examinations revealed liver abscesses and massive intravascular hemolysis caused by Clostridium perfringens as well as other miscellaneous critical pathological findings, including acute renal tubular necrosis, lung edema, and pulmonary fat embolism. In this article, the detailed autopsy results are described and clinicopathologic characteristics on Clostridium perfringens-related sudden death are discussed with a review of the literature.

Keywords: Clostridium perfringens; Death, Sudden; Embolism, Fat; Hemolysis; Sepsis.

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Conflict of interest statement

Conflict of interest: None

Figures

Figure 1
Figure 1. Serum of the patient at presentation.
Figure 2
Figure 2. Non-contrast computed tomography of the abdomen. Irregular-shaped cavities containing abundant gas in the right lobe of the liver.
Figure 3
Figure 3. Microphotographs of the peripheral blood smear. A – A spherocyte showing loss of central pallor, a “dehemoglobinized” ghost cell, and an erythroblast are apparent. Note that intact red cells are no longer identified (Giemsa staining, 1000X); B – “Boxcar-shaped” bacilli are clearly demonstrated in the background of ghost cells and fragments of red cell membrane (Giemsa staining, 1000X).
Figure 4
Figure 4. Abscesses featuring a honeycomb structure with gas bubbles, affecting the right and left lobes of the liver.
Figure 5
Figure 5. Microphotographs of the liver. A – Coagulation necrosis is evident in association with bleb formation. Bacterial proliferation is apparent in the right upper portion (H&E, 100X); B – Gram staining reveals marked proliferation of boxcar-shaped gram-positive bacilli. Note that inflammatory cell infiltration is lacking (400X).
Figure 6
Figure 6. Microphotographs of the bone marrow. A – Necrosis of both hematopoietic cells and fat cells is apparent (H&E, 200X); B – Many boxcar-shaped gram-positive bacilli are confirmed (Gram staining, 400X).
Figure 7
Figure 7. Microphotographs of the lung. A – Eosinophilic transudate around the pulmonary arteriole (H&E, 40X); B – Eosinophilic transudate is observed in the limited area within a pulmonary lobule (H&E, 40X); C – Area of panlobular edema (H&E, 40X); D – Fat globules are demonstrated within the pulmonary arterioles and capillaries of the interalveolar septa (Sudan III staining, 100X).
Figure 8
Figure 8. Aorta: moderate atherosclerosis; endothelium with a burgundy color, indicating massive intravascular hemolysis.

References

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