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Case Report

Rapid Calcification of Myocardium as Sequela from Severe Sepsis

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1University Hospital Wurzburg, Department of Diagnostic and interventional Radiology

Abstract

A rare case of rapid myocardial calcification following severe sepsis is presented. The report outlines the temporal course, imaging findings, and plausible pathophysiologic mechanisms, including septic cardiomyopathy and calcium‑phosphate imbalance. Implications for critical care follow‑up and cardiology evaluation are discussed.

Article Information

  1. Received
  2. Accepted
  3. Published
Journal
Journal of Clinical Case Reports and Images
Volume / Issue
Vol 1, Issue 1
Pages
1–2
ISSN
2641-5518
Type
Case Report
DOI
Published
8 Aug 2017

Academic Editor: Anil TOMBAK, Mersin University Faculty of Medicine

Checked for plagiarism: Yes

Review by: Single-blind

Copyright ©  2017 Andreas S. Kunz, et al

License
Creative Commons License     This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Corresponding author: Andreas S. Kunz, University Hospital Wurzburg, Department of Diagnostic and interventional Radiology —

Competing Interests

The authors have declared that no competing interests exist.

Funding

No specific funding statement was provided by the authors.

Data Availability

No data-availability statement was provided by the authors.

Citation:

Andreas S. Kunz, Matthias Beissert, Thorsten Klink (2017) Rapid Calcification of Myocardium as Sequela from Severe Sepsis. Journal of Clinical Case Reports and Images - 1(1):1-2. https://doi.org/10.14302/issn.2641-5518.jcci-17-1509

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DOI 10.14302/issn.2641-5518.jcci-17-1509

The Case

The reported case shall highlight severe sepsis as possible cause of myocardial calcification, as well as the highly dynamic development thereof within a time span of merely 10 weeks. A 60-year-old male patient had been admitted to hospital for palliative therapy of progressive multiple myeloma, which lately had transformed into plasma cell leukemia. After commencing his third therapy cycle with Elotuzumab, the patient suffered from a pneumogenic sepsis due to staphylococcus infection that required mechanical ventilation for 7 days. Antimicrobial therapy followed antimicrobial susceptibility testing and included Tazobactam, Piperacillin, and Fosfomycin. During his hospital stay, computed tomography images of the chest were acquired initially, i.e. at onset of pneumogenic sepsis (Figure 1.: left panel), as well as after 10 weeks (Figure 1: right panel) to follow-up pneumonia consolidations in both upper lung lobes. Surprisingly, non-contrast enhanced follow-up CT images revealed newly developed calcifications within the outer myocardial layers of the left ventricle.

Figure 1. Non-contrast enhanced CT scans of the chest initially during onset of pneumogenic sepsis (right) and after 10 weeks (left) show rapid development of non-preexisting, extensive myocardial calcifications.
Figure 1. Non-contrast enhanced CT scans of the chest initially during onset of pneumogenic sepsis (right) and after 10 weeks (left) show rapid development of non-preexisting, extensive myocardial calcifications.
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Only very few reports exist describing myocardial calcification as sequela from severe sepsis. Explanations attribute alterations of myocardial microcirculation to cause subsequent tissue necrosis during septic shock and capillary leak and relative capillary stasis.1 Resulting interstitial and intracellular edema, and consecutive mitochondrial destruction and cellular necrosis.2 In other cases, myocardial calcifications have been described as complication resulting from myocarditis.3

In general, myocardial calcifications are associated with myocyte necrosis due to severe infection or inflammation, and can lead to restrictive cardiomyopathy. Differential diagnoses include calcifications of the inner myocardial layers, which can be detected after myocardial infarction, and pericardial calcifications that indicate constrictive pericarditis.

References

  1. 1.Hinshaw L B. (1996) Sepsis/septic shock: participation of the microcirculation. , Crit Care Med 24, 1072-1078.
  1. 2.Hersh M. (1990) Histologic and ultrastructural changes in non-pulmonary organs during early hemodynamic sepsis. , Surgery 107, 397-410.
  1. 3.Wang K Y.(Mar2017,12) Calcifying giant cell cardiomyopathy: a possible new entity: Images in Cardiovascular Pathology. Cardiovasc Pathol. (Epub ahead of print);. 28, 68-70.

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Article Details and Related Research

Journal Clinical Case Reports and Images
Article type Case Report
Published 2017-08-08
DOI 10.14302/issn.2641-5518.jcci-17-1509
ISSN 2641-5518
Authors Andreas S. Kunz, Matthias Beissert, Thorsten Klink
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