Single-Photon Emission Computed Tomography Assessment of Sepsis-Related Myocardial Calcification.

Abstract

A 63-year-old man was admitted to the emergency department with tachypnoea, abdominal pain, hypotension, and altered mental status. Upon examination, the patient had involuntary guarding and localised rebound tenderness in the right lower quadrant, suggestive of peritonitis. The patient had no history of arterial hypertension, diabetes mellitus, or ischaemic heart disease. Arterial blood gas showed elevated lactate (4.1 mmol/L), and laboratory tests were notable for leucocytosis (14.7 × 103/mm3), elevated C-reactive protein (31.4 mg/L), and elevated procalcitonin (1.7 ng/mL), with normal calcium (8.9 mg/dL), phosphorus (4.1 mg/dL), and creatinine (1.27 mg/dL). Abdominal computed tomography (CT) revealed induration of the omentum of the right lower quadrant with bubbles of free air in the subumbilical region, suggesting a ruptured Meckel’s diverticulum. The patient received initial fluid resuscitation, antibiotics (vancomycin and piperacillin–tazobactam), and analgesia. Norepinephrine and vasopressin were initiated as the patient’s blood pressure did not increase with initial fluid resuscitation. The patient underwent an exploratory laparotomy and was hospitalised for sepsis. On the first day of hospitalisation, the patient had elevated troponin I (11.2 ng/mL; laboratory reference range ≤0.04 ng/mL) and N-terminal probrain natriuretic peptide (2,386 pg/mL), with repeated 12-lead electrocardiography showing normal sinus rhythm without ST segmental change throughout hospitalisation. He denied chest pain, tightness, palpitations, or dyspnoea, and his cardiac function remained stable. Three sets of blood cultures with one anaerobic bottle and one aerobic bottle each were collected before initiating empiric antibiotics, with two of the anaerobic bottles growing Escherichia coli 48 hours after incubation. As the patient’s troponin I normalised 4 days later (0.02 ng/mL), without ST segmental changes or wall abnormalities on point-of-care ultrasonography, coronary angiography was not performed. Upon recovery, the patient was referred to our department for further evaluation to clarify the aetiology of cardiac injury. Single-photon emission computed tomography (CT) revealed perfusion defects in the inferior and inferolateral walls, reverse redistribution, and transient dilatation (Figure 1A). The coronary artery calcium score was calculated as low risk, but a hyperdense linear image at the level of the left ventricular (LV) lateral wall was observed (Figure 1B). Cardiac CT angiography (CCTA) was performed, in which Coronary Artery Disease Reporting and Data System 1 was observed (Figure 1C), with LV lateral wall calcification in axial slices (Figure 1D). Three-dimensional reconstruction showed a partial absence of thickness of the LV lateral wall in relation to the calcified tissue (Figure 1E).