A 19-year-old male youth has collapsed at home after complaining of fever and cough for a few days. A day before his demise, his father brought him to a nearby clinic where he was prescribed with fever and cough medications, including antibiotics. Unfortunately, his conditions did not improve, and he was found collapsed in the bathroom. He was immediately brought to a hospital where he was pronounced dead upon arrival at the emergency department. Later, he was brought to the forensic department for a medicolegal autopsy examination. Further history from the family members revealed that he was a healthy teenager with no known medical illness prior to the episode of cough and fever which later led to his premature demise.

Autopsy examination revealed a muscular and large-built male subject, measuring 184 cm in length and 82 kg in weight, with body mass index of 24.2 kg/m2. There was no injury or congenital deformity seen. Postmortem changes such as lividity and rigour mortis were present. Slight bluish discolouration of the lips and nail beds was present, indicating cyanosis. The oral cavity showed natural dentition with good oral hygiene. Internal examination of the skull and the brain showed intact skull and normal brain anatomy. Examination of the thoracic organs showed an intact pericardium, with minimal serous effusion. The heart weighed 475 g, denoting cardiomegaly. There was bulging anterior surface, upper part of the left ventricle observed, which was soft and slightly fluctuant on pressure. Cut section of the heart revealed large vegetations appearing like irregular nodular lesions affecting the left and right coronary cusps of the aortic valve (Fig. 1a). The largest vegetation measured 2 cm × 2 cm, completely disrupting the left coronary cusp. The right coronary cusp mainly displayed ulceration, thickening, and small nodules, as a result of direct spread of the lesion from the adjacent cusp. The non-coronary cusp of the aortic valve was sightly affected, exhibiting a small fibrotic nodule. Further examination of the vegetations at the left coronary cusp revealed a mobile lesion with a necrotic and hollow underneath the area, appearing like a cavity, hidden by the large vegetations (Fig. 1b). The cavity which was present within the left ventricular wall measured 3 cm × 2.5 cm × 1 cm, containing blood clots. The course of the cavity was determined to be at the periannular region and contained within the myocardium. It did not rupture to the epicardial surface. Blood clots which were removed from the cavity weighed approximately 10 g. These findings were consistent with left ventricular pseudoaneurysm, a rare complication of infective endocarditis. The coronary arteries were patent. Subendocardial fibrosis was prominent at the left ventricle. The myocardium surrounding the lesion also appeared soft and haemorrhagic, in keeping with acute myocardial infarction. Examination of the other internal organs such as the lungs, liver, spleen, kidneys, and intestines generally showed congestion, with no gross pathology observed.

Fig. 1
figure 1

A Cut section of the left ventricle of the heart shows a large, mobile vegetations affecting the left coronary cusp of the aortic valve (arrow). The right coronary cusp is slightly affected. B There is a hollow area within the myocardium beneath the vegetations, with an ulcerated opening (arrow). C Cut section of the bulging epicardial surface of the left ventricle revealed large amount of blood clots within the myocardium (arrow). D The pseudoaneurysm contains blood clots and impinges on the coronary artery. The surrounding myocardium is hemorrhagic and soft in consistency, in keeping with acute myocardial infarction (arrows)

Several postmortem specimens were obtained for laboratory investigations. Forensic toxicology analysis showed negative results for alcohol and common drugs, from both the blood and urine samples. Rapid test antigen and polymerase chain reaction (PCR) for COVID-19 were negative. Other infectious disease screening also showed negative results for human immunodeficiency virus (HIV) and hepatitis B and C. Blood and lung tissue specimens were sent for microbiology examination as part of a septic work-up in view of the fever and respiratory symptoms. The results of blood culture showed no growth for both aerobic and anaerobic microorganisms. Culture of the vegetations specimen yielded growth of Granulicatella adiacens sp. anti-streptolysin O titre (ASOT) was 400 IU/mL and reported as positive.

Representative tissue samples from the cardiac lesions were obtained for histology and stained with haematoxylin and eosin (H&E) stains. Microscopically, there are areas of complete destruction of the myocardial layer of the heart wall, beneath the valve. These are covered by fibrofatty tissue that undergoes extensive granulation, haemorrhage with acute and chronic inflammatory cell infiltrations. It subsequently forms a tamponade and therefore architecturally constitutes a formation of a pseudoaneurysm. An extensive haemorrhage is seen in one area of the pseudoaneurysm wall, indicating a rupture. The attached valve tissues are mainly fibrotic and myxomatous with many areas showing necrosis. It is mainly covered by fibrin deposits, infiltrated by mostly acute inflammatory cells with some forming exudates. There fibrin deposits or vegetations are present continuously throughout the internal surface of the pseudoaneurysm lining, which are also mainly infiltrated by neutrophils (Fig. 2). Special stains performed on the sections, namely Ziehl-Neelsen for acid fast bacilli, Grocott’s methenamine silver stain for fungal bodies, and Giemsa and Gram stains for bacterial colonies, show no specific infective agent present.

Correlating the autopsy findings and the laboratory investigation results, the cause of death was certified as aortic valve infective endocarditis complicated with periannular haemorrhage, secondary to pseudoaneurysm.

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