Systemic thromboembolism from a misdiagnosed non‑bacterial thrombotic endocarditis in a patient with lung cancer: A case report

Figures

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  Figure 1.. Baseline CT scan. (A and B) Thoracic CT scan showed a mass in the lower lobe of the right lung, with ipsilateral ilo-mediastinal (subcarinal) and right infra-clavear pathological lymph nodes. (C and D) Abdominal CT scan documented signs of previous, non-datable multiple splenic and renal infarctions (white arrows), likely attributable to an acute/subacute phase of infarction.

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  Figure 2.. Baseline brain MRI. (A-C) Multiple patchy foci of diffusion restriction in the grey matter of the occipital lobes, consistent with acute cerebral infarcts. The multiple patchy foci affected not only the distal territories of the both posterior cerebral arteries but also innumerable tiny foci restricted diffusion in the deep cerebral white matter. (D-F) Star field pattern characteristic of cerebral embolism syndrome. (C and F) Moderate patchy and gyriform enhancement (sign of subacute cerebral infarcts) were evidenced after gadolinium administration. (A and D) Diffusion weighted imaging. (B and E) Apparent diffusion coefficient maps. (C and F) T1-w post gadolinium administration images. (G and H) Overview of the multiple ischemic infarcts as (G) FSE and (H) FLAIR hyperintensities in T2-w images. (I) Susceptibility weighted imaging showed several tiny blooming hypointense foci throughout the hemispheric grey and white matters, characteristic of microbleeds secondary to cerebral embolism syndrome.

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  Figure 3.. Morphological and immunohistochemistry diagnosis of large-cell carcinoma of the lung. (A) Hematoxylin and eosin staining documenting malignant large pleomorphic cells with a moderate to abundant amount of cytoplasm, vesicular nuclei, prominent nucleoli and necrosis. IHC staining of (B) TTF1 and (C) p40 revealed expression of the two markers on pneumocytes (TTF1) and basal cell (p40) only, thus supporting the diagnosis of large-cell carcinoma of the lung. The negativity of TTF1 and p40 precluded the diagnosis of lung adenocarcinoma or squamous cell carcinoma, respectively. Tumors lacked morphological and immunohistochemical evidence of glandular, squamous or neuroendocrine differentiation. (D) Programmed death-ligand 1 expression levels on the surface membrane of 55% of tumor cells. Magnification, (A-C) ×20 and (D) ×40. TTF1, transcription termination factor 1.

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  Figure 4.. Comparison of brain CT scans performed with ~20-days interval. (A and B) At hospitalization. (C, D and E) After 20 days. (A and C) Left antero-inferior cerebellar ischemic infarcts appeared more demarcated and bigger in the most recent exam (B), documenting a new ischemic lesion on the antero-inferior right cerebellar hemisphere in the acute phase of ischemia. (B and D) Bilateral occipital ischemic infarcts too appeared more demarcated and bigger. (E) Another new ischemic lesion in an acute phase was detected in the left postero-superior cerebellar hemisphere.

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  Figure 5.. Radiological and pathological evidence of bowel ischemia. (A and B) Abdominal CT scan performed at the acute onset of abdominal pain and loss of blood stool documented the occlusion of a distal branch of the superior mesenteric artery, accompanied by the thinning of the corresponding ileal loop (red arrows). (C) Hematoxylin and eosin staining at magnification, ×4 of the interface between the intestinal mucosa with hemorrhagic infarction (*on the left) and the wide superficial inflammation (#on the right). (D) Hematoxylin and eosin staining at magnification, ×4 of the mesenteric artery thrombosis in cause of the bowel ischemia.

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  Figure 6.. A transesophageal echocardiogram performed during the second hospitalization revealed a mobile echogenic mass of 0.8×0.6 cm on the atrial surface of the anterior leaflet of the mitral valve, moderate aortic insufficiency and reduced left ventricular ejection fraction by 40%.