PMC4772616_01
Proposed mechanism of PTTM. Microscopic tumor emboli due to disease progression release cytokines and growth factors (e.g., VEGF and PDGF) leading to coagulopathy and vascular remodeling. The latter is responsible for pulmonary hypertension. The involvement of VEGF and PDGF justifies or supports treatment with a tyrosine kinase inhibitor like sunitinib that inhibits VEGF and PDGF pathways.
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F2
PE, these coagulation abnormalities were highly suggestive of a PTTM diagnosis. PTTM is distinct from simple embolic obstruction because it is characterized by (1) the systemic activation of coagulation with the generation of intravascular fibrin and the consumption of procoagulants, leading to a disseminated intravascular coagulation-like picture, present in this case and (2) remodeling of the pulmonary vasculature due to expression of VEGF and PDGF from embolic tumor cells (see fig. 2).
CT of the lungs demonstrates diffuse ground-glass attenuation, bilateral effusions, and scattered pulmonary nodules. The yellow arrows show prominent interlobular septal thickening.
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F3
Chest CT, which had been clear on admission, revealed interlobular septal thickening, diffuse ground-glass attenuation, and bilateral effusions (fig. 3).