Splenic Artery Syndrome (SAS) has emerged as a controversial cause for graft ischemia in orthotopic liver transplant (OLTx) recipients. A complex combination of factors including hepatic artery hypoperfusion and portal hyperperfusion can result in SAS. Clinical and laboratory findings suggest graft ischemia but are generally non-specific. Conventional angiography findings of hepatic artery hypoperfusion with early and rapid filling of the splenic artery are suggestive of the diagnosis in the appropriate clinical setting. Treatment involves proximal splenic artery embolization, surgical splenic artery ligation, or in extreme cases, splenectomy. Most patients with SAS improve clinically following treatment. However, no randomized control trials are available to compare treatment options. Identification of at risk patients with pre-operative CT scans and intra-operative ultrasound has been proposed by some and may allow for prophylactic treatment of SAS.
HighlightsPylephlebitis is a morbid complication of intra-abdominal inflammation.Diagnosis requires high-resolution imaging and bacteremia.Management consists of antibiotic and anticoagulation therapy.
Activation of blood coagulation pathways as a component of an allergic response has been studied in animal models. In patients with allergic diseases, clot qualities have been noted to be different in terms of denser fibrin clot with reduced plasmin-mediated clot lysis. Correlation between occupational hypersensitivity pneumonitis (HP) with thromboembolic events is scarce in the general patient population. We present a case of a 52-year-old man with recurrent venous thromboembolism with HP secondary to bioaerosol exposure in a compost plant. Biochemical evaluation found no evidence of underlying hypercoagulable state, with only remarkable findings of elevated levels of total serum immunoglobulin E and raised Aspergillus sp. IgG antibodies. The patient decided to change his working environment to one without exposure to compost or other fungal elements. His symptoms and pulmonary function tests gradually improved without any subsequent intervention. The patient chose against the advice of his care providers to discontinue warfarin anti-coagulation that had been recommended for lifelong duration after recurrent pulmonary thromboembolism. At a 4-year follow-up he has remained free of any further episodes of venous thromboembolic events without any anti-coagulation. Repeated imaging studies after cessation of exposure demonstrated clearance of multiple lung nodules and improvement in DLco.
Purpose Although MRI identification of new lesions forms the basis for monitoring disease progression in multiple sclerosis patients, how lesion activity relates to longitudinal white matter changes in the brain is unknown. We hypothesized that patients with gadolinium-enhancing lesions would show greater longitudinal decline in fractional anisotropy in major tracts compared to those with stable disease. Methods Thirty patients with relapsing-remitting multiple sclerosis were included in this study – 13 had enhancing lesions at baseline and 17 did not. Each patient underwent at least two 3 Tesla contrast-enhanced MRI scans with a DTI sequence and a median interval of 2.1 years between scans. The forceps major and minor of the corpus callosum and the bilateral corticospinal tracts were selected as the major white matter tracts-of-interest. These tracts were reconstructed using region-of-interest placement on standard anatomical landmarks and a fiber assignment by continuous tracking algorithm using TrackVis (version 0.5.2.2) software. Mixed-effects regression models were used to determine the association between enhancing lesions and subsequent longitudinal change in fractional anisotropy. Results In patients with enhancing lesions, there was greater decline in fractional anisotropy compared to those with stable disease in the forceps major (p=0.026), right corticospinal tract (p=0.032), and marginally in the left corticospinal tract (p=0.050), but not the forceps minor (p=0.11). Conclusion Fractional anisotropy of major white matter tracts declined more rapidly in patients with enhancing lesions, suggesting greater diffuse white matter injury with active inflammatory disease. DTI may provide a means of monitoring white matter injury following relapses.
Chimeric antigen receptor (CAR) T cells targeting the CD19 (cluster of differentiation 19) cell surface glycoprotein have emerged as a highly effective immunologic therapy in patients with relapsed or refractory B‐cell malignancies. The engagement of CAR T cells with CD19 on the surface of neoplastic B cells causes a systemic cytokine release, which can compromise the blood‐brain barrier and cause an immune effector cell‐associated neurotoxicity syndrome (ICANS). In a small proportion of ICANS patients who demonstrate neuroimaging abnormalities, certain distinct patterns have been recognized, including signal changes in the thalami, external capsule, and brainstem, the subcortical and/or periventricular white matter, the splenium of the corpus callosum, and the cerebellum. On careful review of the underlying pathophysiology of ICANS, we noticed that these changes closely mirror the underlying blood‐brain barrier disruption and neuroinflammatory and excitotoxic effects of the offending cytokines released during ICANS. Furthermore, other uncommon complications of CD19 CAR T‐cell therapy such as posterior reversible encephalopathy syndrome, ocular complications, and opportunistic fungal infections can be catastrophic if not diagnosed in a timely manner, with neuroimaging playing a significant role in management. In this narrative review, we will summarize the current literature on the spectrum of neuroimaging findings in ICANS, list appropriate differential diagnoses, and explore the imaging features of other uncommon central nervous system complications of CD19 CAR T‐cell therapy using illustrative cases from two tertiary care institutions.
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