Wunderlich Syndrome: Wonder What It Is.

Wunderlich syndrome (WS) refers to spontaneous renal or perinephric hemorrhage occurring in the absence of known trauma. WS is much less common than hemorrhage occurring after iatrogenic or traumatic conditions. Lenk's triad of acute onset flank pain, flank mass, and hypovolemic shock is a classic presentation of WS but seen in less than a quarter of patients. The majority of patients present only with isolated flank pain and often imaged with an unenhanced CT in the emergency department. The underlying etiology is varied with most cases attributed to neoplasms, vascular disease, cystic renal disease and anticoagulation induced; the etiology is often occult on the initial exam and further evaluation is necessary. Urologists are familiar with this unique entity but radiologists, who are more likely to be the first to diagnose WS, may not be familiar with the imaging work up and management options. In the last decade or so, there has been a conspicuous shift in the approach to WS and thus it will be worthwhile to revisit WS in detail. In our review, we will review the multimodality imaging approach to WS, describe optimal follow up and elaborate on management.

Clinical characteristics and outcomes of splenic infarction in cancer patients: a retrospective, single center report of 206 cases.

Cancer patients have a high risk of thromboembolic events including splenic infarct (SI). However, risk factors for SI in cancer patients are poorly understood, and the utility of systemic anticoagulation in such patients is uncertain. We performed a retrospective cohort study of all cancer patients with SI treated at Yale New Haven Hospital from 2008 to 2017. Central review of radiology imaging was performed to confirm the diagnosis of SI. Baseline differences in variables among patients with and without recurrent SI were compared using Fisher's exact test, Pearson's χ2 test, and t-test. Multivariable regression models were conducted to identify factors associated with recurrent SI. Of 206 patients with cancer and SI, 42 had a prior venous thromboembolic event, while 29 had atrial fibrillation/flutter. At a median follow-up of 11.4 months (range: 0-142.3 months), 152 patients underwent follow-up imaging, with only 6 having recurrent SI. The use of anticoagulation after initial SI was associated with a nonsignificant increase in recurrent SI (p = 0.054) and was not associated with development of venous thromboembolism after SI (p = 0.414). In bivariate analyses, the risk of recurrent SI showed a significant association with lower platelet counts (p < 0.001) and with atrial fibrillation/flutter (p = 0.036). In a multivariable logistic regression model, no variables were identified that were associated with a higher risk of recurrent SI. SI in cancer patients is typically an isolated event with low recurrence risk. Anticoagulation use should be guided by other thromboembolic risk factors.

Villification in the mouse: Bmp signals control intestinal villus patterning.

In the intestine, finger-like villi provide abundant surface area for nutrient absorption. During murine villus development, epithelial Hedgehog (Hh) signals promote aggregation of subepithelial mesenchymal clusters that drive villus emergence. Clusters arise first dorsally and proximally and spread over the entire intestine within 24 h, but the mechanism driving this pattern in the murine intestine is unknown. In chick, the driver of cluster pattern is tensile force from developing smooth muscle, which generates deep longitudinal epithelial folds that locally concentrate the Hh signal, promoting localized expression of cluster genes. By contrast, we show that in mouse, muscle-induced epithelial folding does not occur and artificial deformation of the epithelium does not determine the pattern of clusters or villi. In intestinal explants, modulation of Bmp signaling alters the spatial distribution of clusters and changes the pattern of emerging villi. Increasing Bmp signaling abolishes cluster formation, whereas inhibiting Bmp signaling leads to merged clusters. These dynamic changes in cluster pattern are faithfully simulated by a mathematical model of a Turing field in which an inhibitor of Bmp signaling acts as the Turing activator. In vivo, genetic interruption of Bmp signal reception in either epithelium or mesenchyme reveals that Bmp signaling in Hh-responsive mesenchymal cells controls cluster pattern. Thus, unlike in chick, the murine villus patterning system is independent of muscle-induced epithelial deformation. Rather, a complex cocktail of Bmps and Bmp signal modulators secreted from mesenchymal clusters determines the pattern of villi in a manner that mimics the spread of a self-organizing Turing field.