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Background : : This study investigated the incidence and clinical outcomes of portal and hepatic vein thrombosis (VT) on imaging after transjugular intrahepatic portosystemic shunt (TIPS). Methods : : A retrospective review of records at a single liver transplant center between 2010 and 2018 revealed 423 patients who underwent TIPS. Contrast-enhanced computed tomography and magnetic resonance images within 1 year post-TIPS were available for 138 patients and compared to assess the imaging findings of VT and liver infarction. The associations of VT with overall survival, patient characteristics, stent size, pre- and post- TIPS Model for End-Stage Liver Disease (MELD) scores, and post-TIPS hepatic encephalopathy at 90 days were analyzed. Results : : The prevalence of VT on imaging within 1 year was 63.0% (n = 87). VT within the right portal vein was more common: 41 cases were in the right portal vein, 25 in the posterior portal vein, and two in the anterior right portal vein. Ten patients had VT in the left portal vein. Four had VT in the main portal vein (MPV), and one had shunt thrombosis extending into the superior mesenteric vein. Hepatic VT was seen in the right hepatic vein in 17 patients and in the middle hepatic vein in six patients. VT was associated with liver infarction (n = 9, P = 0.018). There was no relationship between VT and sex, age, cirrhosis etiology, indication for TIPS, stent size, or hepatic encephalopathy at 90 days. VT in the MPV had poorer survival (P < 0.001). Older age (P = 0.028) and higher pre-TIPS MELD score (P = 0.049) were poor prognostic factors. VT was not treated. Conclusion : : Portal and hepatic VTs were common imaging findings after TIPS without worsened clinical outcomes unless VT involved the MPV. VT may cause liver infarction, but infarcts were not independently associated with poorer survival.

Catheter-directed thrombolysis (CDT) for the treatment of acute pulmonary embolism (PE) has gained popularity in recent years, but potential complications during the procedure and their management are not frequently discussed in the literature. In this case report, we describe the clinical dilemma regarding the postoperative anticoagulation management of a 60-year-old male who developed cardiac perforation during a CDT of an acute saddle PE. Early resumption of systemic heparin in such cases may help in clot resolution; however, it can worsen the hemopericardium. On the other hand, delaying restarting heparin may help in healing of the cardiac perforation but can lead to clot propagation. As the chest tube output was minimal initially, anticoagulation was started, which, however, led to disastrous outcome. With limited published medical literature to help guide such a complex situation, it may be prudent to carefully weigh the risks and benefits of resuming systemic heparin versus delaying it for 1–2 days to allow for definitive resolution of the cardiac perforation.

The use of selective serotonin reuptake inhibitors (SSRIs) for the treatment of depression during pregnancy is suggested to increase the incidence of craniofacial abnormalities including craniosynostosis. Little is known about this mechanism, however based on previous data we propose a mechanism that affects cell cycle. Excessive proliferation, and reduction in apoptosis may lead to hyperplasia within the suture that may allow for differentiation, bony infiltration, and fusion. Here we utilized in vivo and in vitro analysis to investigate this proposed phenomenon. For in vivo analysis we used C57BL-6 wild-type breeders treated with a clinical dose of citalopram during the third trimester of pregnancy to produce litters exposed to the SSRI citalopram in utero. At post-natal day 15 sutures were harvested from resulting pups and subjected to histomorphometric analysis for proliferation (PCNA) and apoptosis (TUNEL). For in vitro studies, we used mouse calvarial pre-osteoblast cells (MC3T3-E1) to assess proliferation (MTS), apoptosis (Caspase 3/7-activity), and gene expression after exposure to titrated doses of citalopram. In vivo analysis for PCNA suggested segregation of effect by location, with the sagittal suture, showing a statistically significant increase in proliferative response. The coronal suture was not similarly affected, however there was a decrease in apoptotic activity at the dural edge as compared to the periosteal edge. No differences in apoptosis by suture or area due to SSRI exposure were observed. In vitro results suggest citalopram exposure increased proliferation and proliferative gene expression, and decreased apoptosis of the MC3T3-E1 cells. Decreased apoptosis was not confirmed in vivo however, an increase in proliferation without a concomitant increase in apoptosis is still defined as hyperplasia. Thus prenatal SSRI exposure may exert a negative effect on post-natal growth through a hyperplasia effect at the cranial growth sites perhaps leading to clinically significant craniofacial abnormalities.

Neurodevelopmental disorders can stem from pharmacological, genetic, or environmental causes and early diagnosis is often a key to successful treatment. To improve early detection of neurological motor impairments, we developed a deep neural network for data-driven analyses. The network was applied to study the effect of maternal nicotine exposure prior to conception on 10-day-old rat pup motor behavior in an open field task. Female Long-Evans rats were administered nicotine (15 mg/L) in sweetened drinking water (1% sucralose) for seven consecutive weeks immediately prior to mating. The neural network outperformed human expert designed animal locomotion measures in distinguishing rat pups born to nicotine exposed dams vs. control dams (87 vs. 64% classification accuracy). Notably, the network discovered novel movement alterations in posture, movement initiation and a stereotypy in “warm-up” behavior (repeated movements along specific body dimensions) that were predictive of nicotine exposure. The results suggest novel findings that maternal preconception nicotine exposure delays and alters offspring motor development. Similar behavioral symptoms are associated with drug-related causes of disorders such as autism spectrum disorder and attention-deficit/hyperactivity disorder in human children. Thus, the identification of motor impairments in at-risk offspring here shows how neuronal networks can guide the development of more accurate behavioral tests to earlier diagnose symptoms of neurodevelopmental disorders in infants and children.