Assessing the Impact of Inflammatory Markers and CT Severity Score on Disease Severity of COVID-19 Patients Admitted to ICU at a Tertiary Hospital.

BACKGROUND: In December 2019, SARS-COV-2 infection emerged in Wuhan, China causing COVID-19 and subsequently spread throughout the globe. A great uncertainty is associated with the disease progression, as the risk of severe COVID-19 is not uniform among all the patients. Systemic inflammation has been reported as a predictor for COVID-19 outcomes. Elevated levels of inflammatory markers are shown to be associated with endothelial dysfunction, cytokine storm and coagulopathy in COVID-19. There is a growing body of evidence, that these findings exert influence in the causation of mortality in patients with severe Covid-19. The present study is carried out with an aim to evaluate the clinical outcomes of patients by interrelating their clinical severity with inflammatory markers and CT (Computed tomography) severity score (CTSS). OBJECTIVES: The aim of the study is to correlate COVID-19 severity with inflammatory markers and CT severity score. We also aim to determine the optimal cut-off values for inflammatory markers and CT severity scores in order to establish their interrelationship to the disease severity. MATERIALS AND METHODS: It is a hospital-based retrospective observational study. The study was conducted over a period of four months (July 2020 to October 2020) based on data obtained from the records of patients, admitted with a laboratory confirmed SARS-COV-2 infection. The current study included a total of 84 patients, admitted to ICU with the severe COVID-19.Study tools included serum CRP, serum ferritin, D-dimer, neutrophil-to-lymphocyte ratio (NLR), interleukin-6 (IL-6) and 25-point CT severity score obtained from HRCT (high resolution computerized tomography) chest. RESULTS: Out of 84 patients recruited, 54 patients were survivors and 30 patients were non-survivors (deceased). 78% of the study population was male and 22% was female. For survivors, average CTSS was 12.43 ± 5.7 and whereas average CTSS for non-survivors was 18.87 ± 4.68(p<0001). Average D-dimer was 2.5 ± 1.43 in the survivor group and 3.39 ± 0.95 for non-survivors (p<0.004). Correlation coefficient of CTSS with FiO2 is 0.685 (p<0.0001). The optimal cut-off value for predicting mortality for D-dimer is >2.4 (p<0.0012) and for CTSS is >15 (p<0.0001). CONCLUSION: The disease severity was significantly correlated with CTSS and D- dimer. Severe COVID-19 was also associated with a high NLR (neutrophil to lymphocyte ratio) and moderately elevated inflammatory markers (CRP, Ferritin, IL-6). CTSS >15 and D-dimer >2.4 correlate strongly with mortality. CTSS has the greatest diagnostic accuracy for stratifying the disease severity and predicting the mortality among the markers/ characteristics compared.

Comparing outcomes between patients transferred from a critical access hospital versus directly from scene to a level 1 trauma center.

OBJECTIVES: The aim of this retrospective study was to compare the outcomes of trauma patients directly transported to a level I trauma center (SCENE) versus those who were stabilized at a critical access hospital (CAH) and subsequently transferred. METHODS: Patients were grouped based on their transfer status, interventions performed at CAH and outcomes. Google Maps was used to calculate the distances from the location of injury (LOI). Each transfer group data was analyzed separately to examine associations of different factors on the outcomes. Outcomes were compared using univariate and multivariate analyses and propensity score matching analysis. RESULTS: There were 262 patients in SCENE and 684 in CAH. Compared to SCENE, CAH had higher rates of blunt injury and a greater distance from LOI, whereas lower ISS score and length of stay (LOS) (p < 0.05). The majority of CAH group survived compared to SCENE (p = 0.007). For both groups, baseline factors (e.g., age) were associated with outcomes (p < 0.05). Interestingly, longer LOS in the CAH was associated with an increase in survival (p = 0.009), whereas an increased number of CT/MRI performed was associated with increased LOS (p < 0.05)., and an increased number of procedures was associated with longer LOS and ICU stay (p < 0.05). After matching, the two groups had no significant differences in survival, LOS, or ICU stay (p > 0.05). CONCLUSION: Equivalent overall clinical outcomes were seen in both groups, suggesting that existing trauma system protocols in the West Texas region are functioning well to select appropriate patients for each transfer modality. LEVEL OF EVIDENCE III: Retrospective Analysis.

Clitoral Priapism in a Transgender Male.

INTRODUCTION: Clitoral priapism due to venous outflow obstruction is a rare event and medical emergency. Androgen-induced clitoromegaly in transgender men has not been previously identified as a risk factor. AIMS: Advance current knowledge on identification and treatment of clitoral priapism in the transgender male. METHODS: A 32 year-old presurgical transgender male underwent gender-affirming laparoscopic total hysterectomy and bilateral salpingo-oöphorectomy without incident. Seven days postop, he developed progressive and painful clitoral engorgement that was persistent. Examination and imaging were consistent with clitoral priapism. RESULTS: Clitoral priapism was treated with adrenergic drugs (imipramine and pseudoephedrine) with rapid resolution of symptoms. CONCLUSION: Clitoral priapism is a rare phenomenon usually associated with use of a psychotropic medication. Whether clitoromegaly secondary to androgen administration in transgender men is a risk factor for this rare medical emergency is unknown. Prompt recognition and treatment is paramount. Kusko RE, Singhal E, Kauffman RP. Clitoral Priapism in a Transgender Male. Sex Med 2021;9:100431.

An FGF21-adiponectin-ceramide axis controls energy expenditure and insulin action in mice.

FGF21, a member of the fibroblast growth factor (FGF) superfamily, has recently emerged as a regulator of metabolism and energy utilization. However, the exact mechanism(s) whereby FGF21 mediates its actions have not been elucidated. There is considerable evidence that insulin resistance may arise from aberrant accumulation of intracellular lipids in insulin-responsive tissues due to lipotoxicity. In particular, the sphingolipid ceramide has been implicated in this process. Here, we show that FGF21 rapidly and robustly stimulates adiponectin secretion in rodents while diminishing accumulation of ceramides in obese animals. Importantly, adiponectin-knockout mice are refractory to changes in energy expenditure and ceramide-lowering effects evoked by FGF21 administration. Moreover, FGF21 lowers blood glucose levels and enhances insulin sensitivity in diabetic Lep(ob/ob) mice and diet-induced obese (DIO) mice only when adiponectin is functionally present. Collectively, these data suggest that FGF21 is a potent regulator of adiponectin secretion and that FGF21 critically depends on adiponectin to exert its glycemic and insulin sensitizing effects.