Facebook posts compete for human attention in a zero-sum game; this makes it a challenge for government organizations to engage with their citizens through this medium. In a large-scale longitudinal study we investigate what makes Facebook posts popular (seen by many) and effective (commented, liked, or shared by many) in a nonprofit context: the official Facebook page of a midsized city (Oulu, Finland). We model the competition dynamics that shape the fate of Facebook posts using Structural Equation Modeling. Our analysis reveals that audience demographics, the timing of posts, and the media type of post are significant factors in post reach and effectiveness, and argue that our method can be applied to other contexts to determine which factors can lead to improved government-citizen communication and engagement. Finally, we argue for more actionable research to be conducted on the use of social media by government.
Hyperosmolar Hyperglycemic State (HHS) and Diabetic Ketoacidosis (DKA) are associated with decompensated Diabetes mellitus. On many instances' patients may present with a mixed picture of both conditions. This acute decompensation may result from infarction, medication noncompliance, or infections. With DKA and HHS, hemoconcentration is common due to dehydration. Many nonspecific enzyme values maybe elevated with these conditions, which may cause other underlying pathologies to go unnoticed. Here we report a case of post-COVID HHS/DKA with elevated lipase and features of pancreatitis.CASE PRESENTATION: 52-year-old African-American female with obesity and Type two diabetes presented with nausea, abdominal pain and dizziness of 1 day. She was in the recovery stages of COVID, past 10 days since her diagnosis at the time of admission. She stated that due to altered taste sensation, likely COVID symptom, she was not eating properly, drinking more caffeinated beverages, and less water. Her glucose was >1000 mg/dl, creatinine 1.7, anion gap > 31, elevated betahydroxybutyrate, minimal urine ketones and a bicarb of 13 on admission. Her lipase was >2000 and Amylase >1000. Lab values along with abdominal pain was enough to consider underlying pancreatitis. At that time both DKA/HHS and acute pancreatitis required aggressive fluid hydration, but the patient continued to deteriorate. Fear of fluid overload with tachypnea, along with continued abdominal pain requiring pain medications produced a 'catch 21' with her respiratory status. Ultrasound of the abdomen was unremarkable. CT abdomen did prove acute pancreatitis. Triglycerides were not elevated enough to be the culprit of pancreatitis. She denied use of alcohol or other infections. She was however recovering from SARS-CoV2 infection (>10 days since diagnosis), which may have been the inciting factor for pancreatic inflammation. Her BISAPS score was 4; very severe form of acute pancreatitis with a high mortality risk.DISCUSSION: This case shows how DKA/HHS states can mask pancreatitis. This case also presents an interesting cause of her pancreatitis. Viral etiologies like mumps or coxsackie viruses are known instigators of acute pancreatitis. Given the lack of other etiologies, COVID-19 is likely the trigger to her symptoms. COVID has been known to be a precipitator of DKA in this last year, but little is known in its' involvement in acute pancreatitis. One theory to link pancreatitis to decompensated diabetic states with COVID is cytokine mediated damage to the pancreatic beta cells, causing inflammation of the pancreas and worsening glycemic control precipitating DKA or HHS.CONCLUSIONS: An association of AP with DKA or HHS increases the risk of mortality. It's a rare phenomenon for SARS-Cov2 infection as the provoking factor. More studies should be done on the link of decompensated DM with AP, and how these conditions are affected by COVID-19.
INTRODUCTION: One of the major complications of diabetes mellitus includes hypercoagulability due to platelet hyperactivity, coagulation activation, and hypofibrinolysis. Acute hyperglycemia is hypothesized to exacerbate the coagulation pathway by enhancing the activities of factor VII, VIII and tissue factor pathway inhibitor. The prothrombic state observed in diabetic ketoacidosis (DKA) is due to endothelial activation, augmented activity of platelets, and increased concentration of von Willebrand factor. In the case of inflammatory bowel disease (IBD), however, thrombotic events occur due to an increase in coagulation factors including factor V, VII, VIII, prothrombin, and the thrombin-antithrombin complex. Other studies have noted that the decrease in factor XIII in active Crohn's disease is related to consumption of factor XIII in forming microthrombis. We are presenting a unique case of a STEMI that was provoked by the presence of two hypercoagulable disorders, IBD and DKA. CASE PRESENTATION:The patient is a 41-year-old male with significant PMH of type I diabetes mellitus complicated by gastroparesis and multiple admissions for diabetic ketoacidosis, as well as Crohn's disease not on immunosuppressive therapy. The patient presented with a chief complaint of intractable nausea, vomiting and diffuse, non-radiating abdominal pain. On admission, he was tachycardic, tachypneic, and normotensive. His laboratory studies were consistent with DKA. Abdominal X-ray showed fluid distension in the stomach, similar to previous CT abdomen findings, coinciding with his significant history of gastroparesis. EKG revealed ST elevations in leads II, III, aVF and V3-V6. He underwent a cardiac catheterization, which revealed thrombus in the proximal segment of the right coronary artery with no obvious underlying coronary artery disease. He underwent mechanical thrombectomy only, with no stent deployed. The patient was discharged with goal-directed medical therapy and to continue dual-antiplatelet therapy for one year.DISCUSSION: DKA can cause various complications including hypercoagulability. There are proposed hypotheses for risk of developing thromboembolic disease in both DKA and IBD. The patient had a significant history of recurrent admissions due to DKA with non-specific EKG changes. The patient in this case had a history of Crohn's disease, and was not on any immunosuppressive medications. If the patient's comorbidities had been better controlled, it is possible that the patient would not have suffered this STEMI. CONCLUSIONS:The patient had two hypercoagulable disorders that could have led to formation of the intracoronary thrombus. This case demonstrates the importance of management of chronic diseases and their effects on other organ systems.
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