Role of secondary sepsis in COVID-19 mortality: Observations on patients with preexisting diabetes mellitus and newly diagnosed hyperglycemia.

Diabetics who develop severe acute respiratory syndrome coronavirus 2 (SARS CoV-2) are more likely to have severe disease, higher odds of intensive care requirement and mortality. Fifteen percent of patients have new onset hyperglycemia. We studied the comparative outcomes between prior DM, newly detected hyperglycemia and assessed role of secondary sepsis on mortality. RWe performed a r etrospective study of confirmed SARS-CoV-2 patients at a tertiary care hospital in Chennai, India. Patients were divided as 2 groups (Group 1: With preexisting diabetes mellitus, Group 2: With newly diagnosed hyperglycemia due to newly detected diabetes mellitus or non-diabetic hyperglycemia. Clinical and laboratory data was analysed. Two hundred and thirty eight patients had prior-diabetes mellitus (Group 1) and 40 had newly diagnosed hyperglycemia (Group 2). Thirty four of group 1 and 7 of group 2 patients required intensive care. Mean capillary blood glucose (MCBG) during hospital stay was 207 mg/dl (Group 1) and 192 mg/dl (Group 2). Twentysix patients (9.3%) had secondary sepsis of which sixteen died. Logistic regression identified secondary sepsis(p<0.0001), elevated D-dimer >6 fold (p= 0.0001), elderly p=0.0045), male (p=0.0006), NLR >5 (p=0.01),serum creatinine ≥2 mg/dl (p=0.0004), FiO2 requirement >0.6 in first 48 hours (p=0.001) as mortality predictors.Our study observed a 14.38 % prevalence of newly diagnosed DM or non-diabetic hyperglycemia. Secondary sepsis and >6 fold elevation in D-dimer were strong predictors of mortality. Steroid use possibly contributed to secondary sepsis. Early identification and aggressive management of secondary sepsis are necessary for diabetics.

Comparison of Fasting Insulin Level, Homeostatic Model of Insulin Resistance, and Lipid Levels between Patients with Primary Hypertension and Normotensive Subjects.

BACKGROUND: Hyperinsulinemia and insulin resistance occurs in obese patients with primary hypertension independent of diabetes and obesity. This study was aimed at assessing serum fasting insulin levels, the homeostatic model assessment for insulin resistance (HOMA-IR), and serum lipid levels in non-obese patients with primary hypertension when compared to normotensive subjects. METHODS: This observational study comprised 100 patients over 18 years of age, divided into two groups. The hypertensive group comprised non-obese patients with primary hypertension (n=50); the normotensive group comprised normotensive age- and sex-matched individuals (n=50). Patients with diabetes, impaired fasting glucose, obesity, and other causative factors of insulin resistance were excluded from the study. Serum fasting insulin levels and fasting lipid profiles were measured, and insulin resistance was calculated using HOMA-IR. These data were compared between the two groups. Pearson's correlation coefficient was used to assess the extent of a linear relationship between HOMA-IR and to evaluate the association between HOMA-IR and systolic and diastolic blood pressures. RESULTS: Mean serum fasting insulin levels (mIU/L), mean HOMA-IR values, and fasting triglyceride levels (mg/dL) were significantly higher in the hypertensive versus normotensive patients (10.32 versus 6.46, P<0.001; 1.35 versus 0.84, P<0.001; 113.70 versus 97.04, P=0.005, respectively). The HOMA-IR levels were associated with systolic blood pressure (r value 0.764, P=0.0005). CONCLUSION: We observed significantly higher fasting insulin levels, serum triglyceride levels, and HOMA-IR reflecting hyperinsulinemia and possibly an insulin-resistant state among primary hypertension patients with no other causally linked factors for insulin resistance. We observed a significant correlation between systolic blood pressure and HOMA-IR.

Rare Presentation of Isolated Spontaneous Bacterial Empyema without Concomitant Ascites in a Patient with Cirrhosis.

In decompensated cirrhosis, massive ascites and pleural effusion (hepatic hydrothorax) can be complicated by infection, which manifests either as spontaneous bacterial peritonitis (SBP) or spontaneous bacterial empyema (SBE). SBE is a distinct and often underdiagnosed complication having different pathogenesis and treatment strategy when compared with parapneumonic empyema. Hepatic hydrothorax in the absence of ascites is rare in patients with cirrhosis. The occurrence of SBE without SBP or ascites is even more of a rarity in cirrhosis and carries great morbidity and mortality. Here we report a case of an elderly female patient with cirrhosis (Child-Pugh Class B) who had unusual features of isolated right-sided hepatic hydrothorax without clinically evident ascites and was later diagnosed as having SBE based on imaging of the thorax, pleural fluid analysis, and cultures. The patient was initially treated conservatively with antibiotics, and diuretics, and later pigtail insertion and drainage was done.

Course of COVID-19 Based on Admission D-Dimer Levels and Its Influence on Thrombosis and Mortality.

BACKGROUND: Arterial and venous thrombosis is one of the major complications of coronavirus disease 2019 (COVID-19) infection. Studies have not assessed the difference in D-dimer levels between patients who develop thrombosis and those who do not. METHODS: Our study retrospectively assessed D-dimer levels in all virus confirmed hospitalized patients between May to September, 2020. Patients were divided into three groups: group 1 with normal D-dimer of < 0.5 µg/mL, group 2 with elevation up to six folds, and group 3 with more than six-fold elevation. Statistical analysis was done using SPSS software 23.0. RESULTS: Seven hundred twenty patients (group1 (n = 414), group 2 (n = 284) and group 3 (n = 22)) were studied. Eight thrombotic events were observed. Events were two with stroke, two non-ST elevation myocardial infarction and one each of ST elevation myocardial infarction, superior mesenteric artery thrombosis with bowel gangrene, arteriovenous fistula thrombus and unstable angina. No significant difference (P = 0.11) was observed between median D-dimer levels among patients who developed thrombosis (1.34) and those who did not develop thrombosis (0.91). Twenty-nine patients died. The adjusted odds of death among those with a six-fold or higher elevation in D-dimer was 128.4 (95% confidence interval (CI): 14.2 - 446.3, P < 0.001), while adjusted odds of developing clinical thrombosis was 1.96 (95% CI: 0.82 - 18.2, P = 0.18). CONCLUSIONS: Our study observed a 1.1% in-hospital incidence of clinical thrombosis. While, a six-fold elevation in D-dimer was significantly associated with death; the same was not a strong predictor of thrombosis; an observation which implies that dose of anticoagulation should not be based on absolute D-dimer level.