Background
Diabetic ketoacidosis (DKA) patients present with low serum bicarbonate (HCO3−${\rm{HCO}}_{3}^{-} $), and an increase in its level to ≥15 mEq/L is considered one of the criteria for DKA resolution. Both proton pump inhibitors and histamine‐2 receptor antagonists inhibit downstream functioning of H+/K+ ATPase in the gastric parietal cells, which results in the decreased secretion of HCO3−${\rm{HCO}}_{3}^{-} $ into the bloodstream.
Objectives
We aimed to introduce the hypothesis that DKA patients on acid‐suppressive medications may have a delayed rise in serum HCO3−${\rm{HCO}}_{3}^{-} $ to >15 mEq/L that may cause increased hospital length of stay (LOS) and sought to compare the outcomes of such patients. For the sake of simplicity, conditions requiring acid suppression are grouped under the term peptic ulcer disease (PUD) in this study.
Methods
This is a retrospective study using Nationwide Inpatient Sample employing International Classification of Diseases (ICD‐10) codes for adult patients with a primary diagnosis of DKA. Analyses were performed using STATA, proportions were compared using Fisher exact test, and continuous variables using Student's t‐test. Confounding variables were adjusted using propensity matching, multivariate logistic, and linear regression analyses.
Results
DKA patients with PUD had higher adjusted LOS, intensive care unit admission, and total hospital costs. Mortality and morbidity indicators were similar in both groups. The variables found to be independent predictors of increased LOS were malnutrition, Clostridium difficile infection, pneumonia, Glasgow Coma Scale score of 3–8, and higher Charlson comorbidity score.
Conclusion
We found that Clostridium difficile and pneumonia predicted longer LOS in DKA patients with concomitant PUD, hinting at the possible role of acid suppression in prolonging the LOS in such patients. However, further studies are needed to examine the effect of lesser HCO3−${\rm{HCO}}_{3}^{-} $ generation on LOS.
Background and aimAnticoagulation use for portal vein thrombosis (PVT) in patients with advanced liver disease is controversial. We investigated the effect of anticoagulation on outcomes in patients with PVT with cirrhosis.MethodsWe reviewed National Inpatient Sample data from 2016 to 2018 to identify patients with PVT. Our outcomes were in-hospital mortality, variceal bleeding, hepatic encephalopathy, acute kidney injury (AKI), hepatorenal syndrome (HRS), spontaneous bacterial peritonitis (SBP), sepsis and hospital resource utilisation.ResultsWe included 60 505 patients with PVT, out of whom 6.63% (4015) were on anticoagulation. The overall mortality in the anticoagulation group was 2.12% compared with 9.72% in the no anticoagulation group. The adjusted odds of mortality were low in the anticoagulation group (adjusted OR (AOR) 0.27, 95% CI 0.15 to 0.46, p<0.001). Patients on anticoagulation had 29% lower odds of variceal bleeding (AOR 0.71, 95% CI 0.53 to 0.96, p=0.03). Lower odds of HRS (AOR 0.56, 95% CI 0.37 to 0.85, p=0.01) and AKI (AOR 0.57, 95% CI 0.48 to 0.69, p<0.001) were also seen in the anticoagulation group. Patients in the anticoagulation group also showed lower odds of SBP (AOR 0.62, 95% CI 0.43 to 0.89, p=0.01) and sepsis (AOR 0.57, 95% CI 0.35 to 0.93, p=0.03). Anticoagulation use resulted in shorter hospital stay by 1.15 days (adjusted length of stay −1.15, 95% CI −1.51 to –0.79, p<0.001). The mean difference in total hospital charges between the anticoagulation and the no anticoagulation group was −$20 034 (95% CI −$27 077 to −$12 991, p<0.001).ConclusionOur analysis found that anticoagulation use is safe and associated with better outcomes in patients with PVT with advanced liver disease.
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