Louisiana Via Research Day Book 2026

Case Studies: Section 2

Case Studies: Section 2

100 THE PITFALL OF LIGHT’S CRITERIA: VRE EFFUSION MASQUERADING AS TRANSUDATIVE EFFUSION

101 ACIDOSIS AFTER ANALGESIA: A RARE CASE OF CELECOXIB-INDUCED TYPE 1 RENAL TUBULAR ACIDOSIS

Shekhar Gurung, MD; Dipesh Upreti, MD; Binod Mehta, MD; Muhammad Rashid, MD St. Francis Medical Center, Department of Internal Medicine, Monroe, Louisiana

Shekhar Gurung, MD; Dipesh Upreti MD; Nisheem Pokharel, MD; Edward Cornell Pierce, MD St Francis Medical Center, Department of Internal Medicine, Louisiana

Context: Light’s criteria have been used as a gold standard initial test to differentiate between the transudative and exudative effusion. It relies on the fact that transudative effusions are caused by a change in body mechanics, such as the Starling force in heart failure, whereas exudative effusions are caused by inflammation or malignancy. Though light’s criteria are regarded as very sensitive to identify exudative effusion, they lack the specificity in about 30% of Heart failure-associated pleural effusion. Thus, identifying the etiology of pleural effusion should extend beyond the light’s criteria and focus more on identifying disease-specific markers, including cytology and culture. with reduced ejection fraction and COPD presented with a complaint of shortness of breath. He was hemodynamically stable at the time of presentation with unremarkable CBC, CMP, EKG, Troponin, Elevated BNP, and CT chest demonstrating pleural effusions with loculation on the left, without overt signs of infection. He was subsequently started Report of Case: A 78-year-old male with a past medical history of heart failure

on empiric antibiotics and underwent left sided thoracentesis, draining 2500 mL of cloudy, fibrinous, straw-colored fluid with radiographic resolution; a pigtail catheter was left in place. Pleural fluid analysis suggested a transudative effusion (pleural protein 2.4 g/dL, serum protein 5.4 g/dL, pleural LDH 57 U/L, serum LDH 174 U/L), though the macroscopic appearance was atypical; thus, the antibiotic was continued. Despite drainage, a repeat CT showed persistent effusions, thus requiring the repeat thoracentesis followed by pigtail placement and chemical decortication. The pleural fluid culture eventually showed the growth of Enterococcus faecium (VRE), thus antibiotics were adjusted accordingly. The patient stabilized clinically and was ultimately discharged to long-term acute care (LTAC). Conclusion: This Study highlights the importance of moving beyond the Light’s criteria to identify the cause of Pleural effusion. Though this case was initially thought to be transudative based on light’s criteria and underlying heart failure, the persistent effusion and loculation despite the

adequate diuresis and initial pigtail placement hinted towards a cause beyond heart failure. The growth of vancomycin-resistant enterococci eventually proved the exudative nature of the effusion.

Context: The type 1 RTA results from impairment in acid excretion by the collecting ductal system, leading to non-anion gap metabolic acidosis (NAGMA) in the setting of hypokalemia, positive Urinary anion Gap (UAG), and Urinary pH >5. Due to its asymptomatic nature, the type 1 RTA may go undiagnosed, and its prevalence has been estimated to be 0.46 per 10,000. The Type 1 RTA can be inherited and acquired. NSAIDs are one of the causes for acquired Type 1 RTA. Report of Case: A 42-year-old male with a history of arthritis under celecoxib for 2 years, presented to our facility with complaints of severe weakness of both upper and lower extremities lasting for a day, and inability to move all the extremities for a couple of hours. He denied having nausea, vomiting, diarrhea, recent trauma, use of diuretics, strenuous exercise, or binge carbohydrate consumption before the onset of weakness. He was hemodynamically stable at the time of presentation and had unremarkable CBC, CMP showing NAGMA with potassium of 2.1 mg/dl, normal magnesium, Imaging, and EKG. Further evaluation showed a urine potassium level of

52.5 mmol/L, sodium 94 mmol/L, chloride of 133 mmol/L, and pH of 6. Based on the presence of NAGMA, urine pH >5.5, and a positive UAG, a diagnosis of Type 1 RTA was made. The studies done for the autoimmune panel, Plasma renin aldosterone activity, were unremarkable, leaving only celecoxib as the potential culprit. Thus, Celecoxib was discontinued, and potassium and sodium bicarbonate supplementation continued. His potassium eventually normalized, acidosis was corrected, and he eventually regained his muscle strength. Conclusion: This case illustrates the importance of identifying prolonged celecoxib use as one of the culprits for Type 1 RTA. Though there are cases of NSAIDS, especially Ibuprofen-induced Type 1 RTA, this is the first case that reports the Type 1 RTA in the setting of prolonged Celecoxib use. This study thus highlights the importance of keeping celecoxib as one of the differentials while working up for unexplained hypokalemia and Type 1 RTA and lays a foundation for doing further studies to establish the relationship between celecoxib and Type 1 RTA.

115

114

2026 Research Recognition Day