2026 FSA Podium and Poster Abstracts

Background: Anti-thymocyte globulin is a common immunosuppression agent used during kidney transplants. Thymoglobulin initiates immunosuppression through multiple modalities including T-cell clearance and depletion and through downregulating the expression of molecules and adhesions that allow for T-cell proliferation.

Non-cardiogenic pulmonary edema (NCPE) is a disorder that arises from increased permeability of the lung alveolar-capillary interface leading to excess fluid within the alveoli and interstitial spaces. This is a multifactorial process and can result in increased morbidity and mortality without prompt recognition.

Thymoglobulin has been implicated as a rare cause of NCPE. This has been shown through postmarketing studies through cytokine release syndrome.

Case Description: A 37-year-old woman with end-stage renal disease on hemodialysis via LUE AV fistula and hypertension presented for kidney transplantation. Preoperative dobutamine stress echocardiography was negative for ischemia with preserved left ventricular ejection fraction (60%), moderate concentric LVH, grade II diastolic dysfunction, and a moderately dilated left atrium. RHC demonstrated elevated filling pressures (RA 10 mmHg, RV 50/9 mmHg, PA 44/20 mmHg, PCWP 24 mmHg).

General anesthesia was induced with RSI. Arterial line was placed, and a TAP block was performed. Premedication for rATG included diphenhydramine 50 mg and methylprednisolone 500 mg prior to initiation of thymoglobulin (3 mg/kg). Intraoperative MAPs ranged from 30–110 mmHg.

During emergence, the patient exhibited low tidal volumes and inadequate ventilation despite reversal with neostigmine 3 mg and glycopyrrolate 0.6 mg. Additional sugammadex 200 mg and bronchodilator therapy were administered. She remained hypoxemic and could not be extubated. ABG prior to ICU transfer showed pH 7.31, PaCO2 51 mmHg, PaO2 61 mmHg, HCO3 27 mEq/L. A brief nicardipine infusion was required for hypertension.

CXR and ultrasound revealed moderate to large right and small to moderate left pleural effusions. Repeat echocardiography showed unchanged ejection fraction with severe left atrial dilation and mild tricuspid regurgitation. Broad spectrum antibiotics were initiated; blood cultures remained negative. A right-sided pigtail catheter drained 520 mL of fluid. Despite drainage and supportive care, radiographic findings persisted. The third dose of rATG was withheld. The patient was extubated to high flow nasal cannula on postoperative day (POD) 2 and weaned to lower support by POD 3. Intravenous furosemide 80 mg was administered on POD 3 with further clinical improvement.

Discussion/Conclusion: This case describes suspected rATG-associated NCPE presenting as postoperative hypoxemic respiratory failure. rATG can precipitate cytokine release, increasing alveolar-capillary membrane permeability and leading to capillary leak and pulmonary edema, which may occur during or within 24-hours of infusion. Although this patient had baseline diastolic dysfunction and elevated filling pressures, the timing of respiratory deterioration, lack of infectious source, limited response to pleural drainage, and improvement after withholding further rATG support a permeability mediated process rather than purely cardiogenic or volume-overload etiology.

Kidney transplant candidates are predisposed to volume shifts and cardiopulmonary comorbidities, which can obscure diagnosis. Anesthesiologists should maintain a high index of suspicion for rATG-associated lung injury when unexplained hypoxemia develops perioperatively. Early recognition, supportive respiratory management, and reconsideration of further rATG dosing are critical to improving outcomes.