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Florida Society of Anesthesiologists

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2025 FSA Podium and Poster Abstracts

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P033: ACUTE RESPIRATORY DISTRESS SYNDROME AND SHOCK FOLLOWING DECEASED DONOR KIDNEY TRANSPLANTATION: A CASE OF DELAYED GRAFT FUNCTION AND ANAPHYLAXIS
Eugene Michanine, MD; Rafael Cabrales, MD
Cleveland Clinic Florida

Introduction/Background: Acute respiratory distress syndrome (ARDS) and hemodynamic instability are critical postoperative complications following kidney transplantation, impacting up to 6.6% of ICU-admitted recipients. Patients with complex comorbidities are especially vulnerable. These complications can stem from fluid overload, systemic inflammation, electrolyte disturbances, or anaphylaxis to immunosuppressants like anti-thymocyte globulin (ATG). Delayed graft function (DGF), often from ischemia-reperfusion injury, further elevates risk. Advanced interventions such as venovenous extracorporeal membrane oxygenation (VV-ECMO) and continuous renal replacement therapy (CRRT) may be life-saving when severe ARDS coexists with hemodynamic instability and suspected ATG-induced anaphylaxis. This case emphasizes early recognition and management of these complications in high-risk kidney transplant recipients.

Methods: A 52-year-old male with end-stage renal disease, coronary artery disease, and atrial fibrillation underwent a deceased-donor kidney transplant. Preoperative creatinine was 8.04 mg/dL, with an ASA classification of 4. Blood pressure was initially stable on maintenance crystalloid infusion. 500 mg of methylprednisolone was administered upon induction, and ATG was started shortly after. However, after 20 mg of ATG, mean arterial pressures (MAPs) dropped to 51 mmHg. A dopamine infusion (up to 10 mcg/kg/min) temporarily stabilized MAPs. ATG was discontinued due to suspected anaphylaxis. A total of 3000 mL of crystalloid was infused, with negligible blood loss.

Post-surgery, the patient was extubated but recurrently desaturated, to as low as 65% on supplemental oxygen, requiring intubation in the surgical ICU. Chest X-rays revealed bilateral infiltrates consistent with ARDS (PaO2/FiO2 < 100), and VV-ECMO was initiated for refractory hypoxemia. CRRT was started for oliguria, hypervolemia, and metabolic acidosis. An echocardiogram showed no acute findings. Kidney vasculature was patent on ultrasound. The patient received norepinephrine (up to 10 mcg/min), vasopressin (up to 0.06 units/min), and epinephrine (up to 4 mcg/min) infusions to stabilize hemodynamics. Eventually, creatinine improved from a peak of 8.13 to 1.86 mg/dL with CRRT. On postoperative day 8, subsiding pulmonary infiltrates (Figure 1) and improved respiratory function allowed for ECMO decannulation and extubation.

Results: The patient stabilized following ATG discontinuation and aggressive hemodynamic management with vasopressors and fluids. VV-ECMO for refractory ARDS improved oxygenation, while CRRT supported renal recovery and fluid balance. Over eight postoperative days, pulmonary infiltrates subsided, renal function improved (creatinine decreased from 8.13 to 1.86 mg/dL), and the patient was successfully decannulated from ECMO and extubated.

Discussion/Conclusion: This case highlights the importance of timely ARDS and shock management post-transplant, particularly with suspected ATG anaphylaxis and DGF. Intraoperative vigilance allowed prompt vasopressor use and ATG cessation upon anaphylaxis suspicion. Early VV-ECMO maintained oxygenation in refractory ARDS, aligning with evidence that early ECMO improves survival in high-risk cases. Combining VV-ECMO with CRRT effectively managed fluid balance and supported renal recovery. Ultimately, early multidisciplinary management by anesthesiologists, intensivists, and transplant teams is vital for addressing critical postoperative challenges in high-risk kidney transplant recipients.

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