Background: Propofol infusion syndrome (PRIS) is rare but possibly lethal. Mitochondrial damage is suggested as a potential pathogenesis. However, investigations on the mitochondrial damages in cardiomyocytes in patients with PRIS are insufficient.
Case presentation: A 20-year-old man with Guillain-Barré syndrome had propofol administration for sedation. On day 13, he had hypotension with ST elevation in electrocardiogram, acute kidney injury, hyperkalemia and severe rhabdomyolysis. He was transferred to our ICU on suspicion of PRIS. Administration of noradrenaline and hemodialysis were initiated, and fasciotomy was required for PRIS-rhabdomyolysis. He gradually recovered and was discharged from the ICU on day 30. On day 37, he repeatedly presented sinus bradycardia and conduction disturbance eventually requiring temporary pacing. Cardiac 18F-fluorodeoxyglucose positron emission tomography (18F-FDG PET) on day 67 demonstrated heterogeneous 18F-FDG uptake in left ventricle. Electron microscopic investigation of the endomyocardial biopsy on day 75 revealed abnormal findings in the mitochondria of the cardiomyocytes including myelinization of the cristae. He was discharged with normal cardiac function without arrhythmia on day 192.
Conclusions: This is a case of PRIS with evidence of mitochondrial damage in both morphological and functional aspects. Sustained mitochondrial damage may be a therapeutic target beyond the initial therapy of discontinuing propofol administration.
Keywords: Mitochondria, arrhythmia, cardiac failure