BackgroundDetailed profiles of acute hypothermia and electrocardiographic (ECG) manifestations of arrhythmogenicity were examined to analyze acute hypothermia and ventricular arrhythmogenic potential immediately after portal vein unclamping (PVU) in living-donor liver transplantation (LT).MethodsWe retrospectively analyzed electronically archived medical records (n = 148) of beat-to-beat ECG, arterial pressure waveforms, and blood temperature (BT) from Swan-Ganz catheters in patients undergoing living-donor LT. The ECG data analyzed were selected from the start of BT drop to the initiation of systolic hypotension after PVU.ResultsOn reperfusion, acute hypothermia of < 34℃, < 33℃ and < 32℃ developed in 75.0%, 37.2% and 11.5% of patients, respectively. BT decreased from 35.0℃ ± 0.8℃ to 33.3℃ ± 1.0℃ (range 35.8℃–30.5℃). The median time to nadir of BT was 10 s after PVU. Difference in BT (ΔBT) was weakly correlated with graft-recipient weight ratio (GRWR; r = 0.22, P = 0.008). Compared to baseline, arrhythmogenicity indices such as corrected QT (QTc), Tp-e (T wave peak to end) interval, and Tp-e/QTc ratio were prolonged (P < 0.001 each). ST height decreased and T amplitude increased (P < 0.001 each). However, no correlation was found between ΔBT and arrhythmogenic indices.ConclusionsIn living-donor LT, regardless of extent of BT drop, ventricular arrhythmogenic potential developed immediately after PVU prior to occurrence of systolic hypotension.
Cerebral air embolism is a rare but potentially life-threatening complication. We experienced a living-donor liver transplant recipient who presented with unexpected cerebral air embolism and transient neurologic abnormalities that subsequently developed just after the removal of the pulmonary artery catheter from the central venous access device. One day after the initial event, the patient's neurologic status gradually improved. The patient was discharged 30 days after liver transplantation without neurologic sequelae.
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