Recurrence of fatal venous air embolism

provided the original work is properly cited. CC Venous air embolism (VAE) often occurs in the operating theatre. Squeals have not been reported much in most recovering patients. Our patient recovered from a venous air embolism during surgery but experienced cardiac arrest in the intensive care unit the next day, and died. A review of the chest X-ray revealed pulmonary edema and intracardiac air. A 42-year-old male patient was admitted for surgery on a right occipital brain meningioma. The patient had no specific medical history. The right subclavian vein was cannulated during the preoperative period. In the operating theatre, non-invasive blood pressure, electrocardiograph, pulse oximeter (SpO2), end-tidal carbon dioxide (ETCO2) and central venous pressure (CVP) monitoring were initiated. Anesthesia was maintained with oxygen, air, target-controlled infusion of remifentanil and propofol, and rocuronium with controlled ventilation. The left dorsalis pedis artery was cannulated for continuous arterial blood pressure monitoring (ABP). The surgery was performed in the semi-sitting position. One hour after beginning the surgery, an abrupt CVP elevation from 8 to 18 cmH2O was detected. ETCO2 decreased from 20 to 14 mmHg, and systolic ABP decreased from 110 to 92 mmHg. After injecting 5 mg ephedrine, blood pressure increased but decreased again. Although we suspected a pneumothorax during cannulation of the central line, both lung sounds were symmetrical and a post-procedural X-ray did not reveal a pneumothorax. Sinuses had not been cut yet, but under strong suspicion of a VAE, BP decreased, heart rate (HR) slowed, and ventricular premature complexes occurred. Surgeon sprayed water over the operative field and wrapped the wound with wet surgical pads. The surgery was stopped and the patient was repositioned in the head down position. Aspiration of blood through the central line showed air bubbles. The vital signs stabilized after 1,000 ml of mixed blood and air were aspirated. The cardiologist confirmed that the right heart was enlarged and deviated to the left side on a trans-thoracic echocardiograph (TTE). However, no intracardiac air was detected. When the surgery was being delayed and the surgeon sutured the wound, vital signs became unstable again. We aspirated air from the central line again, and vital signs stabilized. After wound closure, a trans-esophageal echocardiograph (TEE) revealed no intracardiac air. Intracardiac shunts such as foramen ovale were also not detected in TEE. The patient was moved to the ICU without extubation. In the ICU, BP was 140/70 mmHg, HR, 88 beats/min; CVP, 3 cmH2O; and SpO2, 100%. The ventilator was connected with a tidal volume of 450 ml, respiratory rate of 16 breaths/min, fraction of inspiratory oxygen of 1.0, a positive end-expiratory pressure (PEEP) of 5 cmH2O. After a chest X-ray revealed pulmonary edema, the surgeon injected furosemide 20 mg. The Glasgow coma scale score recovered to 9 and after 1 and half hour the patient removed the endotracheal tube accidently. A rebreathing mask with 10 L/min O2 was used, and SpO2 90% was adjusted to 90%. After 30 min, SpO2 decreased to 85% so the patient was reintubated and a diuretic infusion was started. Vital signs were; BP, 140/80 mmHg; HR, 150 bpm; PEEP increased to 7 cmH2O, and fluid was restricted. BP dropped to 70/50 mmHg and a norepinephrine infusion was started 2 hr later. A chest anteroposterior view and brain computed tomography (CT) scan were conducted. The brain CT revealed no other abnormality. Although we increased the norepinephrine dosage, the patient