Fatal air embolism in an infant during vitrectomy – A case report and review of literature

Dear Editor, Venous air embolism (VAE) during the intraoperative period has been commonly described during neurosurgical procedures, where air gets entrained from open and collapsed veins.[1,2] In children, VAE can be fatal due to lower body surface area and poor tolerance to haemodynamic instability.[3] A 1.3-kg, 35-week-old post-conceptional preterm female with no significant birth and neonatal history on topical vancomycin for endophthalmitis was posted for pars plana vitrectomy. After application of standard American Society of Anesthesiologists monitors, anaesthesia was induced with intravenous fentanyl 3 μg/kg, propofol 2 mg/kg, and atracurium 0.5 mg/kg and tracheally intubated with 3.0-mm ID uncuffed tracheal tube. Bilateral air entry was checked, and the patient was manually ventilated. Pupillary dilation was achieved using topical tropicamide (0.5%), and surgery was started using the Geuder posterior vitrectomy system. Air fluid exchange was started via a 5-mm-long, self-retaining 23-G cannula at an air pressure of 40 mmHg. After 40 minutes of surgical time, suddenly end-tidal carbon dioxide (EtCO2) sharply fell from 37 to 20 mmHg, saturation from 99% to 88%, heart rate from 160 to 220 beats per minute, and systolic blood pressure from 100 to 65 mmHg [Figure 1]. After excluding possible mechanical problems with ventilation, the possibility of VAE was strongly suspected. The fraction of inspired oxygen (FiO2) increased to 100%, the intravenous line was checked for possible infusion of air, and the surgeon stopped the intraocular air-fluid exchange. Precordial auscultation revealed a distinct mill wheel murmur. Blood pressure was increased by giving 1.5 mg of intravenous ephedrine. EtCO2 became zero within the next few minutes, and cardiopulmonary resuscitation (CPR) was started with high-quality chest compression and intravenous adrenaline 0.01 mg/kg repeated every 5 minutes. The arterial blood gas sample showed pH as 7.16, partial pressure of carbon dioxide (PCO2) 59 mmHg, partial pressure of oxygen (PO2) 64 mmHg, and bicarbonate 17.1 mmol/L. After 35 minutes of CPR, the patient could not be revived. An autopsy could not be performed as guardians denied consent.Figure 1: Showing vital parameters [heart rate (in beats per minute), peripheral oxygen saturation (SpO2), systolic blood pressure (SBP in mmHg), diastolic blood pressure (DBP in mmHg), and end-tidal carbon dioxide (EtCO2 in mmHg)] with respect to time from the initiation of surgery till cardiopulmonary resuscitationVAE caused by air entrainment through the central retinal vein appears to be the most plausible explanation for the abrupt decrease in PaCO2, hypoxemia, and haemodynamic instability. Anaphylaxis was also considered, but there was no sign of bronchospasm, no urticarial rash, and no temporal association with drug administration.[3-5] A negative pressure gradient or positive pressure insufflations of gas or a liquid-gas mixture can lead to VAE. Air-fluid exchange, with a pressure difference of 20 mmHg (air inflation pressure: 40 mmHg − intraocular pressure: 20 mmHg) through a 23G inflation cannula, would result in a theoretical flow of 1600 mL/min of air, probably which resulted in embolism. This is well above the lethal rate of air entrainment, although the flow created by the air-fluid exchange within the eye is not laminar. A review published on Ocular VAE (OVAE) found 13 case reports, out of which 69% were fatal (9/13), with 8 of 9 deaths occurring on the day of surgery. OVAE may be the most lethal type of surgical air embolization because of its high entrainment pressure and proximity to the heart.[2] Morris et al.[6] simulated vitrectomy through unsutured cannulas on four donor eyes. They withdrew the unsutured cannulas during the air-fluid exchange, producing choroidal detachment that emulated accidental suprachoroidal air infusion from a slipping cannula. This experiment was performed in three eyes, using 25G and 23G systems, under intraocular pressure between 30 mmHg and 60 mmHg. They closed the vortex vein stumps with serrafin clamps in the fourth eye. Initial reports of life-threatening air embolisation through the eye were shocking with a view of the small diameter of the choroidal veins. However, the vortex vein, with its thin walls, can expand substantially under pressure, leading to rapid and fatal entrainment of air, resulting in mortality despite resuscitative efforts. In conclusion, prevention is the only possible treatment that requires precaution during surgery. Literature reports the sole survivor of OVAE cardiac arrest received extra-corporeal life support.[2,6] Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient consented to her images and other clinical information being reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal her identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.