Page 11 - CASA Bulletin of Anesthesiology 2022; 9(3)-1 (1)
P. 11

Vol. 9, No 3, 2022



                   bolus/infusion will be initiated as quickly to restore/maintain hemodynamic stability, and
                   increase CVP to decrease the pressure gradient between the site of air entry and the right
                   heart.
               2.  Anesthesiologists should communicate closely with the surgical team to identify any tract of
                   the air entrainment. Surgeons should compress and repair major vessels to stop bleeding and
                   further air entry. Anesthesiologists should check all central lines and peripheral IV catheters
                   to avoid further air entry into venous circulation.
               3.  If a functional central line is in place, the anesthesia providers should attempt to aspirate
                   entrained VAE as early as possible. Surgeons could withdraw air directly from the right
                   heart. If indicated, the patient can be sent for hyperbaric oxygen therapy to compress and
                   diffuse the air bubbles. In extreme situations and available, cardiopulmonary bypass could be
                   helpful for VAE removal.

                   In addition, it was of note that intraoperative hyperkalemia (6-8mmol/L) and associated
               hypocalcemia (0.47-0.65mmol/L) were discovered immediately prior to the patient’s
               cardiovascular collapse. The patient has received only 6 units of PRBCs that were all
               administered within 35 days of storage. Thus, the team was suspicious of possible concurrent
               intraoperative tumor lysis syndrome. Although tumor lysis syndrome is frequently encountered
               in the patients with hematology-oncology malignancies, in rare instances, it happens in patients
               with solid tumors under general anesthesia undergoing surgery either spontaneously or following
               chemotherapy  . The pathophysiology of tumor lysis syndrome results from the massive release
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               of intracellular ions such as potassium, phosphorus and uric acid and can lead to hyperkalemia,
               hyperphosphatemia and hypocalcemia due to chelation of phosphorus and result in acute kidney
               injury, fatal arrhythmia and death. The acute treatment mainly focuses on IV crystalloid
               hydration and sodium bicarbonate to avoid kidney dysfunction, supplement of calcium,
               hyperventilation, insulin and dextrose to temporarily reduce potassium. In our patient with above
               treatments, her potassium level dropped from 8 to 2.9mmol/L temporarily however, calcium did
               not increase after the administration of 4 gm IV calcium chloride. Further medical therapy would
               have included medications to decrease uric acid, and hemodialysis for persistent hyperkalemia,
               hyperphosphatemia and kidney injury  21-22 .

                   In conclusion, a clinical fatal VAE during liver resection is an extremely rare but life-
               threatening complication during surgery, including major liver resections. Anesthesia providers
               should have a high index of suspicion of possible VAE, be aware of the risk factors and clinical
               signs and promptly initiate management for patients with a VAE.














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