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Intra-flap Thrombosis Secondary to Acute Sickle Crisis
Alison McAnneny MD, Frederick Durden MD, Gregory Pearson MD, Pankaj Tiwari MD
The Ohio State University Medical Center, Columbus, Ohio
2012-01-15
Presenter: Alison McAnneny
Affidavit:
The submitted abstract represents the original work of the resident and attending. It has not been previously presented or published.
Director Name: Michael J. Miller MD
Author Category: Chief Resident Plastic Surgery
Presentation Category: Clinical
Abstract Category: Breast (Aesthetic and Recon.)
How does this presentation meet the established conference educational objectives?
The presentation above highlights a unique microsurgical complication, describes its etiopathology, and suggests strategies for preventing its occurrence in practice. The presenter will review the epidemiology, diagnosis, and pathophysiology of sickle cell diseases, its presence in the plastic surgery literature, and will discuss its implications for free tissue transfer as well as patient risk of perioperative venous thromboembolism.
How will your presentation be used by practicing physicians in the audience?
This presentation will aid practicing physicians in recognizing sickle cell diseases and the increased risks it confers of developing microsurgical complications and peri-operative VTE. The presenter will offer strategies to minimize these risks.
A 40 year-old patient with known sickle cell trait underwent bilateral breast reconstruction with microvascular TRAM flap transfer. Intra-operatively, the patient had arterial anastomotic thrombosis of the right breast flap. By this time, the left breast flap had been harvested and was ischemic, and it was placed on ice. The right anastomosis was successfully revised, and the left breast flap was then anastomosed without complication. On post-operative day two, the patient had significant edema of the left breast flap. Exploration demonstrated no anastomotic thrombosis. The patient also developed a pulmonary embolism and heparin-induced thrombocytopenia. The left breast flap remained swollen with intact cutaneous doppler signals until post-operative day twelve, when the signals were lost. Exploration revealed a thrombosed pedicle. The flap was nonviable, and it was debrided. A specimen was sent to pathology, which demonstrated sickled cells within the flap microvasculature.
Increased erythrocyte sickling occurs in sickle cell trait under conditions of severe tissue hypoxia, acidosis, and hypothermia. Previous reports in the plastic surgery literature highlight the difficulties of free tissue transfer in the sickle cell patient, with complications such as venous thrombosis and total flap loss described.
We believe the left-sided flap failure resulted from prolonged ischemia time (106 minutes) and hypothermia precipitating erythrocyte sickling within the flap, which then caused intra-flap thrombosis that propagated to the pedicle. The right-sided breast free tissue transfer remained well-perfused. While sickle cell diseases are not a contraindication to free tissue transfer, we believe that flap cooling should be contraindicated in this circumstance.
