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We present the case of a patient with arterial thrombosis of a free TRAM flap 11 days after surgery. Initial salvage involved thrombectomy through an arteriotomy using a Fogarty catheter. Subsequent return to the operating theatre was necessary because of further vascular compromise. Thrombectomy was combined with flap thrombolysis and anticoagulation, and the flap remained viable at 6 months. Although rates of successful salvage vary, the literature indicates that flaps are rarely saved if signs of compromise present later than 2 days postoperatively. This case demonstrates that aggressive salvage may be successful even in cases of ‘late’ vascular compromise.
Although microvascular free tissue transfer has gained acceptance as a reliable reconstructive technique, with reported success rates of between 85 and 98%,
Early recognition of compromise and urgent re-exploration are imperative for success, and the majority of successful salvages occur within the first 12–24 h postoperatively.
Betancourt et al examined the timing of critical thrombosis after digital replantation: none of the 21 digits with critical thrombosis beyond 3 days after replantation survived.
A review of the literature failed to find a case of successful free flap salvage more than 6 days postoperatively: Hidalgo and Jones report a recipient artery atherosclerotic obstruction that was reversed on the sixth postoperative day,
We report another case of ‘late’ salvage of a free tissue transfer, 11 days postoperatively.
1. Case report
A 27-year-old female underwent a right modified mastectomy for infiltrating ductal carcinoma and a left simple mastectomy for prophylaxis. Immediate bilateral free TRAM flap reconstruction was performed using the subscapular vascular tree as the recipient vessels; the ischaemia time was less than 2 h. Shortly after releasing the microvascular clamps, we observed bilateral arterial thrombosis, which required revision of the arterial anastomoses, with the removal of platelet plugs from the arterial anastomotic sites and flushing with heparinised (10 U ml−1) Ringer's lactate solution. A 5000 U intravenous bolus of heparin and 30 mg of intravenous ketorolac were given during the revision, and a drip of 10% dextran-40 solution with 10 U ml−1 of heparin at 20 ml h−1 was started. No further anastomotic problems occurred, and the flaps were subsequently well perfused. Laser Doppler was used for postoperative monitoring. The patient was started on 325 mg of aspirin daily, and the dextran infusion was continued for 5 days. The patient was discharged on no medication after an uneventful 7 days in hospital.
On the 11th day after surgery, the patient presented urgently to clinic with a cool violaceous right flap (Fig. 1) . Warm ischaemia time was estimated to be within 5–6 h. She denied any trauma, and inquiry revealed only that she had been smoking during the preceding 3 days.
Figure 1Appearance of the flap at presentation 11 days postoperatively, showing vascular compromise.
The patient was immediately brought to the operating theatre, where the right axilla was re-opened and the pedicle was carefully dissected. The venous anastomosis was patent, but the arterial anastomosis had thrombosed, with proximal extension to the axillary artery. The clot was removed using a Fogarty catheter passed through an arteriotomy, the anastomosis was redone and the patient was given a bolus of 3000 U of intravenous heparin. Unfortunately, shortly after repair, the thrombus recurred, despite systemic anticoagulation, and a second arteriotomy and thrombectomy was required. Patency was observed, and the pedicle was irrigated with 2% lignocaine prior to wound closure. The procedure lasted 5 h. A dextran-heparin infusion was started, and 325 mg of aspirin was given (Fig. 2) .
Figure 2Appearance of the flap after the initial salvage operation.
Poor perfusion of the same flap was detected by laser Doppler 6 h postoperatively, and the patient was again returned to the operating theatre. Secondary re-exploration and thrombectomy was performed. Interestingly, the pedicle was patent, but the appearance of the flap remained unsatisfactory. A total of 30,000 U streptokinase was infused into the flap arterial system via a 30 G needle inserted proximal to the anastomosis. At the same time, the pedicle was filled with heparinised Ringer's lactate and clamped. Adequate bleeding was demonstrated shortly afterwards, and the wound was closed once again. The procedure lasted 1.5 h. The patient was fully anticoagulated using an intravenous heparin drip (1000 U h−1) and restarted on 325 mg of aspirin daily. After an uneventful 8 days stay in hospital, she was discharged with a 6 week course of coumadin anticoagulation.
One year after salvage, the patient has suffered partial necrosis of the lateral aspect of the right flap (Fig. 3) and approximately 20% loss of flap volume. The flap has remained otherwise well, with good wound healing despite chemotherapy (Fig. 4) . The patient has recently been diagnosed with pulmonary metastatic disease.
Figure 3Mild necrosis of the lateral flap margin was treated with serial debridement.
Free flap failure is generally recognised as an ‘early’ complication, occurring within 4–5 days of surgery. Causes are thought to include anastomotic flaws, side-branch injury, vessel spasm, pedicle kinking, haematoma and tight wound closure.
This case adds to the literature describing late vascular compromise as a complication of free tissue transfer.
Through the work of Acland et al, a model of microsurgical thrombosis has been described in which the anastomotic site (zone I) and the downstream microvasculature (zone II) have distinct pathophysiology.
Primary thrombosis in zone I has been vigorously studied, with the focus on vessel-wall injury, subendothelial exposure, platelet adhesion and activation, suture material, flow disturbances and vessel spasm.
Other presumed factors, including extremes of age, radiotherapy, a history of smoking or alcoholism, high ASA grade and ablative surgery, remain disputed.
Secondary thrombosis in zone II is not as well recognised and studied. Hypoperfusion is thought to occur as a result of either embolic showering from the anastomosis or vasospasm secondary to the release of platelet metabolic products, such as thromboxane A2.
Cases thought to be consistent with the latter mechanism have been described as progressive partial free flap failure and occur between 4 h and 6 weeks after surgery.
Identified risk factors include delayed reconstruction of traumatic extremity wounds, established infection, use of vein grafts, refractory vasospasm, hypercoagulable states and intravenous drug use.
The pathophysiology of late arterial thrombosis is not understood, and the aetiology of the vascular compromise in our case is unknown. On initial exploration of the flap, no extrinsic factor was identified, and venous outflow was patent. Given that the flap remained perfused for 11 days postoperatively, thrombosis is unlikely to have been caused by a technical error. The patient gave a history of smoking several days before presentation. Although the role of tobacco in this setting remains unclear, smoking could have induced vasospasm, consistent with the findings of Betancourt et al, in which smoking was associated with late thrombosis of a digital replantation.
Smoking has been shown to cause tissue ischaemia by vasoconstriction, carbon monoxide poisoning and increased carboxyhaemoglobin, and has been associated with platelet dysfunction. There was no evidence of active infection, but subclinical microbial contamination cannot be ruled out.
The flap was successfully perfused following zone I thrombectomy. On subsequent re-exploration, instigated by a decrease in the Doppler monitoring signal, however, the flap remained compromised despite a patent pedicle. That perfusion was only established after streptokinase thrombolysis of the flap microvasculature is consistent with the concept of secondary zone II thrombosis from proximal clot showering and platelet-mediated vasospasm. In retrospect, a hypercoagulability screen could have helped establish the reason for recurrent thrombosis. None the less, the flap was salvaged by removing the thrombus from zone I, thrombolysis in zone II and maintenance of anticoagulation, postoperatively. A combination of modalities was required for correction.
The finding of pulmonary metastatic disease 1 year after her initial surgery indicates persistent disease. A malignancy may lead to unexplained hypercoagulability.
Regardless of the pathophysiology of flap failure, several management options are available after 11 days. Flap survival via neovascularisation has been described following pedicle division 10 days after tissue transfer,
used this approach in cases of late vascular compromise, achieving partial flap survival. However, in our case complete flap necrosis seemed imminent. More aggressive management involves surgical re-exploration of the pedicle and revision of the anastomosis. Wheatley and Meltzer report using Fogarty catheter thrombectomy successfully in six out of seven cases and with partial salvage in the seventh case.
These may be administered systemically or infused to achieve high local concentrations while avoiding systemic complications. Repeated thrombectomy in our case eventually achieved vessel patency despite initial recurrence of thrombosis. The subsequent use of streptokinase thrombolysis and prolonged anticoagulation maintained flap viability with no evidence of significant haematoma formation. In contrast, Wheatley and Meltzer reported that in three out of six cases thrombectomy combined with anticoagulation resulted in a clinically significant haematoma requiring drainage.
Although a multitude of techniques and pharmacologic agents are available to salvage flaps, rapid recognition and re-exploration is widely recognised as a major factor in successful salvage. Hidalgo and Jones achieved a 100% salvage success rate by returning to the operating theatre an average of 1.5 h after identifying compromise.
A period of 7.2 h was found to be associated with a 50% rate of complete flap failure. Although in our case reoperation did not occur until 6 h after the first discovery of compromise, neovascularisation during the 11 days following surgery is likely to have been an important factor in tissue tolerance to ischaemia.
This is one of the few reports of successful salvage of late free tissue transfer compromise. The clinical course was consistent with the phenomenon of secondary thrombosis, and aggressive salvage was achieved without significant haematoma formation. Although, in a review of 990 consecutive free flaps, Kroll et al report that no salvage was achieved at later than 2 days,
we report successful salvage on the eleventh postoperative day. Aggressive attempts at free flap salvage may be successful despite a prolonged interval between the primary procedure and flap failure.
References
Irons G.B
Wood M.B
Schmitt E.H
Experience with one hundred consecutive free flaps.
Division of Plastic and Reconstructive Surgery, Department of Surgery, University of Western Ontario, St Joseph's Health Care, 268 Grosvenor Street, London, Ont. N6A 4L6, Canada.
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