Based on the above findings we propose that the SCM flap be re-classified as type III, instead of type II, as described previously in literature1. A type III flap has two dominant pedicles. According to the findings in this study, the STA is the second dominant pedicle supplying the SCM flap, other than its already established supply from the occipital artery (which serves as its first dominant pedicle). It is evident from the above findings that STA, not only augments the blood supply of the muscle (via occipital artery) but, is also capable of solely supplying the whole muscle in 80% of cases. STA supplied two-thirds of the muscle, including the lower third of the muscle, in 90% cases. In our previous series, we reported a flap loss of 6.25 %, by preserving the SCM branch of STA3, as opposed to the historical 10–30%, reported in literature2. These clinical results are reinforced by our present angiographic study. In situations, where more length of the flap is required, the STA was ligated distal to the SCM branch3. Tiwari et al4 have described their series of 18 successful cases of SCM flaps, of which 3 flaps were done for temporal bone resection defects. In these 3, they detached the muscle from the temporal bone, and none of the muscular branches of occipital artery were preserved. The flap survived solely on the SCM branch from STA, as well as collateral circulation from the branches of occipital and posterior auricular arteries supplying the overlying skin. Wei et al., in their series of 65 patients, emphasized on preserving the SCM branch of STA. They reported partial flap loss of 8 % and did not report any total flap loss. Similarly, Khazaeni in their lone case4, reported sternocleidomastoid myocutaneous flap, for a full thickness cheek defect solely based on the SCM branch of STA, as the occipital branch was ligated during the lymph-node dissection in the same case. Jones et al.2 have very systematically described decrease in the complications of the SCM flap from about 60 % in 1980s5 to present rate of about 2% (2016)6. In their review, they attributed lower complication rates to: 1) suturing skin paddle to underlying muscle so that the perforators can be safeguarded from shearing, while handling the flap 2) to check the skin refill before suturing the flap to the defect 3) preservation of SCM branch of superior thyroid artery.
Hu et al7 in their series of 50 cadaveric muscle specimens, described a branch of STA, that runs down to the clavicle and supplies perforators to perfuse the lower third segment of the muscle. They also stressed on the importance STA in supplying the lower third of the muscle.
The relatively higher loss of the flap in various series may be due to poor underlying perforators to the overlying skin in which case, there is only a partial loss of the skin paddle while the underlying muscle remains healthy. This has been discussed in detail by Jabaley et al.8 where they studied the blood supply of sternocleidomastoid in 3 ways: cadaveric dissection, neck dissections and fluorescein dye testing, after the flaps were raised. They concluded that due to paucity of perforators from the muscle to skin or very narrow caliber capillaries traversing from muscle to overlying skin, there is a greater chance of skin-paddle loss that would eventually heal by re-epithelization with healthy underlying muscle. Another proposed reason for higher flap loss is disrupted venous drainage. As most of the discussions revolve around arterial anatomy of the muscle, venous drainage is often overlooked. SCM is drained by accompanying venous tributaries with each vascular pedicle and additionally by small tributaries to external and anterior jugular vein9. Every effort should be made to preserve maximum venous tributaries to prevent congestion of the flap.
The limitation of our study is a relatively small sample size, that may obviate anatomic variations in the blood supply and this requires larger numbers to be studied. Another drawback is the unaccounted entity of ‘’feeding-vessel” spasm, a phenomenon 10–12 which may get aggravated by flap-handling. In real time surgery, there is always a chance of feeding vessels or perforators ‘going into spasm’ despite rich supply through intramuscular communications. As with all cadaveric studies, it was not possible to study this and it may very well be a cause of flap failure despite angiographic uptake in the lower third of the muscle.