DOI: 10.1097/01.PRS.0000153785.78412.DF
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PMID: 15731709
Issn Print: 0032-1052
Publication Date: 2005/03/01
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Excerpt
In Mathes and Nahai’s well-respected and much-referenced classification of muscle types,1 the authors define dominant vascular pedicles as “those required to ensure viability of muscle following transposition as flaps.” By inference, a minor pedicle such as that seen in type II muscles may be defined as one that cannot ensure viability of muscle after transposition as a flap.
This work was published in 1981, before the first description of free fasciocutaneous flaps such as the anterolateral thigh flap.2,3 As such, the relationships of the dominant and minor pedicles in this type of flap transfer remain undefined.
It has been shown repeatedly that the free fasciocutaneous anterolateral thigh flap will survive on the dominant vascular pedicle to the vastus lateralis, usually the descending branch of the lateral circumflex femoral artery.3,4 However, harvesting the anterolateral thigh flap requires division of the dominant vascular pedicle, leaving the vastus—a type II muscle—in situ with only its minor pedicle intact. Mathes and Nahai’s classification suggests that the minor pedicle cannot sustain the vastus muscle alone, and so it may be reasonable to expect a degree of muscle necrosis and resultant postoperative donor-site problems.
One of the documented strengths of the anterolateral thigh flap is its remarkably good donor-site morbidity, especially when primary closure is achieved.5 This would suggest a minimal degree of muscle necrosis, if any, and gives rise to the following question: Where does the vastus lateralis receive its arterial supply from, after removal of its dominant vascular pedicle?
It may be that the minor pedicle does in fact supply the whole muscle in this situation. However, the lateral circumflex femoral arterial system is highly variable, and in a minority of cases, there may not be a minor pedicle supplying the vastus. Another possibility is that the muscle recruits additional supply from the surrounding tissues. However, this process would presumably take some time, during which the muscle could become ischemic. Indeed, there may in fact be some degree of ischemic muscle damage that has not been recognized, since the individual contribution of the vastus lateralis to the function of the quadriceps femoris is very difficult to quantify in isolation.
The arterial supply to the vastus lateralis—and other type II muscles—after fasciocutaneous free flap transfer remains unclear, and further study may be necessary to clarify the situation.
