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Introduction: The anatomy of the facial artery, its tortuosity, and branch patterns are well documented. To date, a reliable method of identifying the facial artery, based on surface landmarks, has not been described. The purpose of this study is to characterize the relationship of the facial artery with several facial topographic landmarks, and to identify a location where the facial artery could predictably be identified., Methods: Following institutional review board approval, 20 hemifacial dissections on 10 cadaveric heads were performed. Distances from the facial artery to the oral commissure, mandibular angle, lateral canthus, and Manson's point were measured. Distances were measured and confirmed clinically using Doppler examination in 20 hemifaces of 10 healthy volunteers., Results: Manson's point identifies the facial artery with 100% accuracy and precision, within a 3 mm radius in both cadaveric specimens and living human subjects. Cadaveric measurements demonstrated that the facial artery is located 19 mm ± 5.5 from the oral commissure, 31 mm ± 6.8 from the mandibular angle, 92 mm ± 8.0 from the lateral canthus. Doppler examination on healthy volunteers (5 male, 5 female) demonstrated measurements of 18 mm ± 4.0, 50 mm ± 6.4, and 79 mm ± 8.2, respectively., Conclusions: The identification of the facial artery is critical for the craniofacial surgeon in order to avoid inadvertent injury, plan for local flaps, and in preparation of a recipient vessel for free tissue microvascular reconstruction. Manson's point can aid the surgeon in consistently indentifying the facial artery., (Copyright © 2015 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Ltd. All rights reserved.)

The effects of cobalt chloride on ischaemia-reperfusion injury were evaluated in skin flaps. Groin neurovascular island flaps, 3 x 6 cm, were elevated in rats and subjected to primary and secondary ischaemia. Primary ischaemia was produced by 1 hour occlusion of the femoral artery and vein and, 22 hours later, secondary ischaemia was produced by 3 hours venous occlusion. The treatment group received intraperitoneal cobalt chloride (5 or 10 mg/kg) at the time of secondary ischaemia. Flap survival was 80% in the control, 10 to 20% in the cobalt chloride treated, and 20% in the cobalt plus mannitol group. Mannitol (100 mg/kg) failed to prevent the harmful effects of cobalt. Skin flaps exposed to cobalt chloride exhibited increased thiobarbituric acid reactant (TBAR) levels of 20 to 30 times normal. Of the antioxidant enzymes, glutathione peroxidase activity increased by 40% (P < 0.01), whereas glutathione reductase activity decreased by 40% (P < 0.01) in the cobalt exposed groups. Glucose 6-phosphate dehydrogenase activity was not affected.

The effects of diabetes mellitus (DM) on skin flap tolerance to 3 h of secondary venous ischaemia were evaluated. Epigastric island flaps were elevated 3, 6 and 12 weeks after induction of DM in rats. In the non-diabetic control groups, the flap survival was 85% in the 3-week group, 72% in the 6-week, and 78% in the 12-week. In untreated DM groups, the flap survival significantly decreased to 40% in the 3-week group, 25% in the 6-week, and 17% in the 12-week (P < 0.05 in all groups). Flap survival in the DM/insulin group decreased to 31% in the 3-week group. Effects of insulin therapy, however, were observed in later stages of DM: 71% and 62% survival in the 6- and 12-week group, respectively. Significant linear correlations between enzymatic responses and the flap survival were found. The results suggest that DM is detrimental to flap tolerance and is associated with the lack of metabolic responses to secondary ischaemia.

A sacral ulcer is described where ischaemia due to a vascular "steal" syndrome in the gluteal angiotome was the cause of persistent failure of flap reconstruction. Thrombotic obliteration of the abdominal aorta had resulted in the development of collaterals which, paradoxically, deprived the flaps based on standard angiotomes of their major source of blood supply, as they became the major source of perfusion for the legs. Healing of the ulcer was successfully achieved only after aorto-iliac reconstruction. Two other cases of ischaemic sacral ulceration, associated with aortic occlusion, are described.