Polythelia in a 13-year old girl.

We present a rare case of a 13-year old girl with a bilateral polythelia. We would like to draw attention to this particular mammary malformation.

Dietary fish oil reduces microvascular thrombosis in a porcine experimental model.

Microvascular thrombosis plays a significant role in the pathophysiology of ischaemic reperfusion injury. A fish oil-supplemented diet containing n-3 polyunsaturated fatty acids (PUFA) reduces thromboxane A(2) (TxA(2)) synthesis and, thus, vasoconstriction and platelet aggregation. The aim of this study was to elucidate whether n-3 PUFA in a porcine model of ischaemia and reperfusion injury 1) inhibit accumulation of platelets and fibrinogen in ischaemia-reperfusion injured tissue, 2) prolong the bleeding time, and 3) inhibit TxA(2) synthesis. Nine pigs were fed a standard diet supplemented with 7 g n-3 PUFA/day for 3 weeks. Nine pigs on the standard diet served as controls. Unilateral myocutaneous flaps were exposed to ischaemia for a period of 6 hours. Contralateral flaps were nonischaemic. Tissue contents of radioactive-labelled platelets and fibrinogen were measured after 4 hours of reperfusion. Platelet count, serum TxB(2), and the cutaneous bleeding time were measured before and after 3 weeks of diet. In the fish oil group, the accumulation of platelets was significantly reduced in all the myocutaneous flaps, except in the ischaemic skin part, when compared to control animals. Fibrinogen was significantly reduced in nonischaemic flaps, but not in ischaemic flaps. After the feeding period, the level of TxB(2) was significantly lowered in the fish oil group (p<0.01). No difference in the bleeding time was observed. Thus, dietary supplementation with n-3 PUFA inhibits the formation of microvasculatory thrombosis in this model.

Secondary ischemia caused by venous or arterial occlusion shows differential effects on myocutaneous island flap survival and muscle ATP levels.

Ischemia-reperfusion injury is one of the major problems in reconstructive microsurgery. The ischemic insult may be due to an occlusion of either the artery or the vein. Clinical observations have suggested that flap survival is more sensitive to venous stasis than to arterial ischemia. The current study evaluated the viability of the myocutaneous rectus abdominis flap following secondary arterial or venous occlusion and its possible dependency on tissue metabolites and length of the preceding reperfusion period. Forty-eight bilateral 5 X 10 cm myocutaneous rectus abdominis flaps were elevated in 24 pigs and exposed to consecutive periods of primary ischemia (2 hours), reperfusion (1, 4, 8, and 12 hours), and secondary pedicle occlusion (6, 8, 10, 12, 14, or 16 hours) of arterial or venous origin. Muscle adenosine triphosphate (ATP) and glucose-6-phosphate (G6P) were assessed immediately after flap elevation, at the end of primary ischemia, after reperfusion, and at the end of secondary ischemia. Flap viability was assessed 5 days after the operation. Secondary venous occlusion resulted in reduced survival rates as compared with arterial occlusion (9 of 24 versus 20 of 24; p < 0.01), although the average ATP content was higher in flaps subjected to venous stasis [median (25 to 75) percentiles, 3.7 (1.7 to 7.1) micromol/gm protein] than in those subjected to arterial ischemia 1.2 (0.8 to 1.8 micromol/gm protein) (p < 0.01). During reperfusion, muscle ATP decreased from 28.5 (17.9 to 36.6) micromol/gm protein to 15.4 (7.4 to 24.9) micromol/gm protein (p < 0.01) and glucose-6-phosphate from 7.6 (4.1 to 11.6) micromol/gm protein to 1.0 (0.5 to 4.1) micromol/gm protein (p < 0.01). Still, flap survival following secondary arterial ischemia was improved by increasing the reperfusion time from 1 to 8 hours (p < 0.05). No effect of reperfusion time was seen on viability after venous stasis. In conclusion, despite poorer flap survival, venous stasis was less detrimental to tissue ATP level, suggesting that the continued inflow may have supplied substrates for glycolysis. Furthermore, the larger blood volume may have accumulated the glycolytic waste products. After reperfusion, the recovery of aerobic metabolism was far from complete, and cellular glycolytic substrates were nearly exhausted. However, prolongation of the reperfusion time preceding secondary arterial ischemia improved flap survival.