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There is ample evidence of the involvement of free radicals in mediating skin flap necrosis. Dimethyl sulfoxide (DMSO) is a well-tolerated, safe drug that is a powerful scavenger of the hydroxyl free radical. The current study investigated the effect of DMSO on the survival of 9 x 4 cm skin flaps based on the epigastric vessels subjected to primary venous occlusion. Forty-seven skin flaps were elevated and the epigastric vein was occluded by a microvascular clamp for 8 hours. Group 1 received DMSO (1.5 gm/kg) intraperitoneally at reperfusion. Group 2 received saline solution, group 3 received DMSO at reperfusion and every day for 5 days, group 4 received DMSO preoperatively and then as in group 3, and group 5 was the saline solution control for groups 3 and 4. DMSO did not increase percent flap survival when given as a single dose at reperfusion (40.6% +/- 42.7%) compared with saline solution (33.7% +/- 41.2%). When DMSO was continued in the postoperative period, group 3 (86.2% +/- 25.8%) and group 4 (78.0% +/- 32.5%) had significantly better survival than the saline solution control group (32.6% +/- 39.8%) (p < 0.01 and p < 0.03, respectively). There was no significant difference between groups 3 and 4. DMSO administered at reperfusion and postoperatively for 5 days significantly increased flap survival. It is hypothesized that this occurs through scavenging deleterious free radical species. This effect may have clinical significance.

Failure of skin flaps remains a significant clinical problem. The dorsal rat flap, a reliable experimental model, was used to test the efficacy of cimetidine in treating a failing flap. Flaps were elevated in 45 rats divided into three equal groups. Group 1 was a saline control group, Group 2 received cimetidine 250 mg/kg three times a day for 7 days postoperatively, and Group 3 received cimetidine for 1 day before surgery, and then as in Group 2. Necrosis was assessed on the seventh postoperative day. Group 2 had 31.1 +/- 1.3 (mean % +/- SEM) necrosis, significantly better than saline control animals (p less than 0.01) and pretreated animals (p less than 0.05). These results suggest the usefulness of cimetidine in ischemic flap surgery.

Free radicals have been shown to play an important role in hematoma-induced flap necrosis. The present study investigated the effect of deferoxamine, a free radical scavenger and iron chelator, on flap necrosis. A 4 X 2 cm dorsal flap was raised in Fischer inbred rats, and 3 cc of blood from inbred donors was instilled beneath the flap. Saline-treated control animals (Group 1) were compared with two experimental groups. In Group 2, deferoxamine 150 mg/kg was administered 15 minutes before surgery and every 8 hours for 5 days. In Group 3, deferoxamine was given every 8 hours for 3 days before surgery and every 8 hours for 5 days postoperatively. Flap necrosis was assessed on postoperative day 5. Group 2 had significantly less necrosis, 18.6%, than the control group, 64.0% (p less than 0.001). Group 3, with 36.0% necrosis, also showed improvement (p less than 0.05). Group 2 and Group 3 were not significantly different. Deferoxamine, a safe and well-tolerated free radical scavenger, greatly enhanced flap survival, presumably by the neutralization of damaging free radical species and by chelation of iron.

Hypercalcemia associated with head and neck malignancy is not an uncommon occurrence; its causes are multiple. Eight hypercalcemic patients with head and neck malignancy were studied. Serum calcium, serum phosphorus, tubular phosphorus threshold, fasting calcium excretion, plasma 1,25-dihydroxyvitamin D, nephrogenous cyclic adenosine monophosphate (AMP), and immunoreactive parathyroid hormone were measured. Excessive dietary calcium administration in the form of an oral hyperalimentation preparation appeared to be the cause of hypercalcemia in 2 patients. Six patients demonstrated humorally mediated hypercalcemia. These patients resembled patients with primary hyperparathyroidism in having elevated nephrogenous cyclic AMP excretion and reduced proximal tubular phosphorus reabsorption, but they differed from patients with primary hyperparathyroidism by having normal levels of immunoreactive parathyroid hormone, markedly increased fasting calcium excretion, and strikingly reduced mean plasma levels of 1,25-dihydroxyvitamin D. These data strongly suggest that the humoral factor responsible for hypercalcemia in patients with head and neck cancer is not parathyroid hormone, and that patients with hyperparathyroidism can now be distinguished with confidence from those with malignancy-associated hypercalcemia.