Vasospasm is known to have an adverse effect on the survival of free tissue transfers. Prolonged vasoconstriction decreases blood flow to the flap and promotes thrombosis at the anastomotic site. Because of its wide availability and rapid effect, topically applied lidocaine is used by many surgeons to prevent and correct vasospasm. Mucosal absorption of lidocaine is known to be rapid. Absorption by the surgical bed during microvascular reconstruction has not previously been determined. We had three specific aims: (1) to determine whether systemic absorption occurs, (2) if so, to determine the degree of absorption, and (3) to determine whether the type of reconstruction affects the degree of absorption. Twelve consecutive patients were entered into the study, four in a myocutaneous reconstructive group and eight in a fasciocutaneous group. Baseline serum lidocaine levels were drawn. After the initial application of lidocaine, levels were drawn every 30 minutes. Final levels were drawn 120 minutes after the last application. The total amount of lidocaine used ranged from 720 mg to 2600 mg. Application ranged from 7.5 mg/minute to 34.7 mg/minute (2 to 9 times the estimated toxic dose of 4 mg/minute for a patient weighing 70 kg). Results ranged from undetectable (<0.5 microg/ml) to minimal therapeutic levels (1.6 microg/ml). Toxic levels (>6.0 microg/ml) were not encountered. Significant (p < 0.05) differences were found between the fasciocutaneous group, which generally had no detectable serum levels, and the myocutaneous group, which had detectable subtherapeutic to minimally therapeutic levels. Doses considered toxic by intravenous or mucous membrane application may safely be applied topically. Greater absorption was found in the myocutaneous group, which is believed to be a result of the richer absorption surface provided by the muscular tissue.
Otolaryngologists are frequently presented with traumatic or surgical defects that require replacement of missing tissues to achieve optimal functional results. Although autologous or allogeneic tissue, aUoplasts, and metals have been used in various combinations successfully, each of these materials has drawbacks. In an effort to improve and expand our armamentarium, several researchers have demonstrated reproducible results growing cartilage or bone for host tissue replacement using tissue-engineered cell-polymer constructs. Studies have demonstrated that chondrocytes and osteoblasts implanted onto a synthetic mesh can produce mature cartilage or bone when grown subcutaneously in the nude mouse. Tissue produced in this fashion may require additional shaping to be suitable for use in specific defects. To determine whether mature cartilage and bone grown using a standardized cell-polymer construct will reliably retain their shape and tissue integrity after harvesting, shaping and reimplantation, the following study was designed.Using standard tissue-engineering techniques, 25 nude mice were implanted with a 1 cm 2 of synthetic mesh seeded with chondrocytes. Similarly, 25 nude mice were implanted with osteoblast-seeded mesh. After 6 weeks the tissue blocks were removed and carved into a two-dimensional seven-sided figure, similar to an incus. The tissue was photographed for digital analysis and reimplanted in nude mice, for a total incubation time of 20 weeks. At 20 weeks the tissue was again removed. Analysis with digital photography was performed for gross retention of size and shape, with 20% change considered significant. The tissue was also examined histologically for confirmation of mature cartilage and bone in each respective group. In this manner a custom bony or cartilaginous prosthesis could be tissue-engineered. The results of this study will be presented in detail, along with implications for future direction of tissue-engineering studies.
Primary ischemia is the first ischemic insult that occurs in flaps during free tissue transfer. Acute injury resulting from cessation of blood fl0w with subsequent reperfusion is mediated by several pathways, including production of reactive oxygen metabolites (free radicals), prostaglandins, and lipid peroxidases. Lipid peroxidases are produced after injury to cell membranes, which in turn react with adjacent membrane lipids, causing a deleterious chain reaction. Lipid peroxidase inhibitors, such as the lazaroid U74389F, a 21aminosteroid, distribute in the hydrophobic domains of cell membranes and inhibit this process.A study was designed to investigate the significance of lipid peroxidation injury to microvessels in primary ischemia in a skin flap model. Measurements were made in three groups of animals: control, primary ischemia, and primary ischemia with lazaroid pretreatment (3 mg/kg U74389F, Upjohn Co., Kalamazoo, Mich.). Male Sprague-Dawley rats weighing 350 to 450 gm were kept under standard laboratory conditions. A rectangular 3 • 5 cm flap based on the inferior epigastric neurovascular pedicle was raised. Primary ischemia was induced by clamping the vascular pedicle for 150 minutes followed by 120 minutes of repeffusion. The flap was then placed under a customized intravital microscope and measurements of blood flow velocity and vessel diameter were made and analyzed by an image analysis system.Analysis of control group microcirculation data revealed mean red blood cell velocities and vessel diameters of 218 _+ 20.8 ~rrdsec and 17.0 _+ 1.74 ~tm, respectively. Animals subjected to ischemia and reperfusion showed reduced velocities of 165 _+ 17.3 ~tm/sec. Vessel diameters (14.4 _+ 1.12 ~tm) were not significantly different than the control group. The lazaroid pretreated group showed mean velocities and diameters similar to those observed in the control group, 202 +-21.9 ~tm/sec and 17.3 __ 1.21 ~tm, respectively. These data suggest that lipid peroxidation injury is involved in primary ischemia of pedicled flaps and that the 21-aminosteroid, U74389F, attenuates this injury.
Vasospasm is known to have an adverse effect on the survival of free tissue transfers. Prolonged vasoconstriction decreases blood flow to the flap and promotes thrombosis at the anastomotic site. Because of its wide availability and rapid effect, topically applied lidocaine is used by many surgeons to prevent and correct vasospasm. Mucosal absorption of lidocaine is known to be rapid. Absorption by the surgical bed during microvascular reconstruction has not previously been determined. We had three specific aims: (1) to determine whether systemic absorption occurs, (2) if so, to determine the degree of absorption, and (3) to determine whether the type of reconstruction affects the degree of absorption. Twelve consecutive patients were entered into the study, four in a myocutaneous reconstructive group and eight in a fasciocutaneous group. Baseline serum lidocaine levels were drawn. After the initial application of lidocaine, levels were drawn every 30 minutes. Final levels were drown 120 minutes after the last application. The total amount of lidocaine used ranged from 720 mg to 2600 mg. Application ranged from 7.5 mg/minute to 34.7 mg/minute (2 to 9 times the estimated toxic dose of 4 mg/minute for a patient weighing 70 kg). Results ranged from undetectable (<0.5 μg/ml) to minimal therapeutic levels (1.6 μg/ml). Toxic levels (>6.0 μg/ml) were not encountered. Significant ( p < 0.05) differences were found between the fasciocutaneous group, which generally had no detectable serum levels, and the myocutaneous group, which had detectable subtherapeutic to minimally therapeutic levels. Doses considered toxic by intravenous or mucous membrane application may safely be applied topically. Greater absorption was found in the myocutaneous group, which is believed to be a result of the richer absorption surface provided by the muscular tissue. (Otolaryngol Head Neck Surg 1997;117:93–8.)
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