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Biomedical subjects

R W Burk

Publications and source records attributed to R W Burk.

4 recordsLinked to original sources

A modification of the primary nasal correction in the rotation-advancement unilateral cleft lip repair.

Primary correction of the unilateral cleft lip nasal deformity remains a challenge to the cleft surgeon. We wish to present a method of primary nasal correction utilizing presurgical orthopedics with the Latham dentomaxillary advancement appliance, concomitant rotation-advancement cleft lip repair, gingivoperiosteoplasty, and immediate correction of the nasal cartilage distortion with an "open technique" utilizing the rotation-advancement incisions. Direct elevation and suture fixation of the cleft side alar cartilage is performed as well as recreation of the normal upper lateral/lower lateral cartilage relationship, repair of nasal web, and release of the vestibular lining utilizing an L-flap pedicled to the alar base. Details of the operative technique, observations of unilateral cleft nasal anatomy as visualized with the "open technique," and preliminary results are illustrated in patients followed as long as 5 years.

Cartilage↗

Lidocaine and epinephrine levels in tumescent technique liposuction.

The safety of lidocaine dosing in the tumescent technique has been well documented, but there is little evidence regarding the safety of combining tumescent lidocaine infiltration with subcutaneous lidocaine infiltration required in other aesthetic surgery. The safety of lidocaine and epinephrine dosing was investigated in 10 patients undergoing tumescent technique liposuction alone and in 10 patients undergoing tumescent liposuction with concurrent facial and aesthetic breast surgery by determining serum lidocaine and epinephrine levels at 3, 12, and 23 hours following infiltration of the tumescent solution and the subcutaneous lidocaine. The mean lidocaine dose of all patients was 22.3 mg/kg. All patients demonstrated safe lidocaine levels at all intervals, with the highest levels occurring in patients who received intravenous lidocaine at the induction of anesthesia. The peak epinephrine levels occurred at the 3-hour blood draw and were approximately four times physiologic. No patient demonstrated any subjective or objective signs of lidocaine or epinephrine toxicity.

Adult↗

Conceptual considerations in breast reconstruction.

As the therapy for breast cancer evolves, the plastic surgeon must consider the type of mastectomy, the stage of disease, the timing of operations, and the use of adjunctive therapy to continue to provide the best reconstructive option to the patient. All reconstructive results are judged by comparison to the opposite breast, which sometimes should be improved with a conservative reduction or mastopexy. The timing of secondary procedures should be appropriate to avoid interference with adjuvant therapy and provide a lasting result. The plastic surgeon also must be able to follow the reconstructed breast, recognize the pattern of local recurrence, and offer reconstructive options should the therapy require additional resection.

Breast Neoplasms↗

Toxic effects of catecholamines on skin.

The purpose of this study was to examine the effects of catecholamines on skin necrosis independent of their vasoactive effects. Rat abdominal or human breast skin was excised, pinned flat, and incubated at 37 degrees C for 6 hours in a buffered salt solution containing catecholamine. At 0.1 and 6 hours the lactate dehydrogenase (LDH) released from the skin and appearing in the buffer was determined spectrophotometrically. All groups showed similar LDH levels at 0.1 hour. Rat skin treated with greater than or equal to 10(-7) M epinephrine (33 times less than the 1:200,000 used clinically) or greater than or equal to 10(-5) M norepinephrine showed a significant increase in the LDH released at 6 hours versus controls (18.75 +/- 1.25 versus 13.75 +/- 1.25 and 29.25 +/- 2.96 versus 22.00 +/- 1.96 IV, respectively). Total tissue LDH levels were not significantly different at 0.1 or 6 hours. The toxic effect of epinephrine was eliminated by the addition of propranolol or selective beta 2 blockade, but not by alpha or beta 1 blockade. Therefore, this effect appears to be mediated largely by beta 2 receptors. Similar toxic effects were seen in human breast skin treated with 1:200,000 epinephrine and were blocked with propranolol. Phenylephrine at 1:20,000 demonstrated toxicity, but angiotensin II and vasopressin did not. These studies indicate that addition of catecholamine to ischemic rat or human skin accelerates skin death within 6 hours, but that the toxicity can be reversed with beta blockade.

Angiotensin II↗