Tachycardia in breast reconstructive microsurgery: Affirmation of the IMA tachycardia syndrome.

INTRODUCTION: The internal mammary vessels are frequently chosen as recipient vessels for breast free flap reconstruction. We have noticed that when using the internal mammary recipients that these patients have a propensity for tachycardia that was not previously observed. Our aim was to investigate the factors related to perioperative tachycardia in the microsurgical breast reconstruction population and to address whether use of the internal mammary system is a causative factor in tachycardia. METHODS: A retrospective chart review was conducted to identify patients who underwent abdominal-based microvascular breast reconstruction at the Washington University School of Medicine between 2002 and 2012 to identify the presence of tachycardia. After application of exclusion criteria, 76 microvascular abdominal-based free flap reconstructions were identified. The internal mammary (IM) TRAM group (n = 24) and the thoracodorsal (TD) TRAM group (n = 52) were compared. A binomial logistic regression was performed with the presence of tachycardia as the dependent variable. RESULTS: There was a higher incidence of tachycardia in the IM TRAM group when compared to the TD TRAM group (p = 0.004). The variables predictive of tachycardia in our logistic regression model were IMA recipient (p = 0.04), need for transfusion (p = 0.03), and presence of fever (p = 0.01). CONCLUSION: Our study reaffirms that there are several factors that are predictive of tachycardia in the setting of microvascular breast reconstruction. The IMA syndrome should be a recognized cause of tachycardia as using these recipient vessels are shown to be predictive of postoperative tachycardia as shown in our study.

FK506 rescues peripheral nerve allografts in acute rejection.

This study investigated the ability of the immunosuppressant FK506 to reverse nerve allograft rejection in progress. Eighty-four Buffalo rats received posterior tibial nerve grafts from either Lewis or Buffalo donor animals. Allografts were left untreated for either 7, 10, or 14 days before receiving daily subcutaneous FK506 injections (2 mg/kg). Time-matched control animals received either an isograft, an allograft with continuous FK506, or an allograft with no postoperative FK506 therapy. All animals underwent weekly evaluation of nerve function by walking track analysis. Experimental group animals were sacrificed either immediately prior to initiation of FK506 therapy (days 7, 10, or 14), after 2 weeks of immunosuppressive treatment, or 8 weeks postsurgery. Histomorphometric analysis, consisting of measurements of total number of nerve fibers, neural density, and percent of neural debris, demonstrated a statistically significant increase in regeneration in the isograft group relative to the untreated allograft group within 28 days of transplantation. Grafts harvested from animals receiving 2 weeks of FK506 after 7 or 10 days of rejection were histomorphometrically similar to time-matched isografts. By contrast, grafts from animals receiving 2 weeks of FK506 following 14 days without therapy resembled untreated allografts and demonstrated significant histomorphometric differences from isografts at the corresponding time point. Analysis of walking track data confirmed that relative to untreated allografts, functional recovery was hastened in animals receiving an isograft, or allograft treated with FK506. This study demonstrated that when started within 10 days of graft placement, FK506 could reverse nerve allograft rejection in rats evaluated following 2 weeks of treatment.

End-to-side neurorrhaphy and lateral axonal sprouting in a long graft rat model.

OBJECTIVE/HYPOTHESIS: Controversy exists regarding collateral axonal sprouting across an end-to-side neurorrhaphy to provide functional motor reinnervation of a target organ without compromise of the donor nerve. Rat models may be limited in the study of end-to-side repair given potential contamination from the proximal nerve stump of the recipient distal nerve and the use of antagonistic muscle groups for donor and recipient. The current study attempts to address these issues by using a rat model in which an end-to-side coaptation is performed with a long graft interposed between the intact donor tibial nerve and the divided, distal contralateral tibial nerve. MATERIALS AND METHODS: The graft used in proximal end-to-side coaptation consisted of both sciatic nerves in a donor syngeneic animal. The distal repair to the contralateral tibial nerve was done immediately or in a delayed fashion to allow potential motor axons to transverse the graft before division of the recipient tibial nerve. RESULTS: After 24 weeks, axons were noted to transverse the entire distance of the graft and into the contralateral distal posterior tibial nerve. A significant increase in axonal numbers was observed in the immediate repairs compared with the delayed. No animal recovered functional motor ability on the contralateral side as assessed by walking tracks. CONCLUSIONS: These findings suggest the importance of immediate distal neurotrophic factors in encouraging nerve regeneration even in a long graft end-to-side repair. Our model is successful in demonstrating innervation through an end-to-side coaptation but questions its use given the lack of motor recovery.

Need for velopharyngeal management following palatoplasty: an outcome analysis of syndromic and nonsyndromic patients with Robin sequence.

The Robin sequence is a pathogenetically and etiologically heterogeneous condition that can be a nonsyndromic anomaly or one feature of many syndromes. Little information is available regarding the distribution of patients having Robin sequence, with or without associated syndromes, who develop velopharyngeal dysfunction. In order to discern whether patients with Robin sequence, nonsyndromic and/or syndromic, have different velopharyngeal dysfunction rates from those observed among all patients undergoing palatoplasty during the same time period, a retrospective study was undertaken. The charts of 873 patients with overt clefts of the secondary palate managed at a single cleft center between 1978 and 1992 were reviewed. Diagnostic criteria for Robin sequence included cleft palate without cleft lip, microretrognathia, and perinatal respiratory and/or feeding difficulties; 79 such patients (9 percent) were identified from the initial group of 873. Of these, 58 patients (7 percent) were at least 3 years of age and had sufficient follow-up to allow for evaluation of speech outcome by an experienced speech pathologist through a variety of methodologies (videonasendoscopy, speech videofluoroscopy, perceptual speech characteristics). This group comprised the Robin sequence study population. All Robin sequence patients' charts were reviewed by a medical geneticist to confirm the presence or absence of a syndrome. Of the original 873 patients, there were 127 non-Robin sequence patients who were sufficiently cooperative in diagnostic testing to yield definitive information. This group comprised the non-Robin sequence study population. Among nonsyndromic Robin sequence patients, 15 of 34 (44 percent) developed velopharyngeal dysfunction and required velopharyngeal management, while 2 of 24 syndromic patients (8 percent) developed velopharyngeal dysfunction (p = 0.003). Of the 127 non-Robin sequence isolated cleft palate patients, 113 were nonsyndromic, of whom 18 percent (20 of 113) required velopharyngeal dysfunction management, and 14 were syndromic, of whom 64 percent (9 of 14) required velopharyngeal dysfunction management (p = 0.00009). We conclude that nonsyndromic Robin sequence patients have a higher rate of postpalatoplasty velopharyngeal dysfunction than the nonsyndromic non-Robin sequence cleft population. Outcome analysis of velopharyngeal function in cleft patients should take into account patients who have cleft palate in association with Robin sequence, with or without a recognizable syndrome.

Does preexisting posterior pharyngeal wall motion drive the dynamism of sphincter pharyngoplasty?

Lateral speech videofluoroscopic evaluations were videotaped preoperatively and postoperatively for 20 patients who underwent sphincter pharyngoplasty. Randomized videotapes were constructed and subsequently evaluated by speech/language pathologists experienced in assessing patients with velopharyngeal dysfunction. Rating forms assessing various motion parameters of the posterior pharyngeal wall were completed and analyzed statistically. Results showed that the posterior pharyngeal wall configuration postoperatively was less likely to be rated as smooth relative to the preoperative configuration (p = 0.019). No other statistically significant data were obtained, although there was a trend for posterior pharyngeal wall movement rated as discrete preoperatively to be described as generalized postoperatively. We conclude that when comparing preoperative and postoperative parameters, sphincter pharyngoplasty does not significantly affect posterior pharyngeal wall motion. Posterior pharyngeal wall configuration is less likely to be categorized as smooth after sphincter pharyngoplasty relative to the preoperative condition. Although sphincter pharyngoplasty has been shown to improve velopharyngeal function, there is little evidence from this study to suggest that preexisting posterior pharyngeal wall motion causes sphincteric movement.

Hemorrhage from the inferior vena cava versus the ear artery: a comparison of cardiovascular and hormonal responses in conscious rabbits.

There are inherent complications associated with chronic indwelling venous catheters for use as bleed catheters in long term hemorrhage experiments in conscious animals. As an alternative we have developed a protocol for bleeding conscious rabbits using a disposable catheter in the central ear artery. Previously we had bled rabbits through a catheter chronically implanted in the inferior vena cava (IVC); thus, we were interested in any potential differences in the hormonal (vasopressin and renin) and cardiovascular profile during hemorrhage between the IVC and ear artery bleeds. Rabbits underwent two bleeds, 1 week apart, one using the indwelling IVC catheter and the other with an ear artery (EA) catheter. We compared the mean arterial pressure (MAP), heart rate (HR), plasma vasopressin (AVP), and plasma renin activity (PRA) before and during hemorrhage. Baseline cardiovascular and hormonal values were the same, regardless of choice of bleed site. In addition there were no differences between bleed sites in the rate of fall of MAP (slope: IVC, 0.24 +/- 0.05; EA, 0.26 +/- 0.04) and the rate of rise of HR (slope: IVC, -1.37 +/- 0.22; EA, -1.20 +/- 0.19). Finally the AVP and PRA values associated with a MAP of 50 mmHg (1 mmHg = 133.3 Pa) (close to peak levels achieved during the hemorrhage) were also not different between IVC and EA bleeds. Given that the profiles of the bleeds were not different and that surgical implantation, possible infection, and daily flushing were avoided by the use of the EA catheter, we concluded that use of the EA as a site for bleeding conscious rabbits was justified.

Salvaging the failed pharyngoplasty: intervention outcome.

OBJECTIVE: This paper reports on the rates of failure of operations (pharyngeal flap and sphincter pharyngoplasty) performed for management of velopharyngeal dysfunction, and outcome following their revision. DESIGN: Anatomic abnormalities associated with unacceptable vocal resonance and nasal air escape following pharyngeal flap and sphincter pharyngoplasty were critiqued. The results of primary pharyngeal flap were evaluated for 65 patients, and the results of primary sphincter pharyngoplasty were evaluated for 123 patients. All patients were treated for velopharyngeal dysfunction. The definition of surgical failure was based on persistent hypernasality and/or nasal turbulence on perceptual speech evaluation, and incomplete velopharyngeal closure on instrumental evaluation, at least 3 months postoperatively. SETTING: All patients were evaluated and managed at the Cleft Palate and Craniofacial Deformities Institute, St. Louis Children's Hospital, a tertiary cleft care center. PATIENTS, PARTICIPANTS: All patients had failed surgical management initially, either with pharyngeal flap or sphincter pharyngoplasty, and all underwent repeat preoperative and postoperative perceptual speech evaluations; real-time lateral phonation fluoroscopy including still reference views; and flexible nasendoscopy of the velopharynx using standard speech protocols. INTERVENTIONS: Revisional surgery for both procedures consisted of either tightening of the sphincter pharyngoplasty or pharyngeal flap port(s) or reinsertion of the sphincter pharyngoplasty or pharyngeal flaps following dehiscence. MAIN OUTCOME MEASURES: The main outcome measure was normalcy of velopharyngeal function, i.e., elimination of perceptual hypernasality and instrumental evidence of complete velopharyngeal closure. The rates of pharyngeal flap failure and sphincter pharyngoplasty failure were determined for those patients requiring surgical revision. RESULTS: Thirteen of 65 patients (20%) who underwent primary pharyngeal flap required revisional surgery. Of these 13 patients, eight were managed successfully with a single revisional operation. The remaining five patients (38%) continued to exhibit velopharyngeal dysfunction and underwent a second revision consisting of tightening or augmentation of the lateral ports. Speech results were satisfactory in all patients so treated; however, hyponasality with no other airway morbidity occurred in all five. Twenty of 123 patients (16%) who underwent primary sphincter pharyngoplasty required surgical revision. Of these 20 patients, 17 were managed successfully. For both procedures, the principal cause of failure was partial or complete flap dehiscence. CONCLUSIONS: Rates of primary pharyngeal flap failure are roughly equivalent to rates of primary sphincter pharyngoplasty failure. Pharyngeal flap and sphincter pharyngoplasty failures can be salvaged with revisional surgery, which can provide a velopharyngeal mechanism capable of complete closure. Revisional surgery is usually associated with denasal speech.

Effects of FKBP-12 ligands following tibial nerve injury in rats.

The neuroregenerative properties of FK506, an FKBP-12 ligand that inhibits calcineurin, and V-10,367, an FKBP-12 ligand that does not inhibit calcineurin, were evaluated in crush and transection models. Rats were randomly assigned to one of seven groups, including untreated controls and FK506- or V-10,367-treated experimental groups. Following crush or transection nerve injury, animals were assessed with walking tracks, and histomorphometry. FK506-treated animals demonstrated significant functional recovery 11 days following crush and 18 days following transection injury. In untreated and V-10,367 treated animals, nerves recovered 13 days following crush injury, but did not improve significantly prior to sacrifice at 28 days in animals sustaining a transection injury. No statistically significant differences in histomorphometric parameters were identified between any of the groups. The study confirms that FK506 accelerates recovery from tibial nerve injury.

Safe injection of cultured schwann cells into peripheral nerve allografts.

The effects of cultured host Schwann cells on axonal regeneration in peripheral nerve allografts were studied. Fischer rats served as recipient animals and Buffalo rats provided nerve allografts. Animals were randomized into 9 groups. Rats receiving tibial nerve isografts were left untreated (group I), or injected with isogeneic Fischer Schwann cells (group II) or placebo suspension (group III). Allografts obtained from Buffalo rats were left untreated (group IV), or received isogeneic Fischer Schwann cells (group V), 2 mg/kg Cyclosporin A and Fischer Schwann cells (group VI), 5 mg/kg Cyclosporin A (group VII), or 5 mg/kg Cyclosporin A with Schwann cells (group VIII). No Schwann cell tumors were identified 4 or 8 weeks postoperatively. Group IX animals, harvested 3 days postoperatively, demonstrated no evidence of injection injury. Schwann cells modestly improved axonal regeneration in both isografts and allografts and may have a clinical role in the treatment of peripheral nerve allografts.

Predictors of death in nonruptured and ruptured abdominal aortic aneurysms.

PURPOSE: This study evaluated perioperative variables to predict death in nonruptured and ruptured abdominal aortic aneurysm (AAA) surgery. METHODS: A consecutive review of all patients who underwent AAA surgery from January 1984 to December 1993 was carried out. Perioperative variables were analyzed with univariate and multivariate statistical models to predict mortality rates. RESULTS: Four hundred seventy-eight patients with nonruptured AAAs and 157 patients with ruptured AAAs were studied. In patients with nonruptured AAAs, the mortality rate was 3.8%. Using stepwise logistic regression analysis, independent predictors of death were perioperative myocardial infarction (odds ratio [OR], 5.0; p < 0.01), prolonged postoperative ventilation (OR, 4.0; p < 0.01), history of peripheral vascular disease (OR, 2.9; p < 0.01), preoperative renal dysfunction (OR, 2.7; p < 0.01), and history of congestive heart failure (OR, 2.6; p < 0.03). In patients with ruptured AAAs, the mortality rate was 46%. Analysis of preoperative variables using multivariate stepwise logistic regression found predictors of death to be preoperative unconsciousness (OR, 3.1; p < 0.01), advanced age (OR, 1.9; p < 0.01), and cardiac arrest (OR, 1.8; p < 0.05). In patients who survived the initial surgery for ruptured AAA, a second stepwise logistic regression model found independent predictors for subsequent postoperative death to be coagulation disorder (OR, 7.9; p < 0.01), ischemic colitis (OR, 6.4; p < 0.01), inotropic support beyond 48 hours (OR, 4.8; p < 0.01), delayed transport to operating room (OR, 4.6; p < 0.01), advanced age (OR, 4.4; p < 0.01), perioperative myocardial infarction (OR, 4.0; p < 0.05) and postoperative renal dysfunction (OR, 3.7; p < 0.01). CONCLUSION: Prolonged ventilation, perioperative myocardial infarction, a history of peripheral vascular disease, preoperative renal dysfunction, and a history of congestive heart failure are independent predictors of perioperative death in patients with nonruptured AAAs. For patients with ruptured AAAs, mortality rates can be estimated before surgery using age, level of consciousness, and cardiac arrest. For patients who survive the initial surgery for ruptured AAA, subsequent mortality rates can also be predicted.