Current practice: postoperative and return to play trends after ACL reconstruction by fellowship-trained sports surgeons.

PURPOSE: Advances in anterior cruciate ligament (ACL) reconstruction have allowed for many progressions in postoperative management. However, there is no standardized protocol for immediate postoperative management or return to play. Our objective was to evaluate current trends in immediate postoperative and return to sport practices after ACL reconstruction. LEVEL OF EVIDENCE: Cross sectional study, Level IV. METHODS: Surveys were obtained from four large sports fellowship alumni networks. Demographics included years of practice and ACLs performed per year. Postoperative questions included weight bearing status, brace use and continuous passive motion (CPM) use. Return to play included time for return, brace use and metrics used for clearance to sport. RESULTS: A total of 143 surveys were completed (32% response rate). Average years in practice were 15.1 years. Average ACL reconstructions performed per year was 20-50 in 44% and 50-100 in 29%. 26% used CPM in all patients, 8% if concomitant meniscal repair and 66% never. Bracing after surgery was used in 84% and 48% after return to play. Return to play was allowed at 6-9 months in 67% and overall 94% from 6 to 12 months. No consensus on return to play metrics was used, with the hop test being most important followed by specific time point after surgery. CONCLUSION: Immediate weight bearing after surgery is commonplace with intermittent CPM use. Bracing is common postoperatively and half the time with return to play. Return to play is typically allowed after at least 6 months with no consensus on return to sport metrics. Years after fellowship and ACLs performed yearly had no correlation with postoperative practices.

The utility of botulinum toxin A in the repair of distal biceps tendon ruptures.

PURPOSE: The purpose of our study is to report the outcomes and complications in patients who underwent distal biceps tendon repair with the use of Botulinum toxin A (BoNT-A) as an adjunct to surgery. METHODS: A retrospective review of 14 patients who underwent 15 distal biceps tendon repairs was performed. All repaired tendons had their correlating muscle bellies injected intraoperatively with a mixture of 100U of BoNT-A and 10 ml of normal saline. Each patient was evaluated for surgical and post-operative complications and followed with Disabilities of the Arm, Shoulder and Hand (DASH) Disability Scores. RESULTS: The cohort was exclusively male, 14/14 (100%). The mean age at procedure was 52.1 years (range: 29-65 years). Types of injuries repaired included: 12 acute biceps tendon ruptures, one chronic partial (> 50% of tendon) biceps tear, and two chronic biceps ruptures. Average final follow-up was 32.9 months (SD: 19.6; range: 7.07-61.72). Average time to repair of chronic injury was 5.75 months (range: 2-12 months). There were no intraoperative complications, and all patients were discharged home on the day of surgery. Average DASH score at latest follow-up was 4.9 (range: 0.0-12.5). All patients had return of function of paralyzed muscle prior to final follow-up. One patient required an incision and drainage for a deep infection 1 week post-operatively, without any further complications. Another patient required operative removal of heterotopic ossification located around the tendon fixation site, which was the result of a superficial infection treated with antibiotics 2 weeks post-operatively. This patient later healed with improvement in supination/pronation range-of-motion and no further complications. CONCLUSIONS: Injection of BoNT-A is safe and effective to protect distal biceps tendon repair during the early phases of bone-tendon healing. CLINICAL RELEVANCE: BoNT-A may is safe and effective to protect distal biceps tendon repair. The utility of BoNT-A as an adjunct to surgical repair may be applicable to acute or chronic tears as well as repairs in the non-compliant patient without decreases in functional scores after return of function of the biceps muscle. LEVEL OF EVIDENCE: Level 4.

Penetrating mine injury to the heart with a pericardial tamponade.

Cardiac tamponade is a life-threatening emergency. Immediate recognition and surgical intervention is essential to preserve myocardial function and maintain cardiac output. The following is a case report of a penetrating mine injury to the heart with a resulting pericardial tamponade. The positive outcome and the facilities in which the resuscitation and surgical repair occurred make this a unique case report.

Role of bacterial hemolysin production in induction of macrophage Ia expression during infection with Listeria monocytogenes.

The production of a hemolytic exotoxin (Hly) termed listeriolysin O (LLO) is a major determinant of the virulence of the Gram-positive bacterium Listeria monocytogenes. As determined by lethal inoculum size, LLO- strains of L. monocytogenes generally are several orders of magnitude less virulent than their LLO+ counterparts. The generation of protective anti-Listeria T cell immunity also has been shown to depend on the LLO phenotype of the bacteria present during primary infection, although the cellular basis of this observation is not known. The experiments described here address the role of LLO in regulation of the expression of class II MHC (Ia) molecules by murine macrophages. Because Ia expression by macrophages and other APC is thought to be a central factor in the generation of T cells specific for bacterial Ag, we have tested the hypothesis that the failure of LLO- strains to elicit anti-Listeria T cell responses might be secondary to an inability of these strains to stimulate increases in macrophage Ia levels. Our results show that the macrophage Ia response after i.p. injection of L. monocytogenes correlates strongly with the LLO phenotype of the bacteria. The presence of LLO+ organisms, even at very small numbers (as few as 10), elicits a striking increase in Ia expression by peritoneal macrophages. In contrast, even at very high numbers (up to 10(6) per mouse), LLO- bacteria fail to stimulate a strong Ia response. We also have analyzed macrophage Ia expression after injection of lysates of Escherichia coli expressing recombinant LLO protein. Similar to the results obtained with LLO+ and LLO- L. monocytogenes, we have observed Ia induction only with LLO+ lysates. Ia induction by this crude recombinant LLO preparation can be inhibited by cholesterol or heat. Furthermore, supernatants derived from cultures of LLO+ (but not LLO-) L. monocytogenes can cause Ia induction when administered via i.p. injection. Taken together, these findings suggest that the failure of macrophages to respond to LLO- organisms with an increase in Ia expression may be a major underlying cause of the failure of these bacteria to induce Listeria-specific protective T cell immunity. Furthermore, we propose that the induction of macrophage Ia expression in response to bacterial toxins such as Hly may represent one component of a set of early, innate immune mechanisms, and that this induction may provide a critical "bridge" to later, acquired, Ag-specific immune processes.

Lipopolysaccharide responsiveness is an important factor in the generation of optimal antigen-specific T cell responses during infection with gram-negative bacteria.

We previously have found that the endotoxin (LPS) of Gram-negative bacteria is a major determinant of macrophage Ia induction during infection with these organisms. Specifically, i.p. injection of Gram-negative bacteria elicits a striking macrophage Ia response in LPS-responder mice but virtually no response in LPS-low-responder mice. As an extension of these findings, in this report we have tested the hypothesis that the inability of LPS-low responder mice to mount an Ia response during Gram-negative infection may in turn impair their capacity for generation of appropriate antibacterial T cell responses. Our results demonstrate that for a variety Gram-negative organisms (Salmonella typhimurium, Salmonella minnesota, and Escherichia coli), both macrophage Ia induction and the generation of Ag-specific T cell responses are controlled by the lps gene. We also have asked whether the expression of additional toxins (other than LPS) by infecting Gram-negative organisms can "override" this lps gene control of macrophage and T cell responses. We have found that infection of LPS-low-responder mice with an E. coli strain that expresses a hemolytic exotoxin (Hly) leads to the induction of macrophage Ia expression as well as the generation of T cell responses to both the Hly molecule and to other E. coli-associated Ag, whereas no responses are generated during infection with a Hly- strain. This result suggests that LPS-low responder mice have no inherent defect in T cell responsiveness to Gram-negative bacterial Ag but rather that these mice fail to receive an LPS-mediated signal required for the induction of Ia expression and subsequent generation of peritoneal T cell immunity. These findings, when taken together with results presented in the accompanying paper, strengthen the argument that bacterial toxin production (and the ability of the host to respond to the toxin) can represent a critical determinant of the induction of macrophage Ia expression and in turn, of Ag-specific T cell responses during bacterial infection.

Role of listeriolysin-O (LLO) in the T lymphocyte response to infection with Listeria monocytogenes. Identification of T cell epitopes of LLO.

Using a murine model, we investigated the role of the bacterial exotoxin listeriolysin O (LLO) in cellular immunity to Listeria monocytogenes. A correlation between LLO production by infecting bacteria and generation of protective immunity to virulent LLO-producing bacteria was noted. Using isogeneic hemolysin (Hly+ or Hly-) strains of L. monocytogenes, we demonstrated that LLO production by infecting bacteria is required to elicit T cells reactive both to bacteria-associated Ag and to the secreted LLO molecule as measured by IL-2 production in vitro. Distinct sets of T cells specific for largely nonoverlapping pools of antigenic determinants represented by LLO and cell-associated Ag (heat-killed L. monocytogenes) are generated after infection. We have used models for prediction of T cell epitopes based on primary structure of LLO, and synthetic amphipathic LLO peptides were evaluated as Ag in vitro or as immunogenes in vivo. Infection of several strains of mice (H-2k and H-2d) with LLO-producing L. monocytogenes resulted in the generation of T cells that could respond consistently to two peptides, LLO 215-234 and LLO 354-371. Mouse strains lacking expression of I-E molecules (e.g., B10.A(4R) and C57BL/6) responded to LLO but not to the peptides tested. With C3HeB/FeJ mice, antibodies to I-Ek blocked the presentation of LLO 215-234. The importance of the N-terminal portion of LLO 215-234 was evidenced by the drastic reduction in antigenic activity of truncated peptides (e.g., LLO 221-234 and LLO 224-234). LLO 215-234, the strongest and most consistent activator of T cells from L. monocytogenes-immune mice, fit well some models for antigenic peptides in several ways. It could be predicted to form an amphipathic alpha-helix, it contained multiple "Rothbard motifs" (charged residue or glycine, two or three hydrophobic amino acids and then a glycine or polar residue), it had a net charge of +2, and it contained the correct spacing of amino acids (five to six residues between a hydrophobic and basic amino acid) that is characteristic of I-Ek-binding peptides. Immunization with 8 of 10 synthetic LLO peptides generated T cells that recognized the immunizing peptide in vitro, but such T cells were only poorly reactive with LLO. Our results indicate that LLO is an important target Ag for stimulation of CD4+ L. monocytogenes-specific T cells, and that LLO 215-234 is antigenically dominant in C3HeB/FeJ mice.

Role of lipopolysaccharide in induction of Ia expression during infection with gram-negative bacteria.

Lipopolysaccharide (LPS), a major component of the outer membrane of gram-negative bacteria, is known to be a potent modulator of many host immune functions, including the expression of products of the class II major histocompatibility locus (Ia molecules) by macrophages. LPS-mediated Ia induction is controlled by the lps gene. We sought to determine the role of LPS in the induction of Ia expression during infection with gram-negative bacteria. To address this question, we tested a simple prediction: if LPS is the primary determinant of Ia induction during gram-negative infection, then the Ia response to intraperitoneal injection of these organisms should be under the control of the lps gene. We found that while both LPS-responder and LPS-low-responder mice showed strong Ia responses to injection of either a gram-positive bacterium (Listeria monocytogenes) or concanavalin A, only the LPS-responder mice responded strongly to gram-negative organisms or to LPS alone. We interpret these results as strong evidence for the role of LPS as the primary determinant of Ia induction by gram-negative bacteria.