Gregory D. Jay

The Potential for Improved Teamwork to Reduce Medical Errors in the Emergency Department

This article describes emergency department care work teams designed to improve team communication and coordination and reduce error. The core of this teamwork system is the teaching of teamwork behaviors and skills, development of teamwork habits, and creation of small work teams, all of which are key teamwork concepts largely drawn from successful aviation programs. Arguments for enculturating teamwork into ED practice are drawn from a retrospective study of ED malpractice incidents. Fifty-four incidents (1985-1996), a sample of convenience drawn from 8 hospitals, were identified and judged mitigable or preventable by better teamwork. An average of 8.8 teamwork failures occurred per case. More than half of the deaths and permanent disabilities that occurred were judged avoidable. Better teamwork could save nearly

Randomized, prospective trial of bilevel versus continuous positive airway pressure in acute pulmonary edema

3.50 per ED patient visit. Caregivers must improve teamwork skills to reduce errors, improve care quality, and reduce litigation risks.

The secreted glycoprotein lubricin protects cartilage surfaces and inhibits synovial cell overgrowth

OBJECTIVE To evaluate whether bilevel positive airway pressure, by actively assisting inhalation, more rapidly improves ventilation, acidemia, and dyspnea than continuous positive airway pressure (CPAP) in patients with acute pulmonary edema. DESIGN Randomized, controlled, double-blind trial. SETTING Emergency department in a university hospital. PATIENTS Twenty-seven patients, presenting with acute pulmonary edema, characterized by dyspnea, tachypnea, tachycardia, accessory muscle use, bilateral rales, and typical findings of congestion on a chest radiograph. INTERVENTIONS In addition to standard therapy, 13 patients were randomized to receive nasal CPAP (10 cm H2O), and 14 patients were randomized to receive nasal bilevel positive airway pressure (inspiratory and expiratory positive airway pressures of 15 and 5 cm H2O, respectively) in the spontaneous/timed mode that combines patient flow-triggering and backup time-triggering. MEASUREMENTS AND MAIN RESULTS After 30 mins, significant reductions in breathing frequency (32 +/- 4 to 26 +/- 5 breaths/min), heart rate (110 +/- 21 to 97 +/- 20 beats/min), blood pressure (mean 117 +/- 28 to 92 +/- 18 mm Hg), and Paco2 (56 +/- 15 to 43 +/- 9 torr [7.5 +/- 2 to 5.7 +/- 1.2 kPa]) were observed in the bilevel positive airway pressure group, as were significant improvements in arterial pH and dyspnea scores (p < .05 for all of these parameters). Only breathing frequency improved significantly in the CPAP group (32 +/- 4 to 28 +/- 5 breaths/min, p < .05). At 30 mins; the bilevel positive airway pressure group had greater reductions in Paco2 (p = .057), systolic blood pressure (p = .005), and mean arterial pressure (p = .03) than the CPAP group. The myocardial infarction rate was higher in the bilevel positive airway pressure group (71%) compared with both the CPAP group (31%) and historically matched controls (38%) (p = .05). Duration of ventilator use, intensive care unit and hospital stays, and intubation and mortality rates were similar between the two groups. CONCLUSIONS Bilevel positive airway pressure improves ventilation and vital signs more rapidly than CPAP in patients with acute pulmonary edema. The higher rate of myocardial infarctions associated with the use of bilevel positive airway pressure highlights the need for further studies to clarify its effects on hemodynamics and infarction rates, and to determine optimal pressure settings.

Simulation based teamwork training for emergency department staff: does it improve clinical team performance when added to an existing didactic teamwork curriculum?

The long-term integrity of an articulating joint is dependent upon the nourishment of its cartilage component and the protection of the cartilage surface from friction-induced wear. Loss-of-function mutations in lubricin (a secreted glycoprotein encoded by the gene PRG4) cause the human autosomal recessive disorder camptodactyly-arthropathy-coxa vara-pericarditis syndrome (CACP). A major feature of CACP is precocious joint failure. In order to delineate the mechanism by which lubricin protects joints, we studied the expression of Prg4 mRNA during mouse joint development, and we created lubricin-mutant mice. Prg4 began to be expressed in surface chondrocytes and synoviocytes after joint cavitation had occurred and remained strongly expressed by these cells postnatally. Mice lacking lubricin were viable and fertile. In the newborn period, their joints appeared normal. As the mice aged, we observed abnormal protein deposits on the cartilage surface and disappearance of underlying superficial zone chondrocytes. In addition to cartilage surface changes and subsequent cartilage deterioration, intimal cells in the synovium surrounding the joint space became hyperplastic, which further contributed to joint failure. Purified or recombinant lubricin inhibited the growth of these synoviocytes in vitro. Tendon and tendon sheath involvement was present in the ankle joints, where morphologic changes and abnormal calcification of these structures were observed. We conclude that lubricin has multiple functions in articulating joints and tendons that include the protection of surfaces and the control of synovial cell growth.

Homology of lubricin and superficial zone protein (SZP): products of megakaryocyte stimulating factor (MSF) gene expression by human synovial fibroblasts and articular chondrocytes localized to chromosome 1q25.

Objective: To determine if high fidelity simulation based team training can improve clinical team performance when added to an existing didactic teamwork curriculum. Setting: Level 1 trauma center and academic emergency medicine training program. Participants: Emergency department (ED) staff including nurses, technicians, emergency medicine residents, and attending physicians. Intervention: : ED staff who had recently received didactic training in the Emergency Team Coordination Course (ETCC®) also received an 8 hour intensive experience in an ED simulator in which three scenarios of graduated difficulty were encountered. A comparison group, also ETCC trained, was assigned to work together in the ED for one 8 hour shift. Experimental and comparison teams were observed in the ED before and after the intervention. Design: Single, crossover, prospective, blinded and controlled observational study. Teamwork ratings using previously validated behaviorally anchored rating scales (BARS) were completed by outside trained observers in the ED. Observers were blinded to the identification of the teams. Results: There were no significant differences between experimental and comparison groups at baseline. The experimental team showed a trend towards improvement in the quality of team behavior (p = 0.07); the comparison group showed no change in team behavior during the two observation periods (p = 0.55). Members of the experimental team rated simulation based training as a useful educational method. Conclusion: High fidelity medical simulation appears to be a promising method for enhancing didactic teamwork training. This approach, using a number of patients, is more representative of clinical care and is therefore the proper paradigm in which to perform teamwork training. It is, however, unclear how much simulator based training must augment didactic teamwork training for clinically meaningful differences to become apparent.

The role of lubricin in the mechanical behavior of synovial fluid

We have previously identified megakaryocyte stimulating factor (MSF) gene expression by synovial fibroblasts as the origin of lubricin in the synovial cavity. Lubricin is a mucinous glycoprotein responsible for the boundary lubrication of articular cartilage. MSF has a significant homology to vitronectin and is composed of 12 exons. RNA was purified from human synovial fibroblasts and articular chondrocytes grown in vitro from tissue explants obtained from subjects without degenerative joint disease. RT‐PCR was used with multiple complimentary primer pairs spanning the central mucin expressing exon 6 of the MSF gene and individual exons on both the N‐ and C‐terminal sides of exon 6. Exons 2, 4 and 5 appear to be variably expressed by synovial fibroblasts and articular chondrocytes. Lubricating mucin, in the form of MSF, is expressed by both chondrocytes and synovial fibroblasts in vitro. Both lubricin and superficial zone protein (SZP), a related proteoglycan, share a similar primary structure but could differ in post‐translational modifications with O‐linked oligosaccharides which are predominant in lubricin and with limited amounts chondroitin and keratan sulfate found in SZP. Since most of the MSF exons are involved in the expression of lubricating mucin, a strong homology to vitronectin persists. It is therefore appropriate to consider that both SZP and lubricin occupy a new class of biomolecules termed tribonectins. Screening of a human genome bacterial artificial chromsome (BAC) library with a cDNA primer pair complimentary for exon 6 identified two clones. Both clones were complimentary for chromosome 1q25 by in situ hybridization. This same locus was previously implicated in camptodactyl‐arthropathy‐pericarditis syndrome (CAP) by genetic mapping. It is hypothesized that CAP, a large joint arthropathy, may be associated with ineffective boundary lubrication provided by synovial fluid.

Boundary lubrication by lubricin is mediated by O-linked β(1-3)Gal-GalNAc oligosaccharides

Synovial fluid is a semidilute hyaluronate (HA) polymer solution, the rheology of which depends on HA–protein interactions, and lubricin is a HA-binding protein found in synovial fluid and at cartilage surfaces, where it contributes to boundary lubrication under load. Individuals with genetic deficiency of lubricin develop precocious joint failure. The role of lubricin in synovial fluid rheology is not known. We used a multiple-particle-tracking microrheology technique to study the molecular interactions between lubricin and HA in synovial fluid. Particles (200 nm mean diameter) embedded in normal and lubricin-deficient synovial fluid samples were tracked separately by using multiple-particle-tracking microrheology. The time-dependent ensemble-averaged mean-squared displacements of all of the particles were measured over a range of physiologically relevant frequencies. The mean-squared displacement correlation with time lag had slopes with values of unity for simple HA solutions and for synovial fluid from an individual who genetically lacked lubricin, in contrast to slopes with values less than unity (α ≈ 0.6) for normal synovial fluid. These data correlated with bulk rheology studies of the same samples. We found that the subdiffusive and elastic behavior of synovial fluid, at physiological shear rates, was absent in fluid from a patient who lacks lubricin. We conclude that lubricin provides synovial fluid with an ability to dissipate strain energy induced by mammalian locomotion, which is a chondroprotective feature that is distinct from boundary lubrication.

CHARACTERIZATION OF A BOVINE SYNOVIAL FLUID LUBRICATING FACTOR. I. CHEMICAL, SURFACE ACTIVITY AND LUBRICATING PROPERTIES

Lubrication of mammalian joints is mediated by lubricin, a product of megakaryocyte stimulating factor gene (MSF; GenBank accession #U70136) expression. Lubricin (Mr ∼ 240 kDa) is a mucinous glycoprotein which is 50% (w/w) post-translationally modified with β(1-3)Gal-GalNAc incompletely capped with NeuAc, and lubricates apposed cartilaginous surfaces in the boundary mode through an unknown mechanism. Both bovine and human lubricin were purified from synovial fluid and digested with recombinant glycosidases. Released oligosaccharides were identified and quantified by fluorophore assisted carbohydrate electrophoresis (FACE). Corresponding digests of human lubricin were also assayed in a friction apparatus oscillating latex rubber against polished glass at a pressure of 0.35 × 106 N/m2 and the coefficient of friction (μ) was measured. Digestion with α2,3-neuraminidase decreased lubricating ability by 19.3%. Partial removal of β(1-3)Gal-GalNAc moieties by endo-α-N-acetyl-D-galactosaminidase reduced lubricating ability by 77.2%. Human lubricin digested with combined α2,3-neuraminidase and β1-3,6-galactosidase continued to lubricate at 52.2% of its nominal value. Both bovine and human lubricin released 48.6% and 54.4% of total β(1-3)Gal-GalNAc sidechains following digestion with endo-α-N-acetyl-D-galactosaminidase. Biological boundary lubrication by synovial fluid in vitro is provided primarily by extensive O-linked β(1-3)Gal-GalNAc.

Decreased lubricin concentrations and markers of joint inflammation in the synovial fluid of patients with anterior cruciate ligament injury

A lubricating glycoprotein (PSLF) with an apparent molecular weight of 280 kDa was purified from bovine synovial fluid by anion exchange, molecular sieve chromatography, and density gradient centrifugation. Lubrication was measured under boundary conditions as lowering of the coefficient of friction (mu) between oscillating natural latex and polished glass. Lubricating ability was first observed at a concentration of 200 micrograms/ml and became maximal at 260 micrograms/ml. Hydrophobic interfacial tension measurements indicated that at the former concentration, monolayers of PSLF formed. Sugar digestions showed that lubricating ability depends upon the terminal galactose of the molecule. PSLF is similar if not identical to lubricin. It is proposed that a repulsive hydration force is the molecular mechanism for lubricating activity.

Association between friction and wear in diarthrodial joints lacking lubricin

OBJECTIVE To study the effect of anterior cruciate ligament (ACL) injury on lubricin concentrations in synovial fluid (SF) and its correlation with time postinjury, inflammatory cytokines, lubricin-degrading enzymes, and SF proteoglycan content. METHODS SF samples were obtained from both knees of 30 patients with unilateral ACL insufficiency, 32-364 days postinjury. Lubricin, inflammatory cytokines (interleukin-1beta [IL-1beta], tumor necrosis factor alpha [TNFalpha], and IL-6), and catabolic enzymes (procathepsin B and neutrophil elastase) were measured in SF from injured and contralateral (uninjured) joints, by enzyme-linked immunosorbent assay. Sulfated glycosaminoglycan (sGAG) levels in the SF were measured by Alcian blue binding assay. RESULTS SF lubricin concentrations were significantly (P < 0.001) reduced at an early stage following ACL injury when compared with those in the contralateral joint. Within 12 months, the lubricin concentration in the injured knee (slope = 0.006, SE = 0.00010, P < 0.001) approached that in the contralateral knee, which did not change with time (slope = -0.0002, SE = 0.00050, P = 0.71). TNFalpha levels showed a significant negative relationship with log2 lubricin levels. IL-1beta, TNFalpha, IL-6, procathepsin B, and neutrophil elastase concentrations in SF from injured knees were greater in samples from recently injured knees compared with those that were chronically injured. There were no detectable cytokines or enzymes in the SF of contralateral joints. Concentrations of sGAG were significantly (P = 0.0002) higher in the SF from injured knees compared with the contralateral joints. CONCLUSION The decrease in SF lubricin concentrations following ACL injury may place the joint at an increased risk of wear-induced damage as a consequence of lack of boundary lubrication, potentially leading to secondary osteoarthritis. The decrease in SF lubricin was associated with an increase in levels of inflammatory cytokines.