Association of Past and Future Paid Medical Malpractice Claims.

Importance: Many physicians believe that most medical malpractice claims are random events. This study assessed the association of prior paid claims (including a single prior claim) with future paid claims; whether public disclosure of prior paid claims affects future paid claims; and whether the association of prior and future paid claims decayed over time. Objective: To examine the association of 1 or more prior paid medical malpractice claims with future paid claims. Design, Setting, and Participants: This study assessed the association between prior paid claims (including a single prior claim) with future claims; whether public disclosure of prior claims affects future paid claims; and whether the association of prior and future paid claims decayed over time. This retrospective case-control study included all 881 876 licensed physicians in the US. All data analysis took place between July, 2018 and January, 2023. Exposure: Paid medical malpractice claims. Main Outcome and Measures: Association between a prior paid medical malpractice claim and likelihood of a paid claim in a future period, compared with simulated results expected if paid claims are random events. Using the same outcomes, we also assessed whether public disclosure of paid claims affects future paid claim rates. Results: This study included all 881 876 physicians licensed to practice in the US at the time of the study. Overall, 3.3% of the 841 961 physicians with 0 paid claims in the prior period had 1 or more claims in the future period vs 12.4% of the 34 512 physicians with 1 paid claim in the prior period; 22.4% of the 4189 physicians with 2 paid claims in the prior period; and 37% of the 1214 physicians with 3 paid claims in the prior period. The association between prior claims and future claims was similar for high-medical-malpractice-risk and lower-risk specialties; 1 prior-period claim was associated with a 3.1 times higher likelihood of a future-period claim for high-risk specialties (95% CI, 2.8-3.4) vs a 4.2 times higher likelihood for lower-risk specialties (95% CI, 3.8-4.6). The predictive power of a prior paid claim for future claims declined gradually as the time since the prior claim increased, for prior or future periods up to 10 years. Public disclosure did not affect the association between prior and future paid claims. Conclusions and Relevance: In this study of paid medical malpractice claims for all US physicians, a single prior paid claim was associated with substantial, long-lived higher future claim risk, independent of whether a physician was practicing in a high- or low-risk specialty, or whether a state publicly disclosed paid claims. Timely, noncoercive intervention, including education, has the potential to reduce future claims.

Retbindin mediates light-damage in mouse retina while its absence leads to premature retinal aging.

Vision requires the transport and recycling of the pigment 11-cis retinaldehyde (retinal) between the retinal pigment epithelium (RPE) and photoreceptors. 11-cis retinal is also required for light-mediated photoreceptor death in dark-adapted mouse eye, probably through overstimulation of rod cells adapted for low light. Retbindin is a photoreceptor-specific protein, of unclear function, that is localized between the RPE and the tips of the photoreceptors. Unexpectedly, young Rtbdn-KO mice, with targeted deletion (KO) of retbindin, showed delayed regeneration of retinal function after bleaching and were strongly resistant to light-induced photoreceptor death. Furthermore, bio-layer interferometry binding studies showed recombinant retbindin had significant affinity for retinoids, most notably 11-cis retinal. This suggests that retbindin mediates light damage, probably through a role in transport of 11-cis retinal. In Rtbdn-KO mice, retinal development was normal, as were amplitudes of rod and cone electroretinograms (ERG) up to 4 months, although implicit times and c-waves were affected. However, with aging, both light- and dark-adapted ERG amplitudes declined significantly and photoreceptor outer segments became disordered, However, in contrast to other reports, there was little retinal degeneration or drop in flavin levels. The RPE developed vacuoles and lipid, protein and calcium deposits reminiscent of age-related macular degeneration. Other signs of premature aging included loss of OPN4+ retinal ganglion cells and activation of microglia. Thus, retbindin plays an unexpected role in the mammalian visual cycle, probably as an adaptation for vision in dim light. It mediates light damage in the dark-adapted eye, but also plays a role in light-adapted responses and in long term retinal homeostasis.

Amelotin is expressed in retinal pigment epithelium and localizes to hydroxyapatite deposits in dry age-related macular degeneration.

Deposition of hydroxyapatite (HAP) basal to the retinal pigment epithelium (RPE) is linked to the progression of age-related macular degeneration (AMD). Serum-deprivation of RPE cells in culture mimics some features of AMD. We now show that serum-deprivation also leads to the induction of amelotin (AMTN), a protein involved in hydroxyapatite mineralization in enamel. HAP is formed in our culture model and is blocked by siRNA inhibition of AMTN expression. In situ hybridization and immunofluorescence imaging of human eye tissue show that AMTN is expressed in RPE of donor eyes with geographic atrophy ("dry" AMD) in regions with soft drusen containing HAP spherules or nodules. AMTN is not found in hard drusen, normal RPE, or donor eyes diagnosed with wet AMD. These findings suggest that AMTN is involved in formation of HAP spherules or nodules in AMD, and as such provides a new therapeutic target for slowing disease progression.

The klotho-related protein KLPH (lctl) has preferred expression in lens and is essential for expression of clic5 and normal lens suture formation.

KLPH/lctl belongs to the Klotho family of proteins. Expressed sequence tag analyses unexpectedly revealed that KLPH is highly expressed in the eye lens while northern blots showed that expression is much higher in the eye than in other tissues. In situ hybridization in mouse localized mRNA to the lens, particularly in the equatorial epithelium. Immunofluorescence detected KLPH in lens epithelial cells with highest levels in the germinative/differentiation zone. The gene for KLPH in mouse was deleted by homologous recombination. Littermate knockout (KO) and wild type (WT) mice were compared in a wide panel of pathology examinations and were all grossly normal, showing no systemic effects of the deletion. However, the lens, while superficially normal at young ages, had focusing defects and exhibited age-related cortical cataract by slit lamp examination. Whole-lens imaging showed that KO mice had disorganized lens sutures, forming a loose double-y or x instead of the tight y formation of WT. RNA-seq profiles for KO and WT littermates confirmed the absence of KLPH mRNA in KO lens and also showed complete absence of transcripts for Clic5, a protein associated with cilium/basal body related auditory defects in a mouse model. Immunofluorescence of lens epithelial flat mounts showed that Clic5 localized to cilia/centrosomes. Mice mutant for Clic5 (jitterbug) also had defective sutures. These results suggest that KLPH is required for lens-specific expression of Clic5 and that Clic5 has an important role in the machinery that controls lens fiber cell extension and organization.

Cost reductions associated with a quality improvement initiative for patients with ST-elevation myocardial infarction.

BACKGROUND: Efforts to reduce door-to-balloon (DTB) times for patients presenting with an ST-elevation myocardial infarction (STEMI) are widespread. Reductions in DTB times have been shown to reduce short-term mortality and decrease inpatient length of stay (LOS) in these high-risk patients. However, there is a limited literature examining the effect that these quality improvement (QI) initiatives have on patient care costs. METHODS: A STEMI QI program (Cardiac Alert Team [CAT]) initiative was instituted in July 2006 at a single tertiary care medical center located in central Massachusetts. Information was collected on cost data and selected clinical outcomes for consecutively admitted patients with a STEMI. Differences in adjusted hospital costs were compared in three cohorts of patients hospitalized with a STEMI: one before the CAT initiative began (January 2005-June 2006) and two after (October 1, 2007-September 30, 2009, and October 1, 2009-September 30, 2011). RESULTS: Before the CAT initiative, the average direct inpatient costs related to the care of these patients was $14,634, which decreased to $13,308 (-9.1%) and $13,567 (-7.3%) in the two sequential periods of the study after the CAT initiative was well established. Mean DTB times were 91 minutes before the CAT initiative and were reduced to 55 and 61 minutes in the follow-up periods (p < .001). There was a nonsignificant reduction in LOS from 4.4 days pre-CAT to 3.6 days in both of the post-CAT periods (p = .11). CONCLUSIONS: A QI program aimed at reducing DTB times for patients with a STEMI also led to a significant reduction in inpatient care costs. The greatest reduction in costs was related to cardiac catheterization, which was not expected and was likely a result of standardization of care and identification of practice inefficiencies.