Malpractice Litigation Following Traumatic Fracture.

BACKGROUND: Poor clinical outcomes and adverse events following orthopaedic trauma are common, which may lead to litigation. To our knowledge, factors associated with litigation following fracture care have not previously been evaluated. METHODS: A retrospective review of fracture-related malpractice lawsuits from 1988 to 2015 was completed utilizing VerdictSearch (ALM Media Properties), a medicolegal database. Defendant and plaintiff characteristics along with fracture type, allegations, litigation outcomes, and the association of case characteristics with outcomes were analyzed. RESULTS: A total of 561 cases were evaluated; 360 cases were excluded, resulting in a total of 201 cases that were analyzed in detail. The mean age of the plaintiff was 43.1 years (standard deviation [SD],19.4 years). Twenty-four fracture types were represented among the analyzed cases. The most common fractures were of the radius (44), the femur (32), the tibia (30), the ulna (29), the humerus (26), the spine (24), the hip (17), and the fibula (15). Overall, 129 (64.2%) cases resulted in a defense verdict, 41 (20.4%) cases resulted in a plaintiff verdict, and 31 (15.4%) cases resulted in a settlement. For plaintiff verdicts, the mean indemnity payment was $3,778,657 (median, $753,057; range, $89,943 to $27,926,311). For settlements, the mean indemnity payment was $1,097,439 (median, $547,935; range, $103,541 to $9,445,113). The mean indemnity for plaintiff verdicts was significantly greater than the mean indemnity for settlements (p = 0.03). The presence of a neurological deficit was associated with a significantly greater likelihood of a favorable outcome for the plaintiff (52.8% for plaintiffs with neurological deficit versus 32.1% for plaintiffs without neurological deficit; p = 0.019). CONCLUSIONS: This study examined malpractice litigation following traumatic orthopaedic injuries. In cases with decisions for the plaintiff, indemnity payments were on average more than $2.5 million larger than payments for settlements. In fracture cases with neurological deficit, malpractice cases were more likely to result in a favorable outcome for the plaintiff.

In Vivo Hepatic Reprogramming of Myofibroblasts with AAV Vectors as a Therapeutic Strategy for Liver Fibrosis.

Liver fibrosis, a form of scarring, develops in chronic liver diseases when hepatocyte regeneration cannot compensate for hepatocyte death. Initially, collagen produced by myofibroblasts (MFs) functions to maintain the integrity of the liver, but excessive collagen accumulation suppresses residual hepatocyte function, leading to liver failure. As a strategy to generate new hepatocytes and limit collagen deposition in the chronically injured liver, we developed in vivo reprogramming of MFs into hepatocytes using adeno-associated virus (AAV) vectors expressing hepatic transcription factors. We first identified the AAV6 capsid as effective in transducing MFs in a mouse model of liver fibrosis. We then showed in lineage-tracing mice that AAV6 vector-mediated in vivo hepatic reprogramming of MFs generates hepatocytes that replicate function and proliferation of primary hepatocytes, and reduces liver fibrosis. Because AAV vectors are already used for liver-directed human gene therapy, our strategy has potential for clinical translation into a therapy for liver fibrosis.