Evaluating Postoperative Complications and Outcomes of Orthopedic Fracture Repair in Nonagenarian Patients.

INTRODUCTION: The United States and the world are currently experiencing a tremendous growth in the elderly population. Moreover, individuals surpassing the ages of 80 and 90 are also continuing to increase. As this unique division of society expands, it is critical that the medical community best understands how to assess, diagnose, and treat this population. The purpose of this study was to analyze morbidity, mortality, and overall outcome of patients aged 90 years and older after orthopedic surgical fracture repair. Such knowledge will guide patients and their families in making decisions when surgery is required among nonagenarians. METHODS: The trauma registry of our level I academic medical center was queried to identify potential study participants over the past decade. Two hundred and thirty-three surgical procedures among 227 patients were included and retrospectively assessed. Parameters of specific interest were injury type, mechanism of injury (including high energy vs low energy and height of falls), injury severity score, preoperative comorbidities, postoperative complications, length of hospital stay, discharge destination, and postoperative mortality rate. RESULTS: Overall, 4.3% of the cohort died in the hospital following surgery. Of the patients who survived, 89.7% were discharged to a professionally supervised setting. The nonagenarian population displayed a considerable follow-up rate, as 82.8% of individuals returned for their first postoperative office visit. DISCUSSION: Historically, surgical morbidity and mortality are highly associated with this age group. However, the number of nonagenarians in the United States is increasing, as are these surgical procedures. The epidemiologic and clinical findings of our study support this trend and add further insight into the matter. CONCLUSION: This investigation demonstrates that orthopedic surgery is an appropriate treatment in this population with an acceptable complication rate. Furthermore, nonagenarians have the potential to demonstrate a substantial follow-up rate, but postoperative discharge to a professionally supervised setting may be necessary.

Pyloroplasty for Refractory Gastroparesis.

Gastroparesis is a chronic gastric motility disorder in which the pathophysiology mimics a postvagotomy state. Pyloroplasty is beginning to emerge as a successful drainage procedure for refractory gastroparesis. Here we report our experience using pyloroplasty in the surgical management of diabetic and nondiabetic gastroparesis. A retrospective study was performed of 46 patients undergoing pyloroplasty for refractory gastroparesis from January 2010 through December 2013. Gastric emptying scintigraphy and the Gastroparesis Cardinal Symptom Index were assessed pre- and postoperatively. Laparoscopic pyloroplasty was performed in 42 patients, open pyloroplasty in three, and one patient was converted from laparoscopic to open pyloroplasty. Studies were repeated during the six to 12 month postoperative interval. The postoperative gastric emptying scintigraphy improved in 90 per cent of patients and normalized in 60 per cent. Postoperative T½ was significantly reduced (P = 0.001) as was four-hour retention (P < 0.001). The Gastroparesis Cardinal Symptom Index showed statistically significant reduction in symptom severity for all nine categories (P < 0.0005) as well as total symptom score (P < 0.005). No patients developed dumping syndrome. Pyloroplasty is a highly effective therapy for refractory gastroparesis, offering significant reduction in symptom severity, improvement in quality of life, and acceleration of gastric emptying.

Mild hyperglycemia, but not glucagon-like peptide 1 predicts poor outcome after injury.

BACKGROUND: Loss of glucose homeostasis occurs frequently in injured patients. Glucagon-like peptide-1 (GLP-1) is a gut-derived incretin hormone that stimulates insulin and decreases glucagon secretion. The impact of the incretin system on glycemic control in injured patients has not been extensively studied. The aim of this study was to test the hypothesis that glycemic control in injured patients is influenced by circulating levels of GLP-1. METHODS: A prospective, observational pilot study was conducted at a state-designated level 1 trauma center. Patients with injuries requiring admission to the intensive care unit were eligible for inclusion. Patients with preinjury diabetes were excluded. Normoglycemic patients served as the control group. The hyperglycemic group consisted of patients with initial blood glucose levels > 150 mg/dL. Mann-Whitney and χ(2) tests were used for statistical analysis. RESULTS: Eleven controls and 19 hyperglycemic patients entered the study. The study group required ventilation more frequently (P = .047). Hyperglycemia (P = .029), but not GLP-1 level (P = .371), predicted mortality. GLP-1 levels varied greatly in both groups. CONCLUSIONS: GLP-1 levels varied in both control and hyperglycemic groups. Mortality and mechanical ventilation rates were higher in patients with hyperglycemia.

Combination HBV therapy is linked to greater HBV DNA suppression in a cohort of lamivudine-experienced HIV/HBV coinfected individuals.

OBJECTIVES: To determine if highly active antiretroviral therapy (HAART) with combination anti-hepatitis B virus (HBV) therapy compared to HAART with HBV monotherapy leads to greater HBV DNA suppression in an HIV/HBV coinfected cohort. DESIGN: A cross-sectional analysis of 122 HIV/HBV coinfected patients from Australia and the United States. METHODS: Univariate analysis and ordinal logistic regression were used to determine factors associated with an HBV DNA less than 100 IU/ml. RESULTS: The majority of patients were on HAART (85%), had an HIV RNA less than 50 copies/ml, a median CD4 cell count of 438 cells/microl, and had prior or current lamivudine therapy (98%). The majority (89%) of those on HAART were on HBV-active drugs including 54% on tenofovir (TDF) with either lamivudine (LAM) or emtrictabine (FTC), 34% receiving LAM or FTC monotherapy, and 12% on TDF monotherapy. Only 4% of patients in the combination (TDF + LAM/FTC) group had HBV DNA greater than 20 000 IU/ml compared to 54% in the group on no HBV-active therapy, 31% in the LAM or FTC monotherapy group, and 30% in the TDF monotherapy group (P < 0.0001). In an ordinal logistic regression model, monotherapy with either TDF or LAM remained independently associated with higher HBV DNA. CONCLUSION: These data suggest that there may be an advantage to using TDF in combination with LAM or FTC in HIV/HBV coinfection, particularly in the setting of previous LAM experience. Continued prospective follow-up in this study will confirm whether the advantage is sustained longer-term.

CD4+ T cell depletion in an untreated HIV type 1-infected human leukocyte antigen-B*5801-positive patient with an undetectable viral load.

We report a case of a patient infected with human immunodeficiency virus type 1 (HIV-1) for 20 years who has experienced CD4(+) T cell depletion in spite of maintaining undetectable viral loads. Our data suggest that immune activation can cause CD4(+) T cell depletion even when HIV-1 replication appears to be controlled by host factors.

Human immunodeficiency virus-related microbial translocation and progression of hepatitis C.

BACKGROUND & AIMS: Human immunodeficiency virus (HIV)-1 infection has been associated with enhanced microbial translocation, and microbial translocation is a mechanism through which alcohol and some enteric conditions cause liver disease. We hypothesized that HIV promotes liver disease by enhancing microbial translocation. METHODS: We studied human cohorts in which hepatitis C virus (HCV) and HIV outcomes were carefully characterized. RESULTS: HIV-related CD4(+) lymphocyte depletion was strongly associated with microbial translocation as indicated by elevated levels of circulating lipopolysaccharide (LPS), LPS-binding protein, soluble CD14, and fucose-binding lectin (AAL) reactive to immunoglobulin G specific for the alpha-galactose epitope and suppressed levels of endotoxin core antibodies (EndoCAb IgM) in HIV-infected subjects compared with the same persons before they had HIV infection and compared with HIV-uninfected subjects. The same measures of microbial translocation were strongly associated with HCV-related liver disease progression (cirrhosis), eg, LPS, odds ratio, 19.0 (P = .002); AAL, odds ratio, 27.8 (P < .0001); in addition, levels of LPS were elevated prior to recognition of cirrhosis. CONCLUSIONS: Microbial translocation may be a fundamental mechanism through which HIV accelerates progression of chronic liver disease.