McLaren Health Care Corporation is an integrated, managed care health care organization in the Lower Peninsula of Michigan. McLaren operates 14 hospitals, ambulatory surgery centers, imaging centers, a primary and specialty care physician network, commercial and Medicaid HMOs, home health and hospice providers, retail medical equipment showrooms, pharmacy services, and a wholly owned medical malpractice insurance company. McLaren also operates Michigan's largest network of cancer centers and providers, anchored by the Barbara Ann Karmanos Cancer Institute. The Karmanos Cancer Center is the only National Cancer Institute (NCI)-designated comprehensive cancer center in metro Detroit. Its headquarters is in Grand Blanc, Michigan with operations facilities in Michigan, Ohio, and Indiana..
Background: Non-group 1 pulmonary hypertension, also known as secondary pulmonary hypertension (SPH), is predominantly observed among females. However, there is a significant lack of data concerning factors associated with hospitalization among patients diagnosed with SPH. This study aims to provide clinicians with vital insights for the identification of high-risk groups and for the more effective management of contributory risk factors within the female population affected by SPH. Methods: Using the 2019 National Inpatient Sample, we identified female admissions with SPH (n = 648,190), accounting for 3.8% of the total 17,236,228 female admissions. An Artificial Neural Network (ANN) analysis was conducted to evaluate predictive factors. We randomly allocated 3,319,543 patients into training and testing datasets at a ratio of 70:30, comprising 2,323,696 (70%) for training and 995,847 (30%) for testing, to calibrate and validate the performance of the ANN algorithm. Model performance was assessed by comparing misclassification rates between training and testing sets and by the area under the receiver operating characteristic curve (AUC); only internal validation was performed. Results: Females hospitalized with SPH were generally of older age, with a median of 75 years compared to 58 years, and more frequently identified as White (67.7% versus 65.5%) or Black (20.5% versus 15.5%) relative to those without SPH. They also demonstrated a higher prevalence of most atherosclerotic cardiovascular disease (ASCVD) risk factors or their equivalents, including complicated hypertension (50.6% versus 17.8%), diabetes with chronic complications (30.6% versus 13.7%), and hyperlipidemia (50.8% versus 29.2%), as well as other comorbidities such as COPD (43.4% versus 20.2%) and CKD (43.3% versus 14.0%), and exhibited increased all-cause mortality (4.5% versus 1.8%) (p < 0.001). Our ANN model achieved an AUC of 0.823, indicating good predictive capability. The rates of incorrect predictions were comparable in both the testing and training cohorts, at 3.8% each. The factors most strongly associated with a coded SPH diagnosis included age at admission, complicated hypertension, chronic kidney disease, chronic obstructive pulmonary disease, uncomplicated hypertension, prior VTE, race, arthropathies, and AIDS. Conclusions: Our ANN model identified demographic and comorbidity factors associated with a coded SPH diagnosis among hospitalized females, with good discrimination (AUC = 0.823). Because the model classifies the presence of an existing diagnosis rather than predicting future hospitalization, and was validated only internally, external and prospective validation is required before clinical application. Once validated, these factors could support individualized, sex-specific risk stratification for high-risk female populations, consistent with the goals of personalized medicine.
Glenohumeral instability is a common condition encountered by orthopaedic sports surgeons, particularly in young, active athletes. Initial management is nonoperative, consisting of physical therapy, but some patients may still require surgical intervention. Arthroscopic stabilization, via capsulorrhaphy or plication, remains the primary operative approach. Here, we describe our technique, which utilizes an Arthrex double-loaded, knotless 2.6 mm FiberTak soft anchor placed at the 6-o'clock position for labral and capsular repair.
Abstract Introduction Pleural effusions in cirrhosis are usually transudative hepatic hydrothoraces. While hepatic hydrothorax occurs in 5-10% of patients with cirrhosis, the presentation of a chylous-appearing fluid, particularly in the context of recent trauma, represents a significant diagnostic rarity. This presentation raises concern for thoracic duct injury, but may also represent the translocation of chylous ascites. We present a rare case of a massive left-sided effusion with chylous characteristics in decompensated cirrhosis, emphasizing the importance of biochemical differentiation between hepatic hydrothorax and true chylothorax. Case Description A 67-year-old woman with non-alcoholic cirrhosis and prior chylous ascites presented with acute dyspnea after a fall. Chest radiography revealed complete opacification of the left hemithorax. Thoracentesis drained 3 L of milky fluid, followed by re-expansion pulmonary edema requiring non-invasive ventilation. Pleural fluid analysis showed triglycerides 1116 mg/dL, protein 2.4 g/dL, and no lymphocytosis—transudative by Light’s criteria and biochemically similar to her ascitic fluid (SAAG > 2). CT imaging showed no mediastinal pathology, but effusion recurred rapidly (>1.3 L/day) despite prior VATS pleurodesis. The patient developed hepatorenal syndrome, prompting transfer for liver-transplant evaluation. The final diagnosis was refractory hepatic hydrothorax with chylous characteristics, not traumatic chylothorax. Discussion This case illustrates that in cirrhotic patients, a chylous-appearing effusion may reflect chylous ascitic translocation rather than thoracic-duct disruption. The diagnostic clarity rested on the transudative nature of the pleural fluid (protein 2.4 g/dL, meeting Light’s criteria for transudate) and the lack of lymphocytosis, which contrasts with the typical exudative, lymphocyte-predominant profile of a traumatic chylothorax. Elevated triglycerides in transudative pleural fluid mirror the underlying chylous ascites—a rare but recognized manifestation of portal hypertension. Local measures such as pleurodesis often fail when the driving force is persistent portal hypertension. Conclusion This case underscores that in cirrhotic patients with a chylous-appearing pleural effusion, biochemical analysis is paramount to differentiate hepatic hydrothorax from a true chylothorax, thereby preventing misguided and invasive procedures and appropriately directing care towards definitive management of portal hypertension, such as liver transplantation. This abstract is funded by: None