Advocate Christ Medical Center

The biopsychosocial model for providing holistic care after traumatic injury requires consideration of the social factors that influence health outcomes in addition to management of physical wounds. Social drivers of health (SDOH) such as interpersonal safety, food insecurity, housing instability, transportation needs, and utility needs comprise the five domains that the Centers for Medicare and Medicaid Services now require hospitals to screen for. In this article, we will (1) describe the impact of SDOH on injuries and outcomes in trauma patients, (2) describe the value and importance of screening, and (3) provide examples of effective and impactful interventions trauma centers have or may use to improve SDOH in the communities they serve. Through collaboration and intentionality, screening for SDOH can occur at trauma centers, near and far, and serve as a critical step to integrating social care into trauma care.

In the PROACTIVE-HF trial, remote heart failure (HF) management using comprehensive vital signs and seated mean pulmonary artery pressure (mPAP) was safe and resulted in a low reported rate of HF hospitalization (HFH) and all-cause mortality (HFH/D) through 12 months. In this report, we extend the results from the PROACTIVE-HF study through 2 years, stratified by ejection fraction (EF). PROACTIVE-HF was a prospective, multicenter, open-label, single-arm trial evaluating the safety and efficacy of patient management using the Cordella PA pressure sensor system in patients with New York Heart Association class III symptoms, regardless of EF. In the first 24 months, the incidence of HF events (HFE)/D was 0.89 (95% CI 0.81-0.99) events per patient, driven by HFH. Patients with HF with reduced EF had greater HFE/D rates than those with HF with preserved EF (1.0 vs 0.8 events per patient, P = .048). For patients with HF experiencing moderate-to-severe symptoms, management using the Cordella PA sensor system was associated with low event rates and improved health status at 2 years, regardless of EF. Comprehensive remote monitoring of vital signs, seated PAP, and patient-reported symptoms via a digital platform supports sustained benefit for high-risk patients with HF.

Disclosure: D. Kaul: None. M. Paravastu: None. M. Shah: None. R. Patel: None. T. Yasmeen: None. M.H. Kazi: None.Introduction: Lipodystrophy is classified into two main types: generalized and partial, based on the extent of fat loss and further as genetic or acquired, depending on its underlying cause. The prevalence ranges from 1 in 1 million for familial partial lipodystrophy to 1 in 10 million for congenital generalized lipodystrophy. Its manifestation often includes severe metabolic disturbances, including dyslipidemia, insulin resistance, and increased risks of renal, hepatic, and cardiovascular diseases.Clinical Case: A 72-year-old female with type 2 diabetes, chronic kidney disease stage 3, and hyperlipidemia presented with hyperglycemia, severe weight loss, polydipsia, and polyuria. Her diabetes regimen included insulin degludec U-200 (76 units daily), insulin aspart (35 units with meals), and Trulicity (3 mg weekly). She reported missing several doses of insulin and had lost 78 lbs over the past year. On exam, she had generalized subcutaneous fat loss, weighing 54.1 kg with a BMI of 18.68 kg/m². Labs showed a glucose level of 614 mg/dL (normal range: 70-99 mg/dL), without evidence of diabetic ketoacidosis, HbA1c of 8.2% (normal range: 4.5-5.6%), C-peptide of 8.9 ng/mL (normal range: 0.8-3.9 ng/mL), and a triglyceride level of 36 mg/dL (normal range: <=149 mg/dL). Due to severe hyperglycemia, a continuous insulin infusion was started, requiring 931 units over 24 hours plus 100 units of insulin glargine. Given her phenotype and insulin resistance, lipodystrophy was suspected. Leptin was <0.4 ng/mL (normal range: 0.5-15.2 ng/mL), and Cushing syndrome was ruled out with a screening test, confirming generalized lipodystrophy. She was started on metreleptin and discharged with insulin degludec U-200 (90 units twice daily), insulin aspart (60 units three times daily), tirzepatide (2.5 mg weekly), and empagliflozin (25 mg daily).Discussion: Insulin resistance in lipodystrophy arises from the lack of functional adipose tissue, impairing the body’s ability to store excess energy as fat. This leads to ectopic fat deposition in the liver and muscle, disrupting insulin signaling. Leptin replacement therapy is a key treatment, as low leptin levels—due to reduced adipose tissue—contribute significantly to the metabolic abnormalities seen in lipodystrophy. Metreleptin, along with dietary modifications, is the first-line treatment, improving insulin sensitivity, reducing nonalcoholic steatohepatitis, alleviating cardiac hypertrophy, and lowering mortality. Though rare, lipodystrophy requires early recognition for appropriate screening and treatment.Presentation: Monday, July 14, 2025

Insulin lipohypertrophies (LH) consist of soft-tissue nodules caused by insulin's anabolic properties, potentially leading to erratic insulin absorption, hypoglycemia, and uncontrolled diabetes. A thorough physical examination of insulin injection and pump-insertion sites is crucial for detecting such changes in patients with diabetes. Counseling on rotating injection sites helps prevent LH. Here, we present 2 cases of LH, one in a Hispanic man and one in an African American man, both with long-standing type 1 diabetes mellitus.

AimsFollowing HeartMate 3 (HM3) LVAD implantation, acute right heart failure necessitating temporary right ventricular assist device (tRVAD) support has not been extensively described. We examined clinical outcomes in patients with HM3 LVAD stratified by the need for tRVAD support.Methods and resultsThis was a single‐centre, retrospective study of patients who underwent primary HM3 implantation from 2018 to 2022. Patients were placed on tRVAD (concomitant or delayed) support due to clinical deterioration. The primary outcome was 1‐year all‐cause mortality following HM3 implantation using competing risk analysis with heart transplantation acting as the competing event. A matched cohort analysis was also performed to evaluate the primary outcome of patients with and without tRVAD support. Secondary outcomes included an analysis of risk of LVAD‐related adverse events stratified by the presence of tRVAD. Of the 192 patients (median age 60 [49–68] years, 74% male, 37% white), 51 (26%) required tRVAD support. Compared with those with HM3 alone, the tRVAD group had a higher percentage of INTERMACS profile 1 or 2 (49% vs. 27%, P = 0.0005) and had higher rates of pre‐operative VA‐ECMO (28% vs. 5%, P < 0.0001). The tRVAD group had a higher 1‐year all‐cause mortality (33% vs. 3%, adjusted HR [95%CI]: 32.4 [9.51–110], P < 0.0001) compared with the HM3 alone group. In‐hospital mortality for patients with tRVAD was 26% compared with 1% in patients with HM3 alone (P < 0.0001). In the matched cohort analysis, significantly higher risk of both stroke (HR [95% CI]: 5.75 [1.55–21.3], P = 0.009) and dialysis (HR [95% CI]: 13.4 (3.96–45.5), P < 0.0001) was observed in the tRVAD cohort. Compared with concomitant tRVAD support, the delayed tRVAD group did not have a significantly higher risk of adverse events.ConclusionsIn this large single‐centre experience, patients undergoing HM3 LVAD requiring tRVAD support had significantly higher risks of adverse clinical outcomes.