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Background Socioeconomic status affects outcomes in cerebrovascular disease, although its role in the withdrawal of life-sustaining treatments (WLST) remains uncertain. We aim to examine the impact of socioeconomic factors on outcomes including WLST in aneurysmal subarachnoid hemorrhage (aSAH). Methods We conducted a retrospective study of a cohort of consecutive patients with aSAH who were admitted to an academic center from 2016 to 2023. Publicly available data on median neighborhood income by zip code areas were obtained from the US census. Low economic-insurance status (EIS) was defined as using Medicaid or having no insurance or living in a zip code within the lowest two quintiles of household income. High EIS was defined as not using Medicaid and having any other insurance and living in a zip code within the highest two quintiles of household income. The rest of the cohort who was not categorized in the high or low EIS groups was defined as middle EIS. We used multivariable logistic regression analysis to assess the association between socioeconomic and demographic factors and outcomes including WLST, mortality, and 3-month modified Rankin Scale. Results We included 410 patients, with mean age 57.9 years (standard deviation 13.8), who were 65% female, 70% white, 36.8% low EIS, and 35.6% high EIS. Higher EIS was associated with WLST (odds ratio 1.53 per increase in EIS, 95% confidence interval 1.07–2.18; p  = 0.02) when adjusted for other predictors. In addition, a higher quintile of neighborhood income, regardless of insurance status, was associated with higher odds of WLST (odds ratio 1.41 per each quintile increase, 95% confidence interval 1.07–1.86; p  = 0.014). However, there was no association between EIS and 3-month modified Rankin Scale when adjusted for disease severity factors. Conclusions Higher EIS and residing in areas with higher neighborhood incomes were associated with higher odds of WLST in aSAH. Further multicenter studies are needed to investigate the underlying mechanisms that contribute to these associations.

Diabetic cheiroarthropathy (DCA) is a relatively uncommon and underdiagnosed complication of poorly controlled diabetes. It is caused by non-enzymatic glycation of collagen that ultimately leads to microvascular damage and polyarticular stiffness. If diagnosed early, optimal management of serum glucose levels may lessen joint stiffness and prevent microvascular and macrovascular complications associated with diabetes mellitus. We review the case of a 55-year-old male with type 2 diabetes mellitus who was diagnosed with DCA after complaints of chronic joint stiffness and immobility.

Children with Hunter syndrome have a high prevalence of nerve compression syndromes given the buildup of glycosaminoglycans in the tendon sheaths and soft tissue structures. These are often comorbid with orthopedic conditions given joint and tendon contractures due to the same pathology. While carpal tunnel syndrome and surgical treatment has been well-reported in this population, the literature on lower extremity nerve compression syndromes and their treatment in Hunter syndrome is sparse. We report the case of a 13-year-old male with a history of Hunter syndrome who presented with toe-walking and tenderness over the peroneal and tarsal tunnel areas. He underwent bilateral common peroneal nerve and tarsal tunnel releases, with findings of severe nerve compression and hypertrophied soft tissue structures demonstrating fibromuscular scarring on pathology. Post-operatively, the patient's family reported subjective improvement in lower extremity mobility and plantar flexion. In this case, peroneal and tarsal nerve compression were diagnosed clinically and treated effectively with surgical release and postoperative ankle casting. Given the wide differential of common comorbid orthopedic conditions in Hunter syndrome and the lack of validated electrodiagnostic normative values in this population, the history and physical examination and consideration of nerve compression syndromes are tantamount for successful workup and treatment of gait abnormalities in the child with Hunter syndrome.

BACKGROUND: Children with Hunter syndrome have a high prevalence of nerve compression syndromes given the buildup of glycosaminoglycans in the tendon sheaths and soft tissue structures. These are often comorbid with orthopedic conditions given joint and tendon contractures due to the same pathology. While carpal tunnel syndrome and surgical treatment has been well-reported in this population, the literature on lower extremity nerve compression syndromes and their treatment in Hunter syndrome is sparse. OBSERVATIONS: We report the case of a 13-year-old male with a history of Hunter syndrome who ed with and tenderness over the peroneal and tarsal tunnel areas. He underwent bilateral common peroneal nerve and tarsal tunnel releases, with findings of severe nerve compression and hypertrophied soft tissue structures demonstrating fibromuscular scarring on pathology. Post-operatively, the patient's family reported subjective improvement in lower extremity mobility and plantar flexion. LESSONS: In this case, peroneal and tarsal nerve compression were diagnosed clinically and treated effectively with surgical release and postoperative ankle casting. Given the wide differential of common comorbid orthopedic conditions in Hunter syndrome and the lack of validated electrodiagnostic normative values in this population, the history and physical examination and consideration of nerve compression syndromes are tantamount for successful workup and treatment of gait abnormalities in the child with Hunter syndrome.