Radial Artery Pseudoaneurysm From a Squirrel Bite.

Radial artery pseudoaneurysm is a rarelimb-threatening complication that occurs from vascular procedures and direct trauma. We present a rare case of a 74-year-old female who presented to the emergency department with a squirrel bite to her right wrist. Although initially benign-appearing, computed tomography angiography of the right upper extremity showed a pseudoaneurysm at the distal radial artery. The patient was successfully treated with careful compression and rapid resolution was confirmed with an arterial right upper extremity ultrasound that visualized a formed thrombus. Emergency providers should have a high index of suspicion for radial artery pseudoaneurysms in the setting of animal bites to the wrist.

Difficult Intravenous Access Requiring Ultrasound in the Emergency Department: Associations With Delays in Care and Areas for Quality Improvement.

Background Patients with difficult intravenous access (DIVA) requiring ultrasound-guided intravenous (USGIV) access have been associated with delays in treatment, imaging, and disposition in academic emergency department (ED) patient populations. Our objective in this study was to characterize differences in time to intravenous access, imaging, and disposition between patients with DIVA versus those without DIVA requiring USGIV access in a community ED while also assessing for DIVA-associated comorbidities. Methods A cross-sectional, observational analysis was performed on admitted ED patients evaluated from September 2 to September 31, 2022, at a community ED. Patients with DIVA were defined as patients with two failed attempts at traditional intravenous placement. These patients require USGIV placement per institutional protocol. Patients younger than 18 years of age, trauma admissions, repeated visits from the same patient, patients with missing data, and direct hospital admissions were excluded. Continuous variables were recorded with medians and included ED throughput measures of time to vascular access, contrast CT imaging, and disposition. Differences in median times between DIVA patients versus non-DIVA patients were assessed with the Mann-Whitney U-test. Categorical data involving comorbidities were reported as percentages, and differences in proportions between DIVA versus non-DIVA patients were assessed via chi-square tests. Multivariate logistic regression analysis evaluated for correlations between DIVA and times to access, contrast CT imaging, disposition, and significant covariates while adjusting for demographic information. Results A total of 1250 patients were included in this investigation (5.8% associated with DIVA requiring USGIV access). The median age of all subjects was 69 (interquartile range = 58, 79) with no significant difference between the DIVA and non-DIVA groups. Patients with DIVA were more likely to be female in comparison to patients without DIVA (65.3% and 51.2%, respectively, p < 0.05). Patients with a history of end-stage renal disease (ESRD) (p < 0.001), intravenous drug use (IVDU) (p < 0.001), and venous thromboembolism (p < 0.05) had statistically significant associations with DIVA. On regression analysis, patients with DIVA were more likely to have a history of ESRD with an odds ratio (OR) of 3.56 (95% confidence interval (CI): 1.62-7.81) and a history of IVDU with an OR of 14.29 (95% CI: 5.17-39.54). Patients with DIVA were associated with statistically significant greater median times to vascular access, contrast CT imaging, and disposition (p < 0.001 for time to access and disposition and p < 0.01 for time to contrast CT imaging). Conclusion In this study, DIVA cases requiring USGIV access were positively associated with significantly longer times to access, contrast CT imaging, and disposition compared to patients without DIVA at our community ED. Comorbidities such as IVDU and ESRD had statistically significant associations with DIVA requiring USGIV access.

The impact of postresettlement stressors and access to health care on health outcomes in recently resettled refugees in the United States.

This mixed-methods study examines mechanisms connecting the deployment of economic, social, and health care resources to emotional distress and physical health outcomes. Examining such mechanisms is critical for informing strategies, policies, and other interventions for reducing health disparities and improving refugee health in the United States and other resettlement contexts. Data for this study were collected as part of a randomized control trial in a mid-sized city in the Southwestern United States. Two-hundred ninety recently resettled (< 3 years) refugee adults from 143 households were enrolled in the study (36.2% Afghan, 32.8% Iraqi/Syrian, and 31.0% Great Lakes African; 52% women). Qualitative interview data were collected via semistructured interviews. A longitudinal structural equation path model of quantitative data from three time points over 12 months tested hypotheses that emerged from qualitative findings. In semistructured interviews, refugees in the United States (a) attributed the development of worse or new physical health problems to postresettlement stressors related to financial instability and limited social support that contributed to their emotional distress and (b) reported several barriers to accessing health care in the United States, including insufficient knowledge of health care resources, inadequate patient-provider communication, and navigating complex American health insurance systems, all of which exacerbated their physical health problems. Guided by these qualitative findings, longitudinal quantitative data revealed that: (a) postmigration stressors were associated with emotional distress and poor self-reported physical health, (b) emotional distress mediated the association between postmigration stressors and global health satisfaction, and (c) emotional distress was negatively associated with global health satisfaction. Findings document stressors refugees experience in the context of the unique environment created by the American health care system and how these stressors contribute to poor physical health through increased emotional distress. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Compression of the Rectum, Bladder, and External Iliac Vein Due to Hip Arthroplasty-Related Pseudotumor.

A 58-year-old male who underwent left total hip arthroplasty in 1988 for post-traumatic arthritis after an operatively-treated acetabular fracture presented with progressive left hip pain, lower extremity swelling, urinary urgency, constipation, and tenesmus (the feeling of needing to pass stool despite having an empty colon). Imaging demonstrated massive pseudotumor causing iliac vein compression and significant displacement of the rectum and bladder requiring decompression in combination with general surgery followed by revision hip arthroplasty four months later. This case highlights a unique constellation of symptoms due to pseudotumor after total hip arthroplasty, as well as the severity to which pseudotumor can progress, requiring staged decompression with general surgery before revision.

Hyperhomocysteinemia leads to exacerbation of ischemic brain damage: Role of GluN2A NMDA receptors.

Hyperhomocysteinemia has been implicated in several neurodegenerative disorders including ischemic stroke. However, the pathological consequences of ischemic insult in individuals predisposed to hyperhomocysteinemia and the associated etiology are unknown. In this study, we evaluated the outcome of transient ischemic stroke in a rodent model of hyperhomocysteinemia, developed by subcutaneous implantation of osmotic pumps containing L-homocysteine into male Wistar rats. Our findings show a 42.3% mortality rate in hyperhomocysteinemic rats as compared to 7.7% in control rats. Magnetic resonance imaging of the brain in the surviving rats shows that mild hyperhomocysteinemia leads to exacerbation of ischemic injury within 24 h, which remains elevated over time. Behavioral studies further demonstrate significant deficit in sensorimotor functions in hyperhomocysteinemic rats compared to control rats. Using pharmacological inhibitors targeting the NMDAR subtypes, the study further demonstrates that inhibition of GluN2A-containing NMDARs significantly reduces ischemic brain damage in hyperhomocysteinemic rats but not in control rats, indicating that hyperhomocysteinemia-mediated exacerbation of ischemic brain injury involves GluN2A-NMDAR signaling. Complementary studies in GluN2A-knockout mice show that in the absence of GluN2A-NMDARs, hyperhomocysteinemia-associated exacerbation of ischemic brain injury is blocked, confirming that GluN2A-NMDAR activation is a critical determinant of the severity of ischemic damage under hyperhomocysteinemic conditions. Furthermore, at the molecular level we observe GluN2A-NMDAR dependent sustained increase in ERK MAPK phosphorylation under hyperhomocysteinemic condition that has been shown to be involved in homocysteine-induced neurotoxicity. Taken together, the findings show that hyperhomocysteinemia triggers a unique signaling pathway that in conjunction with ischemia-induced pathways enhance the pathology of stroke under hyperhomocysteinemic conditions.

A peptide mimetic of tyrosine phosphatase STEP as a potential therapeutic agent for treatment of cerebral ischemic stroke.

Extensive research over the last two decades has advanced our understanding of the pathophysiology of ischemic stroke. However, current pharmacologic therapies are still limited to rapid reperfusion using thrombolytic agents, and neuroprotective approaches that can reduce the consequences of ischemic and reperfusion injury, are still not available. To bridge this gap, we have evaluated the long-term efficacy and therapeutic time window of a novel peptide-based neuroprotectant TAT-STEP, derived from the brain-enriched and neuron-specific tyrosine phosphatase STEP. Using a rat model of transient middle cerebral artery occlusion (90 min), we show that a single intravenous administration of the peptide at the onset of reperfusion (early) or 6 h after the onset of the insult (delayed) reduces mortality rate. In the surviving rats, MRI scans of the brain at days 1, 14 and 28 after the insult show significant reduction in infarct size and improvement of structural integrity within the infarcted area following peptide treatment, regardless of the time of administration. Behavioral assessments show significant improvement in normal gait, motor coordination, sensory motor function and spatial memory following early or delayed peptide treatment. The study establishes for the first time the therapeutic potential of a tyrosine phosphatase in ischemic brain injury.

Role of AMPA receptors in homocysteine-NMDA receptor-induced crosstalk between ERK and p38 MAPK.

Homocysteine, a metabolite of the methionine cycle has been reported to play a role in neurotoxicity through activation of N-methyl-d-aspartate receptors (NMDAR)-mediated signaling pathway. The proposed mechanisms associated with homocysteine-NMDAR-induced neurotoxicity involve a unique signaling pathway that triggers a crosstalk between extracellular signal-regulated kinase (ERK) and p38 MAPKs, where activation of p38 MAPK is downstream of and dependent on ERK MAPK. However, the molecular basis of the ERK MAPK-mediated p38 MAPK activation is not understood. This study investigates whether α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) play a role in facilitating the ERK MAPK-mediated p38 MAPK activation. Using surface biotinylation and immunoblotting approaches we show that treatment with homocysteine leads to a decrease in surface expression of GluA2-AMPAR subunit in neurons, but have no effect on the surface expression of GluA1-AMPAR subunit. Inhibition of NMDAR activation with D-AP5 or ERK MAPK phosphorylation with PD98059 attenuates homocysteine-induced decrease in surface expression of GluA2-AMPAR subunit. The decrease in surface expression of GluA2-AMPAR subunit is associated with p38 MAPK phosphorylation, which is inhibited by 1-napthyl acetyl spermine trihydrochloride (NASPM), a selective antagonist of GluA2-lacking Ca2+ -permeable AMPARs. These results suggest that homocysteine-NMDAR-mediated ERK MAPK phosphorylation leads to a decrease in surface expression of GluA2-AMPAR subunit resulting in Ca2+ influx through the GluA2-lacking Ca2+ -permeable AMPARs and p38 MAPK phosphorylation. Cell death assays further show that inhibition of AMPAR activity with 2,3-dioxo-6-nitro-1,2,3,4,tetrahydrobenzoquinoxaline-7-sulfonamide (NBQX)/6-cyano-7-nitroquinoxaline-2,3, -dione (CNQX) or GluA2-lacking Ca2+ -permeable AMPAR activity with NASPM attenuates homocysteine-induced neurotoxicity. We have identified an important mechanism involved in homocysteine-induced neurotoxicity that highlights the intermediary role of GluA2-lacking Ca2+ -permeable AMPARs in the crosstalk between ERK and p38 MAPKs.