United States

Background:
Venous malformations (VMs) are congenital slow flow malformations that produce a wide spectrum of disease, from asymptomatic nodules to large painful lesions that cause coagulopathy or death. Current interventions are palliative and recurrence is common; there are no FDA-approved treatments. Discovery of PIK3CA variants in VMs have identified a role for PI3K/AKT/mTOR hyperactivation in VM pathophysiology and led to the repurposing of drugs that inhibit the PI3K pathway. Further development of therapeutics is limited by an incomplete understanding of the mechanism by which PI3K hyperactivation causes VM pathology. Previous work with endothelial cells isolated from patient VMs (VMECs) has shown proteostasis defects, abnormal cell morphology, and hyperproliferation consistent with the clinical presentation of VMs. We hypothesize that protein homeostasis defects in VMECs are downstream of PI3K hyperactivation and that distinct variants affect phenotypic severity.

Methods:
Human umbilical vein endothelial cells (HUVECs) were engineered to express empty plasmid or H1047R, E545K, or E542K pathogenic variants of PIK3CA using a lentiviral system. The resulting cells lines were stained by immunofluorescence for pAKT, CD31, and VECADHERIN and imaged using fluorescence microscopy. Quantification was performed using ImageJ. Statistical analysis was performed using one-way ANOVA with post-hoc Tukey t-test.

Results:
All three PIK3CA variants significantly increased the levels of activated AKT (ANOVA, p&lt;0.0001) confirming effective transduction and function of the transgenes. All three variants led to significantly increased cell size (ANOVA, p&lt;0.0001). The H1047R variant also showed significantly increased number of multi-nucleated cells (post-hoc Tukey t-test, p&lt;0.0001). Abnormal cytoplasmic accumulation of CD31 and VECADHERIN was seen in all three cell variants. Quantification of protein levels showed that H1047R and E542K variants had significantly increased CD31 expression (post-hoc Tukey t-test, p&lt; 0.05 and p&lt;0.005). Only the H1047R and E545K variants had significantly increased VECADHERIN expression (post-hoc Tukey t-test, p&lt;0.005). These changes in protein expression mimic changes observed in patient derived VMECs.

Conclusion:
The introduction of PIK3CA variants that hyperactivate PI3K signaling recapitulated cell morphology and proteostasis defects seen in patient VMECs. The H1047R variant demonstrated the most severe phenotype, which correlates with published clinical data. Disparities between variants may be relevant to understanding both the clinical heterogeneity of VM patients and their differential response to treatment. These data provide compelling evidence that VMEC phenotypes are downstream of PI3K/AKT/mTOR signaling. Future studies of how PI3K hyperactivation causes VMEC dysfunction may uncover novel avenues for therapeutic treatment.

AMA Research Challenge 2025 

PI3K Activation Drives Protein Homeostasis Pathology in Venous Malformations

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Background:
Venous malformations (VMs) are congenital slow flow malformations that produce a wide spectrum of disease, from asymptomatic nodules to large painful lesions that cause coagulopathy or death. Current interventions are palliative and recurrence is common; there are no FDA-approved treatments. Discovery of PIK3CA variants in VMs have identified a role for PI3K/AKT/mTOR hyperactivation in VM pathophysiology and led to the repurposing of drugs that inhibit the PI3K pathway. Further development of therapeutics is limited by an incomplete understanding of the mechanism by which PI3K hyperactivation causes VM pathology. Previous work with endothelial cells isolated from patient VMs (VMECs) has shown proteostasis defects, abnormal cell morphology, and hyperproliferation consistent with the clinical presentation of VMs. We hypothesize that protein homeostasis defects in VMECs are downstream of PI3K hyperactivation and that distinct variants affect phenotypic severity.

Methods:
Human umbilical vein endothelial cells (HUVECs) were engineered to express empty plasmid or H1047R, E545K, or E542K pathogenic variants of PIK3CA using a lentiviral system. The resulting cells lines were stained by immunofluorescence for pAKT, CD31, and VECADHERIN and imaged using fluorescence microscopy. Quantification was performed using ImageJ. Statistical analysis was performed using one-way ANOVA with post-hoc Tukey t-test.

Results:
All three PIK3CA variants significantly increased the levels of activated AKT (ANOVA, p<0.0001) confirming effective transduction and function of the transgenes. All three variants led to significantly increased cell size (ANOVA, p<0.0001). The H1047R variant also showed significantly increased number of multi-nucleated cells (post-hoc Tukey t-test, p<0.0001). Abnormal cytoplasmic accumulation of CD31 and VECADHERIN was seen in all three cell variants. Quantification of protein levels showed that H1047R and E542K variants had significantly increased CD31 expression (post-hoc Tukey t-test, p< 0.05 and p<0.005). Only the H1047R and E545K variants had significantly increased VECADHERIN expression (post-hoc Tukey t-test, p<0.005). These changes in protein expression mimic changes observed in patient derived VMECs.

Conclusion:
The introduction of PIK3CA variants that hyperactivate PI3K signaling recapitulated cell morphology and proteostasis defects seen in patient VMECs. The H1047R variant demonstrated the most severe phenotype, which correlates with published clinical data. Disparities between variants may be relevant to understanding both the clinical heterogeneity of VM patients and their differential response to treatment. These data provide compelling evidence that VMEC phenotypes are downstream of PI3K/AKT/mTOR signaling. Future studies of how PI3K hyperactivation causes VMEC dysfunction may uncover novel avenues for therapeutic treatment.

poster

Introduction: With increases in antimicrobial resistance, stewardship is essential in antibiotic decisions. Infectious diarrhea is a common reason for antibiotic usage. The Gastrointestinal PCR Panel (GPP) is a rapid multiplex molecular test detecting common pathogens causes of infectious diarrhea. Unfortunately, current medical literature contains limited guidance on incorporating GPP results into stewardship decisions. This study investigates the appropriateness of antimicrobial selection in patients with bacterial or parasitic causes of infectious diarrhea. 

Methods: We retrospectively analyzed all positive bacterial or parasitic GPP results from adults (≥18 years) in the Prisma Health Medical System in 2023, excluding patients with concurrent diagnosed infections. We assessed each patient for appropriateness of antimicrobial selection, including antibiotic choices, doses, and durations before and after GPP results. Inappropriate was defined as receiving an ineffective antibiotic, receiving more antibiotics than indicated, indicating but not prescribing treatment, and inappropriate duration of antimicrobial course based on the pathogen, patient’s risk factors, and overall clinical condition.

Results: Of 283 patients, 111 (39.2%) had an inappropriate antimicrobial selection or duration, 29 of which never received an effective antimicrobial despite being warranted. Of the 111, 91 (82.0%) received an inappropriate duration of therapy. Sixty-three patients (56.8%) had an inappropriate antibiotic selection with many receiving unneeded metronidazole. Inappropriate antimicrobial selection or duration occurred frequently in all medical settings: outpatient 7/21 (33.3%), emergency department not admitted 29/68 (42.6%), ED admitted 39/110 (35.5%), and inpatient 36/84 (42.8%). Nineteen of 54 immunocompromised patients (35.2%) received an insufficient duration of therapy. Immunocompromised individuals with Campylobacter (8/8, 100%) and Enteropathogenic E. coli EPEC (4/9, 44.4%) were frequently undertreated. Additionally, patients with Shigella and HIV frequently received an inappropriately short course (5/9, 55.5%). In contrast, immunocompetent individuals frequently received inappropriately long antibiotic courses to treat mild cases of Shigella (4/9, 44.4%), Campylobacter (4/10, 40%), EPEC (5/16, 31.3%), and Enteroaggregative E. coli (EAEC) (2/10, 20%).

Conclusion: Inappropriate antimicrobial therapy for infectious diarrhea was very common in all medical settings. Frequently immunocompromised patients were undertreated while mild infections in immunocompetent patients were overtreated. Many patients received multiple antibiotics when only one antibiotic was indicated.

Future studies:We plan to develop and implement a Prisma Health-specific GPP interpretation guideline to support stewardship via the Prisma Health Stewardship mobile application, with future studies evaluating its impact on prescribing patterns.

Opportunities for antimicrobial stewardship interventions based on Gastrointestinal Pathogen Panel Rapid Diagnostics

Background
Percutaneous coronary intervention (PCI) for chronic total occlusion (CTO) in post-coronary artery bypass grafting (CABG) patients is particularly challenging due to complex anatomy, comorbidities, and limited collateral channels. Hybrid strategies and advanced intravascular imaging are often needed for procedural success.

Case Presentation
A 76-year-old Portuguese male with CAD status post CABG (LIMA-LAD, SVG-OM), type B aortic dissection, AVNRT (s/p ablation), hypertension, hyperlipidemia, thrombocytopenia, and anemia on GDMT presented with exertional angina. Workup revealed inferior wall ischemia secondary to a right coronary artery (RCA) CTO. An initial antegrade PCI in December 2024 achieved proximal RCA stenting but failed to cross the distal CTO, despite subintimal tracking and the use of a Stingray reentry device, limited by the available contrast volume. On January 22, 2025, IVUS-guided PCI of the mid-distal RCA CTO was completed via bilateral femoral access using a Gaia Next 3 wire for true lumen crossing, sequential ballooning, and Synergy XD stent placement. Optimal stent expansion and TIMI III flow were achieved without complications. The patient was discharged on dual antiplatelet therapy and aggressive risk factor modification. Follow-up noted marked symptomatic improvement.

Discussion
This case illustrates the technical complexity of CTO PCI in post-CABG patients, emphasizing the importance of meticulous planning, intravascular imaging, and hybrid strategies. IVUS guidance was critical in achieving optimal outcomes, underscoring its growing role in complex PCI cases.

IVUS-Guided CTO in post-CABG patient using a hybrid approach

Abstract Title: Vagus Nerve Stimulation Ameliorates Inflammatory Skin Diseases through Systemic Anti-Inflammatory Pathways: Evidence from Murine Models of Psoriasis and Atopic Dermatitis
William J. Nahm,1 Ki Joong Kim,2 Eui Namgung,3 Vincent Falanga,4

1) New York University Grossman School of Medicine, New York, NY, USA
2) Department of Oriental Medicine, Daejeon University, Daejeon, ROK
3) Department of Physics, University of California, San Diego, La Jolla, CA, USA
4) Department of Dermatology, Boston University Chobanian and Avedisian School of Medicine, Boston, MA, USA

Background: The cholinergic anti-inflammatory pathway, activated through vagus nerve stimulation (VNS), plays a crucial role in immune response regulation. Although the skin lacks direct vagal nerve (VN) innervation, VNS may influence cutaneous inflammatory disorders through indirect mechanisms. In recent years, VNS has shown promise in modulating rheumatoid arthritis, inflammatory bowel disease, and other conditions, such as cardiovascular disease. This study investigated whether VNS could improve inflammatory skin diseases by modulating systemic inflammatory responses and local inflammatory cytokines.

Methods: Two distinct murine models were employed: C57/BL6 mice with imiquimod-induced psoriasis lesions and NC/Nga mice with dinitrochlorobenzene (DNCB)-induced atopic dermatitis. In the imiquimod model, psoriasis-like lesions were induced by applying imiquimod 5% cream to shaved dorsal skin for seven consecutive days, followed by every other day for six days. The DNCB model involved sensitization with 1% DNCB for seven days, followed by 0.3% DNCB for three days, resulting in marked scaling, crusting, and exudate formation. Cervical VNS (5V/5mA/5Hz/5ms/5min) was administered at 6- and 24-hour pre-sacrifice in the imiquimod model, and 24 hours pre-sacrifice in the DNCB model. Outcomes were assessed through clinical evaluation, histological analysis, immunofluorescence staining, western blotting, and cytokine measurement in plasma and splenic tissue.

Results: The application of imiquimod and DNCB produced psoriatic and eczematous-type clinical inflammation, accompanied by markedly increased epidermal thickening. VNS significantly reduced epidermal thickening and attenuated clinical manifestations in both models. In the imiquimod model, VNS produced a moderate reduction of erythema, scaling, and crusting. The DNCB-induced dermatitis was dramatically ameliorated following VNS treatment. Both models demonstrated significant reduction in pro-inflammatory cytokine expression (TNF-α, IL-6, IL-1β) and decreased CD11b-positive cutaneous macrophage infiltration. Immunofluorescence confirmed decreased epidermal TNF-α expression post-VNS. A single VNS application in DNCB-treated mice resulted in a 32% reduction in plasma TNF-α concentrations (p < 0.01). Notably, the protein levels of TNF-α and IL-1β, which were elevated in splenic tissue in both inflammatory models, were subsequently downregulated by VNS treatment.

Conclusion: These findings establish VNS as a promising therapeutic approach for inflammatory skin diseases. The therapeutic effects appear to be mediated through the modulation of systemic and subsequently local inflammation. These findings suggest that cutaneous inflammatory disorders may be linked to systemic inflammatory processes, providing mechanistic insights into the anti-inflammatory effects of VNS in dermatological conditions. Additionally, VN dysregulation emerges as a potential unifying mechanism underlying the well-established association between inflammatory skin diseases and their systemic comorbidities.

Vagus Nerve Stimulation Ameliorates Inflammatory Skin Diseases through Systemic Anti-Inflammatory Pathways: Evidence from Murine Models of Psoriasis and Atopic Dermatitis

Background: Glaucoma is characterized by the insidious degeneration of Retinal Ganglion Cells (RGCs). Such degeneration can be monitored with the Combined Structure Function Index (CSFI), which can generate an estimated RGC count (eRGCC) to identify early glaucomatous change. In this study, we examine the relationship between enlargement of the Foveal Avascular Zone, a capillary free region of the macula, with decreasing eRGCC, to investigate loss of microvascular integrity as a potential etiology for eRGCC decline.

Methods: Five subjects (9 eyes) underwent comprehensive eye exam, OCT for eRGCC calculation, and OCT-A for FAZ area calculation. Pearson correlation and linear regression were used.

Results: Subjects averaged 55±15 years old, with a mean eRGCC of 892,514± 2,222. A significant negative correlation was found between FAZ and eRGCC (r2 = -0.915, p=0.01). in a linear regression model, FAZ as a predictor explained 5.1% of variance in eRGCC (p=0.010), while age, hypertension, and diabetes account for 93.9% (p=0.002). Every 0.01mm2 rise in FAZ was associated with a 327 eRGCC loss.

Conclusion: Increase in FAZ correlates with eRGCC loss in Glaucoma Suspects, implicating a vascular etiology of Glaucoma.

Increased Foveal Avascular Zone Area Predicts Decreased Estimated Retinal Ganglion Cell Count in Glaucoma Suspects: A Pilot Study

Background
Medial meniscus posterior horn root tears (MMPRTs) are injuries of the knee causing cartilage displacement, leading to accelerated osteoarthritis. MMPRTs are associated with meniscal extrusion, defined as radial displacement >=3 mm of the meniscus. Quantitative MRI, particularly T2 and T2* relaxation time mapping, can distinguish between normal vs. torn or degenerative menisci. This study focuses on 3D T2* mapping in evaluating medial meniscal extrusion between patients before and six months after surgical repair of MMPRTs, compared to healthy controls. We hypothesize that MMPRTs increase T2* values, and that relaxation times correlate with medial meniscus extrusion measurements taken before and after repair.

Methods
This study involved fifteen patients with a unilateral posterior root tear of the medial meniscus and nine healthy controls. Each patient underwent the same MRI protocol twice using a 7T MRI system—once before repair and again six months after repair—while the control group had one scan.

The MRI protocol included T2-weighted turbo-spin echo and 3D SPACE sequences with fat suppression. Multi-echo T2* data were used to fit a mono-exponential signal decay through a two-parametric least-squares fitting routine, with fitting accuracy assessed by normalizing the root mean square error (RMSE) to estimated signal intensity at an echo time of 0 ms.

Manual 3D segmentation was performed on T2*-weighted images using ITK-SNAP to capture the 3D structure of the medial meniscus.

Median T2* values and RMSEs were calculated. Meniscal extrusion was assessed on coronal T2-weighted images with fat suppression by drawing two vertical lines at the peripheral margins of the tibial plateau and the outermost edge of the meniscal body. A linear mixed-effects model was used for comparisons, and Pearson correlation analysis was employed.

Results
Significantly longer T2* values (p<0.05) were observed in the medial meniscus of patients before and six months after repair of the root tear. Post-repair patients showed significantly higher T2* values in the posterior horn of the medial meniscus compared to pre-repair patients. RMSE was below 4.3% for all regions, indicating good reliability. Extrusion measurements in post-repair patients were significantly correlated with T2* values in both pre-repair (r=0.826; p<0.001) and post-repair (r=0.732; p=0.002) patients. 

Conclusion
Findings show strong correlations between T2* mapping and meniscal extrusion, emphasizing the connection between altered structural integrity and tissue laxity. 3D quantitative T2* mapping is a potent tool in evaluating meniscal extrusion in patients with MMPRTs, which can ultimately improve surgical outcomes and patient quality of life.


3D T2* Mapping of Medial Meniscus Extrusion at 7T Before and After Posterior Root Tear Repair

Abstract Title 
Pseudocyesis versus Delusional Pregnancy in a Young Adult with history of Neuroblastoma 

Background 
Pseudocyesis, or false pregnancy, is a rare psychosomatic condition characterized by the belief of being pregnant accompanied by objective signs of pregnancy without actual conception. This condition poses diagnostic challenges, particularly in patients with complex medical histories requiring multidisciplinary care approaches. 

Case Presentation 
We report the case of a 23-year-old female with a history of neuroblastoma who presented with pseudocyesis. The patient experienced multiple emergency department visits over several months, presenting with symptoms consistent with pregnancy including amenorrhea, abdominal distension, and subjective fetal movement. Initial clinical suspicion prompted extensive workup including serial beta-HCG levels and pelvic ultrasounds. Despite repeatedly negative pregnancy tests and imaging studies showing no evidence of intrauterine pregnancy, the patient maintained firm conviction of being pregnant and continued to report symptoms. 

The patient's presentation was complicated by her oncological history, requiring careful consideration of potential malignancy recurrence versus psychiatric etiology. Multiple laboratory investigations and imaging studies were performed to exclude organic causes, including tumor markers and advanced imaging. The persistence of symptoms despite negative objective findings led to psychiatric admission. 

Successful management required close collaboration between primary care physicians, emergency medicine, gynecology, and psychiatry services. This case highlights the importance of early psychiatric involvement in suspected pseudocyesis cases, with primary care physicians serving as essential coordinators of multidisciplinary care. 

Discussion 
This case demonstrates the complexity of diagnosing and managing pseudocyesis, particularly in patients with significant medical histories. The rarity of this condition and the absence of standardized treatment protocols emphasize the critical need for interdisciplinary collaboration between primary care providers and psychiatric services. Primary care physicians are uniquely positioned to identify these cases early, coordinate comprehensive care, and ensure treatment continuity. Early recognition and coordinated care can reduce healthcare utilization, minimize unnecessary testing, and improve patient outcomes in these challenging presentations. 



Pseudocyesis versus Delusional Pregnancy in a Young Adult with history of Neuroblastoma

Background
Invasive mucormycosis is a serious fungal infection that predominantly affects immunocompromised individuals, especially those with diabetes mellitus. Its mortality rate can reach up to 96% despite treatment. Rhino-orbital-cerebral involvement is the most common, but cases of cutaneous mucormycosis, especially in immunocompetent patients, are rare. Factors like trauma, IV drug use, and nosocomial infections increase the risk of infection. Necrotizing fasciitis caused by Rhizopus species is extremely rare without conditions such as uncontrolled diabetes or immunosuppressive therapy. Early recognition and aggressive treatment are crucial, as mucormycosis leads to rapid tissue necrosis, and delayed diagnosis worsens outcomes.
Case Report
A 57-year-old male with schizophrenia and hypertension was found unconscious in a field and brought to the emergency department as a John Doe. Upon admission, he was hyperthermic (107.2°F) and tachycardic, requiring cardioversion. His condition quickly deteriorated into multiorgan dysfunction, including rhabdomyolysis-induced acute kidney injury, disseminated intravascular coagulation (DIC), and necrotizing fasciitis. Blood cultures revealed Pseudomonas, Stenotrophomonas, Enterococcus faecalis, Micrococcus luteus, and Zygomycetes, and histopathology confirmed mucormycosis.
The patient's presentation was complicated by psychiatric instability, as he had not been taking his prescribed medications and was displaying erratic behavior prior to his disappearance. He was intubated, given vasopressors, and started on broad-spectrum antibiotics. As cultures returned, antifungal therapy with Amphotericin B was initiated, later transitioned to isavuconazole. He required multiple rounds of surgical debridement for necrotic tissue, with the largest wound measuring 28 x 18 x 10 cm. His kidney function initially worsened, necessitating hemodialysis, but improved with supportive measures. He also experienced significant difficulty with oral intake, requiring enteral feeding via a PEG tube.
Discussion
This case presents a rare and complex presentation of cutaneous mucormycosis, exacerbated by prolonged environmental exposure, psychiatric illness, and bacterial co-infection. While mucormycosis is often associated with immunocompromised patients, especially those with diabetes, this case shows that other factors, such as trauma and bacterial infection, can also facilitate fungal colonization. The patient’s hyperthermia, rhabdomyolysis, and tissue breakdown provided conditions favorable for fungal growth. Mucormycosis is difficult to diagnose early, especially when bacterial infections mask its characteristic tissue necrosis. This case underscores the importance of early suspicion, rapid antifungal treatment, and a multidisciplinary approach to managing such complex infections. Aggressive debridement and antifungal therapy were key to the patient’s eventual recovery.

Acute Invasive Mucormycosis (Zygomaticus) in Schizophrenic Patient: A Case Report and Literature Review

Background: Developmental facial paralysis (DFP) is a rare congenital condition most often associated with syndromes such as Möbius, CHARGE, and Goldenhar. Isolated cases without syndromic features are uncommon. Chiari I malformation (CM-I), characterized by herniation of the cerebellar tonsils through the foramen magnum, is a structural anomaly of the posterior fossa. To our knowledge, there are no published reports of DFP co-occurring with CM-I. However, posterior fossa abnormalities may hypothetically interfere with cranial nerve development if they
arise during critical periods of neurodevelopment.
Case Presentation: A 37-year-old woman with a lifelong history of right-sided lower motor neuron facial palsy presented with six months of occipital headaches, intermittent neck pain, vertigo, and nausea. Her medical history included idiopathic seizures and chronic gastritis. Neurologic examination revealed an isolated, non-progressive facial palsy without other cranial nerve deficits. Brain MRI demonstrated a 12 mm descent of the cerebellar tonsils below the foramen magnum, consistent with CM-I. She underwent posterior fossa decompression with
suboccipital craniectomy and C1 laminectomy. Postoperative follow-up showed resolution of her new symptoms, but the facial paralysis persisted.
Discussion: This case suggests a possible link between CM-I and isolated DFP. While her facial palsy was congenital and remained unchanged after decompression, the presence of CM-I raises the question of whether altered posterior fossa dynamics may have influenced facial nerve development in utero. Potential mechanisms include mass effect affecting the facial nucleus, cerebrospinal fluid flow disruption, or ischemia due to compromised distal paramedian perforators of the basilar artery. These changes may impair neurogenesis or lead to irreversible nerve injury if present during key embryologic windows. This report highlights a rare clinical
overlap and invites further investigation into how structural posterior fossa anomalies might contribute to isolated cranial nerve deficits.


Posterior Fossa Constraints in a Case of Developmental Facial Palsy with Chiari I Malformation

Background:
The spectrum of vascular access-site complications following cardiac catheterization can vary widely in severity, ranging from simple to complex, and can contribute to significant morbidity with a high economic burden and healthcare costs.
Aim:
The case presentation aimed to describe a post-discharge delayed complication (acute limb ischemia) of cardiac catheterization due to noncalcified plaque.
Case Presentation:
A 58-year-old male with a history of coronary artery disease, diabetes mellitus, and hyperlipidemia underwent cardiac catheterization status-post angioplasty to the right coronary artery via right-femoral artery access. The patient was discharged home post-procedure; however, 8 hours later, he developed a sudden-onset cold foot, worsening numbness, and tingling sensation in his right extremity that prompted him to present to the ER. Physical examination was notable for cold skin in his right leg with diminished dorsalis pedis and popliteal pulses, and a mild loss of “touch sensation” below the level of the knee. The patient was staged “IIa” on the Rutherford Acute Limb Ischemia score. Vitals and labs were within normal limits. CT Angiogram revealed focal high-grade stenosis in the right common femoral artery at the site of a recent arterial puncture from cardiac catheterization. This was likely secondary to nonocclusive, noncalcified plaque that has been disrupted from recent instrumentation. A Heparin drip was initiated and the patient underwent emergent revascularization with a diagnostic angiogram and balloon angioplasty of the right common femoral artery with the placement of a 27mm stent. A completion angiogram showed the resolution of the high-grade stenosis with excellent flow through the profound and superficial femoral artery. 
Discussion:
The risk of access-site complications following cardiac catheterization, although quite low, is increased with the femoral artery, with an incidence estimated to be as high as 17%. Bleeding and bruising are common issues, but blood clots are rare and usually happen due to the breaking of plaque in the arteries or damage to the plaque that leads to a clot. When the severity of limb ischemia is threatening, immediate anticoagulation followed by surgical revascularization is the most appropriate intervention. Thrombosis at the access site of cardiac catheterization can cause critical limb ischemia, particularly with the femoral artery, thus highlighting the need for careful postoperative follow-up. 


Acute Limb Ischemia from Catheter-Induced Plaque Rupture - A Case Report

Background 
People experiencing homelessness (PEH) face dramatically higher traffic collision exposure than housed individuals, with limited published quantification of this disparity. Hit-and-run crashes involving unhoused victims represent a critical knowledge gap, as driver behavior and emergency response patterns remain poorly understood. This pilot study aims to: (1) test whether PEH in Sacramento County have elevated pedestrian hit-and-run (PHAR) fatality risk, and (2) compare injury severity patterns between housed and unhoused victims using postmortem medical examinations. 

Methods 
This mixed-methods retrospective study analyzed Sacramento County pedestrian fatalities using 2020-2024 data for population-level analysis, and January 2024-March 2025 cases for forensic sub-analysis to balance epidemiological rigor with policy-relevant timeliness. 

We calculated relative risk (RR) and population attributable risk percentages (PARP) using Census data, Sacramento Coroner website data, and Sacramento Steps Forward point-in-time homelessness estimates. For injury severity subgroup analysis, we obtained autopsy reports (n = 14) via public records request and applied the Forensic Injury Severity Score Template (FISST), converting descriptive findings to numerical scores, as described by Kim et al (2023). Housing and hit-and-run status was determined through coroner investigation. Given small sample size, we employed descriptive statistics with bootstrapped 95% confidence intervals (CI) and computed Cohen's d (CD) to assess differences between group means. 

Results 
Population-level analysis from 2020-2024 revealed PEH face substantially elevated pedestrian fatality risk compared to housed counterparts (RR 92.2, 95% CI 72.57-117.10), with even higher PHAR fatality risk (RR 113.6, 95% CI 70.62-182.80). PEH were overrepresented in PHAR deaths, accounting for over a third of cases despite representing <1% of the population (PARP = 34.4%). 

FISST scoring analysis of 14 autopsies (seven unhoused, six housed, one excluded outlier: Grubbs’ G= 2.57) demonstrated unhoused victims sustained slightly more severe injuries overall (mean FISST 103.7 vs 84.5, CD= -0.45) with significantly worse chest trauma (mean 34.0 vs 18.0, CD= -1.09) and negligible differences in head/neurological trauma (mean 38.7 vs 37.9, CD = 0.03). Available toxicology analysis was positive in 89% of PHAR victims, with amphetamines detected in three-quarters of those cases. Hit-and-run crashes occurred exclusively at night, with 54.5% of PEH involved in PHAR compared to 33.3% of housed victims. Among all PHAR, 81.8% died within one hour versus 33.3% of non-hit-and-runs. 

Conclusion 
These findings support implementing targeted safety interventions in areas with known unhoused populations, integrating substance harm reduction programs and enhancing nighttime pedestrian safety measures to address Sacramento’s 114-fold disparity in pedestrian hit-and-run fatality risk for PEH. 


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