Conemaugh Memorial Medical Center

Libman-Sacks endocarditis (LSE), or nonbacterial thrombotic endocarditis (NBTE), is a rare condition most commonly associated with systemic lupus erythematosus (SLE), but it may also occur in patients with malignancies. NBTE is an underrecognized cause of cancer-associated embolic strokes of undetermined source. We report the case of a 68-year-old female with metastatic pancreatic adenocarcinoma who presented with acute visual disturbances and headaches. Neuroimaging revealed multiple embolic infarcts in different vascular territories. Transesophageal echocardiography (TEE) identified a mass on the posterior mitral valve, consistent with sterile thrombus formation. Laboratory and imaging studies confirmed advanced pancreatic cancer, creating a hypercoagulable state likely responsible for NBTE. The patient was managed with anticoagulation using low-molecular-weight heparin and palliative chemotherapy targeting the underlying malignancy. Despite these interventions, her clinical course progressed with recurrent embolic events and systemic decline, ultimately necessitating hospice care.This case highlights the diagnostic challenges of NBTE in malignancy, emphasizing the need to consider this condition in patients with multiple embolic strokes of varying ages. Early recognition through neuroimaging and echocardiography is essential for timely anticoagulation and multidisciplinary management. Clinicians should maintain a high index of suspicion for NBTE in patients with prothrombotic cancers, such as pancreatic adenocarcinoma, as prompt diagnosis can guide appropriate therapy and optimize quality of life.

Disclosure: A. Marwat: None. H. Bangash: None.Introduction: Hashimoto’s encephalopathy (HE) is a rare and reversable form of autoimmune encephalitis that predominantly affects females, responds to steroids, and is associated with thyroid autoimmunity. HE typically presents with neuropsychiatric symptoms, including altered mental status (AMS), visual hallucinations, and seizures, along with elevated anti-TPO antibodies. Diagnosing HE can be challenging due to the need to exclude other causes of encephalopathy. This case emphasizes the importance of considering HE in patients with persistent AMS when symptoms fail to resolve after addressing common causes like metabolic encephalopathy Case: A 69-year-old woman with a history of hypothyroidism on levothyroxine presented to the emergency department with subacute onset of (AMS), vivid audiovisual hallucinations, body-wide tremulousness, night terrors, sleep disturbances, and memory deficits. Initial evaluation revealed acute kidney injury (AKI) with a creatinine level of 1.5 mg/dL (baseline: 0.8 mg/dL; normal: 0.6-1.10 mg/dL) and a urinary tract infection (UTI) with WBC >50/HPF (normal: 0-5/HPF) on urinalysis. A provisional diagnosis of metabolic encephalopathy secondary to AKI and UTI was made. However, despite correcting AKI with intravenous fluids and treating the UTI with antibiotics, her mental status failed to improve. Neurology was consulted, and further investigations were performed. Brain MRI showed diffuse cerebral and cerebellar atrophy with T2 hyperintensity in the subcortical region. EEG was limited by artifacts but otherwise normal. Cerebrospinal fluid (CSF) analysis revealed mildly elevated protein at 55.4 mg/dL (normal: 20-40 mg/dL) with no pleocytosis. The CSF autoimmune encephalopathy and multiple sclerosis (MS) panels were negative, and blood cultures were negative. Further testing showed markedly elevated thyroid peroxidase antibodies (anti-TPO) at 7,720 IU/mL (normal: 0-60 IU/mL). TSH was normal at 0.47 µIU/mL (normal: 0.35-4.94 µIU/mL), while free T4 was elevated at 1.83 ng/dL (normal: 0.89-1.76 ng/dL). The exclusion of other causes of encephalopathy, combined with elevated anti-TPO antibodies, neuropsychiatric symptoms, nonspecific T2 subcortical hyperintensity, and CSF protein elevation, led to the diagnosis of Hashimoto’s encephalopathy. The patient was treated with high-dose intravenous Solu-Medrol, 1 g daily for three days, with excellent response and complete neurological recovery. She was discharged on a tapering dose of oral steroids with outpatient neurology follow-up. Conclusion: This case highlights the importance of early recognition and management of the diagnostically challenging HE. Prompt treatment with corticosteroids can result in rapid and significant neurological improvement. Increased clinician awareness is essential.Presentation: Monday, July 14, 2025

Abstract Introduction:Pleural lipomatosis is a rare condition involving abnormal fat accumulation along the pleura. This fatty buildup restricts lung expansion leading to restrictive lung disease (RLD), resulting in shortness of breath due to impaired lung capacity and reduced oxygen exchange. Recognizing pleural lipomatosis as a factor in RLD aids in accurate management for patients with unexplained dyspnea.Case Presentation:A 53-year-old male with a history of asthma, obesity, diastolic heart failure, and pleural lipomatosis presented to our pulmonary clinic with worsening shortness of breath. He reported that he developed shortness of breath 6-7 years ago, but it significantly worsened over the last 2 months. He reported that his shortness of breath has been present at rest and worsened with exertion. He was tried on many inhalers of which none improved his symptoms. His vitals in the clinic were within normal and his BMI was 39. His physical exam showed decreased depth of excursion with inspiration but otherwise unremarkable. He had a recent pulmonary function testing (PFT) that showed a nonspecific decline in FEV1 and FVC, and a restrictive pattern with a moderate reduction in diffusion capacity. He had a CT chest a year ago that showed multiple smoothly marginated pleural thickening when he was diagnosed with pleural lipomatosis. A repeat high-resolution CT chest was ordered which showed increasing prominence of the extra pleural fat, particularly on the right most suggestive of extra pleural fat proliferation with a maximum diameter of 18 mm on the right and 12 mm on the left [Fig. 1]. A walking test showed limitation due to dyspnea but no desaturation. Other workups including echocardiogram, cardiopulmonary exercise stress testing, and sleep study were negative. Patient was referred to a quaternary center for further evaluation by thoracic surgery for possible biopsy and surgical intervention.Discussion:Pleural lipomatosis is an exceedingly rare condition, with fewer than 15 cases reported, and has significant implications due to its association with RLD and progressive dyspnea. In our patient, the pleural fat accumulation likely contributed to restricted lung expansion which likely contributed to dyspnea that persisted despite standard treatments. Known risk factors for pleural lipomatosis include obesity, genetic predisposition and chronic lung diseases. This case shows that progressive pleural lipomatosis should be considered in patients with unexplained dyspnea and confirmed pleural fat on imaging.Conclusion: Early recognition of pleural lipomatosis is crucial, as it allows for targeted management, including surgical evaluation, which may improve outcomes in otherwise treatment-resistant cases.

Abstract Introduction Varicella-zoster virus is a significant cause of neurological infections, including encephalitis and meningitis, with mortality rates between 12% and 15%, particularly high in immunosuppressed patients. Diagnosis relies on clinical presentation, cerebrospinal fluid analysis, and imaging, and early antiviral treatment is essential for recovery. Case Presentation A 71-year-old male with history of pulmonary sarcoidosis on chronic prednisone (10 mg daily) presented following syncope and a fall with head trauma and facial abrasion. He reported multiple recent falls. Physical examination was unremarkable for focal neurological deficits but revealed mildly slowed speech, occasional confusion, and symmetrical weakness in the lower extremities. Initial brain computed tomography was unremarkable.After an inconclusive syncope workup, magnetic resonance imaging of the brain was performed due to vague neurological symptoms, showing scattered periventricular hyperintensities and increased fluid-attenuated inversion recovery signals in the left medial temporal and frontal lobes. Cerebrospinal fluid analysis detected varicella-zoster virus DNA, with protein at 359.7 mg/dL, white blood cells at 325 cells/µL with 99% lymphocytes, red blood cells at 1,450 cells/µL with xanthochromia, and glucose at 57 mg/dL, indicating varicella-zoster virus meningoencephalitis.The patient began intravenous acyclovir therapy. On day three of treatment, he developed worsening lethargy, acute decline in mentation, and inability to protect his airway. Repeat magnetic resonance imaging revealed new parenchymal hemorrhages in the temporal, occipital, and frontal lobes, extensive lesions in the cerebellum and midbrain, and meningeal enhancement. The patient ultimately succumbed to his illness. Discussion In immunocompromised patients, varicella-zoster virus encephalitis often presents atypically, without the classic vesicular rash and with subtler neurological symptoms. This presentation led to an initial focus on other differential diagnoses, including cardiac syncope, peripheral neuropathy, and neurosarcoidosis, all of which were plausible given the patient's syncope, history of sarcoidosis, and neurological findings. Additionally, his advanced age and unclear baseline mentation introduced further complexity, directing the workup toward dementia and peripheral neuropathy. The immunosuppressed status elevates the risk for severe complications, including cerebral hemorrhage, widespread vasculopathy, and rapid neurological decline, all of which can worsen despite aggressive treatment. Although acyclovir slows viral replication, the impaired immune status reduces viral clearance, allowing for progression of cerebral injury and parenchymal hemorrhages. Conclusion This case highlights the critical need for early diagnosis and treatment of varicella-zoster virus encephalitis in immunocompromised patients. Rapid initiation of antiviral therapy based on clinical suspicion can be lifesaving, particularly when typical symptoms are absent.

Since the start of 2020, COVID-19 has profoundly impacted global health. Classically, the disease manifests with pulmonary symptoms such as cough, dyspnea, pneumonia, and respiratory distress. However, it is important to note that in addition to these pulmonary symptoms, COVID-19 can present with extrapulmonary symptoms. This case report involves an 82-year-old male who tested positive for the causative agent of COVID-19 - severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), whose presentation manifested with gastrointestinal symptoms in the form of colonic ileus. This report aims to highlight the pathophysiological mechanisms of COVID-19-associated ileuswhile also delving into the importance of timely intervention to prevent complications like intestinal perforation.

We present the case of a 53-year-old male with complicated left-sided parapneumonic effusion due to Streptococcus intermedius and Prevotella buccae. Management required video-assisted thoracoscopic surgery and partial decortication of the left lung. Complications during the hospital stay were extensive, including sepsis, acute hypoxic respiratory failure, alcohol withdrawal, and transient ischemic attack.

The COVID-19 pandemic prevented centers from providing in-person interactive training programs such as the Rural Trauma Team Development Course. Adapting the course to a virtual platform is an option, yet little is known regarding the feasibility of using this format. This study aimed to evaluate the feasibility of providing a virtual rural trauma development course during COVID-19. This is a descriptive study of emergency medical technicians, nurses, emergency department technicians, and physicians from four rural community health care facilities and local emergency medical services who participated in a virtual Rural Trauma Team Development Course held in November 2021 which was transformed into a virtual platform using live remote interactive lectures, recorded case-based scenarios, and interactive virtual-based questions. The course was evaluated by the changes instituted at the centers based on program recommendations and a participant survey. A total of 41 participants were studied, of whom 31 (75%) returned the emailed postprogram survey. The majority (>75%) of respondents rated the activity as very good, with course objectives met. All four facilities instituted changes following the program, including enhancing policy and procedures, guidelines, advancing performance improvement triggers, and equipment acquisition. Individual-reported participant satisfaction was very high. The Rural Trauma Team Development Course can be provided virtually and is a feasible option for trauma centers to provide initial trauma management in the rural community in a safe pandemic-restrictive atmosphere.

Background and Objectives: With the growing recreational cannabis use and recent reports linking it to hypertension, we sought to determine the risk of hypertensive crisis (HC) hospitalizations and major adverse cardiac and cerebrovascular events (MACCE) in young adults with cannabis use disorder (CUD+). Material and Methods: Young adult hospitalizations (18–44 years) with HC and CUD+ were identified from National Inpatient Sample (October 2015–December 2017). Primary outcomes included prevalence and odds of HC with CUD. Co-primary (in-hospital MACCE) and secondary outcomes (resource utilization) were compared between propensity-matched CUD+ and CUD- cohorts in HC admissions. Results: Young CUD+ had higher prevalence of HC (0.7%, n = 4675) than CUD- (0.5%, n = 92,755), with higher odds when adjusted for patient/hospital-characteristics, comorbidities, alcohol and tobacco use disorder, cocaine and stimulant use (aOR 1.15, 95%CI:1.06–1.24, p = 0.001). CUD+ had significantly increased adjusted odds of HC (for sociodemographic, hospital-level characteristics, comorbidities, tobacco use disorder, and alcohol abuse) (aOR 1.17, 95%CI:1.01–1.36, p = 0.034) among young with benign hypertension, but failed to reach significance when additionally adjusted for cocaine/stimulant use (aOR 1.12, p = 0.154). Propensity-matched CUD+ cohort (n = 4440, median age 36 years, 64.2% male, 64.4% blacks) showed higher rates of substance abuse, depression, psychosis, previous myocardial infarction, valvular heart disease, chronic pulmonary disease, pulmonary circulation disease, and liver disease. CUD+ had higher odds of all-cause mortality (aOR 5.74, 95%CI:2.55–12.91, p < 0.001), arrhythmia (aOR 1.73, 95%CI:1.38–2.17, p < 0.001) and stroke (aOR 1.46, 95%CI:1.02–2.10, p = 0.040). CUD+ cohort had fewer routine discharges with comparable in-hospital stay and cost. Conclusions: Young CUD+ cohort had higher rate and odds of HC admissions than CUD-, with prevalent disparities and higher subsequent risk of all-cause mortality, arrhythmia and stroke.