Extensive Edema Research Articles

No Benefit of 3% Hypertonic Saline Following Experimental Intracerebral Hemorrhage

Intracerebral hemorrhage (ICH) is a stroke subtype with a high mortality rate (~ 40%). After ICH, the mass effect of the hematoma and edema contribute to raised intracranial pressure (ICP) and poor outcome. Endogenous compensatory mechanisms that blunt ICP elevations include redirection of venous blood and cerebrospinal fluid, along with brain tissue compliance (e.g., decreased cell volume, increased cell density); however, these limited reserves can be exhausted after severe stroke, resulting in decompensated ICP that requires careful clinical management. Management strategies can include administration of hypertonic saline (HTS), an osmotic agent that putatively attenuates edema, and thereby ICP elevations. Evidence regarding the efficacy of HTS treatment following ICH remains limited. In this study, adult male rats were given a collagenase-induced striatal ICH and a bolus of either 3% HTS or 0.9% saline vehicle at 2- and 14-hours post-stroke onset. Neurological deficits, edema, ipsilateral cell volume and density (in areas S1 and CA1), and contralateral CA1 ultrastructural morphology were assessed 24 h post-ICH. Animals had large bleeds (median 108.2 µL), extensive edema (median 83.9% brain water content in ipsilateral striatum), and evident behavioural deficits (median 5.4 neurological deficit scale score). However, HTS did not affect edema (p ≥ 0.4797), behaviour (p = 0.6479), cell volume (p ≥ 0.1079), or cell density (p ≥ 0.0983). Qualitative ultrastructural assessment of contralateral area CA1 suggested that HTS administration was associated with paradoxical cellular swelling in ICH animals. Overall, there was no benefit with administering 3% HTS after ICH.

The Effects of VEGF-A and GSTM1/GSTT1 Variants in the Susceptibility to the Chronic Rhinosinusitis with Nasal Polyposis: A Pilot Genetic Study.

Nasal polyps (NPs) are usually part of chronic rhinosinusitis with nasal polyposis (CRSwNP). However, the exact etiology of CRSwNP is still unknown. In addition, the suggested etiological causes are infection, allergy, and immunological disorders, among others, such as genetic predisposition. Moreover, it is also suggested that oxygen-free radicals play a vital role in the pathogenesis of nasal polyposis, and inflammatory cells produce free radicals during phagocytosis, which is the primary source of ROS, controlled by the glutathione S-transferase (GST) system. Although, vascular endothelial growth factor (VEGF) plays an important role in angiogenesis, it is closely interwoven with the mobilization of inflammatory cells. This pilot study evaluated the association between genetic variant VEGF-A (rs28357093) and GSTM1/GSTT1 deletion polymorphism in susceptibility to CRSwNP. A case-control study was conducted with 61 individuals diagnosed with CRSwNP and 100 healthy subjects. VEGF-A (rs28357093) and GSTM1/GSTT1 deletion polymorphisms were genotyped by RFLP-PCR and SYBR Green real-time PCR, respectively. Individuals with allergic rhinitis carriers with AC genotype (rs28357093) presented a 4-fold increased risk to CRSwNP (OR = 4.20, 95% CI = 1.31 to 13.50; p = 0.015). This evidence shows that the increased vascular permeability probably causes an inflamed nasal area leading to extensive edema and polyp growth. On the other hand, no association was verified for each genetic variant by inheritance models. Interestingly, the GSTT1 present genotype showed a protective effect on CRSwNP. In conclusion, additional studies that have larger groups in different geographic localizations may be useful to verify and assess the association between genetic variants and CRSwNP.

12618 A Rare Case Of Diabetic Ketoacidosis Leading To Severe Hypertriglyceridemia-induced Necrotizing Pancreatitis

Abstract Disclosure: E.R. Perez Roman: None. D.A. Lopez Rodriguez: None. K. Ramirez Gorbea: None. M. Sanchez Cordero: None. Y. Garcia Cruz: None. Acute pancreatitis is an acute inflammatory process of the pancreas that if left untreated can become complicated resulting in multiple organ damage and a fatal outcome in approximately 10%-40% of patients. There are well-known causes that can lead to pancreatitis such as alcohol, hereditary disorders, cholelithiasis, prior pancreatitis, and medications. Less frequently, it can be related to poorly controlled diabetes mellitus and diabetic ketoacidosis (DKA), given that in a state of low or deprived insulin, there is a breakdown of triglycerides into toxic fatty acids by pancreatic lipases; this lipotoxicity can result in the development of acute pancreatitis. We present a case of a 50-year-old woman with a past medical history of untreated hyperlipidemia and previous pancreatitis who was transferred to our institution with acute epigastric pain radiating to the back, nausea, and persistent vomiting. Upon arrival, blood glucose was 299 mg/dL, HbgA1c of 11.4%, lactic acid of 3.6 mmol/L, hypocalcemia of 6.0 mg/dl, hypoalbuminemia, and elevated pancreatic enzymes, amylase 869 U/L and lipase 2,493 U/L. The lipid panel was remarkable for total cholesterol of 1,085 mg/dL and triglycerides of 4,369mg/dL. Abdominopelvic CT scan confirmed acute pancreatitis with extensive peripancreatic and regional mesenteric edema. This patient was treated with aggressive IV fluid resuscitation and treated for DKA as per protocol. Despite prompt treatment, the patient rapidly deteriorated, developing pulmonary effusions and impending respiratory failure requiring mechanical ventilation. Her hyperglycemia was challenging to control and in the setting of severe hypertriglyceridemia, insulin requirements were higher, as intravenous insulin is useful in patients with concomitant findings, in the absence of plasmapheresis availability. Despite the marked reduction of triglyceride to 978 mg/dL and a decrease in pancreatic enzymes, multiorgan failure developed. Unfortunately, the patient died. Repeated abdominopelvic CT imaging revealed the progression of the disease to necrotizing pancreatitis involving the pancreatic head, uncinate process, and neck of the pancreas with evidence of a small hypodense lesion at the level of the tail of the pancreas. This case emphasizes the importance of prompt recognition of acute pancreatitis secondary to uncontrolled hyperglycemia with concomitant severe hypertriglyceridemia since it can lead to a worse clinical outcome as seen in our patient who developed rapid progression to necrotizing pancreatitis. It is paramount not to delay treatment with aggressive fluid resuscitation, continuous insulin infusion, and if available, plasmapheresis; as these treatment strategies in conjunction can be life-saving. Presentation: 6/3/2024

LGGL-03 TREATMENT OUTCOMES ON OPTIC GLIOMA: A CASE STUDY

Abstract 11 year old male presented in December 2021 with complaints of headache and visual impairment. On examination [he had] multiple freckles in the right axilla and cafe au lait lesions all over his body with largest being 3cm in the inguinal region. Pretreatment MRI showed minimally enhancing mass seen in the optic chiasm extending anteriorly into the distal optic nerves bilaterally and the optic tract posteriorly with extensive vasogenic edema along the optic pathway into the lateral thalamus and extending into the bilateral lentiform nuclei. H-MR spectroscopy of the mass demonstrated a choline peak. Findings in keeping with optic pathway glioma. The baseline fundoscopy showed a normal anterior segment, slightly pale disc on the posterior segment. The patient was commenced on weekly Vinblastine via chemo port. At 24 weeks of treatment patient was assessed MRI and fundoscopy. MRI showed a mild interval decrease in size of lobulated mass lesion involving the optic chiasma, bilateral optic nerves up to intraorbital segments and optic tracts. The lesion also involves the infundibular stalk and tuber cinereum. No interval change in hyperintense T2/FLAIR signal with no enhancement seen at the lateral geniculate bodies, hippocampi, bilateral lentiform nuclei and lateral thalami. He completed 72 weeks of Vinblastine with good clinical Response. NF 1 can cause tumors to form and optic nerve gliomas that may occur in about 15 percent of children with this disease in about 2/3 of the time the tumors stop growing and disappears however there are some tumors that may require treatment.

Brain microbleeds resulting from presumed extensive fat emboli in a patient with bone marrow necrosis following a sickle cell disease vaso-occlusive crisis.

Acute manifestations of sickle cell disease (SCD) are numerous and multisystemic.Cerebral fat embolism (CFE) is a rare but serious complication of SCD caused by bone marrow necrosis (BMN) during vaso-occlusive crises (VOC). We present the case of a41-year-old man with SCD who developed severe VOC and multi-organ dysfunction.He subsequently experienced neurological deterioration with decreased consciousness and diffuse encephalopathy on serial electroencephalograms. Bone marrow aspiration confirmed BMN. Brain MRI revealed extensive diffuse leukoencephalopathy, vasogenic and cytotoxic edema in the white matter, patchy edema in the cranial vault bone marrow on fat-suppressed FLAIR sequence (a finding consistent with the confirmed BMN), and multiple cerebral microbleeds on susceptibility-weighted imaging consistent with CFE. The management of acute neurological complications of SCD varies depending on the specific complication. Brain MRI plays a crucial role in the accurate diagnosis of these complications to guide appropriate treatment.

Amyloid related imaging abnormalities in the emergency setting.

Since the 2021 FDA approval of the first monoclonal antibody (MAB) therapy for Alzheimer's disease (AD), treatment has progressed from symptom management to targeting and reducing amyloid β plaque burden. While these therapies offer hope of altering the disease course, they come with risks, such as amyloid-related imaging abnormalities (ARIA), which include ARIA-E (edema and effusion) and ARIA-H (hemorrhage). This report details the case of a 64-year-old woman undergoing donanemab treatment who developed severe ARIA, characterized by extensive vasogenic edema and multiple microhemorrhages. The increasing use of MABs necessitates heightened awareness and expertise among emergency radiologists to identify findings of ARIA effectively, ensuring timely and appropriate care for patients undergoing these novel therapies.

Osteochondritis Dissecans of the Medial Femoral Condyle: MRI Findings of Instability.

BACKGROUND: Osteochondritis dissecans (OCD) of the medial femoral condyle (MFC), a common cause of pediatric chronic knee pain, is often found to be stable at arthroscopy. OBJECTIVE: To investigate the performance of MRI for identifying instability of MFC OCD in children. METHODS: This retrospective study included 59 children (37 boys, 22 girls; mean age, 12.5±2.2 years) with 69 MFC OCD lesions, who underwent knee MRI from January 2016 to October 2023. Two radiologists independently reviewed examinations to determine regional findings (effusion, skeletal maturity, secondary physis visibility, progeny composition), as well as direct (osteochondral defect, intraarticular body, cartilage alteration, bone plate disruption, receded ossification front) and indirect (progeny-parent bone interface, radius of curvature, parent-bone low-signal intensity (SI) marginal rim, perilesional marrow edema) findings of instability; disagreements were resolved through consensus. Two investigators assessed an additional indirect finding, cyst(s), in consensus. Demographic characteristics, and lesion volume were collected. The reference standard for lesion stability was arthroscopy (n=52) or follow-up evaluation (based on symptoms and imaging findings) in patients managed conservatively (n=17). Stable and unstable lesions were compared. RESULTS: Forty-nine lesions were stable, and 20 were unstable. Sensitivity and specificity for instability, among features showing significant associations with instability, were 70.0% and 100.0% for skeletal maturity, 75.0% and 75.5% for osteochondral progeny composition, 100.0% and 85.7% for cartilage alteration, 85.0% and 81.6% for presence of progeny-parent bone interface, 30.0% and 100.0% for extensive interface, 90.0% and 34.7% for cyst(s), 45.0% and 91.8% for altered radius of curvature, 80.0% and 89.8% for parent-bone low-SI rim, and 50.0% and 81.6% for extensive perilesional marrow edema. In multivariable analysis, factors independently associated with instability included larger lesion volume and indirect signs (presence of interface, cyst(s), altered radius of curvature, parent-bone low-SI rim, and extensive perilesional marrow edema). Frequency of instability was 0.0%, 7.4%, 16.7%, 75.0%, 83.3%, and 100.0% for lesions with 0, 1, 2, 3, 4, and 5 indirect signs. CONCLUSION: Lesion instability was associated with an increasing number of indirect MRI signs. CLINICAL IMPACT: Assessment of lesion stability by MRI can help guide decisions between arthroscopy and conservative management for MFC OCD in children.

Rare manifestations of cutaneous diphtheria: a case report

BackgroundThis case report presents an exceptionally rare and atypical presentation of diphtheria in a 17-year-old female of Hausa ethnicity residing in an area with an elevated incidence within Kano State, Nigeria. By the end of 39th epidemiological week of 2023, only two cases of cutaneous diphtheria have been reported among 5,811 cases managed at MMSH diphtheria treatment center (DTC), representing approximately 0.035% of all diphtheria cases during that time period.Case presentationA 17-year-old Hausa female presented with a 3-day history of throat discomfort, malaise, and muffled speech. Physical examination revealed a pseudomembrane covering the tonsillar pillars, grade 3 tonsillar enlargement, and an unusual genital manifestation characterized by extensive vulval edema, severe pain, and a large, greyish patch extending into the vaginal introitus. Her medical history was significant for recent exposure to diphtheria and the emotional impact of her sibling's death from the same disease. Diagnostic tests, including throat swab culture and histocytology, confirmed diphtheria in the throat and vulvovaginal regions. The patient was promptly initiated on diphtheria antitoxin, Azithromycin, and innovative sitz baths with hydrogen peroxide. After 4 days of Sitz bath therapy, complete pseudomembrane clearance was observed, and the patient's symptoms resolved.ConclusionThis case underscores the complexity of diphtheria presentations, particularly with rare pseudomembranes in both throat and vaginal regions. The successful management, combining traditional and innovative therapies, highlights the importance of recognizing and addressing unusual manifestations promptly. The potential role of auto-inoculation and the efficacy of interventions like hydrogen peroxide sitz baths warrant further investigation. Overall, this case contributes to the understanding of diverse diphtheria presentations, guiding future clinical strategies for management of diphtheria cases and emphasizing the imperative of comprehensive vaccination efforts.

Integrated transcriptomic and proteomic analyses reveal the effects of chronic benzene exposure on the central nervous system in mice

Benzene exposure is known to cause serious damage to the human hematopoietic system. However, recent studies have found that chronic benzene exposure may also cause neurological damage, but there were few studies in this issue. The aim of this study was to investigate the mechanism of damage to the central nervous system (CNS) by chronic benzene exposure with a multi-omics analysis. We established a chronic benzene exposure model in C57BL/6J mice by gavage of benzene-corn oil suspension, identified the differentially expressed proteins (DEPs) and differentially expressed genes (DEGs) in mice brain using 4D Label-free proteomic and RNA-seq transcriptomic. We observed that the benzene exposure mice had a significant loss of body weight, reduction in complete blood counts, abnormally high MRI signals in brain white matter, as well as extensive brain edema and neural demyelination. 162 DEPs were identified by the proteome, including 98 up-regulated and 64 down-regulated proteins. KEGG pathway analysis of DEPs showed that they were mainly involved in the neuro-related signaling pathways such as metabolic pathways, pathways of neurodegeneration, chemical carcinogenesis, Alzheimer disease, and autophagy. EPHX1, GSTM1, and LIMK1 were identified as important candidate DEGs/DEPs by integrated proteomic and transcriptomic analyses. We further performed multiple validation of the above DEGs/DEPs using fluorescence quantitative PCR (qPCR), parallel reaction monitoring (PRM), immunohistochemistry, and immunoblotting to confirm the reliability of the multi-omics study. The functions of these DEGs/DEPs were further explored and analyzed, providing a theoretical basis for the mechanism of nerve damage caused by benzene exposure.

Study of Biochemical Predictors of Early Neurological Deterioration in Ischemic Stroke in a Tertiary Care Hospital.

Background and objective Early neurological deterioration (END) following acute ischemic stroke (AIS) poses a significant clinical challenge, often leading to increased disability and mortality. This study aimed to investigate the association between specific biomarkers (lactate dehydrogenase (LDH), ferritin,erythrocyte sedimentation rate (ESR),C-reactive protein (CRP), homocysteine) and the occurrence of END in ischemic stroke patients in a tertiary care hospital. Materials and methods Across-sectional hospital-basedstudy was conducted at Dr. D. Y. Patil Medical College and Hospital, Pune, from July 2022 to April 2024. Patients aged 18 and above with confirmed ischemic stroke were included, while those with hemorrhagic stroke, intracranial tumors, mass effect with midline shift, or extensive cerebral edema were excluded. Upon admission, patients were assessed using the National Institutes of Health Stroke Scale (NIHSS) and monitored daily for seven days. Biomarkers, including LDH, ferritin, ESR, CRP, and homocysteine, were measured, and patients were categorized into those with END and without END. Statistical analysis was performed using IBM SPSS Statistics for Windows, Version 20 (Released 2011; IBM Corp., Armonk, New York). Results Out of 100 patients, 12% experienced END. The mean age of patients with END was 53.50 ± 11.20 years, compared to 53.62 ± 11.74 years in those without END (p = 0.790). Males constituted 91.7% of the END group and 73.9% of the non-END group (p = 0.284). A significant association was found between END and alcohol use (41.7% in END vs. 12.5% in non-END, p = 0.010) and tobacco use (41.7% in END vs. 11.4% in non-END, p = 0.010). The mean NIHSS scores were significantly higher in the END group on day 1 (11.58 ± 3.06 vs. 7.69 ± 3.98,p = 0.002) and on day 3 (13.92 ± 3.15 vs. 6.00 ± 3.65, p = 0.001). Biomarker analysis showed a significant difference in the mean vitamin B12 levels between END and non-END groups (93.17 ± 48.58 vs. 183.45 ± 349.33, p = 0.025). Conclusion Our study identified significant predictors of ENDin ischemic stroke patients, including alcohol and tobacco use, higher initial NIHSS scores, and elevated levels of LDH, ferritin, ESR, CRP, and homocysteine, along with low vitamin B12 levels. These findings highlight the importance of routine biochemical assessments and personalized treatment plans in managing AIS, emphasizing lifestyle changes and nutritional support to improve outcomes. Limitations include the single-center design, small sample size, and lack of long-term follow-up data. Future research should validate these findings in larger, multicenter studies and explore their long-term impact on stroke recovery.

Diabetic myonecrosis complicated by emphysematous pyomyositis and abscess caused by Escherichia coli: a case report

BackgroundNecrotizing myopathies and muscle necrosis can be caused by immune-mediated mechanisms, drugs, ischemia, and infections, and differential diagnosis may be challenging.Case presentationWe describe a case of diabetic myonecrosis complicated by pyomyositis and abscess caused by Escherichia coli. A white woman in her late forties was admitted to the hospital with a 1.5 week history of bilateral swelling, weakness, and mild pain of the lower extremities and inability to walk. She had a history of type 1 diabetes complicated by diabetic retinopathy, neuropathy, nephropathy, and end-stage renal disease. C-reactive protein was 203 mg/l, while creatinine kinase was only mildly elevated to 700 IU/l. Magnetic resonance imaging of her lower limb muscles showed extensive edema, and muscle biopsy was suggestive of necrotizing myopathy with mild inflammation. No myositis-associated or myositis-specific antibodies were detected. Initially, she was suspected to have seronegative immune-mediated necrotizing myopathy, but later her condition was considered to be explained better by diabetic myonecrosis with multifocal involvement. Her symptoms alleviated without any immunosuppressive treatment. After a month, she developed new-onset and more severe symptoms in her right posterior thigh. She was diagnosed with emphysematous urinary tract infection and emphysematous myositis and abscess of the right hamstring muscle. Bacterial cultures of drained pus from abscess and urine were positive for Escherichia coli. In addition to abscess drainage, she received two 3–4-week courses of intravenous antibiotics. In the discussion, we compare the symptoms and findings typically found in pyomyositis, immune-mediated necrotizing myopathy, and diabetic myonecrosis (spontaneous ischemic necrosis of skeletal muscle among people with diabetes). All of these diseases may cause muscle weakness and pain, muscle edema in imaging, and muscle necrosis. However, many differences exist in their clinical presentation, imaging, histology, and extramuscular symptoms, which can be useful in determining diagnosis. As pyomyositis often occurs in muscles with pre-existing pathologies, the ischemic muscle has likely served as a favorable breeding ground for the E. coli in our case.ConclusionsIdentifying the etiology of necrotizing myopathy is a diagnostic challenge and often requires a multidisciplinary assessment of internists, pathologists, and radiologists. Moreover, the presence of two rare conditions concomitantly is possible in cases with atypical features.

Acute Corneal Edema in an Arabian Horse: A Case Report

Introduction: Due to the vulnerable position of the eye, eye injuries are very common in horses. Lack of effective and prompt treatment of eye injuries leads to blindness. Most of the trauma to the horse's eye is the blunt type and usually causes more severe injuries than sharp blows. However, in all these cases, at first, acute uveitis with different severities occurred, which requires quick treatment and can have different consequences. Case report: A two-year-old male Arabian horse with a history of ocular trauma for 4 days to the right eye was referred to the large animal clinic of the School of Veterinary Medicine, Shiraz University, Iran. All other clinical signs, including temperature, respiratory rate, appetite, and mental state were normal. Ocular examination revealed extensive corneal edema, elevated intraocular pressure (IOP) detected by palpation of the globe, blepharospasm, conjunctival hyperemia, miosis, and epiphora. Eye disorder was diagnosed as acute corneal edema and traumatic uveitis. Treatment included administration of flunixin meglumine for three days, atropine eye drops once a day, latanoprost eye drops once a day, gentamicin, and ciprofloxacin eye drops three times daily, and eye wash with saline 0.9% solution twice a day. The treatment continued for 2 weeks and resulted in complete healing which confirmed the diagnosis. The treated horse had a positive response to the therapy and fully recovered within 20 days. No relapse or complications were observed during the final check-up. Conclusion: Acute uveitis is a common complication following blunt trauma to the eye and is diagnosed by clinical symptoms. Since this situation could have a devastating consequence on vision, immediate diagnosis and treatment are essential to achieve the desired result. The treatment of these patients is symptomatic treatment based on anti-inflammatory, mydriatic, and antibiotics. Depending on the patient's condition, the use of other drugs, such as intraocular pressure reducers may be helpful and essential to prevent or treat complications, including glaucoma.

OTHR-14. AN ADOLESCENT WITH A RARE SCHWANNOMA LOCALIZATION AND THE IMPORTANCE OF METHYLATION STUDIES

Abstract BACKGROUND Schwannomas are benign nerve sheath tumours, accounting for about 8% of intracranial tumours, with different histologic patterns described. Olfactory nerves are not expected to have Schwann cells, several theories exist about the origin of these tumours. METHODS/RESULTS A 16-year-old boy was admitted to the emergency department due to a first, self-limited, isolated epileptic event. He scored 15 in the GCS and no focal neurological deficits were observed. At that time, he complained about headaches, lasting for 3 months. Brain CT showed a frontobasal heterogeneous mass. MR characterized it as a 43X34X38 mm well-circumscribed mass, with solid and cystic areas, having an intimate relationship with lamina cribosa, with extensive vasogenic oedema surrounding it, causing deviation of adjacent structures. At that time, he was COVID-19 positive. He was submitted to a craniotomy with a transcortical approach, with an apparent total resection. Retrospectively, he became aware of an improved sense of smell after intervention. The histopathological study revealed a tumour composed of sheets and lobules of large, round cells showing immunopositivity for SOX-10 and S100 and with a Ki-67 index of 5-6%. We proceed to a molecular diagnosis, as the morphology was elusive, finding a methylation pattern highly close to those of schwannomas. With this presumptive diagnosis, clinical and radiological follow-up has been done. After two years, he is doing well, without signs of recurrence. CONCLUSIONS Although rare, an olfactory nerve schwannoma should be considered when there is a frontobasal tumour and impaired sense of smell, although in this case, the COVID-19 infection could be responsible for hyposmia. The clinical picture, imaging and histopathology description were not enough to make the diagnosis and, therefore, to plan the post-surgical approach. We emphasize the importance of a comprehensive molecular study, with a methylation classifier, as this tumour exhibits a typical DNA methylation pattern.

Remote Ischemic Conditioning to Reduce Perihematoma Edema in Patients with Intracerebral Hemorrhage (RICOCHET): A Randomized Control Trial.

Background: Early perihematomal edema (PHE) growth is associated with worse functional outcomes at 90 days. Remote Ischemic conditioning (RIC) may reduce perihematomal inflammation if applied early to patients with intracerebral hemorrhage (ICH). We hypothesize that early RIC, delivered for seven days in patients with spontaneous ICH, may reduce PHE growth. Methods: ICH patients presenting within 6 h of symptom onset and hematoma volume < 60 milliliters (mL) were randomized to an RIC + standard care or standard care (SC) group. The primary outcome measure was calculated edema extension distance (EED), with the cm assessed on day seven. Results: Sixty patients were randomized with a mean ± SD age of 57.5 ± 10.8 years, and twenty-two (36.7%) were female. The relative baseline median PHE were similar (RIC group 0.75 (0.5-0.9) mL vs. SC group 0.91 (0.5-1.2) mL, p = 0.30). The median EEDs at baseline were similar (RIC group 0.58 (0.3-0.8) cm vs. SC group 0.51 (0.3-0.8) cm, p = 0.76). There was no difference in the median day 7 EED (RIC group 1.1 (0.6-1.2) cm vs. SC group 1 (0.9-1.2) cm, p = 0.75). Conclusions: Early RIC therapy delivered daily for seven days was feasible. However, no decrease in EED was noted with the intervention.

Challenges in the diagnosis and management of brown widow spider (Latrodectus geometricus) envenomation in dogs

This study reports two cases of araneism in dogs caused by the bite of the brown widow spider (Latrodectus geometricus), one of which resulted in death. The first case presented mild signs, successfully treated with medication and ice packs. The second case, more severe, involved exacerbated local signs such as extensive edema and ecchymosis, and diffuse cutaneous hemorrhage in the affected limb, as well as systemic signs, including vomiting, tetraparesis, ataxia, and epileptic seizure, culminating in renal and hepatic failure, circulatory collapse, and death. The treatments employed were based on the symptoms and included the use of analgesics and anti-inflammatories. The study highlights the importance of early diagnosis and appropriate treatment, including the use of specific antivenoms in more severe cases. It emphasizes the importance of preventive measures, such as the use of insecticides, to prevent future accidents. Awareness of the clinical signs of poisoning and the available treatment options is crucial for healthcare professionals and veterinarians to ensure proper management of these incidents and minimize their consequences.

A case of multidrug-resistant intractable pylephlebitis and intra-abdominal abscess due to perforated appendicitis successfully treated with open abdominal management

BackgroundPylephlebitis, a rare and lethal form of portal venous septic thrombophlebitis, often arises from infections in regions drained by the portal vein. Herein, we report a case of peritonitis with portal vein thrombosis due to acute severe appendicitis, managed with intensive intraperitoneal drainage via open abdominal management (OAM).Case presentationA 19-year-old male with severe appendicitis, liver abscesses, and portal vein thrombosis developed septic shock and multi-organ failure. After emergency interventions, the patient was admitted to the intensive care unit. Antibiotic treatment based on cultures revealing multidrug-resistant Escherichia coli and Bacteroides fragilis and anticoagulation therapy (using heparin and edoxaban) was initiated. Despite continuous antibiotic therapy, the laboratory results consistently showed elevated levels of inflammatory markers. On the 13th day, open abdominal irrigation was performed for infection control. Extensive intestinal edema precluded wound closure, necessitating open-abdominal management in the intensive care unit. Anticoagulation therapy was continued, and intra-abdominal washouts were performed every 5 days. On the 34th day, wound closure was achieved using the anterior rectus abdominis sheath turnover method. The patient recovered successfully and was discharged on the 81st day.ConclusionsAlongside appropriate antibiotic selection, early surgical drainage and OAM are invaluable. This case underscores the potential of anticoagulation therapy in facilitating safe surgical procedures.

Baseline perihematomal edema, C-reactive protein, and 30-day mortality are not associated in intracerebral hemorrhage.

The relationship between baseline perihematomal edema (PHE) and inflammation, and their impact on survival after intracerebral hemorrhage (ICH) are not well understood. Assess the association between baseline PHE, baseline C-reactive protein (CRP), and early death after ICH. Analysis of pooled data from multicenter ICH registries. We included patients presenting within 24 h of symptom onset, using multifactorial linear regression model to assess the association between CRP and edema extension distance (EED), and a multifactorial Cox regression model to assess the association between CRP, PHE volume and 30-day mortality. We included 1,034 patients. Median age was 69 (interquartile range [IQR] 59-79), median baseline ICH volume 11.5 (IQR 4.3-28.9) mL, and median baseline CRP 2.5 (IQR 1.5-7.0) mg/L. In the multifactorial analysis [adjusting for cohort, age, sex, log-ICH volume, ICH location, intraventricular hemorrhage (IVH), statin use, glucose, and systolic blood pressure], baseline log-CRP was not associated with baseline EED: for a 50% increase in CRP the difference in expected mean EED was 0.004 cm (95%CI 0.000-0.008, p = 0.055). In a further multifactorial analysis, after adjusting for key predictors of mortality, neither a 50% increase in PHE volume nor CRP were associated with higher 30-day mortality (HR 0.97; 95%CI 0.90-1.05, p = 0.51 and HR 0.98; 95%CI 0.93-1.03, p = 0.41, respectively). Higher baseline CRP is not associated with higher baseline edema, which is also not associated with mortality. Edema at baseline might be driven by different pathophysiological processes with different effects on outcome.

A case with multiple nodules and mucosal oedema of the trachea and both bronchi induced by IgG4-related disease

BackgroundIgG4-related disease is a systemic fibroinflammatory disease that is mainly seen in older men, and involves multiple organs, such as the pancreas and lungs. However, 75% of patients with IgG4-related lung disease are asymptomatic (if they are symptomatic, they mainly complain of nasal congestion, rhinorrhoea, chest pain, and cough) and are incidentally diagnosed through chest computed tomograph. Although, nodules in the airway and bronchial wall thickening are criteria for diagnosis, it is important that nodules have been reported in peripheral airways in several cases and rarely in the central airway.Case presentationA 74-year-old woman previously diagnosed with Mikulicz’s disease presented with swelling of the eyelid margin on both sides and visual disturbances. Computed tomography revealed extensive multiple nodules and mucosal oedema of the trachea and both bronchi. On flexible bronchoscopy under local anaesthesia, extensive lesions were observed from the middle of the trachea to the carina, extending into both segmental bronchi. The nodules were continuous with the normal respiratory tract mucosa, and the surfaces were smooth with minimal neovascularisation. Due to the solid nature of the lesion, obtaining an adequate amount of specimen was challenging. Therefore, we used a 1.9 mm cryoprobe under intubation, resulting in minimal bleeding. Subsequently, the patient was diagnosed with IgG4-related lung disease.ConclusionsThe present case is very rare because of the presence of multiple nodules, severe mucosal edema of the central airway and the absence of mediastinal lymphadenopathy, ground glass nodules, and lung masses. Therefore, it is important to consider differential diagnoses. Thus, we emphasise the importance of endobronchial cryobiopsy for obtaining an adequate number of tissue specimens in such cases to establish a definitive pathological diagnosis.

Advanced osteoarthritis of the hip as reason for extensive asymmetric leg edema: a rare case report and review of the literature.

An enlarged iliopectineal bursa (IB) can cause pressure on iliofemoral veins. Clinical presentation can manifest as asymmetrical lower extremity edema. This case report demonstrates extensive asymmetrical leg edema caused by femoral vein compression based on iliopectineal bursitis (IB-itis) associated with advanced osteoarthritis (OA) of the left hip joint with an outline of relevant current literature. A female patient presented with left hip pain and edema in the leg. X-ray showed severe OA of the left hip. Computed Tomography (CT) concluded a cystic abnormality at the left iliopsoas muscle associated with the joint consistent with IB-itis, associated with a degenerative left hip joint. Hybrid total hip replacement was performed. At three-month follow-up her left leg showed no longer signs of extensive edema and she walked without the use of walking aids. IB-itis is mostly associated with rheumatoid arthritis (RA). There are no reports which only describe OA as cause of IB-itis. Extensive asymmetrical leg edema can be caused by venous compression of the femoral vein by an IB-itis. If the latter is the consequence of advanced hip OA, a total hip replacement can yield excellent clinical outcomes both functionally and with regard to the edema.

Chemical (Alkali) Burn-Induced Neurotrophic Keratitis Model in New Zealand Rabbit Investigated Using Medical Clinical Readouts and In Vivo Confocal Microscopy (IVCM).

Chemical eye injury is an acute emergency that can result in vision loss. Neurotrophic keratitis (NK) is the most common long-term manifestation of chemical injury. NK due to alkali burn affects ocular surface health and is one of its most common causes. Here, we established a rabbit model of corneal alkali burns to evaluate the severity of NK-associated changes. Alkali burns were induced in NZ rabbits by treating the cornea with (i) a 5 mm circular filter paper soaked in 0.75 N NaOH for 10 s (Mild NK) and (ii) trephination using a guarded trephine (5 mm diameter and 150-micron depth), followed by alkali burn, with a 5 mm circular filter paper soaked in 0.75 N NaOH for 10 s (a severe form of NK). Immediately after, the cornea was rinsed with 10 mL of normal saline to remove traces of NaOH. Clinical features were evaluated on Day 0, Day 1, Day 7, Day 15, and Day 21 post-alkali burn using a slit lamp, Pentacam, and anterior segment optical coherence tomography (AS-OCT). NK-like changes in epithelium, sub-basal nerve plexus, and stroma were observed using in vivo confocal microscopy (IVCM), and corneal sensation were measured using an aesthesiometer post alkali injury. After 21 days, pro-inflammatory cytokines were evaluated for inflammation through ELISA. Trephination followed by alkali burn resulted in the loss of epithelial layers (manifested using fluorescein stain), extensive edema, and increased corneal thickness (550 µm compared to 380 µm thickness of control) evaluated through AS-OCT and increased opacity score in alkali-treated rabbit (80 compared to 16 controls). IVCM images showed complete loss of nerve fibers, which failed to regenerate over 30 days, and loss of corneal sensation-conditions associated with NK. Cytokines evaluation of IL6, VEGF, and MMP9 indicated an increased angiogenic and pro-inflammatory milieu compared to the milder form of NK and the control. Using clinical parameters, we demonstrated that the alkali-treated rabbit model depicts features of NK. Using IVCM in the NaOH burn animal model, we demonstrated a complete loss of nerve fibers with poor self-healing capability associated with sub-basal nerve degeneration and compromised corneal sensation. This pre-clinical rabbit model has implications for future pre-clinical research in neurotrophic keratitis.