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BMC Proceedings 2025, 19(32):EP1
Keywords: Septic shock; lactic acidosis; renal replacement therapy; multidrug-resistant organisms; critical care; tracheostomy
Abstract
Background
Septic shock with extreme acidemia is rare and life-threatening, demanding rapid, coordinated critical-care management. When pH falls to levels typically incompatible with life, therapeutic decisions (airway, vasopressors, renal replacement, and antimicrobials) become uniquely challenging. We report a 71-year-old man with profound acidemia and septic shock to highlight clinical course and management priorities.
Materials and Methods
Single-patient case report. Data were abstracted from the medical record (history, examination, laboratory/ABG trends, imaging, microbiology) and interventions (resuscitation, vasopressors, ventilation, renal replacement therapy, antimicrobials).
Results
A 71-year-old man with hypertension, diabetes, and obstructive sleep apnea presented tachypneic, tachycardic, and hypotensive. Initial arterial blood gas (ABG) showed mixed respiratory/metabolic acidosis (pH 6.8), deteriorating to pH 6.5 despite fluids; he remained conscious (GCS 15/15). Norepinephrine was initiated. Labs indicated renal and hepatic dysfunction with elevated inflammatory markers. He was intubated, admitted to ICU, started on continuous renal replacement therapy (CRRT), later transitioned to intermittent hemodialysis. Prolonged ventilation required tracheostomy on day 15; extubation attempts were unsuccessful. Cultures grew multidrug-resistant Acinetobacter and Klebsiella; antibiotics were escalated per susceptibilities. Despite aggressive, multidisciplinary care, instability persisted due to refractory infection and hemodynamic compromise.
Conclusions
Extreme acidemia in septic shock requires early ABCs, serial ABGs with neurological documentation, immediate broad-spectrum antibiotics and norepinephrine (within 1 hour), and early mechanical ventilation to reduce work of breathing. Consider bicarbonate when HCO₃⁻ <10 mmol/L with hemodynamic compromise, and initiate CRRT early for refractory acidosis or acute kidney injury. Source control and MDR-targeted therapy are pivotal. Further work should refine prognostic thresholds and algorithms for pH <6.8.
Written informed consent for publication in an open-access journal was obtained from the patient.
EP2 Recurrent Pneumococcal Meningitis from Post-Traumatic Frontoethmoidal Encephalocele: A Case ReportYazan Mazen Yaser Saidismail, Ahmed Darweesh, Maryam Al Ani, Nada Alfalasi, Asif Mohamed Salim, Leena AbdelrahmanDepartment of Internal Medicine, Dubai Health, Dubai, United Arab Emirates Correspondence: Yazan Mazen Yaser Saidismail (yazanmelhem2001@gmail.com)BMC Proceedings 2025, 19(32):EP2
Keywords: Recurrent meningitis; Streptococcus pneumoniae; encephalocele; skull defects; CSF leak; endoscopic repair
Abstract
Background
Recurrent bacterial meningitis (≥2 episodes with complete recovery between episodes) warrants evaluation for skull-base defects with CSF leak and for immune deficiencies. In adults, S. pneumoniae often indicates an anatomic breach (e.g., post-traumatic encephalocele/CSF rhinorrhea), whereas Neisseria suggests complement deficiency.
Case Report
We report a case of a 22-year-old man with his second attack of pneumococcal meningitis within a one-year timeframe after sustaining a road traffic accident about 4 years ago. The patient sustained left frontal bone fracture communicating with the left frontal sinus, along with left frontal encephalocele. His current complaint was fever and cough of one-week duration; they were associated with headache, rhinorrhea, vomiting, sore throat, fatigue, and generalized body pain. The patient denied having any past history of recurrent or severe infections, especially during childhood and adulthood. Upon assessment, his temperature was 37.6 °C, and vitals were within normal limits. Physical examination was remarkable for positive neck stiffness. Otherwise, no skin rashes were noted; neurological assessment included a GCS of 15/15, no focal neurological deficits, and intact cranial nerves. Abdomen was soft, lax, and non-tender; spleen was not palpable. Labs were significant for WBC count of 21,100 cells/uL, CRP of 198.7 mg/L, procalcitonin of 0.64 ng/mL, serum glucose (random) of 146 mg/dL, CSF protein of 209 mg/dL, and CSF glucose of 35 mg/dL (with glucose CSF: serum ratio of 0.24). Both blood and CSF cultures were positive for Streptococcus pneumoniae. HIV test was negative. He was empirically treated with IV ceftriaxone and vancomycin, and later tailored to ceftriaxone after the cultures’ susceptibility results were out.
Conclusions and Recommendations
In adults with recurrent pneumococcal meningitis, prompt skull-base imaging for occult CSF leak/encephalocele and parallel immune evaluation are essential. Definitive endoscopic repair plus pneumococcal vaccination can prevent further episodes. Structured pathways that trigger beta-2 transferrin testing and high-resolution CT/MRI after a second episode may reduce diagnostic delay.
Written informed consent for publication in an open-access journal was obtained from the patient.
References
1.Cullu, N., Deveer, M., Karakas, E., Karakas, O., Bozkus, F., & Celik, B. (2015). Traumatic fronto-ethmoidal encephalocele: A rare case. The Eurasian Journal of Medicine, 47(1), 69–71. https://doi.org/10.5152/eajm.2014.50
2.Gressot, L. V., Patel, A. J., Kitagawa, R. S., Clay Goodman, J., & Gopinath, S. P. (2013). Frontal sinus encephalocele: Case report and review of literature. Clinical Neurology and Neurosurgery, 115(10), 2174–2177. https://doi.org/10.1016/j.clineuro.2013.05.035
3.Go, K., Ge, J., Abdelattif, M., & Zaw, M. (2022). Recurrent meningitis in the context of an encephalocele. Cureus, 14(9), e29594. https://doi.org/10.7759/cureus.29594
4.Tebruegge, M., & Curtis, N. (2008). Epidemiology, etiology, pathogenesis, and diagnosis of recurrent bacterial meningitis. Clinical Microbiology Reviews, 21(3), 519–537. https://doi.org/10.1128/CMR.00009-08
EP3 Solitary T9 Plasmacytoma with Concurrent Tuberculous Lymphadenitis Presenting as Acute Myelopathy: A Case ReportAesha Khalid Sharif, Noura Ali AlowaisMohamed bin Rashid University, Postgraduate Medical Education Division, Dubai, United Arab Emirates Correspondence: Aesha Khalid Sharif (aksharif@dubaihealth.ae)BMC Proceedings 2025, 19(32):EP3
Keywords: solitary bone plasmacytoma; spinal cord compression; vertebra plana; FDG-PET lymphadenopathy; tuberculous lymphadenitis; case report.
Abstract
Background
Solitary Bone Plasmacytoma (SBP) is a localized plasma cell neoplasm of bone or soft tissue, without features of myeloma. When managing patients from TB endemic background, FDG-avid lymphadenopathy may trigger your attention to an ongoing infective process rather than metastasis. We report an unusual presentation of T9 SBP causing cord compression with concurrent biopsy-proven tuberculous lymphadenitis.
Case Presentation
A 26 years’ old Nigerian male, with no known medical background, been under police custody for 2 years, presented with 3-month history of progressive bilateral lower limbs weakness, numbness and decreased sensation extending above the level of his umbilicus. He denied any history of recent trauma, back pain, fever, or flu-like symptoms. He reported good appetite. Review of systems was unremarkable. Upon presentation, he was afebrile and hemodynamically stable. His general examination was normal. His neurological examination involving his upper limbs was normal. However, upon examining the lower limbs it was noted that he had hypertonicity, reduced power of both limbs, along with symmetrical decreased sensation to fine touch and pain. Proprioception was impaired and vibration sensation was absent. He had bilateral clonus with equivocal plantar. He exhibited a positive Romberg’s test and a sensory ataxic gait with normal sphincter function. Collectively, labelled as Grade C according to the American Spinal Injury Association (ASIA) scale. Admitted as a case of transverse myelitis, with progressive bilateral hypesthesia up to the level of T6 with imbalance, and inability to walk. Magnetic Resonance Imaging (MRI) with contrast of the thoracic spine reported a T9 vertebra plana causing severe spinal canal stenosis and myelopathy, with abnormal marrow signal of T8 and T10, highly suspicious for neoplastic process with a secondary T9 pathological fracture. In view of his presenting symptoms, he was taken for a life-saving T8-10 combined fusion and partial tumor excision by spine team. Histopathology reported features keeping with plasma cell neoplasm that were diffusely and strongly positive for CD38 and CD117. They showed Kappa restriction, i.e. monoclonal. After discussion with Hematology team, further workup was ordered, and Multiple Myeloma was ruled out. PET CT Scan was preformed which showed “Multiple cervical and mediastinal hypermetabolic lymph nodes”. A biopsy was taken and reported as Chronic Caseating Granulomatous Lymphadenitis - Tuberculous Type confirming the diagnosis of TB lymphadenitis. In TB-endemic settings, FDG-avid nodes should not upstage SBP without biopsy. Histology and marrow studies remain decisive and should be done to avoid misclassification. A combined approach—urgent decompression, local radiotherapy, and antituberculosis treatment—can optimize neurologic and oncologic outcomes.
Written informed consent for publication in an open-access journal was obtained from the patient.
EP4 Safety and Efficacy of BCG Vaccination to Prevent COVID-19: Updated Systematic Review and Meta-analysis of RCTs Ahmed Hosney Nada1,8, Asmaa Zakria Alnajjar2,8, Ismail A. Ibrahim3,8, Talya Mansour4,8, Tuğba Saka5,7, Wael Hafez6,9, Bareera Tanveer Malik7,8 1Faculty of Medicine, Benha University, Egypt; 2Faculty of Medicine Al-Azhar University, Gaza, Palestine; 3Faculty of Health Sciences, Fenerbahce University, Istanbul, Turkey; 4Faculty of Medicine Beirut Arab University, Lebanon; 5Faculty of Medicine İstinye Üniversitesi, İstanbul, Turkey; 6Emirates society of Internal Medicine, EMA, Dubai and NMC Healthcare Abu Dhabi, UAE; 7Faculty of Medicine and Health Sciences, Kassala University, Kassala, Sudan; 8Global Alliance of Young Researchers, Istanbul, Turkey; 9Medical Research and Clinical Studies Institute, The National Research Centre, Cairo, Egypt Correspondence: Wael Hafez (wael.hafez@nmc.ae)BMC Proceedings 2025, 19(32):EP4
Keywords: Bacillus Calmette-Guérin; COVID-19; randomized controlled trials; vaccine efficacy; trained immunity; adverse events
Abstract
Background
Despite the availability of multiple COVID-19 vaccines, challenges remain regarding their prevention and control. The Bacillus Calmette–Guérin (BCG) vaccine has been reported to induce trained immunity, a state of enhanced innate immune responsiveness that may provide non-specific protection against infections such as COVID-19. Although its safety and effectiveness in this setting have been examined in several clinical trials, much remains uncertain. This systematic review and meta-analysis assessed the safety and efficacy of BCG vaccination in COVID-19 prevention.
Methods
This systematic review and meta-analysis followed PRISMA guidelines and was registered in PROSPERO (CRD420251082743). A comprehensive search was conducted in PubMed, Cochrane, Scopus, Web of Science, and Embase databases until March 2024. The primary outcomes included COVID-19 infection rate, mortality, hospitalization rate, and ICU admission. The secondary outcomes focused on adverse events.
Results
Fifteen RCTs with 16,347 participants were included in this study. BCG vaccination did not significantly reduce COVID-19 infection (RR = 1.06, 95% CI [0.96–1.17], p = 0.27), ICU admission (RR = 0.44, 95% CI [0.14–1.42], p = 0.17), or hospitalization rate (RR = 0.90, 95% CI [0.60–1.36], p = 0.62). There were fewer deaths in the BCG group (RR = 0.52, 95% CI [0.25–1.08], p = 0.08). Regarding adverse events, BCG vaccination was strongly associated with erythema and may slightly increase the risk of cough, while other systemic symptoms (nausea, muscle/joint pain, sore throat) showed no significant association.
Conclusion and Recommendations
Across 15 RCTs, early BCG revaccination did not prevent COVID-19 infection, hospitalization, or ICU admission; mortality benefit remains unproven. BCG was generally well tolerated, with more local reactions. Routine use of BCG for COVID-19 prevention is not supported; future trials should stratify by prior BCG status, age, circulating variants, and vaccination context.
EP5 Efficacy of Cellex® in Enhancing Cognitive Function Post-Stroke: A Systematic Review and Meta-Analysis of Clinical Trials Ismail A. Ibrahim1,5, Ahmed Ibrahim2,5, Sohaila Mourad2,5, Bishoy Kamel2,5, Mohamed I. Mohamed2,5, Wael Hafez3,6, Ahmed Hosney Nada4,5 1Faculty of Health Sciences, Fenerbahce University, Istanbul, Turkey; 2Faculty of Medicine, Alexandria University, Alexandria, Egypt; 3Emirates Society of Internal Medicine, EMA, Dubai, UAE; 4Faculty of Medicine, Benha University, Egypt; 5Global Alliance of Young Researchers, Istanbul, Turkey; 6Medical Research and Clinical Studies Institute, The National Research Centre, Cairo, Egypt Correspondence: Wael Hafez (wael.hafez@nmc.ae)BMC Proceedings 2025, 19(32):EP5
Keywords: Cellex; cognitive function; Ischemic stroke; hemorrhagic stroke; systematic review; MMSE; NIHSS; stroke recovery
Abstract
Background
Cognitive deficits after stroke are frequent and predict poor long-term outcomes; however, evidence for adjunct pharmacotherapies is inconclusive. Cellex has been proposed as an add-on therapy; however, individual trials are underpowered. We aimed to investigate the efficacy of Cellex, a novel medication, in improving cognitive function in patients recovering from ischemic or hemorrhagic stroke.
Materials and Methods
This meta-analysis followed PRISMA guidelines and was registered in PROSPERO (CRD42024519134). PubMed, Scopus, Cochrane, Embase, and Web of Science were searched in February 2024 using Medical Subject Headings (MeSH) terms related to Cellex, stroke, and cognition. Eligibility: Studies that enrolled adults (≥18 years) with ischemic or hemorrhagic stroke confirmed by CT/MRI and reported post-stroke cognitive impairment were included. The comparators included placebo and usual care. The exclusion criteria were pre-existing cognitive impairment/dementia, severe comorbidities, other neurodegenerative diseases, Cellex use for non-stroke conditions, or insufficient data. Selection and data extraction: Screening was performed in Rayyan, and data were extracted (study design, sample size, age, follow-up, MMSE, and NIHSS). The risk of bias was assessed using Cochrane ROB-2. Meta-analysis was conducted in RevMan 5.4 using fixed-effects when I2<50% (p>0.1), otherwise random effects were used. Heterogeneity was further addressed through sensitivity analysis using the leave-one-out method.
Results
In our analysis of 11 clinical trials involving 1511 patients, Cellex tended to outperform controls in terms of MMSE scores, showing a mean difference of 1.25 (95% confidence interval [CI] [−0.34, 2.83], p = 0.12). Similarly, for NIHSS scores, Cellex demonstrated a mean difference of 0.58 (95% CI(−0.60, 1.76), p = 0.34]. Two studies underscored the efficacy of Cellex in improving speech function post-stroke, with notable intragroup improvements (p < 0.05). Despite these positive trends, the overall evidence did not decisively support the superiority of Cellex over placebo.
Conclusion and Recommendations
Although Cellex showed promising trends in improving cognitive function post-stroke, its efficacy did not significantly surpass that of the placebo. Further research with larger sample sizes and longer-term outcomes is warranted.
EP6 Acute Kidney Injury Post Palliative Liver Histotripsy Procedure: First Reported Complication in Literature Yousef Boobes1,2, Fatima AlKindi2,3, Dana Kidder1, Philipp Von Breitenbuch4 1Seha Kidney Care, Nephrology, Al Ain, UAE; 2Department of Internal Medicine, College of Medicine and Health Sciences, UAE University, UAE; 3Internal Medicine, Tawam Hospital & Sheikh Tahnoon Bin Mohammed Medical City, Seha, PureHealth, Al Ain, UAE; 4Surgery Department, Tawam Hospital & Sheikh Tahnoon Bin Mohammed Medical City, Seha, PureHealth, Al Ain, UAE Correspondence: Yousef Boobes (boobes@emirates.net.ae)BMC Proceedings 2025, 19(32):EP6
Keywords: AKI, liver histotripsy, cancer, steroid, proteinuria
Abstract
Background
Histotripsy is a novel, non-invasive ultrasound-based technology that enables non-thermal mechanical ablation of tissues. It received FDA approval in 2023 for treating unresectable liver tumors. With a success rate exceeding 90%, histotripsy is considered safe. However, acute kidney injury (AKI) has not previously been reported as a complication.
Materials and Methods
We present two cases of AKI with nephrotic-range proteinuria developing shortly after liver histotripsy. Clinical data and management outcomes were studied. Descriptive analysis was used.
Results
Case 1: A 36-year-old female with cholangiocellular carcinoma and hepatic/lung metastases underwent palliative liver histotripsy. Her medical history included allergies to multiple chemotherapeutic agents and antibiotics. Pre-procedure labs indicated mild anemia and normal renal function (s. creatinine 60 µmol/L). Within 24 hours post-procedure, she was diagnosed to have stage III AKI with oliguria, hyponatremia, and massive proteinuria (PCR: 10.13 g/g; ACR: 673.24 mg/mmol). Serology, autoimmune markers, and renal ultrasound were unremarkable. Without biopsy confirmation, she was treated empirically with intravenous methylprednisolone, followed by a tapering oral course. Creatinine peaked at 663.6 µmol/L and normalized over two weeks. Our clinical diagnosis was acute interstitial nephritis with rapidly reversable podocytopathy.
Case 2: A 64-year-old female with metastatic colon cancer on chemotherapy underwent liver histotripsy. She received two doses of ketorolac prior to the procedure. She initially tolerated the procedure but developed nausea and vomiting the following day. Labs revealed stage III AKI (creatinine: 331.8 µmol/L), hyponatremia, hyperkalemia, metabolic acidosis and proteinuria (PCR: 1.49 g/g). She was managed with IV sodium bicarbonate and patiromer. Without biopsy, a presumptive diagnosis of acute interstitial nephritis with possible glomerular involvement was made. Creatinine peaked at 444.4 µmol/L, and renal function normalized within 10 days following steroid therapy.
Conclusions and Recommendations
Although histotripsy has demonstrated favorable safety outcomes in multicenter trials, these cases highlight a potential association with AKI stage III and proteinuria shortly after the procedure. The clinical features suggest acute interstitial nephritis with transient onset of podocytopathy. Despite the absence of kidney biopsy data, both cases showed rapid improvement with steroids. These findings underscore the need for close renal monitoring post-histotripsy, especially in patients with complex oncologic histories.
Written informed consent for publication in an open-access journal was obtained from the patient.
EP7 A Diagnostic Dilemma: Guillain-Barré Syndrome in the Shadow of Poliomyelitis - Case ReportJafrin Sadiq Abdul Razack1, Ahmad Faud1, Shoaib Shah Ahamed1, Sharanya Suresh Kumar2, Asma Alskaf3 1Medical Intern, Thumbay University Hospital, Ajman, U.A.E.; 2General Practitioner, Thumbay University Hospital, Ajman, U.A.E.; 3Specialist Neurologist, Thumbay University Hospital, Ajman, U.A.E. Correspondence: Jafrin Sadiq Abdul Razack (Sadiq.jafrin@gmail.com)BMC Proceedings 2025, 19(32):EP7
Keywords: Guillain-Barré syndrome; poliomyelitis; acute flaccid paralysis; AIDP; plasmapheresis
Abstract
Background
Guillain–Barré Syndrome (GBS) is an acute immune-mediated polyradiculoneuropathy characterized by rapidly progressive, symmetrical weakness, areflexia, and potential autonomic dysfunction. The most common variant, acute inflammatory demyelinating polyneuropathy (AIDP), can be challenging to identify in patients with pre-existing neurological deficits, such as prior poliomyelitis, where baseline asymmetric weakness and muscle atrophy may obscure new deficits. Accurate differentiation is critical, as management strategies differ and delayed recognition increases morbidity 1,2.
Case Presentation
We report a 51-year-old male with a history of suspected poliomyelitis and residual neurological deficits, who presented with acute right lower limb weakness and inability to ambulate following a gastrointestinal illness. Examination revealed symmetrical lower limb weakness with absent reflexes and preserved sensation. Laboratory tests showed mildly elevated inflammatory markers and creatine phosphokinase. MRI excluded compressive spinal pathology. Nerve conduction studies demonstrated chronic changes from prior anterior horn cell disease with new demyelinating features consistent with AIDP. Cerebrospinal fluid analysis was unremarkable. During admission, the patient developed atrial fibrillation, indicating autonomic involvement. Using standardized diagnostic criteria (Brighton), the multidisciplinary team confirmed GBS (AIDP variant) and initiated plasmapheresis. Following treatment, the patient showed stabilization and partial recovery of motor function. This case highlights the importance of considering superimposed GBS in patients with prior poliomyelitis. Prompt CSF and nerve conduction studies, poliovirus screening when indicated, and early immunotherapy (IVIG or plasmapheresis) with close monitoring of respiratory and autonomic function are essential to optimize outcomes.
Discussion This case underscores the diagnostic dilemma of differentiating AIDP from poliomyelitis in patients with prior neurological disease. While both may present with acute flaccid paralysis, distinguishing features include symmetry of weakness, absence of spinal cord gray matter changes on MRI, demyelinating features on nerve conduction studies, and a favorable response to immunotherapy. Autonomic dysfunction, as observed in this patient, further supports the diagnosis of GBS. Early recognition is crucial, as delayed treatment carries a high risk of morbidity.
Conclusion This case highlights the diagnostic challenge of Guillain–Barré Syndrome (AIDP variant) in a patient with prior poliomyelitis and pre-existing neurological deficits. Careful clinical evaluation, neurophysiological studies, and cerebrospinal fluid analysis, guided by standardized criteria (e.g., Brighton), allowed timely identification of superimposed GBS. Screening for poliovirus can help differentiate recurrent or post-polio deficits. Early immunotherapy with plasmapheresis or IVIG, along with supportive care and physiotherapy, contributed to stabilization and partial recovery of motor function. Clinicians should maintain a high index of suspicion for GBS in patients presenting with new or progressive weakness, even in the context of prior neurological disease, to ensure prompt treatment and optimize outcomes.
Written informed consent for publication in an open-access journal was obtained from the patient.
References
1.Khan, S. A., Das, P. R., Nahar, Z., & Dewan, S. M. R. (2024). An updated review on Guillain-Barré syndrome: Challenges in infection prevention and control in low- and middle-income countries. SAGE Open Medicine, 12, Article 20503121241239538. https://doi.org/10.1177/20503121241239538
2.Bellanti, R., & Rinaldi, S. (2024). Guillain-Barré syndrome: A comprehensive review. European Journal of Neurology, 31(8). https://doi.org/10.1111/ene.16365
EP8 Short-Term Dexketoprofen–Associated Acute Kidney Injury in a Patient with Type 2 Diabetes: Case ReportJafrin Sadiq Abdul Razack1, Sarah Elkhawaga2, Noel George Cherian1, Ahmad El-Ouweini3 1Medical Intern, Thumbay University Hospital, Ajman, U.A.E.; 2Pharm D Graduate, Gulf Medical University, Ajman, U.A.E.; 3Clinical Assistant Professor of Pharmacy Practice and Critical Care Clinical Pharmacist, Dubai Medical College, Dubai, U.A.E. Correspondence: Jafrin Sadiq Abdul Razack (sadiq.jafrin@gmail.com)BMC Proceedings 2025, 19(32):EP8
Keywords: Non-steroidal anti-inflammatory drugs; dexketoprofen; acute kidney injury; diabetes mellitus; hemodialysis; case report
Abstract
Background Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used for postoperative pain management but can precipitate acute kidney injury (AKI) via hemodynamic or interstitial mechanisms, especially in patients with underlying risk factors. While NSAID-induced AKI is usually associated with prolonged use or pre-existing renal disease, severe renal impairment may also occur after short-term exposure. We report a case of KDIGO stage 3 AKI following five days of dexketoprofen use in a patient with type 2 diabetes.
Materials and Methods
This is a case report of a 46-year-old male with moderately controlled type 2 diabetes who underwent fistulectomy and received dexketoprofen for postoperative analgesia. Baseline renal function was normal. Clinical evaluation, laboratory investigations (serum creatinine, urea, pancreatic enzymes), urine output monitoring, and imaging studies were performed to identify the cause of AKI. Management included cessation of NSAIDs, intravenous fluid therapy, and initiation of hemodialysis when renal function deteriorated.
Results Five days postoperatively, the patient presented with fever, epigastric pain, nausea, and vomiting. Laboratory evaluation revealed serum creatinine of 9.18 mg/dL, urea 89.37 mg/dL, and elevated pancreatic enzymes. Urine output declined progressively, and imaging excluded obstructive causes. Despite supportive therapy, renal function continued to worsen, necessitating hemodialysis via a temporary catheter. After multiple ICU dialysis sessions, the patient’s renal function gradually improved, returning to baseline levels prior to discharge in stable condition.
Conclusions and Recommendations
This case demonstrates that NSAID-induced AKI can occur even after short-term administration, particularly in patients with diabetes. Clinicians should exercise caution when prescribing NSAIDs postoperatively, closely monitor renal function, and intervene promptly if impairment develops. Awareness of this risk may prevent severe renal complications and guide safer analgesic practices.
Written informed consent for publication in an open-access journal was obtained from the patient.
EP9 Guillain-Barré Syndrome Axonal Variant Complicated by Hemodynamic Crashes During Plasmapheresis: A Case ReportHadeel Ali, Tahlil Ibrahim, Ahmed Abdalla, Doaa Elhassan, Alaa AhmedMedical Interns, Thumbay University Hospital, Ajman, UAE Correspondence: Hadeel Ali (hadeelahmed.2000@gmail.com)BMC Proceedings 2025, 19(32):EP9
Keywords: Guillain-Barré Syndrome, Axonal Neuropathy, Autonomic Dysfunction, Plasmapheresis, Case Report
Abstract
Background
Guillain-Barré Syndrome (GBS) is an acute immune-mediated neuropathy associated with rapid motor weakness and potential autonomic complications 1. While the demyelinating type is most common, axonal variants such as acute motor axonal neuropathy (AMAN) often cause more severe deficits and prolonged recovery 2. Autonomic instability, including arrhythmias and hemodynamic crashes, may complicate treatment 3. This report describes a diagnostically challenging case of axonal GBS in a patient with underlying muscular dystrophy, further complicated by cardiac arrhythmias and hypotensive episodes during plasmapheresis.
Materials and Methods
We present a single-patient case report of a 51-year-old male, a known case of hypertension and muscular dystrophy who developed acute progressive weakness. Neurological assessment, MRI imaging, laboratory tests, and electrophysiological studies were performed. Cerebrospinal fluid (CSF) analysis and spinal MRI were used to exclude alternative diagnoses. The patient underwent plasmapheresis with concurrent cardiac monitoring.
Results
Nerve conduction studies confirmed axonal polyneuropathy consistent with axonal GBS, despite normal CSF findings. The patient’s weakness progressed to quadriparesis, and he developed atrial fibrillation requiring amiodarone and anticoagulation. Plasmapheresis sessions were complicated by recurrent bradycardia and hypotension, necessitating temporary cessation and fluid resuscitation. After five sessions, gradual motor improvement was noted in the upper limbs, though the patient remained ICU-dependent for mobility and was initiated on structured physiotherapy.
Conclusions and Recommendations
This case highlights the importance of early electrophysiologic testing when GBS is suspected but CSF findings are inconclusive. Recognition and management of autonomic instability are critical, particularly during plasmapheresis. Clinicians should maintain a high index of suspicion for axonal GBS in atypical presentations and adopt a multidisciplinary approach to optimize outcomes.
Written informed consent for publication in an open-access journal was obtained from the patient.
References
1.Kuwabara, S., & Yuki, N. (2013). Axonal Guillain–Barré syndrome: Concepts and controversies. The Lancet Neurology, 12(12), 1180–1188. https://doi.org/10.1016/S1474-4422(13)70215-1
2.Leonhard, S. E., Mandarakas, M. R., Gondim, F. A. A., et al. (2019). Diagnosis and management of Guillain–Barré syndrome in ten steps. Nature Reviews Neurology, 15(11), 671–683. https://doi.org/10.1038/s41582-019-0250-9
3.Yuki, N., & Hartung, H.-P. (2012). Guillain–Barré syndrome. The New England Journal of Medicine, 366(24), 2294–2304. https://doi.org/10.1056/NEJMra1114525
EP10 Isolated Ulnar Artery Occlusion with Concurrent Internal Jugular Thrombosis in Severe Iron-Deficiency Anemia: Case ReportZahraa Haider1, Aya Alsabbah2, Noor Alhaboobi1, Touseef Kazmi3 1College of Medicine, University of Sharjah, Sharjah, UAE; 2Dubai Health, Dubai, UAE; 3Rashid Hospital, Dubai Health, Dubai, UAE Correspondence: Zahraa Haider (zahraalhaboobi@gmail.com)BMC Proceedings 2025, 19(32):EP10
Keywords: iron-deficiency anemia; reactive thrombocytosis; ulnar artery occlusion; internal jugular vein thrombosis; hypercoagulability; case report
Abstract
Background
Severe iron deficiency anemia (IDA) can be accompanied by reactive thrombocytosis and platelet hyper reactivity, which may increase thrombotic risk, particularly in women of reproductive age 1. While arterial events related to thrombotic risk in severe IDA are rare, occasional reports describe thrombotic events such as abdominal aortic thrombosis and jugular or cerebral venous thrombosis 1,2. Chronic IDA may predispose young women to thrombotic events in the absence of traditional risk factors or trauma, though isolated ulnar artery occlusion remains rare 3. This case report highlights the association between severe IDA, thrombocytosis, and thrombotic events in a young, otherwise healthy woman.
Materials and Methods
A 41-year-old woman presented with bluish discoloration of her right index and middle fingers, along with a 2-week history of headache, dizziness, nausea, and visual blurring. Work-up revealed severe microcytic hypochromic anemia (Hb 6.7 g/dL, MCV 59 fL, iron 13 µg/dL, TIBC 509 µg/dL), prompting blood transfusion and IV iron therapy, which improved Hb to 8.1 g/dL. Referred to rheumatology for suspected Raynaud’s phenomenon, she returned with worsening ischemia, and imaging confirmed right ulnar artery occlusion and partial thrombosis of the right internal jugular vein. An embolectomy was performed, and anticoagulation therapy was initiated. A thrombophilia and autoimmune work-up revealed low activated protein C resistance (APCR).
Results
The patient’s vascular status improved post-embolectomy, with laboratory values normalizing. Notably, her platelet count was elevated above normal (442 × 10⁹/L), consistent with reports of young women experiencing simultaneous arterial and venous thromboses in severe IDA with thrombocytosis. Reactive thrombocytosis significantly elevates thrombotic risk, reinforcing the need for early recognition, as IDA with thrombocytosis doubles the risk of thrombosis.
Conclusions and Recommendations
Severe IDA can create a prothrombotic milieu, increasing the risk of both arterial and venous thromboses. Clinicians should maintain high suspicion for thrombosis in severe IDA and evaluate for embolic sources and thrombophilia. Treatment with rapid iron repletion, standard antithrombotic therapy, and follow-up imaging is recommended. Avoid prothrombotic exposures until iron stores recover. Prospective studies should investigate whether expedited iron repletion or prophylaxis reduces thrombotic events.
Written informed consent for publication in an open-access journal was obtained from the patient.
References
1.Valiyaveettil, D., & Harish, R. (2014). Iron deficiency anemia with thrombocytosis: A rare association. Indian Journal of Hematology and Blood Transfusion, 30(4), 304–306. https://doi.org/10.1007/s12288-013-0306-3
2.Keung, Y. K., & Owen, J. (2004). Iron deficiency and thrombosis: Literature review. Clinical and Applied Thrombosis/Hemostasis, 10(4), 387–391. https://doi.org/10.1177/107602960401000412
3.Akins, P. T., Glenn, S., Nemeth, P. M., & Derdeyn, C. P. (1996). Carotid artery thrombus associated with severe iron-deficiency anemia and thrombocytosis. Stroke, 27(5), 1002–1005. https://doi.org/10.1161/01.STR.27.5.1002
EP11 Isolated Pupil-Sparing Third Nerve Palsy as a Relapse of PR3-ANCA Vasculitis: Case ReportJoudi Habbal1, Hamda Ali1, Emad Khater2 1Department of Internal Medicine, SEHA- Sheikh Khalifa Medical City; 2Department of Nephrology, SEHA- Sheikh Khalifa Medical City Correspondence: Joudi Habbal (judymh99@gmail.com)BMC Proceedings 2025, 19(32):EP11
Keywords: ANCA-associated vasculitis; PR3-ANCA; oculomotor (third) nerve palsy; cranial neuropathy; neuro-vasculitis; case report
Abstract
Background
Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a rare autoimmune disorder targeting small- and medium-sized vessels. Neurological involvement occurs in approximately 15–20% of patients, most commonly as peripheral neuropathy or mononeuritis multiplex. Isolated cranial nerve palsy is exceptionally rare. It occurs in fewer than 2%, with the third cranial nerve infrequently affected.
Case Presentation
We report a unique case of a 66-year-old male with a 17-year history of biopsy-proven pauci-immune necrotizing crescentic glomerulonephritis and cANCA positivity, previously treated with cyclophosphamide and maintained on azathioprine. He presented with a three-day history of left-sided periorbital pain, ptosis, and binocular diplopia, without systemic symptoms. Neurological examination revealed isolated left third cranial nerve palsy with impaired adduction and ptosis; pupils were spared. ESR was 4 mm/hr and CRP was 1.34 mg/L. MRI/MRA brain excluded ischemia, aneurysm, or compressive lesions. Serum cANCA was elevated (164 RU/mL), with negative pANCA. Given his AAV history, absence of alternative etiologies, and supportive serology, an isolated cranial mononeuritis multiplex flare was diagnosed. He was treated with oral prednisolone (25 mg/day) and continued azathioprine (50 mg/day), resulting in gradual resolution of ptosis and improvement in diplopia over three weeks.
Discussion
This case demonstrates the importance of considering AAV in patients with cranial nerve deficits, even in the absence of systemic symptoms. Unlike typical systemic flares, this presentation occurred with low inflammatory markers and no other organ involvement, highlighting the need for vigilance in neurological assessment. Prompt recognition and immunosuppressive therapy may prevent irreversible deficits.
Conclusion and Recommendations
Clinicians should consider AAV flare in the differential diagnosis of unexplained cranial nerve palsy, even in the absence of systemic symptoms or elevated inflammatory markers. This case underscores the need for heightened clinical suspicion for AAV-related neuropathy in patients with compatible history. Early identification facilitates targeted therapy and favourable neurological outcomes.
Written informed consent for publication in an open-access journal was obtained from the patient.
EP12 Adult Taenia Infection Presenting with Lower Gastrointestinal Bleeding: Case Report Esraa Abdulla Ibrahim OckbaDepartment of Internal Medicine, Dubai Health, Dubai, United Arab Emirates Correspondence: Esraa Abdulla Ibrahim Ockba (esraaaockba@gmail.com)BMC Proceedings 2025, 19(32):EP12
Keywords: Taenia Saginata; Taeniasis; Gastrointestinal Hemorrhage; Iron-Deficiency Anemia; Colonoscopy; Praziquantel.
Abstract
Background
Taenia species are cestode parasites for which humans are the definitive host, typically acquired by ingesting raw or undercooked meat containing larval cysts.1 Taenia saginata is the most common human tapeworm.2 Adult worms rarely invade the intestinal mucosa, so infection is usually asymptomatic. When symptomatic, patients may present with nonspecific gastrointestinal complaints such as abdominal discomfort, nausea, or diarrhea.3,4. Gastrointestinal bleeding is an uncommon complication which may occur from mucosal irritation or ulceration at the ileocecal region where proglottids adhere or transit.1 We report this case to highlight Taenia infection as a potential culprit for lower gastrointestinal bleeding.
Materials and Methods
We present a case report of a 29-year-old female with no comorbidities presented with 4 days of melena, dizziness, and fatigue. She denied abdominal pain, nausea, vomiting, diarrhea, hematemesis, or other bleeding sites. She had a similar episode 3 months prior, managed with supportive transfusion. Dietary history included intermittent raw meat intake. On examination, she was pale, tachycardic, and hypotensive, with melena on rectal exam. Admission labs (Table 1) revealed severe hypochromic microcytic anemia (Hb 3.5 g/dL) and low ferritin (7.9 ng/mL). Stool examination was negative for ova or parasites. She was stabilized and transfused with three units of packed red blood cells.
Results
Upper GI endoscopy revealed H. pylori–associated non-bleeding erosive gastropathy (Figure 1 A, B), for which eradication therapy was advised. Due to ongoing melena, colonoscopy revealed a 30-cm tapeworm in the cecum and terminal ileum, morphologically suggestive of Taenia saginata (Figure 1 C). The retrieved tapeworm specimen is shown in Figure 1D. The patient received a single 600 mg dose of praziquantel and iron therapy, after which melena resolved and hemoglobin improved to 9.9 g/dL at discharge.
Conclusions and Recommendations
Adult Taenia infection can present with lower GI bleeding, particularly with ileocecal involvement, and may be missed by a single stool examination. When endoscopy reveals cestode segments, obtain species confirmation (morphology ± PCR) to distinguish T. saginata from T. solium, treat with weight-based praziquantel or niclosamide, and arrange stool re-examination at 1–3 months. Prevention through proper cooking of raw meat and reinforcement of household hygiene is essential.
Written informed consent for publication in an open-access journal was obtained from the patient.
References
1.Settesoldi, A., Tozzi, A., & Tarantino, O. (2017). Taeniasis: A possible cause of ileal bleeding. World Journal of Clinical Cases, 5(12), 432–436. https://doi.org/10.12998/wjcc.v5.i12.432
2.Braseth, A. L., Elliott, D. E., & Ince, M. N. (2021). Parasitic infections of the gastrointestinal track and liver. Gastroenterology Clinics of North America, 50(2), 361–381. https://doi.org/10.1016/j.gtc.2021.02.011
3.Paniker, S. G. C. J. (2018). Paniker’s textbook of medical parasitology (8th ed.). Jaypee Brothers Medical Publishers.
4.Craig, P., & Ito, A. (2007b). Intestinal cestodes. Current Opinion in Infectious Diseases, 20(5), 524–532. https://doi.org/10.1097/qco.0b013e3282ef579e
Table 1 (abstract EP12). Laboratory results on admission Fig. 1 (abstract EP12).
Endoscopic and colonoscopic images: A and B: Upper gastrointestinal endoscopy showing H. pylori–associated erosive gastroduodenopathy. C: Colonoscopic image showing a 30-cm tapeworm in the terminal ileum. D: Retrieved tapeworm specimen after treatment
EP13 Diabetic Ketoacidosis as the Initial Presentation of Undiagnosed Diabetes in an Adult: Case Report Aia Nana, Dhurgadharshini SudhakarAcademic Health Center, Thumbay University Hospital, Ajman, UAE Correspondence: Aia Nana (aiabna3na3@gmail.com)BMC Proceedings 2025, 19(32):EP13
Keywords: diabetic ketoacidosis; undiagnosed diabetes; adult-onset diabetes; LADA; ketosis-prone type 2 diabetes; case report.
Abstract
Background
Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes mellitus, occasionally presenting as the first manifestation in previously undiagnosed individuals. In adults, DKA may reflect type 1 diabetes, latent autoimmune diabetes in adults (LADA), or ketosis-prone type 2 diabetes, requiring early etiologic work-up.
Materials and Methods
A 40-year-old male with no known comorbidities presented to the emergency department with severe abdominal pain, nausea, generalized weakness, increased thirst and urination, and breathing difficulty for four days. Clinical evaluation and laboratory investigations, including venous blood gas analysis, were conducted.
Results
Laboratory investigations revealed markedly elevated random blood glucose (GRBS, 491 mg/dL, positive urine ketones (3+), severe metabolic acidosis (venous pH 7.11), and an elevated anion gap (18.4 mmol/L). The patient was diagnosed with DKA and required admission to the intensive care unit for further management. He received 1.5 L isotonic crystalloid in the first hour, insulin 0.1 U/kg/h with potassium protocol; the anion gap closed at 12 hours, transitioned to subcutaneous insulin; length of stay was 4 days; no cerebral edema or hypoglycemia.
Conclusions and Recommendations
DKA should be considered in adults with compatible symptoms even without known diabetes. Immediate protocolized management (fluids, insulin, electrolytes) and early classification testing (autoantibodies, C-peptide) enable a safe transition to outpatient care and tailored long-term therapy. Diabetes surveillance in high-risk population (GRBS, HbA1c) and health awareness programs on diabetes and DKA presentation is essential for better outcomes
Written informed consent for publication in an open-access journal was obtained from the patient.
EP14 Sarcoidosis presenting with Uveitis and Granulomatous Interstitial Nephritis: Case ReportBasel Al HaykiDepartment of Nephrology, Ibn Al Nafees Hospital, Manama, Bahrain Correspondence: Basel Al Hayki (drbasel2002@hotmail.com)BMC Proceedings 2025, 19(32):EP14
Keywords: sarcoidosis; uveitis; granulomatous interstitial nephritis; renal sarcoid; corticosteroids; case report
Abstract
BackgroundSarcoidosis is a multisystem inflammatory disease characterized by noncaseating granulomas. While pulmonary involvement is most common, extrapulmonary manifestations such as ocular sarcoidosis and renal sarcoid are under-recognized. Granulomatous interstitial nephritis (GIN) is a rare renal manifestation of sarcoidosis and can be the initial or sole manifestation.
Case PresentationA 47-year-old Bahraini male with no prior medical history presented with progressive blurred vision and was diagnosed with bilateral anterior uveitis. He was treated with local corticosteroids, resulting in partial symptom improvement.Due to incidentally found elevated creatinine (143 µmol/L), he was referred to nephrology. He had no systemic complaints. Review of systems was negative for fever, rash, weight loss, joint pain, cough, or neurological symptoms. Physical examination and vital signs, including blood pressure, were normal.
Laboratory FindingsSerum creatinine: 143 µmol/LESR: 2 mm/hrUrinalysis: RBCs 6–8/HPF, WBCs 2–3/HPF, protein 1+Albumin-to-creatinine ratio (ACR): 4.82 mg/mmolANA, anti-dsDNA, ANCA (c/p), anti-CCP: NegativeHIV, Hepatitis B/C, VDRL, TP-PA, RPR: NonreactiveSerum calcium and liver enzymes: NormalACE level: ElevatedQuantiFERON TB: Negative
ImagingRenal ultrasound: Normal-sized kidneys with preserved echogenicityChest X-ray: NormalCT scan (thorax, abdomen, pelvis): Enlarged mesenteric lymph nodesECG and echocardiogram: Normal
Renal BiopsyHistology revealed tubulointerstitial nephritis with noncaseating granulomas, mild tubular atrophy, and interstitial fibrosis. Glomeruli were unremarkable.
Diagnosis
The differential diagnosis was sarcoidosis and tubulointerstitial nephritis with uveitis (TINU) Given the constellation of granulomatous interstitial nephritis, uveitis, CT scan confirming the presence of lymphadenopathy, and elevated ACE levels with exclusion of infectious and autoimmune causes, a diagnosis of sarcoidosis was made.
Treatment and Follow-up The patient was initiated on prednisolone 60 mg daily with complete recovery of eye symptoms and uveitis and renal function within few weeks with plan gradual tapper of steroids.
Conclusions and Recommendations In adults presenting with unexplained uveitis and interstitial nephritis, consider sarcoidosis early. Prompt renal biopsy, advanced thoracic imaging, and metabolic assessment are essential. Multidisciplinary input and early systemic corticosteroids are critical, with steroid-sparing agents for recurrent or dependent cases.
Written informed consent for publication in an open-access journal was obtained from the patient.
EP15 Hidden Danger: Acquired Methemoglobinemia Following Dapsone TherapyMusab Ahmed, Ahmed Usama, Chryslene Abraham, Rayana Ahmed, Mohamed MohamedkhairThumbay University Hospital, Ajman, UAE Correspondence: Musab Ahmed (dr.musabahmed1@gmail.com)BMC Proceedings 2025, 19(32):EP15
Keywords: methemoglobinemia; dapsone; saturation gap; methylene blue; co-oximetry; G6PD deficiency
Background
Methemoglobinemia is a disorder in which hemoglobin iron is oxidized from ferrous (Fe2⁺) to ferric (Fe3⁺), impairing oxygen binding and delivery to tissues. It may be congenital or acquired, the latter often from oxidizing drugs such as dapsone. Symptoms range from mild fatigue to life-threatening hypoxia. A hallmark finding is the “saturation gap”, where SpO₂ is low despite a normal or elevated PaO₂ on arterial blood gas.
Case Presentation
A 38-year-old male with dermatitis herpetiformis on dapsone for one month presented with one week of headache, dyspnea, fatigue, and grayish skin and nail discoloration. He was tachycardic and hypoxic (SpO₂ 87% on room air), with normal chest exam, ECG, CXR, and PFTs. In the ED, SpO₂ dropped to 79% despite oxygen via non-rebreather mask. ABG on oxygen revealed pH 7.40, Hb 12.3 g/dL, lactate 1.5 mmol/L, PaCO₂ 38 mmHg, PaO₂ 188 mmHg, SaO₂ 96.6% (co-oximetry), and MetHb 12.9%, confirming a saturation gap and the diagnosis of dapsone-induced methemoglobinemia. He received IV methylene blue (1.8 mg/kg in D5W) and was admitted to ICU and placed on oxygen support. His SpO₂ improved to 95% on room air within 24h. Dapsone was discontinued and therapy adjusted.
Discussion
Dapsone is a well-recognized cause of acquired methemoglobinemia, with up to 15% of treated patients developing elevated MetHb levels. Diagnosis requires high suspicion when hypoxia is disproportionate to clinical findings, especially when a saturation gap exists between SpO₂ on pulse oximetry and SaO₂ on co-oximetry. Treatment includes discontinuation of the offending agent, administration of methylene blue (1–2 mg/kg IV), and screening for G6PD deficiency to avoid hemolysis. Vitamin C and dextrose may be used as adjuncts. Newer multi-wavelength co-oximeters facilitate earlier detection.
Conclusions and Recommendations
In dapsone-treated patients with unexplained hypoxia or cyanosis unresponsive to oxygen, methemoglobinemia should be suspected and confirmed with co-oximetry. Management involves discontinuing the offending drug, screening for G6PD deficiency, and administering methylene blue (1–2 mg/kg IV, repeat if needed), while monitoring for rebound. Patients should also be counseled on early symptom recognition, advised to avoid other oxidant medications, and considered for periodic MetHb monitoring during therapy initiation or dose escalation.
Written informed consent for publication in an open-access journal was obtained from the patient.
EP16 Early Childhood Infections and Pediatric Movement Disorders: A Narrative Review of Clinical Links and Mechanisms (2020–2024)Mohamed Taha1, Mohamed Mohamed2, Mohamed Khalifa2, Mohamed Mohamedkhair2,3, Musab Ahmed2,3 1Faculty of Medicine, University of Medical Science and Technology, Khartoum, Sudan; 2Faculty of Medicine, National University, Khartoum, Sudan; 3Thumbay University Hospital, Ajman, UAE Correspondence: Mohamed Taha (mohameddyaeldin@gmail.com)BMC Proceedings 2025, 19(32):EP16
Keywords: Pediatric movement disorders; Sydenham chorea; PANDAS/PANS; postinfectious autoimmunity; basal ganglia; streptococcal infections.
Background
Early childhood infections are increasingly recognized as potential triggers for pediatric movement disorders. Evidence suggests that selected infections and post-infectious immune responses may precipitate pediatric movement disorders such as Sydenham chorea, largely through basal ganglia–directed autoimmunity and related mechanisms. Associations differ by pathogen, geography, and diagnostic criteria, and remain controversial for entities such as PANDAS/PANS. For this review, we defined early childhood as ages 0–8 years and synthesized recent human data (2020–2024) on clinical presentations, immune mechanisms, and outcomes.
Materials and Methods
We conducted a targeted narrative review of studies published between January 2020 and April 2024. Databases screened included PubMed, Embase, and Web of Science. Search terms combined childhood infection, post-infectious autoimmunity, and movement disorders. Eligible studies included human cohorts, clinical trials, and meta-analyses describing pediatric movement disorders linked to infectious or post-infectious mechanisms. Nine studies were identified for synthesis.
Results
Recent reports highlight pathogen-specific associations between infections and pediatric movement disorders. Dystonia has been described in Japanese encephalitis, CNS tuberculosis, and neurocysticercosis, while ataxia has emerged in children with SARS-CoV-2 infection. Autoantibodies targeting dopamine receptors and other neural components have provided immune-mediated explanation, though vasculopathy, inflammation, and space-occupying lesions may also contribute. Reported treatments include corticosteroids and botulinum toxin, with outcomes varying by infection type and severity.
Conclusions and Recommendations
Recent studies suggest pathogen-specific and mechanism-dependent links between infection and pediatric movement disorders—robust for Sydenham chorea, less certain for PANDAS/PANS, and variable for direct CNS infections. Clinicians should document antecedent infections, use standardized diagnostic criteria and severity scales, and tailor therapy to the mechanism: antimicrobials for active infection, immunomodulation for post-infectious autoimmunity, and symptomatic treatment such as botulinum toxin for focal dystonia. Research priorities include prospective cohorts with clear diagnostic criteria, biobanking, standardized outcome measures, and controlled trials for immunomodulatory therapies in well-defined subgroups.
EP17 ECMO for ARDS in the COVID-
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