Case Reports in Critical Care最新文献

{"title":"Case Report: Sepsis With Multisystemic Amyloid Light-Chain Amyloidosis.","authors":"Mehtap Selçuk, Galip Emre Kılıçaslan, Sinem Keskin Kayalar, Ismail Cinel","doi":"10.1155/crcc/6794847","DOIUrl":"10.1155/crcc/6794847","url":null,"abstract":"<p><strong>Introduction: </strong>Systemic light-chain (AL) amyloidosis is a complex disorder characterized by extracellular fibril deposition, leading to severe multisystem dysfunction. When sepsis superimposes on preexisting organ impairment, early clinical recognition becomes particularly challenging yet critical.</p><p><strong>Methods: </strong>We present a case of a 60-year-old female who presented with generalized edema, dyspnea, and cardiac/renal involvement, subsequently diagnosed with AL amyloidosis based on laboratory, imaging, bone marrow biopsy, and Congo red staining findings.</p><p><strong>Results: </strong>Following chemotherapy with bortezomib and cyclophosphamide, the patient experienced transient cardiac arrest, received an implantable cardioverter defibrillator, and subsequently developed massive ascites. Upon developing <i>Pseudomonas guariconensis</i> bacteremia, she progressed to septic shock requiring intensive care unit admission, mechanical ventilation, vasopressor support, and targeted antimicrobial therapy. Through aggressive supportive care and source control, hemodynamic stabilization was achieved, allowing successful extubation and transfer to the general ward.</p><p><strong>Conclusions: </strong>Superimposed sepsis on severe, multi-organ amyloidosis significantly complicates diagnosis and management. High clinical vigilance, early infection recognition, and prompt targeted therapy are essential to prevent fatal outcomes in patients with preexisting chronic organ dysfunctions.</p>","PeriodicalId":52357,"journal":{"name":"Case Reports in Critical Care","volume":"2026 ","pages":"6794847"},"PeriodicalIF":0.0,"publicationDate":"2026-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13700113/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149276863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Euglycemic SGLT2 Inhibitor-Associated Ketoacidosis in a Nondiabetic Patient: A Case Report.","authors":"Carmelo Zinnato, Teresa Roatta, Giacomo Berta, Roberto Penso, Vincenzo Russotto","doi":"10.1155/crcc/3970190","DOIUrl":"https://doi.org/10.1155/crcc/3970190","url":null,"abstract":"<p><p>We present the case of a 62-year-old nondiabetic woman receiving dapagliflozin for dilated cardiomyopathy presenting to the emergency department with severe hypoxemic respiratory failure because of suspected cardiogenic pulmonary edema. Despite treatment, she remained symptomatic and required intubation and intensive care admission. After intubation, high-anion-gap metabolic acidosis was unmasked. After exclusion of other common causes, SGLT2 inhibitor-associated ketoacidosis due to dapagliflozin was suspected. Marked ketonuria confirmed the diagnosis despite the absence of hyperglycemia. Dapagliflozin was discontinued, and intravenous insulin, glucose infusion, and early enteral nutrition were initiated. Metabolic acidosis resolved completely within 24 h. The patient was successfully extubated and discharged from the intensive care unit 48 h later. SGLT2 inhibitor-associated ketoacidosis should be considered in patients receiving sodium-glucose cotransporter-2 inhibitors who develop otherwise unexplained high-anion-gap metabolic acidosis, irrespective of diabetic status or blood glucose concentration. Fasting and acute illness are relevant precipitating factors; prompt drug withdrawal, carbohydrate administration, insulin therapy, and nutritional support can lead to rapid resolution.</p>","PeriodicalId":52357,"journal":{"name":"Case Reports in Critical Care","volume":"2026 ","pages":"3970190"},"PeriodicalIF":0.0,"publicationDate":"2026-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13695839/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149276898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An Unusual Presentation of Invasive Group A <i>Streptococcus</i>-A Review of Epidemiology and Challenges in Management.","authors":"Fatima Hakak, Blake W Jackson, Michael Addidle, Ulrike Buehner","doi":"10.1155/crcc/6007143","DOIUrl":"https://doi.org/10.1155/crcc/6007143","url":null,"abstract":"<p><p>Invasive Group A <i>Streptococcus</i> (iGAS) infection is a disease state with increasing incidence internationally. This case report outlines a patient with severe septic shock from Group A beta-haemolytic<i>Streptococcus</i> within a provincial intensive care unit (ICU) in New Zealand. Consequently, this case has prompted discussion on the local change in epidemiology for Group A beta-haemolytic <i>Streptococcus</i> (GAS) and a review of the evidence of recognised interventions for iGAS and Streptococcal toxic shock syndrome (STSS).</p>","PeriodicalId":52357,"journal":{"name":"Case Reports in Critical Care","volume":"2026 ","pages":"6007143"},"PeriodicalIF":0.0,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13650736/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149171716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracorporeal Cooling in Heat Stroke Induced Takotsubo Cardiomyopathy.","authors":"Maja Mačković, Nikolina Marić, Petar Pekić, Nikola Udiljak, Zrinka Planinić","doi":"10.1155/crcc/9589641","DOIUrl":"https://doi.org/10.1155/crcc/9589641","url":null,"abstract":"<p><p>Heat stroke is a life-threatening condition characterized by elevated core body temperature (≥ 40°C) and central nervous system (CNS) dysfunction, resulting from body's inability to adequately dissipate heat. It can lead to multiorgan failure, including the cardiovascular system. Takotsubo cardiomyopathy (TCM), also known as stress-induced cardiomyopathy, is an acute syndrome of transient global or regional ventricular dysfunction, most commonly apical ballooning, mimicking acute coronary syndrome, typically occurring after severe physical or emotional stress. Although individually well-described, the combination of severe heat stroke as a trigger for TCM is rare. This case report describes a female patient with severe heat stroke who developed TCM and, due to persistent hyperthermia unresponsive to conventional cooling methods, was successfully cooled using prolonged intermittent hemodiafiltration. It also highlights the importance of timely recognition of atypical complications such as TCM in patients with cardiovascular instability and demonstrates the potential role of hemodialysis as an effective cooling method in cases of refractory hyperthermia.</p>","PeriodicalId":52357,"journal":{"name":"Case Reports in Critical Care","volume":"2026 ","pages":"9589641"},"PeriodicalIF":0.0,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13636670/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149118326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disseminated Varicella Zoster and Multiorgan Failure Requiring ECMO Support in a Patient With Evans Syndrome.","authors":"Rachel E Gahagen, Riad Lutfi, Mara E Nitu, Jatinder K Dhami, John C Christenson, Daniel T Cater","doi":"10.1155/crcc/2103304","DOIUrl":"https://doi.org/10.1155/crcc/2103304","url":null,"abstract":"<p><p>Visceral disseminated varicella-zoster virus (VD-VZV) infection is an uncommon but potentially life-threatening manifestation of varicella infection that primarily affects immunocompromised patients. When hematogenous dissemination occurs, the risk of significant organ dysfunction and death increases considerably. The disease develops through systemic viral spread to visceral organs, resulting in widespread multisystem involvement. Patients with Evans syndrome may be at increased risk because of underlying immune dysregulation and the frequent need for immunosuppressive treatment. We report the case of a 5-year-old unvaccinated child with Evans syndrome who developed severe multiorgan failure secondary to VD-VZV infection. The patient's condition was refractory to medical management but was successfully supported with venoarterial extracorporeal membrane oxygenation (VA-ECMO), without bleeding complications despite profound thrombocytopenia. A modified anticoagulation strategy and aggressive platelet support were used. The patient was successfully decannulated after 8 days of ECMO without major hemorrhagic complications and subsequently recovered renal and hepatic function. This case highlights the fulminant nature of VD-VZV infection in an unvaccinated patient with Evans syndrome. It demonstrates that survival is possible with timely initiation of antiviral therapy and extracorporeal support.</p>","PeriodicalId":52357,"journal":{"name":"Case Reports in Critical Care","volume":"2026 ","pages":"2103304"},"PeriodicalIF":0.0,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13624837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149118355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-Dose Inhaled Colistin-Aminoglycoside Combination Therapy in Critically Ill Patients With Multidrug-Resistant <i>Pseudomonas aeruginosa</i> Hospital/Ventilator-Associated Pneumonia: A Case Report and Literature Review.","authors":"Thang Nguyen Ngoc, Cuong Duong Cao, Thang Vu, Soan Hoang, Quyet Nguyen","doi":"10.1155/crcc/9472232","DOIUrl":"10.1155/crcc/9472232","url":null,"abstract":"<p><strong>Background: </strong>Multidrug-resistant <i>Pseudomonas aeruginosa</i> (MDR PA) ventilator-associated pneumonia (VAP) and hospital-associated pneumonia (HAP) are associated with high morbidity and limited therapeutic options. Intravenous antibiotics often achieve inadequate pulmonary concentrations. Aerosolized delivery permits high local drug exposure, but data on combined inhaled polymyxin-aminoglycoside therapy remain limited.</p><p><strong>Case report: </strong>We describe three critically ill patients with HAP/VAP due to MDR PA. All received adjunctive high-dose inhaled colistin immediately followed by inhaled amikacin or tobramycin, in addition to systemic therapy. Dosing was individualized based on renal function. Nebulization was optimized using inspiratory-synchronized delivery. All patients demonstrated clinical improvement, reductions in inflammatory markers (though with a transient rise in one or more markers in two patients), radiologic resolution, and eventual microbiologic eradication, despite isolates reported as resistant to the aminoglycoside and colistin used in vitro. No nephrotoxicity, bronchospasm, or device-related complications were observed clinically, despite doses exceeding those commonly reported, although formal ototoxicity surveillance was not performed. However, because all patients also received concurrent systemic antibiotics, a specific causal contribution from inhaled therapy cannot be fully established.</p><p><strong>Conclusions: </strong>Dual inhaled colistin-aminoglycoside therapy may represent a pharmacokinetically rational adjunctive strategy in selected patients with MDR PA HAP/VAP. High intrapulmonary concentrations achieved through aerosolization may overcome resistance while maintaining acceptable systemic safety. Prospective PK-guided studies are warranted.</p>","PeriodicalId":52357,"journal":{"name":"Case Reports in Critical Care","volume":"2026 ","pages":"9472232"},"PeriodicalIF":0.0,"publicationDate":"2026-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13617312/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149076579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Seizure due to Lamotrigine Underexposure During High-Volume CRRT for Hyperammonaemia: A Case Report.","authors":"Michael C van Herwerden, Jan H Elderman, Laurent M A Favie, Margreet Wagenmakers","doi":"10.1155/crcc/9950547","DOIUrl":"10.1155/crcc/9950547","url":null,"abstract":"<p><strong>Background: </strong>Hyperammonaemic decompensation in urea cycle disorders (UCDs) is a medical emergency that requires prompt intervention. Continuous renal replacement therapy (CRRT) is an effective strategy for acute ammonia clearance, but it may significantly alter the pharmacokinetics of administered drugs.</p><p><strong>Case presentation: </strong>A woman in her 40s with argininosuccinate lyase (ASL) deficiency and long-standing, well-controlled epilepsy treated with lamotrigine presented with a hyperammonaemic crisis and was treated with high-volume continuous venovenous haemodialysis (CVVHD). She developed a generalised tonic-clonic seizure shortly after cessation of CVVHD. Serum lamotrigine declined from 12.7 to 6.0 mg/L over approximately 12 h, corresponding to an apparent elimination half-life of 11.5 h. Lamotrigine was measurable in the effluent (2.9 mg/L), giving a saturation coefficient of 0.48 and an extracorporeal clearance of 38.4 mL/min during the high-volume phase. The seizure was attributed to the abrupt underexposure of lamotrigine in a previously seizure-free patient.</p><p><strong>Conclusion: </strong>This case underscores the clinical significance of extracorporeal clearance of antiseizure medications during CRRT in patients with UCDs. Drug selection should consider both ammonia-modifying and dialysability profiles. Therapeutic drug monitoring and pre-emptive dose adjustment, or the addition of a second intravenously available agent, should be considered when high-volume dialysis is initiated in a patient receiving a dialysable antiseizure medication.</p>","PeriodicalId":52357,"journal":{"name":"Case Reports in Critical Care","volume":"2026 ","pages":"9950547"},"PeriodicalIF":0.0,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13595043/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149026755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polymyxin B and the Pulmonary Peril: A Case Series of Acute Respiratory Failure.","authors":"Lovely Thomas, John Victor Peter, Binu Susan Mathew, Sara Jose, Lisa Merin Joseph, Jeethu Joseph Eapen, Sirish Chandra Srinath Patloori, Binila Chacko","doi":"10.1155/crcc/5569011","DOIUrl":"10.1155/crcc/5569011","url":null,"abstract":"<p><strong>Background: </strong>The neurotoxicity potential of polymyxin B is underrecognized.</p><p><strong>Results: </strong>Four critically ill patients treated with polymyxin B for suspected or confirmed nosocomial Gram-negative infections developed acute hypercapnic respiratory failure temporally associated with polymyxin B administration. Respiratory support escalated from room air or low-flow oxygen to noninvasive or invasive mechanical ventilation after one, two, five, and seven doses of polymyxin. No alternative explanation for the abrupt deterioration was identified after clinical evaluation. Following cessation of polymyxin (<i>n</i> = 3) or dose reduction (<i>n</i> = 1), all patients were liberated from ventilation within 60 h. Measured polymyxin concentrations were above the therapeutic range in all patients; however, the delayed timing of sampling, measured at variable intervals after the respiratory events, limits conclusions regarding causality and dose-dependent toxicity.</p><p><strong>Conclusion: </strong>Polymyxin B should be considered as a potential cause of acute hypercapnic respiratory failure in critically ill patients when no alternative explanation is apparent. Both idiosyncratic susceptibility and drug accumulation may contribute, although the delayed timing of drug concentration measurements precludes firm conclusions regarding dose-dependent toxicity. Further prospective studies are required to define the mechanisms and risk factors.</p>","PeriodicalId":52357,"journal":{"name":"Case Reports in Critical Care","volume":"2026 ","pages":"5569011"},"PeriodicalIF":0.0,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13594767/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149026720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pan-Neurofascin Antibody-Associated Nodopathy: A Critical Guillain-Barré Syndrome Mimic in the Differential Diagnosis-Report of Two Cases.","authors":"Andrea Nemethova, Willem De Ridder, Ingrid Baar, Alicia Alonso-Jimenez","doi":"10.1155/crcc/2662185","DOIUrl":"10.1155/crcc/2662185","url":null,"abstract":"<p><p>Guillain-Barré syndrome (GBS) is an acute autoimmune polyradiculoneuropathy typically characterized by an ascending sensorimotor deficit with potential involvement of bulbar and respiratory muscles that may necessitate intensive care admission and mechanical ventilation. Standard treatment includes supportive care, management of complications such as weakness, immobility, respiratory failure, autonomic dysfunction and pain, along with early initiation of immunotherapy-either intravenous immunoglobulin (IVIg) or plasma exchange (PE). However, lack of significant clinical improvement following immunotherapy should prompt consideration of alternative diagnoses, including pan-neurofascin antibody-positive autoimmune nodopathy (panNF + AN). In this report, we present two patients presenting with a severe GBS-like neuropathy. Initial treatment with IVIg resulted in either no response or only transient, mild improvement, followed by rapid clinical deterioration to near-complete tetraplegia, respiratory failure, and autonomic and cranial nerve involvement. Both patients were unresponsive to further treatment with a second course of IVIg, PE and corticosteroids. Subsequent diagnostic evaluation revealed the presence of pan-neurofascin antibodies, confirming panNF + AN. This prompted initiation of treatment with rituximab, which resulted in sustained and complete clinical recovery in both cases. A transient or mild clinical response-or an initial lack of response-to standard GBS-treatment followed by rapid and severe deterioration in cases initially presenting as GBS should be considered a red flag warranting evaluation for AN-associated antibodies. Recognition of this important GBS mimic is critical, as it requires an alternative treatment approach with rituximab, which has been associated excellent clinical outcomes.</p>","PeriodicalId":52357,"journal":{"name":"Case Reports in Critical Care","volume":"2026 ","pages":"2662185"},"PeriodicalIF":0.0,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13589164/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149009380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Atypical Presentation of Undiagnosed Crouzon's Syndrome With Pansinusitis, Orbital Cellulitis, and Altered Mentation Successfully Managed With Functional Endoscopic Sinus Surgery: A Case Report.","authors":"Parul Issar, Shivam Galav, Raunaq Goel, Ashesh Bhushan","doi":"10.1155/crcc/8887878","DOIUrl":"10.1155/crcc/8887878","url":null,"abstract":"<p><strong>Background: </strong>Crouzon's syndrome is a rare autosomal dominant craniosynostosis disorder characterized by midfacial hypoplasia due to premature fusion of the coronal and sagittal sutures. Facial features are typical in the form of a hypoplastic maxilla, shallow orbits, and mandibular prognathism. The condition is usually diagnosed during infancy or early childhood because of characteristic craniofacial features. Delayed diagnosis during adolescence is uncommon, and severe infective complications as the initial presentation are exceedingly rare.</p><p><strong>Case summary: </strong>A 14-year-old boy with no known craniofacial diagnosis presented to the emergency department with fever, headache, altered mentation, and left eye swelling. Examination revealed proptosis, chemosis, and purulent discharge from the left eye, along with midfacial hypoplasia and shallow orbits. Computed tomography and magnetic resonance imaging demonstrated extensive pansinusitis, orbital cellulitis, frontal bone osteomyelitis, and craniosynostosis-related craniofacial abnormalities. Initial empirical antimicrobial therapy was started and subsequently escalated following the isolation of carbapenem-resistant <i>Pseudomonas aeruginosa</i>. Owing to progressive disease, urgent functional endoscopic sinus surgery (FESS) was performed. The patient demonstrated rapid clinical improvement with resolution of orbital swelling and recovery of neurological status. Subsequent genetic testing confirmed an FGFR2 mutation, establishing the diagnosis of Crouzon syndrome.</p><p><strong>Conclusion: </strong>This case highlights a rare late presentation of previously undiagnosed Crouzon syndrome with life-threatening infective complications. Recognition of craniofacial dysmorphism in patients presenting with severe sinonasal infections is essential for timely diagnosis and multidisciplinary management. Culture-directed antimicrobial therapy combined with appropriately planned FESS can result in excellent clinical outcomes.</p>","PeriodicalId":52357,"journal":{"name":"Case Reports in Critical Care","volume":"2026 ","pages":"8887878"},"PeriodicalIF":0.0,"publicationDate":"2026-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13570442/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148956975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}