Successful management of protracted anaphylaxis-induced severe acute respiratory distress syndrome masquerading as non-ST elevation myocardial infarction: a rare case report

Successful management of protracted anaphylaxis-induced severe acute respiratory distress syndrome masquerading as non-ST elevation myocardial infarction: a rare case report | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Successful management of protracted anaphylaxis-induced severe acute respiratory distress syndrome masquerading as non-ST elevation myocardial infarction: a rare case report Hanh-Duyen Bui-Thi, Vu Hoang Vu, Khang Duong Nguyen, Thanh-Son Do-Truong, and 4 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-6917956/v1 This work is licensed under a CC BY 4.0 License Status: Published Journal Publication published 28 Jan, 2026 Read the published version in BMC Cardiovascular Disorders → Version 1 posted 12 You are reading this latest preprint version Abstract Background Prolonged anaphylaxis, especially symptoms that last several days, can lead to misdiagnosis and delays in treatment, especially when patients present with complications such as acute respiratory distress syndrome (ARDS) and secondary myocardial injury. A thorough review of medical history is very important for accurate diagnosis. Early recognition and intervention are essential for managing both the allergic response and pulmonary-cardiac injury. Case presentation: We present the case of a 70-year-old woman with no significant medical history who developed rapid respiratory failure and extremely elevated troponin levels. The patient was initially diagnosed with non-ST-segment elevation myocardial infarction (NSTEMI) complicated by pulmonary edema, and the patient's condition continued to worsen despite coronary intervention. A reevaluation revealed that anaphylaxis was potentially triggered by the recent use of floctafenine and meloxicam, which were taken as painkillers four days before admission. The administration of epinephrine led to a marked improvement in her condition, and she was successfully discharged without further complications. Conclusion Protracted anaphylaxis, especially when complicated by ARDS and myocardial injury mimicking NSTEMI, requires careful diagnostic consideration. Clinicians must thoroughly evaluate patient history, particularly recent medication use, to avoid misdiagnosis. Epinephrine remains a crucial treatment in such cases, and prompt administration can be life-saving. This case highlights the diagnostic challenges of protracted anaphylaxis and the importance of comprehensive clinical assessment and timely intervention. Clinical trial number: not applicable. Anaphylaxis acute myocardial infarction acute respiratory distress syndrome myocardial injury protracted anaphylaxis floctafenine meloxicam nonsteroidal anti-inflammatory drug epinephrine Figures Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Figure 6 I. Background Anaphylaxis is a severe, potentially life-threatening allergic reaction that can occur rapidly. It involves multiple organ systems, including the skin, respiratory, cardiovascular and gastrointestinal systems ( 1 ). Timely diagnosis and prompt intervention are crucial in anaphylaxis, as respiratory distress and cardiac arrest can develop rapidly, often within minutes. Typically, anaphylaxis presents symptoms rapidly, usually within minutes to a few hours after exposure to an allergen( 1 ). However, there are instances where symptoms can persist over a more extended period, ranging from several hours to days. Protracted or prolonged anaphylaxis can be challenging to diagnose correctly because the extended time frame might lead clinicians to consider other diagnoses. This delay can result in inappropriate treatment, which poses significant dangers to the patient​. Moreover, anaphylaxis can present with atypical symptoms and signs, such as elevated troponin levels, that mimic acute myocardial infarction ( 2 ). This can lead to unnecessary vascular intervention and delays in the diagnosis and treatment of anaphylaxis. Myocardial injury in individuals experiencing anaphylaxis may first present as a mild increase in cardiac markers without any noticeable symptoms but can progress to severe chest discomfort, abrupt myocardial infarction, and cardiogenic shock. Despite the burden of these phenomena, complete epidemiological data on anaphylaxis triggered by drugs are not available. The prevalence of the disorder has been estimated to range from 0.04–3.1% ( 3 , 4 ). Recent investigations have reported that the occurrence and intensity of drug-induced anaphylaxis are relatively high ( 5 , 6 ). Respiratory and cardiovascular problems have been demonstrated to be linked to a poor prognosis because of their potential impact on compensatory mechanisms in anaphylaxis, leading to low blood pressure or low oxygen levels ( 7 , 8 ) and death. This report presents an interesting case with protracted anaphylaxis-induced acute respiratory distress syndrome (ARDS) and extremely increased troponin T levels masquerading as non-ST elevation myocardial infarction due to floctafenine and meloxicam. We also performed a literature review on this matter. We searched PubMed with the following keywords: ((Anaphylactic) OR (anaphylaxis)) AND ((floctafenine) OR (meloxicam)). There were 3 results, with 2 studies included in the final review. One study was excluded because of duplication. II. Case presentation A 70-year-old female patient was admitted to the hospital due to dyspnea. One day prior to admission, the patient, who was in a seated position, suddenly experienced dyspnea. The dyspnea remained consistent regardless of body position and progressively worsened over time, without accompanying symptoms such as chest pain, fever, or cough. The patient was admitted to the emergency department and exhibited severe difficulty breathing. Her heart rate was 122 beats per minute (bpm), her blood pressure was 170/80 mmHg, and her SpO 2 was 73% with ambient air. The physical examination revealed that the patient was conscious and alert and had regular breathing sounds with crackles in both lungs. The patient also had swelling in both lower extremities, but no abnormalities were detected in other organs. An electrocardiogram (ECG) revealed a sinus rhythm, with no specific changes observed in the ST-T segment. The blood test results revealed high levels of high-sensitivity troponin T (hs-TnT), with values of 5076.7 ng/L (< 15.6 ng/L) and 4163.7 ng/L (after 1 hour); NT-proBNP, 15,254 ng/mL; urea, 67 mg/dL; creatinine, 1.81 mg/dL; and mildly elevated liver enzymes, with 76 U/L GOT and 48 U/L GPT. The patient was diagnosed with acute pulmonary edema due to non-ST-segment elevation myocardial infarction on the second day, with a Killip III classification indicating a very high risk. The patient was treated with 4 tablets of aspirin (81 mg), 2 tablets of ticagrelor (90 mg), and 40 mg of atorvastatin with increasing doses of furosemide and nitroglycerine. Despite these efforts, the patient’s condition continued to worsen. The patient was intubated and placed on mechanical ventilation. Therefore, she was taken to the DSA room for coronary angiography. The results of the coronary angiography revealed that the left coronary artery was the dominant system. There was 80% stenosis in the left anterior descending artery (LAD) I, and the right coronary artery (RCA) II was completely blocked. However, RCA II receives a blood supply from collateral circulation originating from the LAD (Fig. 1 ). Percutaneous coronary intervention was conducted via a single drug-eluting stent, 3.0 × 18 mm, in LAD I. Postoperative coronary blood flow reached the TIMI III level without evidence of dissection, thrombus, or residual stenosis. At the 5-hour mark following the procedure, the patient remained on mechanical ventilation under deep sedation and muscular relaxation, with no hypotension. The ventilator settings were as follows: positive end-expiratory pressure (PEEP) of 14 cmH 2 O, fraction of acquired oxygen (FiO 2 ) of 100%, tidal volume (VT) of 400 mL, and respiratory rate (f) of 20 bpm. However, her SpO 2 level reached only 60–70%, with a maximum of 73%. Her blood pressure was normal. The physical examination revealed a consistent cardiac rhythm and normal breath sounds bilaterally. The blood test results indicated that the hs-Troponin T level increased to 12,910 ng/L, the CK-MB level increased to 66 U/L, and the procalcitonin level was 0.26 ng/mL. The chest X-ray revealed widespread consolidation of the right lung and half of the left lung (Fig. 2 and Fig. 3 ). At this time, the inquiry revolved around whether the patient's issues were solely non-ST-segment-elevation myocardial infarction accompanied by acute pulmonary edema and the reason for her lack of improvement following successful coronary intervention, despite the implementation of optimized mechanical ventilation. Upon reviewing the patient’s medical history, we found that four days prior to admission, she had experienced an injury to her left leg in an accident, leading to the use of floctafenine and meloxicam as painkillers. Two days later, she developed mild facial edema, which subsequently progressed to involve the entire body. The edema worsened, and dyspnea one day prior to admission led to her presenting to the emergency department. Consequently, anaphylaxis due to nonsteroidal anti-inflammatory drugs (NSAIDs) and complications arising from multiple organ failure were considered. After 15 hours of admission (8 hours postcoronary intervention), we decided to administer epinephrine at a concentration of 1 mg/ml. Half of an ampoule was given intramuscularly twice at 5-minute intervals. After the injection, there was a marked improvement in vital signs, with the SpO 2 increasing from 73–97% within minutes, despite unchanged ventilator settings (PEEP 14 cmH 2 O, FiO 2 100%). The patient was subsequently transferred to the intensive care unit (ICU), where a continuous infusion of epinephrine was initiated at a rate of 0.1 mg/h. The ventilator parameters were adjusted to VT 360 mL, PEEP 14 cmH 2 O, f 26 l/p, and FiO 2 65%. The patient's blood pressure was 111/53 mmHg, her heart rate was 100 pm, and her SpO2 reached 99%. The peak troponin concentration was 41,077 ng/mL upon ICU admission and was reduced to 10,461 ng/mL after 1 day, after which it continued to decrease. In the following days, the dosage of epinephrine gradually decreased. Serial chest X-rays revealed significant improvement, with resolution of bilateral lung consolidation (Fig. 4 and Fig. 5). Additionally, she was also prescribed desloratadine 5 mg along with anti-H1 medication. The patient was gradually weaned off the ventilator and successfully extubated after 5 days. After GI bleeding stabilized, which occurred before ICU admission, she received 40 mg of methylprednisolone intravenously daily. She was successfully discharged from the ICU after 10 days and discharged from the hospital after a 16-day stay. Her discharge medication included 16 mg of methylprednisolone, 5 mg of desloratadine, 75 mg of clopidogrel, 40 mg of atorvastatin and 40 mg of pantoprazole. After 20 months, the patient's condition remained stable, with no reported incidents (Fig. 6 ). III. Discussion According to the 2020 World Allergy Organization Anaphylaxis (WAO), anaphylaxis is a serious systemic hypersensitivity reaction that typically begins quickly and may be fatal. Severe anaphylaxis has the potential to be life-threatening, as it can compromise the airway, breathing, and circulation. It may present with or without typical skin features or circulatory shock. Anaphylaxis can be diagnosed in the following two clinical contexts: ( 1 ) acute onset of an illness, occurring within minutes to several hours, with concurrent involvement of the skin, mucosal tissue, or both, and at least one of the following: (i) respiratory compromise; (ii) reduced blood pressure or associated symptoms of end-organ dysfunction; or (iii) severe gastrointestinal symptoms, especially after exposure to nonfood allergens. ( 2 ) Acute onset within minutes to several hours of hypotension, bronchospasm, or laryngeal involvement after exposure to a known or highly probable allergen for that patient if typical skin symptoms and signs are absent ( 9 ). Despite rare presentations, such as persistent anaphylactic reactions and ARDS, which we discuss later, our case still demonstrated some typical signs of anaphylaxis. Our patient experienced skin lesions and severe respiratory symptoms after taking NSAIDs. According to the 2020 World Allergy Organization and the 2021 European Academy of Allergy and Clinical Immunology guidelines, both are presentations of anaphylaxis in the first clinical context. Moreover, the patient's respiratory failure rapidly improved only after adrenaline administration, despite not responding to other interventions. Typical clinical manifestations of anaphylaxis generally emerge within minutes to hours following exposure to an allergenic agent. Without prompt acute intervention, the condition can be fatal. Prolonged (protracted) anaphylaxis is defined as the presence of symptoms and/or clinical findings that meet the criteria for anaphylaxis and persist for at least four hours ( 10 ). It is different from refractory anaphylaxis, which is defined as the continuation of anaphylaxis symptoms despite the administration of at least three appropriate doses of epinephrine or the initiation of an epinephrine infusion ( 11 ). Protracted anaphylaxis in the absence of treatment is rarely observed and often results in misdiagnosis. The incidence of protracted episodes of anaphylaxis is 3–8% ( 12 , 13 ). Vinuya RZ et al. reported a case of a young male patient who presented with skin, respiratory, and persistent gastrointestinal involvement after consuming clams over a 14-hour period. These symptoms persisted for three days prior to admission. The patient's symptoms resolved after the administration of antihistamine H1, anti-H2, or fluids without the use of adrenaline. Elevated serum tryptase levels were observed on the fourth and fifth days of illness. The serum clam-specific immunoglobulin E (IgE) level was negative at admission but was found to be lowly positive several months later ( 14 ). To the best of our knowledge, this case represents the second reported instance of protracted anaphylaxis lasting several days before diagnosis and treatment. Myocardial injury-associated anaphylaxis includes three clinical scenarios: ( 1 ) Kounis syndrome; ( 2 ) secondary acute myocardial infarction or ischemia following epinephrine administration due to anaphylaxis; and ( 3 ) acute myocardial infarction type 2 ( 15 ). Kounis syndrome is defined as the simultaneous occurrence of acute coronary syndrome alongside conditions that trigger mast cell activation. This involves the interplay of various inflammatory cells and is associated with allergic reactions, hypersensitivity responses, and anaphylactic attacks. Kounis syndrome has three variants. Type I EHBD occurs in patients with normal or nearly normal coronary arteries and no coronary artery disease risk factors. Acute allergic reactions can cause coronary artery spasms, which may lead to myocardial infarction with elevated cardiac enzymes and troponins or without increased cardiac enzymes and troponins. Type II involves patients with preexisting but inactive atheromatous disease. Acute allergic reactions can trigger coronary artery spasm, plaque erosion, or rupture, resulting in myocardial infarction. Type III is associated with stent thrombosis following hypersensitivity reactions to drug-eluting stents. Thrombus pathology reveals the presence of eosinophils and mast cells ( 16 , 17 ). Epinephrine remains the cornerstone of treatment for anaphylaxis; however, its administration is associated with potential adverse cardiovascular events, including coronary artery vasospasm that can precipitate secondary myocardial infarction ( 18 ). The incidence of these cardiovascular complications varies according to the route of administration. A study by Campbell et al. demonstrated that the bolus intravenous route is associated with a significantly greater risk of adverse cardiovascular events than the intramuscular route is (10% vs 1.3%; odds ratio 8.7 [95% CI, 1.8–40.7], P = 0.006) ( 19 ). In this case, the patient experienced a type 2 myocardial infarction secondary to severe hypoxemia, which initially led to a misdiagnosis of type 1 myocardial infarction. Although the respiratory system is one of the four main organs affected by anaphylaxis, with an incidence of approximately 70% ( 20 ), anaphylaxis-induced ARDS is rare. The exact incidence rate remains undetermined, as it has only been documented in case studies. NSAIDs are a major cause of anaphylaxis ( 21 ); however, ARDS due to NSAID-induced anaphylaxis is extremely rare ( 22 , 23 ). The pathophysiology underlying NSAID-induced anaphylaxis progressing to ARDS involves a complex interplay of immune mechanisms, leading to a systemic inflammatory response, increased vascular permeability, and fluid extravasation into the interstitial space. Management strategies for anaphylaxis-induced ARDS typically involve a combination of general ARDS and anaphylaxis treatment protocols. The primary cause of drug anaphylaxis is typically antibiotics, which are responsible for 35.5–66.6% of cases ( 24 ). NSAIDs and other analgesics remain important anaphylactic causes, accounting for 21.5–28.5% of the total. Within this category, NSAIDs accounted for 11.5%, opiates accounted for 8.7%, and regional anesthetics accounted for 1.3%. In clinical practice. Floctafenine, a compound derived from anthranilic acid, is an NSAID that possesses both analgesic and anti-inflammatory properties. Floctafenine exhibits analgesic activity comparable to that of moderate analgesics in acute situations. In laboratory studies, floctafenine has been demonstrated to hinder the production of PGE2 and PGF2a. In the literature, we documented a case in which the administration of a single capsule of floctafenine resulted in the onset of a widespread rash and rapid loss of consciousness within 30 minutes ( 25 ). In 1996, a review of drug-associated anaphylaxis within 20 years in the Netherlands ( 26 ) reported 936 cases, of which 345 cases were probable anaphylaxis, 485 were possible anaphylaxis, and 106 were unlikely. Among them, 12 cases (7 of which were probable) were related to floctafenine, and two cases died. Meloxicam, on the other hand, is rarely reported in relation to anaphylaxis compared with floctafenine. This case underscores several important clinical points. First, the symptoms of anaphylaxis can persist for several days before being recognized and treated, increasing the risk of misdiagnosis or delayed intervention. Furthermore, angioedema may be mistaken for generalized edema in patients with renal or cardiac failure. Cardiac injury, which manifests as markedly elevated troponin I levels due to anaphylaxis-induced severe hypoxemia, is another potential diagnostic pitfall. Notably, even in severe cases of anaphylaxis, stable hemodynamics may be preserved despite multiorgan failure. Rapid improvement following adrenaline administration in the context of profound pulmonary impairment caused by anaphylaxis highlights the essential role of epinephrine, which has significant therapeutic efficacy in such cases. IV. Conclusion This case underscores the complexity of diagnosing and managing protracted anaphylaxis, particularly when myocardial injury presents in a manner resembling non-ST elevation myocardial infarction. The overlap in clinical manifestations between anaphylaxis-induced hypoxemia and type 1 myocardial infarction increases the risk of misdiagnosis and inappropriate interventions. Clinicians must take a thorough medical history, paying particular attention to medication administration, to ensure accurate diagnosis and effective treatment. Declarations Ethics approval and consent to participate Ethics approval was not required for this case report as it involves a single patient and does not constitute research. Consent for publication Written informed consent was obtained from the patient for the publication of this case. Availability of data and materials The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request Competing interests The authors declare that they have no competing interests. Funding Not applicable. Authors' contributions HDBT made substantial contributions to the conception and design of the work; VHV, KDN, and NNKT have drafted the work; STTD, HT, DTB, BNG and BQT substantively revised it. All authors read and approved the final manuscript. Acknowledgements Not applicable. 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Bui","email":"","orcid":"","institution":"University Medical Center Ho Chi Minh City","correspondingAuthor":false,"prefix":"","firstName":"Dung","middleName":"The","lastName":"Bui","suffix":""},{"id":492838605,"identity":"5e85fddc-f419-4bf6-a6b6-73810875f4c4","order_by":7,"name":"Binh Quang Truong","email":"","orcid":"","institution":"University Medical Center Ho Chi Minh City","correspondingAuthor":false,"prefix":"","firstName":"Binh","middleName":"Quang","lastName":"Truong","suffix":""}],"badges":[],"createdAt":"2025-06-18 01:23:11","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-6917956/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-6917956/v1","draftVersion":[],"editorialEvents":[{"content":"https://doi.org/10.1186/s12872-026-05565-7","type":"published","date":"2026-01-28T15:58:14+00:00"}],"editorialNote":"","failedWorkflow":false,"files":[{"id":88135299,"identity":"bae21c2f-2bba-4678-9f54-367d3ee9c2a0","added_by":"auto","created_at":"2025-08-01 21:37:11","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":315448,"visible":true,"origin":"","legend":"\u003cp\u003eThe coronary angiogram revealed 80% LAD I stenosis (left) and chronic total occlusion of RCA II (right).\u003c/p\u003e","description":"","filename":"floatimage1.png","url":"https://assets-eu.researchsquare.com/files/rs-6917956/v1/cbb853c832d74e924cf41798.png"},{"id":88135817,"identity":"e7d94bbf-0e07-4b9a-bb15-9e76f3f6e1d2","added_by":"auto","created_at":"2025-08-01 21:45:14","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":112622,"visible":true,"origin":"","legend":"\u003cp\u003eChest X-ray at admission\u003c/p\u003e","description":"","filename":"floatimage2.png","url":"https://assets-eu.researchsquare.com/files/rs-6917956/v1/0a22fe1aae3615aeacdf25ac.png"},{"id":88135816,"identity":"a68c8333-b80d-4439-9ca4-c83271260118","added_by":"auto","created_at":"2025-08-01 21:45:14","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":124555,"visible":true,"origin":"","legend":"\u003cp\u003eChest X-ray obtained 2 hours after coronary intervention revealed consolidation of the right lung and half of the left lung.\u003c/p\u003e","description":"","filename":"floatimage3.png","url":"https://assets-eu.researchsquare.com/files/rs-6917956/v1/0c1dbfdace1442133ba10c46.png"},{"id":88135300,"identity":"5bb7efbf-927a-4fd6-995f-9edf2bd0ad5f","added_by":"auto","created_at":"2025-08-01 21:37:11","extension":"png","order_by":4,"title":"Figure 4","display":"","copyAsset":false,"role":"figure","size":113269,"visible":true,"origin":"","legend":"\u003cp\u003eChest X-ray 2 days after admission\u003c/p\u003e","description":"","filename":"floatimage4.png","url":"https://assets-eu.researchsquare.com/files/rs-6917956/v1/2cf6968627c9612e5b0937d7.png"},{"id":88135305,"identity":"03ecade6-7f63-4a79-9a05-69303911e775","added_by":"auto","created_at":"2025-08-01 21:37:11","extension":"png","order_by":5,"title":"Figure 5","display":"","copyAsset":false,"role":"figure","size":95066,"visible":true,"origin":"","legend":"\u003cp\u003eChest X-ray 5 days after admission\u003c/p\u003e","description":"","filename":"floatimage5.png","url":"https://assets-eu.researchsquare.com/files/rs-6917956/v1/a2c80e69f63a3ec3ced39a30.png"},{"id":88135311,"identity":"2a8695b2-6866-4c96-947a-6e9d25a7357b","added_by":"auto","created_at":"2025-08-01 21:37:11","extension":"png","order_by":6,"title":"Figure 6","display":"","copyAsset":false,"role":"figure","size":170544,"visible":true,"origin":"","legend":"\u003cp\u003eSummary timeline of the diagnosis and management\u003c/p\u003e","description":"","filename":"floatimage6.png","url":"https://assets-eu.researchsquare.com/files/rs-6917956/v1/9210b8bdc74425aef5940231.png"},{"id":101691955,"identity":"47545641-9747-4356-9cd0-ede06c6e3de0","added_by":"auto","created_at":"2026-02-02 16:16:29","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1429900,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-6917956/v1/bd127a4a-1cf4-4cd7-8066-8fa3ff8eb8f7.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Successful management of protracted anaphylaxis-induced severe acute respiratory distress syndrome masquerading as non-ST elevation myocardial infarction: a rare case report","fulltext":[{"header":"I. Background","content":"\u003cp\u003eAnaphylaxis is a severe, potentially life-threatening allergic reaction that can occur rapidly. It involves multiple organ systems, including the skin, respiratory, cardiovascular and gastrointestinal systems (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e). Timely diagnosis and prompt intervention are crucial in anaphylaxis, as respiratory distress and cardiac arrest can develop rapidly, often within minutes. Typically, anaphylaxis presents symptoms rapidly, usually within minutes to a few hours after exposure to an allergen(\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e). However, there are instances where symptoms can persist over a more extended period, ranging from several hours to days. Protracted or prolonged anaphylaxis can be challenging to diagnose correctly because the extended time frame might lead clinicians to consider other diagnoses. This delay can result in inappropriate treatment, which poses significant dangers to the patient​.\u003c/p\u003e\u003cp\u003eMoreover, anaphylaxis can present with atypical symptoms and signs, such as elevated troponin levels, that mimic acute myocardial infarction (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e). This can lead to unnecessary vascular intervention and delays in the diagnosis and treatment of anaphylaxis. Myocardial injury in individuals experiencing anaphylaxis may first present as a mild increase in cardiac markers without any noticeable symptoms but can progress to severe chest discomfort, abrupt myocardial infarction, and cardiogenic shock.\u003c/p\u003e\u003cp\u003eDespite the burden of these phenomena, complete epidemiological data on anaphylaxis triggered by drugs are not available. The prevalence of the disorder has been estimated to range from 0.04\u0026ndash;3.1% (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e). Recent investigations have reported that the occurrence and intensity of drug-induced anaphylaxis are relatively high (\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e). Respiratory and cardiovascular problems have been demonstrated to be linked to a poor prognosis because of their potential impact on compensatory mechanisms in anaphylaxis, leading to low blood pressure or low oxygen levels (\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e) and death.\u003c/p\u003e\u003cp\u003eThis report presents an interesting case with protracted anaphylaxis-induced acute respiratory distress syndrome (ARDS) and extremely increased troponin T levels masquerading as non-ST elevation myocardial infarction due to floctafenine and meloxicam. We also performed a literature review on this matter. We searched PubMed with the following keywords: ((Anaphylactic) OR (anaphylaxis)) AND ((floctafenine) OR (meloxicam)). There were 3 results, with 2 studies included in the final review. One study was excluded because of duplication.\u003c/p\u003e"},{"header":"II. Case presentation","content":"\u003cp\u003eA 70-year-old female patient was admitted to the hospital due to dyspnea. One day prior to admission, the patient, who was in a seated position, suddenly experienced dyspnea. The dyspnea remained consistent regardless of body position and progressively worsened over time, without accompanying symptoms such as chest pain, fever, or cough. The patient was admitted to the emergency department and exhibited severe difficulty breathing. Her heart rate was 122 beats per minute (bpm), her blood pressure was 170/80 mmHg, and her SpO\u003csub\u003e2\u003c/sub\u003e was 73% with ambient air. The physical examination revealed that the patient was conscious and alert and had regular breathing sounds with crackles in both lungs. The patient also had swelling in both lower extremities, but no abnormalities were detected in other organs. An electrocardiogram (ECG) revealed a sinus rhythm, with no specific changes observed in the ST-T segment. The blood test results revealed high levels of high-sensitivity troponin T (hs-TnT), with values of 5076.7 ng/L (\u0026lt;\u0026thinsp;15.6 ng/L) and 4163.7 ng/L (after 1 hour); NT-proBNP, 15,254 ng/mL; urea, 67 mg/dL; creatinine, 1.81 mg/dL; and mildly elevated liver enzymes, with 76 U/L GOT and 48 U/L GPT. The patient was diagnosed with acute pulmonary edema due to non-ST-segment elevation myocardial infarction on the second day, with a Killip III classification indicating a very high risk. The patient was treated with 4 tablets of aspirin (81 mg), 2 tablets of ticagrelor (90 mg), and 40 mg of atorvastatin with increasing doses of furosemide and nitroglycerine. Despite these efforts, the patient\u0026rsquo;s condition continued to worsen. The patient was intubated and placed on mechanical ventilation. Therefore, she was taken to the DSA room for coronary angiography.\u003c/p\u003e\u003cp\u003eThe results of the coronary angiography revealed that the left coronary artery was the dominant system. There was 80% stenosis in the left anterior descending artery (LAD) I, and the right coronary artery (RCA) II was completely blocked. However, RCA II receives a blood supply from collateral circulation originating from the LAD (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). Percutaneous coronary intervention was conducted via a single drug-eluting stent, 3.0 \u0026times; 18 mm, in LAD I. Postoperative coronary blood flow reached the TIMI III level without evidence of dissection, thrombus, or residual stenosis.\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003cp\u003eAt the 5-hour mark following the procedure, the patient remained on mechanical ventilation under deep sedation and muscular relaxation, with no hypotension. The ventilator settings were as follows: positive end-expiratory pressure (PEEP) of 14 cmH\u003csub\u003e2\u003c/sub\u003eO, fraction of acquired oxygen (FiO\u003csub\u003e2\u003c/sub\u003e) of 100%, tidal volume (VT) of 400 mL, and respiratory rate (f) of 20 bpm. However, her SpO\u003csub\u003e2\u003c/sub\u003e level reached only 60\u0026ndash;70%, with a maximum of 73%. Her blood pressure was normal. The physical examination revealed a consistent cardiac rhythm and normal breath sounds bilaterally. The blood test results indicated that the hs-Troponin T level increased to 12,910 ng/L, the CK-MB level increased to 66 U/L, and the procalcitonin level was 0.26 ng/mL. The chest X-ray revealed widespread consolidation of the right lung and half of the left lung (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e and Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003e). At this time, the inquiry revolved around whether the patient's issues were solely non-ST-segment-elevation myocardial infarction accompanied by acute pulmonary edema and the reason for her lack of improvement following successful coronary intervention, despite the implementation of optimized mechanical ventilation.\u003c/p\u003e\u003cp\u003eUpon reviewing the patient\u0026rsquo;s medical history, we found that four days prior to admission, she had experienced an injury to her left leg in an accident, leading to the use of \u003cb\u003efloctafenine and meloxicam\u003c/b\u003e as painkillers. Two days later, she developed mild facial edema, which subsequently progressed to involve the entire body. The edema worsened, and dyspnea one day prior to admission led to her presenting to the emergency department. Consequently, anaphylaxis due to nonsteroidal anti-inflammatory drugs (NSAIDs) and complications arising from multiple organ failure were considered.\u003c/p\u003e\u003cp\u003eAfter 15 hours of admission (8 hours postcoronary intervention), we decided to administer epinephrine at a concentration of 1 mg/ml. Half of an ampoule was given intramuscularly twice at 5-minute intervals. After the injection, there was a marked improvement in vital signs, with the SpO\u003csub\u003e2\u003c/sub\u003e increasing from 73\u0026ndash;97% within minutes, despite unchanged ventilator settings (PEEP 14 cmH\u003csub\u003e2\u003c/sub\u003eO, FiO\u003csub\u003e2\u003c/sub\u003e 100%). The patient was subsequently transferred to the intensive care unit (ICU), where a continuous infusion of epinephrine was initiated at a rate of 0.1 mg/h. The ventilator parameters were adjusted to VT 360 mL, PEEP 14 cmH\u003csub\u003e2\u003c/sub\u003eO, f 26 l/p, and FiO\u003csub\u003e2\u003c/sub\u003e 65%. The patient's blood pressure was 111/53 mmHg, her heart rate was 100 pm, and her SpO2 reached 99%. The peak troponin concentration was 41,077 ng/mL upon ICU admission and was reduced to 10,461 ng/mL after 1 day, after which it continued to decrease.\u003c/p\u003e\u003cp\u003eIn the following days, the dosage of epinephrine gradually decreased. Serial chest X-rays revealed significant improvement, with resolution of bilateral lung consolidation (Fig. \u003cspan class=\"InternalRef\"\u003e4\u003c/span\u003e and Fig. 5). Additionally, she was also prescribed desloratadine 5 mg along with anti-H1 medication. The patient was gradually weaned off the ventilator and successfully extubated after 5 days. After GI bleeding stabilized, which occurred before ICU admission, she received 40 mg of methylprednisolone intravenously daily. She was successfully discharged from the ICU after 10 days and discharged from the hospital after a 16-day stay. Her discharge medication included 16 mg of methylprednisolone, 5 mg of desloratadine, 75 mg of clopidogrel, 40 mg of atorvastatin and 40 mg of pantoprazole. After 20 months, the patient\u0026apos;s condition remained stable, with no reported incidents (Fig. \u003cspan class=\"InternalRef\"\u003e6\u003c/span\u003e).\u003c/p\u003e"},{"header":"III. Discussion","content":"\u003cp\u003eAccording to the 2020 World Allergy Organization Anaphylaxis (WAO), anaphylaxis is a serious systemic hypersensitivity reaction that typically begins quickly and may be fatal. Severe anaphylaxis has the potential to be life-threatening, as it can compromise the airway, breathing, and circulation. It may present with or without typical skin features or circulatory shock. Anaphylaxis can be diagnosed in the following two clinical contexts: (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e) acute onset of an illness, occurring within minutes to several hours, with concurrent involvement of the skin, mucosal tissue, or both, and at least one of the following: (i) respiratory compromise; (ii) reduced blood pressure or associated symptoms of end-organ dysfunction; or (iii) severe gastrointestinal symptoms, especially after exposure to nonfood allergens. (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e) Acute onset within minutes to several hours of hypotension, bronchospasm, or laryngeal involvement after exposure to a known or highly probable allergen for that patient if typical skin symptoms and signs are absent (\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e). Despite rare presentations, such as persistent anaphylactic reactions and ARDS, which we discuss later, our case still demonstrated some typical signs of anaphylaxis. Our patient experienced skin lesions and severe respiratory symptoms after taking NSAIDs. According to the 2020 World Allergy Organization and the 2021 European Academy of Allergy and Clinical Immunology guidelines, both are presentations of anaphylaxis in the first clinical context. Moreover, the patient's respiratory failure rapidly improved only after adrenaline administration, despite not responding to other interventions.\u003c/p\u003e\u003cp\u003eTypical clinical manifestations of anaphylaxis generally emerge within minutes to hours following exposure to an allergenic agent. Without prompt acute intervention, the condition can be fatal. Prolonged (protracted) anaphylaxis is defined as the presence of symptoms and/or clinical findings that meet the criteria for anaphylaxis and persist for at least four hours (\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e). It is different from refractory anaphylaxis, which is defined as the continuation of anaphylaxis symptoms despite the administration of at least three appropriate doses of epinephrine or the initiation of an epinephrine infusion (\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e). Protracted anaphylaxis in the absence of treatment is rarely observed and often results in misdiagnosis. The incidence of protracted episodes of anaphylaxis is 3\u0026ndash;8% (\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e, \u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e). Vinuya RZ et al. reported a case of a young male patient who presented with skin, respiratory, and persistent gastrointestinal involvement after consuming clams over a 14-hour period. These symptoms persisted for three days prior to admission. The patient's symptoms resolved after the administration of antihistamine H1, anti-H2, or fluids without the use of adrenaline. Elevated serum tryptase levels were observed on the fourth and fifth days of illness. The serum clam-specific immunoglobulin E (IgE) level was negative at admission but was found to be lowly positive several months later (\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e). To the best of our knowledge, this case represents the second reported instance of protracted anaphylaxis lasting several days before diagnosis and treatment.\u003c/p\u003e\u003cp\u003eMyocardial injury-associated anaphylaxis includes three clinical scenarios: (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e) Kounis syndrome; (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e) secondary acute myocardial infarction or ischemia following epinephrine administration due to anaphylaxis; and (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e) acute myocardial infarction type 2 (\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e). Kounis syndrome is defined as the simultaneous occurrence of acute coronary syndrome alongside conditions that trigger mast cell activation. This involves the interplay of various inflammatory cells and is associated with allergic reactions, hypersensitivity responses, and anaphylactic attacks. Kounis syndrome has three variants. Type I EHBD occurs in patients with normal or nearly normal coronary arteries and no coronary artery disease risk factors. Acute allergic reactions can cause coronary artery spasms, which may lead to myocardial infarction with elevated cardiac enzymes and troponins or without increased cardiac enzymes and troponins. Type II involves patients with preexisting but inactive atheromatous disease. Acute allergic reactions can trigger coronary artery spasm, plaque erosion, or rupture, resulting in myocardial infarction. Type III is associated with stent thrombosis following hypersensitivity reactions to drug-eluting stents. Thrombus pathology reveals the presence of eosinophils and mast cells (\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e, \u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e). Epinephrine remains the cornerstone of treatment for anaphylaxis; however, its administration is associated with potential adverse cardiovascular events, including coronary artery vasospasm that can precipitate secondary myocardial infarction (\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e). The incidence of these cardiovascular complications varies according to the route of administration. A study by Campbell et al. demonstrated that the bolus intravenous route is associated with a significantly greater risk of adverse cardiovascular events than the intramuscular route is (10% vs 1.3%; odds ratio 8.7 [95% CI, 1.8\u0026ndash;40.7], P\u0026thinsp;=\u0026thinsp;0.006) (\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e). In this case, the patient experienced a type 2 myocardial infarction secondary to severe hypoxemia, which initially led to a misdiagnosis of type 1 myocardial infarction.\u003c/p\u003e\u003cp\u003eAlthough the respiratory system is one of the four main organs affected by anaphylaxis, with an incidence of approximately 70% (\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e), anaphylaxis-induced ARDS is rare. The exact incidence rate remains undetermined, as it has only been documented in case studies. NSAIDs are a major cause of anaphylaxis (\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e); however, ARDS due to NSAID-induced anaphylaxis is extremely rare (\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e, \u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e). The pathophysiology underlying NSAID-induced anaphylaxis progressing to ARDS involves a complex interplay of immune mechanisms, leading to a systemic inflammatory response, increased vascular permeability, and fluid extravasation into the interstitial space. Management strategies for anaphylaxis-induced ARDS typically involve a combination of general ARDS and anaphylaxis treatment protocols.\u003c/p\u003e\u003cp\u003eThe primary cause of drug anaphylaxis is typically antibiotics, which are responsible for 35.5\u0026ndash;66.6% of cases (\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e). NSAIDs and other analgesics remain important anaphylactic causes, accounting for 21.5\u0026ndash;28.5% of the total. Within this category, NSAIDs accounted for 11.5%, opiates accounted for 8.7%, and regional anesthetics accounted for 1.3%. In clinical practice. Floctafenine, a compound derived from anthranilic acid, is an NSAID that possesses both analgesic and anti-inflammatory properties. Floctafenine exhibits analgesic activity comparable to that of moderate analgesics in acute situations. In laboratory studies, floctafenine has been demonstrated to hinder the production of PGE2 and PGF2a. In the literature, we documented a case in which the administration of a single capsule of floctafenine resulted in the onset of a widespread rash and rapid loss of consciousness within 30 minutes (\u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e). In 1996, a review of drug-associated anaphylaxis within 20 years in the Netherlands (\u003cspan citationid=\"CR26\" class=\"CitationRef\"\u003e26\u003c/span\u003e) reported 936 cases, of which 345 cases were probable anaphylaxis, 485 were possible anaphylaxis, and 106 were unlikely. Among them, 12 cases (7 of which were probable) were related to floctafenine, and two cases died. Meloxicam, on the other hand, is rarely reported in relation to anaphylaxis compared with floctafenine.\u003c/p\u003e\u003cp\u003eThis case underscores several important clinical points. First, the symptoms of anaphylaxis can persist for several days before being recognized and treated, increasing the risk of misdiagnosis or delayed intervention. Furthermore, angioedema may be mistaken for generalized edema in patients with renal or cardiac failure. Cardiac injury, which manifests as markedly elevated troponin I levels due to anaphylaxis-induced severe hypoxemia, is another potential diagnostic pitfall. Notably, even in severe cases of anaphylaxis, stable hemodynamics may be preserved despite multiorgan failure. Rapid improvement following adrenaline administration in the context of profound pulmonary impairment caused by anaphylaxis highlights the essential role of epinephrine, which has significant therapeutic efficacy in such cases.\u003c/p\u003e"},{"header":"IV. Conclusion","content":"\u003cp\u003eThis case underscores the complexity of diagnosing and managing protracted anaphylaxis, particularly when myocardial injury presents in a manner resembling non-ST elevation myocardial infarction. The overlap in clinical manifestations between anaphylaxis-induced hypoxemia and type 1 myocardial infarction increases the risk of misdiagnosis and inappropriate interventions. Clinicians must take a thorough medical history, paying particular attention to medication administration, to ensure accurate diagnosis and effective treatment.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eEthics approval was not required for this case report as it involves a single patient and does not constitute research.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWritten informed consent was obtained from the patient for the publication of this case.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003cstrong\u003eAvailability of data and materials\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe datasets used and/or analysed during the current study are available from the corresponding author on reasonable request\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no competing interests.\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable.\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;\u003cstrong\u003eAuthors\u0026apos; contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eHDBT made substantial contributions to the conception and design of the work; VHV, KDN, and NNKT have drafted the work; STTD, HT, DTB, BNG and BQT substantively revised it. All authors read and approved the final manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eRossi CM, Lenti MV, Di Sabatino A. Adult anaphylaxis: A state-of-the-art review. European Journal of Internal Medicine. 2022;100:5-12.\u003c/li\u003e\n\u003cli\u003eLieberman P, Simons FER. Anaphylaxis and cardiovascular disease: therapeutic dilemmas. Clinical \u0026amp; Experimental Allergy. 2015;45(8):1288-95.\u003c/li\u003e\n\u003cli\u003eKlein JS, Yocum MW. Underreporting of anaphylaxis in a community emergency room. J Allergy Clin Immunol. 1995;95(2):637-8.\u003c/li\u003e\n\u003cli\u003eRisk of anaphylaxis in a hospital population in relation to the use of various drugs: an international study. 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World allergy organization anaphylaxis guidance 2020. World allergy organization journal. 2020;13(10):100472.\u003c/li\u003e\n\u003cli\u003eGolden DB. Patterns of anaphylaxis: acute and late phase features of allergic reactions. Novartis Found Symp. 2004;257:101-10; discussion 10-5, 57-60, 276-85.\u003c/li\u003e\n\u003cli\u003eDribin TE, Sampson HA, Camargo CA, Jr., Brousseau DC, Spergel JM, Neuman MI, et al. Persistent, refractory, and biphasic anaphylaxis: A multidisciplinary Delphi study. J Allergy Clin Immunol. 2020;146(5):1089-96.\u003c/li\u003e\n\u003cli\u003eOya S, Nakamori T, Kinoshita H. Incidence and characteristics of biphasic and protracted anaphylaxis: evaluation of 114 inpatients. Acute Med Surg. 2014;1(4):228-33.\u003c/li\u003e\n\u003cli\u003eLimb SL, Starke PR, Lee CE, Chowdhury BA. Delayed onset and protracted progression of anaphylaxis after omalizumab administration in patients with asthma. J Allergy Clin Immunol. 2007;120(6):1378-81.\u003c/li\u003e\n\u003cli\u003eVinuya RZ, Simon MR, Schwartz LB. Elevated serum tryptase levels in a patient with protracted anaphylaxis. Ann Allergy. 1994;73(3):232-4.\u003c/li\u003e\n\u003cli\u003eKounis NG. Kounis syndrome: an update on epidemiology, pathogenesis, diagnosis and therapeutic management. Clin Chem Lab Med. 2016;54(10):1545-59.\u003c/li\u003e\n\u003cli\u003eKounis NG, Mazarakis A, Tsigkas G, Giannopoulos S, Goudevenos J. Kounis syndrome: a new twist on an old disease. Future Cardiol. 2011;7(6):805-24.\u003c/li\u003e\n\u003cli\u003eVu VH, Nguyen KD, Nguyen CD, Truong BQ. A Case of Kounis Syndrome Presenting as Coronary Artery Spasm Associated with Acetaminophen Infusion. Am J Case Rep. 2021;22:e934190.\u003c/li\u003e\n\u003cli\u003eTan PZ, Chew NWS, Tay SH, Chang P. The allergic myocardial infarction dilemma: is it the anaphylaxis or the epinephrine? J Thromb Thrombolysis. 2021;52(3):941-8.\u003c/li\u003e\n\u003cli\u003eCampbell RL, Bellolio MF, Knutson BD, Bellamkonda VR, Fedko MG, Nestler DM, Hess EP. Epinephrine in anaphylaxis: higher risk of cardiovascular complications and overdose after administration of intravenous bolus epinephrine compared with intramuscular epinephrine. J Allergy Clin Immunol Pract. 2015;3(1):76-80.\u003c/li\u003e\n\u003cli\u003eKhan NU, Shakeel N, Makda A, Mallick AS, Ali Memon M, Hashmi SH, et al. Anaphylaxis: incidence, presentation, causes and outcome in patients in a tertiary-care hospital in Karachi, Pakistan. Qjm. 2013;106(12):1095-101.\u003c/li\u003e\n\u003cli\u003eAun MV, Blanca M, Garro LS, Ribeiro MR, Kalil J, Motta AA, et al. Nonsteroidal anti-inflammatory drugs are major causes of drug-induced anaphylaxis. J Allergy Clin Immunol Pract. 2014;2(4):414-20.\u003c/li\u003e\n\u003cli\u003eKumar V, Kamath V, Ganguly S. A Case of Noncardiogenic Pulmonary Edema and Pleural Effusion following Diclofenac Administration. APIK Journal of Internal Medicine. 2021;9(1):48-51.\u003c/li\u003e\n\u003cli\u003e\u0026Ouml;zbek AE, Divrikoğlu YS, Yılmaz S, Aytaş N, \u0026Ccedil;elik E. Nonsteroidal anti-inflammatory drug-induced acute respiratory distress syndrome. Am J Emerg Med. 2018;36(10):1929.e1-.e2.\u003c/li\u003e\n\u003cli\u003eRegateiro FS, Marques ML, Gomes ER. Drug-Induced Anaphylaxis: An Update on Epidemiology and Risk Factors. International Archives of Allergy and Immunology. 2020;181(7):481-7.\u003c/li\u003e\n\u003cli\u003eJonkhoff AR, Stricker BH. [Anaphylactic reactions following administration of floctafenine]. Ned Tijdschr Geneeskd. 1990;134(17):863-5.\u003c/li\u003e\n\u003cli\u003eVAN DER KLAUW MM, WILSON JHP, STRICKER BHC. Drug-associated anaphylaxis: 20 years of reporting in the Netherlands (1974\u0026ndash;1994) and review of the literature. Clinical \u0026amp; Experimental Allergy. 1996;26(12):1355-63.\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-cardiovascular-disorders","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bcar","sideBox":"Learn more about [BMC Cardiovascular Disorders](http://bmccardiovascdisord.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bcar/default.aspx","title":"BMC Cardiovascular Disorders","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Anaphylaxis, acute myocardial infarction, acute respiratory distress syndrome, myocardial injury, protracted anaphylaxis, floctafenine, meloxicam, nonsteroidal anti-inflammatory drug, epinephrine","lastPublishedDoi":"10.21203/rs.3.rs-6917956/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-6917956/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eBackground\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eProlonged anaphylaxis, especially symptoms that last several days, can lead to misdiagnosis and delays in treatment, especially when patients present with complications such as acute respiratory distress syndrome (ARDS) and secondary myocardial injury. A thorough review of medical history is very important for accurate diagnosis. Early recognition and intervention are essential for managing both the allergic response and pulmonary-cardiac injury.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCase presentation:\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWe present the case of a 70-year-old woman with no significant medical history who developed rapid respiratory failure and extremely elevated troponin levels. The patient was initially diagnosed with non-ST-segment elevation myocardial infarction (NSTEMI) complicated by pulmonary edema, and the patient's condition continued to worsen despite coronary intervention. A reevaluation revealed that anaphylaxis was potentially triggered by the recent use of floctafenine and meloxicam, which were taken as painkillers four days before admission. The administration of epinephrine led to a marked improvement in her condition, and she was successfully discharged without further complications.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusion\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eProtracted anaphylaxis, especially when complicated by ARDS and myocardial injury mimicking NSTEMI, requires careful diagnostic consideration. Clinicians must thoroughly evaluate patient history, particularly recent medication use, to avoid misdiagnosis. Epinephrine remains a crucial treatment in such cases, and prompt administration can be life-saving. This case highlights the diagnostic challenges of protracted anaphylaxis and the importance of comprehensive clinical assessment and timely intervention.\u003c/p\u003e\n\u003cp\u003eClinical trial number: not applicable.\u003c/p\u003e","manuscriptTitle":"Successful management of protracted anaphylaxis-induced severe acute respiratory distress syndrome masquerading as non-ST elevation myocardial infarction: a rare case report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-08-01 21:37:06","doi":"10.21203/rs.3.rs-6917956/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2025-10-31T11:15:34+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-08-18T21:53:56+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-08-17T13:40:20+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"196030524357029150424065271189102819661","date":"2025-08-08T18:28:41+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"309242020176436021545639639700659933954","date":"2025-08-08T14:31:02+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-08-06T03:30:13+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"98565627112343978083892899734374492924","date":"2025-08-03T22:35:57+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2025-07-29T06:49:49+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2025-06-27T12:45:34+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2025-06-27T08:54:54+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2025-06-27T08:51:51+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Cardiovascular Disorders","date":"2025-06-18T01:13:19+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-cardiovascular-disorders","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bcar","sideBox":"Learn more about [BMC Cardiovascular Disorders](http://bmccardiovascdisord.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bcar/default.aspx","title":"BMC Cardiovascular Disorders","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"998dffb7-e526-4a9f-97ff-4f479cd244ef","owner":[],"postedDate":"August 1st, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"published-in-journal","subjectAreas":[],"tags":[],"updatedAt":"2026-02-02T16:16:11+00:00","versionOfRecord":{"articleIdentity":"rs-6917956","link":"https://doi.org/10.1186/s12872-026-05565-7","journal":{"identity":"bmc-cardiovascular-disorders","isVorOnly":false,"title":"BMC Cardiovascular Disorders"},"publishedOn":"2026-01-28 15:58:14","publishedOnDateReadable":"January 28th, 2026"},"versionCreatedAt":"2025-08-01 21:37:06","video":"","vorDoi":"10.1186/s12872-026-05565-7","vorDoiUrl":"https://doi.org/10.1186/s12872-026-05565-7","workflowStages":[]},"version":"v1","identity":"rs-6917956","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-6917956","identity":"rs-6917956","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}