Diagnosis Of Anaphylactic Shock Research Articles

Anaphylactic shock after mistletoe therapy

Life-threatening side effects of mistletoe therapy are mostly negated by physicians working in complementary medicine. This article reports on a case of life-threatening anaphylactic shock after carrying out mistletoe therapy. In patients with a carcinoid syndrome (flushes, diarrhea, bronchoconstriction) the diagnosis of anaphylactic shock can be masked by the findings of a neuroendocrine neoplasm. Before a planned complementary medicine mistletoe therapy patients should also be well-informed on rare life-threatening side effects.

Anaphylaxis shock with laryngeal edema: a case report

Anaphylaxis is a serious systemic or hypersensitivity reaction that rapid in onset and affect airway, breathing, and/or circulatory problems, and that is usually associated with skin and mucosal changes. Laryngeal edema is observed in 40-50% of death cases. A 49-year-old Asian female came to emergency department with chief complaint of difficulty to breath since 30 minutes ago after took cefixime and also common cold drug (Combination of paracetamol, glyceryl guaifenesin, phenylephrine, and Chlorpheniramine maleate). She also complained difficulty to speak and feeling strangulated on her neck. She ever had an allergic reaction, when she was child after suffering fever and common cold, but didn’t remember the name of the medication. History of food allergies was denied. On physical examination revealed, dyspnea and minimal tachycardia. Present of laryngeal edema, on auscultation stridor and wheezing on both lungs. Diagnosis of anaphylactic shock was made, and immediately giving epinephrin and followed by corticosteroid and antihistamine. The signs and symptoms of anaphylaxis might differ from patient to patient and impact the skin, gastrointestinal tract, respiratory system, and heart. Anaphylaxis fatal cases rise when laryngeal edema and cardiovascular organ involvement occur. The most frequent triggers are produced by food, venom from insects, and prescription drugs. The risk of death in anaphylaxis patients is decreased with prompt treatment. It is necessary to assess and maintain breathing, circulation, and airways in addition to determining the cause. Anaphylaxis can be potentially lethal or life-threatening, thus prompt identification and appropriate treatment are necessary.

ЭТИОЛОГИЧЕСКИЕ И КЛИНИЧЕСКИЕ ОСОБЕННОСТИ АНАФИЛАКТИЧЕСКОГО ШОКА У ПАЦИЕНТОВ, ГОСПИТАЛИЗИРОВАННЫХ В КЛИНИКУ ЭКСТРЕННОЙ МЕДИЦИНЫ

Introduction. Anaphylaxis is a severe generalized hypersensitivity reaction affecting more than one organ system that can start very quickly and symptoms can be severe or life-threatening. The profile of triggers and cofactors for anaphylaxis is age dependent and varies across geographies. The clinical manifestations of anaphylaxis are diverse, one of its most severe clinical phenotypes is anaphylactic shock. Aim. To assess the significance of various groups of triggers, cofactors and clinical features of anaphylactic shock in patients hospitalized in the Department of Allergology and Immunology of the Kazan City Clinical Hospital No. 7. Material and methods. A retrospective analysis of 107 medical records of inpatients hospitalized in the Department of Allergology and Immunology of City Clinical Hospital No. 7 with a diagnosis of anaphylactic shock (T78.0, T78.2, T80.5, T88.6) was carried out for three calendar years (from 01.01.2018 to 31.12.2020). Statistical data processing was carried out using the Statistical Package for Social Sciences (v.18.0). Results and discussion. It has been shown that medicines were the most common trigger for anaphylactic shock in hospitalized patients, while food and insect bites led to the development of shock much less frequently and with approximately the same frequency. The vast majority of patients did not have concomitant diseases, and also did not take concomitant therapy, which are risk factors for the severe course of anaphylaxis. Skin changes were the most frequent symptom, supplementing the clinic of anaphylactic shock, followed, approximately with equal frequency, by gastrointestinal and respiratory symptoms, neurological symptoms were most rarely recorded. Conclusion. To verify the trigger as the cause of anaphylactic shock, it is necessary to conduct an allergological examination after the resolution of its symptoms. To assess the influence of exogenous and endogenous cofactors on the occurrence of anaphylaxis and the severity of its course, it is necessary to conduct prospective studies.

Anaphylactic shock with pulmonary eosinophilic infiltration due to honeybee attack in a donkey: case report

ABSTRACT A case of a donkey attacked by Africanized honeybee is reported here with clinical signs of agitation, dehydration, congestion of the ocular mucous membranes, tongue edema, tachycardia and inspiratory dyspnea, and progression to death. At necropsy, diffuse, severe subcutaneous edema at face and cervical regions and severe diffuse pulmonary hyperemia with abundant edema without parenchymal collapse were observed. Microscopically, marked, diffuse deep dermis and panniculus carnosus edema and marked diffuse alveolar edema, with moderate population of eosinophils predominantly around larger caliber vessels were noted. The final diagnosis of anaphylactic shock was supported by history, clinical signs, and anatomic pathology findings. This is the first report of a honeybee attack with pulmonary eosinophilic infiltration in a mammal.

Trends, characteristics, and incidence of anaphylaxis in 2001-2010: A population-based study

Anaphylaxis is a potentially life-threatening systemic allergic reaction. We aimed to determine the incidence rate and causes of anaphylaxis during a 10-year period in Olmsted County, Minnesota. Using the resources of the Rochester Epidemiology Project, a comprehensive records linkage system, we performed a population-based incidence study in Olmsted County, Minnesota, from 2001 through 2010. All cases with a diagnosis of anaphylactic shock and 20% of cases with related diagnoses were manually reviewed. The relationships of age group, sex, and year of anaphylaxis with incidence rates were assessed by fitting Poisson regression models. Six hundred thirty-one cases of anaphylaxis were identified. The median age was 31years (interquartile range, 19-44years). The overall age- and sex-adjusted incidence rate was 42 (95% CI, 38.7-45.3) per 100,000 person-years. There was a significant increase in the overall incidence of anaphylaxis during the study period, with an average increase of 4.3% per year (P<.001). In addition, there was a 9.8% increase per year in the incidence rate of food-related anaphylaxis. Food-related anaphylaxis was most common in children aged 0 to 9years, venom-related anaphylaxis was most common in those 20 to 39years of age, and medication-related anaphylaxis was most common in those 30 to 39years of age. The overall incidence rate of anaphylaxis was 42 per 100,000 person-years from 2001-2010 in Olmsted County, Minnesota. The incidence of anaphylaxis increased over time,and several inciting triggers were uniquely associated withdifferent age groups.

Severe anaphylaxis reaction from dipyrone without a history of hypersensitivity. Case report

IntroductionThe safety of dipyrone has been the object of numerous debates, since severe allergic reactions to it can occur with an estimated incidence of 1 in 5000 parenteral administrations. Clinical findingsWe report the case of one patient who, after an infusion with dipyrone, presented coughing, pharynx itch, dyspnea, generalized cyanosis, and decreased consciousness. The diagnosis of anaphylactic shock without a history of hypersensitivity to the medication was made, and despite treatment with orotracheal intubation, adrenaline, hydrocortisone, sodium chloride, and sodium bicarbonate, it was fatal for the patient. ConclusionCases of severe hypersensitivity without antecedents can be present in patients, which makes it important to recognize this risk in our patients.

Reacción de anafilaxia grave por dipirona sin antecedente de hipersensibilidad. Informe de caso

IntroductionThe safety of dipyrone has been the subject of several debates; severe allergic reaction can occur; its incidence is 1 in 5.000 parenteral administrations. Clinical findingsA case of a patient who following an infusion with dipyrone has a cough, pharyngeal pruritus, dyspnea, cyanosis and generalized impairment of consciousness. The diagnosis of anaphylactic shock by dipyrone in a patient without hypersensitivity precedent is reported, despite treatment with endotracheal intubation, adrenaline, hydrocortisone, sodium chloride and sodium bicarbonate, which proved fatal. ConclusionSerious cases of hypersensitivity may occur in patients with no history of it; it is important recognized this risk in our patients.

Suspected Anaphylactic Shock Associated with Rocuronium in an Infant: A Case Report

We report a case of severe anaphylactic shock in a 5-month-old infant who was scheduled to undergo an external inguinal hernia repair under general anesthesia. Rocuronium used for anesthesia induction was the most likely cause of anaphylaxis. High levels of serum tryptase and histamine detected in the blood sample collected during the anaphylactic reaction confirmed the diagnosis of anaphylactic shock. The patient’s clinical status improved within 90 min of intervention by the intravenous injection of vasopressors and a steroid. Surgery was canceled, and the patient stayed in the pediatric intensive care unit (PICU) under artificial ventilation for 5 h before safe extubation. The patient achieved full recovery the next day, without any sequelae. The rescheduled surgery was successfully completed 5 months later under general anesthesia without the use of neuromuscular blocking agents.

Cetirizine‐induced anaphylaxis: a rare adverse drug reaction

A 30-year-old female patient was prescribed oral cetirizine 10 mg at night for the treatment of chronic idiopathic urticaria. Within 15 min of oral ingestion of cetirizine 10 mg, the patient experienced severe pruritis and urticarial eruption all over the body. She developed severe breathlessness and was unable to speak. The patient became restless, disoriented and lost consciousness. She was rushed to the emergency room. Her pulse and blood pressure were unrecordable and air entry was decreased in both lungs. A diagnosis of anaphylactic shock was made. Cardiopulmonary resuscitation was started and epinephrine 0.5 mg of 1:10 000 was given intravenously. She also received intravenous crystalloid. After approximately 30 min, the pulse rate increased to 100 beats min−1 and blood pressure to 124/80 mmHg. Hydrocortisone 100 mg was then given intravenously. The patient remained haemodynamically stable. She had no previous history of allergic reactions to any drug. There was no history of concomitant use of any other medication or alcohol intake, nor of previous exposure to cetirizine or any other piperazines. The patient received only one oral dose of cetirizine. The causality assessment of the adverse drug reaction (ADR) by Naranjo Algorithm was 7, putting it in a ‘probable’ ADR category [1]. The ADR was reported to the peripheral pharmacovigilance centre of the state under the National Pharmacovigilance Programme, India. Histamine-1 (H1) receptor antagonists have an established and valued place in the symptomatic treatment of various immediate hypersensitivity reactions. Nevertheless, it is a little known fact that although H1 receptor antihistamines are used in the treatment of drug-mediated allergy, they themselves can provoke allergic reactions. Although they have shown good tolerance in humans, no currently available antihistaminic is completely free from potential adverse effects under all circumstances [2]. There have been several reports of cetirizine causing multiple fixed drug eruptions and urticaria [3–6]. However, anaphylaxis due to oral ingestion of cetirizine is extremely rare. All the available H1 receptor antagonists are reversible competitive inhibitors of the interaction of histamine with H1 receptors. Cetirizine, a human metabolite of hydroxyzine, is a selective H1 receptor antagonist belonging to the second-generation piperazine class. Cetirizine is well absorbed orally and is excreted in the urine mainly in the unmetabolized form. Many drug reactions attributable to allergic phenomena respond to therapy with H1 antagonists, particularly those characterized by itch, urticaria, and angio-oedema; serum-sickness reactions also respond to intensive treatment. In humans, during hypersensitivity reactions, oedema formation and itch are effectively suppressed by histamine antagonists. Other effects, such as hypotension, are less well antagonized. This may be explained by the participation of other types of histamine receptors and by effects of other mast cell mediators such as prostaglandins, eicosatetratenoic acid derivatives, leukotrienes and others. Prophylactic treatment with a H1 antagonist may reduce symptoms of the hypersensitivity reaction to a tolerable level. However, in a patient with known hypersensitivity to cetirizine, repeat administration of cetirizine or hydroxyzine is contraindicated [7]. The exact mechanism by which cetirizine can cause anaphylaxis is not known, but may be linked to the piperazinic ring that is well known as an antigen [8]. Also, cetirizine has no effect on mast cell activation [9]. In conclusion, even though the safety of cetirizine has been widely established, there is an extremely rare chance of it causing anaphylaxis. Cetirizine may be used in the treatment of anaphylaxis. Hence this possibility (and similarly with other antihistamines) needs to be considered in the differential diagnosis of a patient not responding to treatment or deteriorating. Cetirizine may also mimic the underlying disease that led to its intake [10].

Anaphylactic Shock with Multiorgan Failure in a Cyclist after Intravenous Administration of Actovegin

Letters4 March 2008Anaphylactic Shock with Multiorgan Failure in a Cyclist after Intravenous Administration of ActoveginLuis Maillo, MDLuis Maillo, MDFrom Hospital Ramón y Cajal, 28039 Madrid, Spain.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-148-5-200803040-00022 SectionsAboutVisual AbstractPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Background: Actovegin (Nycomed Pharma, Zurich, Switzerland) is a calf-blood extract free of proteins and filtrated to remove prions. It is marketed in some countries for the treatment of cerebrovascular and metabolic disorders, peripheral flow disorders, burns, and wounds (1–4) and is used by some athletes to improve blood oxygenation without raising hematocrit, purportedly by promoting glucose and oxygen uptake by cells (5, 6). Actovegin has been banned by the International Olympics Committee since 2000.Objective: To report a case of anaphylaxis with use of Actovegin.Case Report: A 22-year-old man who was an amateur cyclist with no significant medical history self-injected intravenous Actovegin, 5 mL, over 5 minutes the night before a competition. He had administered the drug 1 year earlier with no consequences. Ten minutes later, the patient developed fever with rigors, abdominal pain, and vomiting. Three hours later, after taking anti-inflammatory medication with no effect, the patient presented to the emergency department. He was conscious and oriented, with a blood pressure of 100/60 mm Hg, heart rate of 87 beats/min, temperature of 37.9 °C, and normal oxygen saturation. His physical examination was normal except for epigastric and right upper quadrant pain with hepatomegaly on palpation. Initial blood analysis showed a blood urea nitrogen level of 19.3 mmol/L, creatinine level of 106.76 μmol/L (1.4 mg/dL), alanine aminotransferase (ALT) level of 566 U/L, aspartate aminotransferase (AST) level of 335 U/L, lactate dehydrogenase (LDH) level of 6.46 µkat/L, and bilirubin level of 15.74 μmol/L (0.92 mg/dL). Hemoglobin level was 138 g/L, leukocyte count was 2.1 × 109 cells/L, and platelet count was 133 × 109 cells/L. His electrocardiogram and chest radiograph were normal. During his stay in the emergency department, his blood pressure decreased to 77/50 mm Hg and liver test values increased to 824 U/L ALT, 564 U/L AST, and13.62 µkat/L LDH.The patient was transferred to the intensive care unit, where he was sleepy but still conscious. He remained hypotensive despite a fluid challenge and required dopamine, 10 μg per kg of body weight per minute, to maintain his blood pressure. He received nasal oxygen at 2 L/min. His arterial blood gas values were pH, 7.42; PCO2, 30 mm Hg; PO2, 164 mm Hg; and HCO3, 20 mmol/L. On arrival at the intensive care unit, his blood analysis showed a glucose level of 8.55 mmol/L (154 mg/dL), creatinine level of 109.8 µmol/L (1.44 mg/dL), ALT level of 796 U/L, AST level of 633 U/L, LDH level of 11.00 µkat/L, lactic acid level of 2.44 mmol/L, prothrombin activity of 47%, activated cephalin time of 62 seconds, international normalized ratio of 1.6, and fibrinogen level of 4.38 µmol/L. The rest of the blood analysis, including amylase, creatinine phosphokinase, and ammonia, were normal. A urine toxicology screening was negative.The patient was given an empirical antibiotic for a temperature of 38 °C. Thoracic–abdominal computed tomography showed enlargement of the inferior vena cava with increase of the suprahepatic veins. A follow-up abdominal ultrasonography showed hepatomegaly and moderate ascites but no Budd–Chiari syndrome. Indirect and direct antiglobulin testing (Coombs test) were normal.Over time, the patient's hepatic profile and coagulopathy normalized, and dopamine therapy was titrated downward and discontinued. After 2 days of supportive treatment, the patient was discharged from the intensive care unit to the general ward with a diagnosis of anaphylactic shock after intravenous administration of Actovegin, hypoxic hepatitis, and prerenal acute renal failure.Discussion: Although this case is no more than a hypersensitivity reaction type I (anaphylactic shock), it highlights the life-threatening adverse effects that may accompany administration of performance-enhancing (“doping”) substances. The particular drug in this case was Actovegin, a substance with few indications that is marketed in a few countries. It was allegedly used by some cyclists in the 2000 Tour de France because it has properties similar to those of erythropoietin without raising hematocrit. Life-threatening anaphylaxis revealed that this individual had been doping, but most cases remain unknown. We think the medical community should be aware of the problem, especially because these substances are prescribed by physicians and very few articles describe these cases in the scientific literature (7, 8).Conclusion: Intravenous Actovegin can cause life-threatening anaphylaxis.Luis Maillo, MDHospital Ramón y Cajal28039 Madrid, Spain

Fístula de quiste hepático hidatídico a vena porta: revisión de la literatura

En la bibliografía hay solamente 3 publicaciones sobre la invasion de la vena porta por quiste hidatídico. Es una complicación infrecuente que se debe tener en cuenta en el diagnóstico del shock anafiláctico. El motivo de consulta puede ser variado; desde dolor abdominal y fiebre relacionados con el quiste hasta complicaciones como la hipertensión portal por la cavernomatosis, o una reacción anafiláctica por la fuga de material antigénico del quiste. Entre las pruebas diagnósticas, la ecografía Doppler y la tomografía computarizada identifican quistes hepáticos e imágenes compatibles con cavernomatosis, pero la resonancia magnética detecta la presencia de múltiples vesículas hijas intraportales y la comunicación entre el quiste residual y la vena porta. El tratamiento de elección es la intervención quirúrgica, con extirpación del quiste e instilación de soluciones escolicidas, además de tratamiento con albendazol, comenzando 4 días antes de la extirpación y manteniéndolo durante más de 4 semanas. We have found only 3 publications in the literature that describe portal vein invasion by a hydatid cyst. This complication is very uncommon but should be kept in mind in the diagnosis of anaphylactic shock. Clinical presentation can vary from abdominal pain and fever to portal hypertension or anaphylactic reaction due to leaking of antigenic material from the cyst. Ultrasound and computed tomography scan can identify hydatid cysts and cavernomatosis, but magnetic resonance imaging shows the presence of multiple daughter vesicles replacing the lumen of the portal vein and a communication between the residual cyst and the portal vein. The treatment of choice is surgery, including removal of the cyst and local instillation of scolicide solution. In addition to surgery, administration of albendazole is recommended. Administration should begin 4 days before extirpation and should be continued for more than 4 weeks.

Serum tryptase levels in adverse drug reactions

We evaluated the usefulness of individual tryptase levels and variations after adverse drug reactions in 64 patients. Our aim was to find a tool for the diagnosis of drug allergy. Thirty-seven subjects were confirmed to have drug allergy, 12 had nonsteroidal anti-inflammatory drug (NSAID) reactions, five had negative controlled drug challenges (NAAR), and 10 had symptoms after placebo intake (PLA). Serum tryptase levels greatly increased after anaphylactic shocks (2242%) and anaphylaxis (710.5%). Patients with allergic urticaria and those with idiosyncratic responses to acetylsalicylic acid (ASA) exhibited a small increase in serum tryptase (49.5% and 38.2%, respectively). In the other two groups (NAAR and PLA), no variation in this serum protease was observed. The time of appearance of the serum tryptase peak differed considerably among patients with similar clinical reactions (from 30 min to 6 h) and was independent of the latent period, severity of symptoms, or the amount of tryptase released. We conclude that serum tryptase determinations are helpful in the diagnosis of anaphylactic shock and anaphylaxis, but serial measurements may be needed to confirm mast-cell participation in milder reactions.

Anaphylactoid Reaction in a Surgeon to Surgical Rubber Gloves

Anaphylactoid Reaction in a Surgeon to Surgical Rubber Gloves