Project description:We report a case of Kounis syndrome that led to shock after protamine administration during percutaneous coronary intervention (PCI). A man in his 50s was admitted to the nearest hospital following the onset of acute myocardial infarction. Coronary angiography showed a single-vessel lesion in the left anterior descending artery (LAD). He was admitted for PCI. After heparin administration, the procedure was completed by implantation of a coronary stent with the usual procedure. For hemostasis, following protamine administration, the patient went into shock. Subsequently, electrocardiography showed bradycardia with ST-segment elevation at leads II, III, aVF, and V3-6. Cardiopulmonary resuscitation was started immediately. As pulseless electrical activity continued, extracorporeal membrane oxygenation (ECMO) was introduced. Coronary angiography demonstrated coronary spasm in the LAD. He was withdrawn from the ECMO on day 7. His intradermal tests were positive for protamine in the convalescent phase. The patient was diagnosed with protamine shock and type I Kounis syndrome. Protamine shock is not uncommon, but Kounis syndrome may be hidden in it. Thus, similar cases should not be treated as a simple protamine shock. <Learning objective: This case report aimed to determine 1) the mechanism of protamine shock and its risk factors, and 2) the pathogenesis and type of Kounis syndrome in a patient who developed protamine shock, and 3) the significance of ST-elevation during anaphylactic shock.>.
Project description:RationaleLocal anesthesia is a widely used technique for emergency wound closure, with lidocaine among the most commonly employed local anesthetics. Allergic reactions to lidocaine are rare, with anaphylaxis being even more uncommon.Patient concerns and diagnosisThis report describes a 72-year-old male patient who presented with a right foot injury and underwent wound suturing under lidocaine local anesthesia. Although the procedure went smoothly, the patient developed dizziness, cold sweats, hypotension, and bradycardia 30 minutes later, leading to a diagnosis of anaphylaxis due to lidocaine allergy.Interventions and outcomesImmediate treatment for anaphylactic shock was initiated, including intramuscular administration of adrenaline, fluid resuscitation, anti-inflammatory agents, antihistamines, oxygen therapy, and symptomatic supportive care. Within 20 minutes of active treatment, the patient's symptoms were effectively controlled. The patient was safely discharged after 24 hours of observation. Health education was provided to enhance self-management skills.LessonsAlthough rare, anaphylaxis induced by lidocaine can be fatal. Early recognition, prompt intervention, thorough preoperative assessment, and careful postoperative monitoring are critical to improving survival rates.
Project description:BackgroundAcute myocardial infarction (AMI) can be induced by several factors. However, AMI induced by Kounis syndrome (an allergic reaction) is extremely rare and is highly susceptible to misdiagnosis.Case summaryA 70-year-old man presented after suffering an allergic reaction that caused chest pain triggered upon eating ice cream. Troponin I was found to be elevated, and an electrocardiogram showed ST-segment elevation. The diagnosis was AMI. He underwent two coronary angiographies, with one intravascular ultrasound during hospitalization showing no evidence of atherosclerotic coronary artery disease. The final diagnosis was vasospastic myocardial infarction due to Kounis syndrome. The patient was then treated with hydrocortisone and intravenous antihistamines, and his chest pain symptoms resolved.ConclusionAllergic reactions (such as Kounis syndrome) can cause serious damage to the heart. Physicians should be alert to the consequences and avoid misdiagnosis.
Project description:Immune-mediated acute coronary syndrome, also known as Kounis syndrome (KS), is an underrecognized and challenging diagnosis. In this case report, we present a case of cardiac arrest secondary to iodinated contrast allergy requiring emergent cardiac catheterization and hemodynamic support secondary to type 2 KS. KS necessitates a high index of clinical suspicion by the treating physician in order to address both the hypersensitivity reaction and its cardiac implications.Learning objectivesKounis syndrome (KS) is a clinically distinct entity from anaphylaxis; managing KS in the same way as anaphylaxis can worsen cardiac demand and ischemia. In addition, KS may present as coronary vasospasm or plaque rupture; regardless, percutaneous coronary intervention (PCI) should be performed as worse outcomes have been described in cases where PCI is not performed or delayed.
Project description:Patent blue is one of the most used dyes for the identification of sentinel lymph nodes in breast cancer. This report describes a case of an anaphylactic shock reaction to patent blue dye in a patient with cross-reactivity to methylene blue. Therefore, after allergy confirmation, the operation was repeated avoiding blue dye and an alternative labelling technique with 99mTc albumin nanocolloids was used.
Project description:Anaphylactic shock is characterized by elevated immunoglobulin-E (IgE) antibodies that signal via the high affinity Fc epsilon receptor (Fc epsilonRI) to release inflammatory mediators. Here we report that the novel cytokine interleukin-33 (IL-33) potently induces anaphylactic shock in mice and is associated with the symptom in humans. IL-33 is a new member of the IL-1 family and the ligand for the orphan receptor ST2. In humans, the levels of IL-33 are substantially elevated in the blood of atopic patients during anaphylactic shock, and in inflamed skin tissue of atopic dermatitis patients. In murine experimental atopic models, IL-33 induced antigen-independent passive cutaneous and systemic anaphylaxis, in a T cell-independent, mast cell-dependent manner. In vitro, IL-33 directly induced degranulation, strong eicosanoid and cytokine production in IgE-sensitized mast cells. The molecular mechanisms triggering these responses include the activation of phospholipase D1 and sphingosine kinase1 to mediate calcium mobilization, Nuclear factor-kappaB activation, cytokine and eicosanoid secretion, and degranulation. This report therefore reveals a hitherto unrecognized pathophysiological role of IL-33 and suggests that IL-33 may be a potential therapeutic target for anaphylaxis, a disease of considerable unmet medical need.
Project description:BackgroundKounis syndrome is the occurrence of acute coronary syndrome precipitated by an allergic reaction in the presence or absence of underlying coronary artery disease. The syndrome is explained by the effect of released inflammatory mediators on the coronary arteries and platelets.Case summaryWe report an uncommon case of Kounis syndrome Type II in a 65-year-old man 24 h after being bitten by a hymenoptera. Clinical context, electrocardiogram, coronary angiography, and enhanced cardiac magnetic resonance imaging (MRI) imaging modality are presented.DiscussionAwareness and understanding of this syndrome is essential for starting early and appropriate therapy, thereby preventing life-threatening events. Accordingly, we highlight the importance of enhanced cardiac MRI to complete the assessment of this entity.
Project description:Kounis syndrome (KS) is an acute coronary disorder associated with anaphylactic reactions. The purpose of this report is to identify the features of KS triggered by contrast media on the basis of our experience and from literature review. We have described a case and literature review of KS triggered by injection of contrast media. Including the present case, we reviewed eleven cases of KS. Six cases developed KS in diagnostic radiology departments. KS could be induced by intravenous injection of contrast media in the radiology department. Radiologists should recognize this critical condition to ensure appropriate management.
Project description:Coronary stent thrombosis is a life-threatening condition induced by multiple factors, including allergic reactions. A 64-year-old man presented with stent thrombosis in the left anterior descending artery and multiple cardiorespiratory arrests immediately after the first dose of the BNT162b1 mRNA vaccine. He underwent emergent percutaneous coronary intervention. Anaphylaxis-induced stent thrombosis, or type III Kounis syndrome, is a highly possible diagnosis. Cardiogenic shock can hide the skin manifestations of anaphylaxis, making this syndrome challenging to diagnose. This clinical case underscores the importance of surveillance for at least 30 minutes after vaccine administration, especially in patients at risk.
Project description:Haemocoagulase injection is a mixture of purified enzymes isolated from the venom of Bothrops atrox, which is used for the prevention and treatment of haemorrhage. It is a relatively safe pharmacological agent that does not require a skin test prior to administration. However, following a literature search, 14 reported cases of anaphylactic shock caused by haemocoagulase injection were identified, including one lethal case in China. Using SDS-PAGE and protein identification, four primary components in haemocoagulase injection were characterized, including one metalloproteinase, which may be a thromboplastin-like enzyme, and two serine proteinases, which may be thrombin-like enzymes. Administering concentrated haemocoagulase injections failed to provoke a positive skin reaction in allergic patients. Basophil activation tests revealed that haemocoagulase injections did not upregulate cluster of differentiation 63 or C-C chemokine receptor type 3 expression. These findings suggest that haemocoagulase injection may cause fetal anaphylaxis. Although it is difficult to determine a clear conclusion without being able to evaluate the patients that underwent haemocoagulase injection-induced shock, it is unlikely that the venomous components of haemocoagulase injection cross-react with common allergens in allergic patients. It is possible that haemocoagulase injection-induced anaphylaxis is caused by its additive components, such as mannitol and succinylated gelatin.