TITLE OF CASE A successful termination of bidirectional ventricular tachycardia followed by intravenous lidocaine. KEY CLINICAL MESSAGE Bidirectional ventricular tachycardia, once a hallmark of severe digitalis toxicity, can also result from causes like catecholaminergic polymorphic VT, aconite poisoning, genetic channelopathies, myocarditis, and myocardial infarction. While electrical cardioversion is recommended for unstable VT, tailored treatments, including intravenous lidocaine, may be effective for BVT-associated myocardial infarction. INTRODUCTION Bidirectional ventricular tachycardia (BVT) is a rare and life-threatening arrhythmia with a limited differential diagnosis, including digitalis toxicity, catecholaminergic ventricular tachycardia, aconite poisoning, hereditary channelopathy syndromes, myocarditis and myocardial infarction[1 2]. The precise cause of BVT remains poorly understood. Current guidelines for ventricular tachycardia management typically recommend beta-blockers, propafenone, or flecainide[3]. However, intravenous lidocaine has not been previously recognized as a treatment for BVT. We report a case of a patient presenting to the emergency department with chest pain and hypotension, diagnosed with unstable BVT, which was successfully treated with intravenous lidocaine, restoring normal sinus rhythm. The patient was stabilized, transferred to the cardiac care unit, and later diagnosed with myocardial infarction after cardiac catheterization. The pathophysiology of BDVT is similar to other forms of ventricular tachycardia, involving delayed afterdepolarization, reentry, and automaticity. Given that lidocaine is effective for ventricular tachycardia associated with MI, it may also be beneficial in BVT cases associated with myocardial infarction. KEYWORDS Ventricular, Tachycardia, Myocardial Infarction, Lidocaine, Acute Coronary Syndrome. CASE HISTORY/EXAMINATION An Asian male who was in his 40s with a significant medical history of morbid obesity (BMI of 31), ischemic cardiomyopathy, and a decreased left ventricular ejection fraction (19%) without a prior history of cardiac arrhythmias visited the ED with 30 minutes of central chest discomfort radiating to the left arm. The patient was alert with a blood pressure of 90/69 mmHg, a heart rate of 167 beats per minute, a respiratory rate of 22 breaths per minute, and a capillary refill time of less than 2 seconds. No signs of heart failure were observed. A 12-lead electrocardiogram (ECG) showed significant tachycardia with a rate of 164 beats per minute and bidirectional QRS morphology strongly suggestive of BVT as shown in Figure 1. Following the initial evaluation, the patient remained hypotensive, requiring continuous cardiac monitoring and immediate cardiology consultation with the differential diagnosis of ischemic cardiomyopathy-related VT, acute myocardial infarction, and toxin-related BVT. The patient was subsequently treated with 100 mg of intravenous lidocaine over three minutes instead of synchronized electrical cardioversion since it could worsen his ventricular ejection fraction. Five minutes after lidocaine had been administered, the ECG returned to sinus rhythm as shown in Figure 2 with a blood pressure of 120/58 mmHg. Laboratory studies revealed a troponin-T level of 520 ng/L, while the test results were unremarkable. Digoxin level was not determined due to the absence of a history of drugs or toxin-related ingestion. INVESTIGATIONS Laboratory studies revealed a troponin-T level of 520 ng/L, while the test results were unremarkable. Digoxin level was not determined due to the absence of a history of drugs or toxin-related ingestion. DIFFERENTIAL DIAGNOSIS

DRESS Syndrome Without Eosinophilia Presented with Extensive Skin Rash and Acute Respiratory FailureNattanicha Chaisrimaneepan, MD1, Corley Pruneda MD2, Marwan Elmassry MD1, and Mahmoud Abdelnabi, MD, MSc11 Department of Internal Medicine, Texas Tech University Health Science Center, Lubbock, Texas2 Dermatology Department, Texas Tech University Health Sciences Center, Lubbock, TexasCorresponding author: Nattanicha Chaisrimaneepan, MD Department of Internal Medicine, Texas Tech University Health Sciences Center, 3601 4th St., Lubbock, TX 79430 (e-mail: nattanicha.chaisrimaneepan@ttuhsc.edu)

EBV-associated CNS Infection in an Immunocompetent Adult: A Case Report and Literature ReviewGwyn Srifuengfung, MD1, Pichatorn Suppakitjanusant, MD1, Nattanicha Chaisrimaneepan, MD21Department of Neurology, Texas Tech University Health Sciences Center, Lubbock, TX, USA2Department of Medicine, Texas Tech University Health Sciences Center, Lubbock, TX, USACorresponding author: Nattanicha Chaisrimaneepan, MDDepartment of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX, USA3601 4th St, Lubbock, TX 79430Email: nattanicha.chaisrimaneepan@ttuhsc.eduDisclosure: All the authors declare no conflict of interest.Verbal and written consent was obtained from the patient to publish his case.AbstractEpstein-Barr virus (EBV) infections typically manifest with respiratory symptoms, lymphadenopathy, and, rarely, central nervous system (CNS) involvement. We report an uncommon case of an immunocompetent 18-year-old male with altered mental status due to EBV-associated CNS infection. The patient, with a recent history of infectious mononucleosis, presented with fever and meningeal irritation signs. Initial investigations revealed leukocytosis, atypical lymphocytes, and positive heterophile antibodies, but a head CT scan was normal. Empirical treatment for bacterial meningitis was initiated. Results of further assessments, including a positive EBV serology, a consistent cerebrospinal fluid analysis and positive EBV DNA in the CSF led to the diagnosis of EBV-associated CNS infection-more specifically meningoencephalitis. Neuroimaging, including MRI, showed no abnormalities. The patient improved with supportive care and a four-day course of acyclovir. We discussed the challenges in diagnosing EBV-associated CNS infection, emphasizing the role of CSF PCR in confirming the diagnosis. The importance of ruling out other infections is highlighted, and the heterogeneity in the mechanism of infection is explored. The case underscores the significance of recognizing an isolated, active EBV infection in young adults with altered mental status, especially when more common causes have been excluded.Keywords: Epstein-Barr virus, CNS infection, aseptic meningitis, altered mental status, CSF PCR, viral encephalitis.

IntroductionStatin belongs to a medication class of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) inhibitor. It is the most significant drug used for lipid-lowering and cardiovascular disease prevention1. A wide range of statin myopathy has been reported including myalgia, myopathy, myositis, or rhabdomyolysis. Statin-induced immune-mediated necrotizing myopathy (IMNM) is a relatively rare side effect with an incidence of 2 or 3 of every 100,000 patients taking statins2. Many different findings help differentiate toxic non-inflammatory effects from immune-mediated myopathy due to statins1. We report a case of statin-induced IMNM with oropharyngeal involvement.

IntroductionCoccidioidomycosis, known as Valley Fever, is the disease caused by the inhalation of arthroconidia from the soil-dwelling dimorphic fungi,Coccidioides immitis and Coccidioides posadasii [1]. In the United States, coccidioidomycosis is endemic to the southwestern part of the country, with most cases located in the San Joaquin Valley of California and Southern Arizona. The incidence of coccidioidomycosis is approximately 10,000 cases reported annually [1,2]. Coccidioidomycosis may affect any demographic, but primarily affects those aged 40-60 years old and has a slight male predominance. Clinical manifestations range from asymptomatic to disseminated infection depending on the patient’s immune status.Cutaneous manifestations in coccidioidomycosis can be classified as reactive or organism-containing lesions in secondary or primary cutaneous infection [3]. Sweet syndrome, or acute febrile neutrophilic dermatosis, is an inflammatory, non-infectious skin reaction rarely observed as one of the reactive skin manifestations of coccidioidomycosis. Patients with Sweet syndrome clinically present with fever, leukocytosis with neutrophilia, and painful erythematous papules, plaques, pustules, and nodules commonly appearing on the upper limbs, trunk, head, and neck [4]. Here, we present a case of coccidioidomycosis associated with Sweet’s syndrome.