Legionnaires Disease in Immunocompromised Host

Legionella bacteria are aerobic, pleomorphic, gram negative bacilli found in fresh water environments and are usually transmitted through inhalation aerosols from contaminated water or soil. Legionnaire’s disease is a severe form of pneumonia caused by legionella species and can be community acquired or hospital acquired. The reported incidence of Legionnaires’ disease is approximately 1.4–1.8 cases per 100,000 persons and immunocompromised state is a very important risk factor. Some of the other important risk factors include old age, impaired cellular immunity, hematologic malignancies, solid organ transplantation, splenectomy, tumor necrosis factor-alpha inhibitors, chronic respiratory disease, diabetes and end stage renal disease. Legionella pneumophila serotype 1 is the most commonly reported cause of human Legionella infections. The pathogenesis of legionnaire’s disease involves invasion of alveolar macrophages and cell mediated immunity is the primary means of immune control. The prevalence of Legionnaires disease has risen possibly from increased awareness and reporting. The symptoms of the disease are nonspecific requiring a high index of suspicion in vulnerable hosts, as effective treatment could be life-saving. Sensitivity of urinary antigen testing is lower in immunocompromised patients because of higher likelihood of infections caused non L. pneumophila species. Extrapulmonary manifestations and higher mortality are particularly more common in immunocompromised patients than in immunocompetent hosts

A Review of the Incidence Diagnosis and Treatment of Spontaneous Hemorrhage in Patients Treated with Direct Oral Anticoagulants

Anticoagulation carries a tremendous therapeutic advantage in reducing morbidity and mortality with venous thromboembolism and atrial fibrillation. For over six decades, traditional anticoagulants like low molecular weight heparin and vitamin K antagonists like warfarin have been used to achieve therapeutic anticoagulation. In the past decade, multiple new direct oral anticoagulants have emerged and been approved for clinical use. Since their introduction, direct oral anticoagulants have changed the landscape of anticoagulants. With increasing indications and use in various patients, they have become the mainstay of treatment in venous thromboembolic diseases. The safety profile of direct oral anticoagulants is better or at least similar to warfarin, but several recent reports are focusing on spontaneous hemorrhages with direct oral anticoagulants. This narrative review aims to summarize the incidence of spontaneous hemorrhage in patients treated with direct oral anticoagulants and also offers practical management strategies for clinicians when patients receiving direct oral anticoagulants present with bleeding complications

Sudden Death in Athletes

Sudden death in athletes has been a tragic occurrence in the fields of sports medicine, cardiology, primary care, and pediatrics. By far the most common cause of unexpected death for a younger athlete on the competitive field is cardiac illness; usually that of congenital etiology. However, the use of anabolic steroids, peptide hormones, and stimulants have led to the emergence of acquired heart disease in younger and middle-aged athletes. In contrast, sudden death in an older athlete is typically due to atherosclerotic coronary artery disease. There are a variety of congenital heart illnesses that occur in the general population. Most of them categorize into structural and non-structural varieties. Congenital structural heart disease will generally affect blood flow within the heart and flow from the heart. Examples include hypertrophic obstructive cardiomyopathy (HOCM), arrhythmogenic right ventricular dysplasia (ARVD), and coronary artery anomalies. Non-structural heart disease involves defects in the electrical system of the heart which may induce unstable and dangerous arrhythmias. Examples include long QT syndrome, Brugada syndrome, Wolff-Parkinson-White (WPW) syndrome and catecholaminergic polymorphic ventricular tachycardia (CPVD). Other congenital structural and non-structural heart diseases exist and have been described previously in the setting of physical activity and athletics. Also, drug-induced cardiac effects are of important notice. Anabolic steroids and peptide hormones induce structural changes in the heart. Stimulants can cause dangerous arrhythmias. These conditions can clinically manifest as syncope/pre-syncope, and in some instances can present as a sudden, unexpected death. The associated mortality underscores the importance of early screening and identification of existing heart disease in athletes. Many athletes with pre-existing heart disease are often asymptomatic with a cardiac arrest being the initial manifestation of underlying pathology. The challenging aspect of identifying affected athletes is adequately screening the general population without excessive and unnecessary invasive testing. A thorough sports physical examination including an assessment of personal history, family history, physical exam, and an electrocardiogram can be a useful screening tool in asymptomatic and low-risk athletes. Higher risk athletes, such as those who have abnormal findings or have symptoms, may require more extensive testing. Upon arriving at a diagnosis, an athlete will undergo risk stratification. Then, a long-term treatment regime is initiated to minimize the risk of sudden cardiac death. Medical management is a common option, while surgical intervention is reserved for specific cases. Inserting an implantable cardioverter-defibrillator (ICD) is appropriate for anyone considered to be at risk for cardiac arrest secondary to a fatal arrhythmia. The decision to continue or abandon the sport of choice results from shared decision making between the physician and patient. The purpose of this article is to review the causes of sudden death in athletes with a significant focus on the most common etiologies in younger athletes and their presentation and evaluation

Pemetrexed Induced Life-threatening Anaphylaxis.

Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related death. The American Society for Clinical Oncology (ASCO) recommends platinum based regimens as the first-line of treatment for NSCLC. Pemetrexed, an antifolate agent, has been approved by the ASCO for the treatment of advanced non-squamous NSCLC and has been shown to be efficient for first-line, maintenance and second- or third-line treatment in this subgroup. It is administered intravenously over 10 minutes and is usually well tolerated with a very few side effects. There have been a few cases of anaphylaxis reported with pemetrexed use and most of the patients presented only with cutaneous manifestations. We present a patient with stage IV adenocarcinoma of the lung who developed a severe life threatening anaphylactic reaction requiring ventilatory support after administration of pemetrexed