Bottom Line: Vijay and Fattah1 state that Lemierre’s syndrome typically presents in young adults who were previously healthy. In a case series of 222 patients who fit the “Lemierre’s syndrome case presentation, the median age was 19 years and 89% of patients were aged 10 to 35 years.”2 Its four key elements are “primary oropharyngeal infection within 4 weeks, suppurative thrombophlebitis of the internal jugular (IJ) vein, metastatic septic emboli, and [a] causal association with F necrophorum.” It should be “suspected in those with a recent history of oropharyngeal infection presenting with fever and rigors, with or without evidence of metastatic lesions, particularly respiratory symptoms (pleuritic chest pain, dyspnoea, haemoptysis).” Penicillin/beta-lactamase inhibitor, penicillin plus metronidazole, and carbapenem” are “appropriate empirical antibiotic regimens….There are no controlled trials to guide management, but most sources recommend between 2–6 weeks of antibiotics in total.” Review article provides four computed tomography pulmonary angiogram (CTPA) images with red arrows that indicate locations of multiple peripheral nodular lesions.
1. Vijay V, Fattah Z. Lesson of the month 1: Lemierre‘s syndrome: a reminder of the ‘forgotten disease.’ Clin Med (Lond). 2018 Feb;18(1):100-102. doi:10.7861/clinmedicine.18-1-100.
2. Riordan T. Human infection with Fusobacterium necrophorum (Necrobacillosis), with a focuson Lemierre’s syndrome. Clin Microbiol Rev. 2007 Oct;20(4):622-59. doi:10.1128/CMR.00011-07.
The Bottom Line: The mechanisms for fever-induced bradycardia are not completely understood. It is well known that many infectious agents can cause acute myocarditis and induce cardiac conduction abnormalities. One study suggested that relative bradycardia due to a specific disease has no predictive value in making a diagnosis. However, another suggests that relative bradycardia in a single patient can be helpful in arriving at a tentative diagnosis.
Mittal J, Estiverne C, Kothari N, Reddi A. Fever and Relative Bradycardia: A Case Presentation and Review of the Literature. Int J Case Rep Short Rev. 2015;1(1): 004-008.
In many noninfectious and infectious conditions, the heart rate does not increase with a rise in temperature. This phenomenon is called pulse-temperature deficit which many clinicians refer to as relative bradycardia. A caveat to this rule is that a patient must have a temperature of at least 102 F in order to better appreciate this pulse temperature relationship
The Bottom Line: Inflammatory idiopathic myopathies (IIM) are a group of rare autoimmune diseases characterized by proximal skeletal muscle weakness, raised muscle enzymes and extramuscular organ involvement, most frequently the lungs, resulting in interstitial lung disease (ILD). Numerous autoantibodies are associated with the disease, many linked to different clinical phenotypes. Polymyositis predominantly presents with proximal symmetrical muscle weakness, while dermatomyositis is characterized by skin and muscle involvement; both are associated with extramuscular features.
Clark, K., & Isenberg, D. (n.d.). A review of inflammatory idiopathic myopathy focusing on polymyositis. European Journal of Neurology., 25(1), 13-23.
The main aims of treatment are to suppress inflammation, improve muscle power and prevent chronic damage to muscles and extramuscular organs. However, there is a lack of robust data to guide treatment. Glucocorticoids remain the mainstay of treatment in IIM. Initial dosing is approximately 0.5 mg/kg of prednisolone, but the many side effects of steroids encourage a reducing regime over the first 2 months. Methotrexate and azathioprine are often used as first line disease modifying anti-rheumatic drugs. A Cochrane review found insufficient evidence of improved efficacy using one DMARD (methotrexate, azathioprine or cyclosporine) in combination with corticosteroids in preference to another.
Examples for extrinsic esophageal compression are found in inflammatory, postoperative and neoplastic mediastinal diseases, but also in substernal strumae, cervical spondylitis and vertebral osteophytes. Vascular esophageal compression syndromes are typically caused by an aberrant origin of the right subclavian artery far left in the aortic branch and course of this “A. lusoria” anterior or posterior of the esophagus. In addition, similar forms of esophageal compression can result from a congenital right-sided aorta, aortic aneurysms and conditions of left atrial enlargement.
Werner, C., Rbah, R., & Böhm, M. (n.d.). Cardiovascular dysphagia. Clinical Research in Cardiology : Official Journal of the German Cardiac Society., 95(1), 54-56.
Radiological imaging revealed an extrinsic esophageal compression as the cause of the patient’s complaints, for example, due to a mediastinal tumor. However, computed tomography of the chest showed a rare case of cardiovascular compression as the cause of dysphagia in this case. The patient turned down the option of endoscopic examination at the time.
The Bottom Line: Myocardial infarction (MI) is caused by prolonged myocardial ischemia, a condition where atherosclerotic plaques limit coronary flow reserve. About 25% of patients exhibiting symptoms of acute cardiac ischemia (ACI) will have a myocardial infarction.
Lanza GA, Crea F. Overview of Management of Myocardial Ischemia: a Mechanistic-Based Approach. Cardiovasc Drugs Ther. 2016 Aug;30(4):341-349.
Simel DL, Goodacre SW, Kristin L. “Myocardial Infarction”. The Rational Clinical Examination: Evidence-Based Clinical Diagnosis. Eds. David L. Simel & Drummond Rennie. New York, NY: McGraw-Hill.
Diagnosing a patient with MI should be based on whether the patient is exhibiting symptoms (i.e. chest pain, shortness of breath, cardiac arrest, abdominal pain) rather than whether the patient exhibits any risk factors for MI. The most beneficial methods to detect acute myocardial infarction are by observing changes in the Q waves or observing ST-segment elevation or depression on an ECG by the bedside; if ECG results are normal or non-diagnostic, measuring the patient’s symptoms using predictive models can be useful in diagnosing MI.
Posted in EUH
The Bottom Line: Early treatment is of paramount importance for patients with crescentic GN. The current approach is based on a combination of corticosteroids and cytotoxic drugs with the aims of quenching the active inflammation and abating the cellular response and the antibody production
The etiology and the initial pathogenetic factors are different in the three types, but the final mechanisms leading to crescent formation and the renal symptoms and signs are similar.
Moroni, G., & Ponticelli, C. (n.d.). Rapidly progressive crescentic glomerulonephritis: Early treatment is a must. Autoimmunity Reviews, 13(7), 723-729.
The term crescentic glomerulonephritis (GN) refers to a pathologic condition characterized by extracapillary proliferation in > 50% of glomeruli. Clinically crescentic GN is characterized by a nephritic syndrome rapidly progressing to end stage renal disease (ESRD).
Posted in VA
Bottom Line: “Microscopic colitis is a common cause of chronic watery diarrhea, particularly in the elderly. The accompanying symptoms, which include abdominal pain and fatigue, can markedly impair patients’ quality of life. Diagnosis is based upon characteristic histologic findings of the colonic mucosa….Two recent randomized studies have confirmed the effectiveness of oral budesonide for both induction and maintenance treatment of microscopic colitis and is now endorsed by the American Gastroenterological Association as first-line treatment.”
Reference: Cotter TG, Pardi DS. Current approach to the evaluation and management of microscopic colitis. Curr Gastroenterol Rep. 2017 Feb;19(2):8.