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Pericardium
Published in Mary N. Sheppard, Practical Cardiovascular Pathology, 2022
Trauma may also cause pericarditis with early onset following injury or, as more frequently encountered in clinical practice, result in a delayed inflammatory reaction. Dressler syndrome, also called late post-myocardial infarction syndrome, is a well-recognized post-cardiac injury syndrome where pericarditis is preceded by acute coronary syndrome, with a delayed inflammatory response usually several weeks after the initial event. It is believed to occur secondary to formed antimyocardial antibodies as a delayed autoimmune process causing symptoms of pericarditis in the late post-myocardial infarction stage. When first described, its incidence was estimated at 5–7% of myocardial infarctions, but it has become an uncommon entity with the many improvements achieved in the management of acute coronary syndrome. In developed countries, idiopathic or so-called viral pericarditis is the most common diagnosis. In a biopsy study including 259 patients with a large pericardial effusion, the underlying cause was identified by molecular and immune-histological methods mainly as autoreactive/lymphocytic (i.e. idiopathic or viral, 35%), malignant (28%), traumatic (i.e. post-cardiac surgery, 15%) and viral (12%). The aetiological spectrum is different in developing countries, with a high prevalence of tuberculosis (70% of pericarditis in sub-Saharan Africa, and ≥90% when associated with HIV infection).
Cardiology
Published in Paul Bentley, Ben Lovell, Memorizing Medicine, 2019
PericarditisEarly pericarditis represents infarction of the pericardiumDressler syndrome is due to autoantibodies against sarcolemma + subsarcolemma of myocytes
Iatrogenic tracheobronchial and chest injury
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
Marios Froudarakis, Demosthenes Makris, Demosthenes Bouros
The pathogenesis of the post-CABG effusion remains obscure. The pathogenesis of early effusions is probably related to trauma during surgery that results in bleeding into the pleural space. Late pleural effusions probably have a different pathogenesis. Because of the late presentation, it is unlikely to be related to blood in the pleural space at the time of surgery. The high lymphocyte count suggests an immunologic aetiology similar to postcardiotomy syndrome and Dressler syndrome. It has been suggested that late lymphocytic pleural effusions after CABG may represent a subset of patients with a variant of, or a limited type of, postcardiotomy syndrome involving only the pleura. However, several other factors may also contribute to the formation of effusions in patients undergoing CABG. These may include congestive heart failure, pulmonary embolism, atelectasis and the use of drugs such as amiodarone, procainamide hydrochloride, and beta-adrenergic blocking agents. It is therefore important to include these in the differential diagnosis of effusions occurring in patients who have undergone CABG. Patients should be managed initially with therapeutic thoracocentesis and an anti-inflammatory agent such as indomethacin which is particularly useful in late pleural effusions, where an immunologic basis for the effusion is speculated. However, if the effusion recurs, a second therapeutic thoracocentesis with the possible addition of oral prednisone therapy for a brief period is recommended. When the effusion continues to recur, appropriate investigations to exclude other causes of effusion and then more aggressive measures such as tube thoracostomy with pleurodesis should be considered.70,71
Pericardial Anatomy, Interventions and Therapeutics: A Contemporary Review
Published in Structural Heart, 2021
Reza Reyaldeen, Nicholas Chan, Saberio Lo Presti, Agostina Fava, Chris Anthony, E. Rene Rodriguez, Carmela D. Tan, Walid Saliba, Paul C Cremer, Allan L. Klein
Post-cardiac injury syndrome (PCIS) is a complex, heterogenous group of immune-mediated disorders related to pericardial, epicardial and myocardial inflammation following an inciting event, most often following surgical or procedural trauma, iatrogenic or accidental injury and finally, post-myocardial infarction.32 The reason for this heterogeneity relates to the variable chronology of presentation, differing etiology and severity of disease. For this reason, the exact incidence of PCIS is difficult to determine, but has been reported to be in the order of 15–30% in the post-cardiac surgery population, <5% in the peri-infarction group and <1% in the late post-infarction group, also known as Dressler syndrome.32,33 Furthermore, the incidence of pericardial complications after percutaneous coronary intervention is rare, reported as <0.5%, and between 1% and 5% for other interventional procedures, which is highly dependent on the type and complexity of procedure and use of anticoagulation.32,34 While it would stand to reason that interventional procedures employing direct pericardial contact are most likely to induce PCIS along with cardiac surgery, there are reports of other interventions such as transcatheter edge-to-edge mitral valve repair and transcatheter aortic valve replacements also causing similar presentations.35,36 The mechanism remains unclear, and whether this is related to transient pericardial irritation or injury, or representative of underlying autoimmunity is unknown. Thus, a high degree of suspicion should be maintained for PCIS in patients following any cardiac intervention.