Sandbox:Usman Ali Akbar: Difference between revisions
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* It has been suggested that pericardial damage due to different etiological factors leads to triggering of innate immune response especially due to autoimmune disease primarily mediated by cytokines ( e.g IL-1). | * It has been suggested that pericardial damage due to different etiological factors leads to triggering of innate immune response especially due to autoimmune disease primarily mediated by cytokines ( e.g IL-1). | ||
* The autoinflammatory mechanism resulting from activation of inflammasome by any etiological agent in patient with immunocompromised immune system. | * The autoinflammatory mechanism resulting from activation of inflammasome by any etiological agent in patient with immunocompromised immune system. | ||
* This results into release of various cytokines predominately IL-1 that recruits neutrophils and macrophages to the damaged area. | * This results into release of various cytokines predominately IL-1 that recruits neutrophils and macrophages to the damaged area. <ref name="pmid32238419">{{cite journal| author=Cacoub P, Marques C| title=Acute recurrent pericarditis: from pathophysiology towards new treatment strategy. | journal=Heart | year= 2020 | volume= | issue= | pages= | pmid=32238419 | doi=10.1136/heartjnl-2019-316481 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32238419 }} </ref> | ||
== Epidemiology and Demographics == | == Epidemiology and Demographics == | ||
Revision as of 01:00, 5 June 2020
Acute Pericarditis
Overview
Acute pericarditis can be defined as inflammation of pericardial sac. Pericardial sac is composed of two layers visceral and parietal layers which is separated by a space called pericardial space. Acute pericarditis can be divided based on difference in etiology, i.e Viral, bacterial, autoimmune,neoplastic or idiopathic. It presents with history of chest pain which is sharp , pleuritic and improved by leaning forward and sitting up. There is pericardial friction rub that can be heard by placing diaphragm of the stethoscope over Left Sternal Border. Acute Pericarditis can be diagnosed by proper history and physical exam. The initial modality of testing is usually ECG ,Chest X-ray and cardiac biomarkers. Acute pericarditis is a relatively benign condition and can be managed by addressing the specific etiology. For acute idiopathic and viral pericarditis , symptomatic treatment including colchicine and NSAIDs is usually given. Glucocorticoids is usually reserved for patients having contraindications for treatment with NSAIDs
Historical Perspective
Classification
Acute Pericarditis can be classified based on etiology into following categories
- Idiopathic
- Infectious ( Viral, Bacterial and fungal etc)
- Post-myocardial infarction ( Dressler's Syndrome)
- Pericarditis due to drugs and toxins
- Malignancy associated pericarditis
- Autoimmune mediated ( e.g SLE)
Pathophysiology
The pathophysiology of acute pericarditis generally depends upon the etiological agent causing the disease.
- It has been suggested that pericardial damage due to different etiological factors leads to triggering of innate immune response especially due to autoimmune disease primarily mediated by cytokines ( e.g IL-1).
- The autoinflammatory mechanism resulting from activation of inflammasome by any etiological agent in patient with immunocompromised immune system.
- This results into release of various cytokines predominately IL-1 that recruits neutrophils and macrophages to the damaged area. [1]
Epidemiology and Demographics
The incidence of acute pericarditis in hospitalized patients is 0.1 to 0.2 percent. [2]
References
- ↑ Cacoub P, Marques C (2020). "Acute recurrent pericarditis: from pathophysiology towards new treatment strategy". Heart. doi:10.1136/heartjnl-2019-316481. PMID 32238419 Check
|pmid=value (help). - ↑ Kytö V, Sipilä J, Rautava P (2014). "Clinical profile and influences on outcomes in patients hospitalized for acute pericarditis". Circulation. 130 (18): 1601–6. doi:10.1161/CIRCULATIONAHA.114.010376. PMID 25205801.