Page created on December 1, 2018. Last updated on May 12, 2019 at 12:33
Myocarditis, inflammation of the myocardium, can be divided into two groups: Those that are secondary to infections (non-immune/infectious type), and those that are secondary to immune reactions (immune-mediated type).
Myocarditis is by definition an acute inflammation, however despite this are actually lymphocytes the most important type of leukocyte in this disease. Histologically can focal lymphocyte accumulations be seen, along with focal cell necrosis.
The inflammation leads to myocyte injury and later myocardial fibrosis. Macroscopically will the myocardium become flabby and spotted. Mural thrombi can be present.
Immune-mediated myocarditis is often seen in:
- Rheumatic fever
- Side effect of certain drugs
Infectious myocarditis most commonly occurs due to viral infection by the Coxackie virus, however cytomegalovirus, HIV and influenza can also cause it. Less commonly can it be caused by bacteria, fungi, protozoa and helminths (parasites).
Pericarditis is one of the two pathologies of the pericardium (the other being pericardial effusion). Pericarditis is rarely primary, and when it is is it most commonly caused by viral infection. Secondary pericarditis is the most common, and is usually secondary to a thoracic and systemic disease.
Five types exist, based on what type of acute inflammation it includes. They are:
- Serous pericarditis occurs in SLE, rheumatoid arthritis, scleroderma and viral infection
- Fibrinous pericarditis is the most common type. It occurs in uraemia, SLE, rheumatic fever and acute myocardial infarction. The fibrinous exudate can either undergo resolution (be removed by macrophages) or undergo organization (become dense fibrinous scar tissue).
- Purulent pericarditis occurs in bacterial infection, often secondary to haematogenous spread from pneumonia or pleuritis.
- Haemorrhagic pericarditis occurs in neoplastic involvement of the pericardium, such as a tumor growing into the pericardium
- Caseous pericarditis occurs in fungal infections and tuberculosis.
The most important clinical consequence is the potential for the fibrinous or serous exudate to fill the pericardial space (pericardial effusion) and cause pericardial tamponade. Another important consequence is that the fibrinous, purulent or caseous exudate can become organized and turn into dense fibrinous scar tissue, a condition called chronic pericarditis. If the fibrosis is so extreme that the heart can’t expand normally during diastole is the condition called constrictive pericarditis.
Abnormal fluid accumulation in the pericardium is called pericardial effusion and is the second pathology of the pericardium. Aside from pericarditis can it be caused by:
- Serous effusions
- Congestive heart failure
- Serosanguineous (both blood and serous fluid)
- Chest trauma
- Ruptured myocardial infarct
- Aortic dissection
- Mediastinal lymphatic obstruction
The consequence is potentially pericardial tamponade, but it depends on both the amount of fluid and the how fast the effusion accumulated. The pericardial space usually contains 30 – 50 mL of serous fluid, but it can hold as much as 1000 mL if the effusion happens slowly enough to give the pericardium time to stretch. If the effusion develops rapidly is as little as 250 mL enough to cause fatal pericardial tamponade.
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