Dressler syndrome

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Dressler's syndrome
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Dressler syndrome
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Dressler syndrome is a secondary form of pericarditis that occurs in the setting of injury to the heart or the pericardium (the outer lining of the heart). It consists of fever, pleuritic pain, pericarditis and/or pericardial effusion.

Dressler syndrome is also known as postmyocardial infarction syndrome[1] and the term is sometimes used to refer to post-pericardiotomy pericarditis.

It was first characterized by William Dressler at Maimonides Medical Center in 1956.[2][3][4]

It should not be confused with Dressler's syndrome of

haemoglobinuria named for Lucas Dressler, who characterized it in 1854.[5][6]

Presentation

Dressler syndrome was historically a phenomenon complicating about 7% of myocardial infarctions,

pleuritic), pericarditis (usually evidenced by a pericardial friction rub, chest pain worsening when recumbent, and diffuse ST elevation with PR segment depression), and/or pericardial effusion. The symptoms tend to occur 2–3 weeks after myocardial infarction but can also be delayed a few months. It tends to subside in a few days, and very rarely leads to pericardial tamponade.[8] Elevated ESR
is an objective but nonspecific laboratory finding.

Causes

It is believed to result from an

]

Diagnosis

Differential diagnosis

Dressler syndrome needs to be differentiated from pulmonary embolism, another identifiable cause of pleuritic (and non-pleuritic) chest pain in people who have been hospitalized and/or undergone surgical procedures within the preceding weeks.[citation needed] ischaemic heart disease.

Treatment

Dressler syndrome is best treated with high-dose aspirin. In some resistant cases,

NSAIDs, though once used to treat Dressler syndrome, are less advocated and should be avoided in patients with ischemic heart disease. One NSAID in particular, indomethacin, can inhibit new collagen deposition, thus impairing the healing process for the infarcted region. Other NSAIDS should be used only in cases refractory to aspirin. Heparin should be avoided because it can lead to hemorrhage into the pericardial sac, leading to tamponade. The only time heparin could be used with pericarditis is with coexisting acute MI, in order to prevent further thrombus formation.[9]

References

External links