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P398 ACUTE PERICARDITIS COMPLICATED BY RAPID DEVELOPMENT OF CONSTRICTION: A CASE REPORT
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Abstract
A 57–years–old man with no previous cardiovascular history presented with fever, hypotension, dyspnoea at rest and chest pain. The electrocardiogram showed sinus tachycardia, PR–segment depression and diffuse concave–upwards ST–segment elevation. Elevated C–reactive protein and low pro–BNP level were found at lab tests, procalcitonin and troponin were negative. Chest X–ray showed bilateral pleural effusion. Transthoracic echocardiogram (TTE) revealed mild–to–moderate serofibrinous pericardial effusion with initial diastolic collapse of right chambers, suggesting cardiac pre–tamponade. Because of the exiguity of liquid component, pericardiocentesis was not performed, patient was stabilized by fluid–challenge with hypertonic solution. Ibuprofen and colchicine were started. Left thoracentesis was performed removing one liter of fluid overall compatible with transudate. Cytological and microbiological examinations were negative. Despite of initial clinical improvement, the patient showed kidney failure and worsening of lung failure; perianal abscess was detected causing sepsis and requiring surgical drainage and antibiotic therapy with vancomycin and piperacillin/tazobactam. Culture exams were negative. After ibuprofen replacement with indomethacin a repeated TTE showed reduced pericardial effusion, but also respiratory variation in ventricular filling with signs of interventricular dependence. Cardiac magnetic resonance showed thickening and high signal intensity of pericardial layers on T2 weighted imaging and ventricular septal shift on free–breathing cine sequences, suggesting effusive–constrictive pericarditis. Left and right cardiac catheterization demonstrated ventricular “dip and plateau” pattern and ventricular discordance. Considering the lack of clinical improvement on medical therapy, off–bypass pericardiectomy was performed. Incomplete adhesion between the two pericardial layers and thick gelatinous material were found. After surgery patient experienced rapid clinical improvement; cardiac index increased from 1.5 to 3.5 L/min/m2. Effusive–constrictive pericarditis is a rare and dreaded complication of acute pericarditis. Surgery, when appropriated, is crucial for prognosis. In our case initial response to anti–inflammatory therapy with reduced pericardial effusion unmasked constrictive physiology in an effusive–constrictive pericarditis. Clinical management was complicated by sepsis which could have played a role in constriction developing.
Oxford University Press (OUP)
Title: P398 ACUTE PERICARDITIS COMPLICATED BY RAPID DEVELOPMENT OF CONSTRICTION: A CASE REPORT
Description:
Abstract
A 57–years–old man with no previous cardiovascular history presented with fever, hypotension, dyspnoea at rest and chest pain.
The electrocardiogram showed sinus tachycardia, PR–segment depression and diffuse concave–upwards ST–segment elevation.
Elevated C–reactive protein and low pro–BNP level were found at lab tests, procalcitonin and troponin were negative.
Chest X–ray showed bilateral pleural effusion.
Transthoracic echocardiogram (TTE) revealed mild–to–moderate serofibrinous pericardial effusion with initial diastolic collapse of right chambers, suggesting cardiac pre–tamponade.
Because of the exiguity of liquid component, pericardiocentesis was not performed, patient was stabilized by fluid–challenge with hypertonic solution.
Ibuprofen and colchicine were started.
Left thoracentesis was performed removing one liter of fluid overall compatible with transudate.
Cytological and microbiological examinations were negative.
Despite of initial clinical improvement, the patient showed kidney failure and worsening of lung failure; perianal abscess was detected causing sepsis and requiring surgical drainage and antibiotic therapy with vancomycin and piperacillin/tazobactam.
Culture exams were negative.
After ibuprofen replacement with indomethacin a repeated TTE showed reduced pericardial effusion, but also respiratory variation in ventricular filling with signs of interventricular dependence.
Cardiac magnetic resonance showed thickening and high signal intensity of pericardial layers on T2 weighted imaging and ventricular septal shift on free–breathing cine sequences, suggesting effusive–constrictive pericarditis.
Left and right cardiac catheterization demonstrated ventricular “dip and plateau” pattern and ventricular discordance.
Considering the lack of clinical improvement on medical therapy, off–bypass pericardiectomy was performed.
Incomplete adhesion between the two pericardial layers and thick gelatinous material were found.
After surgery patient experienced rapid clinical improvement; cardiac index increased from 1.
5 to 3.
5 L/min/m2.
Effusive–constrictive pericarditis is a rare and dreaded complication of acute pericarditis.
Surgery, when appropriated, is crucial for prognosis.
In our case initial response to anti–inflammatory therapy with reduced pericardial effusion unmasked constrictive physiology in an effusive–constrictive pericarditis.
Clinical management was complicated by sepsis which could have played a role in constriction developing.
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