Abstract
Abstract Myopericarditis is defined as inflammation of the heart muscle and pericardium, which can be caused by infectious agents, toxins, or immunological reactions. The most recognized cases are secondary to cardiotropic viral infections. Escherichia coli rarely causes myopericarditis and is secondary to the septic dissemination of bacteria or myocardial toxicity of endotoxins. We describe a case of bacterial sepsis due to Escherichia coli which caused myocardial damage with pericardial effusion. 32 year old woman without cardiovascular risk factors, suffering from congenital immunodeficiency for IG type A, B–cell NH lymphoma undergoing chemotherapy treatment, Hashimoto‘s thyroiditis. The patient arrives for dyspnoea and fever. The ECG showed mild PR depression and an over diffuse ST in all leads with low voltage QRS and increased TNI. PA 120/70 mmHg, HR 74 b / m, FR of 15 acts / m. ETT showed diffuse hypokinesia with FE40% and moderate, circumferential, corpuscular and hyperechoic pericardial effusion without signs of cardiac tamponade. CRP, ESR, Procalcitonin, Leukocytes were elevated, hypothyroidism and low gamma globulin values. The serology of pericardiotropic viruses is negative. Chest x–ray of mild bilateral pleural effusion. Urine culture was performed for pollakiuria, dysuria, fever: positive for Escherichiacoli. After gamma globulin replacement therapy, levothyroxine and targeted antibiotic therapy, the patient presents clinical and laboratory improvement and improvement in FE with persistence of pericardial effusion. Pericardiocentesis is performed with drainage of 800 ml of serous–looking liquid with coarse fibrin shoots. Cytological examination of the liquid shows a blood serum aspect with a carpet of granulocytic inflammatory elements. The patient was discharged after therapy with colchicine, prednisone, levothyroxine sodium, indomethacin, ramipril, omeprazole. The ECG showed an evolved ischemic type pattern. Conclusion Very rare cases of Escherichia coli cystitis complicated by myo–pericarditis have been described in the literature. Presumably hypothyroidism and congenital IgA immunodeficiency contributed to favoring and worsening the formation of the effusion. However, further studies are still needed to clarify the mechanisms of myocardial damage, although reversible during this type of bacterial infection.
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