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A 20 years old female student of cinematography was admitted to our department with clinical and echocardiography signs of cardiac tamponade. The disease started one month prior admission, with fever up to 38°C, followed by dry cough. She had no signs of arthritis, no skin rash, and she did not take any medication before symptoms occurred. She had no previous medical history, was physically active and a non-smoker.
However, she was exposed to the intensive and prolonged emotional stress due to the disagreement with her family regarding the topic of her studies and the selection of Belgrade University instead of Toronto where her parents live.
Initially, she was treated with Ciprofloxacin and Ceftriaxone after the chest X-ray showed signs of pneumonia and bilateral pleural effusions. Since the therapy had no effect, she was admitted to pulmonology department, sub-febrile and with progressive pleural effusions. Laboratory analyses revealed high sedimentation rate ranging 88-94 mm/h, C-reactive protein (CRP) 107-131 mg/l, fibrinogen 8.8 μmol/L, leukocytes 9.6x109/l, platelets 528-613x109/l, D-dimer 2050-3079 U/l, aspartate aminotransferase (AST) 112 U/l, alanine aminotransferase (ALT) 109 U/l, alkaline phosphatase 171 U/l, gamma glutamyl transferase 163 U/l, she was HIV, HBsAg, HCV negative, with positive IgG antibodies on Mycoplasma pneumoniae (175.6, IgM 0.33). Among the tumour markers she had mildly elevated Ca 125 (526), but normal Ca 72-4 and CEA. Diagnostic puncture of pleural effusion revealed 50 ml of serous pleural effusion (sterile exudate with negative direct microscopy on acid-fast stain). MRI of the pelvis and abdomen as well as gynaecology examination were unremarkable. MSCT of the thorax showed small bilateral pleural effusion and discretely enlarged lymph glands (11-14 mm) retrosternaly, around the thoracic aorta and in subcarinal region with small amount of pericardial effusion. Pleural puncture was performed once again with the pleural biopsy, this time 500 ml of sero-haemorrhagic fluid was obtained. The microbiology examination of the pleural effusion samples was again BK and Löwenstein negative and no malignant infiltration was detected in both cytology examination of the fluid and the biopsy samples. Although pericardial effusion was rather small, due to the fast accumulation our patient became progressively hypotensive, tachycardic, and orthodyspnoic and subsequently an emergency pericardiocentesis had to be performed in the sitting position providing an immediate clinical relief although only 400 ml of serous exudate was evacuated (Figure 1).
During further hospitalisation she was haemodynamically stable with no recurrence of tamponade but continuously moderately febrile with peeks up to 38.6°C (with high sedimentation rate and parameters of inflammation, high leucocytes with relative lymphopenia, thrombocytosis, low urea and cholesterol and anaemia of chronic disease). She felt exhausted with occasional chest pain. Except minor but persistent bilateral pleural effusion other clinical findings were unremarkable.
Figure 1. Rapidly evolving, small pericardial effusion causing acute cardiac tamponade with a dramatic clinical presentation. Left-sided figure demonstates a circulary pericardial effusion in the anterior-posterior view after evacuation of 100 ml of effusion and injection of 30 ml of angiographic contrast media intrapericardially using the intercostally placed 7F catheter. Right-sided figure reveals a normal heart shadow after evacuation of 400 ml of serous effusion.
Drainage of pericardial effusion lasted for 5 days, during which she received Cephtriaxone intravenously. She had no recurrences of pericardial effusion for about a month, when a 5-6 mm small pericardial effusion was again detected with signs of organisation. Immediately after pericardiocentesis Colchicine (0.5 mg BID) with Cephtriaxone and Gentamycin were administered. With this therapy she was not febrile for three days, but then developed diarrheic syndrome. Vancomycin, Ciprofloxacin, Metronidazole, and Nystatin were given and after diarrhoeas stopped Vancomycin was switched to Teicoplanin.
No test to Clostridium difficile came back positive. In the meantime an extensive diagnostic work-up was preformed (Tables 1-3).
Table 1. Extensive laboratory evaluation of a young patient with prolonged febrile condition after acute cardiac tamponade
Table 2. Results of the immunology tests performed as a part of aetiological valuation of a young patient with prolonged febrile condition after acute cardiac tamponade.
ANA - antinuclear antibodies, ANCA – Anti-neutrophil cytoplasmic antibodies , Ab – antibodies,
RF – rheumatoid factor
Table 3. Comprehensive diagnostic evaluation
What would be your diagnosis and suggestion for treatment?
Diagnosis, case resolution and treatment
According to the recommendations of the American rheumatology association (1), our patient fulfilled 4 of 11 criteria for diagnosis of systemic lupus erythematosus:
1. Polyserositis, 2. Haematological manifestations-relative lymphopenia, 3. Immunology manifestations with positive anti-dsDNK antibodies and 4. Positive antinuclear antibodies. However, initial clinical presentation was obscured, most probably with a viral infection accompanied (high CRP, cardiac tamponade), initially negative anti-nuclear antibodies, and gastrointestinal side-effects of applied antibiotic and tuberculostatic medications. In addition, signs of organisation of the chronic pericardial effusion with an unexplained, prolonged low-grade fever also suggested a possibility for tuberculous pericarditis (2-4)(excluded only by a favourable 2-year clinical course after a rapid discontinuation of tuberculostatic medications due to the subacute pancreatitis). After the proper management of acute cardiac tamponade (2, 5) our patient was haemodynamicaly stable, but only after initiation of low-dose steroid treatment our she became afebrile (very quickly) and all signs of poliserositis disappeared (pericardial and both pleural effusions and ascites). With adequate physical therapy, the signs of subatelectasis in portions of previous encapsulated pleural effusion also disappeared. Patient was discharged three months after the admission, in stabile condition, afebrile two weeks prior discharge, with no symptoms what so ever, and normal laboratory parameters, on low fat and protein diet and suggestion for regular controls of gastroenterologist and rheumatologist and on low doses of corticosteroids (Methylprednisolone 16 mg once daily with Chloroquine). Signs of pancreatitis resolved during the further 3 months. During the subsequent 2-year follow-up no recurrences of pericardial effusion and no progression of the systemic autoimmune diseases was noted despite the steroid treatment was subsequently reduced to 4 mg of methylprednisolone once daily) with no signs of constriction or any other complication.
Systemic lupus erythematosus (SLE) is chronic inflammatory disease of unknown aetiology that targets joints, kidneys, lungs, nervous system, seroses, and other organs. The prevalence among other systemic diseases is 20-80 on 100.000 cases (1,6). SLE may cause a pericardial effusion in about 30% of cases [1,2]. Although it may be recurrent, pericardial effusion is most often small (6). Cardiac tamponade occurs as initial manifestation of the disease occurs in less than 1% of cases (6-9). In our registry of 1200 patients with pericardial effusion this was the first cardiac tamponade in a patient with SLE. As in our case, when SLE is properly diagnosed and treated, involvement of the pericardium has a good prognosis (2,3). For recurrent forms an alternative treatment option would be intrapericardial instillation of triamcinolone (10).
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