HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History
54-year-old woman. No known allergies. No cardiovascular risk factors or toxic habits. Bilateral pneumonia due to COVID-19, requiring hospital admission and treatment with high-dose corticoid. During admission she reported lumbar pain and was diagnosed by CT scan with a fracture of L2, being treated conservatively. She was discharged 4 days before the current episode. On treatment with omeprazole 20 mg every 24 hours, dexamethasone 2 mg every 24 hours, metamizole 575 mg every 8 hours if required due to pain and enoxaparin 40 mg every 24 hours.

Current illness
Patient presented to the emergency department with progressive dyspnoea for 48 hours with central thoracic pressure that improved with sitting. The pain does not change with inspiration. The patient reports progressive swelling of the lower limbs and increased abdominal perimeter since discharge from hospital for COVID-19 pneumonia (4 days ago). She denies fever or dysthermic sensation. Pain with mechanical characteristics persists in the upper lumbar region, secondary to L2 fracture during the previous admission.

Physical examination
Blood pressure 100/50 mmHg, heart rate 104 bpm, temperature 36.2 oC, oxygen saturation 96% basal. General condition fair, tachypneic at rest. Mucocutaneous pallor. Jugular ingurgitation and positive hepatojugular reflux. Cardiac auscultation: rhythmic heart sounds, no murmurs or pericardial friction rub. Pulmonary auscultation: hypoventilation in the left base, without other superimposed sounds. Abdomen soft, slightly painful in the mesogastrium and right hypochondrium, without abdominal defence and with preserved peristalsis; doubtful signs of ascites. No signs of peritoneal irritation. Extremities: bilateral tibial and malleolar oedema with no signs of deep vein thrombosis (DVT). Pain on mobilisation of the lower limbs with positive Lasegue's sign. Pain on palpation in the spinous processes of L2- L4. Venoclysis scar on the left wrist.

COMPLEMENTARY TESTS
Admission CBC: CRP 21.45 mg/dl, glucose 157 mg/dl, urea 42 mg/dl, creatinine 0.72 mg/dl, triglycerides 126 mg/dl, serum total cholesterol 187 md/dl, troponin 6.7 ng/ml (normal values < 12.3 ng/ml), NT-proBNP 1.057, chlorine 104 mEq/l, sodium 139 mEq/l, potassium 4.7 mEq/l, amylase 110 U/l, lipase 97 U/l, alkaline phosphatase 153 U/l, GGT 304 U/l, LDH 322 U/l, GOT 150 U/l, GPT 244 U/l, ESR 97 mm. Leukocytes 15,700 μl with left shift, haemoglobin 11.8 g/dl, haematocrit 28.7%, platelets 178,000/μl. INR 1.04. D-dimer 5,600. Emergency electrocardiogram (ECG): sinus tachycardia at 109 bpm. Slightly lowered PR in inferior and lateral face. Narrow QRS. Concave inframilimetric ST elevation in V3-V6, DI, DII and aVF. No other acute repolarisation abnormalities. Chest X-ray, portable AP: cardiothoracic index 0.5-0.6, slightly increased. Normal pulmonary vascularisation. Bronchiectasis in LII. No signs of cardiac decompensation or pneumonic consolidation. SARS-CoV-2 serology on admission: Ig G and Ig M positive. Blood cultures on admission: positive for methicillin-sensitive Staphylococcus aureus (SAMS). Pericardial fluid analysis: red blood cells 572,800/mm3, leukocytes 16,992/mm3 (86.9% segmented), ADA 63.6 IU/l, glucose < 0.10 g/l, LDH 5,432 IU/l, protein 52.9 g/l. Initial echocardiogram: severe pericardial effusion predominantly posterior and lateral to the LV with maximum separation of pericardial sheets. There is some evidence of haemodynamic repercussions such as collapse of the right atrium (RA) and dilated inferior vena cava (IVC) (21 mm and with practically abolished inspirophasic variations), but there are no significant variations in valvular flows. Fibrin mantle over right chambers and thin fibrin tracts lateral to LV. No significant pleural effusion visualised. Normal biventricular function. No valvular alterations of interest. Pulmonary artery systolic pressure (PSAP) 45 mmHg. Echocardiogram in the evolution: sinus tachycardia. Hyperdynamic LVEF. Paradoxical septal motion with diastolic notch, without contractile asymmetries. Right ventricle (RV) not dilated. Slightly depressed RVEF. No valvulopathies of interest. No images of endocarditis. Moderate pericardial effusion, circumferential, predominantly posterolateral, with maximum separation of pericardial sheets of 11 mm in the posterior sac, 13 mm in the lateral sac at the level of the atrioventricular (AV) groove, 7 mm in the apex, 7 mm adjacent to the RA and in the anterior sac to the RV, with a fibrin mantle in the anterior sac. Echocardiographic signs of haemodynamic repercussions: significant respirophasic variations in transmitral flow (50%) and transtricuspid flow (55%) and dilatation of the IVC, without cavity collapse. Echocardiographic data suggestive of constrictive physiology: protodiastolic notch of the interventricular septum, "reverse ring" (lateral E wave < septal E wave) and respirophasic variations in suprahepatic vein flow, with reverse diastolic flow in expiration. Bilateral pleural effusion. Control echocardiogram: biventricular systolic function preserved. No notable valvulopathies. Estimated normal PSAP. No images suggestive of endocarditis. Slight pericardial effusion, predominantly posterolateral, with no haemodynamic repercussions or evidence of constrictive physiology at present. Thoracoabdominal CT scan: pericardial effusion with enhancement of the visceral and parietal pericardium in the venous phase suggestive of associated pericarditis and right heart failure with congestive liver and vesicular oedema. Bilateral pleural effusion with passive lower lobe atelectasis. Multiple abscesses in both psoas muscles. Erosion of the upper plateau of the vertebral body of L3, to assess L2-L3 spondylodiscitis or compression fracture. Magnetic resonance imaging (MRI) of the shoulder: septic arthritis of both shoulders. Lumbar MRI: study compatible with L2-L3 infectious spondylodiscitis with involvement of L3 and, to a lesser extent, L2, and right anterior peridural extension and L3, right L2-L3 and L3-L4 foraminal extension with potential effect on the emerging roots. Abscesses in both psoas, multiple on each side, with the largest one on the right side reaching 7.5 cms. Laboratory tests at discharge: CRP 1.43, creatinine 0.66 mg/dl, urea 42 mg/dl, cholesterol 175 mg/dl, chlorine 102 mEq/l, sodium 137 mEq/l, potassium 4.5 mEq/l, albumin 3.2 g/dl, alkaline phosphatase 75 U/l, GGT 59 U/l, GOT 14 U/l, GPT 12 U/l, LDH 156. Leukocytes 6,500/ μl, haemoglobin 10.3 g/dl, platelets 265,000/ μl, ESR 76.

CLINICAL COURSE
The patient was initially seen in the emergency department of our hospital. Given the signs of heart failure predominantly on the right and the central thoracic pain, together with the elevation of acute phase reactants in the laboratory tests, it was decided to admit the patient for further investigation. During her stay in the ED, the patient presented a peak fever of 38.2oC and blood cultures were taken. The echocardiogram on admission showed severe pericardial effusion with signs of echocardiographic repercussions, but no clinical signs at that time. Blood cultures showed growth of SAMS. Suspicion of purulent pericarditis led to subxiphoid pericardial drainage and antibiotic therapy was started with cefazolin and daptomycin. Pericardial fluid cultures were sterile but the biochemical characteristics of the fluid were infectious. The patient's symptoms did not clearly improve despite drainage of the pericardial fluid, so a transesophageal echocardiogram (TEE) was requested to rule out the presence of endocarditis and to evaluate the progression of the effusion. This TEE showed constrictive physiology data suggestive of effusive-constrictive pericarditis. In addition to the cardiorespiratory symptoms, the patient presented pain in the upper lumbar region, both shoulders and left lower extremity. In view of the suspicion of septic foci, the study was completed with thoracoabdominal CT and magnetic resonance imaging of both shoulders and lumbar region. Imaging studies confirmed the presence of septic arthritis in both shoulders, spondylodiscitis at L2-L3 and multiple abscesses in bilateral psoas. The patient also presented a lesion on the left lower extremity compatible with cellulitis.

Due to the persistence of fever, despite targeted antibiotherapy, the abscesses in the psoas muscle were drained and SAMS was again isolated in the fluid culture. The control echocardiogram showed slight pericardial effusion with no signs of haemodynamic compromise or constrictive physiology. Slow evolution of the patient, with progressive disappearance of the different infectious foci and clinical improvement without new episodes of fever. Periodic blood cultures were negative. Finally, after 8 weeks of intravenous antibiotics, she was discharged for outpatient follow-up. Treatment at discharge was omeprazole 20 mg every 24 hours, dexketoprofen 25 mg every 12 hours, colchicine 0.5 mg every 24 hours, paracetamol 1 g every 8 hours and bemiparin 7,500 IU every 24 hours.

DIAGNOSIS
Persistent SAMS bacteraemia with multiple foci (purulent pericarditis, multiple psoas abscesses, spondylodiscitis, cellulitis, bilateral septic shoulder arthritis). Effusive-constrictive pericarditis resolved with medical treatment.
