HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
A 66-year-old woman consulted for dyspnoea and oedema in the lower limbs.

History
No known drug allergies.
She denies toxic habits.
Cardiovascular risk factors: dyslipidaemia. Type 2 diabetes under treatment with oral antidiabetics with good control (last HbA1c 6.8%).
Permanent atrial fibrillation anticoagulated with warfarin.
Rheumatic valvular heart disease with severe mitral stenosis and moderate double aortic lesion, operated on 19-June-18. Mitral and aortic valve replacement with mechanical prostheses. Postoperative period uncomplicated, except for anaemia which required transfusion of 1 red blood cell concentrate. Discharged from hospital on 28 June 2018.
Home treatment after surgery: omeprazole 20 mg daily, carvedilol 6.25 mg every 12 hours, pravastatin 40 mg daily, warfarin 10 mg according to haematology guidelines and gliclazide 30 mg every 12 hours.

Present illness
Patient admitted from the emergency department for progressive dyspnoea until minimal effort and oedema in the lower limbs 2 weeks after being discharged following valve replacement surgery. She associated two-pillow orthopnoea and paroxysmal nocturnal dyspnoea crises. The patient denied non-adherence to treatment or dietary transgressions. On arrival at the emergency department, atrial flutter was observed with rapid ventricular response and congestive data on examination, and the patient was admitted to hospital by the cardiology department.

Physical examination
General condition preserved. Conscious and oriented. Well hydrated and perfused. Pallor of skin and mucous membranes. Blood pressure 125/80 mmHg. Eupneic at rest, with basal oxygen saturation 94%. Heart rate 100 bpm. No jugular ingurgitation or hepatojugular reflux. Cardiorespiratory auscultation: arrhythmic heart at about 100 bpm. Prosthetic metallic click. No audible murmurs. Good pulmonary ventilation with slight crackles in both lung bases, with no other added pathological sounds. Abdomen: no masses or megaliths, not painful on deep palpation. No evidence of peritoneal irritation. Oedema up to the knees with fovea.

COMPLEMENTARY TESTS
Laboratory tests in the emergency department:
Haemogram: 7430 leucocytes with normal formula, haemoglobin 9 g/dl, MCV 90.60 fl, platelets 179000.
Coagulation: INR 2.07.
Biochemistry: normal renal function and ionogram. C-reactive protein 58.1 mg/l. NT-proBNP 1404 pg/dl.
Serial myocardial damage enzymes: CK 36 - 22 U/l, ultrasensitive troponin T 28 - 31 ng/l.
Electrocardiogram: atrial flutter with variable ventricular response around 120 bpm. Normal axis. Narrow QRS. Good R progression in precordial leads. Negative T waves V4-V6, without other repolarisation alterations.
Transthoracic echocardiography: non-dilated left ventricle with mild concentric hypertrophy. Dilated left atrium. Normal right chambers. Sections of aorta studied within normality. Valves: normopositioned mechanical mitral prosthesis and no nodding, with preserved disc mobility, no signs of insufficiency and mean gradient 4 mmHg (video 1). Normopositioned mechanical aortic prosthesis with no pitching, preserved disc mobility, no insufficiency jets and normal anterograde gradients (maximum velocity 2.3 m/sec). Preserved left ventricular systolic function estimated at 60% by biplane Simpson, without segmental contractility disorders. Preserved right ventricular systolic function. Absence of pericardial effusion.

CLINICAL EVOLUTION
Initial evolution was favourable after intravenous diuretic treatment and transfusion of blood products. However, on the sixth day of admission, the patient's platelet count dropped from 160,000 to 23,000. Given the suspicion of heparin-induced thrombopenia (HIT), it was decided to replace this drug with fondaparinux and antiplatelet factor IV antibodies were requested, which were found to be positive. After replacing heparin with fondaparinux, platelets progressively rose to normal, allowing the reintroduction of warfarin, his usual anticoagulant therapy. During treatment with fondaparinux, there were no haemorrhagic or thrombotic complications. Before discharge, a new echocardiogram was performed and both prosthetic valves were found to be normally functioning and showed no evidence of thrombosis.
Intercurrently, the patient presented with micturition symptoms with dysuria, frequency of urination and urinary urgency; a urine culture showed E. coli producing extended-spectrum beta-lactamase (E. coli BLEE+). Given the patient's high comorbidity and the risk of endocarditis in the event of bacteraemia due to the recent implantation of two mechanical prostheses, it was decided to start broad-spectrum antibiotherapy with ertapenem. Two days after starting treatment with ertapenem, the patient developed generalised polyarthralgia, predominantly in the lower limbs, and non-pruritic skin lesions, which progressively worsened, some of them acquiring a bull's-eye morphology. Suspecting toxicoderma due to ertapenem, we replaced this drug with fosfomycin, and the symptoms resolved completely within 48 hours. A skin biopsy was obtained with a result of small-vessel leukocytoclastic vasculitis compatible with genuine serum sickness or sickness associated with taking the drugs, findings consistent with the initial suspicion of ertapenem-induced toxicoderma.

DIAGNOSIS
Decompensation of heart failure in association with:
Subacute normocytic anaemia in probable relation to surgery. Atrial flutter with rapid ventricular response.
Heparin-induced thrombopenia (HIT).
BLEE+ E. coli urinary tract infection.
Small vessel leukocytoclastic vasculitis secondary to administration of carbapenemics (ertapenem).
