PERSONAL HISTORY
Allergy to sulphonamides and acetylsalicylic acid. Cardiovascular risk factors: dyslipidaemia under pharmacological treatment. No diabetes mellitus. No arterial hypertension (AHT). No toxic habits.
Cardiological history: severe symptomatic aortic stenosis. Aortic valve replacement was performed in May 2008 with implantation of St. Jude No 19 mechanical aortic prosthesis. Last control echocardiography in 2012: normofunctioning prosthesis with preserved LVEF. Other history of interest: Bronchial asthma under inhaled treatment with good control. Macular thrombosis and vitreous detachment in the right eye, treated with laser in 2015. Pelvic fracture in August 2017 (right ischium and coccyx) resolved. L1 impingement fracture in 2016.
Surgical interventions: replacement of total right hip prosthesis one month ago due to fracture of the neck of the right femur. Previous medication: omeprazole 20 mg (1-0-0), enalapril 20 mg (1-0-0), ecomcor 2.5 mg (1/2-0-1/2), atorvastatin 10 mg (0-0-1), acenocoumarol according to haematology guidelines (after hip surgery, in bridging therapy with low molecular weight heparins (dose: enoxaparin sc 40 mg c/24 hours).  

CURRENT DISEASE
Patient presented to the emergency department with a sudden increase in dyspnoea. She reported clinical symptoms of upper respiratory symptoms 3-4 days previously, with cough and increased expectoration, which was treated with azithromycin. Discharged 1 month ago after admission for hip replacement.

PHYSICAL EXAMINATION
Vital signs on arrival at the emergency department: blood pressure (BP) 98/56 mmHg; SatO2 92% with oxygen therapy by VentiMask at 35%. Temperature 36.2 ̊C. Weight 68 kg. Height 162 cm. Conscious, oriented and cooperative. Well hydrated and perfused. Tachypneic on speech. Cannot tolerate decubitus. Cardiac auscultation: rhythmic heart rhythms, prosthetic metallic click with systolic murmur III/VI, and systolic murmur in mitral focus II-III/VI. Pulmonary auscultation: coarse crackles up to midfields. Abdomen: soft, not painful on palpation. No palpation of masses or megaliths, peristalsis preserved. Normal percussion. Lower extremities: oedema with fovea up to the knees. No signs of deep vein thrombosis (DVT).

COMPLEMENTARY TESTS
Laboratory tests: biochemistry: glucose 246 mg/dl. Urea 38 mg/dl. Creatinine 0.93 mg/dl (GFR 59 ml/min). CRP 0.96. Troponin T ultrasensitive 256 ng/dl. Haemogram 14,500 leucocytes (7,900 N, 5,400 L, 900 M, 200 E). Hb 10.8 mh/dl and MCV 88.2. Platelets 553,000. Coagulation: INR 1.70. Prothrombin rate 39.8%.
Electrocardiogram (ECG): sinus rhythm at 90 bpm. Left bundle branch block (LBBB) already present in previous ECGs. No other alterations. Chest X-ray: cardiomegaly. Bilateral pleural effusion. Pulmonary vasculation in relation to pulmonary oedema.
Transthoracic echocardiography (TTE): left ventricle with concentric hypertrophy (septum 12 mm), abnormal septal motion with septal akinesia and moderately affected global systolic function. LA of 17.3 cm2. Valve prosthesis in aortic position poorly visualised, with severe regurgitation (THP 160ms) and obtaining a max gradient of 94 mmHg (mean 59 mmHg). Fibrocalcified mitral valve mostly posteriorly with at least moderate regurgitation (grade III), reaching the atrial roof. Normal sized right chambers with TAPSE of 12 mm and moderate TR with a calculated PsAP of 32 mmHg + PVC. No pericardial effusion. IVC of 18 mm with inspiratory collapse < 50%.
Transesophageal echocardiogram: metallic prosthesis in aortic position with very reduced disc mobility, low echogenic density material is observed at disc level. Severe stenosis with velocities greater than 5 ms/s and severe insufficiency. Moderate mitral insufficiency. Left ventricle (LV) not dilated, mild hypertrophy, moderately impaired systolic function. Non-dilated right ventricle (RV) with normal function.

CLINICAL COURSE
The patient is a 76-year-old woman admitted with acute pulmonary oedema. Emergent TTE was performed and showed a moderately affected left ventricular ejection fraction (LVEF) with severe aortic stenosis and insufficiency secondary to dysfunction of the mechanical aortic valve prosthesis. Given his history of previous surgery with under-therapeutic doses of anticoagulation, acute-subacute prosthetic thrombosis was suspected on admission as the main aetiology. For this reason, a TEE study was completed which led to this diagnosis.
Medical treatment was started with intravenous diuretics. The patient evolved unfavourably and was haemodynamically unstable, requiring vasoactive support, so given the situation of cardiogenic shock, emergency aortic valve replacement surgery was decided. Emergent surgery was performed, in which a St Jude aortic prosthesis no 19 blocked by the presence of two small clots of less than 5 mm in both hinges was visualised. The prosthesis was explanted and the annulus was enlarged with a pericardial patch in the non-coronary leaflet towards the mitral annulus in order to implant the Magna Ease No 19 biological prosthesis. He presented with an episode of ventricular fibrillation that reverted after defibrillation, so it was decided to re-enter CPB and implant intra-aortic balloon counterpulsation (IABP) via the right femoral artery with insufficient haemodynamic response and severe left ventricular dysfunction; finally it was decided to implant a peripheral femoro-femoral venoarterial extracorporeal membrane oxygenator (ECMO). Poor evolution during the days following surgery, in a situation of cardiogenic shock refractory to maximum support measures, evolving towards multi-organ failure, finally dying.

DIAGNOSIS
Heart failure in a situation of acute pulmonary oedema. Acute thrombosis of mechanical aortic prosthesis with stenosis and severe insufficiency secondary to anticoagulation underdosage after hip surgery. Aortic valve replacement with implantation of a biological prosthesis. Refractory cardiogenic shock. ECMO implantation. Multi-organ failure. Death.
