HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
Male, 78 years old.

PERSONAL HISTORY
No known drug allergies.
Cardiovascular risk factors (CVRF): hypertension (HT), diabetes mellitus with poor metabolic control with target organ damage, dyslipidaemia.

Cardiovascular history:
Rheumatic fever in childhood. Rheumatic mitro-aortic valve disease. Mitral valve replacement on three occasions:
Surgery for severe mitral stenosis in 2006. St Jude metal mitral prosthesis.
Mitral valve replacement with biological prosthesis due to valve thrombosis (2007).
Mitral and aortic valve replacement with biological prosthesis (2018) due to mitral prosthetic degeneration and moderate aortic stenosis. Recent admission (discharged one week ago) after prolonged admission (30-day stay) due to clinical heart failure, deterioration of renal function in this context and complications of the critically ill patient.
Atrial fibrillation. Frequency control strategy. Under treatment with sintrom and bisoprolol.
Coronary arteries without lesions in coronary angiography (October 2018).

Other history:
Chronic kidney disease of diabetic aetiology. Baseline creatinine 1.4 mg/dl (glomerular filtration rate [GFR] 47 ml/min/1.73 m2).
Moderate sleep apnoea-hypopnoea syndrome (SAHS), without treatment with continuous positive airway pressure (CPAP) due to poor tolerance.
Prostatectomy due to prostate carcinoma.

Usual treatment:
Acenocoumarol 4 mg. DTS 15 mg. Recent stable INR controls.
Spironolactone 50 mg (1 tablet every 24 hours).
Bisoprolol 2.5 mg (1 tablet every 24 hours).
Simvastatin 20 mg (1 tablet daily).
Omeprazole 40 mg (1 tablet per day).
Furosemide 40 mg (two tablets at breakfast, one at lunch and one at dinner).
Slow insulin 18 IU per day.
Rapid insulin (6-8-8 IU per day).
Metamizole 575 mg (1 amp every 8 hours if pain).
Baseline: independent for basic activities of daily living (BADL). He goes out on a daily basis. Manages her medication. Does not meet frailty criteria (robust). KATZ A.

CURRENT ILLNESS
He presented with worsening functional class, with dyspnoea on minimal effort, increased oedema in the lower limbs and orthopnoea which led him to sleep in a sitting position the night before admission. Recent admission (discharged 7 days ago) from another centre following mitral and aortic valve replacement surgery. The patient reported congestive symptoms a few days after discharge. He acknowledges salt intake in his usual diet at home, and has also started taking non-steroidal anti-inflammatory drugs (NSAIDs) as a result of pain secondary to musculoskeletal pathology exacerbated after the recent admission.

PHYSICAL EXAMINATION
Blood pressure (BP) 140/80 mmHg, heart rate (HR) 120 bpm, Sat 93% with nose glasses.
Head and neck: no jugular venous engorgement
Cardiac auscultation: arrhythmic, no murmurs.
Pulmonary auscultation: crackles in both bases.

COMPLEMENTARY TESTS
Blood tests: haemoglobin 10.3 mg/dl. Urea 62 mg/dl. Creatinine 1.8 mg/dl (GFR 39 mg/ml/1.73 m2), NT-proBNP 4550 pg/ml. Iron profile: total Fe 136, ferritin 150 g/l; IST 18%. TSH 2.1.
HbA1C 7.9%. Albumin 2.6 mg/dl. Prealbumin 13 mg/dl.
ECG: atrial fibrillation at 140 bpm. QRS 110 msg. Normal axis. No repolarisation alterations.
Chest X-ray: cardiomegaly. Vascular redistribution. Bilateral pleural effusion. Previous sternotomy sutures.
Echocardiogram: left ventricle with normal size, with concentric hypertrophy of moderate degree, without significant alterations of segmental contractility and with preserved global systolic function. Right ventricle with preserved size and function.
Both atria severely dilated. Mitral biological prosthesis with no signs of dysfunction.
Aortic biological prosthesis with no signs of dysfunction. Trivial IT allowing estimation of systolic pulmonary pressure of 35 mmHg. Aortic root and proximal ascending aorta of normal size. Inferior vena cava severely dilated and no respiratory changes. Absence of pericardial effusion.

CLINICAL EVOLUTION
Poor evolution during the first days with persistence of congestive data despite high doses of loop diuretic (furosemide 180 mg per day, in intravenous boluses), control of water intake (less than 1.5 litres per day) and controlled salt intake at meals (dose of 2 g sodium chloride per day). The patient presented progressive deterioration of renal function in consecutive analyses, with creatinine levels of up to 2.6 mg/dl (GFR 24 ml/min/1.73 m2). In view of this worsening renal function, with glomerular filtration rates below 30 ml/h, it was decided to discontinue treatment with spironolactone.
As a strategy, given that positive water balances persisted daily with worsening congestive data (third tone, increased crackles, worsening peripheral oedema), a combination diuretic strategy was decided upon. Bolus doses of loop diuretics were discontinued and replaced by intravenous infusion of furosemide, and thiazide diuretics (hydrochlorothiazide) and carbonic anhydrase inhibitor diuretics (acetazolamide) were added to the treatment. Due to the history of recent prolonged hospitalisation and data of protein malnutrition, the nutrition service was contacted and protein-rich nutritional supplements were started.
Twelve hours after initiating this new treatment strategy, the patient persisted with neutral balances. The patient presented clinical deterioration compatible with acute pulmonary oedema, which required admission to the coronary unit and ventilatory support with non-invasive mechanical ventilation. At this point, different therapeutic options were considered. Various pharmacological treatment options were considered, including increasing the dose of thiazide diuretics, prescribing hypertonic saline perfusion together with loop diuretic perfusion and even a more invasive strategy was considered, contacting the nephrology department to schedule haemodiafiltration sessions if necessary. The patient was reluctant to this last option, so it was decided to wait for a diuretic response in the following hours, adding hypertonic saline perfusion to the treatment (perfusion of 100 ml of 0.9% physiological saline with the addition of 1 ampoule of 20% ClNa).
Finally, the patient started with a good diuretic rhythm, achieving negative water balances. A few days later, the improvement of congestion data was evident, with improvement of pulmonary auscultation and reduction of peripheral oedema, cardiac auscultation free of third tone. All this was accompanied by an analytical improvement in renal function, until creatinine levels before admission returned to normal. All this good evolution finally allowed the patient to be discharged from hospital.

DIAGNOSIS
Decompensation of heart failure.
Probable dietary transgression/NSAID intake.
Preserved LVEF.
Biological normofunctioning mitral and aortic prosthesis.
Atrial fibrillation anticoagulated with acenocoumarol.
Impaired renal function in patients with chronic kidney disease (CKD). Probable cardio-renal syndrome.
Normocytic normochromic anaemia.
Diuretic resistance syndrome.
