Extract

Background

The surviving sepsis campaign recommends that every patient must receive 30 cc/kg fluid for the resuscitation from sepsis-induced hypoperfusion within the first 3 h.1 In an acute clinical scenario, it is very difficult to know the right amount of fluid to give to a patient with sepsis. Sepsis sometimes coexists with hypervolaemia in patients with congestive heart failure or pulmonary hypertension; furthermore many conditions mimic sepsis by meeting criteria for systemic inflammatory response syndrome including anaphylaxis, aspiration, bowel obstruction, colitis, hypovolemia, pancreatitis, pulmonary embolism, GI bleeding, heart failure, acute coronary syndrome, spinal cord injury, toxic overdose, medication effect and vasculitis. If these conditions are not considered, there is potential for increased mortality and morbidity.2

Case presentation

A 30-year-old male patient presented to the emergency department with a 3-week history of shortness of breath on exertion, coughing white sputum and feeling generally unwell. He had been initially treated as lower respiratory tract infection by his GP and was given antibiotics with no improvement. Initial observations revealed O2 saturations of 93%, respiratory rate of 25, blood pressure 85/45, a heart rate of 120, temperature 37.8 and the patient appeared slightly pale. Initially, sepsis was suspected and IV fluids started (500 ml of Hartmann’s) in accordance with the local sepsis bundle. His chest X-ray showed a mildly enlarged heart but was otherwise clear. A focused cardiac ultrasound as part of the RADiUS protocol for dyspnoea was initially performed. POCUS echo performed in the emergency department (Figure 1) demonstrated dilated cardiomyopathy with a visual ejection fraction 10%, mitral regurgitation and suspected distal thrombus. Fluids were immediately stopped and 40 mg of IV furosemide administered. The patient was subsequently admitted to CCU. A formal echocardiogram confirmed the diagnosis. The patient was treated with Ramipril, Bispoprolol and Eplerenone and underwent a cardiac viability MRI which showed evidence of non-ischaemic cardiomyopathy with an EF of 6%. His renal function also started to deteriorate secondary to his cardiogenic shock and he was started on dopamine. Renal function improved and the dopamine was weaned down but unfortunately he started to become overloaded again and it was increased again to 10 mg/h prior to discharge to the cardiac reference Hospital. Currently, the patient is awaiting cardiac transplant.

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