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Patient with fever, cough, shortness of breath, diarrhoea, nightmares, rhabdomyolysis and gradually worsening kidney function

An 89-year-old man with a history of paroxysmal atrial fibrillation, a pacemaker (inserted in 2006 due to sick sinus syndrome), ischemic heart disease, mild chronic renal failure, allergy to penicillin, bronchiectasis .... developed a cough that had started about 20 days ago. The cough worsened in the last week and fever and diarrhea (~2 per day) occurred. Gradually weakness, headache and then progressively worsening shortness of breath settled in the last 24 hours.


His medication included antihypertensives (angiotensin receptor blocker and diuretics), aspirin, a statin (rosuvastatin), and amiodarone, which had replaced sotalol 2 months ago because of arrhythmias during pacemaker control. He took nothing extra for the new onset symptoms other than simple antipyretics for the last week. On clinical examination, the patient appeared ill and had respiratory distress (40 breaths/min, SO2 86%, accessory muscle use) that worsened when lying down. On auscultation of the lungs there were bilateral auscultations, but mainly in the right lung. The patient had tachycardia (120 beats/min) and complete arrhythmia with an irregular pulse. The cardiogram showed atrial fibrillation with no other serious abnormalities. The patient was unable to get up and stand while having a fairly good level of communication. Neurological examination was unremarkable. From the abdomen there was flatulence (gas in the bowel) and increased bowel sounds. The skin showed no changes. He reported no pain anywhere in his body. From the blood tests, the patient showed an increase in white blood cells (13300/µL), polymorphonuclear (86%), an increase in C reactive protein (23.3 mg/dl), worsening of renal function (creatinine 2.9 mg/dl, urea 140 mg /dl), rhabdomyolysis (muscle destruction, CPK 10600 IU/L), increased myocardial enzymes (troponin 164 pg/dl, CK-MB 213 IU/L, SGOT 240 IU/L) but without liver function disorder . The patient underwent cardiac ultrasound which showed good cardiac function and contractility. Chest computed tomography showed diffuse ground-glass imaging bilaterally, areas of fibrosis and interstitial edema as well as bronchiectasis bilaterally. He was placed on IV antibiotics for a possible respiratory infection, hydration and urine alkalinization (which was soon discontinued as it was not effective) for the rhabdomyolysis, and on anticoagulants and β-blockers for the atrial fibrillation. Amiodarone and statin were discontinued.


The patient recovered quickly, his general condition improved but the inflammation markers remained high as well as the white blood cell count. Respiratory function also improved (30 breaths per minute) but hypoxaemia persisted when the oxygen mask was removed and worsened with any attempt by the patient to move. On the 5th day of hospitalization, the patient's level of consciousness had improved significantly and when the patient was informed of the discontinuation of amiodarone he reported that after its initiation he started having vivid dreams and nightmares, which disappeared on admission to the hospital. At that point the antibiotic treatment was changed and cortisone was added to the treatment for possible toxicity due to amiodarone. In the following days respiratory function improved significantly (20 breaths/min, SO2 91% without oxygen) and diarrhea was discontinued. Inflammation markers started to improve gradually. The patient started to feel better and was able to stand up and walk.

After 12 days of hospitalization the patient was discharged from the hospital in good condition with home oxygen, antibiotics, cortisone and anticoagulants. On examination performed a few days later, the patient was in much better condition, and his respiratory function remained stable. Drug toxicity is a fairly common cause of hospitalisation. Amiodarone is one of the most commonly used drugs in cardiology. Its effectiveness is proven, but it sometimes causes significant side effects such as nightmares, nephropathy, nephropathy, pneumonitis, thyroid disease, hepatitis, pancreatitis, corneal deposition and in combination with other drugs such as statins can cause or predispose to rhabdomyolysis.

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