Abstract

We describe a patient with acute disseminated encephalomyelitis following leptospira infection. This case highlights the importance of complete investigation for diagnosis and early treatment, leading to a better prognosis and reduction in morbidity and mortality.

Introduction

Leptospirosis-induced acute disseminated encephalomyelitis (ADEM) has rarely been reported in the literature with almost all cases originating from Asian countries. We describe a case of ADEM after leptospirosis acquired in the Netherlands.

Case report

We describe a 69-year-old male patient with a previous medical history of non-erosive gastritis, osteoporosis, depressive disorder and pneumonia requiring mechanical ventilation five months prior to presentation. This pneumonia was complicated by delirium and a cryptogenic organising pneumonitis requiring long-term, high-dose steroids. On presentation, his medication consisted of venlafaxine 75 mg, prednisone 5 mg and calcium carbonate/colecalciferol 500 mg/440 units, all once daily. During a heat wave in the Netherlands with maximal temperatures of 37.5 ⁰C, the patient complained of severe abdominal pain with loss of appetite and uncontrollable vomiting. After a day he visited his general practitioner who considered gastritis and started metoclopramide 10 mg three times daily, omeprazole 40 mg twice daily and ranitidine 150 mg twice daily. The prednisone was discontinued. Due to persistent complaints he was seen in the emergency department of his local hospital four days later. An ECG and laboratory tests were performed showing reassuring results and he was discharged home without a classifying diagnosis and prescribed oxycodone. In the following three days, his symptoms worsened in combination with darkened urine, oliguria and marked confusion with erratic behaviour and fever. The patient presented again to the same hospital and laboratory testing now showed severe rhabdomyolysis with creatine kinase 148,795 U/l (0-171 U/l), urea 25 mmol/l (2.5-6.4 mmol/l), creatinine 494 µmol/l (53-119 µmol/l), aspartate aminotransferase 2912 U/l (0-35 U/l), alanine aminotransferase 564 U/l (0-45 U/l), lactate dehydrogenase 2955 U/l (0-248 U/l), and a C-reactive protein of 65 mg/l (0-10 mg/l). There was a mild leukocytosis of 14.4 x 109 /l (4.0-10 x 109 /l) and mild thrombocytosis of 579 x 109 /l (150-400 x 109 /l). CT angiography of the abdomen showed no apparent pathology besides possible infiltrate of the right lower lobe of the lung, for which a short three-day course of cefuroxime was started. No definite cause was found for this rhabdomyolysis and the confused state was thought to be caused by delirium. Hyperhydration with balanced solutions, frusemide and sodium bicarbonate solution was commenced. The differential diagnosis with these findings was cryptogenic organising pneumonia, hypersensitivity pneumonitis (extrinsic allergic alveolitis) due to known activity with birds, or iatrogenic pneumonitis following the use of venlafaxine, which was withdrawn. After hyperhydration, the rhabdomyolysis and acute kidney injury improved. No renal replacement therapy was necessary. Severe confusion resulted in exhaustion making sedation and mechanical ventilation necessary. Prior to intubation, tremors and myoclonus were witnessed. Lumbar puncture was performed, showing a clear aspect with normal glucose and lactate but an increased white blood cell count (20 x 106 /l (3-14 x 106 /l)) and a high protein (1620 mg/l (206-629 mg/l). Blood cultures and liquor cultures remained sterile. A gastroscopy and colonoscopy were performed but showed no abnormalities.