ECE2018 Poster Presentations: Pituitary and Neuroendocrinology Clinical case reports - Pituitary/Adrenal (38 abstracts)
Acute hyponatraemia complicating therapy of acute hepatic porphyria need immediate correction before become symptomatic: a case report
Dragan Tesic 1 , Predrag Petrovic 2 , Tatjana Pesic 3 , Edita Stokic 1 , Milioca Medic 1 , Milena Mitrovic 1 , Dragana Tomic/Naglic 1 , Tijana Icin 1 , Ivana Bajkin 1 & Mirjana Tomic 2
1Clinic of Endocrinology, Diabetes and Metabolic Diseases Clinical Centre of Vojvodina, Novi Sad, Serbia; 2Emergency Center Clinical Centre of Vojvodina, Novi Sad, Serbia; 3Clinic of gastroenetrology and hepatology Clinical Centre of Vojvodina, Novi Sad, Serbia.
Introduction: Acute hepatic porphyria is a relatively rare metabolic disorder. Its typical clinical manifeastations are abdominal symptoms and/or troubles belonging to the cerebral oedema. Clinical picture of acute abdomen is frequent and unsuccessful surgical treatment leads to the diagnosis of porphyria.
Case description: Female, born in 1987, presented in emergency surgical unit as appendictis. She was operated but the problems did not disappear. After 3 days, the patient was readmitted with abdominal pain, vomiting and lack of wind and stools, weaknesses. The urine was reddish and at the end porfobilinogen in urine was confirmed.The day before the admittance to the hospital sodium level was 134 mmol/l and on the day of admittance 128 mmol/l. Therapy with 1000 ml 5% glucosae and 1000 ml Ringer solution was administered. Tommorow morning, the patient was with similar troubles but her Na was 116 mmol/l. She was considered to be acute asymptomatic hyponatraemia. 10% glucose solution plus 20 ml 50% glucose was continued plus 0.9% NaCl.The next morning she started to feel bowel movements and since one week ago she started to feel better. However, suddenly patient developed seizures, with foam on mouth, circulatory collaps and respiratory arrhest. Na at that moment was 113 mmol/l. Patient was successfully reanimated. That day received 10 g/24 h od sodium chloide and only 3g as ‘bolus‘. On that therapy tomorrow morning Na was almost unchanged, as it was the case during the whole previous day (110–116 mmol/l). So we decided to give 3g NaCl (125 ml of 3% SolNaCl) on 2–3 h, a total of 12 g. during the day and Na raised to 120 mmol/l, with desired +7 mmol/l rise per day. Next day Na was 130 mmol/l with the need of only one dose of 3 g NaCl. We confirmed acute hepatic porphyria by porphobilinogen of 67, uroporphyrin 455 and coproporhyrin 1333 mmol/l in urine. During the treatment pottassiium level was between 3.1–3.5 mmol/l.
Discussion: The aim of this case report is to emphasize the importance of rapid correction of acute hyponatriaemia, whatever its cause is. Sodium incerase have to be not more than 10 mmol/l/24 h. We do not have to wait hyponatraemia symptomaticity as it was in our case report. As we are affraid of cardiac arrhythmias in case od low potassium, we shoud escape raised intracranial pressure symptomts of low sodium. Patients syster, also with porphyria, died suddenly when she was 20 y. old.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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