Conference Papers
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This collection contains abstracts of conference papers, presented at local and international conferences by the staff of the Faculty of Medicine
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Item Familial thrombocytopaenia in three male siblings(Sri Lanka Medical Association, 2017) Amarasena, P.; Premawardhena, A.P.; Herath, H.R.B.M.; Seneviratne, S.L.INTRODUCTION & OBJECTIVES: Familial thrombocytopaenia is uncommon. Specific molecular defects have been identified in some families. We describe three male siblings with thrombocytopaenia and other immune related findings. The parents are healthy and non-related. METHODS: Clinical and investigative findings were obtained from the brothers and their parents. RESULTS: Case 1: A 15 year old male presented with spontaneous ecchymotic patches and oral mucosal bleeding. Platelet count was 1000/mm3, mild hepatomegaly was present on ultrasonography and IgA was raised. As the response to IV methyl-prednisolone was poor, IVIG, prednisolone and azathioprine were used. He has had recurrent RT infections and as his latest platelet counts are suboptimal, Rituximab is being considered. Case 2: A 19 year old male was found to have thrombocytopaenia whilst being investigated for a large scalp haematoma aged 2 years. He had been treated with oral prednisolone and needed pulse IV dexamethasone. Presently he is off steroids and the platelet count is 54000/mm3. Serum IgM is reduced and IgA is raised. He has chronic bilateral lower limb eczema, an atrio-fascicular accessory pathway and gets recurrent RT infections. Case 3: A 12 year old male had fever, cervical lymphadenopathy and hepatosplenomegaly aged 3 years. He then developed AIHA and thrombocytopaenia. The thrombocytopaenia persisted and was treated with prednisolone and cyclosporine. Aged 9 years, he developed SLE and a year later, class IV lupus nephritis was found on renal biopsy. CONCLUSION: An AR or XR genetic cause is likely in this family. The identification of the exact molecular defect may help with selecting appropriate medications to target abnormal immune pathways.Item Outcome of management of yellow oleander poisoning in a Base Hospital setting(Sri Lanka Medical Association, 2001) Seneviratne, S.L.; de Silva, C.E.; Fonseka, M.M.D.; Gunatilake, S.B.; de Silva, H.J.Abstract AvailableItem Outcome of envenomation due to snake bite during pregnancy(Sri Lanka Medical Association, 2001) Seneviratne, S.L.; de Silva, C.E.; Fonseka, M.M.D.; Gunatilake, S.B.; de Silva, H.J.Abstract availableItem Post mortem findings in yellow oleander poisoning(Sri Lanka Medical Association, 2001) Seneviratne, S.L.; de Silva, C.E.; Fonseka, M.M.D.; Gunatilake, S.B.; de Silva, H.J.INTRODUCTION: Death from yellow oleander poisoning (YOP) is mainly due to cardiac toxicity caused by its effect on the conducting system leading to bradyarrhythmias. Whether other organ systems are involved in YOP is not clear. No post-mortem studies of death due to YOP have been documented. OBJECTIVE: To study post-mortem (PM) abnormalities following YOP. METHODS: Post-mortems were performed on patients with YOP who died after admission to Base Hospital, Polonnaruwa (BHP), over a 20 month period from January 1998 to August 1999. Written consent was obtained from relatives for the PM examination. RESULTS: Thirty seven PMs were performed during the study period. There were 21 males and the age range was from 13 to 70 years. Twenty three patients died within 24 hours of admission while ten and two died on the 2" and 3rd days respectively. Two patients died after 72 hours of hospital stay. Almost all subjects (35) had myocardial and pericardial haemorrhages. Congested kidneys were found in 24 (64.8%) while nine had a congested liver. Cerebral oedema was found in 16(43.2%). No abnormalities were found in the lungs and other intra- abdominal organs. CONCLUSION: Deaths occur early in fatal YOP. Myocardial and pericardial haemorrhages were seen in almost all PMs and could have resulted from cardio-pulmonary resuscitation, at least in some patients. PM abnormalities seen in kidneys and brain were probably secondary to hypoperfusion following cardiac arrhythmias. YOP does not seem to cause direct damage to organ systems other than the heart. Further work needs to be done to determine the effects of YOP on the cardiac conducting tissue.