Browsing by Author "Buckley, N."

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    Delayed psychological morbidity in victims of snakebite envenoming
    (Sri Lanka Medical Association, 2010) Williams, S.S.; Wijesinghe, C.A.; Jayamanne, S.F.; Buckley, N.; Dawson, A.; Lalloo, D.G.; de Silva, H.J.
    OBJECTIVES: We assessed delayed somatic symptoms, depressive disorder, post-traumatic stress disorder (PTSD) and impairment in functioning among snakebite victims. The psychological impact of snakebite on its victims has not been systematically studied. METHODS: The study had qualitative and quantitative arms. In the quantitative arm, 88 persons who had systemic envenoming following snakebite from the Polonnaruwa District were randomly identified from an established research database and interviewed 12 to 48 months (mean 30) after the incident. 88 persons with no history of snakebite, matched for age, sex, geograpical location and occupation acted as controls. A modified version of the Beck Depression Inventory, Post-Traumatic Stress Symptom Scale, Hopkins Somatic Symptoms Checklist and Sheehan Disability Inventory, together with a structured questionnaire were administered. In the qualitative arm, focus group discussions among snakebite victims explored common somatic symptoms attributed to envenoming. Results: Snakebite victims had more symptoms as measured by the modified Beck Depression Scale (mean 19.1 vs 14.4) and Hopkins Symptoms Checklist (38.9 vs. 28.2) compared to controls (p<0.001). 48(54%) victims met criteria for depressive disorder compared to 13(15%) controls. 11(12.5%) victims also met criteria for PTSD. 24(27%) claimed that the snakebite caused a negative change in their employment; 9(10.2%) had stopped working. 15(17%) victims claimed residual physical disability, and themes identified in the qualitative arm included blindness, tooth decay, body aches, tiredness and weakness. CONCLUSIONS: Snakebite causes delayed psychological morbidity, a complication not previously documented.
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    Mechanisms underlying early rapid increases in creatinine in paraquat poisoning
    (Public Library of Science, 2015) Mohamed, F.; Endre, Z.; Jayamanne, S.; Pianta, T.; Peake, P.; Palangasinghe, C.; Chathuranga, U.; Jayasekera, K.; Wunnapuk, K.; Shihana, F.; Shahmy, S.; Buckley, N.
    BACKGROUND: Acute kidney injury (AKI) is common after severe paraquat poisoning and usually heralds a fatal outcome. The rapid large increases in serum creatinine (Cr) exceed that which can be explained by creatinine kinetics based on loss of glomerular filtration rate (GFR). METHODS AND FINDINGS: This prospective multi-centre study compared the kinetics of two surrogate markers of GFR, serum creatinine and serum cystatin C (CysC), following paraquat poisoning to understand and assess renal functional loss after paraquat poisoning. Sixty-six acute paraquat poisoning patients admitted to medical units of five hospitals were included. Relative changes in creatinine and CysC were monitored in serial blood and urine samples, and influences of non-renal factors were also studied. RESULTS: Forty-eight of 66 patients developed AKI (AKIN criteria), with 37 (56%) developing moderate to severe AKI (AKIN stage 2 or 3). The 37 patients showed rapid increases in creatinine of >100% within 24 hours, >200% within 48 hours and >300% by 72 hours and 17 of the 37 died. CysC concentration increased by 50% at 24 hours in the same 37 patients and then remained constant. The creatinine/CysC ratio increased 8 fold over 72 hours. There was a modest fall in urinary creatinine and serum/urine creatinine ratios and a moderate increase in urinary paraquat during first three days. CONCLUSION: Loss of renal function contributes modestly to the large increases in creatinine following paraquat poisoning. The rapid rise in serum creatinine most probably represents increased production of creatine and creatinine to meet the energy demand following severe oxidative stress. Minor contributions include increased cyclisation of creatine to creatinine because of acidosis and competitive or non-competitive inhibition ofcreatinine secretion. Creatinine is not a good marker of renal functional loss after paraquat poisoning and renal injury should be evaluated using more specific biomarkers of renal injury