診療に必要な情報が瞬時に確認できるオンラインツール | 今日の臨床サポート

	1:	Delayed-onset encephalopathy and coma in acute organophosphate poisoning in humans.
		著者: John Victor Peter, Appaswamy T Prabhakar, Kishore Pichamuthu 雑誌名: Neurotoxicology. 2008 Mar;29(2):335-42. doi: 10.1016/j.neuro.2008.01.004. Epub 2008 Jan 21. Abstract/Text The objective of the study was to describe the clinical characteristics and course of delayed-onset organophosphate (OP) poisoning. In our clinical experience, we have noticed patients with onset of deep coma 4-7 days after hospital admission, clinical features that have not been previously described. We set up a prospective observational study over 1 year to formally characterize this observation. Thirty-five patients admitted to the intensive care unit (ICU) with severe OP poisoning and treated with atropine and supportive therapy were followed up. Oximes were not administered. Three patients developed delayed-onset coma after presenting with normal or near normal Glasgow coma score (GCS). They developed altered conscious state rapidly progressing to deep coma, 5.0+/-1.0 (mean+/-S.D.) days after OP ingestion. The GCS persisted at 2T for 4.3+/-2.1 days despite the cessation of sedative drugs at the onset of coma. During this period, the patients had miosed non-reacting pupils and no clinically detectable cortical or brainstem activity. Computed tomography of the brain and cerebrospinal fluid analysis were normal. Electroencephalogram showed bihemispheric slow wave disturbances. Two patients required atropine during this period to maintain heart rate and reduce secretions. In all three patients, no metabolic, infective or non-infective cause of altered conscious state was identified. With supportive therapy the GCS improved to 10T in 8.0+/-2.0 days. All patients survived to hospital discharge. Three other patients who developed a reduction in GCS (3T-7T) by 4.7+/-1.2 days but not progressing to coma and recovering (GCS 10T) in 3.3+/-0.6 days may have manifested delayed-onset encephalopathy. Delayed-onset coma appears to have a distinct clinical profile and course with complete resolution of symptoms with supportive therapy. Although persistent cholinesterase inhibition is likely to have contributed to the manifestations, the mechanism of coma and encephalopathy need to be explored in further trials. The good outcomes in these patients suggest that therapy should not be limited in OP-poisoned patients developing profound coma or encephalopathy during hospitalization.   Neurotoxicology. 2008 Mar;29(2):335-42. doi: 10.1016/j.･･･

	2:	Predicting outcome in acute organophosphorus poisoning with a poison severity score or the Glasgow coma scale.
		著者: J O J Davies, M Eddleston, N A Buckley 雑誌名: QJM. 2008 May;101(5):371-9. doi: 10.1093/qjmed/hcn014. Epub 2008 Mar 4. Abstract/Text BACKGROUND: Organophosphorus (OP) pesticide poisoning kills around 200,000 people each year, principally due to self-poisoning in the Asia-Pacific region. AIM: We wished to assess whether patients at high risk of death could be identified accurately using clinical parameters soon after hospital admission. DESIGN: We evaluated the usefulness of the International Program on Chemical Safety Poison Severity Score (IPCS PSS) and the Glasgow Coma Score (GCS) prospectively for predicting death in patients poisoned by OP pesticides. METHODS: Data were collected as part of a multicenter cohort study in Sri Lanka. Study doctors saw all patients on admission, collecting data on pulse, blood pressure, pupil size, need for intubation and GCS. RESULTS: Of the patients, 1365 with a history of acute OP poisoning were included. Receiver operating characteristic (ROC) curves were calculated for the IPCS PSS and GCS on admission. The IPCS PSS and GCS had similar ROC area under the curves (AUC) and best cut points as determined by Youden's index (AUC/sensitivity/specificity 0.81/0.78/0.79 for IPCS PSS > or = grade 2 and 0.84/0.79/0.79 for GCS < or = 13). The predictive value varied with the pesticide ingested, being more accurate for dimethoate poisoning and less accurate for fenthion poisoning (GCS AUC 0.91 compared with 0.69). CONCLUSION: GCS and the IPCS PSS were similarly effective at predicting outcome. Patients presenting with a GCS < or = 13 need intensive monitoring and treatment. However, the identity of the organophosphate must be taken into account, since the half of all patients who died from fenthion poisoning only had mild symptoms at presentation.   QJM. 2008 May;101(5):371-9. doi: 10.1093/qjmed/hcn014. ･･･

	3:	Severity index of paraquat poisoning.
		著者: Y Sawada, I Yamamoto, T Hirokane, Y Nagai, Y Satoh, M Ueyama 雑誌名: Lancet. 1988 Jun 11;1(8598):1333. Abstract/Text   Lancet. 1988 Jun 11;1(8598):1333.