急性二氯乙烷中毒 Acute occupational 1,2-dichloroethane poisoning

1、1Acute occupational 1,2-dichloroethane(1,2-DCE) poisoning 2General Profile Application and Exposure： Widely use in electronics manufacture, shoes manufacture, ，Industrial production, such as rubber , resin, paint, synthetic fiber and vinyl-chloride ,ect.Mainly used as organic solvent and glue in Chi

2、na.3General Profile Mechanism of Poisoning ： Attack induced by increasing free radicals Cells suffocation induced by interference to the metabolism of brain cells Brain edema type: vasogenic cerebral edema (at first), mixed cerebral edema (mainly);4 Cause acute and subacute poisoning epidemic types:

3、 sporadic ,seldom outbreak Central nervous system damage is the main manifestations . High cranial pressure syndrome occurs initially and follows by disturbance of consciousness.A few patient can have secondary epilepsy.5 Widespread brain damage that involves the whole brain,especially in the cerebe

4、llum and extrapyramidal Brain edema last a long period and often occur repeatedly; A few patient can have secondary epilepsy May be accompaniedby liver, kidney and heartdamage.clinical manifestations6Case introduction Female，46y， worker of a shoes factory Occupational history ： 2009.062010.01, Shoes

5、 modeling (放港宝), attach shoe materials, exposed to thinners (banana oil) 。 Working 1012h/day, in a small house with windows closed in cold winter, no fresh air， No mask or other protective equipments, one more worker in the same position.78Walkthrough investigation: 2010.01.09-12, Result of Air Test

6、 in modeling workshop: Max concentration of 1,2-DCE 7.4mg/m3。 Result of material analysis : 1,2-DCE can be found in thinners (banana oil) 9 Chief complaint:Headache for 9 days with limb convulsion for 8 daysHistory of present illness: 2010.01.04 had progressive headache with nausea 2010.01.05 had se

7、vere headache and vomit after lunch took some pills for cold by herself , but still got worse develop to aphasia and limb convulsion limb convulsion shook her twice in an hour, 10-60 seconds every time . With lost consciousness, eyes on the turn , limb stiffness. Sent to general hospital but continu

8、ed getting worse, limb convulsion occurred more often with the longer lasting time. .10 2010.01.08 Transferred to the Infectious disease department (tertiary general hospital) Intracranial pressure (ICP) 150mmH2O， CSF test was normal. Head MR was no change； Treatment: reduce intracranial pressure 、a

9、nti-infection Effect: slightly relieved After special Consultation ，the patient was presumptive diagnosed as Acute DCE poisoning and sent to our hospital.11Physical examination Specialized examination of nervous system: Tired，clear， active position: ； neck stiffness, dysarthria , inflexible eye move

10、ment 、no nystagmus Pupils: equal roundness, same size2.5mm, delay reaction； Muscle tension normal, but low muscle strength failure in finger nose test 、heel-knee-tibia test 。 physiological reaction normal, no pathological reaction 12Laboratory findings 2010.01.05 Head CT :No change found 2010.01.07

11、Head MRI :spot-like cerebral ischemia in semiovale. 2010.01.15. Head CT :No change found13影像学检查1月6日MR检查：半卵园中心可疑点状缺血。1月5日CT检查：涉及半卵园中心各个层面密度均正常。14Laboratory findings ALT 43IU/L、GGT 51IU/L、GLU 7.3mmol/l、C3 1.7g/l、C4 0.54g/l。 2010.01.14 EEG：abnormal. 2010.03.02 Head MRI：(slight) multiple demyelinating l

12、esions in semiovale and corona radiata (induced by poisoning)15Discharge & follow-up After 2 years treatment in our hospital, the patient remained: Alalia, upper limb intentional tremor , failure in finger nose test Muscle tension was high, but muscle strength was normal Normal pupil reaction, flexi

13、ble eye movement, no nystagmus physiological reaction normal, no pathological reaction tests of the liver and kidney functions was normal16 The most outstanding imaging characteristics of 1,2-DCE poisoning is diffuse brain white matter demyelinating, which may last 6 months to 1 year or more But at

14、very early stage, imaging test may be normal ,then comes up with cerebral edema, which last longer than cerebrovascular disease Imaging characteristic of 1,2-DCE poisoning17Imaging characteristic of 1,2-DCE poisoning (CT)Showed extensive low density focus (edematiclesions) in bilateral cortical area

15、s, basal ganglia, thalamus. Swelling gyri and compressed sulci.18Imaging characteristic of 1,2-DCE poisoning (MRI)T1WI: symmetry low signal in superficial white matter of frontal and temporal area, but the deep white matter is normalT2WI: symmetry high signal in superficial white matter of frontal a

16、nd temporal area 19Imaging characteristic of 1,2-DCE poisoning (MRI)MRI T1WI：low signalMRI T2WI： high signal MRI FLAIR： diffuse high signal in bilateral cortical areas20Diagnosis 1. Clear exposure to 1, 2 DCE (found in patients biological test and material samples) 2. The clinical manifestations of

17、central nervous system damage (brain edema, disturbance of consciousness, ataxia, epilepsy, etc.) 3. May be accompanied by liver and kidney damage 4. Head imaging examination (visible brain alba change, early change of cerebral edema). 5. Eliminate nervous system lesions caused by other reasons21Gen

18、eral Principle Rescue Principle: Closely observe, early perceive and timely treatment ， prevent relapse Medicine Principle: Early detection, early diagnosis, early treatment and adequate entire course medicine (No specific antidote) 22Treatment Early symptomatic treatment Dehydrate therapy (Progress

19、ive, whole course, adequate ) Glucocorticoid therapy (large dose pulse therapy) Anti-free radical treatment Hyperbaric oxygen (HBO) (earlier, better) Intensive nursing service Anti-infective treatment Supportive treatment (anti-epilepsy ) Physiotherapy & functional exercise23Prognosis Death may occur in severe poisoning patients of cerebral hernia Patient may have kinds of sequelaes with delay in treatment, such as epilepsy, ataxia, myoclonus, but seldom intelligence damage Some patients may recovery, leaving cerebrovascular and nerve