NEUROTOXICOSIS Bodnar R.Ya.

1. NEUROTOXICOSIS Bodnar R.Ya.

2. Mercury poisoning Industrial uses. Pathogenesis of Mercury poisoning. Clinical picture. Diagnosis. Treatment. Tetraethyllead poisoning Industrial uses. Pathogenesis of Tetraethyllead poisoning. Clinical picture. Diagnosis. Treatment. Manganesepoisoning Industrial uses. Pathogenesis of Manganese poisoning. Clinical picture. Diagnosis. Treatment. PLANNEUROTOXICOSIS

3. MERCURY POISONING

4. MERCURY POISONING • Mercury has been used commercially and medically for centuries. • In the past it was a common constituent of many medications. It isstill used in hospitals in thermometers and blood-pressure cuffs and commerciallyin batteries, switches, and fluorescent light bulbs. • Large quantities of metallicmercury are employed as electrodes in the electrolytic production of chlorine andsodium hydroxide from saline. • These uses still give rise to accidental and occupationalexposures.

5. MERCURY POISONING • Today, however, exposure of the general population comes from three major sources:fish consumption, dental amalgams, and vaccines. • Each has its own characteristicform of mercury and distinctive toxicologic profile and clinical symptoms. • Dental amalgamsemit mercury vapor that is inhaled and absorbed into the bloodstream. • Dentistsand anyone with an amalgam filling are exposed to this form of mercury. • Liquid metallicmercury (quicksilver) still finds its way into homes, causing a risk of poisoning fromthe vapor and creating major cleanup costs. • Humans are also exposed to two distinct butrelated organic forms, methyl mercury (CH3Hg+) and ethyl mercury (CH3CH2Hg+).

6. MERCURY POISONING • Fish are the main if not the only source of methyl mercury, since it is no longer used asa fungicide. • In many countries, babies are exposed to ethyl mercury through vaccination,since this form is the active ingredient of the preservative thimerosal used in vaccines. • Whereas removal of certain forms of mercury, such as that in blood-pressurecuffs, will not cause increased health risks, removal of each of the three major sourcesdescribed in this article entails health risks and thus poses a dilemma to the health professional.

7. MERCURY POISONING • Exposure to mercury from dental amalgams and fish consumption has been a concernfor decades, but the possible risk associated with thimerosal is a much newer concern. • These fears have been heightened by a recent recommendation by the EnvironmentalProtection Agency (EPA) that the allowable or safe daily intake of methyl mercury bereduced from 0.5 μg of mercury per kilogram of body weight per day, the threshold establishedby the World Health Organization in 1978,to 0.1 μg of mercury per kilogramper day.

8. In nature, mercury vapor (Hg0), a stable monatomic gas,evaporates from the earth’s surface (both soil and water)and is emitted by volcanoes Anthropogenicsources include emissions from coal-burning power stationsand municipal incinerators. After approximatelyone year, mercury vapor is converted to a soluble form(Hg2+) and returned to the earth in rainwater. It may beconverted back to the vapor form both in soil and in waterby microorganisms and reemitted into the atmosphere.Thus, mercury may recirculate for long periods.Mercury attached to aquatic sediments is subject to microbialconversion to methyl mercury (MeHg), whereuponit enters the aquatic food chain. It reaches its highestconcentrations in long-lived predatory fish, such assharks. The Global Cycle of Mercury

9. Panel indicates the routes of transfor-mation tomethyl mercury as originally The Global Cycle of Mercury

10. Panel depicts the increase in mercury concentrationsin feathers of fish-eating birds in Sweden. The periodcovered by these data corresponds approximately to thegrowth of industrialization in Sweden. The Global Cycle of Mercury

12. Acute MERCURY poisoning • Acute mercury poisoning occurs rarely. • It arises up after contact with large quantitiesof mercury.

13. Acute MERCURY poisoning The main symptoms of the acute poisoning are • hypersalivation, • inflammation and formation of ulcers of mucous of the mouth, • swelling of salivary glands, • increase of submandibular lymph nodes, • inflammation of gums, • nausea, • vomiting, • diarrhea, • tenesmus, • intestinal colic.

15. Acute MERCURY poisoning • Necrotizing nephrosis with acute renal failure often develops. • acute bronchitis, • pneumonia. • Very often liver, nervous system are affected. • In blood: hemolysis, leukocytosis, increase of ESR (to 30-50 mm/h), increase of blood protein, nitrogen.

16. Mercury poisoningNecrotizing nephrosis

17. Acute MERCURY poisoning • After the acute poisoning: • a chronic diseases of kidneys, • chronic colitis, • hepatitis • astheniс syndrome. • After the treatment may be complete recovery.

18. Chronis MERCURY poisoning • Occurs after contact with mercury during 8-10 years. • Clinical symptoms develop gradually and are characterized by affection of the NERVOUS SYSTEM. • According to the degree of expressiveness of pathological process chronic poisoning is divided into 3 stages: INITIAL (FUNCTIONAL), MODERATE AND SEVERE.

19. MERCURY POISONINGDIAGNOSIS Early typical symptoms: • irritability, • weakness, • Gingivitis • stomatitis. Confirmation of diagnosis is mercury determination in urine and feces. Presence of mercury in urine without proper clinical symptoms indicates a “mercury carriage”.

20. MERCURY POISONINGTreatment -Todestroymercury and excrete it from organism antidotes are recommend: Unitiol, Sucsimer, sodium thiosulphate. - Most effective is Unitiol (sodium 2,3-dymercaptopropansulfonat) - 5%5-10 ml (0,05 g or 5% 1 ml per 10 kg of patient’s weight). 1 day - 2-4 injections, next 6-7 days –1 injection/ day. - Its sulfhydryl groups formuntoxic complexes with poison and are excreted with urine.

21. MERCURY POISONINGTreatment • Sodium thiosulphate 30% 5-10 ml i/v slowly. • Drugs which improve metabolism and blood supply of brain (Pyracetam, Stugeron). • Glucose 40% 20 ml +Vit. C, • Vit.B 1, B 12, B 6. • Tranquilizers. • Symptomatic therapy.

22. TETRAETHYLLEAD POISONING

23. TETRAETHYLLEADPOISONING • TEL is an oily transparent liquid which contains a 64,07 % of lead, • well dissolves in organic solvents (ether, alcohol, benzol, petrol and other) and in fats.

24. TETRAETHYLLEADPOISONING • ТЕL is applied as antidetonate. • A dangerous contact with TEL may occur -at its producing, - mixing with a fuel, - at cleaning of petrol cisterns. • Tetraethyllead is a strong neurotrop poison.

25. TETRAETHYLLEADPOISONING

26. TETRAETHYLLEADPOISONING

27. TETRAETHYLLEADPOISONING • Tetraethyllead Poisoning is characterized by neurological symptoms.

28. Toxic affection of cerebral neurocytes

29. ACUTE TETRAETHYLLEADPOISONING • in 1-3 hours after a contact with ТЕL the first symptoms of the acute poisoning appear. • According to the degree of expressiveness of clinical manifestations there are three STAGES of the acute poisoning by ТЕL: - INITIAL, - PRECULMINATION, - CULMINATION.

30. CHRONICTETRAETHYLLEADPOISONING • is observed in workers who worked in contact with ТЕLduring long period. • A clinic develops gradually and can be poorly expressed. • According to thedegree of expressiveness of clinical manifestations there are three STAGES of the chronic poisoning: • I-st (initial), • II-nd • III-rd.

31. ACUTETELPOISONINGTreatment • To wash up skin (with warm water and soap), to make gastric washing,to use absorbents. • Patients with acute TEL poisoning need complete rest, hypnotic medicines from the group of barbituratus (phenobarbital, barbital sodium or etaminal sodium). • At hyperexcitability barbamil (i/m or i/v) or hexenal are prescribed. • hypertensive solution of glucose i/v, Vitamine therapy. • Warm baths are recommended before sleep.

32. CHRONIC TELPOISONINGTreatment • Treatment of patients with the chronic form of TEL poisoning is appointed taking into account expressiveness of clinical manifestations. • For such patients - drugs which influence on a tissue metabolism (glutamine acid, glucose, vitamins C, B1, B2, ATF, riboxin), - tranquilizers (Diasepam, Tazepam) are recommended.

33. MANGANESEPOISONING

34. Manganesepoisoning • The occupational manganese poisoning occurs among workers who work - on the manganese mines, - in metallurgical industry at steel making , -special alloys producing (ferromanganese – to 80 % of manganese, mirror cast-iron – to 15 % of manganese), - at making of electrodes and gumboils which are used for the electric welding, - in chemical and lacquer-paint industry, - in agriculture (stain of seed for stimulation of plant growth), - in rubber industry. - Most dangerous is ground and sifting of pound ore, because a lot of small disperse dust of manganese appear.

35. VARIANTS OF CLINICAL COURSE

36. Manganesepoisoning - The oxides of manganese are quickly absorbed. - In blood manganese circulates as an unsteady complex with plasma proteins. - Manganese is deposited in bones, cerebrum, parenchyma organs. - It is excreted from the organism with feces and urine. - Manganese may cause bronchial asthma and eczema because of its allergic influence.

37. Manganesepoisoning Pathogenesis • Manganese, as a microelement, takes part in biological processes of organism. • It influences on metabolic processes, depresses cholinesterase activity, affects metabolism of serotonin. • At the protracted and systematic getting into the organism it has a direct influence on nervous tissue, and causes vascular violations, increase capillary permeability. • It changes activity of enzymes of nervous cells, depresses the biosynthesis of catecholamines, intensifies protein metabolism.

38. Manganesepoisoning Pathogenesis The action of manganese is divided into two phases. • I phase – cholinergic – is characterized by predominance of cholinergic influence. • II phase – phase of areactivity – injury of acetylcholinoreactive structures. • A manganese influences on the function of thyroid, cardiovascular system, gastrointestinal tract, liver and other.

39. Acute Manganesepoisoning • In industry acute manganese poisoning occurs rarely. • It arises up at breathing in large quantitiesof dust which contains manganese. • Manganese poisoning causes severe disorders of blood circulation, dyspnea, frequent syncopes. • In easy cases of poisoning irritation of the mucous of respiratory tracts, cough, and headache are observed.

40. CHRONIC MANGANESE POISONING • Clinical picture of the chronic manganese poisoning is characterized by three stages. • !!! The special feature of clinical course of chronic manganese poisoning is inclination to its progress after stopping contact with a metal.

41. MANGANESE POISONINGDIAGNOSIS • Special attention is paid to early diagnosis of chronic manganese poisoning. • It’s necessary to find out a professional route, • sanitary description of labor conditions (manganese concentration in the workplace, • duration of contact during work day, experience of work, influence of other harmful professional factors), • to analyse results of biochemical investigations (level of manganese in blood, urine, saliva, milk).

42. MANGANESE POISONING • A decline of patient activity, dormancy of psychical processes, insufficient critical relation to the state of organism predetermine the late appeal of patients for medical help.

43. Handwriting in different stages of manganese poisoning

44. MANGANESE POISONINGTreatment • Glucose40 % + Vit.C (300-500 mg) i/v, • vitamin B1 (40-50 mg), • 0,25 % novocaine 10-15 ml (15-20 injections). • At appearance of Parkinsonism signs it is necessary to prescribe antiparkinsonism cholinolytics (Cyklodol, Norakin, Amedin, Tropacin, tab. “Korbella”). • Tropacinum – is effective antiparkinsonism cholinolytical drug (10-20 mg 1-2 times per a day after meal). “Karbella” decrease tremor and diminish tonus of muscles (1 tablet before sleep).

45. MANGANESE POISONINGTreatment • medical gymnastics • bath (36-37C, duration - 20 minutes, course of treatment - 10 baths) • Application of ozocerite on spine (20-25 minutes 7-10 days)).

46. THANK YOU FOR ATTENTION !