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Common Environmental Toxins By ANNERIE HATTINGH 18 February 2009.

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Presentation on theme: "Common Environmental Toxins By ANNERIE HATTINGH 18 February 2009."— Presentation transcript:

1 Common Environmental Toxins By ANNERIE HATTINGH 18 February 2009

2 Common Environmental Toxins 1.Hydrocarbons 2.Inhaled toxins 3.Pesticides 4.Heavy Metals

3 Hydrocarbons Introduction: One of most frequently reported poisonings Presentation to ED classified into 4 types: 1.) Accidental ingestion, - most common - in children less 5yrs 2.) Intentional inhalation, - abuse of volatile hydrocarbons - recreational 3.) Accidental inhalation / exposure, - household or workplace 4.) Massive oral ingestion, - suicide attempts

4 Hydrocarbons Pharmacology: Diverse group of organic compounds Contain hydrogen and carbon Most are petroleum distillates (e.g. gasoline) - derived from crude oil and coal - turpentine derived from pine oil 2 Main categories (classified by structure) (i) Aliphatics – straight chain hydrocarbons ~ paraffin (lamp oil) ~ mineral turpentine ~ thinners ~ petrol ~ diesel ~ benzine

5 Hydrocarbons Pharmacology: (ii) Aromatics – ring structure hydrocarbons ~ lubricating oil ~ liquid paraffin ~ baby oil ~ suntan oils ~ petroleum jelly ~ grease Hydrocarbons commonly used as solvent base for toxic chemicals like insecticides and metals

6 Hydrocarbons Pathophysiology: 3 main target organs effected: # CNS # Lungs # Heart Most acute damage in the lungs Potential for acute toxicity depends on 4 characteristics 1.) Viscosity (resistance to flow) low viscosity = high toxicity eg. Lubricants + mineral oil * high viscosity + low toxicity Furniture oil * low viscosity + high toxicity + aspiration

7 Pathophysiology: 2.) Volatility (capacity of liquid to turn into gas) - displaces alveolar O 2 - petrol 3.) Surface tension 4.) Chemical side chains - often high toxicity - e.g.. Heavy metals Hydrocarbons

8 Pathophysiology: LUNG DISEASE: Fatalities after ingestion, accompanied by aspiration 1ml in trachea can cause chemical pneumonitis Mechanisms 1)Penetrates lower airways ~ produces bronchospasm + inflammation 2)Displaces alveolar O2 (volatile hydrocarbon) 3)Inhibits surfactant 4)Damaging alveoli and capillaries

9 Hydrocarbons Pathophysiology: These effects cause: Alveolar disfx Vent / Perfusion mismatch Hypoxia Resp. failure

10 Hydrocarbons CNS: Narcotic – like effects: ~ euphoria ~ disinhibition ~ confusion Usually substance abusers - recreational use Single exposure with rapid onset of intoxication + recovery Chronic use causes: ~ peripheral neuropathy ~ cerebellar degeneration ~ neuropsychiatric disorders ~ dementia ~ chronic encephalopathy

11 Hydrocarbons CARDIAC: Sudden death Sudden physical activity during / after intentional inhalation Myocardial sensitization to endogenous + exogenous catecholamines Precipitates vent. dysrythmias + myocardial dysfx

12 Hydrocarbons Clinical presentation: 4 typical presentations: 1.) Accidental ingestion: Usually toddlers Reused beverage containers storing hydrocarbon Mild Sx include ~ tachypnoea ~ dyspnoea ~ bronchospasm ~ fever within 6 hours

13 Hydrocarbons Clinical presentation:(cont.) 1.) Accidental ingestion:(cont.) Severe poisonings ~ early resp. Sx ~ cyanosis ~ grunting ~ coughing ~ repeated vomiting ~ these findings suggests aspiration Change in mental status ~ direct CNS effect OR ~ caused by hypoxia

14 Hydrocarbons Clinical presentation: 2.) Intentional inhalation: Substance abuse Mechanisms include: - “bagging”- hydrocarbon poured into bag/container + deeply inhaled - “huffing” - inhaling through a saturated cloth - “sniffing” Mostly volatile hydrocarbons - petrol - paint - glue

15 Clinical presentation: 2.) Intentional inhalation: (cont.) Presentation: - sudden cardiac arrest - CNS intoxication with euphoria, agitation, hallucinations + confusion Chronic abusers similar to long-term alcoholics - peripheral neuropathy - cerebellar degeneration - encephalopathy Hydrocarbons

16 Clinical presentation: 3.) Accidental dermal exposure or inhaled resp. exposure: In workplace / home Not life threatening Asymptomatic or transient non-specific symptoms Sx resolve with fresh air / removal from offending environment 4.) Intentional ingestion / intravenous injection: Rare Suicide attempts Used in combination with other substances Massive oral ingestion not associated with significant morbidity Hydrocarbons

17 Diagnosis: Clinically History from parents / family / bystanders Contact local poison control centre to identify product CXR: - radiographic changes can occur within 30 min - findings of chemical pneumonitis include: 1.) bilat. perihilar infiltrates 2.) gradually: forms patchy infiltrates 3.) finally: large areas of consolidation Pulse oximetry ABG Hydrocarbons

18 Management: Observe for 4 – 6 hours (even if asymptomatic) If any Sx present: do CXR, pulse oximetry, ABG Supportive care Gastric lavage should be avoided - increased risk of aspiration No antidote If any Sx present suggestive of aspiration – admit for 24 hour observation Manage resp. complications appropriately – give O 2, intubate + ventilate if necessary No prophylactic A/B!!

19 1.Smoke inhalation 2.Cyanide 3.Carbon monoxide INHALED TOXINS

20 Introduction: Inhalation injury common Fires in enclosed spaces like homes / factories Injury typically irritant in nature Heated particulate matter + absorbed toxins injure normal mucosa Carbon monoxide + Cyanide poisoning often associated with smoke inhalation - these are systemic ( not resp.) toxins Smoke inhalation

21 Principles: Fires involves variable fuels + burning conditions - character of smoke not always identified Irritant toxins are produced which damages the airway mucosa Clinical presentation: Morbidity + mortality related to resp. tract damage - thermal / irritant in nature Time between smoke exposure + onset of Sx – highly variable May always be delayed Depend on degree + nature of exposure Smoke inhalation

22 Clinical presentation: (cont.) Cough + stridor - thermal + irritant induced laryngeal injury Cough, stridor + bronchospasm - caused by soot + irritant toxins in the airways Subsequently – a cascade of: - airway inflammation - acute lung injury with pulm. edema - resp. failure Burned nasal hair + soot in the sputum suggest substantial exposure Always consider CO + cyanide inhalation - in pt`s exposed to filtered / distant smoke ( different room) OR - relatively smokeless combustion Smoke inhalation

23 Management: Rapid assessment of the airway + early intubation mandatory (prior to deterioration!!) Supportive care Intraveneous fluid resuscitation Maintenance of adequate oxygenation - suctioning + pulm. toilet Admit to ICU / transfer to Burn Centre Smoke inhalation

24 One of the most rapidly acting poisons Causes: 1.) Smoke inhalation: - most common - compounds containing carbon + nitrogen produce hydrogen CN gas when burned - natural compounds (silk + wood) produces HCN as a combustion product - burning of household furniture + plastics also causes HCN gas Cyanide

25 Causes: (cont.) 2.) Intentional poisoning: - uncommon - cyanide salts in hospitals + labs 3.) Industrial exposure: - Occupations with easy access to cyanide * chemists * jewelers * pest control * mineral refining * photography * electroplating * dying + printing Cyanide

26 Pathophysiology: Cyanide inhibits mitochondrial cytochrome oxidase + blocks electron transport ( binding with ferric iron Fe 3+ ) aerobic metabolism + O 2 utilization decreases Lactic acidosis occurs as a consequence of anaerobic metabolism O 2 cellular level is grossly hampered Cyanide rapidly absorbed from: - stomach - lungs - mucosal surfaces - skin Cyanide

27 Clinical presentation: Sx appear seconds to minutes after exposure HCN gas can lead to cardioresp. arrest + death within minutes Onset of effects after ingestion / skin contamination: - much slower (several hours) - early signs: i) dizziness ii) bronchospasm iii) dyspnoea iv) confusion v) paresis - Later: i) cardiovasc. collapse ii) seizers iii) coma

28 Prognostic features: 1.) Ingestion of few hundred mg of cyanide salt = FATAL 2.) Pt`s surviving to reach the hospital after HCN inhalation - unlikely to have suffered significant poisoning 3.) Lactic acidosis + pulm. edema = severe poisoning Cyanide

29 Management: Avoid mouth – to – mouth resuscitation! Give 100% O 2 - tight fitting facemask - ventilate via ET tube if necessary O 2 contributes to reversal of cyanide-citochrome complex Skin contamination – wash thorough with soap + H 2 O Antidote therapy: - given ASAP, if available - Regimens: 1.) dicobalt edetate ~ toxic ~ only given in confirmed cyanide poisoning Cyanide

30 Management: (cont.) 2.) Nitrate / Sodium Thiosulphate Regimen ~ safer ~ antidote kit with: * amyl nitrate * sodium nitrate * sodium thiosulphate ~ Nitrates oxidizes Hb to MetHb - which has greater affinity for cyanide - leading to dissociation of cyanide citochrome complex ~ Thiosulphate mediates conversion of cyanide to less toxic substance - excreted in urine Cyanide

31 Management: (cont.) Doses: 1.) Inhalation of 0.3ml amyl nitrate (emptied on a gauze) 2.) Then 10ml Sodium Nitrate given ivi over 3min. 3.) 50ml 50% Sodium Thiosulphate given over 10min. Cyanide

32 Most common cause of poison - + fire – related deaths Generated through incomplete combustion of all carbon – containing products Sources: 1.) Smoke inhalation 2.) Poorly maintained domestic gas appliances 3.) Deliberate inhalation of car exhaust fumes Carbon Monoxide

33 Pathophysiology: Intense tissue hypoxia + cell injury caused by 2 mechanisms: 1.) Interrupts electron transport in the mitochondria (like cyanide), leading to anaerobic metabolism 2.) Reduces O2 delivery by: - competing with O 2 for binding to Hb (CO has much higher affinity for Hb, than O 2 !) - Shifting the HbO 2 dissociation curve to the left

34 Carbon Monoxide Pathophysiology: (cont.) REMEMBER!! Affinity of fetal Hb for CO even higher than that of adult Hb! Therefore fetal exposure higher than that of predicted maternal exposure!

35 Carbon Monoxide Clinical presentation: Hypoxia without cyanosis Myocardium + Brain mostly affected ( high O 2 consumption) Sx include: - dizziness - convulsions - headaches - coma - confusion - cardio/resp. dysfx + death - chest pain - dyspnoea - palpitations - syncope

36 Carbon Monoxide Clinical presentation: (cont.) COHb levels correlate poorly with clinical features – only used to confirm exposure “cherry – red” skin + mucus membranes found post mortem

37 Carbon Monoxide Complications: Outcome depends on degree + duration of peripheral tissue hypoxia 1.) CNS: - cerebral, cerebellar + midbrain fx affected 2.) Myocardium: - ischemia + infarction 3.) Skeletal muscle: - rhabdomyolysis - myoglobinuria

38 Carbon Monoxide Complications:(cont.) 4.) Skin: - erythema - severe blistering

39 Carbon Monoxide Management: AIM: minimize + Rx Complications Admit to ICU Give 100% O 2 - tight fitting facemask - ventilate via ET-tube if necessary ( O 2 decreases half life of COHb) Continuous cardiac monitoring Pulse oximeter useless!! - cannot distinguish COHb from HbO2

40 Carbon Monoxide Management:(cont.) Hyperbaric O 2 preferred only if readily available in: - unconscious pt - severe metabolic acidosis - pregnancy - COHb level 25 – 40% - neurological signs Supportive care: - Rx arrhythmias - correction of acid base + electrolyte abnormalities - Rx convulsions

41 Carbon Monoxide Management:(cont.) Ensure F/U as neuropsychiatric squeal may take many weeks to evolve!

42 Pesticides 1.) Organophosphates + Carbamates 2.) Paraquat + Diquat Poisoning

43 Organophosphates + Carbamates Poisoning commonly seen in: - accidental ingestion (kids) - suicide attempts - agricultural workers - pest control Introduction: Potent cholinesterase inhibitors Accumulation of acetylcholine (Ach) Indirect stimulation of nicotinic + muscarinic receptors

44 Organophosphates + Carbamates Introduction: (cont.) Absorbed through: - skin - inhalation - ingestion Carbamate + OP poisoning clinically indistinguishable Differences: - OP forms irreversible complex with cholinesterase - Carbamate complex reversible, with shorter duration of action ( less than 24 h) - Carbamates penetrates blood-brain barrier poorly, therefore less CNS effects

45 Organophosphates + Carbamates Clinical presentation: Minutes to 12 hours after exposure 1.) Muscarinic effects: (post ganglionic) - hyper secretion (sweating, salivation + bronchial secretions) - constricted pupils - bradycardia + hypotension - vomiting + diarrhoea - urinary incontinence - bronchoconstriction - Also commonly referred to SLUDGE syndrome:

46 Organophosphates + Carbamates Clinical presentation: (cont.) S – salivation L – lacrimation U – urinary incontinence D – diarrhoea G – G.I cramps E – emesis

47 Organophosphates + Carbamates Clinical presentation: (cont.) 2.) Nicotinic effects: (preganglionic) - muscle weakness - fasciculations - resp. muscle weakness NB: Sometimes nicotinic effects overrides muscarinic effects! Causes: - tachycardia - hypertension - dilated pupils

48 Organophosphates + Carbamates Clinical presentation: (cont.) 3.) CNS effects: - restlessness - anxiety - headaches - convulsions - coma

49 Complications: Mortality + Morbidity caused by: 1.) Seizers / Coma 2.) Pulm. hypersectretion 3.) Resp. muscle weakness Organophosphates + Carbamates

50 Diagnosis: 1.) Clinically (cholinergic syndrome) 2.) Cholinesterase level Organophosphates + Carbamates

51 Management: 1.) Decontamination: - remove contaminated clothing - activated charcoal within 1-2 hours 2.) Supportive care: NB airway management! - suctioning of secretions - O 2 - ventilate via ET-tube if necessary ( avoid Scoline / succinylcholine!!!) ( may have extremely prolonged duration) Organophosphates + Carbamates

52 Management:(cont.) 3.) Definitive Rx: - Atropine administration! - ASAP - test dose 1mg adults, 0.01mg/kg children - then: 0.05mg/kg (2-4mg) given every 15 min - until full atropinisation achieved - maintenance: iv infusion of 0.05mg/kg/hour - high doses required sometimes - control of bronchial / oral secretions indicates adequate therapy Organophosphates + Carbamates

53 Management:(cont.) 3.) Definitive Rx: - Atropine administration! - reduce dose slowly - do not stop abruptly - Cholinesterase reativator: - e.g. obidoxime - early Mx of moderate – severe OP poisoning - atropine always given first - Contraind. in carbamate poisoning Organophosphates + Carbamates

54 Paraquat + Diquat Most toxic herbicide known ( weed-killers ) Multiorgan toxicity Death due to delayed pulm. fibrosis + resp. failure

55 Paraquat + Diquat Pathophysiology: - Cytotoxic O 2 radicals generated - selectively accumulates in the lungs - Lungs major target organs (except diquat) - also liver, kidneys, heart + CNS - Absorption: * skin * GIT * resp. tract

56 Paraquat + Diquat Clinical presentation: 1.) Chemical burns of oropharynx 2.) Esophageal perforation + mediastinitis (extreme cases) 3.) N + V 4.) Skin irritation 5.) Resp. injury: - high doses cause dyspnoea, ARDS + rapid multiorgan failure - progressive pulm. Injury over 1 – 3 weeks with irreversible pulm. fibrosis

57 Paraquat + Diquat Management: Aggressive early decontamination Gastric lavage Activated charcoal Rx resp. complications appropriately BUT high insp. O 2 concentration worsens resp. toxicity!!! Use low FiO 2 mixtures with CPAP + PEEP

58 Heavy Metal Toxicity -Uncommon dx -Exceptions: 1.) acute iron toxicity (intentional / unintentional) 2.) lead exposure -Unrecognized / inappropriately Rx result in significant morbidity + mortality -Other examples: arsenic, mercury, cadmium.

59 Heavy Metal Toxicity -Toxicity depends on: 1.) ? Metal 2.) Total dose absorbed 3.) Acute/Chronic exposure 4.) Age – children more susceptible to toxic effects + prone to accidental exposures 5.) Route of exposure - e.g. Elemental mercury, not dangerous if ingested / absorbed through skin - disastrous if inhaled / injected

60 Heavy Metal Toxicity -Sources: Exposure through: * Diet supplements * Medications ( herbal remedies ) * Environment * Occupational / Industrial ( most acute presentation) * Ingestion of non food items e.g.Toys, paint chips, ballistic devices, fishing sinkers, curtain weights * Retained bullets ( rarely causes lead toxicity)

61 Heavy Metal Toxicity Pathophysiology: -Remains relatively constant for all heavy metal toxidromes -Binds to O 2, Nitrogen + sulphydryl groups in proteins -Result in: ALTERATIONS OF ENZYMATIC ACTIVITY -Nearly all organ systems involved: * CNS * PNS * Haemapoietic * GIT * Cardiovasc. * Renal

62 Heavy Metal Toxicity Clinical presentation: -History NB! * diet * occupation * hobbies -Nausea, persistent vomiting, diarrhoea, abd. pain -Dehydration -Metal salts = corrosive

63 Heavy Metal Toxicity Clinical presentation: (cont.) -Acute high dose exposures: Encephalopathy ( leading cause of mortality!) Cardiomyopathy Dysrhythmias ATN Metabolic acidosis -Chronic exposures: Anaemia “Mees lines” on nails (horisontal hypopigmented lines across all nails) Subtle neurological signs

64 Heavy Metal Toxicity Diagnosis: -History -FBC -U+E -LFT -Urine analysis -LFT -AXR in ingested heavy metals - some radio opaque

65 Heavy Metal Toxicity Management: (in Emergency Room) 1.) Decontamination ( MOST NB!) * removal from source of exposure * gastric lavage if ingested 2.) Resuscitation: - supportive care - airway protection - Rx arrhythmias - replace fluids + electrolytes

66 Heavy Metal Toxicity Management:(cont.) (in Emergency Room) 3.) Chelation: * rarely indicated in emergency setting * possible exceptions: Lead encephalopathy! * routine chelation not recommended! * Always in conjunction with Medical toxicologist + Local Poison Centre. * Chelation Rx supplies sulphydryl groups for heavy metals to attach to + be eliminated from the body.

67 Heavy Metal Toxicity Management:(cont.) (in Emergency Room) Excamples: -Dimercaprol (mercury + arsenic) -Calcium disodium edetate (acute / chronic lead poisoning) -Penicillamine (mercury, arsenic, lead, copper poisoning) All available in SA!

68 References 1.) Rosen’s Emergency Medicine Online: Part Four, Environment + Toxicology; 2228 – ) SAMF( 8’th Edition): Emergency treatment of poisoning; ) Soghoian S, Sinert R. Heavy Metal Toxicity. eMed: Jul. 2008;


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