Management of Acute Poisoning ANISH FINAL
-
Upload
anish-joshi -
Category
Documents
-
view
49 -
download
3
Transcript of Management of Acute Poisoning ANISH FINAL
![Page 1: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/1.jpg)
Management of Unknown Acute Poisoning
Dr. ANISH JOSHIMD, FNB CRITICAL CARE,
INDIAN DIPLOMA IN CRITICAL CARE,
FELLOW OF COLLEGE OF CHEST PHYSICIANS,
FELLOW OF COLLEGE OF CRITICAL CARE MEDICINE
![Page 2: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/2.jpg)
2
Agents commonly responsible for acute Poisoning
Pesticides:Organophosphates, Carbamates,
Organochlorines, Synthetic pyrethroids, Rodenticides, Herbicides, Fumigants, Unlabelled powders sold by hawkers
Household chemicalsAcids, Bleach,Grain preservatives, Drain
cleaners,Naphthalene balls, CuSO4, Cosmetics
![Page 3: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/3.jpg)
3
Agents responsible for acute Poisoning contd.
Industrial Chemicals
Irritant gases like Chlorine and Ammonia, Acid fumes like Oleum, MethHb forming agents such as Nitrobenzene, Solvents like acetonitrile, Intermediates released during the manufacture of Dyes and Pharmaceuticals
![Page 4: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/4.jpg)
4
Pharmaceuticals
Sedatives and hypnotics (mostly benzo-diazepines) either alone or in combination with alcohol, phenobarbital, Chlorquine, antidepressants, drugs used in treatment of major psychotic disorders like schizophrenia, OTCs, antihistaminics, Mixed ingestions
Agents responsible for acute PoisoningAgents responsible for acute Poisoning contd.contd.
![Page 5: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/5.jpg)
5
Plant Poisonings
Datura, Argemone (Epidemic dropsy)
Plants with digitalis like effect Animal Toxins
Snake bites, scorpion bites
Agents responsible for acute Poisoning contd.
![Page 6: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/6.jpg)
6
4 situations
1. History of ingestion(mostly), poison is known and treatment is known
2. History of ingestion, poison is known but the physician is not very confident about the treatment
3. History of ingestion but poison is unknown
4. ? Poisoning e.g pt is unconscious
![Page 7: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/7.jpg)
7
Situation 1 – does not need any discussion
Situation 2 – Ask the Poison Center
Tel: + 91 - 79 - 2755 35 94 / 95 (10 am – 5.30 pm), Monday to Friday
At other times – see website www.inchem.org
Situation 1 & 2Situation 1 & 2
![Page 8: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/8.jpg)
8
Situation 3 and 4
1. First attend to the patient then poison
Resuscitate the patient without contaminating yourself
2. Be patient with the relatives and insist on seeing the empty container or a leaflet
3. Location and occupation of the patient can be a pointer to the poison
![Page 9: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/9.jpg)
9
Management Guidelines
If the patient is unconscious and poisoning is doubtful then look for other causes such as Trauma or Metabolic causes ( Poisoning and trauma may co-exist)
Symptom complexes or Toxidromes may help
![Page 10: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/10.jpg)
10
Gastrointestinal decontamination
Induction of emesis, Syrup of Ipecac not available & its role is being questioned in countries where it is available
Gastric lavage is the only way to remove unabsorbed poison, but it needs to be with care, aspiration pneumonitis common, should not be done with ingestions of corrosive substances and hydrocarbon ingestions
![Page 11: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/11.jpg)
What is a Toxidrome?
Several clinically recognizable features, s/s, phenomena or characteristics which often occur together, so that presence of one feature alerts the physician to the others
Narrows the differential diagnosis to a specific class of poisons
11
![Page 12: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/12.jpg)
Toxidrome Features Drugs/Toxins Drug Treatment
“DUMBELS” D -DiarrhoeaU- Urinary frequency,
M- miosis,
B - bradycardia, bronchorrhoea bronchoconstriction,
E - emesis,
L - lacrimation
S – salivation
OrganophosphatesCarbamatesPhysostigminePilocarpine
Atropine
Oximes for Organophosphates
The Cholinergic ToxidromeThe Cholinergic Toxidrome
12
![Page 13: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/13.jpg)
The Anticholinergic ToxidromeThe Anticholinergic Toxidrome
Toxidrome Features Drug Toxin Drug Treatment
Hot as HareDry as a boneRed as a beet Mad as a hatter
Altered mental statusSedationMydriasisTachycardiaFeverDry skinDry mucous membranesDecreased bowel sounds FlushingUrinary Retention
AntihistaminicsAtropineBaclofenBenztropineDaturaTCAPhenothiazinesScopolamine
For life threatening events use Physostigmine*Not indicated for TCA as it may worsen conduction disturbances
*not available in India
13
![Page 14: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/14.jpg)
Sedative Hypnotic ToxidromeSedative Hypnotic Toxidrome
Features Drug Toxin Drug Treatment
Slurred speechConfusionStupor ComaApnoea
AnticonvulsantsAntipsychoticsBarbituratesBenzodiazepinesEthanolOpiates
NaloxoneFlumazenilUrinary alkalinization for Phenobarbital
14
![Page 15: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/15.jpg)
Narcotic ToxidromeNarcotic Toxidrome
Features Drug Toxin Drug Treatment
Altered Mental StatusSlow shallow breathsMiosisBradycardiaHypotesionHypothermiaDecreased Bowel Sounds
DextromethorphanOpiatesPentazocinePropoxyphene
Naloxone
15
![Page 16: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/16.jpg)
Extrapyramidal ToxidromeExtrapyramidal Toxidrome
Features Drug Toxin Drug Treatment
RigidityTremorOpisthotonusTrimusHyperreflexiaChoreoathetosis
HaloperidolPhenothiazinesRisperidoneOlanzapine
DiphenhydramineBenztropine
16
![Page 17: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/17.jpg)
Serotonin ToxidromeSerotonin Toxidrome
Features Drug Toxin Drug Treatment
IrritabilityHyperreflexiaFlushing DiarrheaDiaphoresisFeverTrismusTremorMyclonus
FluoxetineParoxetineSertralineTrazodoneClomipramine
BenzodiazepinesWithdrawal of drugCyprohepatidine (?)
17
![Page 18: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/18.jpg)
Solvent ToxidromeSolvent Toxidrome
Features Drug Toxin Drug TreatmentLethargyConfusionHeadacheRestlessnessIncoordinationDepersonalization
HydrocarbonsTolueneAcetoneNaphthaleneChlorinatedHydrocarbons
Withdrawal of toxinAvoid catecholamines
18
![Page 19: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/19.jpg)
EpileptogenicEpileptogenic
Features Drug Toxin Drug Treatment
TremorsHyperreflexiaTonic clonic seizuresHyperthermiaMay mimic stimulant patterns
Organochlorine pesticides like Endosulfan, LindaneIsoniazidCamphorStrychninePhencylidineCocaineXanthines
Antiseizure medicationsPyridoxine for IsoniazidAvoid phenytoin for theophyllineInduced seizures
19
![Page 20: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/20.jpg)
Hallucinogenic ToxidromeHallucinogenic Toxidrome
Features Drug Toxin Drug Treatment
HallucinationsPsychosisPanicFeverMydriasisHyperthermiaSynesthesia*
AmphetaminesCannabinoidsCocaineLSDPhencyclidine(May present with miosis)
Benzodiazepines
* Synesthesia :One sensory experience described in terms of * Synesthesia :One sensory experience described in terms of another sensory experience.another sensory experience.
20
![Page 21: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/21.jpg)
Limitations of diagnosis based on toxidromes
Toxidromes are most clinically useful when the patient has been exposed to a single drug.
Many toxidromes have several overlapping features.
For example, anticholinergic findings are highly similar to sympathomimetic findings, with one exception being the effects on sweat glands: anticholinergic agents produce warm, flushed dry skin, while sympathomimetic produce diaphoresis.
21
![Page 22: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/22.jpg)
Limitations of diagnosis based on toxidromes
Toxidrome findings may also be affected by individual variability, comorbid conditions, and co-ingestants.
For example, tachycardia associated with sympathomimetic or anticholinergic toxidromes may be absent in a patient who is concurrently taking ᵝ blockers.
When multiple drugs have been ingested, conflicting clinical effects may negate each other and cloud the clinical picture.
22
![Page 23: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/23.jpg)
Pesticide Poisoning
Commonest cause of Self-poisoning or Deliberate self-harm (DSH)
Accidental poisoning : may occur in children Occupational poisoning: In farmers during
spraying or pesticide formulatorsRoutes of exposure:
Most pesticides can be absorbed by all routes including dermal route and inhalation route, though toxicity and mortality are highest when ingested for self-harm as usually persons take a large amount
23
![Page 24: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/24.jpg)
Insecticides
Organophosphates e.g.malathion, chlorpyriphos, monocrotophos, dimethoate, phorate, quinalphos, ethion, Fenthion
Carbamates: Propoxur, Carbaryl Organochlorines: DDT, BHC,
Lindane, Endosulfan Synthetic pyrethroids: Cypermethrin,
Deltamethrin, Fenvalerate Neonicotinoids: Imidacloprid
24
![Page 25: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/25.jpg)
Organophosphates
Some are also used nerve agents for terrorist attacks
Sarin gas was released in the Tokyo subway system by the Aum Shinrikyo Cult, creating more than 5,000 victims and causing 12 deaths. (1995)
25
![Page 26: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/26.jpg)
Organophosphorus pesticides inhibit the enzyme Organophosphorus pesticides inhibit the enzyme
acetylcholinesteraseacetylcholinesterase in synapses and on RBC membranes, in synapses and on RBC membranes,
and and butyrylcholinesterasebutyrylcholinesterase in plasma. in plasma. Although acute butyrylcholinesterase inhibition does Although acute butyrylcholinesterase inhibition does
not seem to cause clinical features, not seem to cause clinical features, acetylcholinesteraseacetylcholinesterase
inhibition results in accumulation of acetylcholine and inhibition results in accumulation of acetylcholine and
overstimulation of acetylcholine receptors in synapses of the overstimulation of acetylcholine receptors in synapses of the
ANS, CNS, and N-M junctions. ANS, CNS, and N-M junctions.
26
![Page 27: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/27.jpg)
NN
Autonomic Nervous SystemAutonomic Nervous System Somatic Central Somatic Central
ParasympatheticParasympathetic Sympathetic Sympathetic
NN NN NN
ACAChh ACAChh ACAChhACAChh
ACAChh
MM
MM
ACAChh ACAChh
AA AA
EpinephrineEpinephrine NorepinephrineNorepinephrine
NN
ACAChh
Sweat GlandsSweat Glands
GlandsGlandsBladderBladder
GutGutHeartHeart
HeartHeartBlood PressureBlood Pressure Neuromuscular Neuromuscular
JunctionJunction
BrainBrain
AutonomicAutonomicGangliaGanglia
End End OrganOrgan
MM
27
![Page 28: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/28.jpg)
Acute Cholinergic Crisis
Clinical features depend on the type of receptors stimulated by acetylcholine and their location
Muscarinic receptors (parasympathetic): diarrhoea, urinary frequency, miosis, bradycardia, bronchorrhoea and bronchoconstriction, emesis, lacrimation, salivation (DUMBELS), hypotension & cardiac arrhythmias
28
![Page 29: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/29.jpg)
Nicotinic (sympathetic)
Tachycardia
Mydriasis
Hypertension
Sweating
Nicotinic (N-M Jn) Muscular weakness
Paralysis
Fasciculation
29
Acute Cholinergic Crisis
Tacchycardia can also be caused by hypovolaemia, Tacchycardia can also be caused by hypovolaemia, hypoxia, previous doses of atropine, and alcohol hypoxia, previous doses of atropine, and alcohol
withdrawalwithdrawal
Nicotinic & Muscarinic (CNS)Nicotinic & Muscarinic (CNS) ConfusionConfusion AgitationAgitation ComaComa Respiratory failureRespiratory failure
![Page 30: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/30.jpg)
Result of Result of centrally or peripherally mediated centrally or peripherally mediated mechanisms. mechanisms. Occurs during the acute cholinergic crisis (type I Occurs during the acute cholinergic crisis (type I paralysis) or during an apparent recovery phase paralysis) or during an apparent recovery phase (intermediate syndrome, or type II paralysis). (intermediate syndrome, or type II paralysis). Weakness of neck flexors Weakness of neck flexors is an early sign of is an early sign of significant muscle weakness.significant muscle weakness.
Respiratory failure in OP poisoningRespiratory failure in OP poisoning
30
![Page 31: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/31.jpg)
Causes of High Case Fatality
High toxicity Difficulty in transporting patients over long
distances from rural areas Lack of treatment facilities at PHC & even
district hospitals Lack of training in management of pesticide
poisoning
31
![Page 32: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/32.jpg)
Diagnosis
Ask the relatives. Clinical picture, smell of pesticides or solvents Typical s/s When in doubt quantification of butyrylcholinesterase
or acetylcholinesterase is helpful. Cholinesterase ≤ 80% of the lower reference range is
probably indicative. In very severe poisonings, may be zero
Source: Eddleston et al;Lancet online August, 2007Source: Eddleston et al;Lancet online August, 200732
![Page 33: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/33.jpg)
Variable onset: Most patients develop severe toxicity within six hours. Patients remaining asymptomatic for 12 hours after ingestion are unlikely to develop major clinical toxicity
Exceptions exist with some highly lipophilic organophosphorus compounds (most importantly fenthion), which produce only subtle cholinergic features initially then progressive muscle weakness, including respiratory failure requiring intubation
Source: Managing acute organophosphorus pesticide poisoning. Darren M Roberts, Source: Managing acute organophosphorus pesticide poisoning. Darren M Roberts, Cynthia K Aaron; BMJ,2007Cynthia K Aaron; BMJ,2007
Diagnosis
33
![Page 34: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/34.jpg)
Principles of Treatment
ABC, Oxygen Muscarinic antagonist (Atropine) Acetylcholinesterase reactivator (Oxime) Gastric decontamination only after
patient has been fully resuscitated and stabilized
Careful observation for changing atropine needs, respiratory function and recurrence of cholinergic crisis
34
![Page 35: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/35.jpg)
Initial Stabilization Medical emergency Start two I/V lines. Give I/V saline to keep SBP ≥ 80
mm of Hg Patient should be placed in left lateral position with
neck extended Watch out for convulsions and give I/V diazepam Record a baseline GCS
35
![Page 36: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/36.jpg)
Gastric lavage
Gastric lavage is useful if done within 1-2 hours First aspirate and then do a lavage with 200-300
ml of tap water Comatosed patients should be intubated prior
to lavage with a cuffed endotracheal tube Do not carry out lavage in an unwilling
conscious patient
36
![Page 37: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/37.jpg)
Skin Decontamination
If there is suspicion of dermal exposure, remove all clothes and wash the skin thoroughly with soap and plenty of warm water
Give special attention to skin folds, hair, nails and areas like axillae and groins
Use adequate personal protection like gloves and apron
37
![Page 38: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/38.jpg)
Antimuscarinic agents
Atropine Before giving atropine, record pulse rate, BP, pupil
size, presence of sweat and auscultatory findings Give 1-3 mg bolus of atropine depending on
severity and then loading dose of PAM After 5 minutes of atropine, check all parameters
again and if no improvement has taken place double the dose of atropine
Continue to review every 5 minutes and doubling doses of atropine
Once the patient is stable start an infusion of atropine with 10-20% of the total dose needed to stabilize the patient38
![Page 39: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/39.jpg)
Antimuscarinic agents
Target end-points Target end-points ::
•Clear chest on auscultation with no wheezeClear chest on auscultation with no wheeze
•HR ≥ 80 per minuteHR ≥ 80 per minute
•Pupils no longer pinpointPupils no longer pinpoint
•Dry axillaeDry axillae
•SBP ≥ 80 mm HgSBP ≥ 80 mm Hg
39
![Page 40: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/40.jpg)
Aim of Atropine Therapy:
• No need to aim for a heart rate of 120-140/min.No need to aim for a heart rate of 120-140/min.
• Tachycardia can be caused by hypoxia, agitation, Tachycardia can be caused by hypoxia, agitation, alcohol withdrawal, pneumonia, hypovolemia and fast alcohol withdrawal, pneumonia, hypovolemia and fast oxime administration & are not a C/I for atropineoxime administration & are not a C/I for atropine
• Glycopyrrolate: Glycopyrrolate: In patients with atropine toxicity, but In patients with atropine toxicity, but it it does not counteract CNS effects of OPsdoes not counteract CNS effects of OPs
40
![Page 41: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/41.jpg)
Glycopyrrolate
• Similar outcomes using continuous infusion.Similar outcomes using continuous infusion.
• Ampoules of 7.5 mg can be added to 200 ml of saline Ampoules of 7.5 mg can be added to 200 ml of saline and infusion can be titrated to drying of secretions. and infusion can be titrated to drying of secretions. Atropine can be added as a bolus if heart rate goes below Atropine can be added as a bolus if heart rate goes below 60/min.60/min.
• It may be used where the secretions are difficult to It may be used where the secretions are difficult to control.control.
• Or when it is difficult to differentiate altered level of Or when it is difficult to differentiate altered level of consciousness due to atropine toxicity or relapse of OP consciousness due to atropine toxicity or relapse of OP poisoningpoisoning41
![Page 42: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/42.jpg)
Why Oximes have been shown to be ineffective in some studies ?
Reasons could be Insufficient dose or duration High dose of poison and rapid reinhibition of
reactivated enzyme Ageing of inhibited AChE Poor affinity for the particular OP-AChE complex
Many patients in the trials presented late and had taken dimethyl pesticides
42
![Page 43: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/43.jpg)
Pralidoxime in the blood might required to be higher to antagonise the toxic effects of many pesticides.
Thus a bolus-loading infusion followed by a maintenance infusion might be the best regimen.
On this basis, the WHO has proposed that patients be given about 30 mg/kg pralidoxime salt as a loading dose, followed by an infusion of at least 8 mg/kg/h (in a 50 kg south Asian patient this is roughly equivalent to 1–2 g bolus followed by 0·5 g/h).
Dose of Oximes
43
![Page 44: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/44.jpg)
Oximes
• Pralidoxime is the only oxime available in India.Pralidoxime is the only oxime available in India.
• Dose: Give 2gm I/V over 20-30 minutes and then an Dose: Give 2gm I/V over 20-30 minutes and then an infusion of 0.5-1gm/hour till atropine is not needed infusion of 0.5-1gm/hour till atropine is not needed for 12-24 hours and the patient has been extubated.for 12-24 hours and the patient has been extubated.
• Treatment for poisoning with dimethyl pesticides Treatment for poisoning with dimethyl pesticides must be started much earlier than for other diethyl must be started much earlier than for other diethyl pesticidespesticides
• Rapid infusion may cause vomiting, tachycardia and Rapid infusion may cause vomiting, tachycardia and diastolic hypertensiondiastolic hypertension
44
![Page 45: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/45.jpg)
Benzodiazepines
• Patients poisoned with OP frequently develop agitated Patients poisoned with OP frequently develop agitated delirium. delirium.
•Cause: Pesticide itself, atropine toxicity, hypoxia, Cause: Pesticide itself, atropine toxicity, hypoxia, alcohol, and medical complications.alcohol, and medical complications.
• Diazepam Diazepam is first line of treatment for seizures with OP is first line of treatment for seizures with OP poisoning though seizures are uncommon in well poisoning though seizures are uncommon in well oxygenated patientsoxygenated patients
45
![Page 46: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/46.jpg)
Carbamate Pesticides
Commonest is Baygon which is used as a household pesticide
Clinical picture similar to OP poisoning but CNS toxicity is less
Plasma and RBC cholinesterase may be depressed for short time but quickly recover
Prognosis good
46
![Page 47: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/47.jpg)
Carbamate Pesticides
Atropine, Role of PAM is not clear Complications mostly due to aspiration
pneumonitis (while doing gastric lavage). Many carbamate formulations are made in
petroleum product base. Pulmonary oedema and poor oxygenation may not respond to Atropine and such cases have to be managed as cases of ARDS
Carbamates used for agricultural purpose such as Carbofuran, Aldicarb and Methomyl are highly toxic47
![Page 48: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/48.jpg)
Organochlorine pesticides
Examples are DDT, BHC, Lindane, Endosulfan DDT and BHC already discontinued except for
public health programs Endosulfan is one of the most commonly used
agricultural pesticides Patient will present with convulsions No lab test available for diagnosis Treat with Diazepam, Phenobarbital or other
anticonvulsants
48
![Page 49: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/49.jpg)
Fumigants: Aluminium phosphide (AlP):
It is available as 3 gm tablets known as Celphos, Alphos, Quickphos
It is used for storage of wheat On coming in contact with moist air or
gastric contents, releases Phosphine (PH3) gas
It is highly toxic and even ½ tablet can be fatal
There is no antidote49
![Page 50: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/50.jpg)
Aluminium phosphide
Signs and Symptoms: Epigastric pain, retrosternal burning, vomitus
smells of decaying fish Severe hypotension or shock is the cardinal
feature & is often unresponsive to vasopressors Cardiac arrhythmias and metabolic acidosis Liver damage, Renal failure and ARDS may
develop after 24-48 hours Patient remains conscious till the end
50
![Page 51: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/51.jpg)
Though there are not many published reports, but administration of coconut oil (about 200 ml) has been reported to prevent release of phosphine gas. Role of gastric lavage is not clear
Give I/V fluids and vasopressors like dopamine There is no antidote After giving this first aid, shift the patient to an ICU This is one poisoning where quick first aid can
make a difference
Aluminium phosphideAluminium phosphideAluminium phosphide
51
![Page 52: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/52.jpg)
Ethylene dibromide (EDB)
Sold as a liquid in an ampoule Used for grain storage Causes hepatic and renal damage Initially patient may present with
vomiting and drowsiness, second day pt. may look better, but next day s/s of hepatic damage and anuria develop
Treatment symptomatic, no antidote, high fatality
52
![Page 53: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/53.jpg)
Rodenticides
Types:
1. Single dose : Zinc phosphide, Thallium, Red squill, Sodium monofluroacetate, Barium salts like carbonate, hydroxide and chloride
2. Multiple dose: Warfarins and Superwarfarins
53
![Page 54: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/54.jpg)
Zinc phosphide
It is greyish powder, smells of decaying fish Toxicity is similar to ALP but it is slower in
onset as release of phosphine is slow S/S are nausea, vomiting, shock, oliguria,
metabolic acidosis, pulmonary oedema, hepatotoxicity, ECG changes, convulsions, coma
No specific antidote, treatment is supportive and symptomatic
54
![Page 55: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/55.jpg)
Barium salts
Interfere with Na-K pump and cause paralysis of muscles
Barium carbonate can cause toxicity at a dose of 0.5 gm and Barium chloride is toxic in a dose of 1-10 gm.
S/S repeated vomiting, loose motions and abdominal pain
Tightness of muscles of face and neck, muscle tremors, difficulty in breathing
55
![Page 56: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/56.jpg)
Convulsions and cardiac arrhythmias Wide complex tachyarrhythmias including
VPCs, VT & VF Perioral paraesthesias which may spread
to other parts of body Ascending quadriparesis Hypokalaemia is common
Barium salts s/s contd.
56
![Page 57: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/57.jpg)
Gastric lavage followed by instillation of magnesium sulphate to form insoluble barium sulphate
Do not give mag sulphate by I/V route as ppt of barium sulphate may cause renal failure
Monitor arrhythmias and adequately treat hypokalaemia
Rx.
57
![Page 58: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/58.jpg)
Warfarins and Superwarfarins
They are coumarin derivatives and are used as anticoagulants
Inhibiting vitamin K dependent clotting factors II, VII, IX and X causing ↑ PT
Superwarfarins like bromadiolone, brodifacoum, difenacoum and diaphacinone are more potent and have a long duration of action
Bleeding may occur as petechial hemorrhages, haematuria, and occult blood in stools
58
![Page 59: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/59.jpg)
Toxicity is monitored by serial measurements of PT
Effect is usually seen after 48 hours and for most ingestions no treatment is required
Vitamin K1 is given by I/V route if PT is prolonged 10 mg upto 5 times a day (Do not give K3 or K4)
FFP / BT
Warfarins and Superwarfarins
59
![Page 60: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/60.jpg)
Corrosive PoisoningCorrosive Poisoning
• An average home contains a dozen different cleaning An average home contains a dozen different cleaning products. products. • Responsible for a large number of accidental and Responsible for a large number of accidental and intentional poisoningsintentional poisonings• Three types:Three types:
ACIDACIDALKALIALKALIOXIDIZING AGENTSOXIDIZING AGENTS
• > 100-150 ml is massive poisoning> 100-150 ml is massive poisoning
60
![Page 61: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/61.jpg)
61
![Page 62: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/62.jpg)
62
![Page 63: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/63.jpg)
Endoscopy
63
![Page 64: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/64.jpg)
Treatment of Corrosive Poisoning
64
![Page 65: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/65.jpg)
65
![Page 66: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/66.jpg)
When to start feeding ?
66
![Page 67: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/67.jpg)
Poisoning with Sedative /Hypnotic drugs
Can be easily detected by urine drug screens Relatively safe drugs unless ingested with other
sedatives like alcohol or TCAs The elderly are more sensitive to the CNS
depressant effect and those suffering from COPD are more susceptible to respiratory effects.
Paradoxical reactions of agitation, aggression, hallucinations and combativeness may uncommonly occur; children are more susceptible.
67
![Page 68: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/68.jpg)
Treatment of Benzodiazepine Overdose:
Close observation and supportive care Secure airway and adequate ventilation Flumazenil is a specific antidote, but is very short
acting. Should not be routinely used. Flumazenil may precipitate seizures in case TCA are
also taken with BZD Induction of acute withdrawal in those suffering
benzodiazepine dependence may also trigger seizures or pulmonary aspiration.
68
![Page 69: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/69.jpg)
Acute Methemoglobinemia
69
![Page 70: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/70.jpg)
Clinical Presentation
• Methemoglobin is an abnormal hemoglobin Methemoglobin is an abnormal hemoglobin • Usual reduced Ferrous state (Fe2Usual reduced Ferrous state (Fe2++) of the heme ) of the heme
iron is oxidized to Ferric form (Fe3iron is oxidized to Ferric form (Fe3++))• Deeply cyanosed yet completely asymptomatic Deeply cyanosed yet completely asymptomatic
at Meth-Hb conc. less than 10-15%. at Meth-Hb conc. less than 10-15%. • At higher concentrations, signs and symptoms At higher concentrations, signs and symptoms
of anoxia appearof anoxia appear
70
![Page 71: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/71.jpg)
Clinical Presentation
Meth-Hb levelsMeth-Hb levels Signs and SymptomsSigns and Symptoms20-30%20-30% Headache, fatigue, nauseaHeadache, fatigue, nausea30-45%30-45% DOE, lethargy & tachycardiaDOE, lethargy & tachycardia50-70%50-70% Arrhythmias, coma, Arrhythmias, coma,
seizures, resp. distress,seizures, resp. distress,lactic acidosislactic acidosis
>70%>70% Cardiovascular collapse,Cardiovascular collapse,DeathDeath
Anemic patients have symptoms at lower meth-Hb Anemic patients have symptoms at lower meth-Hb levelslevels
71
![Page 72: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/72.jpg)
Treatment
-Supportive: OSupportive: O22, decontamination of skin, , decontamination of skin, - Antidote : Methylene blue Antidote : Methylene blue if Meth-Hb levels are if Meth-Hb levels are ≥ 30% or patient is showing s/s of anoxia≥ 30% or patient is showing s/s of anoxiaDose: Dose: 1mg/kg body wt of 1% solution slowly over 1mg/kg body wt of 1% solution slowly over a period of 5 minutesa period of 5 minutes. Repeat after 1 hour if . Repeat after 1 hour if patient is still symptomatic. Some chemicals may patient is still symptomatic. Some chemicals may need many doses but need many doses but do not exceed 7 mg/kgdo not exceed 7 mg/kg
72
![Page 73: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/73.jpg)
Role of Intensivist
All poisoning requires intensive care atleast for initial time period
Multiorgan involvement & Multimodality treatment
Real time critical decisions Cordination with other superspecialities (if
required)
73
![Page 74: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/74.jpg)
Thankyou !Thankyou !
74
![Page 75: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/75.jpg)
Paracetamol (Lethal dose:7.5-10 gm)
Mechanism of toxicity
At therapeutic doses, 90% of acetaminophen is converted to non-toxic glucuronide and sulfate conjugates and 5% is excreted in the urine unchanged.
The other 5% is oxidized in the liver by P450 enzymes to NAPQI(N-acetyl-p-benzoquinoneimine). At therapeutic amounts glutathione binds with NAPQI to form a non-toxic conjugate
75
![Page 76: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/76.jpg)
In overdose, glucuronide and sulfate conjugation becomes saturated and an increased proportion of NAPQI is formed. Glutathione levels are depleted.
NAPQI remains in its toxic form in the liver. This can cause hepatocellular damage
76
![Page 77: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/77.jpg)
Four phases
PHASE 1 (0.5 to 24 hours): Few s/s: malaise, anorexia, nausea, vomiting, pallor
PHASE 2 (24 to 72 hours): Right upper quadrant pain may appear indicating hepatic damage with
associated raised hepatic transaminases. INR increases. Renal function may begin to deteriorate
PHASE 3 (72 to 96 hours): Continuing hepatic centrilobular necrosis with associated coagulation defects,
hypoglycemia, metabolic acidosis, and jaundice. Renal failure and cardiac complications frequently occur. Hepatic encephalopathy and death may ensue.
PHASE 4 (4 days to 2 week): If phase 3 is survived complete resolution of hepatic and renal function is
usual.
77
![Page 78: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/78.jpg)
Treatment
Decontamination with activated charcoal is effective within 2 hours
Rapid measurement of plasma acetaminophen (paracetamol) level is necessary.
N-acetylcysteine is a life-saving antidote, and while its efficacy declines after approximately eight hours of the acetaminophen (paracetamol) ingestion, it should be administered to all patients with a potentially toxic overdose, regardless of time
78
![Page 79: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/79.jpg)
79
![Page 80: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/80.jpg)
Antidote
N-acetylcysteine:
Administer: 150 mg/kg in 200 mL diluent IV D5 or NS over 15 minutes
Followed by 50 mg/kg in 500 mL diluent IV over 4 hours
Followed by100 mg/kg in 1,000 mL diluent IV over 16 hours
80
![Page 81: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/81.jpg)
Antidote Endpoint
At the end of the infusion regimen the patient’s hepatic transaminases, INR and S.creat. should be determined. If these are normal, or normalizing, further N-acetylcysteine is not required.
If not, the infusion must continue at a rate of 100 mg/kg in 1,000 mL diluent over 16 hours, until hepatic transaminase levels and INR decline and renal function improves.
Supportive care
81
![Page 82: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/82.jpg)
82
Chloroquine – acutely toxic drug
Many cases with chloroquine ingestion Dramatic toxicologic syndrome GI upset followed by cardiotoxicity manifested
as hypotension, vasodilatation, ECG abnormalities particularly QRS widening and cardiovascular collapse
Acute ingestions of 5 gm or more may be fatal
![Page 83: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/83.jpg)
83
Chloroquine (contd.)
Life saving treatment regimen for acute chloroquine intoxication
Epinephrine infusion which begins at a rate of 0.25 ug/kg per minute, rapid-sequence intubation, mechanical ventilation, diazepam 2 mg/kg, and immediate GI decontamination
![Page 84: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/84.jpg)
84
Examples of toxidromes
Sedative/hypnotic: coma, decreased reflexes, hypotension, hypothermia, dilated or small pupils
examples: sedatives, barbiturates Tricyclic antidepressants: initially agitated
then coma, resp., dilated pupils, QT interval prolongation, conduction defects, hyperreflexia, convulsions,,
![Page 85: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/85.jpg)
85
Organophosphorus pesticides
Most are agricultural pesticides, highly toxic, absorbed by all routes including skin
Signs and symptoms typical, often patient needs ventilatory support for days
High doses of atropine needed, dose determined by clinical signs mainly drying of secretions
Dose of PAM still not definite, some recommend continuous infusion
![Page 86: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/86.jpg)
86
Organophosphorus pesticides (contd.)
Plasma and RBC cholinesterase good markers for diagnostic purpose, no prognostic value
Some patients may develop intermediate syndrome after 2-3 days characterized by weakness of neck flexors & proximal limb muscles, cranial nerve palsy and paralysis of respiratory muscles, needs good ventilatory and general support, prognosis good
![Page 87: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/87.jpg)
87
Organophosphorus pesticides (contd.)
OPIDN (organophosphate induced delayed neuropathy) may occur in few cases, takes long time to recover
Prognosis of OP poisoning is good and patients make a complete recovery if treatment is not delayed
Some Ops like Chlorpyrifos have a very long effect and may need hospitalization for weeks
Other common OPs are Dimethoate, Monocrotophos and Phorate
![Page 88: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/88.jpg)
88
Carbamate Pesticides
Commonest is Baygon which is used as a household pesticide
Clinical picture similar to OP poisoning but CNS toxicity is less
Plasma and RBC cholinesterase may be depressed for short time but quickly recover
Prognosis good
![Page 89: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/89.jpg)
89
Carbamate Pesticides (contd.)
Complications mostly due to aspiration pneumonitis (while doing gastric lavage)
Atropine is the only recommended treatment but PAM does not seem to do any harm
Carbamates used for agricultural purpose such as Carbofuran, Aldicarb and Methomyl are highly toxic
![Page 90: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/90.jpg)
90
Organochlorine pesticides
Examples are DDT, BHC, Lindane, Endosulfan Endosulfan is the most commonly used
agricultural pesticide Patient will present with convulsions No lab test available for diagnosis Treat with Diazepam, Phenobarbital or other
anticonvulsants
![Page 91: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/91.jpg)
91
Fumigants: Aluminium phosphide (AlP): known as
Celphos, highly toxic, high fatality, patient presents with shock, cardiac arrhythmias, severe metabolic acidosis, later on renal failure and liver damage, ARDS
Treatment is supportive, treat metabolic acidosis, shock and arrhythmias
Role of Magnesium sulfate to treat arrhythmias is controversial
![Page 92: Management of Acute Poisoning ANISH FINAL](https://reader033.fdocuments.us/reader033/viewer/2022061302/54e6bda44a795981528b46f3/html5/thumbnails/92.jpg)
92
Fumigants (contd.)
Ethylene dibromide (EDB): sold as a liquid in an ampoule, used for grain storage, causes hepatic and renal damage
Initially patient may present with vomiting and drowsiness, second day pt. may look better, but next day s/s of hepatic damage and anuria develop
Treatment symptomatic, no antidote, high fatality