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Management of Unknown Acute Poisoning



Agents commonly responsible for acute Poisoning

Organophosphates, Carbamates, Organochlorines, Synthetic pyrethroids, Rodenticides, Herbicides, Fumigants, Unlabelled powders sold by hawkers

Household chemicals
Acids, Bleach,Grain preservatives, Drain cleaners,Naphthalene balls, CuSO4, Cosmetics

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

Agents responsible for acute Poisoning contd.

Sedatives and hypnotics (mostly benzodiazepines) 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 Poisoning contd.

Plant Poisonings Datura, Argemone (Epidemic dropsy) Plants with digitalis like effect Animal Toxins Snake bites, scorpion bites

4 situations


3. 4.

History of ingestion(mostly), poison is known and treatment is known History of ingestion, poison is known but the physician is not very confident about the treatment History of ingestion but poison is unknown ? Poisoning e.g pt is unconscious

Situation 1 & 2

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

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

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

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


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


The Cholinergic Toxidrome

Toxidrome Features Drugs/Toxins Drug Treatment
Oximes for Organophosph ates


D -Diarrhoea U- Urinary frequency,

M- miosis,

B - bradycardia,
Killer Bs

Organophosphates Carbamates Physostigmine Pilocarpine

bronchorrhoea bronchoconstriction,

E - emesis, L - lacrimation S salivation


The Anticholinergic Toxidrome

Hot as Hare Dry as a bone Red as a beet Mad as a hatter

Altered mental status Sedation Mydriasis Tachycardia Fever Dry skin Dry mucous membranes Decreased bowel sounds Flushing Urinary Retention

Drug Toxin
Antihistaminics Atropine Baclofen Benztropine

Drug Treatment
For life threatening events use Physostigmine* Not indicated for TCA as it may worsen conduction disturbances *not available in India

TCA Phenothiazines Scopolamine


Sedative Hypnotic Toxidrome


Drug Toxin

Drug Treatment

Slurred speech Confusion Stupor Coma Apnoea

Anticonvulsants Antipsychotics Barbiturates Benzodiazepines Ethanol Opiates

Naloxone Flumazenil Urinary alkalinization for Phenobarbital


Narcotic Toxidrome


Drug Treatment Altered Mental Status Dextromethorphan Naloxone Slow shallow breaths Opiates Miosis Pentazocine Bradycardia Propoxyphene Hypotesion Hypothermia Decreased Bowel Sounds

Drug Toxin

Extrapyramidal Toxidrome

Features Rigidity Tremor Opisthotonus Trimus Hyperreflexia Choreoathetosis

Drug Toxin Haloperidol Phenothiazines Risperidone Olanzapine

Drug Treatment Diphenhydramine Benztropine


Serotonin Toxidrome
Features Irritability Hyperreflexia Flushing Diarrhea Diaphoresis Fever Trismus Tremor Myclonus

Drug Toxin Fluoxetine Paroxetine Sertraline Trazodone Clomipramine

Drug Treatment Benzodiazepines Withdrawal of drug Cyprohepatidine (?)

Solvent Toxidrome

Lethargy Confusion Headache Restlessness Incoordination Depersonalization

Drug Toxin
Hydrocarbons Toluene Acetone Naphthalene Chlorinated Hydrocarbons

Drug Treatment
Withdrawal of toxin Avoid catecholamines


Features Tremors Hyperreflexia Tonic clonic seizures Hyperthermia May mimic stimulant patterns Drug Toxin Organochlorine pesticides like Endosulfan, Lindane Isoniazid Camphor Strychnine Phencylidine Cocaine Xanthines Drug Treatment Antiseizure medications Pyridoxine for Isoniazid Avoid phenytoin for theophylline Induced seizures


Hallucinogenic Toxidrome

Features Hallucinations Psychosis Panic Fever Mydriasis Hyperthermia Synesthesia*

Drug Toxin Amphetamines Cannabinoids Cocaine LSD Phencyclidine (May present with miosis)

Drug Treatment Benzodiazepines

* Synesthesia :One sensory experience described in terms of another sensory experience.


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.


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 blockers. When multiple drugs have been ingested, conflicting clinical effects may negate each other and cloud the clinical picture.


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 formulators Routes 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



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



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)


Organophosphorus pesticides inhibit the enzyme acetylcholinesterase in synapses and on RBC membranes, and butyrylcholinesterase in plasma. Although acute butyrylcholinesterase inhibition does not seem to cause clinical features, acetylcholinesterase inhibition results in accumulation of acetylcholine and overstimulation of acetylcholine receptors in synapses of the ANS, CNS, and N-M junctions.

Autonomic Nervous System

Parasympathetic Sympathetic



Autonomic Ganglia





End Organ


Sweat Glands



Epinephrine Norepinephrine Heart Blood Pressure

Glands Bladder Gut 27 Heart

Neuromuscular Junction

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


Acute Cholinergic Crisis

Nicotinic (sympathetic) Tachycardia

Nicotinic (N-M Jn) Muscular weakness

Mydriasis Hypertension Sweating

Paralysis Fasciculation

Nicotinic & Muscarinic (CNS)

Tacchycardia can also be caused by hypovolaemia, hypoxia, previous doses of atropine, and alcohol withdrawal

Confusion Agitation Coma Respiratory failure


Respiratory failure in OP poisoning

Result of centrally or peripherally mediated mechanisms. Occurs during the acute cholinergic crisis (type I paralysis) or during an apparent recovery phase (intermediate syndrome, or type II paralysis). Weakness of neck flexors is an early sign of significant muscle weakness.


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



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, 2007


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, Cynthia K Aaron; BMJ,2007

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


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


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


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


Antimuscarinic agents
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 38 the patient

Antimuscarinic agents
Target end-points :

Clear chest on auscultation with no wheeze

HR 80 per minute Pupils no longer pinpoint Dry axillae SBP 80 mm Hg

Aim of Atropine Therapy:

No need to aim for a heart rate of 120-140/min. Tachycardia can be caused by hypoxia, agitation, alcohol withdrawal, pneumonia, hypovolemia and fast oxime administration & are not a C/I for atropine Glycopyrrolate: In patients with atropine toxicity, but it does not counteract CNS effects of OPs


Similar outcomes using continuous infusion. Ampoules of 7.5 mg can be added to 200 ml of saline and infusion can be titrated to drying of secretions. Atropine can be added as a bolus if heart rate goes below 60/min.

It may be used where the secretions are difficult to control.

Or when it is difficult to differentiate altered level of consciousness due to atropine toxicity or relapse of OP 41poisoning

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





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 12 g bolus followed by 05 g/h).


Pralidoxime is the only oxime available in India.

Dose: Give 2gm I/V over 20-30 minutes and then an infusion of 0.5-1gm/hour till atropine is not needed for 12-24 hours and the patient has been extubated. Treatment for poisoning with dimethyl pesticides must be started much earlier than for other diethyl pesticides
Rapid infusion may cause vomiting, tachycardia and diastolic hypertension

Patients poisoned with OP frequently develop agitated
delirium. Cause: Pesticide itself, atropine toxicity, hypoxia, alcohol, and medical complications. Diazepam is first line of treatment for seizures with OP poisoning though seizures are uncommon in well oxygenated patients


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


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 toxic

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


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 tablet can be fatal There is no antidote

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


Aluminium phosphide Aluminium phosphide

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


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





Single dose : Zinc phosphide, Thallium, Red squill, Sodium monofluroacetate, Barium salts like carbonate, hydroxide and chloride Multiple dose: Warfarins and Superwarfarins


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


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


Barium salts s/s contd.

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



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


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


Warfarins and Superwarfarins

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


Corrosive Poisoning
An average home contains a dozen different cleaning

products. Responsible for a large number of accidental and intentional poisonings Three types: ACID ALKALI OXIDIZING AGENTS > 100-150 ml is massive poisoning





Treatment of Corrosive Poisoning



When to start feeding ?


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.

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.


Acute Methemoglobinemia


Clinical Presentation
Methemoglobin is an abnormal hemoglobin Usual reduced Ferrous state (Fe2+) of the heme iron is oxidized to Ferric form (Fe3+) Deeply cyanosed yet completely asymptomatic at Meth-Hb conc. less than 10-15%. At higher concentrations, signs and symptoms of anoxia appear

Clinical Presentation
Meth-Hb levels 20-30% 30-45% 50-70% Signs and Symptoms Headache, fatigue, nausea DOE, lethargy & tachycardia Arrhythmias, coma, seizures, resp. distress, lactic acidosis Cardiovascular collapse, Death


Anemic patients have symptoms at lower meth-Hb levels


-Supportive: O2, decontamination of skin, - Antidote : Methylene blue if Meth-Hb levels are 30% or patient is showing s/s of anoxia Dose: 1mg/kg body wt of 1% solution slowly over a period of 5 minutes. Repeat after 1 hour if patient is still symptomatic. Some chemicals may need many doses but do not exceed 7 mg/kg


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)


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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


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


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.



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




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


Antidote Endpoint

At the end of the infusion regimen the patients 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


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


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


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,,


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


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


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


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


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


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


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


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