General principles of poisoning treatment,
specific antidotes of medicines, and the
mechanisms of their effects
Jana Nováková, M.D., Ph.D.
Jan Juřica, PharmD., Ph.D.
Pharmacology vs. Toxicology
• Interconnection of both disciplines
• They study the effects of chemicals on biological systems
Pharmacology - therapeutically useful effects, drugs
Toxicology - adverse, harmful (toxic) effects, poisons and toxins
Paracelsus (1493-1548):
“All substances are poisonous; there is none which is not a
poison. The right dose differentiates a poison and a remedy”
Causes of poisoning
1. drugs - 52%
2. Industrial Products - 30% (chemicals for cleaning, organic solvents,
cosmetics etc.)
3. plants - 8%
4. Pure bulk chemicals -5%
5. funghi - 2%
6. Animal poisons (snakebite) -1%
7. others -1%
General principles of acute poisoning treatment
Treatment has to be provided as quickly as possible but
always with judgment so that therapeutical procedures do
not cause worsening of the patient´s state or even death
!!!
General principles of poisoning treatment:
• eliminate the substance from organism as quickly as possible
(= decontamination)
• antidote (rapid counteraction for poison by means of specific
actions);
„a drug, chelating substance, or a chemical that
counteracts (neutralizes) the effects of another drug or
a poison“
• vital functions + symptomatic treatment
1. Elimination of unabsorbed toxic substances
from organism
• Gastric lavage and administration of emetic,
preferably within 1 hour of intoxication (the first
treatments should be done prior to transportation
to the hospital)
• An average patient arrives only after 3 hours
1. Elimination of unabsorbed toxic substances
from organism
Induced vomiting
• in p.o. poisoning within 4 hours
• within 8 hours after anticholinergic agents
• within 12 hours of pylorospasm inducing agents (eg, salicylates)
• the patient is conscious, without spasms
• Syrup of ipeca (emetin)- non-reg., apomorphine (s.c.)
• mechanic stimulation of pharynx
• (red-eyed treefrog secretion)
Can not evacuate whole stomach content (max 30-50%) !
• DO NOT INDUCE VOMITING IF ACIDS OR ALKALI WERE INGESTED
OTHER CONTRAINDICATIONS OF INDUCED VOMITING:
• Somnolence and loss of consciousness
• Intoxication with foaming agents
• Intoxication with hydrocarbons
• Attacks of spasms
• Alimentary intoxications in small infants
1. Elimination of unabsorbed toxic substances
from organism
Adsorbents
• With poisons ingested p.o.
• Charcoal (adsorbing carbon = Carbo adsorbens) / diosmectit  large
active surface
• 50 – 100 g in 5 – 10% suspension, possibly with stomach tube, then
repeatedly 50 g per 4 hours
• Up to 2.5 g/kg
+: paracetamol, salicylic acid, diazepam, amphetamine
– methyl/ethylalcohol, Li, strong acids and alkali
Toxic substances that are poorly
adsorbable by Charcoal
• acids
• alkali
• chlorates
• chlorids
• cyanides
• nitrates
• ethanol
• ethylenglycol
• isopropanol
• methanol
• fluorides
• iron
• ferrous sulphate
• potassium
• sodium
• detergents
1. Elimination of unabsorbed toxic substances from
organism
• KMnO4 – oxidation of strychnine and cyanides (light pink solution)
• Lime water - Ca(OH)2 - binds F- and oxalic acid into insoluble salts
• Flour/starches –binds iodine into insoluble iodides
• Paraffin oil binds phenols and organic solvents (benzene, toluene)
• Liquid paraffin (Paraffinum subliquidum –
100 – 300 ml)  it is a non-resorbable fatty substance  decreases
resorption of poisons soluble in fats (simple and halogenated
hydrocarbons)
1. Elimination of unabsorbed toxic substances
from organism
Gastric lavage
• In p.o. intoxications within 4 hours
• The patient is conscious, without spasms
• when unconscious, ONLY in lying position and intubated
• warm water (37°C), saline(preparation: 2 teaspoons of salt
per 1 litre water), 300 ml
• Sample for toxicological analysis
• In the end (the last lavage) add adsorbent (30 g of
activated carbon) or a laxative (Na2SO4)
1. Elimination of unabsorbed toxic substances from
organism - PEG - laxative , GIT dialysis
• PEG - polyethylene glycol in ionic solutions
• 4 liters / 2 hours
• until the evacuated rectal content is clear
Indications (toxic and lethal doses):
• rugs bound poorly by charcoal: iron, lithium
Retarded tablets: theophylline, calcium blockers verapamil,
diltiazem!
1. Elimination of unabsorbed toxic substances
from organism
Increasing the intestinal passage
The patient is conscious, with no spasms
• Administration of big doses of strong and quick-acting laxatives
• Sodium sulphate (20 – 30 g with a large volume of water)
• Mannitol (ca 50g per 1 litre water; 0.5 – 1 litre is administered p.o.)
• Castor oil (20 – 30 ml)
• CI in poisons soluble in fats!!! (castor oil bile secretion
and resorption of fats)
1. Elimination of unabsorbed toxic
substances from organism
Total intestinal lavage
• Large-volume solution (25 ml/kg)
• Through stomach tube, until clean solution flows off
• Without resorption, does not cause diarrhoea
• It only rinses the intestine
• polyethylenglycol + NaSO4, NaCl
1. Elimination of absorbed toxic
substances from organism
Forced osmotic diuresis
• Infusion of saccharide solutions (20% mannitol; possible
combination with furosemide), physiological solution
• Up to several litres / day
• CI: brain and lung oedema, heart failure, anuria
1. Elimination of absorbed toxic substances
from organism
Forced alkali diuresis
• Speeds up elimination of slightly acidic poisons
• Alkalinisation of urine and blood (pH 7.5 – 9.0)
• NaHCO3 solutions
• I: salicylates, barbiturates, sulphonamides,
antipsychotic drugs,...
• CI: pulmonary oedema, shock, serious impairment of
kidneys
1. Elimination of absorbed toxic substances
from organism
Forced „acidic“ diuresis
Speeds up elimination of slightly alkalinic poisons
• Acidification of blood and urine
• 5% Glc solutions with ammonium chloride in i.v. infusion
• I: amphetamines, quinine, quinidine, nicotine, morphine,...
• CI: serious impairment of kidneys
1. Elimination of absorbed toxic substances
from organism
Peritoneal dialysis
• dialysis solution via catheter into abdominal cavity
• Intestinal mucosa and peritoneum serve as a membrane
• Replacement after 2 hours
• I: unavailability of haemodialysis in case forced diuresis cannot
be applied
• For poisoning with some analgesics, hypnotics, barbiturates,...
• -: low efficiency, risk of infection
1. Elimination of absorbed toxic substances
from organism
Haemodialysis/CRRT
• I: salicylates, barbiturates, alcohols, ethylenglycol,
toluene, mushrooms
•Acute renal failure – e.g. rapidly progressing glomerulonephritis
•hypercalemia > 6 mmol/l that cannot be managed by conservative therapies
•hypercalcaemia > 3.5 mmol/l
•hyperuricemia > 1000 μmol/l
• uncorrectable metabolic acidosis, pH < 7.1
•hyperhydrating with heart failure
•oligouria lasting more than 3 days
INDICATION OF HAEMODIALYSIS
Indication for dialysis (sooner in diabetics):
•urea > 30 mmol/l,
•creatinine 600–800 μmol/l,
•Creatinine clearance < 0.25 ml/s.
Patient on dialysis
Diseases that lead to dialysis are as follows:
• diabetic nephropathy,
• hypertension nephropathy,
• chronic glomerulonephritis,
• rapidly progressing glomerulonephritis (RPGN) – when irreversible fibrotic changes occur,
•Autosomal dominant polycystic disease of kidneys.
INDICATION OF HAEMODIALYSIS – cont.
1. Elimination of absorbed toxic substances from
organism
Haemoperfusion
• Perfusion of blood through a capsule
containing sorbents
• I: barbiturates, theophylline,
phenothiazines, paracetamol, salicylates,
phenobarbital, carbamazepine
• +: highly efficient
Haemodialysis, haemoperfusion
Indication (on fulfilment of at least 3 criteria):
• Clinical picture of severe intoxication (deep unconsciousness, hypotension,
hypothermia, hypoventilation in intoxications with depressant substances)
• Clinical state can only be influenced by a complex resuscitation care
• Clinical state becomes worse despite complex resuscitation care
• Protracted unconsciousness with pulmonary complications (pneumonia, diffuse
alveolar damage, COPD)
• Proven high plasmatic level of toxic substance that can be eliminated applying
available methods
Haemodialysis, haemoperfusion
Contraindication of extracorporeal elimination methods:
• Effective antidote is available
• The toxic substance is quickly metabolised and its metabolites
are not toxic
• Toxicity appears quickly and irreversibly
• Intoxication is caused by a substance with low toxicity
• The toxic substance has a large distribution volume
• Shock
• Severe haemocoagulation disorders
• Novel (Commercial RMP) – decreases the free fraction of lipophilic drugs
in serious intox. (Intralipid®)
• for the treatment of severe arrhythmias (e.g. ventricular tachycardia,
atrial fibrillation, cardiac conduction systém block, asystole)
• in lipid soluble drugs
• if conventional therapy fails.
• Free drug fraction - binding by lipid emulsion a
• reducing the pharmacological effect
• commonly used to treat a topical toxicity of local anaesthetics
• Cardiotoxicity of local anesthetics, some beta-blockers, TCA
Lipidic (micro)emulsions
• however, the blood in the blood abolishes the possibility of
hemodialysis or ECMO - hence this therapy is preferated over lipids
when other options fail
Lipidic (micro)emulsions
2. Neutralization of poison through
administration of antidote
• Antidote – a substance that neutralises the effect of poison
• specific (using antagonistic effects of pharmaceuticals – antidotes that can
counteract the effects of poison either partly or completely)
• Non-specific (adsorption – activated – medicinal carbon = carbo adsorbens –
carbo activatus – carbo medicinalis)
RATIO OF CARBON : TOXIC SUBSTANCE = 10 : 1
(usually 50g / 3 – 4h; most often intoxications with medicines, chemicals)
• It is necessary to administer antidote as quickly as possible
• Dosage according to plasmatic level of toxin
2. Neutralization of poison through administration of
antidote
• Decrease bioavailability of the toxic substance
• Increase rate of elimination of (especially non-transformed) toxic
substance
• Slow down biotransformation of the toxic substance leading to
activation of the tox. substance
• Incr. rate of biotransformation to inactive metabolite
• Influence the distribution of the toxic substance within the organism
https://www.annemergmed.com/article/S0196-0644(17)30657-1/fulltext
Specific Antidotes
Specific antidotes
• (http://www.farmakologie.net/lecbaotrav.php)
Lékové informační centrum 3. LF UK (Information
Centre for Pharmaceutical Drugs at the Third Faculty
of Medicine, Charles University)
3. Symptomatic treatment
• Check vital signs
• Intubation
• Entry into bloodstream
• Support of CVS (inotropics, vasopressors)
• Therapy of spasms
Welcome at the website of the Toxikologické informační střediskoTIS).
Acute poisoning - what to do?
Dial +420 224 91 92 93 or 224 91 54 02
To receive advice on first aid and what to do next.
Prepare:
• precise information on the accident
• full name
• birth identification number
• health insurance company
• healthcare professional also their IČP (organization identification number)
In order to facilitate the consultation, the doctors are asked to calculate (provided it can be
ascertained) the quantity of medication (active substance) that intoxicated the patient. Also
please try to estimate or find out the body weight of the patient.
Toxicological Information Centre
--
Toxicological Information Centre
• A 24/7 nationwide telephone medical information service to consult cases of acute
human and animal intoxications
• For both laypersons and doctors
• The goal of the TIS is to decrease the number and severity of intoxications and to
favourably effect the course of accidents. The Centre provides information on the
chemical composition of commercial products and on the therapy of acute
intoxications with these products
• It does not deal with:
the influence of chemical compounds on foetus
cancerogeneity
adverse effects of medicinal drugs
impact of chemical compounds on the environment
Toxicological Information Centre
• 120 00 Praha 2, Na Bojišti 1
• http://www.tis-cz.cz/
• E-mail: tis@vfn.cz
• Phone: +420 224 91 92 93 or +420 224 91 54 02
• Snakebite poisoning
Anaesthesiology and Resuscitation Clinic
1st FM CU in Prague and VFN in Prague
Praha 2
Phone: 224 962 243
• Lékové informační centrum (Information Centre for
Pharmaceutical Drugs)
Lékárna FN U sv. Anny
Brno
Phone: 543 182 175-7
• Poisoning causes 10% of deaths !!!
• Coincidence
• Suicide
• Criminal act
• Abuse of habit-forming substances
• Occupational injury
• ...
• 2/3 of all intoxications are related with children!
• Most frequent entry: p.o. or inhalation
Intoxication with drugs (in German hospitals in 2011)
• T50 = other medications, not further specified
• Mental and behavioral disturbances due to acute intoxication with: F10.0 = alcohol (ethanol)
• F11.0 = opioids
• F13.0 = hypnotics, sedatives
• F15.0 = stimulants
• F19.0 = multiple substance use
T39 = analgesics (ca. 40% 4-aminophenol
derivatives)
T42 = hypnotics (ca. 50%
benzodiazepines) and antiepileptic drugs
T43 = antidepressants, neuroleptic drugs,
psychotropic substances (not further
classified)
T40 = narcotics, methadone,
hallucinogens (especially morphine and
codeine)
Dtsch Arztebl Int. 2013 Oct; 110(41): 690–700.
General overview of neurologic
symptomatology at unknown
poison intoxication
 Convulsion – spasmso skeletal muscles: substances with
excitatory effects (strychnine, HCN, organophosphates,
psychotomimetics, psychostimulants [caffeine included!])
 Excited state – states similar to ebriety (often during intoxication
with solvents, benzine, alcohol, atropine, scopolamine, PS-lytics,
cocaine, hashish, fly agaric [amanita muscaria])
 Hallucination, delirious states – analeptics,
atropine(Atropa belladonna), scopolamine, panther mushroom
(also causes states of confusion), organophosphates, ergot
alkaloids, yohimbine
 Manifestations of depression – sedation, somnolence,
sopor to comatose states with depression of breath and blood
circulation – hypnotics, „narcotics“, sedatives, antipyretics,
analgesics, codeine antitussives, alcohol, CO, poisoning...
• Vision disorders – atropine (transitory disorder – mydriasis,
focusing disorder), H2S, As, myorelaxants (focusing disorder),
alcohol (vision hallucinations), amphetamines (tactile
hallucinations: bedbugs creeping below one´s skin →
excoriation),
• Hearing disorders – streptomycine (and other AMG - at
doses), quinine and salicylates (transitory worsening of
hearing, tinnitus)
Intoxication with medicines
Intoxication with medicines
Most often: sedatives, hypnotics, analgesics
Causes of death:
• Injury to CNS – psychotropics
• Injury to CVS – cardioglycosides antiasthmatic drugs
• Liver injury – paracetamol, nimesulide, pretease inhibitors,
TOXICITY of MEDICATIONS
1. ANALGESICS:
a) paracetamol 10 - 15 tb. (15 – 20 tb. of Panadol 500mg →
serious to lethal intoxication)
– hepatotoxicity; it changes into N-acetyl-p-benzochinone
imine(minor metabolite) =hepatotoxic
– GIT problems (vomiting, renal failure)
– Th.: activated carbon + N-acetylcysteine
b) salicylates: breath stimulation, hyperventilation,
– alkalosis = brain and lung oedema
– Th.: alkalizing of urine + activated carbon +
haemodialysis
c) opioids – see Psychopharmaceuticals
2. PSYCHOTROPICS
a) antipsychotic (neuroleptic) drugs, TCA antidepressants
– depressed consciousness, sedation, somnolence, sopor
(it is difficult to wake up the patient), coma + increased muscle
tone, convulsions, cardiotoxicity
– Th.: act. carbon, laxatives, symptomatic treatment antidote =
physostigmine – mitigates anticholinergic symptoms, haemoperfusion
b) psychostimulants (amphetamines, cocaine)
– endogenous catecholamine secretion, stimulation of
sympathetic nervous system
– euphoria, hallucination, unconsciousness, hypertension, arrythmia
c) opioids
– euphoria, breath depression, miosis, BP decrease, heart rate decrease,
apnoe, coma
– Th.: naloxone
2. PSYCHOTROPICS
d) Hypnotics, sedatives
– BZD:
– CNS depression
– Th.: flumazenil
– BARBITURATES:
– CNS depression
– Th.: charcoal, alkali forced diuresis, haemoperfusion
Selected CVS pharmaceuticals and the
related intoxications
Beta-blockers (BB)
• AE: bronchial asthma, shortness of breath
• heart failure, bradycardia, blocking of transmission of
impulses in the heart
• hypoglycaemia
• peripheral circulation disorders, sleeping disorders,
depression (lipophile substances)
• fatigue, cold extremities, dizziness, paresthesia
• skin rashes, fever, and other manifestations of allergy
(rare)
• sudden interruption of therapy – „rebound phenomenon“
Intoxication with BB:
• hypotension
• bradycardia
• A-V blocks
• ventricular dysrhythmias (ventricular tachycardia to fibrillation)
• pulmonary oedema, renal failure (at prolonged hypotension)
• diplopia, mydriasis
• bronchoconstriction, shortness of breath, cyanosis
• spasms or CNS depression
Therapy of intoxication with BB:
• gastric lavage at potentially lethal doses (within 2 to 3h from
ingestion), in patients with spasms and comatous patients
• Add Carbo adsorbens (50-100g) to the last dose of lavage
• At hypotension Trendelenburg position + i.v. liquids on a massive
scale
• At persisting hypotension – dopamine or NA
• At bradycardia atropine i.v. (some cases require a temporary
stimulation)
• At hypoglycaemia – i.v. glucose (or glucagon)
Selected CVS pharmaceuticals and the
related intoxication
ACE Inhibitors (ACEI) AE:
• hypotension (usually reacts to dose modification)
• cough
• hypercalcaemia
• decrease in renal functions to acute renal failure
• angioneurotic oedema
• neutropenia - rarely
• liver function abnormalities
Intoxication with ACEi:
• hypotension
• hypercalcaemia (mainly in patients with acute renal function abnormalities)
• renal function abnormalities (important factors of severity are as follows: dose,
age of the patients, concomitantly administered medications -NSAIDs, diuresics)
• Increase in nitrogen compounds (haemodialysis)
• oliguria, anuria
Therapy of intoxication :
• discontinuation ACEI (or NSAIDs, diuresics)
• rehydration (saline, ballanced inf. solution – ringer/ ringer lactate)
• persisting hypotension – catecholamines ( dopamine, dobutamine,
NA)
• Gastric lavage, administration of adsorbents
• monitoring of BP, electrolytes, and creatinine
• vital functions (breath, ECG)
Prognosis of intoxication:
• promising with early diagnose
• promising in patients with nitrogen compounds retention who
have no significant hypotension
• hypotension – impairment of renal tissue + ischemia
• unfavourable at concomitant administration of NSAIDs and
diuretics
• Unfavourable in elderly patients, at dehydration, in inflammatory
complications and other comorbidities
Intoxication with anticholinergic drugs
• Anticholigics (atropin, TCA, antihistaminics, antipsychotics)
• HOT as a hare (hypertermia)
• RED as a beet (flush)
• DRY as a bone (dry skin, mucosas)
• BLIND as a bat (mydriasis)
• MAD as a hatter (delirium)
• tachycardia, urinary retention
• urine, absence of peristalsis
Intoxication with serotonergic drugs –
serotonergic toxidrome
• Serotonin increrase within CNS (antidepressants MAOIs, SSRIs, triptans,
TCAs, ecstasy, dextromethorphan, opioids, prokinetics)
• mydriasis, agitation / coma, confusion, hallucinations,
• tachycardia, hypertension, hyperthermia, tremor, hyperreflexia,
• convulsions, tachypnea, diaphoresis
Th.: discontinue 5-HT agonists,
Symptomatic treatment: lorazepam, propranolol, cyproheptadine
Selected CVS pharmaceuticals and the related intoxication -
Digoxine
Pharmacokinetics of digoxine
• 60 - 75% absorbed from GIT
• t 1/2 = 36 hours
• 75 % renal elimination (both GF and efflux transport)
• therap.plasm. [0.6-2.0 nmol/L]
• binding to albumine 20 - 40%
• metabolised < 20%
Increased plasm. concentration of digoxine
• Dose not corresponding with muscle mass
• Decreased renal excretion
- hypocalemia < 3 mmol/l
- chinidin, amiodaron
- decreased GFR - elderly, renal failure
• Decrease of extraren. clearence - AA
• Decrease of intestinal degradation – broad spectrum ATB
Signs of intoxication with digoxine
• GIT
- anorexia, nausea, vomiting, diarrhoea
• CNS
- fatigue, depression, yellow vision
• HEART
- arrythmia
Arrythmia at treatment with digoxine
• Ventricular extrasystoles (VES) (bigeminia)
• atrial tachycardia with block
• AV tachycardia
• SA and AV blocks
Treatment of intoxication with digoxine
• discontinue digoxine
• adjust plasm. levels of potassium
• SV tachycardia, tachyFis - phenytoin
• VES and KT – lidokain, mesokain, phenytoin
• bradycardia and blocks – temporary stimulation (try
atropine prior to that!)
• to renew a stable rhythm – chinidin, prokainamid
• DIGIDOT - ovine PL against DG
Risks of treatment with digoxine
• status after AMI
• thyreopathy
• hypoxemia (lung disease)
• drug interaction (chinidin, CAA, ATB )
• older age (lower GF and muscular mass)
• changes in K and Ca concentrations
• other – obesity, renal failure
Mushroom poisoning
• Quite frequent in this country
• Less frequent after ingestion of edible mushrooms
that developed toxic products due to metabolic
processes
• Death cap mushroom – Amanita Phalloides
=phaloidine, amanitine alpha, beta, gamma, ...
• Most frequently confused with champignons
POISONING with Amanita phalloides "destroying angel“- „death cap“
A quarter to half of mushroom of average 30 - 35 g mass causes a serious
poisoning in an adult person !
• Lethal intoxication – caused by ingestion of only 1 mushroom (children are
more sensitive!!!)
• prognosis: very serious especially in children, death rate 60 - 80% !!!
POISONING with Amanita phalloides "destroying angel“- „death cap“
• Th.:
• gastric lavage.
• forced diuresis
• PNC G (displaces amanitine from its binding to serum albumine)
• silymarine → hepatoprotective – 20 mg/kg/day in 4 infusions, other
hepatoprotectives,
• CRRT- haemoperfusion
• charcoal
Symptoms of muscarine intoxication
• Typical for excessive stimulation of PS (?):
• (identification of muskarine in plasma, but in a very low
concentr.)
• salivation, lacrimation, sweating
• bradycardia, hypotension
• Decr. breathing (bronchoconstriction, hypersecretion of
bronchial glands)
• Diarrhoea (hypermotility and hypersecretion in the GIT)
• Muscular tremor
Poisoning with amanita results from joint action of muscarine,
ibotenic acid with muscimole and also mykoatropine (but
atropine poisoning symptoms may be also present (PL effects)
Plants
• Nearly all plants that are used in traditional medicine can be
toxic in higher doses (primarily in children)
• „red berries“ – common rue, perfoliate honeysuckle (or fly,
Japanese h.), bittersweet – solanum, common yew, lily-of-the-
valley
• „blue berries“ – privet (Ligustrum), common juniper, deadly
nightshade (Atropa Belladonna)
• Datura, daffodil, raw and green haricot beans = toxic dose 3-10
beans
Poisoning with organophosphates (insecticides)
Cholinergic crisis (organophosphates, carbamates, pilocarpine)
i AChE – SLUDGE-M:
salivation, lacrimation, urination, diarrhea/diaphoresis,
emesis, miosys.
Bradycardia, bronchosecretion
AchE INHIBITORS
SHORT-TERM
(REVERSIBLE)
LONG-TERM
(IRREVERSIBLE)
Competitive inhibition
of enzyme
„Ageing“ of the
inhibitor + enzyme complex
COVALENT BOND
Poisoning with organophosphates (insecticides)
• Irreversible inhibition of Ach-esterase – cumulation of Ach
• Late neurotoxic effects – 1-2 weeks (paresis of extremities)
• Th.:
• atropine – antagonist on Ach receptors
• reactivators of Ach-esterase (trimedoxin, pralidoxim)
• reversible inhibitors of AchE
• symptomatol. treatment (e.g. treatment of spasms – BZD)
Intoxication with organic solvents and alcohols
• ethylalcohol (alcohol, ethanol)
– alcohol → (alcohol dehydrogenase) → acetaldehyde + acetic acid +
CO2 + H2O
– Th.:artificial respiratory support, glc infusion, BZD (to dampen
restlessness+ convulsions), fomepizol (competitive inhibiton of ADH)
methylalcohol (methanol)
– methanol → ADH → formaldehyde + CO2 + H2O +
+ formic acid
• Metabolic acidosis
• Damaged eye
• Th.: gastric lavage, laxatives, paraffine, ethylalcohol, fomepizol, haemodialysis
• organic solvents: petrol, trichlorethylene, toluen, xylen, benzene,
hexane...
– Th.: paraffine oil – not absorbed