ANTIDOTE THERAPY

Antidote
Toxicant Toxic dose Toxic effect Mechanism of toxicity
Name Mechanism
Cyanide 200 mg Headache, nausea, Binding to cellular Hydroxocobalamin Hydroxocobalamin and
sodium/potassium dyspnea, and cytochrome oxidase, it hydrochloride, cyanocobalamin are analogs
salt confusion. Syncope, blocks the aerobic utilization thiosulfate, sodium of vitamin
seizures, coma, of oxygen nitrite, sodium B12 that have been used for
agonal respirations, thiosulfate the treatment of pernicious
and cardiovascular anemia. Hydroxocobalamin
collapse ensue rapidly rapidly exchanges
after heavy exposure its hydroxyl group with free
cyanide to produce nontoxic,
stable cyanocobalamin.
When administered to
patients with cyanide
poisoning, it rapidly improves
the heart
rate and systolic blood
pressure and decreases
acidemia.
Sodium nitrite, amil nitrite:
forming methaemoglobin and
binds the cyanide to release
its binding to haemoglobin
Thiosulfate, sodium
thiosulfate accelerates the
conversion of cyanide to
thiocyanate.
Paracetamol 6-7 g/day in adult Hepatotoxicity NAPQI formation exceeding N-Acetylcysteine NAC serving as a glutathione
200 mg/kg BW in Early: anorexia, the glutathione (GSH) (NAC) precursor, leading to
children nausea, vomiting
 After 24-48h: AST & NAPQI covalently bind the increased GHS availability &
ALT begin to rise liver cells causing prevents pct toxicity
hepatic necrosis hepatotoxicity NAC also serve as GSH
become evident. substitute, combining with
Encephalopathy, NAPQI & being converted to
metabolic acidosis, & cysteine & mercaptate
increasing PT/INR conjugates
indicate a poor
prognosis

Organophosphate Diarrhoea, urination, Inhibit AChE (found in Atropine sulfate, Atropine – antimuscarinic
insecticide miosis, bradycardia, synaptic junction & RBC) & pralidoxime chloride agent
bronchospasm, PChE. These enzymes breaks (2-PAM) Pralidoxime – enzyme
emesis, lacrimation, down acetylcholine. reactivator
lethargy, salivation,
seizures
Carbon monoxide 1200 ppm (0.12%) headache, dizziness, CO binds to haemoglobin Oxygen, hyperbaric Breathing 100% oxygen
and nausea with an affinity 250 times speeds the elimination of CO
With that of oxygen, resulting in from
more severe reduced oxyhaemoglobin haemoglobin to
exposures, impaired saturation and decreased approximately 1 hour
thinking, syncope, blood oxygen-carrying
coma, convulsions, capacity
cardiac
arrhythmias,
hypotension, and
death may occur.
Ethylene glycol 1.0–1.5 mL/kg During the first few Metabolized by alcohol Ethanol, Fomepizole Saturate the enzyme
(alcohol) hours after acute dehydrogenase to alcohol dehydrogenase and
ingestion, the victim glycolaldehyde, prevent metabolism of
may appear which is then metabolized to ethylene glycol to its toxic
intoxicated as if by glycolic, glyoxylic, and oxalic metabolites
ethanol acids. These acids,
 After a delay of 4–12 along with excess lactic acid,
hours, evidence of are responsible for the anion
intoxication by gap metabolic acidosis.
metabolic products Oxalate readily precipitates
occurs, with anion with calcium to form
gap acidosis, insoluble calcium oxalate
hyperventilation, crystals. Tissue injury is
convulsions, coma, caused by widespread
cardiac conduction deposition of oxalate
disturbances, and crystals
arrhythmias. Renal and the toxic effects of
failure is common but glycolic and glyoxylic acids
usually reversible.
Pulmonary oedema
and cerebral oedema
may also occur.
Hypocalcaemia with
tetany has been
reported
Opioid Lethargy, coma The binding of opioids & its Naloxone Competitive antagonist at the
receptor causing sedation & hydrochloride receptor
respiratory depression →
respiratory failure → death
Warfarin Cause ecchymoses, Inhibit vitamin K 2,3-epoxide Vitamin K Directly reverse the effect of
subconjunctival reductase and vitamin K warfarin
haemorrhage, quinone reductase, two
bleeding gums, or enzymes responsible for the
evidence of internal conversion
haemorrhage. The of vitamin K to its active
most immediately form
life-threatening
complications are
massive GI bleeding
and intracranial
haemorrhage.