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Envenomation and Intoxication
Envenomation and Intoxication
Envenomation and Intoxication
INTOXICATION
Bayu Lestari
ENVENOMATION
Entering of venom from venomous animal or plant into the body
Caused by snakebite, scorpion bite, spider bite, insect bite, or marine
animal.
Snakebite are the most common cause of envenomation
SNAKEBITE ENVENOMATION
Etiology: Elapidae (cobras, king cobras, coral snakes, sea snake),
Viperidae (typical viper, pit viper)
VENOM COMPOSITION
Zinc metalloproteinase haemorrhagins: damage vascular endothelium,
bleeding
Procoagulant enzymes: stimulate blood clotting consumption
coagulopathy paradoxical bleeding
Phospholipase A2: damage RBC, mitochondria, leukocytes, platelets,
peripheral nerve endings, skeletal muscle, endothel
Acetylcholinesterase: found in elapid venoms, doesnt contribute to their
neurotoxicity
Hyaluronidase: promotes the spread of venom
Neurotoxins: such as cobrotoxin bind to Ach receptor, crotoxin release
Ach at nerve endings
EPIDEMIOLOGY
In 2008 Kasturiratne et al. estimated 237 3791184 550 envenomings
with 15 38557 636 deaths in the Asia-Pacific Region
Peak incidence: children and elderly
Some snake-bite is an occupational disease
SYNDROMIC APPROACH
SYNDROMIC APPROACH
MANAGEMENT OF SNAKE-BITES
FIRST AID
-FIELD SETTING
Retard systemic absorption of venom immobilized-pressure method,
pressure pad method
Preserve life and prevent complications
Control distressing or dangerous early symptoms including respiratory
paralysis and shock
Transport to hospitals
Dont do:
Tight (arterial) torniquets
Interfere bite wound (incisions, rubbing, vigorous cleaning, massage,
application of herbs or chemicals)
PRESSURE IMMOBILIZATION
METHOD
PRESSURE PAD
FIRST AID
SIGN OF DANGER
ANTIVENOM THERAPY
ANTIVENOM THERAPY
ANTIVENOM REACTION
Antivenom could lead to anaphylaxis reaction, pyrogenic reactions, or
serum sickness reactions
However, skin or conjunctival test didnt need to performed
Antivenom administration should be prepared with adrenalin for first line
treatment in anaphylaxis reaction
INTOXICATION
Clinical syndromes caused by administration of toxic dose of drugs/
substance
General evaluation:
recognition of poisoning
identification of agents involved
assessment of severity
prediction of toxicity
GENERAL- MANAGEMENT
provision of supportive care
prevention of poison absorption
enhancement of elimination of poison
administration of antidotes (should know the toxicants first)
SUPPORTIVE CARE
ABC
Vital signs, mental status, and pupil size
Pulse oximetry, cardiac monitoring, ECG
Protect airway
Intravenous access
cervical immobilization if suspect trauma
Rule out hypoglycaemia
HISTORY
Pill bottles
Alcohol
Drug history including access
Remember OTC drugs
Suicide note
National Poisons Information Centre *
EXAMINATION
Physiologic excitation
anticholinergic, sympathomimetic, or central hallucinogenic
agents, drug withdrawal
Physiologic depression
cholinergic (parasympathomimetic), sympatholytic, opiate, or
sedative-hypnotic agents, or alcohols
Mixed state
polydrugs, hypoglycemic agents, tricyclic antidepressants,
salicylates, cyanide
PREVENTING ABSORPTION
Gastric Lavage
Not in unconscious patient unless intubated (risk aspiration)
Flexible tube is inserted through the nose into the stomach
Stomach contents are then suctioned via the tube
A solution of saline is injected into the tube
Recommended for up to 2 hrs in TCA & up to 4hrs in Salicylate OD
Induced Vomiting
Ipecac - Not routinely recommended
Risk of aspiration
PREVENTING ABSORPTION
Activated Charcoal
Adsorbs toxic substances or irritants, thus inhibiting GI
absorption
Addition of sorbitol laxative effect
Oral: 25-100 g as a single dose
Repetitive doses useful to enhance the elimination of certain
drugs (eg, theophylline, phenobarbital, carbamazepine, aspirin,
sustained-release products)
ELIMINATION OF POISONS
Renal elimination
Medication to stimulate urination or defecation may be given to try to flush
the excess drug out of the body faster.
Forced alkaline diuresis
Infusion of large amount of NS+NAHCO3
Used to eliminate acidic drug that mainly excreted by the kidney eg
salicylates
Serious fluid and electrolytes disturbance may occur
Need expert monitoring
Hemodialysis or haemoperfusion:
Reserved for severe poisoning
Drug should be dialyzable i.e. protein bound with low volume of
PARACETAMOL
Widely available
Potential toxicity underestimated
Toxicity unlikely to result from a single dose of less than 150 mg/kg
in child or 7.5 to 10 g for adult
Toxicity is likely with single ingestions greater than 250 mg/kg or
those greater than 12 g over a 24-hour period
Virtually all patients who ingest doses in excess of 350 mg/kg
develop severe liver toxicity unless appropriately treated
FACTORS INFLUENCING
TOXICITY
Dose ingested
Excessive cytochrome P450 activity due to induction by chronic
alcohol or other drug use eg carbamazepine, phenytoin, isoniazid,
rifampin
Decreased capacity for glucuronidation or sulfation
Depletion of glutathione stores due to malnutrition or chronic
alcohol ingestion
Acute alcohol ingestion is not a risk factor for hepatotoxicity and
may even be protective by competing with acetaminophen for
CLINICAL FEATURES
Stage I (0.5 to 24 hours)
No symptoms; N&V Malaise
Stage II (24 to 72 hours)
Subclinical elevations of hepatic aminotransferases (AST, ALT), right upper
quadrant pain, with liver enlargement and tenderness. Elevations of
prothrombin time (PT), total bilirubin, and oliguria and renal function
abnormalities may become evident
Stage III (72 to 96 hours)
Jaundice, confusion (hepatic encephalopathy), a marked elevation in hepatic
enzymes, hyperammonemia, and a bleeding diathesis hypoglycemia, lactic
acidosis, renal failure 25%, death
Stage IV (4 days to 2 weeks)
Recovery phase that usually begins by day 4 and is complete by 7 days after
overdose
PARACETAMOL OVERDOSE
The risk of toxicity is best predicted by relating the time of ingestion
to the serum paracetamol concentration
The dose history should not be used as studies have found no
correlation
Peak serum concentrations reached within 4 hrs following overdose of
immediate-release preparations
May be delayed with extended releases preparations or drugs that
delay gastric emptying (eg, opiates, anticholinergic agents) are
coingested
Check level at >= 4 hrs
N-ACETYLCYSTEINE
Antidote MOA: a glutathione precursor
Limits the formation and accumulation of NAPQI
Powerful anti-inflammatory and antioxidant effects
IV infusion or oral tablets (also oral methionine)
150mg/Kg over 15 min; 50mg/Kg over next 4 hrs; 100mg/kg over
next 16 hrs up to 36hrs
Beyond 8 hours, NAC efficacy progressively decreases
S/Es nausea, flushing, urticaria, bronchospasm, angioedema, fever,
chills, hypotension, hemolysis and rarely, cardiovascular collapse
It is better to contact the local liver transplant centre earlier than this.
PT > 20 sec at 24 hr
PT > 40 sec at 48 hr