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ENVENOMATION AND

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

SIGNS AND SYMPTOMS


Local: fang marks, pain, bleeding,
bruising, blistering, infection,
necrosis, lymphangitis or lymph
node enlargement

SIGNS AND SYMPTOMS


Systemic:

General: nausea, vomiting, malaise, abdominal pain


CV: dizziness, faintness, shock, arrhythmias, pulmonary edema
Bleeding disorders cerebral haemorrhage, hemoptysis, SCH
Cerebral arterial thrombosis
Neurological: paresthesia, ptosis
Rhabdomyolisis, renal failure, endocrine disorders

SYNDROMIC APPROACH

SYNDROMIC APPROACH

LONG TERM COMPLICATIONS


Local: chronic ulceration, osteomyelitis, malignant transformation
(squamous cell carcinoma)
Systemic: Chronic kidney disease, chronic panhypopituitarism or diabetes
insipidus, chronic neurological deficits

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

PARACETAMOL OVERDOSE TREATMENT


Activated charcoal within four hours of ingestion
May reduce absorption by 50 to 90 percent
Single oral dose of one gram per kilogram

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

PARACETAMOL OVERDOSE TREATMENT


At the end of NAC infusion, a blood sample should be taken for
determination of the INR, plasma creatinine and ALT. If any is
abnormal or the patient is symptomatic, further monitoring is
required
Patients with normal INR, plasma creatinine and ALT and who are
asymptomatic may be discharged from medical care. They should
be advised to return to hospital if vomiting or abdominal pain
develop or recurrent

Indications for liver transplantation

Liver transplantation is life-saving for fulminant hepatic necrosis

The indications for liver transplantation are:


1 - Acidosis (pH < 7.3), or
2 - PT > 100 sec
3 - Creatinine > 300 mcg/l
4 - Grade 3 encephalopathy (or worse)

It is better to contact the local liver transplant centre earlier than this.

Grossly abnormal prothrombin times should trigger referral:

PT > 20 sec at 24 hr

PT > 40 sec at 48 hr