basic concepts of poisoning management n some poisoning cases

1. BY

2. .

3. .
What is it that is not a poison?
All things are poisons and nothing is without
poison. It is the dose only that makes a thing not
a poison
Paracelsus(1493-1541),the Renaissance“ father of
toxicology ” in his third defense

4. “ sola dosis facit venenum”
the dose makes the poison

5. .
•ACUTE POISONING: is the exposure to a poison on one
occasion or during a short period of time..symptoms
develop in close relation to exposure
•CHRONIC POISONING is long-term repeated or
continuous exposure to a poison where the symptoms do
not occur immediately or after each exposure…the pt
gradually becomes ill or becomes ill after a latent period
PHYSICAL FINNDINGS IN SPECIFIC TOXIDROMES
•Moisis: Opiates cholinergics , barbiturates,pontine stroke
•Mydriasis : Sympathomimetics , anticholinergics
•Dry skin: anticholinergics
•Blisters: barbiturates, corbon monoxide poisoning

6. .
• Toxidrome /toxic syndrome: constellation of
clinical examination findings that assists in the
diagnosis and treatment of patient with
exposure to an unknown agent.
Toxicologic physical examination:
• vital signs
• pupillary diameter
• skin findings
• bowel sounds
• urinary retention

7. .
CLASSIFICATION:
Five general toxidromes
 sympathomemitic: (hypertention,tachycardia,
Pupillary dilatation,diaphoresis)….cocaine and amphetamines
and beta agonists and vesopressors
 Cholinergic: (bradycardia,respiratory depression,decrreased
oxygen saturation,pinpoint pupil and SLUDGE syndrome,seizures
or coma)…organophosphate
 Anticholinergic: antimuscarinic syndrome
(tachycardia and hyperthermia, CNS effects like agitation,
dellirium, seizures and other peripheral effects like mydriasis,
dry flushed skin, urine retention and decreased intestinal
motility)..atropine,scopolamine and antihistamines
 Opiate:(respiratory depression and oxygen desaturations in
conjunction with miosis, decreased intestinal motility and coma
 Sedative hypnotic: sedative picture or coma with normal vital
signs

8. .
Diagnostic testing:
Laboratory studies
 FSBG
 Blood chemistry
 Serum drug screening
 Urine drug screening
 Blood gas
ECG
Imaging particularly abdominal radiograph..useful in the
following ingestions
Chloral hydrate
Heavy metals
iron
Phenothiazine
Enteric coated preparation
Sustained release preparation

9. .

10. 1.GENERAL MANAGEMENT
• History(what, How much,What else, When,why)
• physical findings(look, feel and smell)
• ABC
• DEFG(don’t ever forget the glucose) altered mental status/coma
• investigations
2.SPECIFIC MANAGEMENT
A.DECREASING DRUG ABSORPTION
1.Induced vomiting using epecac(given within 1-2hrs),more useful for
use at home and never recommended in children
2.Gastric lavage rarely used,useful within first hour of ingestion.
-should only b used in those with altered mental status when epecac
is dangerous bcz of possible aspiration
-should b preceded by endotracheal intubation
Both lavage and epecac are contraindicated with ingestion of
caustic substances such as alkalies and acids

11. .
3.ACTIVATED CHARCOAL,THE ADSORBANT:
-usually given within one hour
-safe for all patients
-give repeated doses
-dose 50-100grams
Charcoal doesn’t bind to PHAILS
Pesticides
Heavy metals
Acids/alkali/alcohol
Iron
Lithium
Solvents
• Whole bowel irrigation with GoLYTeLY(polyethylene
glycol)+electrolyte solution..for large volume pill ingestion+slow
release tabs such as iron n lithium
• Cathartics ..useful only when used with charcoal, speed transit
time

12. B)ANTAGONIZING THE EFFECT OF POISON e.g
-NAC (paracetamol)
-DESFERRIOXAMINE(iron)
-NALAXONE(Opiates)
C)INCREASING ELIMINATION
-Multiple doses of charcoal..gastrointestinal dialysis
-Forced diuresis… salicylates and phenobarbital
-Haemodialysis..used when liver and renal failure limits the
excretion of substances from the body and those with sever
symptoms (coma, hypotension or apnea)..
Following things can b removed by haemodialysis
isoprapanol.,salicylates,theophylline,uremia,methanol, barbiturtaes
,lithium and ethylene glycol (remember by mneumonic.I
STUMBLE)
REMEMBER: Give nalaxone ,dextrose and thiamine to any pt
presenting with altered mental status or coma

17. 1.ACETAMINOPHEN TOXICITY
• One the few toxins with known toxicity level, about
140mg/kg is usually sufficient to cause serious toxicity.
• Hepatotoxic level=7.5 to 10gm while in those with liver
disease and thus with depleted glutathione stores
hepatotoxic dose is less(4gm/day).
• Metabolism
conjugation conjugation
sulpher acetaminophen glucoronic acid
moiety(NONTOXIC) p450 moiety(NONTOXIC)
NAPQI (toxic) NAC
glutathione
Cysteine and mercapturic acid(NONTOXIC)

18. Clinical findings
4 PHASES
PHASE-1 PHASE-2 PHASE-3(hepatic phase)
first 24 hours 24 to 72 hours 72 to 96 hours
Asymptomatic Right upper quadrant pain
n tenderness
Hepatic necrosis
Jaundice
Nausea n vomiting Hypotension due to volume
loss AND tachycardia
Hypoglycemia
malaise Rise in transaminases n
bilirubin
Hepatorenal syndrome
Hepatic encephalopathy
fatigue Oliguria in some patient Multi organ failure
diaphoresis Anorexia and n/v Coagulopathy with
spontaneous bleeding

19. .DIAGNOSIS:
• Hx of ingestions
• Drug level.. After 4hrs of ingestion because by that time drug has been
completely absorbed
• Plot the level on Rumack-Matthews Nomogram..relates drug level to time of
ingestion….predicts the risk of hepatotoxicity
-150mg/dl at 4hrs is possibly toxic
• LFTs,Urea and creatinine, Serum electrolytes and Glucose level
• PT /INR
• Urine analysis for haematuria and proteinuria
• ECG for detection of co-ingestants
MANAGEMENT
• Gastric decontamination using activated charcoal and should b given in
repeated doses
• Gastric lavage should not b given..
• N-acetylecysteine….preferably given within 8hours
1.FDA approved oral administration
- First give loading dose of 140mg per kg then after 4hours, 70mg per kg
every four hours for about 17 doses n treatment duration is 72hrs

20. .
IV administration:
150mg/kg over 30-60minutes
50mg/kg over 4hours
100mg/kg over 16hours
. Methionine: 2.5gram orally 4 doses at 4hours interval
Never forget the assessment for progression of liver failure
while managing the pt
Prognostic markers are blood PH, PT/INR, serum creatinine,
serum bicarbonate n sever hepatic encephalopthy

21. .
4 8 12 16 20 24
5
500
150
100
50
10
Hours after acetaminophen ingestion
.
late
Not valid after
24hous
Serumlevel(mcg/ml)

22. 2.Organophosphate(OP) toxicity
• Diverse group of chemicals used in domestic and
industrial settings…
• EXAMPLES are as follows
1.insectisides- malathion , parathion etc..
2.Nerve gases like sarin, soman etc
3.Ophthalmic agents- echothiophate, isoflurophate
4.antihemintics-trichloron
5.herbicides-merphos ,tribufos
Primary mechanism of action is inhibition of
acetylcholinesterase(AchE) and has both nicotinic and
muscarinic effects.

23. MECHANISM OF OP TOXICITY AND TREATMENT WITH OXIME

24. .
NICOTINIC EFFECTS:
• Muscle weakness
• Muscle cramping and
fasciculation
• Decreased respiratory
derived due to
diaphramatic failure
CNS EFFECTS:
• Anxiety
• Restlessness n tremors
• Seizures and even coma
MUSCARINIC EFFECTS:
(Recall with DUMBELS
SYNDROME)
• Diarrhea/diaphoresis
• Urinary incontinence
• Miosis
• Bradycardia/bronchospas
m/bronchorrhoea
• Emesis
• Lacrimation
• Salivation

25. .
DIAGNOSIS
• Clinical diagnosis
• RBC cholinesterase level for confirmation ,plasma cholinesterase can also b
used
test-mate ChE field test (kit) measures RBC AChE and plasma AChE within
4mints
• Do all the baselines
TREATMENT AND MANAGEMENT
Close monitoring for oxygen saturation,ECG,blood
gases,temperature,urea,electrolytes and glucose
• Optimizing oxygenation before atropine is recommended to
minimize the potential for dysrhythmia
• Ventilatory support
• Atropine(0.6-2mg iv) reverses ach-induced bradycardia,
bronchospasm,bronchorrhea and hypotension
• Pralidoxime(2-PAM) which restores cholinesterase activity and
reverses both nicotinic and muscarinic effects.
• Benzodiazepine(2gm iv over 4mints)for seizures,to reduce
agitations,to sedate pt during mechanical ventilation

26. .
Intermediate syndrome
OPIDN(mixed sensory/motor polyneuropathy)

27. .
. A 56years old military man has been attacked
with nerve gas. He presents with
lacrimation,salivation ,urination , defecation and
shortness of breath. His pupils are constricted
what is first step in management of this
patient
a. Atropine
b. Decontaminate the pt
c. Remove his clothing
d. Pralidoxime
e. No therapy is effective

28. 3.OPOIDS TOXICITY
• Opoids toxicity is predominently respiratory related, via
depressant effects on respiratory centers in the brain stem.
• Death can occur from respiratory acidosis.
• Examples of opoids are morphine, oxycodone ,tramadol,
herion,fentanyl,methadone
CLINICAL FINDINGS
• Mild intoxication: euphoria, drowziness and constricted pupils
• More severe intoxication may cause hypotension,
bradycardia, constipation, hypothermia, coma and respiratory
arrest
TREATMENT
• General treatment already discussed
• Specific Rx: Nalaxone, an opoid antagonist
- 0.2-2mg iv and repeat as needed to awaken the patient.

29. 4.TCAs and other antidepressant
• TCAs have anticholinergic and cardiac depressant properties
(quinidine-like sodium channel blockage)
• Newer antidepressants like paroxitine ,sertraline ,fluoxetine
and citalopram do not generally produce quinidine-like
cardiotoxic effects
CLINICAL FINDINGS
• Quick onset with rapid deterioration is common
• Anticholinergic effects ( dry mouth, tachycardia, dilated pupils
and flushed skin and decreased peristalsis)
• Cardiotoxic effects include QRS complex widening, AV-block
ventricular arrhythmia and hypotension
• Life threatening hyperthermia bcz of impairment sweating
• CNS effects include altered mental status or confusion and
seizures, myoclonus and respiratory depression

30. .
Diagnosis:
-clinical
-Drug level..limited role
-EKG
TREATMENT:
• AC..1gm/kg
• hyperventilation
• NaHCO3:Cardio toxic sodium channel-depressant TCAs
effects may respond to sodium bi-carbonate which provides
large sodium load that alleviates depression of sodium-
dependent channels
• NOREPINEPHRINE
• Lidocaine
• Benzodiazipine
• Prolongation of QT interval is usually treated with iv
magnesium or overdrive pacing

31. 5.CORBON MONOXIDE POISONING
(odorless, colorless and tasteless gas)
• Source: exposure to various forms of burning material
such as gasoline , wood and natural gas and with
entrapment in fire and smoke inhalation
• Binds to hemoglobin about 250 times more avidly than
oxygen thus reduce oxygen carrying capacity, resulting
in tissue hypoxia and anaerobic metabolism
Clinical findings:
• Flue like symptoms
• Dyspnea, tachypnea, headache, chest pain, arrhythmia
and hypotension and early neurologic symptoms (
headache, nausea, blurry vision and dizziness) and late
symptoms like confusion, seizures and syncope.

32. Cont…CO
• COHb level gives an indication of severity of the
exposure
<10%: may occur in city dwellers who r smokers
20-30%: mild symptoms
30-50%:moderate to sever symptoms
>50-60%:may be fatal
• Influenza is Most common misdiagnosis
• Always think of CO poisoning when the entire family
members presents with “Flue” symptoms without fever
• Diagnosis depends on specific measurement of arterial
or venous COHb saturation
• Routine pulse oximetory is not useful bcz it will nt
detect difference b/w oxyhemoglobin and COHb

33. .MANAGEMNET
- removal from source exposure
-100% oxygen administration
-hyperbaric oxygen in severe case
 COHb level>25%
 MI
 CNS abnormalities other than headache
 pregnancy when COHb >15%
- EKG
- avoid excessive iv fluid
- diazepam for seizure if present
- vasopressor for hypotension
Co has half life of 4-6hrs which decreases to 40-80 minutes
on 100% oxygen ant to 15 minutes with hyperbaric oxygen