Nowell Benedict C. Catbagan, MD, FPCP
Clinical Toxicology
BGHMC Poison Control Unit
Department of Internal Medicine
Baguio General Hospital and Medical Center


Almost 4,000 cases of poison cases recorded.


88.9% occurred AT HOME!
38% involved children 9 years old and below

93.44% were due accidental by nature

77.66% of poisoning involving adolescents were intentional by nature

2015 – 72.86%

2014 – 60.39%

The home as a poison trap? Because we tend to take our storing of household chemicals for granted…

The home as a poison trap? Because we tend to take our storing of household chemicals for granted…

The home as a poison trap? Because we tend to take our storing of household chemicals for granted…

The home as a poison trap? Because we tend to take our storing of household chemicals for granted…

Managing the Poisoned Pediatric
Patient: What’s the Difference?

Children are NOT small adults.

Numerous anatomic and physiologic characteristics unique in the pediatric patient affects the Absorption, Distribution,
Metabolism and Elimination (ADME) of certain drugs/ toxicants.

Managing the Poisoned Pediatric
Patient: What’s the Difference?

Absorption

Gastric

Gastric emptying time delayed in neonates and infants (6-8 hrs compared to 2 hrs in adults) until 6th to 8th month of life.

Weakly acidic, non-ionized drugs better absorbed in stomach of infants

Poorly absorbed: oral erythromycin, phenytoin, phenobarbital, paracetamol

Rectal

Paracetamol with good absorption and delay in children


Diazepam more rapidly absorbed
Percutaneous

Absence of histamine in neonatal skin until 3rd wk of life

Skin testing in neonates to detect allergy to penicillin will not be informative

Managing the Poisoned Pediatric
Patient: What’s the Difference?

Distribution

Neonates and infants with lower protein binding (PB) than adults


Highly PB drugs with greater systemic effect

Salicylates, phenytoin, valproic acid

Highly PB drugs easier displace bilirubin from albumin  kernicterus
Drugs/Toxicants more easily traverse the Blood Brain Barrier in neonates/infants


Incomplete development of the BBB
Increased membrane permeability

Incomplete brain myelinization

Managing the Poisoned Pediatric
Patient: What’s the Difference?

Metabolism

Maturation of drug metabolizing enzymes occurs longitudinally

The very young have very low activity

Cardiovascular collapse in chloramphenicol associated
“gray baby syndrome”

Cause for caution for drugs that have wider therapeutic index in adults

3rd generation cephalosporins, captopril and morphine

Managing the Poisoned Pediatric
Patient: What’s the Difference?

Elimination

Neonates with GFR 30-40% of adult value; reaches adult levels by 3 months of age

Estimation of renal function necessary for determining dose regimen for drugs with extensive renal clearance

Ceftazidime, famotidine, aminoglycosides


Emergency stabilization

Clinical evaluation

Elimination of the poison

Enhancing elimination of absorbed substance

Administration of antidotes

Supportive therapy and observation

Disposition

Emergency Stabilization

“FIRST: PROTECT
YOURSELF…”

At least Level D PPE

Esp. if patient is not yet externally decontaminated

Emergency Stabilization


Emergency Stabilization

Maintain adequate A irway

Provide adequate
B reathing /ventilation

Maintain adequate C irculation

Treat D rug - or toxicant-induced
CNS disturbances.

Correct metabolic abnormalities
( E lectrolyte s, glucose, acid-base)

Emergency
Stabilization

Check and clear obstruction; remove foreign bodies

Endotracheal intubation if indicated

Regular suctioning of bronchial secretions

Emergency
Stabilization

Check ABGs

Rule out common toxicants that can cause hypoxia

Alcohol

Cyanide

Organophosphates

Carbon monoxide

Opiates

Emergency
Stabilization

Deliver oxygen as to patient need

DO NOT give Oxygen for the ff. poisonings:

WATUSI – flammable and may explode in the presence of Oxygen

PARAQUAT – increased risk of pulmonary fibrosis

ZINC PHOSPHIDE – increased oxidative stress and release of Free Radicals

Emergency
Stabilization

Hypotensive patients

NSS (10 to 20 ml/kg)

Maintenance fluids


Adults – NSS, D
5
Acetated Ringer’s solution

Pediatric - D
5
0.3% NaCl
Pressors if indicated

Treat Drug Induced CNS disturbances convulsions and coma
Emergency
Stabilization

Convulsions in poisoned patients may be due to:

Direct convulsant effect of the poison

E.g. Isoniazid, mefenamic acid, ASA, organoPO4 pesticides

Cerebral hypoxia from the respiratory or cardiovascular depressive effect of the toxicant

E.g. Opiates, alcohol

Hypoglycemia

E.g. Severe alcohol intoxication

Treat Drug Induced CNS disturbances convulsions and coma
Emergency
Stabilization

Convulsions in poisoned patients may be due to:

Severe muscle spasm due to spinal or peripheral effects on the mechanism controlling muscle tone

Decreased seizure threshold in an epileptic patient

E.g. phenobarbital

Withdrawal reactions in patients with substance dependence

E.g. ethanol

Treat Drug Induced CNS disturbances convulsions and coma

Management of Seizures

Diazepam

Adult: 5 mg SIVP

Pedia: 0.3 mg/kg/dose SIVP

Max dose of 20 mg
Emergency
Stabilization

If given beyond 20 mg, airway must be secured

Exception: alcohol withdrawal

Phenobarbital – for benzo- resistant seizures

10 – 15 mg/kg IV SIVP

Treat Drug Induced CNS disturbances convulsions and coma

Management of Seizures

Phenytoin

Adult: 2.5 to 10 mg/dose (usual: 4-5 mg)

Pedia: 0.05 – 0.1 mg/kg/dose, max of 4 mg

Used with extreme caution in toxin induced seizures

Ineffective in Alcohol Withdrawal seizures

Should be considered as a last resort agent
Emergency
Stabilization

Treat Drug Induced CNS disturbances convulsions and coma

Management of Seizures of Unknown Etiology

Pyridoxine (Vit B6)
Emergency
Stabilization

Antidote for Isoniazid (INH) Toxicity

Quickly check for current history of treatment for TB or access to anti-TB drugs

MOT of INH: inhibits enzyme w/c converts pyridoxine to pyridoxal phosphate and increases its excretion
 decreased GABA formation  seizures

Seizure dose of INH: 80-120 mg/kg

Treat Drug Induced CNS disturbances convulsions and coma

Management of Seizures of Unknown
Etiology

Pyridoxine (Vit B6) for Isoniazid Toxicity

Available in Vit B Complex formulation

Tribimin (B
1
100 mg, B
6
50 mg, B
12
5 mg)

Neurobion 5000 (B
1
100 mg, B
6
100 mg, B
12
5 mg)

Empirical Dose

Adult: 5 gm IV

Pedia: 100 mg/kg IV
Emergency
Stabilization

Treat Drug Induced CNS disturbances convulsions and coma

Management of Seizures of Unknown
Etiology

Pyridoxine (Vit B6) for Isoniazid Toxicity

If IV prep not available: may give orally but double the computed dose for IV

B
1 should not exceed 1 gm per dose in adults, 20 mg/kg in pediatric patients

Increased risk for anaphylactoid reactions to thiamine

May equally divide dose, administer 10-15 minutes apart
Emergency
Stabilization

Treat Drug Induced CNS disturbances convulsions and coma

Management of Seizures of Unknown
Etiology

Pyridoxine (Vit B6) for Isoniazid Toxicity

Once patient improves, maintain on oral Vitamin B
Complex (with Vit B6 at 10 mg/kg/day in 3 divided doses for 3-6 weeks
Emergency
Stabilization

Treat Drug Induced CNS disturbances convulsions and coma

Management of Coma of Unknown Etiology

100% Oxygen

Carbon monoxide, Hydrogen Sulfide, Cyanide

Thiamine (Vit. B complex 100mg)

Alcohol intoxication – prevent Wernicke’s enc

Glucose (D50 50-100ml, D10 1-2ml/kg/dose)

Hypoglycemic Agents, Toxic Alcohols

Naloxone ( 400 mcg IV every 3 minutes, up to 2 mg)

Opiates

Caution in chronic opiate users: may induce withdrawal seizures

If > 2 mg given with no response: other etiology must be considered
Emergency
Stabilization

Correct metabolic abnormalities
( E lectrolytes, glucose, acid-base)
• Toxicants causing
Hypokalemia:
• A lkalinizing agents
• (NaHCO
3
)
• B ronchodilators
• theophylline, salbutamol
• C orticosteroids
• D iuretics
• furosemide
Emergency
Stabilization
• Toxicants causing
Hyperkalemia:
• A CE inhibitors
• B eta blockers
• C ardiac glycosides
• C yanide
• O ral potassium
• P otassium-sparing diuretics

Correct metabolic abnormalities
( E lectrolytes, glucose, acid-base)
• Treatment of hypokalemia
• KCl solution
• Treatment of Hyperkalemia
• Glucose-insulin infusion
• 50 mL D50 and 10 units of regular insulin
• Sodium bicarbonate
• Follow after glucose infusion at 1 mEq/kg/dose
• 10% calcium gluconate
• An alternative to sodium bicarbonate
• Dialysis
• For intractable hyperkalemia
Emergency
Stabilization

Correct metabolic abnormalities
( E lectrolytes, glucose, acid-base)
Emergency
Stabilization
• Hypomagnesemia
• diuretics, aminoglycosides, cardiac glycosides, chronic alcohol abuse.
• Hypocalcemia
• “ watusi ”, jatropha seed ingestion
• complication of bites and stings of animals e.g. sea urchins, spiders.
• Hypoglycemia
• alcohol intoxication
• salicylates

Correct metabolic abnormalities
( E lectrolytes, glucose, acid-base)
Clinical
Evaluation

ABG’s: check and treat Metabolic Acidosis
• M Methanol
• E Ethylene glycol
• T Toluene, theophylline
• A Alcoholic ketoacidosis
• L Lactic acidosis
• A
• C
• I
• D
Aminoglycosides
Cyanide, CO
Isoniazid, iron
Diabetic ketoacidosis
• G Grand mal seizures
• A Aspirin (salicylates)
• P Paraldehyde, Phenformin

Tx: Sodium bicarbonate, Hemodialysis

General Principles

Emergency stabilization

Clinical evaluation

Elimination of the poison

Enhancing elimination of absorbed substance

Administration of antidotes

Supportive therapy and observation

Disposition

Complete Clinical Evaluation
•
•
•
•
Clinical
Evaluation

Good History Taking
Clinical
Evaluation
• Information to be Elicited:
• Type and amount
• Time of exposure
• Mode of exposure
• Intake of other substances
• Circumstances prior to poisoning
• Current medications
• Past medical history
• Any home remedies taken

Good History Taking
Clinical
Evaluation
• Asymptomatic patient DOES NOT mean NO
POISONING!
• Toxicants with Delayed Manifestations
• Ethylene glycol 6 hours
• Salicylates
• Paracetamol
• Paraquat
• Methanol
• Coumatetralyl
12 hours
36 hours
48 hours
48 hours
72 hours

Physical Examination
• Evaluate general status
• Examine skin
• Characterize odor of patient’s breath
• Auscultate the lungs
• Listen to patient’s heart
• Check the abdomen
• Do a complete neuro exam
Clinical
Evaluation

Physical Examination
Clinical
Evaluation
• Evaluate general status
• Toxicants causing
Hypertension
• C Cocaine
• T Theophylline
• S Sympathomimetics
(amphetamine, PPA)
• C Caffeine
• A Anticholinergics
• N Nicotine
• Toxicants causing
Hypotension
• C Clonidine
• R Reserpine and other anti-HTNs
• A Antidepressants
• S Sedativehypnotics
• H Heroin and other opiates

Physical Examination
Clinical
Evaluation
• Evaluate general status
• Toxicants causing
Hyperventilation
• C arbamates
• O rganophosphates
• M ethanol
• E thylene Glycol
• T heophylline
• S alicylates
• Toxicants causing
Hypoventilation
• C lonidine
• O pioids
• Heavy M etals
• B eta-Blockers
• A romatic hydrocarbon
• S edatives

Physical Examination
Clinical
Evaluation
• Evaluate general status
• Toxicants causing
Mydriasis
• Toxicants causing
Miosis
• A ntihistamines/
Antidepressants
• S ympathomimetics
(MAP, cocaine)
• I soniazid
• A nticholinergics
• C holinergics/
Clonidine
• O piates/
Organophosphates
• P henothiazines/
Pilocarpine
• S edative-hypnotics

Physical Examination
Clinical
Evaluation
• Examine the Skin
• Look for needle tracks , bruises , bite/sting marks
• Diaphoresis - carbamate and organophosphate pesticides, salicylate, amphetamine
• Jaundice - a delayed manifestation of paracetamol and other hepatotoxic agents
• Dry skin and hyperpyrexia - atropine and other anticholinergic agents
• Flushing – anticholinergics, alcohol, cyanide

Complete Physical Examination
• Characterize the odor of patient’s breath
• Bitter almonds - Cyanide
• Fruity odor - Isopropyl alcohol
• “Oil of wintergreen” - Methylsalicylate
• Rotten eggs - Sulfur dioxide/ Hydrogen sulfide
• Garlic – Organophosphate
• Mothballs – Naphthalene
Clinical
Evaluation

Complete Physical Examination
Clinical
Evaluation
• Auscultate the Lungs
• Edema – organophosphate pesticides, INH, opiates, betablockers, TCADs
• Aspiration pneumonia – hydrocarbon
(kerosene)

Complete Physical Examination
• Listen to the Heart
• Toxicants causing
Tachycardia
• I Iron
• C Carbon monoxide/ Cyanide
• O Organochlorines
• P Phenothiazine
• E Ethylene Glycol/ Ethanol
• F Free-base cocaine
• A Anticholinergics/
Antihistamines/ Amphetamines
• S Sympathomimetics/
Salicylates/ Solvents
• T Theophylline
Clinical
Evaluation
• Toxicants causing
Bradycardia
• P Propranolol and other beta-blockers
• A Anticholinesterases
• C Clonidine/ Calcium
Channel Blockers/
Codeine and other opioids
• E Ethanol
• D Digitalis

Complete Physical Examination
Clinical
Evaluation
• Check the Abdomen
• Organomegaly – enlarged liver in Paracetamol toxicity
• Bowel Sounds – hyperactive in organoPO4 pesticide exposure
• Do a complete neuro examination
• Glasgow Coma Scale
• Always rule out head trauma – loss of consciousness secondary to a toxicant  fall  head injury

Check for Toxidromes

Signs and symptoms which when taken collectively can characterize a suspected toxicant

These groups of manifestations are observed to occur consistently with particular poisons

Seizures + coma + metabolic acidosis
Clinical
Evaluation

Anticholinergic/ Antidepressant
Toxidrome
Clinical
Evaluation
• Hyperthermia: “hot as a hare”
• Dry mucosa: “dry as a bone”
• Flushed skin: “red as a beet”
• Dilated pupils: “blind as a bat”
• Confusion/delirium: “mad as a hatter”

Cholinergic Toxidrome
• D iarrhea, diaphoresis
• U rination
• M iosis
• B radycardia, bronchoconstriction, bronchorrhea
• E mesis
• L acrimation
• S alivation, sweating
Clinical
Evaluation

Sympathomimetic Toxidrome
• M
• T
• H
• H
• S
Clinical
Evaluation

Laboratory Examinations
Clinical
Evaluation

General Laboratory Examinations

Complete blood count

Urinalysis (with pregnancy test for females)

Blood chemistries: FBS, BUN, Creatinine, electrolytes

Liver function test (AST, ALT)

Bleeding Parameters (PT, PTT)

Arterial blood gas

Chest/Abdominal x-ray

12-L ECG

Laboratory Examinations

Radio-opaque Toxicants

Heavy Metals (Lead, Mercury,
Arsenic)

Iron and Iodides

Enteric Coated Salicylates
Clinical
Evaluation

Laboratory Examinations

Specimen Collection

Blood/ Urine for qualitative/quantitative level determination

Total serum iron (TSI), Serum Paracetamol

Pharmacokinetic profile of toxicant dictate timing of collection

Paracetamol

Blood sample should only be taken on or after the peak plasma concentration time (4 hours post exposure)
Clinical
Evaluation

Laboratory Examinations


Bedside Toxicology Tests


Test kits for illicit drugs

Methamphetamine, THC, MDMA
Colorimetric Tests

Ferric Nitrate Test for Salicylates

Positive Result: Purple Color
Advanced Methods of Toxicant Detection

Mass Spectrometry (MS)

Gas Chromatography (GC MS)

Liquid Chromatography (LC MS)


Inductively Coupled Plasma Ionization (ICP MS)
Atomic Spectrometry (AS)
Clinical
Evaluation

General Principles

Emergency stabilization

Clinical evaluation

Elimination of the poison

Enhancing elimination of absorbed substance

Administration of antidotes

Supportive therapy and observation

Disposition

Elimination of the Poison
•
•
•
•
•
•
External Decontamination
Emptying the Stomach/ Gut Decontamination
Administer Single Dose Activated Charcoal
Administer Cathartics
Use of Demulcents/ Neutralizing Agents
Whole Bowel Irrigation

External Decontamination Elimination of the
Poison
•
•
•
Discard the patient’s clothing
Give patient a bath
• Mild Alkaline Soap
• “Perla White”
Perform Eye
Decontamination
• Irrigate with PNSS for
15 minutes

Emptying the Stomach/ Gut
Decontamination
Elimination of the
Poison
➢
Induction of Emesis
➢
Use of syrup of Ipecac
➢
No longer routinely recommended in the hospital setting
➢ can cause prolonged vomiting
➢ can delay administration of activated charcoal
➢ potential complications including pulmonary aspiration

Emptying the Stomach/ Gut
Decontamination
➢
Gastric Lavage
Elimination of the
Poison
➢
Using irrigating solution (PNSS)
➢
May be beneficial if done within 1 hour post ingestion
➢
Contraindication
➢
Depressed sensorium with unprotected airway
➢
Ingestion of corrosive substances
➢
Ingestion of hydrocarbons
➢
Patients at risk of hemorrhage or gastrointestinal perforation

Administer Single Dose Activated
Charcoal
➢
Activated charcoal
Elimination of the
Poison
➢
“Activated” Carbonaceous material
- adding acid and steam  very fine particle size with increased overall surface area and adsorptive capacity
➢
Not “digested”: stays within the GI tract and is eliminated with the adsorbed toxin on bowel movement

Administer Single Dose Activated
Charcoal
➢
Activated charcoal
Elimination of the
Poison
➢
“ Very effective in decreasing absorption by binding the drugs on the surfaces of the charcoal particles when given within 1 hour post ingestion
➢
Can still be given up to 4 hrs post ingestion for:
➢
Slow release prep pharmaceuticals
➢
Co-ingestion of drugs that delay gastric emptying (e.g. opioids)
➢
Drugs that produce pharmacobezoars (e.g.
Enteric coated aspirin)

Administer Single Dose Activated
Charcoal
➢
Activated charcoal
Elimination of the
Poison
➢
Given at a ratio of about 10 parts charcoal to 1 part poison (10:1)
➢
Adult: 50-100 g in 100-200 mL water
➢
Pedia: 1 g/kg in water as 1:3 dilution to make a slurry, or 30 to 50 g in 100 mL water

Administer Single Dose Activated
Charcoal
➢
Activated charcoal
Elimination of the
Poison
➢
Contraindications

Gastrointestinal tract is not anatomically intact

Unprotected airway

Ingestion of corrosive substances

Administer Single Dose Activated
Charcoal
➢
Activated charcoal
➢
Substances NOT Adsorbed by Activated
Charcoal
➢
C yanide/Caustics
➢
A lcohol
➢
L ithium
➢
I ron
➢
P etroleum Distillates
Elimination of the
Poison

Administer Cathartics Elimination of the
Poison
➢
Cathartics
➢
Drugs that increase GI motility, eliminating the ingested toxicant before being absorbed systemically
➢
Sodium Sulfate
➢
Dose
➢
Adult: 15 g in 100 mL water
➢
Pedia: 250 mg/kg given as 10% solution

Administer Cathartics
➢
Cathartics
➢
Usually has no role in poison management when used alone, except in
Kerosene/Hydrocarbon ingestions
Elimination of the
Poison

Administer Cathartics
➢
Cathartics
➢
Contraindications

Caustic ingestion

Poisoning from drugs/chemicals which are readily absorbable

In patients with paralytic ileus


In patients with severe fluid and electrolyte disturbances
In patients with congestive heart failure (do not use sodium containing cathartics)
Elimination of the
Poison

Kerosene/Hydrocarbon Poisoning
➢
Management
➢
Do not induce vomiting – hydrocarbons easily volatilize  chemical pneumonitis
➢
Do not give activated charcoal – hydrocarbons not adsorbable
➢
Give sodium sulfate
Elimination of the
Poison
➢
Alternatives:
➢
Soap Sud Enema – shavings from ¼ bar of mild alkaline soap in 1 li of water
➢
Laxatives – e.g. Lactulose, Bisacodyl

Use of Demulcents/ Neutralizing
Agents
➢
Demulcents
Elimination of the
Poison
➢
An agent that forms a protective film when administered onto a mucous membrane surface
➢
Limited use in poisoning
➢
Narrow therapeutic window: within 30 minutes to 1 hr post ingestion
➢
Raw egg whites commonly used
➢
Pedia: 4-6 egg whites
➢
Adults: 8-12 egg whites

Use of Demulcents/ Neutralizing
Agents
➢
Neutralizing Agent
Elimination of the
Poison
➢
Sodium Bicarbonate
➢
Used in Iron Ingestion and Red Tide poisoning
➢
Dose: 2 vials of 8.4% sodium bicarbonate in 1 Li water to make a 2% solution, as lavage
➢
Alternative: 1 tbsp. in 1 liter of water

Poisoning sec. to Caustic
Substances
➢
➢
➢
Can be highly acidic
(Muriatic Acid) or highly alkaline (Sodium Hydroxide)
Predictors of significant GI mucosal injury
➢
Drooling, pain on swallowing, epigastric pain
➢
Toxicant pH: <3 of >10
Always rule out pneumoperitoneum: do an upright chest/abdominal xray
Elimination of the
Poison

Poisoning sec. to Caustic Substances
➢
Management
➢
Demulcents if within 30 min to 1 hr post ingestion
➢
No Emesis/ No NGT/ NPO
➢
Start H2 blockers/Proton Pump Inhibitors
➢
Refer for endoscopy within 24-48 hrs
➢
Determine extent of GI mucosal injury
➢
Determine need for surgical intervention
➢
Predict probability for stricture formation
Elimination of the
Poison

Poisoning sec. to Caustic Substances Elimination of the
Poison
➢
Management
➢
DO NOT give neutralizing agents (i.e. NaHCO3 for acid exposure or Vit C for alkali)
➢
Reaction is exothermic  release of heat and CO2  aggravate chemical injury, increase risk of rupture

Whole Bowel Irrigation Elimination of the
Poison
• Polyethylene glycol (PEG)
•
•
•
Electrolyte solution used to expel poisons that are poorly absorbed by activated charcoal (e.g. iron) and sustained-release and entericcoated drugs
Not routinely used
Dose:
•
•
Adults: 2 Li/hr
Pedia: 500 ml/hr

General Principles

Emergency stabilization

Clinical evaluation

Elimination of the poison

Enhancing elimination of absorbed substance

Administration of antidotes

Supportive therapy and observation

Disposition

Enhanced Elimination of Absorbed
Substance
•
•
•
•
•
•
•

Multiple Dose Activated Charcoal
Enhanced
Elimination

Modes of Action:


Enhance the pre-absorptive elimination of drugs which decrease gastric motility, and sustained-release agents that have erratic absorption in the gastrointestinal tract

E.g. Anticholinergics, phenytoin
Gut dialysis of drugs

Lipophilic


Low protein binding capacity

Small volumes of distribution

Long half-lives

Barbiturates, aspirin, phenytoin
Interrupting enterohepatic recirculation

Multiple Dose Activated Charcoal
Enhanced
Elimination

Substances with Enterohepatic Recirculation
• Aspirin
• Digoxin
• Paracetamol
• Phenytoin
• Salicylate
• Anticoagulants
• Carbamazepine
• Methamphetamine
• Phenobarbital
• Organochlorine
Pesticides

Multiple Dose Activated Charcoal
Enhanced
Elimination

Dose:

Adult 50-100g in 100-200ml of water

Pedia: 0.5-1 g/kg

Every 4-6 hrs for at least 48 hrs, or until with signs of clinical improvement

Ensure patient has at least 1 bowel movement per day during MDAC

AE: intestinal obstruction sec to AC

Ion Trapping
•
•
•
Ionizing weak acids or bases  inhibit passive renal tubular reabsorption
Alkalinization Therapy
•
•
Salicylates, Phenobarbital, Isoniazid
DOSE: 1 mEq/kg/dose IV NaHCO3 every 6 hrs to titrate urine pH within 7.5-8.5
Acidification Therapy
•
•
For weakly basic toxicants, e.g. MAP, Phenytoin
DOSE: 500 – 1000 mg of Vitamin C IV to titrate urine pH < 5.5-6.0
Enhanced
Elimination

Extracorporeal Elimination
Enhanced
Elimination
• Hemoperfusion
• Large volumes of the patient's blood are passed over an adsorbent substance (AC) in order to remove toxic substances.
• barbiturates, carbamazepine, theophylline, glutethimide, quinidine, paraquat

Extracorporeal Elimination
Enhanced
Elimination
• Dialysis – effective for:

Amanita phalloides

Antifreeze/ Brake Fluid (ethylene glycol)

Heavy metals in soluble compounds

Heavy metals after chelation

Methanol

General Principles

Emergency stabilization

Clinical evaluation

Elimination of the poison

Enhancing elimination of absorbed substance

Administration of antidotes

Supportive therapy and observation

Disposition

Antidotes

Seldom necessary in poisoning

Benefit outweighs potential harm

Indication depends on clinical status, laboratory results, pharmacodynamics of toxicant

Antidotes

Mechanisms

Inert complex formation

Accelerated detoxification

Reduction in conversion to more toxic compounds

Competitive inhibition at receptor sites

Bypassing the effects of the poison

Antibody interacting with poison

Antidotes

Chelating agents

Facilitate the formation of a stable complex with the poison, which can be readily excreted

E.g. Heavy metal poisoning

Lead, Arsenic, Methylmercury,
Cadmium, Copper

Deferoxamine for Iron Toxicity




Caustic to GI Tissue

Directly hepatotoxic

Generates free radicals  oxidative stress

Inhibits cellular respiration  H + accumulates  metabolic acidosis


Management

No Activated Charcoal – iron cannot be adsorbed

If less than 1 hr post ingestion or if iron tablets are seen in X-ray: give NaHCO3 lavage

2 vials of NaHCO3 8.4% in 1 li of water

May repeat until gut radiopacities disappear


Antidote: Deferoxamine

10-15 mg/kg/hr to a max of 6 gms/day

Best given at 6 hrs postingestion up to 24 hrs

Check for “vin rose” color change in urine – due to deferoxamine-iron complex being excreted

Antidotes

Enhanced formation of a non-toxic or less toxic compound

Na thiosulfate + cyanide 
Thiocyanate (less toxic)

N-Acetylcysteine for
Paracetamol – converts NAPQI  less toxic conjugates


Suggested Toxic Dose: 150 mg/kg

MOT: Hepatocellular toxicity through the formation of N-acetyl p-benzoquinomine
(NAPQI)

Monitor AST/ALT, including bleeding parameters

N-Acetylcysteine: glutathione precursor  increase metabolism of NAPQI to non-toxic conjugates


Dose:

IV

Phase 1: 150 mg/kg in 200 cc D5W x 1 hr

Phase 2: 50 mg/kg in 500 cc D5W x 4 hrs

Phase 3: 100 mg/kg in 1 Li D5W x 16 hrs

Oral:

Loading dose: 140 mg/kg

Succeeding doses at 70 mg/kg every 4 hrs for a total of
17 doses

Best started at 6-8 hrs post ingestion: 100% efficacious

Antidotes

Inhibits formation of metabolites which are more toxic than the parent compound

Ethanol for methanol or ethylene glycol poisoning

Ethanol competes for the same enzyme that metabolizes methanol and ethylene glycol to more toxic compounds

Phenytoin in malathion

Antidotes

Competes for the receptor sites where the poison attaches thereby dislodging from the receptors

Atropine for organophosphate or carbamate poisoning

Binds to muscarinic receptors thereby blocking the action of acetylcholine



Oxygen for cyanide poisoning

Synergistic antidotal action when given with sodium nitrite and sodium thiosulfate

Pyridoxine for INH poisoning

Pyridoxine is a needed cofactor for the synthesis of GABA which is depleted in INH poisoning
Antidotes

Antidotes


Digoxin-specific antibody fragments
(Digibind) for digitalis poisoning

Binds digoxin, limiting the cardiotoxic effects

Cobra antivenom for cobra envenomation

Neutralizes the venom

General Principles

Emergency stabilization

Clinical evaluation

Elimination of the poison

Enhancing elimination of absorbed substance

Administration of antidotes

Supportive therapy and observation

Disposition


Problems in the critically ill poisoned patients






Depressed sensorium
Impaired ventilation
Impaired cough reflexes
Prone to aspiration
Immobility
Fluid, electrolyte and other metabolic problems

GOOD SUPPORTIVE AND NURSING CARE IS
IMPORTANT!








Intravenous fluids: replacement and maintenance
Frequent blood and urine pH determination: acidification and alkalinization therapy
Prevention of aspiration
Prevention of decubitus ulcer
Treatment of electrolyte, metabolic and temperature problems
Monitoring of vital signs
Monitoring of input and output

General Principles

Emergency stabilization

Clinical evaluation

Elimination of the poison

Enhancing elimination of absorbed substance

Administration of antidotes

Supportive therapy and observation

Disposition


Observation: at least 24 hours

Frequent re-evaluation

Psychiatric Evaluation: for suicidal patients and substance abusers

Suicide, Homicide, Escape, Assault risk assessment and precaution


Referral to support groups/ rehab centers

Childhood poisoning: referral to
Social Services for suspicion of abuse or neglect

Domestic Abuse: referral to WCPU

Family counselling and education


Criteria :

Absolute identification

Time and amount of ingestion is known

Amount ingested relative to px’s wt is less than the smallest amt known or predicted to induce toxicity

Time elapsed since ingestion is greater than the longest predicted interval between ingestion and peak toxicity

Detailed hx includes no symptoms or signs of toxicity













Air fresheners
Antacids
Antibiotic ointments
Antiperspirants
Ashes (wood, fireplace, cigarette)
Baby products
Ballpoint pen inks
Calamine lotion
Cat/Dog Food
Chalk
Charcoal
Clay












Contraceptives
(without Iron)
Corticosteroids
Cold Packs
Cosmetics
Crayons
Dessicants
Disposable Diapers
Douches
Erasers
Felt Tip Markers
Gums
Paint (Acrylic/Latex)







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




Paste/Glue
Pencil lead
(graphite)
Petroleum jelly
Plastics
Rust
Rubber cement
Shampoo (nonmedicated)
Shaving cream
Shoe polish
Silica gel
Soaps (for bathing)
Styrofoam






Sunscreen
Toothpaste
Vaseline
Vitamins (w/o Iron)
Watercolor paint
Zinc oxide (for Diaper
Rash)



NATIONAL POISON MANAGEMENT AND CONTROL
CENTER (UP-PGH)

SUN: 09228961541


Direct Line: (02) 5241078
UP-PGH Trunk Line: (02) 5548400 local 2311

Email: uppoisoncenter@gmail.com
BGHMC POISON CONTROL UNIT


BGHMC Trunkline: (074)4424216 or (074)6617932, local 396
Email: bghmcpcu@gmail.com


Poisonings remain to be an important but underreported health issue in the country.

Poisonings among the pediatric population remains to be primarily accidental in nature, however a rise in intentional poisonings among adolescents are observed

When initially managing a poisoned patient:

Protect yourself first!

Treat the patient, not the poison!

Do not treat a pediatric patient like a small adult.


Good history taking and physical examination is essential.

External/gut decontamination can remove >80% of the toxic agent at the onset.

Antidotes are rarely used, and at times not needed.

Good supportive management is key.





N. Cortes-Maramba , et al, “Algorithms of Common Poisonings”, 3 rd edition, National Poison Management and Control Center, 2011
N. Dando, “Developmental Pharmacology”, Powerpoint presentation for Tox Pharma students, Department of Pharmacology and
Toxicology, College of Medicine, UP Manila, 2016
L. Nelson, et al, “Goldfrank’s Toxicologic Emergencies”, 10 th edition,
2015
M. Shannon, et al, “Haddad and Winchester’s Clinical Management of Poisoning and Drug Overdose”, 4 th edition, 2007

Thank you for listening!