GENERAL MEASURES

IN THE MANAGEMENT
OF POISONING
CHARLOTTE ANNE V. TIU
EMERGENCY MEDICINE
GENERAL APPROACH TO THE
POISONING PATIENT
• Emergency stabilization
• Clinical evaluation
• Minimizing absorption of the poison
• Enhancing elimination of the
absorbed poison
• Administration of antidotes
• Supportive therapy and observation
• Disposition
I. EMERGENCY STABILIZATION
• Life-saving measures should take priority

ABCs of Life Support for Poisoned Patients

Airway -maintain adequate airway

Breathing - provide adequate oxygenation/ventilation

Circulation - maintain adequate circulation

Drugs- or toxicant-induced CNS disturbances. Treat

convulsions, coma

Electrolytes - correct metabolic abnormalitites

A. Maintain adequate airway
-assess for airway patency
-decreasing sensorium due to worsening intoxication
may compromise airway patency
- obstructed airway - supine position, chin-lift or jaw-
thrust maneuver, remove foreign bodies
-r/o cervical fracture before endotracheal intubation
B. Provide adequate oxygenation /
mechanical ventilation
• ABG -assess ventilation
• PO2 <80% - give O2 inhalation
• Bronchospasm - give bronchodilators
 Important:
Oxygen - contraindicated in
the initial management of
watusi poisoning and paraquat
posoning

Watusi is a flammable
substance which can explode
in the presence of oxygen.
Oxygen administration in
paraquat poisoning can cause
pulmonary fibrosis
C. Maintain adequate circulation RECOMMENDED IV FLUIDS
• Hypotension <SBP <80mmHg in less than 40y.o. &
<90mmHg in over 40y.o) HYPOTENSIVE PATIENTS
• Elevate legs 15cm from horizontal plane to increase
NSS
Crystalloid
venous return from the heart
• Fluid challenge – NSS 220ml adults; 10ml/kg for ADULT MAINTENANCE
children D5NSS
D5AR

PEDIATRIC MAINTENANCE
D5 0.3 NaCl

Severe poisoning cases

Maintenance drips and fluid challenge may be
ineffective
Severe hypotension – insert central venous line,
monitor hydration status, infuse plasma expanders
Still unsuccessful – start dopamine or norepinephrine
drip in D5.
D. Treat CNS disturbances – convulsions and coma
Convulsions may be due to:
1. Direct convulsant effect of the poison
TOXICANTS COMMONLY ASSOCIATED WITH CONVULSIONS
• AMINOPHYLLINE • LITHIUM
• AMPHETAMINES • MAO INHIBITORS
• CARBON MONOXIDE • MEFENAMIC ACID
• COCAINE • ORGANOPHOSPHATES
• CYANIDE • SALICYLATES
• ETHYLENE GLYCOL • STRYCHNINE
• HYPOGLYCEMIC AGENTS • THEOPHYLLINE
• INH • TCA
• LEAD • WITHDRAWAL OF NARCOTICS.
DIAZEPAM OR ETHANOL

2. Cerebral hypoxia from respiratory or cardiovascular depressive effect of the toxicant

3. Hypoglycemia
4. Severe muscle spas, d/t spinal or peripheral effects on the mechanism controlling muscle tone
5. Withdrawal reactions in patients with substance dependence
6. Decreased seizure threshold in epileptic patients

TREATMENT
• Etiology, metabolic or secondary
effect of an ingested poison
• Adequate tissue oxygenation
should be maintained
MANAGEMENT OF SEIZURES
General management of seizures
Diazepam
Adult: 5 mg slow IV push
Pedia: 0.3 mg/kg/dose slow IV push
Every 2 to 5 mins (max 20 mg)
>20 mg  intubation and artificial respiratory support
may have to be done before giving additional doses.
Never dilute diazepam with any fluid
Lorazepam
Adult: 2.5 to 10 mg/dose Usual dose is 4 to 5
mg/dose
Pedia: 0.05 to 0.1 mg/kg/dose IV up to maximum of 4
mg/dose Repeat twice at intervals of 15 to 20 mins prn.
 MANAGEMENT OF SEIZURES

Management of uncontrolled seizures

Phenytoin
Loading dose: 15 to 20 mg/kg slow IV push
Adult: Give at a rate not to exceed 50 mg/min
Pedia: Give at a rate not to exceed 1 mg/kg/min

Maintenance dose:
Adult: 100 mg PO or IV every 6 or 8 hrs
Pedia: 5 to 7 mg/kg/day in divided doses

Phenytoin  NEVER be diluted in dextrose containing fluids to avoid crystallization. Flush IV

line with normal saline solution if phenytoin is administered through a D5-containing solution

Diazepam and phenytoin  poorly absorbed and are ineffective when given through the
intramuscular route. In emergency situations, lorazepam is particularly useful since it can be
given IV or IM.
 MANAGEMENT OF SEIZURES
Management of seizures of unknown etiology

Unresponsive to conventional drug therapy, give:

Pyridoxine (B6) therapeutic trial
Adult: 5 g IV
Pedia: 80 to 120 mg/kg/dose

Known INH toxicity

 give in 5 to 10 g increments until cessation of seizures is achieved
 MANAGEMENT OF COMA

Coma of unknown etiology

100% oxygen
 possible poisoning with ASPHYXIANTS (such as carbon monoxide, hydrogen sulfide) and
cyanide

Thiamine (or Vitamin B complex if pure thiamine is not available)

 alcohol intoxication to prevent Wernicke’s encephalopathy
 Dose: 100 mg IV, followed by 50-100 mL of D50-50

Glucose  suspected hypoglycemia-induced coma

 Adult: 50-100 mL Dextrose 50%
 Pedia: 1-2 mL/kg/dose Dextrose 10%

Naloxone  opioid/opiate toxicity

 Give initial dose of 400 mcg IV every 3 minutes
 does not respond to up to 2 mg, then overdose from other drugs should be investigated
 Total dose of 10 mg is seldom necessary
 For neonates and infants, 10 to 100 mcg/kg/dose IV, IM, SC to be repeated if necessary after 2
to 3 minutes up to 3 times.
E. CORRECT METABOLIC ABNORMALITIES
• HYPOKALEMIA
• Theophylline overdose, salbutamol, terbutaline
• Stimulate Na/K pump forcing K into the cells, causing hypokalemia
• Forced alkaline diuresis – Furosemide

Causes of Hypokalemia Treatment of Hypokalemia

Alkalanizing agent Potassium chloride up to 40mEq/hr; do
Bronchodilators (Theophylline, not exceed 60mEq/hr
Salbutamol)
Corticosteroids
Diuretics
• HYPERKALEMIA
• Beta-blockers and cardiac glycosides  inhibit
Na/K pump, allowing K to leak into the ECF
• ACEi  angiotensin-aldosterpone inhibition
Hypomagnesemia
• Common in diuretics, xanthines, aminoglycosides, cardiac glycosides, chronic alcohol abuse
• Digoxin-induced due to inhibition of Na-K pumps in the renal tubules
• Poor nutrition, ketosis, GI losses, hypoaldosteronism
Hypocalcemia
• Common in watusi and jatropha seed ingestion
• Complication of bites and stings of animals such as
sea urchins and spiders
Hypothermia
<30C rectal temp
Overdose of
several toxicants
Only supportive
measures needed

Hyperthermia
>40C rectal temp
Immediately cool
to body temp
Hypoglycemia
• Common in alcohol intoxication and
salicylate toxicity
• Caused by prolonged glucose utilization
and depletion of hepatic glycogen
stores
II. CLINICAL EVALUATION

Chief complaint General status Bedside toxicology

PHYSICAL EXAM

LAB EXAM
HISTORY
Pertinent Symptoms Skin Specimen collection
Type & Amount Breath odor (blood, urine)
Time of exposure Auscultate lungs General lab exams
Mode of exposure Listen to heart
Intake of other Check abdomen
substances Complete neurological
Circumstances prior exam
Past Medical Hx &
Current meds
Home remedies done
Cutaneous bullae Edema

SKIN FINDINGS

LUNG FINDINGS
• Barbiturates, CO • Pesticides, INH, opiates, beta
Diaphoresis blockers, TCADs
• Carbamate, organophosphate, Aspiration pneumonia
salicylate, amphetamine • Kerosene ingestion
Jaundice
• Paracetamol, hepatotoxics
Dry skin, hyperpyrexia
• Atropine, anticholinergics
TCADs
Flushing
• Anticholinergics, alcohol,
cyanide
Forrest Test
• For phenothiazine
overdose Specimen Collection:
Blood
• POSITIVE: deep purple 5-10ml heparinized. Keep tubes in ice
color after 6-7 drops of Urine
12N sulfuric acid and 2 Sealed container (-20C)
drops 10% ferric chloride For paracetamol toxicity, sampling done on
to 2ml patient’s acidified 4th hour post-ingestion
urine
CBC
Anemia, leukocytosis
UA
Urine pH, SG
FBS, BUN, Crea, Electrolytes
Metabolic abnormalities
ABG
Acid-base disturbance,
hypoxemia
ECG
arrhythmias
LFTs, PT, aPTT
hepatotoxicity
CXR Upright
Aspiration pneumonia,
pulmonary edema, perforated
ulcer
Abdominal XR
Radio-opaque drugs, ruptured
viscus
III. ELIMINATION OF THE POISON

A. External decontamination
B. Emptying the stomach
C. Administer single-dose activated charcoal
D. Administer cathartic
E. Use demulcents / neutralizing agents
F. Whole bowel irrigation
A. External decontamination
• Done in an area outside ER
• Wear PPE (gloves, face mask, plastic or vinyl apron)
• Discard patient’s clothing (70% if poison) and place in
impermeable, double layered bag
• Eye contamination: Irrigate eye with free flowing water for
30 mins
• Avoid neutralizing solutions which may cause further injury
due to resultant exothermic reaction

B. Empty the stomach

1. Induction of Emesis
Only if within 1 hour of ingestion
Consider only if:
No absolute CI
Amount ingested can lead to toxicity
Definitive treatment will be delayed
Mechanical emesis
Large pills that do not disintegrate
Ingestions by infants and small children where large-bore
tubes cannot be used safely
Drink 1-2 glasses warm water then apply pressure on
posterior pharynx

2. Gastric lavage
• ingested potentially life-
threatening amounts of
poison within 1-4 hrs of
ingestion
• No benefit if used alone
• Anticipate risk for
aspiration pneumonia
• Always protect airway
Do not perform
gastric lavage if the
patient:
• ingested caustics or
Trendelenburg kerosene unless a more
position with head toxic substance is
Insert a nasogastric Give lukewarm or
turned to the left combined with
tube (Fr. 16 for Aspirate gastric tepid water: Adult: kerosene, or the
while inserting the
adults or an contents. Check for 50 to 60 mL Pedia: ingested kerosene is > 2
appropriately sized
nasogastric tube.
presence of blood, 10 to 20 mL. Repeat mL/kg
Afterwards, place
tube for pediatric
patient to the left
tablets, etc. until return flow is • depressed sensorium
with unprotected airway
patients). clear.
lateral decubitus • frank convulsions is at
position. risk of hemorrhage or
gastrointestinal
perforation
• is uncooperative
C. Activated charcoal
• Decreases absorption of drugs
by binding them on the
surfaces of charcoal particles
• Only if within 1hr of ingestion

• Trendelenburg and left lateral

decubitus position.
• Effective adsorption, give a
ratio of about 10 parts
charcoal to 1 part poison.
 Adult: 50 to 100 g of activated
charcoal in 100 to 200 mL
water
 Pedia: 1 g/kg in water as 1:3
dilution, or 30 to 50 g in 100
mL water
D. Cathartics
• Hasten intestinal elimination of unabsorbed toxic agent
• No role when used alone

Sodium sulfate
Adult: 15 g in 100 mL water
Pedia: 250 mg/kg given as 10% solution

 should be administered after charcoal lavage. If no bowel

movement occurs in 30 minutes to 1 hour, another dose may
be given. If there is still no bowel movement, do not give
another dose of sodium sulfate. Consider giving soap suds
enema instead.
E. Demulcents / Neutralizing agents
1. Raw Egg White
For mild caustic ingestion and “watusi” poisoning
Adult: 8-12 eggs
Pedia: 4-6 eggs

2. Sodium bicarbonate
Neutralizing agent in iron toxicity and red tide poisoning
NaHCO3 (8.4%): 1 vial in 250 mL for a 2% solution
Baking soda: 1 heaping tsp in 100mL water makes 5%
solution

F. Whole Bowel Irrigation

Flushes poison down GIT, removing and preventing
further absorption of toxicant
Propylene Glycol (PEG) is the electrolyte solution
used
Recommendation is to not routinely use this
procedure
IV. ENHANCING ELIMINATION OF ABSORBED
POISONS
A. Multiple-dose activated charcoal
B. Forced diuresis
C. Alkalinization therapy
D. Acidification therapy
E. Dialysis and hemoperfusion
A. Multiple-dose activated charcoal
Effective in poisoning from carbamazepine, dapsone,
phenobarbital, quinine and theophylline
Beneficial in:
Enhancing preabsorptive elimination of drugs which
decrease gastric motility, and sustained-release agents that
have erratic absorption in GIT
Gut dialysis of drugs that are lipophilic, have low protein-
binding capacity, have small volumes of distribution, and
long half-lives
Interrupting enterohepatic circulation
CI: caustics and petroleum distillates
Steps:
Give activated charcoal every 4-8 hours.
Exercise gut caution due to risk of intestinal
impaction, gut obstruction, and pulmonary
aspiration
Ensure bowel movement is observed daily
B. Forced diuresis D. Acidification therapy
• No longer recommended Ionizes weak bases (i.e. amphetamines, PCP,
• many drugs are metabolized in liver phenytoin, theophylline)
• Appropriate rehydration will suffice Can produce metabolic acidosis, rhabdomyolysis,
and renal failure
C. Alkalinization therapy Beneficial in methamphetamine toxicity
• Ionizes weak acids (i.e. salicylates, barbiturates, INH, 2,4- Ascorbic acid
dichlorophenoxyacetic acid) Adult: 1g IV q6 hrs until urine pH <5.5
• Inhibits passive renal tubular reabsorption of non-ionized Pedia: 20mg/kg IV q6 hrs until urine pH <5.5
molecules
• Sodium bicarbonate
• (8.4%) at 1 mEq/kg/dose or
1ml/kg/dose IV until urine pH is 7.5-8.5
E. Dialysis & Hemoperfusion
Employed in:
• Life-threatening poisoning
• Electrolyte & acid-base disturbances
• Dialysable toxins with poor body
clearance and high plasma toxin
concentration
• Underlying kidney or liver problems
Peritoneal Dialysis
Useful in short-term dialysis (i.e. severe salicylate
toxicity, ethylene glycol, or methanol ingestion)
Hemodialysis
Much more effective than peritoneal, including
lithium and isopropanol
Hemoperfusion
Poisoning from barbiturates, carbamazepine,
theophylline, glutethimide, quinidine, paraquat
Activated charcoal- most popular adsorbent in
hemoperfusion
V. ADMINISTRATION OF ANTIDOTES
• Use of specific antidotes is
seldom necessary except when
their administration is beneficial
and life-saving
• Dependent on the assessment of
the patient’s clinical state, lab
results, and pharmacodynamics
of the substance
6 MECHANISMS OF ACTION OF
ANTIDOTES:
A.Inert complex formation
B.Accelerated detoxification
C.Reduction in conversion to more toxic
compounds
D.Competitive inhibition at receptor sites
E. Bypassing the effects of the poison
F. Antibodies interacting with poisons
A. Inert Complex Formation Chelating Agents
• Used in heavy metal poisoning
• Facilitate formation of stable complex with a
5- or 6-membered ring, and incorporation of
a sulfide bond
B. Accelerated Detoxification D. Bypassing poison effects
Enhances rapid detoxification in the central Synergistic antidotal action
compartment, preventing distribution to cells i.e. Oxygen, Na thiosulfate and Na nitrite vs Cyanide;
i.e. thiosulfate in cyanide toxicity Pyridoxine vs INH toxicity
E. Antibodies
C. Reduction in Conversion Reverse the binding of compounds to receptors
Inhibit conversion to more toxic metabolite i.e. Digi-Fab at cardiac receptors; Antivenin vs venom
i.e. Ethanol inhibits conversion of methanol; phenytoin
prevents conversion of malathion to malaoxon

D. Competitive Inhibition
Blockade of receptor sites in CNS (i.e. Naloxone), or of
Ach at muscarinic receptors (i.e. Atropine)
VI. SUPPORTIVE THERAPY AND OBSERVATION

• Give IV fluids for maintenance and

replacement
• Test blood and urine pH when alkaline
and acid therapy are employed
• Provide intensive nursing care
• Treat metabolic disturbances
• Monitor VS
• Monitor I&O
VII. DISPOSITION
• Poisoned patient should be observed for
at least 24 hours, even if asymptomatic
• Refer for psychiatric evaluation if suicidal
• For substance abusers, consider referral to
support groups or rehab centers upon
discharge
• Consider possibility of child abuse
• Family counseling and education should
be initiated in hospital and continued
during OPD follow up