1. Update on Medical Emergencies Course, Terengganu
Acute Poisoning
and Drug Overdose
Dr. Rashidi Ahmad
MD (USM), MMED (USM), FADUSM, AM
Dept. Emergency Medicine
School of Medical Sciences
USM Health Campus
8th December 2007
2. Objectives
• Understanding poison
• Develop methodical approach to Poisoned
Patients
• Characterize Toxidromes & its
management
• Evidence-Based GI Decontamination
• Learn Antidotes
4. Poison
“Substance that when introduced into, or absorbed
by a living organism destroys life or injures
health”
(Oxford Dictionary)
“Poisons and medicines are oftentimes the same
substance given with different intents”
(Peter Mere Latham; 1789 – 1875)
5. “What is it that is not a poison?
All things are poison 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.
6.
7. 7 Mechanisms of Toxicity
1. Interfere with O2 transport or tissue utilization of
oxygen (i.e: cyanide, CO)
2. Affect lungs (paraquat)
3. Affect cardiovascular system (TCA, Ca++ channel
blockers)
4. Affect CNS (cocaine, sedatives)
5. Affect ANS (organophosphates)
6. Direct local damage (acids, bases)
7. Delayed effects on liver or kidneys
(acetaminophen, metals)
10. Two Sources of Data
• Data from Dr. Rozlan Ishak, Environmental
Health, Unit Disease Control Division, MOH
(1999)
• Data from the Occupational Health Unit of the
MOH (1997-2000)
• Data from the National Poison Centre,
Universiti Sains Malaysia
(1995 to 2002)
11. Site of Exposure
1997 1998 1999 2000
HOME 357 400 684 767
WORKPLACE 83 115 136 136
OTHERS 15 20 50 68
MISSING 253 11 18 75
TOTAL 708 546 888 1,046
14. Ethnic Group
1997 1998 1999 2000
MALAY 229 170 393 399
CHINESE 137 106 173 175
INDIAN 254 159 177 290
OTHERS 87 110 136 159
MISSING 1 1 9 23
TOTAL 708 546 888 1,046
15. Ethnic difference of Chemical Poisoning in Malaysia in 1999
6000
4843
5000
No. of Cases
3630
4000
3000
2000 984 952 910 1161
1000 34 24 340 283
0
Malays / Chinese Indians Others Missing Data
Bumiputra
Ethnicity in Malaysia
Male Female
16. Female
Male
ak
aw
Sar
ah
Sab
Gender Difference in Poisoning in Malaysia, 1999
an
ant
Kel u
gan
eng
Ter
ang
Pah
or
States in Malaysia
Joh
laka bila
n
Me
Sem pur
er i um
Neg aL
ual
PK
W.
or
ang
Sel
ak
Per ang
Pin
au
Pul
ah
Ked
lis
Per
0
1200
1000
800
No. of Cases 600
400
200
31. Preclinical phase
• Follows exposure before s/sx
• History guides management
• Aim: to reduce or prevent toxicity
• Decontamination is a priority
32. Toxic phase
• Period from onset to peak of manifestation of
toxicity clinical or laboratory
• PE guides treatment
• Aim: to shorten or lessen the severity of toxicity
• Priority: stabilize airways, breathing and
circulation and consider antidote
33. Resolution phase
• From peak toxicity to recovery
• Clinical status guides management
• Major goal: shorten the duration of toxicity &
supportive care
35. Approach to the Poisoned Patient
• ABC’s are always first !
• Most Patients Do Fine
- Majority of poisoned patients require
only supportive Rx
• But, those who don’t … often present with
undifferentiated AMS
36. Approach to the Poisoned Patient
• Approach to AMS
• Toxicologic History
• Toxicologic Physical Exam
• Toxicologic Labs
Think Toxins in any patient with AMS !
37. Approach to AMS
• A – Airway (mental status, suicidal trauma)
• B – Breathing (resp depression, pulm oedema, ARDS)
• C – Circulation (dysrhythmias, CV depression)
• D – Dysfunction CNS (hypoglycemia, alcohol, opiate
& benzodiazepine overdose, seizure control)
• E – Exposure (hyperthermia)
38. “Coma Cocktail” in toxin induce AMS
• Use of D50%, thiamine, nalaxone, flumazenil
• Toxin-induced LOC is generally well-tolerated and
achieving "arousal" of the patient does not
necessarily improve outcome.
• ? cost-effectiveness and risks of the coma cocktail
39. • D50% & thiamine should probably be given to
patients with AMS from unknown causes.
• Strongly suspected opiate overdose: Naloxone is
indicated. Lack of response to 10 mg of naloxone
generally excludes opioid toxicity
• Flumazenil should be used mainly for reversal of
therapeutic conscious sedation.
Hoffman RS, et al. The poisoned patient with altered consciousness.
Controversies in the use of a "coma cocktail." JAMA 1995;274:562-9
40. • Reversal of BZD intoxication with flumazenil is
a/w significant toxicity in patients with
benzodiazepine dependence or coingestion of
proconvulsant medications (TCA)
• May be useful to reverse excessive sedation
when BZDs are used for procedural sedation.
Toxicology in ECC. Circulation. 2005;112:IV-126-IV-132
41. Toxicology history
• Risk assessment
- to predict the likely clinical course and potential
complications
- To allow the clinician to make specific decisions
about all subsequent management steps
(appropriate supportive care and monitoring; screening and
specialized testing; decontamination; enhanced elimination;
antidotes and disposition)
42. Toxicology History
• Goal is Identification of Etiologic Agent(s)
• Use all Available Resources
- Pill bottles
- Pre-hospital personnel
- Family and Friends
- Medical Records
- Past medication and medical history
• Assess for Suicidal Behavior
- Must assume suicidal until proven otherwise
- Low threshold for Psychiatric consultation
43. Evaluation of Toxicity
• Evaluate the SATSC
– Substance
– Amount
– Time since ingestion
– Symptoms
– Co-morbid
• Regional Poison Control Center
44. Toxicology PE
• Vitals, Vitals, Vitals !
- Measure accurately
- Measure often
- Temp, HR, BP, RR, Pulse Ox
• Assess for Signs of Trauma
• “Skin” exam is critical
- Diaphoresis ?
- Trauma (scalp, elsewhere) ?
• Odor!!
• Pupil examination
45.
46. Odor Poison
Sweet/fruity Ketone, alcohol
Almond Cyanide
Gasoline Hydrocarbon
Garlic Organophospate
Wintergreen Methylsalicylate
Pear Chloral hydrate
John J. Marini, Arthur P. Wheeler. Critical care Medicine.
The essentials – Textbook 2006
47. Toxicology laboratory
• Mainly to assess the severity
• Asymptomatic Patients
- Acetaminophen Level – the “Silent” killer
• Toxin Identified/Strongly Suspected
- Testing based on suspected toxin
- Consider acetaminophen level as well
• In any patient with Undifferentiated AMS
- Blood: CBC, Chem 7, LFT’s, CPK, Serum osm
- Urine: U/A, UPT, UTox
- Tox-Specific: Acet, ASA,
48. Toxicology laboratory
• Most poisonings can be managed appropriately
without extensive laboratory studies.
• “Tox screens" rarely helpful.
- Undetected: bromide, carbon monoxide, chloral hydrate,
clonidine, cyanide, organophosphates, tetrahydrozoline,
beta-blockers, calcium-channel blockers, clonidine,
colchicine, digitalis, and iron.
• PCM screening helps especially in multiple
medications in intentional overdose.
53. Urine toxicology
Drug Durations in the urine
Drug Duration
Amphetamines 48 hours
Alcohol 12 hours
Barbiturates 10-30 days
Valium 4-5 days
Cocaine 24-72 hours
Heroin 24 hours
Marijuana 3-30 days
Methaqualone 4-24 days
Phencyclidine 3-10 days
Methadone 3 days
54. Toxidromes
• Constellation of Physical Findings
- Provides Clues
- Narrows Differential Diagnosis
• Beware: Many Exceptions Exist!
- Poly-drug Overdoses
- Overlapping and confusing mixed syndromes
55. Autonomic Nervous System
• Parasympathetic (PNS)
- “Rest and Digest”
- Mediated by Acetylcholine
- Muscarinic and Nicotinic Receptors
• Sympathetic (SNS)
- “Fight or Flight” response
- Mediated by Catecholamines
- Sympathetic Cholinergic: Sweating
66. GHB: Date rape drug
“Georgia homeboy, liquid ectasy, or grievous bodily harm”
• Developed as anesthetic agent. GABA analog
• Symptoms: bradycardia, hypothermia,
hypoventilation, somnolence, vomiting,
myoclonic jerking
• Treatment
– Conservative mx
– Intubation
– Careful exam for sexual assault
67. Ketamine: “K”, “special K”
• Developed as an anesthetic, structurally resemble
PCP
• Acts on all six neurotransmitter systems
– Anticholinergic: dry skin, miosis
– Dopamine/norepinephrine: agitation, delusions
– Opioid: pain perception alterations
– Serotonin: perceptual changes
– GABA receptor inhibition: excitation
• Treatment
– Benzodiazepines/haloperidol
– Supportive care
– Can consider urine alkalinization
68. Treatment of acute poisoning
• Primary goal - keep concentration of poison as low
as possible by preventing absorption and increasing
elimination
• Secondary goal - counteract toxicological effects at
effectors site, if possible
70. Principle of GI decontamination
• Toxins poorly absorbed in stomach, toxins well
absorbed in SI
• Decrease amount in stomach, therefore less
presenting to SI for absorption
• Maximum benefit: present soon after the ingestion.
• Delayed presentation + without symptoms -
probably does not contribute to the outcome
• Drugs with delayed absorption/reduce GI motility,
activated charcoal may reduce the final amount
absorbed.
?? Prehospital GI decontamination of toxic ingestions
71. Methods of GI decontamination
• Gastric
- Ipecac
- Activated Charcoal
- Single dose vs multi-dose
- Gastric Lavage
• Gastro-Intestinal
- Cathartics
- Whole Bowel Irrigation
73. Ipecac
• Little evidence that ipecac prevents drug absorption
or systemic toxicity
• No convincing data that it significantly alters the
clinical outcome of patients who are awake and
alert on presentation to the ED.
• Considered only in fully alert patients
• Never indicated after hospital admission
• CI: corrosives, petroleum products, or antiemetics,
high risk of seizures or altered consciousness.
Vale JA, Meredith TJ, Proudfoot AT. Syrup of ipecacuanha: is
it really useful? BMJ 1986; 293:1321–1322
74. Ipecac
• No evidence from clinical studies that ipecac
improves the outcome of poisoned patients and
its routine administration in the emergency
department should be abandoned.
• Insufficient data to support or exclude ipecac
administration soon after poison ingestion.
• Ipecac may delay the administration or reduce
the effectiveness of activated charcoal, oral
antidotes, and whole bowel irrigation.
Krenzelok AP et al. J Toxicol Clin Toxicol. 2004;42(2):133-43.
75. Single-dose activated charcoal
• Should not be administered routinely
• The effectiveness of activated charcoal decreases
with time; the greatest benefit is within 1 hour of
ingestion.
• Consider if a patient has ingested a potentially
toxic amount of a poison: insufficient data to
support or exclude its use after 1 hour of ingestion.
• There is no evidence that the administration of
activated charcoal improves clinical outcome.
Chyka PA et al. J Toxicol Clin Toxicol. 1997;35(7):721-41.
76.
77. Substances that are not absorb by charcoal
Mnemonic: CHARCOAL
Caustics & corrosive
Heavy metals
Alcohol & glycols
Rapidly absorbed substances
Cyanide
Other insoluble drugs
Aliphatic hydrocarbobs
Laxatives
78. Multiple-dose activated charcoal
• Consider only if a patient has ingested a life-
threatening amount of:
- carbamazepine
- dapsone
- phenobarbital
- quinine
- theophylline
• Insufficient clinical data: salicylate, amitriptyline,
dextropropoxyphene, digitoxin, digoxin, disopyramide, nadolol,
phenylbutazone, phenytoin, piroxicam, and sotalol
79. • The need for concurrent administration of
cathartics remains unproven and is not
recommended.
• Cathartics should not be administered to young
children because of the propensity of laxatives to
cause fluid and electrolyte imbalance.
Jefrey B, et al. Clinical Toxicology, 37(6), 731–751 (1999)
80. Gastric lavage
• Reported complication:
– Aspiration pneumonia - most
common
– Laryngospasm with cyanosis
– Kinking of lavage tube in
eosphagus
– Esophageal perforation
Reid et al Arch Dis Child 1970
Mattew et al Br Med J 1966
81. “Gastric lavage should not be employed routinely, if ever, in
the management of poisoned patients.”
J Toxicol Clin Toxicol 2004;42:7:933.
82. Evidence based protocols
• Ipecac
- is effectively obsolete
• Charcoal
- agent of choice for most poisons
- Best if used within one hour
• Lavage
- Narrow indications
- principally for potentially serious amounts of agents not
adsorbed by charcoal within half hour ingestion
Bateman DN. Gastric decontamination--a view for the millennium.
J Accid Emerg Med. 1999 Mar;16(2):84-6
83. Cathartics
• Use alone - not recommended as a method of gut
decontamination.
• Conflicting data: combine with activated charcoal:
• No clinical studies have been published to
investigate the ability of a cathartic, with or without
activated charcoal, to reduce the bioavailability of
drugs or to improve the outcome of poisoned
patients.
Donna Seger, et al. CLINICAL TOXICOLOGY.
Vol. 42, No. 3, pp. 243–253, 2004
84. Whole bowel irrigation (WBI)
• No conclusive evidence WBI improves outcome
• Consider: potentially toxic ingestions of sustained-
release or enteric-coated drugs.
• Insufficient/theoretical data for iron, lead, zinc, or
packets of illicit drugs
• CI: bowel obstruction, perforation, ileus, hemodynamic
instability or unprotected airways.
• A single dose of charcoal prior to WBI does not
decrease the binding capacity of charcoal
Hoffman RS. J Toxicol Clin Toxicol. 2000;38(7):689-90
89. Risk assessment
• Distinct cognitive step (predict the likely clinical
course and potential complications for the
individual patient at that particular presentation)
• Quantitative
• Takes into account:
– Agent(s)
– Dose(s)
– Time since ingestion
– Current clinical status
– Patient factors
90. Summary
• Supportive care and monitoring
• Investigations
– Screening (ECG, paracetamol)
– Specific
• Decontamination
• Enhanced elimination
• Antidotes
• Disposition
91. Conclusion
• Intoxication manifestation is very challenging (non
specific, AMS, no hx of intoxication, masked by
other conditions)
• Methodical approach/toxidrome helps
• Decontamination methods are vital – indications
determined by type of poisons, conscious level, risk
of aspiration, hemodynamic stability, time factor
• Antidote: gold standard
92. Build me newer molecules,
O my Soul -
As the swift seasons roll
Let each new compound
Safer than the last
Avoid the reactions observed in the past
………………..
The Pharmacologic Principles of
Medical Practice (1954)