This document discusses childhood poisoning. It begins by outlining the objectives, which are to recognize common causes of childhood poisoning, understand the general principles of diagnosis and management, and provide guidance to prevent accidental poisoning. The document then covers general principles of diagnosis and management. It outlines the approach to a poisoned patient and discusses specific compounds commonly involved in pediatric poisoning like paracetamol, salicylates, iron, and more. It provides details on diagnosis, mechanisms of toxicity, and management strategies for several common toxic exposures in children.

1. CHILDHOOD
POISONING
Eunice Jade P. Oconer

2. › Identify the common etiologies of poisoning in the Philippines
setting
› To list down the general principles in diagnosis and
management of poisoning
› To illustrate the approach to a poisoned patient
› Recognize the clinical manifestations of childhood poisoning
› Discuss the pathophysiology, diagnosis and management of
common toxicants
› Provide anticipatory guidance for the prevention of accidental
poisoning
OBJECTIVES

3. I. Poisoning
II. General Principles
III. Approach to a Poisoned
Patient
IV. Principles of
Management
a. Decontamination
b. Enhanced Elimination
c. Antidotes
d. Supportive Care
OUTLINE
V. Common Compounds in
Pediatric Poisoning
› Paracetamol/Acetaminophen
› Salicylates
› Iron
› Caustics
› Hydrocarbons
› Organophosphates/Carbamates
› Lead
VI. First Aid for Acute Poisoning

4. › Exposure to a chemical or other agent that adversely
affects functioning of an organism.
› Ingestion of or contact with a substance that can
produce toxic effects
› Common occurrence in childhood
› Half of the cases of poisoning happens in ages 5 years
or younger
› Routes of exposure can be ingestion, injection,
inhalation or cutaneous exposure.
POISONING

5. CHILD POISONING
It is commonly occurs in & around the household
› Household items, Kerosene, Insecticides, Rat
killers, Naphthalene balls, Cosmetics, Bleaching
agents, Personal Care products
› Drugs: pain relievers, thinks medicine as “candy”

7. GENERAL PRINCIPLES IN
DIAGNOSIS & MANAGEMENT
OF POISONING

8.  Diagnosis is usually based on a high index of suspicion
 Confirm that there is a toxic exposure by a good history
and thorough physical examination
 Diagnosis of poisoning is almost always clinical
 Look for clues as to what was taken
 Where the child was found
 Smell the chemical
 Know approximately when the substance was ingested
 Estimate how much was taken and it is better to
overestimate than underestimate
GENERAL PRINCIPLES IN DIAGNOSIS &
MANAGEMENT OF POISONING

9.  Look for toxidromes or cluster of toxic symptoms
 Laboratory test most often do not help; sometime
they are just confirmatory of your findings
 Start life-saving measures immediately
 Done simultaneously while doing the history
and Physical Examination
 Give the antidote at once if there is a need. Do not
delay.
 Primum Non Nocere (Do no/further harm)
GENERAL PRINCIPLES IN DIAGNOSIS &
MANAGEMENT OF POISONING

10. APPROACH TO THE
POISONED PATIENT

11. ›Airway
›Breathing
›Circulation
›Mental Status
STABILIZE THE PATIENT

12. Specific:
ABC’s of Toxicology:
› Airway
› Breathing
› Circulation
› Drugs
› Draw blood
› Decontaminate
› Expose / Examine
› Full vitals / Monitoring
› Give specific antidotes / treatment

13. 1. History
 Is it intentional, unintentional, exploratory?
 Witnessed?
 Onset of symptoms
 Presence of sudden alteration of mental status, multiple
system organ dysfunction
2. Description of the exposure
 Brand, generic, chemical, specific ingredients along with
concentrations
 Timing
 Amount
INITIAL EVALUATION

14. 3. Symptoms
4. Past Medical History
5. Social History
6. Physical Examination
INITIAL EVALUATION

15. I - Iron
C - Carbon monoxide, Cyanide
O - Organophosphates
P - Phenothiazines
E - Ethylene Glycol, Ethanol
F - Free base cocaine
A - Anticholinergic, Antihistamines
S - Sympathomimetic, Salicylates, Solvents
T - Theophylline
When a patient has TACHYCARDIA it is often
associated with “I COPE FAST ”

16. P - Propanol
A - Anticholinesterase
C - Clonidine, Calcium Channel Blockers
E - Ethanol
D - Digitalis
BRADYCARDIA is often associated with
“PACED”

17. C - Cocaine
T - Theophylline
S - Sympathomimetic
C - Caffeine
A - Anticholinergic
N - Nicotine
HYPERTENSION is often associated with
“CT SCAN”

18. C- Clonidine
R- Reserpine
A- Antidepressants
S- Sedative- Hypnotics
H- Heroin
HYPOTENSION is often associated with
“CRASH”

19. 7. Toxidromes - for patient whom you are
unaware of the history; based on clustering of
symptoms that are usual for certain toxicants
8. Laboratory Evaluation
INITIAL EVALUATION

22. SCREENING LABORATORY CLUES IN
TOXICOLOGIC DIAGNOSIS

23. ELECTROCARDIOGRAPHIC FINDINGS IN
POISONING

24. PRINCIPLES OF
MANAGEMENT

25. GOAL: Prevent absorption of the toxic
substances
Regardless of the decontamination method
used, the efficacy of the intervention decreases
with increasing time since exposure.
DECONTAMINATION

26. Remove contaminated clothing and particulate matter
by flushing using NSS (~10-20 min) or tepid water
Protective gear for treating clinicians
Some chemicals, particularly alkaline corrosives, may
require much longer periods of flushing.
For dermal exposures, mild soap and water can be
used.
DERMAL AND OCULAR DECONTAMINATION

27.  Most likely effective in the first hour after an acute ingestion
 >1 hour after ingestion may be considered in some instances,
but may consider other ways aside from GI decontamination.
 Methods of GI decontamination:
1. Induced emesis with Syrup of Ipecac
2. Gastric lavage
3. Single-dose activated charcoal
4. Whole Bowel Irrigation
GI DECONTAMINATION

28. 1. INDUCED EMESIS WITH SYRUP OF IPECAC
a. Contraindications of induced emesis:
Decreased sensorium
Impaired gag reflex leading to aspiration
Late pregnancy that may induce preterm labor for
adolescent pregnancy
Caustics and hydrocarbons, convulsants,
arhythmogenic agents
Cardiac disease or aneurysm
Methods of GI Decontamination

29. GASTRIC LAVAGE
 Benefit is between 6-12 hours post ingestion in those who took
the drug with slow gastric emptying or slow released
preparations.
 May be done when you know the drug.
 Insert an NGT to the patient; place him in a trendelenburg
position with head turned towards the left and the body in left
lateral decubitus. Infuse lukewarm or tepid water, repeating until
the fluid becomes clear in the NGT.
 Contraindications:
 Caustics
 Convulsions/ seizures
Methods of GI Decontamination

30. SINGLE-DOSE ACTIVATED CHARCOAL
 Adsorbent that binds organic substances such as drugs, chemicals,
toxins and hormones on the surface thus preventing absorption in
the GIT
 Avoided after ingestion of a caustic substance
 Dose: 1g/kg in children or 50-100g in adolescents and adults
 Best utilized during the 1st hour of post ingestion.
 Can be combined with water, flavor or administered via NGT due to
the taste, it is poorly tolerated by children
 Substances poorly absorbed by activated charcoal:
 Alcohols, Caustics (alkalis & acids), Cyanide, Heavy Metals (e.g.
lead), Hydrocarbons, Iron, Lithium
Methods of GI Decontamination

31. WHOLE BOWEL IRRIGATION
Highly effective in getting rid of substances not
usually adsorbed by charcoal and lavage by
flushing the ingested substances down the GIT
Best for sustained-release preparations,
concretions of tablets, transdermal patches and
drug packets.
This is given by drinking it or thru NGT until rectal
flow is clear. Thus, measure the output of the
patient.
Methods of GI Decontamination

32. WHOLE BOWEL IRRIGATION
Polyethylene glycol electrolyte solution is
used.
Contraindication: Ingestion of caustic
substances, fluid and electrolyte
imbalance, paralytic ileus, congestive heart
failure
Methods of GI Decontamination

33.  Generally accomplished by moving the patient
to fresh air or, if necessary, administering
oxygen.
 In addition to supportive care, a few specific
antidotes are used for some specific inhaled
toxins
INHALED TOXIN DECONTAMINATION

34. A. MULTIPLE-DOSE ACTIVATED CHARCOAL
 0.5g/kg every 4-6 hours for < 24hrs until there is
significant clinical improvement
 Interruption of enterohepatic recirculation and
“GI dialysis”
ENHANCED ELIMINATION

35. B. URINARY ALKALINIZATION
 Use Sodium Bicarbonate (NAHCO3), which is
incorporated into IV fluids
 Goal: Urine pH of 7.5-8.0
 Used for: Salicylate, methotrexate toxicity,
barbiturate, and amphetamines
 Adverse effects: hypokalemia and hypocalcemia
 Contraindication: Patients with fluid volume
overload, such as patients with CHF or renal
problems
ENHANCED ELIMINATION

36. C. DIALYSIS
Toxins amenable to dialysis have the ff. properties:
Low volume of distribution
Low molecular weight
Low degree of protein binding
High degree of water solubility
ENHANCED ELIMINATION

39. PARACETAMOL/ACETHAMINOPHEN
POISONING

40. › Most widely used analgesic and antipyretic in
pediatrics
› Common causes of acute overdose
› Therapeutic dose: 10-15mg/kg/dose.
› After ingestion of paracetamol, 90% is
metabolized to its inactive sulfate and
glucoronide conjugates.
PARACETAMOL (ACETOMINOPHEN)

41. STAGE Time after
ingestion
CHARACTERISTICS
I 0-24 hrs
Gastrointestinal irritation
Nausea, vomiting or dizziness
Labs typically normal, except for
acetaminophen levels (elevated)
II 24-48 hrs
Latent period
 Resolution of earlier symptoms
 Hepatic tenderness and Hepatomegaly
 Elevated bilirubin, prothrombin time
 Hepatic enzymes start to elevate (AST/ALT
and alkaline phosphatase);
 Oliguria
Classic stages in the Clinical Course of
Paracetamol Toxicity

42. STAGE Time after
ingestion
CHARACTERISTICS
III 72-96 hrs
Hepatic failure
 Severe hepatotoxicity – jaundice, coagulopathy,
hypoglycemia, recurrent nausea and vomiting and
encephalopathy ensue
 Transaminases are markedly increased (AST rises
to 20,000-30,000 IU/Liter)
 Peak liver function abnormalities multisystem
organ failure and potential death
IV
4 days –
2wk
Recovery or death
 Most patients recover completely
 Progressive encephalopathy, renal failure,
bleeding and hyperammonemia leading to death
 Clinical recovery precedes histologic recovery
Classic stages in the Clinical Course of
Paracetamol Toxicity

43. Toxicity results from accumulation of toxic
metabolites: N-acetyl-pbenzoquinoneimine (NAPQI)
relative to endogenous glutathione
Toxic single dose is 150 mg/kg
At therapeutic dose:
 90% of acetaminophen is conjugated and renaly
excreted.
 2-4% is metabolized via P450 enzymes to NAPQI
NAPQI is quickly conjugated to gluthatione to a
non toxic metabolite
MECHANISM OF TOXICITY

44. In an overdose, glutathione stores are depleted,
NAPQI accumulates leading to hepatotoxicity
Single acute toxic dose: (taken as single dose)
 >200 mg/kg – children
 >7.5-10g – adolescents & adults
 If there is repeated administration at
supratherapeutic doses, which is >75mg/kg/day
for consecutive days could lead to hepatic injury
or failure.
MECHANISM OF TOXICITY

45. Serum Paracetamol assay within 4 hours post-ingestion
Electrolytes, RBS, BUN, Creatinine, Liver transaminases,
Prothrombin time, Bilirubin levels
If a toxic ingestion is suspected, a serum paracetamol
level should be measured 4 hrs after the reported time of
ingestion.
Paracetamol levels obtained <4 hrs after ingestion are
difficult to interpret and cannot be used to estimate the
potential for toxicity.
Not helpful in patients with chronic exposure to
paracetamol.
DIAGNOSIS

49.  Gastric Decontamination
 NGT, activated charcoal, sodium sulfate cathartic
 Specific Therapy
 Antidote: 20% N-Acetylcysteine (NAC)
 Loading dose: 140mg/kg; After 4 hrs, you can give
70mg/kg
 The standard administration of NAC is a 3 stage infusion
giving a total dose of 300mg/kg:
 Phase I: 150 mg/kg in 1 hr
 Phase II: 50 mg/kg in 4 hrs
 Phase III: 100 mg/kg in 16 hrs
MANAGEMENT

50. SALICYLATES POISONING

51.  ASA, Methylsalicylate (oil of wintergreen), salicylic
acid.
 Aspirin – still used for pediatric groups with
rheumatoid arthritis and Kawasaki disease.
 Commonly found in household.
 Toxic dose:
 Acute: 150-200 mg/kg (mild); 300-500 mg/kg
(severe/ fatal)
 Chronic: 100 mg/kg/day for 2 or more days.
SALICYLATES

52.  Inhibits Kreb’s cycle and blocks carbohydrate and lipid
metabolism causing lactic acidosis.
 Uncouples oxidative phosphorylation & interruption of glucose
and fatty acid metabolism leading to metabolic acidosis
 Central stimulation of the respiratory center leading to
hyperventilation and secondary respiratory alkalosis
 Alters platelet formation by prolonging prothrombin time
(protime)
 Pulmonary and cerebral edema (mechanism unknown).
MECHANISM OF TOXICITY

54. Toxicologic exam:
 Determining drug level 6 hours post-ingestion can confirm both
diagnosis and severity of poisoning, however, plasma salicylate level
concentration poorly correlates with signs and symptoms because
toxicity is directly related to concentration of free drug which
depends on total plasma concentration and degree of protein
binding.
 Serum/urine salicylate assay
 Serial serum salicylate levels should be closely monitored
(every 2 hours initially) until they are consistently down
trending.
 Salicylate absorption in overdose is often unpredictable and
erratic, and levels can rapidly increase into the highly toxic
range.
DIAGNOSIS

55.  ABC’s of life support
 Decontamination - prevent further absorption
 Can also give activated charcoal at 1g/kg
 Primary mode of therapy: Alkalinization therapy
 IV Bicarbonate infusion 1mmol/kg/hr, after initial
slow bolus of 2 mmol/kg (keep urine pH >7.5)
 Supportive therapy
MANAGEMENT

56. IRON POISONING

57.  One of the most common causes of childhood
poisoning mortality
 Toxic dose: 20 mg/kg elemental iron
 Remember: Measure elemental iron for toxicity, not
dosage.
Sulfate – 20% elemental iron
Gluconate – 12% elemental iron
Fumarate – 33% elemental iron
IRON

58.  Toxicity occurs when serum iron exceeds total iron binding
capacity (TIBC), causing an increase in free circulating iron,
which causes damage to GIT, heart, and liver.
 Iron is corrosive to the GI mucosa and may lead to intestinal
ulceration, edema, and possibly perforation.
 Accumulates in the mitochondria and tissues to produce
cellular damage and systemic toxicity.
 Causes vasodilatation and increased capillary permeability
leading to hypotension.
 Early hypovolemia and mitochondrial damage, results in
lactic and citric acid accumulation, causing metabolic
acidosis.
MECHANISM OF TOXICITY

59. STAGE 1 (INITIAL PERIOD)
 30 min to 6 hours
 symptoms of nausea, vomiting, abdominal pain,
and diarrhea (Hallmark of iron poisoning)
 corrosion in GIT: hemorrhage, ulceration,
transmural inflammation, necrosis of bowel wall,
infarction.
STAGE 2 (LATENT/QUIESCENT STAGE)
 6-24 hour period following the resolution of GI
symptoms and before overt systemic toxicity.
CLINICAL COURSE

60. STAGE 3 (RECURRENT PERIOD)
 24-48 hours post-ingestion
 Shock results from hypovolemia, vasodilation, and poor cardiac
output.
 Iron directly inhibits oxidative metabolism at cellular level causing
tissue ischemia.
 Iron-induced coagulopathy worsens bleeding and hypovolemia.
 Lethargy, hyperventilation, seizure, coma.
STAGE 4
 4-6 weeks following ingestion
 Gastric outlet obstruction secondary to strictures and scarring
from injury.
 Rarely occurs
 Do endoscopic evaluation.
CLINICAL COURSE

61. Toxicologic exam:
 Serum iron level taken at least 4-6 hours post-ingestion
(<500 μg/dL 4-8 hr: low risk; >500 μg/dL indicate that
significant toxicity)
 Check TIBC (Total Iron Binding Capacity)
General exam:
 CBC, blood typing, RBS, BUN, creatinine, urinalysis,
serum electrolytes, ABG, liver function tests, fecalysis
with occult blood, plain abdomen (abdominal x-ray to
see radio-opaque materials, which are undissolved iron
tablets).
DIAGNOSIS

62.  ABC’s of life support
 Decontamination: NAHCO3 lavage.
 Antidote: DEFEROXAMINE 10-15 mg/kg/hr IV
infusion
 Whole bowel irrigation
 Charcoal is of no benefit
 Supportive therapy
MANAGEMENT

63. CAUSTICS POISONING

64. › Cause direct damage to tissues upon contact.
› Acid ingestion produces coagulation necrosis
resulting in eschars which tend to self-limit further
damage.
› Alkali causes liquefaction necrosis.
› Remember: aCid=Coagulation, aLkali=Liquefaction
› Solubility of alkali allow further penetration hence,
injury is more severe than that of acids
CAUSTICS POISONING

65. Common Available Acids

66. Common Available Alkali

67.  Factors to consider in establishing the degree of
damage are:
 pH - strong acids pH below 2; Strong alkali pH
above 12
 Concentration
 Molarity
 Volume
 Contact time
 Premorbid condition of the stomach
 Ulceration of necrotic tissues may lead to perforation,
peritonitis, strictures, and stenosis in the esophagus,
stomach or pylorus

68. Special precautions
DO NOT insert NGT if more than 30 min have
elapsed since ingestion.
DO NOT attempt lavage
DO NOT induce vomiting
DO NOT give any neutralizing agents because
the reaction can evolve CO2 which can
aggravate the chemical injury to the stomach
and cause rupture

69. ABC’s of life support.
Use copious amounts of water to decontaminate
the eyes/skin exposed to acid/alkali spills or
vomitus.
Put patient on NPO, give IV fluids
Start antacids
Refer for emergency endoscopy
Supportive therapy: acute abdomen, shock, upper
airway obstruction, upper GI bleeding
TREATMENT

70. HYDROCARBON POISONING

71. Kinds of hydrocarbons:
 Aliphatics: Gasoline, naphthalene,
kerosene, turpentine, mineral seal oil,
heavy fuel oil
 Aromatics: benzene, toluene, xylene
 Halogenated: Methylene chloride,
carbon tetrachloride,
tetrachloroethylene
HYDROCARBONS

72.  Majority of cases are due to the petroleum distillates
 Most ingestions are accidental chiefly because they
are STORED IN THE WRONG CONTAINERS
 Aspiration of even small amounts is serious and
potentially life threatening.
 Have high volatility (ability of the subs to become a
gas) and low surface tension (ability of the subs to
resist flow) , hence are commonly aspirated and
produce pulmonary injury
HYDROCARBONS

73.  Hydrocarbons are poorly absorbed in the GIT, and just cause
abdominal pain and discomfort. However, drinking large
amounts may cause convulsions, coma and death
 Initial manifestations:
 Cough, shortness of breath, dyspnea, often a few minutes
after ingestion or 6 hours post ingestion
 Caution must be taken because aspiration pneumonia is likely to
occur, especially when there is vomiting.
 Aspirated kerosene inhibits surfactant, leading to alveolar
instability, early distal airway closure, V/Q mismatches and
subsequent hypoxemia
 Can also cause direct CNS effects leading to coma and seizures
MECHANISM OF TOXICITY

74.  Decontaminate – wash skin with soap/water
 Give cathartics
 DO NOT GIVE ACTIVATED CHARCOAL because it
does not offer any benefit
 Treatment is generally supportive: aspiration
pneumonia (give antibiotics), gastritis (give H2
blocker), hypoprothrombenemia, seizures (give
anticonvulsants)
MANAGEMENT

75. ORGANOPHOSPHATES/CARBAMATE
POISONING

76. ORGANOPHOSPHATES/CARBAMATE
POISONING

77.  Most pediatric poisoning occurs because of unintentional
exposure to insecticides.
 These inhibit the action of Acetylcholinesterase (ACHe) by
phosphorylating the active or esteric site of the enzyme
preventing the degradation of acetylcholine, leading to
accumulation of Acetylcholine (Ach) at receptor sites.
 Net effect is a decrease in the activity of the enzyme leading
to acetylcholine excess
 Enzymes affected include ACHe or red blood cell
cholinesterase, pseudocholinesterase (found in plasma), and
neurotoxic esterase (nervous system)
 If left untreated, organophosphates form a permanent bond
to these enzymes, inactivating them in a process called aging
MECHANISM OF TOXICITY

78. S - salivation
L - lacrimation
U - urination
D - diarrhea
G - GI cramps
E - emesis
MANIFESTATIONS
 D - diarrhea
 U - urination
 M - miosis
 B - bradycardia
 E - emesis
 L - lacrimation
 S - salivation

79. Severity System Involved
Mild Mainly Muscarinic
Moderate Muscarinic and Nicotinic
Severe Muscarinic, Nicotinic, and CNS
CLINICAL FEATURES DEPEND ON THE
SEVERITY

81. Toxicological exam: RBC cholinesterase
 Mild poisoning: Depression in cholinesterase
activity to 20-50%
 Moderate poisoning: Activity to 10-20%
 Severe poisoning - <10% of cholinesterase
enzyme activity
 General examinations: ABG, ECG, Na, K, Cl,
CBC, RBS, BUN, Creatinine, LFT, protime,
Urinalysis, amylase
DIAGNOSIS

82.  ABC’S of life support
 Decontamination
 Clothing removed, skin washed with running water and soap
 Activated charcoal lavage, emesis
 Enhanced elimination
 Antidotes
 Atropine: blocks the muscarinic manifestations: 0.01-0.05
mg/kg; can be used for both organophosphates and
carbamates;
 Pralidoxime: regenerates acetylcholinesterase at muscarinic,
nicotinic and CNS sites: 20-40 mg/kg dissolved in NSS and
infused over 30 mins; not necessarily used for carbamates
because the enzyme degrades spontaneously
MANAGEMENT

83. LEAD POISONING

84.  Environmental toxicant that can be fatal
 Children has increased exposure and
vulnerability
 Battery making/burning, paints, ceramics or
toys glazed with lead, soldering, make-up, eye
brow pencil, hair dye, air pollutants.
 Ingestion, inhalation and dermal absorption.
 Bones–90% of total body lead burden
LEAD

85.  Impairs heme biosynthesis
 Inhibits ferrochelatase
 Elevated free erythrocyte protoporphyrin levels
 Segmental demyelination of peripheral nerves
 Decreased motor nerve conduction velocity
 Rapidly absorbed in the GI tract especially in an
empty stomach. Peak concentration occurs
within 30mins to 1 hr upon ingestion.
MECHANISM OF TOXICITY

86. Usually occur after chronic exposure
Anorexia, vomiting, colicky abdominal
pain, arthralgias, headache, weakness,
anemia, motor neuropathy, wrist drop,
hearing impairment, encephalopathy,
mental retardation, hyperactivity, school
failure, antisocial behavior
MANIFESTATIONS

87. Toxicologic Exam:
› Severe lead poisoning: > or equal to 70 mg/dL
› Blood lead level: 1 specimen of > 10mg/dl (venous blood)
› Or 2 capillary blood levels (prick) of > 10mg/dl (capillary
blood) checked twice, 12 hours apart
General examinations:
› CBC, Liver function tests, Renal function tests, serum
electrolytes, RBS, EMV-NCV, IQ tests, x-ray of abdomen and
long bones (check for red-liner), urinalysis, serum iron, TIBC.
› Do peripheral blood smear to check for RBC stippling---high
lead levels in the blood.
DIAGNOSIS

88. › Removal from exposure
› Identification of source
› Diazepam for seizures
› Laboratory monitoring
› Iron supplement
› Ascorbic acid to increase iron absorption
MANAGEMENT

89. most common gas involved in pediatric
exposures is carbon monoxide (CO)
CO is a colorless, odorless gas produced during
the combustion of any carbon-containing fuel.
The less efficient the combustion, the greater
the amount of CO produced.
Wood-burning stoves, old furnaces, and
automobiles are a few of the potential sources
of CO.
CARBON MONOXIDE

90.  CO binds to hemoglobin with an affinity >200 times that of
oxygen, forming carboxyhemoglobin (COHb).
 CO displaces oxygen and creates a conformational change in
hemoglobin that impairs the delivery of oxygen to the tissues,
leading to tissue hypoxia.
 CO binds to cytochrome oxidase, disrupting cellular respiration.
 CO displaces nitric oxide (NO) from proteins, allowing NO to
bind with free radicals to form the toxic metabolite
peroxynitrate.
 NO is also a potent vasodilator, in part responsible for clinical
symptoms including headache, syncope, and hypotension.
MECHANISM OF TOXICITY

91. › Early symptoms are nonspecific and include headache,
malaise, nausea, and vomiting.
› At higher exposure levels, patients can develop mental
status changes, confusion, ataxia, syncope,
tachycardia, and tachypnea.
› Severe poisoning is manifested by coma, seizures,
myocardial ischemia, acidosis, cardiovascular collapse,
and potentially death.
› On exam, patients might have cherry-red skin.
MANIFESTATION

92. Administration of 100% oxygen to enhance
elimination of CO.
Severely poisoned patients might benefit from
hyperbaric oxygen (HBO), which decreases the half-
life of COHb to 20-30 minutes.
Sequelae of CO poisoning include persistent and
delayed cognitive effects.
Prevention of CO poisoning should involve
educational initiatives and the use of home CO
detectors.
TREATMENT

93. THANK YOU!