Carbon Monoxide poisoning presentation auditorium of ED Farwaniya hospital, state of Kuwait.

1. Case 1
 A 67-year-old man sought medical help after three days of
light-headedness, vertigo, stabbing chest pain, cough, chills
and headache. His wife had experienced similar symptoms over
the past week.
 He was admitted, evaluated and discharged with a diagnosis of
viral syndrome.
 Ten days later he returned to the ER with vertigo, palpitations
and nausea but was sent home for outpatient follow up.
 Four days later he again returned to the ER with diarrhea and
severe chest pain, collapsing to the floor. He was admitted to
the Coronary Care Unit with acute myocardial infarction.
 Among the results of a routine arterial blood gas analysis, it was
found that his COHb levels were 15.6%.
 A COHb level then obtained on his wife was 18.1%. A rusted
furnace was found to be the source.

2. Case 2
 A 69-year-old man came to the ER after days of confusion,
nausea, vomiting, intermittent syncope, hallucinations and
shortness of breath. An arterial blood gas measurement found
an oxygen saturation of 89%.
 He was admitted to the coronary care unit with a diagnosis of
acute myocardial infarction.
 The next day a COHb level was measured and normal. While
the patient was hospitalized he invited his sister and daughter-in-
law to stay in his home.
 They both arrived at the ER the next morning with headaches,
vomiting, and vertigo.
 Their COHb levels on initial observation were 28% and 32%.
After investigation, the man’s gas water heater was faulty.

3.  Yasser Diab

4. What Is Carbon Monoxide?

 Carbon monoxide is a colorless, odorless, tasteless, and
initially non-irritating toxic gas, it is very difficult to be to
detected.
 Carbon monoxide consists of one carbon atom and one
oxygen atom, connected by a triple bond that consists of
two covalent bonds as well as one dative covalent bond.
 Carbon monoxide is a product of incomplete combustion
of organic matter due to insufficient oxygen supply to
enable complete oxidation of carbon atom to form carbon
dioxide (CO2).

6. Sources of carbon monoxide

 Endogenous
a. Normal heme catabolism by heme oxygenase.
b. Increased in hemolytic anemia, sepsis.
 Exogenous
a. Incomplete combustion of carbonaceous fossil fuel
b. House fires
c. Automobile exhaust
d. Propane-powered vehicles (forklifts, ice skating rink resurfacers)
e. Gas-powered furnaces, ovens, fireplaces
f. Heaters
g. Indoor grills
h. Camp stoves
i. Boat exhaust
j. Cigarette smoke
k. Methylene chloride: a Solvent found primarily in paint remover
Endogenously converted to carbon monoxide after inhalational
exposure

7. Worldwide, the largest source of carbon monoxide is natural in
origin, due to photochemical reactions in the troposphere that
generate about 5×1012 kilograms per year.(Weinstock 1972)
 Other natural sources of CO include volcanoes, forest fires,
and other forms of combustion.

8.  Half-life: it is the time required for half the quantity of a drug
or other substance to be metabolized or eliminated.
 CO half-life on 21% room air O2: 4-6 hours.
 CO half-life on 100% O2:80 minutes.
 CO half-life with hyperbaric O2: 22 minutes.

9. Carbon monoxide molecule:


10. Who Is at Risk?
 EVERYONE, especially:
 People using alternate heat sources during power
outages
 Elderly.
 Unborn babies, infants.
 People living in poorly vented crowded houses.

11.  People with chronic heart disease, anemia, or respiratory
problems.
 Personnel at fire scenes (fire-fighters/rescue workers)
 Individuals involved into camping activities (Kuwait and Gulf
region).
 Industrial workers at pulp mills, steel foundries and plants
producing formaldehyde and coke.

12. Incidence increase
generaly in winter because:

Insufficient ventilation
 Generators used inside during a power outage
 Gas or kerosene heater in room without proper
ventilation
 Stoves or fireplaces that are improperly vented.
 Cars or trucks idling in a garage
 Improper use
 Using charcoal grills indoors
 Heating homes with gas ovens

13. Why carbon monoxide

CO binds to:
Hemoglobin Myoglobin
Cytochrome
oxidase
Brain lipids
is dangerous?

14. Hemoglobin:
  The affinity between hemoglobin and carbon monoxide is
approximately 230 times stronger than the affinity
between hemoglobin and oxygen so hemoglobin binds to
carbon monoxide in preference to oxygen.
 Hemoglobin is a tetramer with four oxygen binding sites.
The binding of carbon monoxide at one of these sites
increases the oxygen affinity of the remaining three sites,
which causes the hemoglobin molecule to retain oxygen
that would otherwise be delivered to the tissue.
 This situation is described as carbon monoxide shifting
the oxygen dissociation curve to the left.

16.  Because of the increased affinity between hemoglobin
and oxygen during carbon monoxide poisoning, little
oxygen will actually be released in the tissues.
 This causes hypoxic tissue injury resulting in relative
functional anemia.
 This decreases the amount of oxygen carried by the
hemoglobin, and forming carboxyhemoglobin (COHb).

17. 

18. 

19. Cardiac myoglobin:

 Carbon monoxide also binds to the cardiac myoglobin. It
has a high affinity for myoglobin, about 60 times greater
than that of oxygen.
 Carbon monoxide bound to myoglobin may impair its
ability to utilize oxygen.This causes reduced cardiac
output and hypotension, which may result in brain
ischemia.
 Carbon monoxide has double effect on the heart, hypoxia
and direct toxicity.

20. Cytochrome oxidase:
 Carbon monoxide binds to mitochondrial cytochrome

oxidase C and P450 with less affinity than oxygen, so it
is possible that it requires significant intracellular
hypoxia before binding.
 This binding interferes with aerobic metabolism and
efficient adenosine triphosphate (ATP) synthesis. Cells
respond by switching to anaerobic metabolism, causing
anoxia, lactic acidosis, and eventual cell death.
 The rate of dissociation between carbon monoxide and
cytochrome oxidase is slow, causing a relatively
prolonged impairment of oxidative metabolism.

21. Brain lipid peroxidation:
  CO may cause leukocyte-mediated inflammatory
changes in the brain, a process that may be inhibited by
hyperbaric oxygen therapy.
 Following severe intoxication, patients may display
central nervous system (CNS) pathology, including
white matter demyelination.
 This leads to edema and focal areas of necrosis

22. Clinical picture
 Signs and symptoms
usually vague and non-specific.
You must
ALWAYS
maintain a
high index of
suspicion for
CO poisoning!

23. Acute exposure Chronic

exposure
Delayed effect
 Headache: dull, frontal, and continuous
(most common) (Hampson et al 2002)
 General: Malaise, flu-like symptoms,
fatigue.
 Central: Drowsiness, weakness,
agitation, confusion, Visual
disturbance, syncope, seizures, Fecal
and urinary incontinence, Memory and
gait disturbances, coma
 Circulatory: Dyspnea on exertion, Chest
pain, palpitations.
 Other: Nausea , vomiting , diarrhea,
Abdominal pain
 Headache,
dizziness,
anorexia, apathy,
insomnia, and
personality
disturbance
 Polycythemia
and
cardiomegaly,
likely secondary
to chronic
hypoxia
(Penney 1988)
DNS or delayed
neurological
sequalae in the
form of
impairment of
cognitive
functions.
Clinical picture of CO poisoning:

24. Giuseppe et al 2011

25. Clinical severity:(Ernst et al 2008)

Mild
< 15 - 20%
Headache
Nausea, Vomiting
Dizziness, Blurred vision
Moderate
21 - 40%
Confusion, Syncope
Chest pain, Dyspnea
Weakness
Tachycardia, Tachypnea
Rhabdomyolysis
Severe
41 - 59%
Palpitations, Dysrhythmias
Hypotension
Myocardial ischemia, Cardiac arrest
Respiratory arrest
Noncardiogenic pulmonary edema
Seizures, Coma
FATAL >60% Death

27. Delayed Neurological Sequelae(DNS):
 The delayed neurological sequelae may occur in up to 50% of
poisoned people after 2 to 40 days (Lewis et al 2002).

 It is difficult to predict who will develop delayed sequelae;
however, advanced age, loss of consciousness while poisoned,
and initial neurological abnormalities may increase the chance
of developing delayed symptoms
 include difficulty with higher intellectual functions, short-term
memory loss, dementia, amnesia, psychosis, irritability, a
strange gait, speech disturbances, Parkinson's disease-like
syndromes, cortical blindness, and a depressed mood.
 Depression may even occur in those who did not have pre-existing
depression.(Roohi et al 2001)

28. Concentration Symptoms (Goldstein et al 2008)
35 ppm (0.0035%)
Headache and dizziness within six to eight hours of constant
exposure
100 ppm (0.01%) Slight headache in two to three hours
200 ppm (0.02%) Slight headache within two to three hours; loss of judgment
400 ppm (0.04%) Frontal headache within one to two hours
800 ppm (0.08%)
Dizziness, nausea, and convulsions within 45 min; insensible
within 2 hours
1,600 ppm (0.16%)
Headache, tachycardia, dizziness, and nausea within 20 min; death
in less than 2 hours
3,200 ppm (0.32%)
Headache, dizziness and nausea in five to ten minutes. Death
within 30 minutes.
6,400 ppm (0.64%)
Headache and dizziness in one to two minutes. Convulsions,
respiratory arrest, and death in less than 20 minutes.
12,800 ppm (1.28%)
Unconsciousness after 2–3 breaths. Death in less than three
minutes.

30. Historical hint:
In addition to the Holocaust
during World War II,
German Nazis used gas
vans to kill an estimated
700,000 prisoners by carbon
monoxide poisoning. This
method was also used in the
gas chambers of several
death camps.

31. Differential diagnosis
 Carbon monoxide has been called a "great mimicker" due to the

presentation of poisoning being diverse and nonspecific.
 Headaches (migrain, cluster, tension.. Etc)
 Flu-like viral syndromes
 Depression
 Chronic fatigue syndrome
 Acute cronary syndrome
 Acute respiratory distress syndrome
 Altitude sickness,
 Lactic acidosis,
 Diabetic ketoacidosis,
 Meningitis or encephalities.
 Methemoglobinemia,
 Or opioid or toxic alcohol poisoning
(Shochat et al 2009)

32. 
Management

33. Diagnosis
• The diagnosis of CO poisoning is a clinical one, the common
definition requires: (Neil B. Hampson 2012).

 History of recent CO exposure,
 The presence of symptoms consistent with CO poisoning,
 And demonstration of an elevated carboxyhemoglobin
level
• Laboratory testing requires a blood sample (arterial or venous)
and laboratory analysis on a CO-Oximeter.

34. 

35. Emergency Department Evaluation
 Patients with confirmed or strongly suspected CO poisoning may be
triaged according to their clinical status with Special attention be paid
to airway management.

 Attention should be paid for co morbidities (burns, trauma, other
inhalational injuries…..)
 Intubation of the comatose patient or, if necessary, for airway
protection (ie ..laryngeal edema)
 Vital signs and a directed neurologic examination should be done
immediatly, and the patient should have continuous cardiac monitoring.
An IV catheter should be inserted.
 Non-invasive co-oximetry may be useful at triage to rapidly identify
patients with significant CO exposure.

36.  ECG and cardiac monitoring because of the potential for
myocardial ischemia or dysrhythmia. Ventricular dysrhythmias
or ST-segment changes are sometimes seen. (Anderson et al
1967).

38. RAD-57
Finger tip
carboxyhemo
globin
saturation
monitor
(SpCO%)
(Masimo RAD-57
Portable CO
oximeter)

39. Breath CO monitor

40. Patient evaluation
It is directed at making the diagnosis, estimating the severity
of poisoning, and identifying 
end-organ damage. Questions
to ask include:
• Where was the patient found, and under what circumstances?
• Was there clear evidence of CO exposure?
• Was there loss of consciousness?
• Was there evidence of trauma?
• Was a fingerstick glucose determination performed?
• Was noninvasive co-oximetry performed?
• Was prehospital ECG performed?
• Was there evidence of attempted self-harm or suicidal intent?

41.  In addition to standard medical history, ask about symptoms
consistent with end-organ dysfunction or damage. These include:
 Headaches
 Alterations in mentation
 Difficulty performing simple mathematical tasks
 Visual changes
 Syncope
 Other focal neurologic symptoms, or seizure.
 All patients, regardless of age or health status, should be asked about
the presence of
 chest pain
 shortness of breath
 dyspnea on exertion,
 palpitations, or lightheadedness.
 Female patients should be asked about the possibility of pregnancy.
 All patients with CO poisoning should be questioned directly
regarding suicidal intent.

42. Physical examination
 General: for burns and coexistent trauma, evaluation of the
oropharynx for edema and soot, neck for stridor.

 Vital signs: for arrythmia, Hypotension that may indicate
cardiogenic shock due to ischemia, or it may be related to
acidosis or other Co-inhalants, such as cyanide.
 Skin: Classic cherry red skin is rare, usually detected
postmortem (ie, "When you're cherry red, you're dead"); pallor
is present more often.
 Pulmonary examination: for small airway obstruction as
wheezing in patients who are exposed to smoke or have
inhaled other irritants. Also “cardiac wheezing” or crackles
signifying myocardial depression secondary to smoke
inhalation.

43.  Cardiac examination: new gallop may represent acute diastolic
dysfunction.
 Neurological: Cranial nerves, motor, and sensory examination
performed to detect any focal neurologic deficits.
 cerebellar function tests may also detect abnormalities not
evident on gross examination.
 Gait testing is a must, because ataxia can be a presenting
sign of neurotoxicity and may be missed if the patient is not
observed while ambulating.
 Ophthalmologic
Flame-shaped retinal hemorrhages
Bright red retinal veins (a sensitive early sign)
Papilledema
Homonymous hemianopsia.

44. Diagnostic Studies

Co-oximetry:
 SpCO measured with the RAD-57 was not a substitute
for standard blood COHb measurement. However,
noninvasive pulse CO-oximetry could be useful as a
first-line screening test, enabling rapid detection and
management of CO-poisoned patients in the
emergency department. (Mustapha et al, RCj 2013)
 So,It cannot be considered the standard of care.

45. Carboxyhemoglobin level:
 Normal circulating levels in the blood are 0% to 3%, and are
higher in smokers. Carbon monoxide levels cannot be
assessed through a physical exam. (Roth and Herkner 2010).
 Done for all patient with known or suspected CO poisoning
 The relationship between COHb levels and poisoning
severity is generally poor; accordingly, this should be
obtained while initiating empiric treatment (Harper et al
2004).
 A COHb level greater than 3% in non-smokers or greater
than 10% in smokers suggests an abnormal CO exposure.

46. ABG and serum lactate:
Lactic acidosis due to increased anaerobic cellular metabolism in
the setting of tissue hypoxia (Sokal et al 1985)
Cardiac Biomarkers: if: (MMWR 2004)
 Patients have ECG changes suggestive of ischemia,
 Symptoms consistent with myocardial ischemia.
 History of coronary artery disease.
 Age greater than 65 years.
Pregnancy testing:
As elimination of CO from fetal hemoglobin takes over
3 times as long as it does for the mother. (Hill EP et al 1977)

47. Other tests:
 Creatinine kinase, urine myoglobin: Nontraumatic
rhabdomyolysis
 Complete blood count: mild leukocytosis/ DIC-TTP
 Electrolytes and glucose level : Lactic acidosis, hypokalemia,
and hyperglycemia with severe intoxication
 BUN and creatinine levels :Acute renal failure secondary to
myoglobinuria
 Liver function tests : Mild elevation in fulminant hepatic
failure
 Urinalysis : Positive for albumin and glucose in chronic
intoxication
 Methemoglobin level : normal 0-12% ,Included in the
differential diagnosis of cyanosis with low oxygen saturation
but normal PaO2
 Toxicology screen :volatile alcohols, salicylates, acetaminophen
levels, if altered mental status or in patients who present after a
suicide attempt.
 Ethanol level : A confounding factor of intentional and
unintentional poisonings

48. Chest Radiography:
 pulmonary edema, aspiration pneumonitis, pneumothorax, or
other underlying preexisting condition such as (COPD).
 Changes such as ground-glass appearance, perihilar haze, and
intra-alveolar edema imply a worse prognosis than normal
findings.
CT scan:
head and cervical spine if suspected trauma or altered mental status,
For patients who will be undergoing HBO therapy for concealed
hemorrhage.

51.  Admission should be considered for patients :
 with symptoms of moderate or severe CO poisoning, such as
altered mental status or persistent neurologic or cardiovascular
dysfunction. (with or without COHb >20%).
 These patients may have comorbidities, such as concurrent
cardiac ischemia, burns, or hemodynamic instability, each of
which requires specialized care.

53. 1-Normobaric oxygen
 It is a 100% oxygen given at atmospheric pressure using non
rebreather mask, It is the mainstay of treatment.

 It is continued until the patient is asymptomatic and HbCO levels are
below 10%. In patients with cardiovascular or pulmonary
compromise, lower thresholds of 2% have been suggested.
 Calculate a gross estimate of the necessary duration of therapy using
the initial level and half-life of 30-90 minutes at 100% oxygen
 Carbon monoxide is competitively displaced from hemoglobin and
eliminated from the body via the pulmonary circulation.
 CO half-life is inversely proportional to the fraction of inspired
oxygen. The elimination half-life is approximately 300 minutes on
room air, 90 minutes on reservoir “non-rebreather” facemask, and 30
minutes breathing HBO.(Ernst A et al 1998)

54. 2-Hyperbaric oxygen therapy (HBO):
 HBO is defined as 100% inspired oxygen delivered at greater

than 1.4 atm of pressure in a special chamber.
 Treatment regimens usually involve 100% oxygen at 2.4-3
atm for 90-120 minutes.
 It is supposed that HBO is benificial
o Increased elimination of HbCO
o Remove CO from cytochrome oxidase, inhibit adherence
of neutrophils on vascular endothelium, and prevent the
downstream effects of lipid peroxidation (Thom et al
1993)
o Certain studies proclaim major reductions in delayed
neurologic sequelae, cerebral edema, pathologic central
nervous system (CNS) changes, and reduced cytochrome
oxidase impairment.

55. Indications for hyperbaric oxygen therapy in carbon
monoxide poisoning: (Hampson 2001)
Currently Accepted Indications
1) Neurologic findings
a. Altered mental status
b. Coma
c. Focal neurologic deficits
d. Seizures
2) Pregnancy with CO-Hgb levels > 15–20%
3) History of loss of consciousness
Relatively Considered for:
a. Cardiovascular compromise (ischemia,
infarction,dysrhythmia)
b. Metabolic acidosis
c. Extremes of age
d. Elevated CO-Hgb level (>25–40%)
e. Abnormal neuropsychometric testing results
f. Persistent symptoms despite normobaric oxygen

59. Controverse about HBO therapy:
With:
Hyperbaric oxygen should at least be considered in all cases of serious acute
CO poisoning and normobaric 100% oxygen continued until the time of
hyperbaric oxygen administration. (Weaver et al 2007).
Daily 100-minute treatments with 100% oxygen in a hyperbaric chamber–60
minutes at 2.8 atmospheres for 3 days, extended to 6 days if there were
neurological abnormalities. (Scheinkestel et al 1999).
CO-poisoned patients who received three hyperbaric oxygen treatments
within 24 hours of presentation manifest approximately one-half the rate of
cognitive sequelae at 6 weeks, 6 months, and 12 months after treatment as
those who were treated with normobaric oxygen. (Weaver et al 2007).

60. 
Aginst:
The use of HBO therapy in CO poisoning
remains controversial (Juurlink et al 2005)
There is insufficient evidence to support the
use of hyperbaric oxygen for treatment of
patients with carbon monoxide poisoning
(Buckley et al 2011).

62. The American College of Emergency Physicians
(ACEP) clinical policy final recommendations are:
1. Hyperbaric oxygen therapy is a therapeutic option
for CO-poisoned patients; however, its use cannot be
mandated.
2. No clinical variables, including carboxyhemoglobin
levels, identify a subgroup of CO poisoned patients for
whom hyperbaric oxygen therapy is most likely to
provide benefit or cause harm. (wolf et al 2008)

63. 3-Treatment of complications
 Arrythmias: managed according to ACLS protocol.
 Acidosis : it is not recommended to treat acidosis with a PH above

7.15 because it results in a rightward shift in the oxyhemoglobin
dissociation curve, increasing tissue oxygen availability. Acidosis
generally improves with oxygen therapy.
 Treatment of potentially coexistent inhalational cyanide toxicity
using cyanide antidote kit and cyanocobalamine.
 Treatment of delayed neurological sequalae.

64. COPD patients:
  Patients with carbon monoxide poisoning and a
significant smoking history – even if not formally
diagnosed with COPD – have regular ABG analysis
during treatment to ensure that they are not developing
a dangerous respiratory acidosis.
 Carbon dioxide retention in such patients limits the use
of uncontrolled high-flow oxygen, and thus in certain
circumstances early intubation may need to be
considered. The use of hyperbaric oxygen therapy in
such patients should be considered only with extreme
caution. (Tristan et al 2008)

65. Pregnancy
 Fetal hemoglobin has a 10 to 15% higher affinity for carbon
monoxide than adult hemoglobin, causing more severe
poisoning in the fetus than in the adult (omaye et al 2002)

 In utero fetus are more vulnerable to CO toxicity because of the
natural leftward shift of the dissociation curve of fetal
hemoglobin.
 Acute, severe CO poisoning is associated with high maternal
and fetal mortality.
 Steady state levels of COHb in the fetus are higher than in
maternal blood. It takes longer to reach steady-state, and fetal
elimination of CO is also prolonged.
 For these reasons, many centers advocate hyperbaric treatment
for pregnant females with a cohb level greater than 20% or
signs of fetal distress (decreased or absent fetal movement or
fetal bradycardia) . (elkharrat et al 1991)

66. Discharge:

Patients who did not have:
1. loss of consciousness.
2. who have complete recovery from any symptoms,
3. whose COHb level has returned to normal (Asymptomatic patients
with levels below 10% may be discharged).
4. and who have no evidence of end-organ damage (ECG changes,
elevated cardiac biomarkers, neurological deficits)
may be safely discharged to home. (Lavonas EJ et al 2007)
 An observation unit stay would be a useful option for stable
patients requiring prolonged NBO therapy.
 Only those patients showing signs of significant end-organ
toxicity will require hospitalization, with or without HBO therapy.

68. Key message (Neil et al 2011)
I. Basic pathophysiology:

Several mechanisms of CO toxicity exist, in addition to relative
hypoxemia from carboxy hemoglobin (COHb) formation.
II. Diagnosis
a. Symptoms: Nonspecific. Most common are headache,
dizziness, nausea/vomiting, confusion, fatigue, chest pain,
shortness of breath, and loss of consciousness.
b. Signs: Cherry red discoloration is rare.
c. Role of carboxy hemoglobin level: Confirms clinical diagnosis.
Correlates poorly with symptoms or prognosis
d. Pre diagnosis management: Administer 100% oxygen while
waiting for COHb level.

69. III. Management
a. Normobaric oxygen therapy:
If chosen for treatment, 100% oxygen by nonrebreather facemask or
endotracheal tube until COHb normal (,3%) and patient asymptomatic
(typically 6 h)
b. Selection for hyperbaric oxygen (HBO) therapy:
Currently not completely clarified. Poisoned patients with loss of
consciousness, ischemic cardiac changes, neurological deficits,
significant metabolic acidosis, or COHb.25% warrant HBO2. More mildly
poisoned patients may be treated accordingly.
c. Goals of HBO2therapy:
Prevent neurocognitive sequelae
d. Optimal HBO protocol:
Unknown. Recommend retreatment of persistently symptomatic patients
to a maximum of 3 treatments.
e. Intentional poisonings:
Coingestion of other toxins commons. Consider toxicological screening
f. Concomitant cyanide poisoning:
Suspect if CO source is house fire. Consider empiric treatment if pH 7.20
or plasma lactate.10 mmol/L.

70. IV. Patient follow-up
a. Accidental poisoning: Follow-up in 4–6 wk to screen for
cognitive sequelae
b. Intentional poisoning: Psychiatric follow-up mandatory in
light of high rate of subsequent completed suicide
V. Prevention
a. Public education: Educate about proper generator use and risk
from combustion of fuels indoors
b. CO alarms: Encourage minimum of 1 per home, located near
sleeping area. Replace alarms every 5–7 yr, as per manufacturer’s
instructions

71. 
Thank you

72. References

 Diagnosis And Management Of Carbon Monoxide
Poisoning In The Emergency Department, February
2011 Volume 13, Number 2:
Heikki Nikkanen, MD, FAAEM, FACMT Attending
Physician, Brigham and Women’s Hospital, Department of
Emergency Medicine, Boston, MA
Aaron Skolnik, MD Chief Resident, Harvard Affiliated
Emergency Medicine Residency,
Brigham and Women’s Hospital Department of Emergency
Medicine, Boston, MA

73.  Goldstein M (December 2008). "Carbon monoxide poisoning".
Journal of Emergency Nursing: JEN: Official Publication of the
Emergency Department Nurses Association 34 (6): 538–542.
doi:10.1016/j.jen.2007.11.014. PMID 19022078.
 Roohi F, Kula RW, Mehta N (July 2001). "Twenty-nine years
after carbon monoxide intoxication". Clinical Neurology and
Neurosurgery 103 (2): 92–95. doi:10.1016/S0303-8467(01)00119-
6. PMID 11516551
 Hampson NB, Hampson LA (March 2002). "Characteristics of
headache associated with acute carbon monoxide poisoning".
Headache 42 (3): 220–223. doi:10.1046/j.1526-4610.2002.02055.x.
PMID 11903546.
 Omaye ST (Nov 2002). "Metabolic modulation of carbon
monoxide toxicity". Toxicology 180 (2): 139–50.
doi:10.1016/S0300-483X(02)00387-6. PMID 12324190

74. Sokal JA, Kralkowska E. The relationship between exposure
duration, carboxyhemoglobin, blood glucose, pyruvate, and
lactate and the severity of intoxication in 39 cases of acute
carbon monoxide poisoning in man. Arch Toxicol.1985;57:196-
199.(Prospective, descriptive study; 39 patients
Ernst A, Zibrak JD. Carbon monoxide poisoning. N Engl J
Med.1998;339:1603-1608. (Review article)
Juurlink DN, Buckley NA, Stanbrook MB, et al. Hyperbaric
oxygen for carbon monoxide poisoning. Cochrane Database
Syst Rev.2005;(1):CD002041. (Meta-analysis)

75. Thom SR. Functional inhibition of leukocyte B2 integrins by
hyperbaric oxygen in carbon monoxide-mediated brain injury in rats.
Toxicol Appl Pharmacol.1993;123:
248-256. (Animal study)
Elkharrat D, Raphael JC, Korach JM, et al. Acute carbon monoxide
intoxication and hyperbaric oxygen in pregnancy. Intensive Care
Med. 1991;17:289-292. (Prospective study; 44 patients)
Lavonas EJ. Carbon monoxide poisoning. In: Shannon M, Borron S,
Burns M, eds. Haddad and Winchester’s Clinical Management of
Poisoning and Drug Overdose.Philadelphia, Pa: Elsevier; 2007:1297-
1307. (Textbook chapter) Diagnosis And Management Of Carbon
Monoxide Poisoning In The Emergency Department

76. Wolf SJ, Lavonas EJ, Sloan EP, et al. Clinical policy: critical issues in the management of adult
patients presenting to the emergency department with acute carbon monoxide poisoning. Ann
Emerg Med.2008;51(2);138-152. (Clinical policy)
Harper A, Croft-Baker J. Carbon monoxide poisoning: undetected by both patients and their
doctors. Age Ageing.2004;33:105-109
Anderson EF, Allensworth DC, DeGroot WJ. Myocardial toxicity from carbon monoxide
poisoning. Ann Internal Med.1967;67:1172-1182
Centers for Disease Control and Prevention. Carbon monoxide poisonings resulting from open-air
exposures to operating motorboats - Lake Havasu City, Arizona, 2003. MMWR.2004;53(15);314-
318
Hill EP, Hill JR, Power GG, et al. Carbon monoxide exchanges between the human fetus and
mother: a mathematical model. Am J Physiol.1977;232:H311-H323.

77.  Carbon monoxide poisoning in a patient with carbon dioxide retention: a
therapeutic challenge,Tristan RA Lane,corresponding author1 WilbyJ
Williamson,1 and Joshua M Brostoff1,Cases J. 2008; 1: 102.Published
online Aug 18, 2008. doi: 10.1186/1757-1626-1-102.
 Buckley NA, Juurlink DN, Isbister G, Bennett MH, Lavonas EJPublished
Online:13 April 2011There is insufficient evidence to support the use of
hyperbaric oxygen for treatment of patients with carbon monoxide
poisoning.
 Buckley NA, Juurlink DN, Isbister G, Bennett MH, Lavonas EJ.
Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database
Syst Rev. Apr 13 2011;4:CD002041.

78.  Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning,
Weaver et al 2002,N Engl J Med 2002; 347:1057-1067October 3,
2002DOI: 10.1056/NEJMoa013121.
 Hyperbaric oxygen for carbon monoxide poisoning Nick A
Buckley1,*,David N Juurlink2,Geoff Isbister3,Michael
H,Bennett4,Eric J Lavonas5 Editorial Group: Cochrane Injuries
Group Published Online: 13 APR 2011,Assessed as up-to-date:
6 JUN 2010,DOI: 10.1002/14651858.CD002041.pub3
 Practice Recommendations in the Diagnosis, Management,
and Prevention of Carbon Monoxide Poisoning
 Neil B. Hampson1, Claude A. Piantadosi2, Stephen R. Thom3,
and Lindell K. Weaver4,2012 the American Thoracic Society.

79.  Penney DG. Hemodynamic response to carbon monoxide.
Environ Health Perspec 1988;77:121–30.