Carbon monoxide poisoning diagnosis and treatment.

1. CARBON MONOXIDE POISONING
Done by: Leena Al-Mubiden

2. OVERVIEW
• Carbon monoxide (CO) is a colorless, odorless gas produced by
incomplete combustion of carbonaceous material.
• The atmospheric concentration of CO is generally
below 0.001 percent
• Binds to the iron of heme with approximately 240 times the affinity
of oxygen.
• Clinical presentation in patients with CO
poisoning ranges from headache and dizziness to coma
and death.
• CO oximetry gold standard for diagnosis
• Hyperbaric oxygen therapy can significantly reduce the morbidity
of CO poisoning, but a portion of survivors still suffer significant
long-term neurologic and affective sequelae.
• Two thirds of patients eventually recover completely.

3. PATHOPHYSIOLO
GY
• Cardiac
ischemia
• Cerebral edema

4. WHAT ARE THE MOST COMMON
CAUSES OF CARBON MONOXIDE (CO)
TOXICITY?
• Most fatalities from CO toxicity result from fires.
• but stoves, portable heaters, and automobile exhaust cause
approximately one third of deaths.
• Cigarette smoke is a significant source of CO.
• Other sources of CO exposure include the following :
• Propane-fueled forklifts
• Inhaling spray paint
• Swimming behind a motorboat
• Methylene chloride (dichloromethane) is an industrial solvent
and a component of paint remover. Inhaled or ingested methylene
chloride is metabolized to CO by the liver, causing CO toxicity in the
absence of ambient CO.

6. CLINICAL
PRESENTATI
ON

7. • For nonfatal nonintentional non–fire-related
exposures,
• the most common symptom was headache (37%)
• followed by dizziness (18%) and nausea (17%).
• However, any of the following symptoms should alert
suspicion in the winter months, especially when the
patient has a history compatible with CO exposure and
when more than one patient in a group or household
presents with similar complaints

8. Malaise, flulike
symptoms,
fatigue
Dyspnea on
exertion
Chest pain,
palpitations
Lethargy Confusion Depression
Impulsiveness Distractibility
Hallucination,
confabulation
Agitation
Nausea,
vomiting,
diarrhea
Abdominal pain
Headache,
drowsiness
Dizziness,
weakness,
confusion
Visual
disturbance,
syncope, seizure
Fecal and
urinary
incontinence
Memory and gait
disturbances
Bizarre
neurologic
symptoms,
coma

9. • Other classical signs
• Cherry-red skin: after exposure to
high levels (rare and usually seen
postmortem)
• Fundoscopic findings: bright red
retinal vessels, retinal hemorrhage
s, papilledema (indicative
of cerebral edema)
Chronic exposure also produces the above
symptoms; however, patients with chronic
CO exposure may present with loss of
dentition, gradual-onset neuropsychiatric
symptoms, or, simply, recent impairment
of cognitive ability.

10. DIAGNOSIS
• Three criteria should be present to confirm acute poisoning, but symptoms vary widely
and the history of exposure is not always evident.
• Any symptoms of CO poisoning
• Exposure to CO source
• Abnormal COHb level on venous/arterial CO oximetry
• > 3–4% in nonsmokers
• > 10–15% in smokers
• Start 100% oxygen immediately if clinical suspicion for CO poisoning is high
• Diagnostic workup should not delay oxygen administration

11. •CO oximetry with spectrophotometry
Gold standard for diagnosis
•The COHb level is used to guide
therapeutic decisions.
• Findings on arterial blood gas measurement include the
following:
• Partial pressure of oxygen (PaO2) levels should remain
normal; oxygen saturation is accurate only if directly
measured but not if calculated from PaO2, which is
common in many blood gas analyzers.
• Metabolic acidosis occurs secondary to lactic acidosis
from ischemia.

12. ADDITIONAL STUDIES
• Screen for affected organs and toxic coingestions.
• Inhalation injury: airway examination (e.g., direct laryngoscopy)
• Cardiac toxicity
• All patients: ECG and cardiac monitor for 4–6 hours
• Findings may include signs of myocardial ischemia and/or arrhythmias.
• Select patients :
• cardiac enzymes and echocardiography
• Findings may include increased troponin and/or cardiac hypomotility.

13. • Neurological toxicity: CT/MRI brain
• Indications :
• Symptomatic patients (e.g., altered mental status)
• Unconscious patients
• Retinal hemorrhage (good indicator of CNS toxicity)
• Findings
• The globus pallidus is commonly affected
• White matter changes
• Cerebral edema

14. MANGMENT
• Patients often arrive in critical condition or comatose,
which requires an ABCDE approach
• Oxygen therapy:. Oxygen therapy is considered first-
line treatment.
• Administer 100% oxygen immediately
via nonrebreather facemask.

15. HYPERBARIC OXYGEN (HBOT) :
• Hyperbaric oxygen therapy (HBOT) is breathing 100%
oxygen while under increased atmospheric pressure.
• The treatment of CO poisoning with hyperbaric oxygen
therapy (HBOT) is based upon the theory that oxygen
competitively displaces CO from hemoglobin. While
breathing room air, this process takes about 300 minutes.
While on a 100% oxygen nonrebreather mask, this time is
reduced to about 90 minutes. With HBOT, the time is
shortened to 32 minutes.
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

16. INDICATIONS:
• The following are considered relative indications: COHb > 25%
• Pregnant women with a COHb > 20%
• CO level >25 percent
• Neurological manifestations (e.g.,
confusion, loss of consciousness, seizures, focal
neurological deficits
• Severe acidosis (pH < 7.15)
• Evidence of end-organ ischemia

17. • Secure airway: Consider early intubation in
patients with inhalation injury or severely
impaired mental status
• Evidence of cardiac toxicity
(e.g., arrhythmias, ischemia): urgent
cardiology consult, continuous cardiac
rhythm monitoring
• Suspicion of intentional poisoning
• Evaluate for suicidal ideation
• Obtain a psychiatric consultation and
consider involuntary psychiatric hold.

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