Carbon Monoxide Poisoning

Carbon Monoxide
Poisoning
Morning Report
January 7, 2009

Sources of Carbon Monoxide
Car exhaust fumes (#1 cause of CO-related death)
Smoke from fires (#2)
Furnaces
Gas-powered engines (idling boats)
Home water heaters
Wood stoves/ gas stoves/ space heaters
Paint removers (containing methylene chloride)
Tobacco smoke
Pool heaters

Pathophysiology
Curve shifts LEFT
O2 delivery to tissues
…Tissue hypoxia ensues

Historical Clues
Co-inhabitants with similar symptoms at same onset
Symptoms recur and do not follow a regular 7-10
day viral course
Alternative heating devices (space heaters, gas
stoves), wintertime (idling auto with snow blocked
exhaust pipe)
Improves when away from site
Absence of sore throat/fever/URI symptoms
Illness or death of a family pet

Environmental Exposure History
Community (urban vs.rural/near industrial sites)
Home (heating sources, location of bedrooms,
fireplaces, wood stoves)
Hobbies (especially hockey, ice skating)
Occupation (industrial sites w/ inadequate
ventilation, auto repair shops, loading docks)
Personal (screen for depression/suicidal ideation)
Diet
Drugs (especially tobacco)

Clinical Presentation
COHb 20%
Headache
Dizziness
Weakness/myalgia
Nausea/vomiting
Shortness of breath
Visual changes
Chest pain
COHb >40%
Confusion
Syncope
Pulmonary edema
Coma
Seizures
COHb >60%
Cardiac ischemia
Death
Classic Triad “cherry red lips,
cyanosis & retinal hemorrhages”

Delayed Neuropsychiatric Syndrome
Delayed onset of neurologic symptoms after apparent
recovery from acute CO intoxication
Occurs 3-240 days (mean 20) in up to 50% of patients
The development of DNS correlates poorly with COHb levels
Symptoms: cognitive and personality changes, parkinsonism,
dementia, psychosis, movement disorders
Imaging will often show abnormalities within the globus
pallidus and the deep white matter
Recovery occurs in 50-75% of affected persons within one
year

Diagnosis
Carboxyhemoglobin level
Measured directly via co-oximetry
A low level does not rule out acute intoxication
ABG- metabolic acidosis (and co-oximetry)
PaO2 may be normal!
BMP- anion gap metabolic acidosis
EKG

Management
100% O2
Half-life of COHb :
Room air: 4-5 hrs
100% oxygen: 90 min
Hyperbaric oxygen: 20-30 min
Ventilatory support if needed
Cardiac monitoring
Most CO poisonings can be managed in the ED
COHb levels >25% admission is recommended

Hyperbaric Oxygen Therapy
HBO involves exposure to 100% FiO2 under supraatmospheric
conditions (2.5-3.0 atm)
May be beneficial in preventing the late
neurocognitive deficits (DNS)
Results of clinical trials vary widely
Most authorities recommend HBO if:
COHb >30%
LOC, acute neurological deficits
Pregnant women with COHb >15%

Take Home
CO poisoning results in nonspecific sx…HA,
dizziness, weakness, N/V
SaO2 and PaO2 may be normal…

References
Abelsohn, A, Sanborn MD., Jessiman, BJ. Identifying and managing
adverse environmental health effects: Carbon monoxide poisoning.
CMAj. 2002; 166 (13): 1685-1690
Armin Ernst, MD and Joseph D. Zibrak, MD. Carbon Monoxide
Poisoning. NEJM 1998; 339:1603-1608.
Juurlink DN, Stanbrook MB, McGuigan MA. Hyperbaric oxygen for
carbon monoxide poisoning. Cochrane Database Syst Rev 2005; 1:
CD002041
Weaver LK, et al. Hyperbaric oxygen for acute carbon monoxide
poisoning. NEJM 2002; 347: 3. Reviewed in: The Peds CCM Evidence-
Based Journal Club, 2003.