Carbon Monoxide Poisoning
4/11/10
PY Mindmaps
- colourless, odourless gas produced by incomplete combustion of carbonaceous material
- impaired O2 delivery to tissue c/o avid binding of CO to Hb
- 250x more than O2 + left shift of oxy-Hb dissociation curve
- CO binds to myocardial myoglobin -> depression
- CO binds to cytochrome P450 -> causes lipid peroxidation and leukocyte mediated
inflammatory changes in the brain (limited by hyperbaric O2)
HISTORY
Acute poisoning
- CNS: malaise, confusion, depression, impulsiveness, hallucinations, agitation, headache,
drowsy, visual disturbance, syncope, seizure, bizarre neurological symptoms, coma
- GI: abdominal pain, N+V, diarrhoea
- RESP: SOB, chest pain, palpitation
Chronic exposures
- all above
- gradual onset of neuropsychiatric symptoms and cognitive symptoms
High risk exposures
-
fires
stoves
portable heaters
automobile exhaust
cigarette
charcoal grills
propane fuelled forklifts
gas powered concrete saws
inhaling spray paint
swimming behind a motor boat
solvents and paint removers (metabolised to CO in liver)
EXAMINATION
- vitals: tachycardia, hyper/hypotension, hyperthermia, tachypnoea
- cherry red skin (“when you’re cherry red, you’re dead”)
- ophthalmological signs: flame-shaped haemorrhages, bright red retinal veins, papilloedema,
homonymous hemianopsia
- pulmonary oedema
- neurological: amnesia, confabulation, emotional liability, decreased cognition, coma, gait
disturbance, apraxia, agnosia, blindness, psychosis.
Jeremy Fernando (2011)
INVESTIGATIONS
- HbCO -> elevated levels are significant, but low levels do not rule out exposure
- ABG: PaO2 should be normal, SpO2 only accurate if measured (not calculated from PaO2)
- FBC: mild leukocytosis
- lactate: tissue hypoxia
- hyperglycaemia
- hypokalaemia
- CK: rhabdomyolysis
- acute renal failure from myoglobinuria
- LFT derangement
- MetHb: in differential for cyanosis with low SpO2 but normal PaO2
- ethanol: polypharmacy OD
- cyanide level: (industrial fire, cyanide exposure)
- urine: +ve for albumin and glucose in chronic intoxification
- CXR: pulmonary symptoms
- CT head: in patients who’s symptoms don’t rapidly resolve (basal ganglia low densities) ->
poor outcome
- ECG: sinus tachycardia
MANAGEMENT
Resuscitate
- FiO2 1.0 (continue until patient asymptomatic or CO level < 10%)
- cardiac monitoring
- intubate the comatosed patient
Acid-base and Electrolytes Abnormalities
- metabolic lactic acidosis -> do not aggressively treat as this will shift oxy-Hb dissociation
curve to right -> encourage O2 off loading
Specific Treatment
- O2 via NRB
- transfer to hyperbaric facility (severe intoxication or persistent symptoms after 4 hrs)
- hyperbaric O2 (3 ATM) will decrease the half life of carboxyHb from 6 hours -> 20 minutes
- if associated with cyanide intoxification and nitrites use -> sodium thiosulphate 12.5mg IV
(this will prevent left shift of oxy-Hb curve)
Underlying Cause
- if intentional -> psychiatric referral
- work or home environment assessment
Jeremy Fernando (2011)