Carboxyhemoglobinemia

Epidemiology

Leading cause of death by poisoning in the USA

Etiology

Portable heaters/ wood stoves/ gasoline engines: CO generated by incomplete combustion of fuel
Smoke Inhalation (see [[Smoke Inhalation]]): accounts for most cases of lethal CO intoxication
Paint remover: solvent methylene chloride is metabolized to CO

Physiology

Carbon monoxide (CO) inhalation, rapid absorption in lungs with avid binding to Hb in pulmonary capillaries (Hb binds to CO with 210x affinity of that for O2), myoglobin in muscle, and mitochondial cytochrome oxidase
Physiologic effects:
- Decrease in Hb’s oxygen-carrying capacity: results in tissue hypoxia
- Shift of oxygen dissociation curve to left: impairs oxygen unloading at tissues
- Decrease in myoglobin oxygen-carrying capacity:
- Impaired cellular respiration: with resultant anaerobic metabolism an dlactic acidosis
Cardiac effects:
- Increased afterload:
- Increased cardiac output:
- Decreased coronary endothelial vasodilation in vessels with atheroma:
- Enhanced platelet adhesiveness:
- Increased blood viscosity (due to capillary leak and hemoconcentration): with resultant decreased myocardial oxygen delivery

Diagnosis

EKG: may show ischemic arrhythmias
- Ventricular ectopy
- A-Fib
ABG: metabolic (lactic) acidosis
- Normal pO2:
- Normal or decreased pCO2:
- Direct (ABG) co-oximetry SaO2: decreased
- Pulse oximetry SaO2: normal
- COHb Level by Co-Oxemtry: diagnostic (levels as low as 2-4% may decrease exercise tolerance and precipitate angina in patients with CAD)
  - 20-30%: usually associated with mild symptoms
  - 30-50%: usually associated with moderate symptoms
  - 50-60%: usually associated with severe symptoms
  - >60%: often fatal
CK/LDH: may be elevated (reflecting rhabdomyolysis)
Lactate: increased
CXR: normal or may show pulmonary edema

Clinical

10% COHb: Headache
20% COHb: Headache/Dyspnea
30% COHb: Nausea/Dizziness/Impaired Judgement
40% COHb: Confusion/Syncope
50% COHb: Coma/Seizures
60% COHb: Hypotension/Resp Failure
70% COHb: Death

Toxidrome:
-Neuro (CNS injury occurs due to hypoxia, hypotension, leukocyte adherence with protease release): headache/ emotional lability/ impaired judgement/ clumsiness/ vis-ual field defects, blindness/ altered MS/ seizures/ resp-iratory depression/ cerebral edema (with papilledema or optic atrophy)
–Up to 30% of cases with LOC have persistent neuro changes (ranging from altered personality to blindness to Parkinson’s) up to 1-3 weeks after exposure
-Cardiac: angina (may precipitate MI)/ myocarditis/ syncope/ arrhy-thmias/ hypotension/ CHF

-Pulmonary:
a) Cyanosis (more common than “cherry red” skin): “Cherry Red” Appearance of Lips and Skin is an insensitive sign associated with carboxyhemoglobinemia
b) Dyspnea/Tachypnea/ Hyperventilation:
c) ALI/ARDS:

-Other: fatigue/ generalized weakness/ N/V/D/ “cherry red” skin and mucous membranes (occurs rarely)/ conversion reaction/ blisters or bullae (over pressure points)/ rhabdomyolysis

Treatment

Supplemental Oxygen:

Oxygen (100%): administer until COHb is <10% and symptoms have resolved (treat infants and pregnant females for hrs longer due to higher affinity of fetal Hb for CO)/ may require mechanical ventilation in comatose patients
Inhibits CO binding to Hb and CO is subsequently excreted through the lungs (half-life depends on treatment, but half-life with methylene chloride exposure is considerably longer)
In RA, COHb half-life: 4-6 hrs
On 100% O2: COHb half-life: 40-80 min

Hyperbaric Oxygen (HBO)

At 2-3 atm, decreases CO-Hb half-life (to 15-30 min) and provides increased disssolved oxygen to prevent tissue hypoxia/ may be required in some severe cases or cases unresponsive to 100% oxygen
In comatose cases, proven to shorten duration of coma (may also prevent delayed sequelae)
Consider in cases with coma/neuro deficits/pregnancy/acidosis/chest pain/COHb >30%

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