β οΈ Carbon Monoxide (CO) Poisoning
π· 1. What is Carbon Monoxide?
- Colorless, odorless, tasteless gas
- Produced by incomplete combustion of carbon-containing fuels (e.g., gas stoves, car exhausts, fires, generators)
- A major cause of accidental poisoning worldwide
π· 2. Sources of Exposure
Source Type |
Examples |
Household |
Gas heaters, stoves, poorly vented appliances |
Environmental |
Vehicle exhaust in closed garages |
Fire-related |
Smoke inhalation in burns |
Occupational |
Mines, furnaces, industrial plants |
π· 3. Pathophysiology of CO Poisoning
Carbon monoxide is toxic via multiple mechanisms:
π©Έ 1. Carboxyhemoglobin Formation
- CO has ~200β250Γ affinity for Hb vs oxygen
- Forms Carboxyhemoglobin (COHb) β reduces Oβ carrying capacity
β 2. Leftward Shift of Oxy-Hb Curve
- Decreases oxygen unloading at tissues β tissue hypoxia
π§ 3. Direct Cellular Toxicity
- CO binds cytochrome oxidase in mitochondria β impairs oxidative phosphorylation
- CO induces lipid peroxidation, leukocyte activation, and nitric oxide (NO) release, causing vasodilation, hypotension, and CNS damage.
- Causes lactic acidosis, free radical injury
π§ 4. Delayed Neurotoxicity
- Neuroinflammation, demyelination β delayed encephalopathy
π· 4. Clinical Features
β±οΈ Acute Presentation (dose-dependent)
COHb Level |
Symptoms |
<10% |
Often asymptomatic |
10β20% |
Headache, nausea, dizziness |
20β30% |
Confusion, ataxia, dyspnea |
30β40% |
Severe headache, chest pain, vomiting |
>40% |
Seizures, coma, death |
π§ Key Signs
- Cherry red skin/mucosa (rare, late finding)
- Tachycardia, hypotension
- Confusion, seizures, coma
- Metabolic acidosis with raised lactate
π· 5. Diagnosis
π§ͺ Arterial Blood Gas (ABG):
- Normal PaOβ despite hypoxia!, cyanosis absent
- May show metabolic acidosis (β lactate)
π©Έ COHb Level:
- Gold standard
- Detected via CO-oximetry
- Normal: <2% (nonsmokers), <10% (smokers)
- Toxic: >10β15%
π Pulse oximetry is unreliable: It overestimates SpOβ (can’t distinguish oxy-Hb vs COHb)
π· 6. Management
π§― A β Immediate Removal
- Remove from source
- Ensure patient & responder safety
π¨ B β 100% Oxygen Therapy
- High-flow Oβ via non-rebreather mask
- Increases CO elimination (reduces half-life of COHb):
Mode |
COHb Half-Life |
Room air |
4β6 hours |
100% oxygen |
1β1.5 hours |
Hyperbaric oxygen (HBO) |
~20 minutes |
π C β Hyperbaric Oxygen (HBO) Therapy
- Indications:
- COHb >25% (>15% in pregnancy)
- Loss of consciousness
- Severe acidosis (pH <7.1)
- Neurologic deficits, cardiac ischemia
- Benefits:
- Faster CO clearance
- Prevents delayed neurological sequelae
π΄ Why HBOT in Pregnancy?
β’ Fetal hemoglobin has higher affinity for CO, leading to fetal hypoxia.
π· 7. Investigations
Test |
Findings |
ABG |
Metabolic acidosis, β lactate |
COHb (via co-oximetry) |
β levels |
ECG |
ST-T changes, arrhythmias |
Troponins |
May be elevated |
MRI Brain (if encephalopathy) |
Basal ganglia changes (esp. globus pallidus) |
π· 8. Complications
Immediate |
Delayed |
Hypoxia, cardiac arrest |
Delayed neuropsych sequelae (DNS) |
Myocardial ischemia |
Cognitive deficits, memory loss |
Arrhythmias |
Parkinsonism-like syndrome |
Pulmonary edema |
Depression, psychosis |
π· 9. Delayed Neurological Sequelae (DNS)
- Seen in ~15β40% of survivors
- Develops 3β21 days post exposure
- Symptoms: memory loss, mood changes, psychosis, Parkinsonism
- MRI Brain: demyelination, basal ganglia changes
- Prevention: Early HBO therapy
β Avoid Succinylcholine for Intubation
β’ Risk of hyperkalemia in CO-induced muscle damage
β ECG & Cardiac Monitoring
β’ Myocardial ischemia is common (CO-induced hypoxia & vasodilation)
β’ Check troponins in high-risk patients
β Seizure Control
β’ Benzodiazepines for seizures (avoid phenytoin due to CO-induced cardiac effects)
π· 10. Prognosis
- Good with early recognition and treatment
- Poor in delayed diagnosis, prolonged exposure, CNS involvement
π· 11. Prevention
- CO detectors in homes
- Regular maintenance of appliances
- Educate about safe heating/cooking practices
π Summary Mnemonic: βCO-POISONβ
- C β Carboxyhemoglobin formed
- O β Oxygen affinity β, tissue delivery β
- P β Pulse ox unreliable
- O β Oxygen therapy (100% Oβ, HBO)
- I β Investigation = COHb levels
- S β Sequelae (neuro, cardiac)
- O β Occupational/environmental exposure
- N β Neurological signs: headache β coma
MCQs on Carbon Monoxide Poisoning
Q1. What is the most reliable test for diagnosing carbon monoxide poisoning?
A) Pulse oximetry
B) Serum lactate
C) Carboxyhemoglobin level
D) Arterial blood gas
β Answer: C) Carboxyhemoglobin level
Q2. Which of the following is a classic MRI finding in delayed CO poisoning?
A) Diffuse white matter lesions
B) Bilateral globus pallidus lesions
C) Unilateral temporal lobe hyperintensity
D) Pontine hemorrhage
β Answer: B) Bilateral globus pallidus lesions
Q3. Which of the following is the best treatment for severe carbon monoxide poisoning?
A) 100% oxygen via nasal cannula
B) Hyperbaric oxygen therapy
C) High-dose steroids
D) Alkalinization with sodium bicarbonate
β Answer: B) Hyperbaric oxygen therapy