2. INTRODUCTION
• CO is produced by incomplete combustion of
carbonaceous material
• It is a colorless, tasteless, non-irritative and odorless
gas and lighter than air
• Sources- tobacco smoke, house fires, automobile
exhaust, coal gas, industrial processes, etc.
3. ACTION
• CO has got 250 times more affinity for Hb and combines
reversibly with hemoglobin to form carboxyhemoglobin
(COHb).
• It inhibits the electron transport by blocking cytochrome
A3 oxidase and cytochrome P450 and hence intracellular
respiration
• CO affinity to myoglobin is about 40 times greater than
oxygen, which may cause direct myocardial depression.
4. SIGNS AND SYMPTOMS
COHb(%) SIGNS AND SYMPTOMS
0-10 No symptoms
10-20 Breathlessness, mild headache
20-30 Throbbing headache, irritability, emotional instability
30-40 Severe headache, nausea, vomiting, dizziness
40-50 Increasing confusion, hallucination, rapid respiration
50-70 Weak thready pulse, hypotension , irregular respiration, convulsions
>80 Rapid death from respiratory arrest
5. Fatal dose and period
COHb(%) Severity of poisoning
10-30 Mild
30-40 Moderate-severe
>40 Very severe
Severity of CO poisoning
CO concentration (%) Fatality (hours)
0.2 4
0.4 1
10 ½
6. CHRONIC POISONING
• Patients present with bizarre behavioral abnormalities,
declining intellect, memory disturbances, chronic cough
or diarrhea.
• It is often misdiagnosed as chronic fatigue syndrome,
viral, bacterial, pulmonary, gastrointestinal infection or
immune deficiency.
7. Delayed neuropsychological sequelae in CO poisoning
Neurological sequelae Cognitive and psychological sequelae
Gait and motor disturbances Cognitive impairment
Bradykinesia Concentration deficit
Intention tremor Memory loss
Postural instability Personality changes
Cortical blindness Insomnia
Hearing loss, tinnitus, vertigo Anxiety
Recurrent headache Depression
Fecal/urinary incontinence Extreme emotional lability
Dysphasia , dyspraxia Psychosis
8. DIAGNOSIS
• Carboxyhemoglobin level – normally it is 0 to 5 %
• Pulse oximetry
• ECG: ST depression or elevation, T-wave flattening or
inversion
• Chest radiograph- perihilar haze, intra-alveolar oedema
9. DIFFERENTIAL DIAGNOSIS
• Alcoholic intoxication
• Diabetic/Insulin coma
• Cerebral hemorrhage
• Head injury
• Uremia
• Barbiturates/Narcotic poisoning
10. TREATMENT
• Remove the victim from source of exposure
• Maintain patent airway, fresh air and orthobaric oxygen by tight-
fitting high-flow reservoir face mask or endotracheal tube
• Blood transfusion, if required
• Gastric lavage
• Mannitol 500ml IV as 20% solution over 15 min, followed by
500 ml of 5% dextrose over next 4hr.
• IV fluids, inotropic agents
• Antibiotics and symptomatic treatment.
11. POSTMORTEM FINDINGS
EXTERNAL
• Cherry red coloration of skin, mucous membranes, PM
staining, blood, tissues and internal organs.
• Fine froth at the nostrils/mouth
• Blisters of skin over dependent areas or bony pressure
points
12. POSTMORTEM FINDINGS
INTERNAL
• Lung: edema and congestion
• Heart : petechial hemorrhages, myocardial necrosis
• Rhabdomyolysis
• CNS: Neuronal hypoxic injury, Punctiform hemorrhages
and softening of cerebral cortex and corpus striatum
13. MEDICO-LEGAL ASPECTS
• Common mode of committing suicide
• Accidental poisoning
• Masochistic sexual asphyxia
• Homicide - rare
14. REFERENCES
Biswas G. Asphyxiants , In: Review of Forensic Medicine and
Toxicology, 4th edition, Jaypee Brothers Medical Publishers (P)
Ltd, 2019.p.595-597.
Reddy N. Asphyxiants ,In: The Essentials of Forensic Medicine
& Toxicology, 34th edition, Jaypee Brothers Medical Publishers
(P) Ltd,2017.p.576-579.
Rao N G. Asphyxiants ,In: Textbook of forensic medicine &
toxicology, 2nd edition, Jaypee Brothers Medical Publishers (P)
Ltd, 2010.p.545-547.
