Specific Poisonings

Carbon Monoxide

The commonest sources are smoke inhalation, poorly maintained domestic gas appliances and deliberate inhalation of car exhaust fumes. Causes intense tissue hypoxia by two mechanisms:

1. interrupts electron transport in mitochondria;
2. blocks tissue 02 delivery both by competing with 02 for binding to Hb (Ka CO 220-fold > 02) and altering the shape of the Hb02 dissociation curve (less sigmoidal).

Presentation

• Signs of hypoxia without cyanosis NB 'cherry-red' most obvious post mortem.
• Symptoms & signs correlate with % COHb:
  
  < 30% causes only headache and dizzyness
  50-60% produces syncope, tachypnoea, tachycardia and fits.
  > 60% causes increasing risk of cardiorespiratory failure and death.

Complications

Sites at particular risk are:

• CNS - cerebral, cerebellar or midbrain (Parkinsonism and akinetic-mutism)
• Myocardium - ischaemia/infarction
• Skeletal muscle - rhabdomyolysis/myoglobinuria
• Skin - erythyema to severe blistering.

NB

1. Anaemia, increased metabolic rate (e.g. children) and underlying ischaemic heart disease all increase susceptibility to CO.
2. Neurological recovery depends on the duration of hypoxic coma: complete recovery has been reported in young subjects (under 50) after up to 21 hrs versus 11 hrs in older ones.

Management

• Pa02 may be normal. Metabolic acidosis indicates severe poisoning. Pulse oximetry unhelpful even misleading. Give 02 by mask. If comatose then IPPV with Fi02=1 (t1/2 COHb 320 mins on room air vs 80 mins at 100%)*. Also consider if severely acidotic or evidence of myocardial ischaemia.
• Control fits with IV diazepam.

* Hyperbaric 02 will shorten the washout of COHb further (half-life of 25 mins at 2 atmospheres), but access and transfer times to a hyperbaric chamber makes this often an impractical option. Ventilatory stimulation by adding C02 (4- 7%) to the inspired 02 also reduces washout times (to <15 mins) but worsens the metabolic acidosis.

NB Neuropsychiatric sequelae may take many weeks to evolve.