Write a short note on carbon monoxide poisoning and salicylate poisoning.

Carbon Monoxide Poisoning

Sources: incomplete combustion — charcoal and coal braziers (angithi) used for indoor heating, faulty gas geysers in bathrooms, generator exhaust, house fires, and smoke inhalation. In India, bathroom water-heater deaths and winter brazier deaths are a recurring pattern.

Mechanism:

• CO binds haemoglobin with 240 times the affinity of oxygen, forming carboxyhaemoglobin (COHb), which cannot carry oxygen.
• It shifts the oxygen dissociation curve to the left, impairing oxygen release to tissues — so tissue hypoxia is worse than the reduction in oxygen content alone would suggest.
• It binds cytochrome c oxidase, impairing cellular respiration, and myoglobin, causing myocardial depression.

Clinical features: non-specific and easily misdiagnosed as viral illness or food poisoning.

• Mild: headache (the commonest symptom), nausea, dizziness, fatigue, poor concentration.
• Moderate: confusion, ataxia, visual disturbance, chest pain, dyspnoea, tachycardia.
• Severe: seizures, coma, myocardial ischaemia and arrhythmia, lactic acidosis, rhabdomyolysis, death.
• "Cherry-red" skin is a late, unreliable and usually post-mortem sign — do not rely on it.
• A history of several household members falling ill simultaneously, or symptoms that improve on leaving the house, is the single strongest clue.
• Delayed neuropsychiatric sequelae — appearing days to weeks after apparent recovery, with cognitive impairment, parkinsonism, personality change and memory loss.

Investigations:

• COHb level by co-oximetry on arterial or venous blood (levels correlate poorly with severity but confirm exposure)
• pulse oximetry is falsely normal, since standard oximeters cannot distinguish COHb from oxyhaemoglobin
• arterial blood gas with lactate
• ECG and troponin
• CT or MRI brain in severe cases, which may show bilateral globus pallidus lesions.

Management:

• Remove from the source immediately.
• High-flow 100% oxygen via a non-rebreathing mask — this is the treatment. It reduces the half-life of COHb from around 4–5 hours on room air to about 1 hour, and shorter still on 100% oxygen. Continue until the patient is asymptomatic and COHb has fallen substantially.
• Intubation and ventilation with 100% oxygen for coma or respiratory failure.
• Hyperbaric oxygen is considered for loss of consciousness, neurological deficit, myocardial ischaemia, very high COHb levels, and pregnancy (fetal haemoglobin binds CO avidly and the fetus is at high risk), though evidence for benefit on long-term outcomes remains debated and availability in India is limited.
• Treat acidosis, seizures and myocardial ischaemia; monitor for delayed sequelae with neuropsychological follow-up.
• Prevention is the real answer: ventilation of rooms using braziers, servicing of gas appliances, and never siting a geyser inside a closed bathroom.

Salicylate (aspirin) Poisoning

Mechanism — a uniquely mixed acid-base picture:

• Direct stimulation of the respiratory centre produces respiratory alkalosis (early).
• Uncoupling of oxidative phosphorylation and inhibition of Krebs cycle enzymes produce high anion gap metabolic acidosis with lactate and ketoacid accumulation, plus hyperthermia.
• The classic result in adults is a mixed respiratory alkalosis with metabolic acidosis — a combination that is virtually diagnostic. Children develop metabolic acidosis earlier, without the alkalotic phase.

Clinical features: nausea, vomiting, epigastric pain, tinnitus and deafness (early and characteristic), hyperventilation, sweating, fever, dehydration. Severe poisoning causes agitation, confusion, seizures, coma, non-cardiogenic pulmonary oedema, hypoglycaemia (and low CNS glucose despite a normal blood level), hypokalaemia and renal failure.

Investigations:

• serum salicylate level, repeated — a single level may be misleading, as sustained-release and enteric-coated preparations continue to be absorbed and levels may rise for many hours
• arterial blood gas and serum electrolytes
• blood glucose
• renal function
• coagulation profile
• paracetamol level, since combined preparations and mixed overdoses are common.

Management:

• Resuscitation — airway, breathing, circulation; correct dehydration with intravenous fluids; correct hypokalaemia, which is essential for effective urinary alkalinisation.
• Activated charcoal if presentation is early, and repeated doses for sustained-release preparations.
• Urinary alkalinisation with sodium bicarbonate — the mainstay. Alkalinising the urine traps ionised salicylate in the tubule and markedly increases excretion. Target an alkaline urine pH while monitoring serum potassium and pH closely.
• Haemodialysis — indicated for very high salicylate levels, altered mental status, seizures, pulmonary oedema, renal failure, refractory acidosis or clinical deterioration despite treatment.
• Glucose should be given for altered mental status even when blood glucose is normal, because CNS glucose may be low.
• Correct hyperthermia with cooling; avoid intubation where possible — paralysing a patient removes their compensatory hyperventilation and can cause a catastrophic fall in pH; if intubation is unavoidable, maintain high minute ventilation.