Carbon monoxide and cyanide poisoning

• Carbon monoxide (CO) and hydrogen cyanide are two gases that poison by stopping the body using oxygen: CO by stealing the red cell's oxygen-carrying capacity and cyanide by stopping the cell's mitochondria.
• CO comes mainly from fires and faulty heaters or engines. Cyanide comes mainly from smoke in enclosed fires, and also from some industrial chemicals, plants and drugs. A victim dragged from a fire can have both.
• Neither gives many warning signs. CO is odourless and colourless; cyanide has a faint bitter-almond smell that most people cannot detect. Headache, confusion, dizziness, breathlessness and collapse are common to both.
• A normal pulse oximeter does not exclude CO poisoning, and pulse oximetry is misleading after certain antidotes. The correct tests are co-oximetry (and, for cyanide, clinical assessment plus lactate). ^[4]
• The base of treatment is 100% oxygen for CO and supportive care with the right antidote for cyanide. Hydroxocobalamin is the first-line antidote for confirmed cyanide poisoning. ^[1][6]

By the end of this page you should be able to:

1. List the common sources of carbon monoxide and cyanide poisoning and explain why a fire victim may have both.
2. Explain how CO produces tissue hypoxia: its effect on haemoglobin (affinity, left shift of the oxygen dissociation curve) and its direct cellular toxicity.
3. Explain how cyanide stops cellular respiration at cytochrome oxidase and why this produces lactic acidosis.
4. Recognise the clinical features of each, including the late and unreliable signs, and know which bedside finding is not reliable.
5. Choose and interpret the right investigation: co-oximetry for CO, and clinical signs plus lactate for cyanide.
6. Outline the treatment of each: 100% oxygen and the place of hyperbaric oxygen for CO; hydroxocobalamin, and the sodium nitrite plus sodium thiosulfate sequence, for cyanide, with correct adult doses and cautions.
7. Recognise delayed neurological sequelae after CO poisoning and how follow-up is arranged.

Both conditions are medical emergencies. They share a feature that makes them dangerous: the gas is invisible (CO) or has poor warning properties (cyanide), and the early symptoms are non-specific, so the diagnosis is easily missed unless the exposure is considered.

Carbon monoxide poisoning is one of the commonest serious poisonings worldwide. It occurs as accidental or intentional exposure, and is a leading cause of death from poisoning in many countries. Reported annual exposures are in the tens of thousands in large populations, with a large share of fatal cases being suicides from motor-vehicle exhaust and, increasingly, charcoal burning. Smoke inhalation is also a major source. ^[2]

Cyanide poisoning is rarer as a single-agent event, but it is common in enclosed-space fires, where burning plastics, wool and other nitrogen-containing materials release hydrogen cyanide. Smoke-inhalation victims are therefore often exposed to both CO and cyanide at once. Cyanide also comes from some industrial chemicals (for example, fumigants and metal-plating chemicals), hydrogen cyanide gas, cyanogenic plants, prolonged nitroprusside infusion, and ingestion of cyanogenic compounds such as amygdalin in apricot kernels. ^[4][5]

Older adults, infants, pregnant women, and people with chronic heart, lung or blood disease are more vulnerable to the effects of tissue hypoxia in both poisonings. ^[2]

CO is produced by incomplete combustion of carbon-containing fuel whenever there is not enough oxygen. Common sources include: ^[2]

• House fires and smoke inhalation (often combined with cyanide).
• Faulty domestic heaters, boilers, furnaces and water heaters, especially with poor ventilation.
• Petrol and diesel engines in enclosed spaces: running a car in a garage, indoor use of petrol generators, and exhaust from recreational boats.
• Solid-fuel burning: charcoal grills, barbecues and camp stoves used indoors or in tents, wood-burning or kerosene stoves, and wood pellet stores.
• Recreational exposure: waterpipe (shisha) smoking in enclosed rooms.
• Occupational exposure: mining, steelmaking, pulp and paper, and work with petrol-powered tools such as power washers in garages.

CO has poor warning properties: it is odourless, colourless and non-irritating, so people can be poisoned without realising. ^[2]

• Enclosed-space fires (the commonest cause of significant cyanide exposure in the general population): burning wool, silk, plastics and nitrogen-containing materials release hydrogen cyanide. ^[4]
• Industrial and occupational exposure: electroplating, mining, fumigation, chemical synthesis, and plastics manufacture.
• Chemical agents: hydrogen cyanide (AC) is a chemical warfare agent.
• Plants and food: cassava, lima beans, apricot kernels and other cyanogenic plants (releasing cyanide after ingestion), which matter most in low-resource settings.
• Drugs: prolonged infusion of sodium nitroprusside can release cyanide.

A useful clinical rule: every patient rescued from a serious enclosed-space fire should be treated as possibly poisoned by both CO and cyanide until proven otherwise. ^[1]

The mechanism has two parts: a haematological problem and a direct cellular problem. ^[1]

1. Haemoglobin stealing. CO diffuses rapidly across the alveolar membrane and binds to the iron in haem with an affinity 210 to 300 times that of oxygen. ^[1][3] The binding also changes the haemoglobin molecule so that it holds on to its remaining oxygen more tightly. The result is a leftward shift of the oxygen dissociation curve: less oxygen is picked up in the lungs for a given inspired pressure in the presence of competing CO, and, crucially, less oxygen is released to the tissues. ^[1] The result is tissue hypoxia even when the arterial oxygen pressure looks normal.

2. Direct cellular toxicity. Inside cells, CO binds to other haem-containing proteins such as myoglobin in muscle and myocardium, and to cytochrome oxidase in mitochondria. This impairs cellular respiration directly. CO also activates neutrophils, promotes lymphocyte proliferation, damages mitochondria and causes lipid peroxidation. The resulting oxidative stress, inflammation and cell death resemble a reperfusion injury, particularly in organs with no oxygen reserve: the brain and the heart. ^[1]

Because CO is cleared from the blood faster than from tissue, injury can develop or worsen after the blood level has fallen. ^[1]

Cyanide is a mitochondrial poison. ^[4][5]

Cellular respiration stops. Cyanide binds the ferric iron of cytochrome a3, a component of the cytochrome c oxidase complex (complex IV) in the inner mitochondrial membrane. ^[4][5] This is the final step of the electron transport chain, so oxidative phosphorylation stops. The cell cannot use oxygen and is forced into anaerobic metabolism. ^[4][5]

Lactic acidosis develops. Anaerobic metabolism produces lactate, which accumulates and causes a severe high-anion-gap metabolic acidosis. ^[4][5] A plasma lactate concentration of 8 mmol/L or more is listed among the common signs of isolated cyanide poisoning. ^[4][5] In smoke-inhalation victims, CO also contributes to lactate, so a lactate of 10 mmol/L or more is taken as indicative of cyanide poisoning in that setting. ^[4][5]

Energy failure produces the clinical picture. Without ATP, organs with high oxygen demand fail first: the brain (confusion, seizures, coma) and the heart (tachypnoea early, then bradypnoea and apnoea, arrhythmias, vascular collapse). Cyanide is also a cellular asphyxiant: venous blood is unusually bright red because tissues have not extracted its oxygen, although this is not a reliable sign. ^[4][5]

Symptoms are non-specific and depend on the concentration and duration of exposure. They can resemble influenza. ^[1][2]

Mild to moderate: headache (often described as a "tight band"), dizziness, weakness, nausea and vomiting, chest pain or palpitations, breathlessness, irritability and difficulty concentrating. ^[2]

Severe: malaise, severe headache, visual disturbance, ataxia, confusion, altered mental status, memory and cognitive disturbance, syncope, seizures, coma and death; tachycardia, tachypnoea, hypotension; arrhythmias; myocardial ischaemia or infarction; metabolic acidosis; non-cardiogenic pulmonary oedema. ^[2]

Cherry-red skin is described as a sign of severe poisoning, but it is a late and unreliable finding. It is absent in most patients and should not be waited for. ^[1]

Cardiac involvement is important. In moderate to severe poisoning, a large share of patients show elevated cardiac biomarkers or electrocardiographic changes, and cardiac involvement predicts long-term mortality. ^[1] In severe poisoning it is worth performing an ECG and measuring cardiac troponins. ^[1]

Severity does not track the blood level well. The initial carboxyhaemoglobin concentration correlates poorly with how ill the patient is, so clinical picture and exposure history matter most. ^[1][3]

Delayed neurological sequelae (DNS) are a particular worry. New symptoms can appear days to weeks after an initially good recovery: personality change, mood disorder, memory loss, difficulty concentrating, sleep disturbance, executive dysfunction, Parkinsonism, ataxia, dementia, and other disabling hypoxic brain-injury signs. ^[1][3] A longer exposure (more than 24 hours) and age over 36 are recognised risk factors for developing neuronal late sequelae. ^[1] Because damage can appear after a symptom-free interval, all discharged patients should be warned and followed up. ^[2]

Onset is rapid, within minutes of exposure, and the course is short. ^[4]

Symptoms: headache, confusion, dyspnoea, chest tightness, nausea. Signs: altered mental status (confusion, disorientation), seizures or coma, dilated pupils, tachypnoea progressing to hyperpnoea and then bradypnoea or apnoea, hypertension early then hypotension, cardiovascular collapse, vomiting, and plasma lactate of 8 mmol/L or more. ^[4][5]

Smoke inhalation makes diagnosis harder. Many smoke-inhalation victims have burns and trauma as well, and confusion may be due to CO or cyanide. Not all smoke-inhalation victims have cyanide poisoning. Useful clues are an enclosed-space fire, soot around the mouth, nose and throat, altered mental status, and a lactate of 10 mmol/L or more. Hypotension is highly suggestive but present in only a small proportion of cases. ^[4]

Important caution with sodium nitrite. In patients with smoke inhalation and concurrent CO, care is needed with antidotes that form methaemoglobin, because they can worsen tissue oxygen delivery. ^[5]

Measure carboxyhaemoglobin with a CO-oximeter. This is the key confirmatory test. The CO-oximeter uses multiple wavelengths and can be used on venous or arterial blood. ^[2] It reports the percentage of haemoglobin saturated with CO.

Carboxyhaemoglobin levels (approximate guides, not strict rules): ^[2]

• Non-smokers: a level above 2% supports poisoning. ^[2]
• Smokers: a level above 9% supports poisoning. ^[2]
• Severity: levels do not track severity well, so treat the patient, not the number. ^[1][3]

Do not trust a conventional (two-wavelength) pulse oximeter. It cannot tell oxyhaemoglobin from carboxyhaemoglobin and will look normal (or near-normal) in a seriously poisoned patient. ^[2] Multi-wavelength (pulse) CO-oximeters exist and can be useful, but their precision is limited, and they are not a substitute for blood testing. ^[1]

Supporting tests: ECG and cardiac troponin in moderate or severe cases, because cardiac injury is common; arterial blood gas for acid-base status; chest X-ray for pulmonary oedema; pregnancy testing in women of childbearing age. ^[2] CT head or MRI is recommended after loss of consciousness or cardiopulmonary signs. ^[2]

Remember the timing problem: once the patient has been breathing room air for some hours, the carboxyhaemoglobin falls naturally and becomes less useful. ^[2]

There is no widely available, rapid confirmatory test, so diagnosis is clinical. ^[4][5]

Lactate is the most useful laboratory clue: 8 mmol/L or more in isolated poisoning, and 10 mmol/L or more in a smoke-inhalation victim (because CO contributes to the lactate). ^[4][5] Do not delay treatment to get a result if suspicion is high. ^[4]

Blood cyanide levels can be measured in specialised laboratories and are useful for documentation, but results come too slowly to guide initial treatment. ^[4] A pretreatment sample may be useful before the antidote is given, because sampling after hydroxocobalamin is inaccurate. ^[4]

Pseudo-acidosis and other causes of lactate elevation (shock, seizures, exercise, other toxins) should be considered before attributing a high lactate to cyanide alone.

There is no single diagnostic cut-off. A diagnosis is made from a suggestive history and physical findings plus a raised carboxyhaemoglobin in a symptomatic patient. Other conditions can mimic or coexist: smoke inhalation lung injury, trauma, hypothermia, stroke, infection, or intoxication with other agents. ^[2]

Hyperbaric oxygen considerations. No single indication is accepted everywhere. One consensus approach selects patients with any of: impaired consciousness or coma; cardiac ischaemia; neurological deficits; metabolic acidosis; pregnancy; or a carboxyhaemoglobin above 25% (some guidance uses a 25 to 30% range). ^[1][2] An American systematic review concluded that randomised trials do not establish whether hyperbaric oxygen reduces adverse neurological outcomes, so hyperbaric oxygen cannot be routinely recommended on current trial evidence; it may still be justified in selected, more severely poisoned patients. ^[3]

There is no formal scoring system. Treatment is started on strong clinical suspicion in a compatible setting, because the condition kills within minutes. ^[4][5]

1. Remove from the source and keep yourself safe (rescuers need breathing apparatus in enclosed fires).
2. 100% oxygen as early as possible. This is the most important treatment. Give by tight-fitting mask with a reservoir at 15 L/min, by CPAP mask in alert patients, or by mechanical ventilation if needed. ^[1][2]
3. Continue until symptoms resolve or poisoning is no longer detectable (carboxyhaemoglobin under 3%). ^[1]
4. Standard emergency care: airway, breathing, circulation, intravenous fluids, monitoring, ECG and troponin, and treatment of seizures.
5. Assess for combined cyanide poisoning in anyone pulled from a fire. ^[1]

Elimination kinetics. The half-life of carboxyhaemoglobin is about 320 minutes in room air, about 74 minutes on 100% normobaric oxygen, and about 20 minutes at 2.5 bar hyperbaric oxygen. Five half-lives using 100% oxygen removes most of the CO, which is why oxygen must be given for several hours. ^[1][3]

Hyperbaric oxygen (100% oxygen at 2 to 3 atmospheres) clears CO faster and, in animal studies, may limit inflammation and lipid peroxidation. In humans, however, randomised trials have produced conflicting results and high risk of bias has been present in all of them; a pooled analysis does not show a statistically significant reduction in neurological sequelae, and current reviews cannot routinely recommend hyperbaric oxygen on trial evidence alone. ^[3] The position of several emergency and toxicology groups is to consider hyperbaric oxygen for selected high-risk patients: ^[1][2]

• neurological deficits;
• cardiac ischaemia or myocardial injury;
• loss of consciousness or coma;
• metabolic acidosis;
• pregnancy;
• a very high or rising carboxyhaemoglobin;
• age over 36 or exposure longer than 24 hours as additional risk factors for delayed sequelae. ^[1]

Timing matters. If hyperbaric oxygen is used, it should be started within six hours of exposure, and never after 24 hours. ^[1] Pregnant women are a special case: saturation and elimination are slower on the fetal side, fetal carboxyhaemoglobin can be far higher than the mother's, and maternal 100% oxygen alone may not protect the fetus. Hyperbaric oxygen is therefore usually considered even at lower carboxyhaemoglobin levels in pregnancy. ^[1][2]

Warn every patient about delayed neurological problems and tell them what to do if these appear (memory or concentration problems, clumsiness, behaviour change, Parkinsonism). Arrange a follow-up medical and neurological examination in about two weeks. ^[2] In one guidance set, a cognitive examination at four to six weeks is advised. ^[1]

1. Remove from the source with appropriate protection.
2. Support airway, breathing and circulation without delay: high-flow oxygen, ventilation, and fluids and vasopressors if needed. ^[4][5] Cyanide poisoning is treated with oxygen and antidotes, but ventilation and haemodynamic support come first.
3. Administer an antidote when suspicion is high.
4. Check for the cyanide plus carbon monoxide combination in every fire victim and treat both. ^[1]
5. Monitor blood pressure during antidote infusion and for 24 to 48 hours after treatment. ^[5]
6. Decontaminate if the exposure was dermal or by ingestion (remove contaminated clothing, wash skin, gastric lavage as appropriate). ^[4]

Hydroxocobalamin (vitamin B12a) is the first-line antidote for confirmed cyanide poisoning and the most commonly used antidote by current practice. ^[6][4] It binds each cyanide ion by replacing its hydroxo ligand, forming non-toxic cyanocobalamin, which is excreted in the urine. ^[4]

Adult dose: 5 g given intravenously over 15 minutes. ^[4] If response is inadequate, a second 5 g (total 10 g) may be given; the second dose may be given faster (15 minutes in a patient in extremis) or over up to 2 hours depending on condition. ^[4] A vial is reconstituted to 200 mL with 0.9% sodium chloride (5% glucose or lactated Ringer is compatible if saline is not available). ^[4]

Advantages: rapid onset and a safety profile that is better than sodium nitrite in the setting of smoke inhalation, because sodium nitrite can worsen hypoxia. ^[6][4]

Cautions and side effects: transient blood pressure rise, anaphylaxis, acute renal injury (usually reversible, but monitor renal function for 7 days), red-brown skin colour lasting up to 2 weeks, red urine lasting up to 5 weeks, and an acneiform rash 7 to 28 days later. At high doses it interferes with many colour-based blood tests (creatinine, bilirubin, ALT and others) and with pulse oximetry for up to a day or more, so record results before treatment. ^[4] Hydroxocobalamin is physically and chemically incompatible with sodium thiosulfate, sodium nitrite, ascorbic acid and blood products: do not run them through the same intravenous line. ^{[4] [6]}

Use in pregnancy is lifesaving for mother and fetus; cyanide readily crosses the placenta, and treatment should not be withheld. ^{[4] [2]}

Although hydroxocobalamin is first-line for confirmed poisoning, its routine use in a smoke-inhalation victim without confirmed cyanide poisoning is controversial. Current evidence is largely retrospective and low-quality, with no randomised controlled trials, and two recent systematic reviews report similar mortality with or without it, along with a possible association with acute kidney injury (probably reflecting how ill the patients were rather than direct drug toxicity). ^[6] European expert consensus does recommend it for suspected cyanide poisoning in smoke-inhalation victims, and United States paramedicine practice varies. ^[6] Because blood cyanide testing is slow, the decision must rest on risk, clinical picture, and institutional or poison-centre guidance. ^[4][6]

Used either as an alternative to hydroxocobalamin or in combination with it in some regimens, and still specified in many emergency kits. ^[5]

Mechanisms. Sodium nitrite oxidises haemoglobin to methaemoglobin, which has a higher affinity for cyanide than cytochrome oxidase does; cyanide moves from the mitochondrion to methaemoglobin, forming cyanomethaemoglobin, and cellular respiration resumes. Sodium thiosulfate is a sulphur donor that is converted by the enzyme rhodanese into thiocyanate, which is relatively harmless and is excreted in urine. ^[5]

Adult dose: sodium nitrite 300 mg (10 mL of 3% solution) intravenously at 2.5 to 5 mL per minute, followed immediately by sodium thiosulfate 12.5 g (50 mL of 25% solution) intravenously; then flush the line. ^[5] A second course at half dose is given if signs of poisoning return. ^[5] Paediatric doses are weight (or surface-area) based, and anemia reduces the sodium nitrite dose proportionally. ^[5]

Cautions. Sodium nitrite can cause life-threatening hypotension and methaemoglobinaemia and should be used with caution in patients with smoke inhalation (because it can worsen hypoxia), anemia, or cardiac or respiratory compromise. ^[5] Methaemoglobin levels should be kept below 30%; levels up to 58% have been reported after two 300-mg doses. ^[5] Do not give blood products or hydroxocobalamin through the same line. ^[5][4] Patients are monitored for 24 to 48 hours. ^[5]

• Delayed neurological sequelae (see above), which may start days to weeks later and can include dementia, Parkinsonism and focal deficits. ^[1][3]
• Cardiac events: elevated troponin, arrhythmia, myocardial infarction, and increased long-term cardiovascular risk. ^[1]
• Anoxic brain injury in severe cases.
• Pulmonary (non-cardiogenic oedema) and renal injury.

• Severe anoxic brain injury.
• Death within minutes without treatment.
• Complications of antidotes: methaemoglobinaemia and hypotension with sodium nitrite; renal impairment and assay interference with hydroxocobalamin. ^[4][5]

Prognosis depends on how long and how heavily the patient was exposed, how quickly oxygen or an antidote is given, and whether there is cardiac or neurological injury.

Carbon monoxide. Outcome correlates poorly with the initial carboxyhaemoglobin level. ^[1][3] In pooled trials, about 29% (hyperbaric oxygen) to 34% (normobaric oxygen) of patients still had symptoms or signs at 4 to 6 weeks. ^[3] A substantial minority with moderate or severe poisoning show cardiac involvement, which predicts higher long-term mortality. ^[1] Long-term cohort studies describe raised risks of dementia, diabetes and cardiovascular events, and higher long-term mortality, after CO poisoning. ^[1] A retrospective analysis suggested that hyperbaric oxygen reduced acute and one-year fatality, but this is not randomised evidence. ^[1]

Cyanide. With prompt treatment, many patients recover fully. In patients who present in cardiac arrest, only a small proportion survive. ^[4] Survivors of severe poisoning can be left with memory, cognitive or cerebellar deficits. ^[4]

• Carbon monoxide detectors in homes (with battery or hard-wired alarms), checked regularly, and replacement before expiry. ^[2]
• Never run engines or generators indoors, including in garages or near open windows or air conditioners. ^[2]
• Vent fuel-burning appliances properly and have them inspected.
• Keep grills, barbecues and camp stoves out of the home and tent.
• Water safety: prevent fumes entering boat cabins and vehicle tailgate areas.
• Occupational ventilation and monitoring in high-risk workplaces.
• Safe food preparation: soak and cook cassava and other cyanogenic foods properly; limit bitter-apricot-kernel ingestion. ^[4]

There is no general screening programme for CO poisoning outside specific outbreak or disaster settings.

Cyanide crosses the placenta and carbon monoxide can produce fetal carboxyhaemoglobin levels above the mother's, so both are emergencies for mother and fetus. ^[1][4] Treatment must not be withheld because of pregnancy. For CO, 100% oxygen should be given aggressively and hyperbaric oxygen is usually considered even at lower maternal carboxyhaemoglobin levels. ^[1][2] For cyanide, hydroxocobalamin is appropriate in pregnancy. ^[4]

Children are more vulnerable to tissue hypoxia at lower carboxyhaemoglobin levels. ^[1] Evidence for hyperbaric oxygen in children is limited and retrospective. For cyanide, no paediatric dose of hydroxocobalamin is established, although 70 mg/kg has been used in non-United States practice. ^[4] Sodium nitrite can be dangerous in young infants. ^[5]

Age over 36 raises the risk of delayed neurological sequelae after CO poisoning, and older adults are more likely to have cardiac comorbidity. ^[1]

The central clinical scenario is the smoke-inhalation victim. Give oxygen for both, support the airway and circulation, and administer hydroxocobalamin when cyanide is suspected, while not overlooking the CO poisoning. ^[1][6]

• Oxygen is the antidote for CO. If hyperbaric facilities are unavailable, aggressive normobaric 100% oxygen given for long enough (hours, guided by carboxyhaemoglobin or symptoms) still helps. ^[1][2]
• A CO-oximeter is the key piece of laboratory equipment for diagnosis. Where it is absent, treat on clinical suspicion and exposure history. ^[2]
• A pulse oximeter cannot exclude CO poisoning. ^[2]
• Cyanide antidotes may be unavailable. Hydroxocobalamin is costly. Sodium nitrite and sodium thiosulfate (or even amyl nitrite) are the fallbacks in many kits. Supportive care (oxygen, ventilation, fluids) remains the backbone. ^[5]
• Cassava and cyanogenic plant poisoning is a treatment problem in some regions: decontamination, supportive care, and cheap antidotes where available.
• Poison centres can guide dosing and antidote selection when both gases are suspected in a single victim.

• Carbon monoxide and cyanide both stop cells using oxygen, but in different ways: CO impairs delivery and release, cyanide stops mitochondrial respiration.
• CO is produced by incomplete combustion; common sources are fires, faulty heaters and engines, and charcoal or generators used indoors. ^[2]
• Cyanide most often comes from enclosed-space fires, and a fire victim may have both. ^[1][6]
• CO binds haemoglobin 210 to 300 times more tightly than oxygen and shifts the oxygen dissociation curve to the left; it also damages mitochondria and promotes inflammation and cell death. ^[1][3]
• Cyanide binds cytochrome a3, stopping aerobic metabolism and producing lactic acidosis; lactate is usually 8 mmol/L or more in isolated poisoning and 10 mmol/L or more in smoke inhalation. ^[4][5]
• CO symptoms are non-specific (headache, dizziness, confusion, chest pain, nausea); cherry-red skin is a late, unreliable sign. ^[1][2]
• Cyanide acts within minutes (headache, confusion, seizures, coma, tachypnoea then apnoea, collapse). ^[4]
• A normal conventional pulse oximeter does not exclude CO poisoning; use co-oximetry. ^[2]
• CO is cleared about five-fold faster on 100% oxygen (half-life about 74 minutes) than in air (about 320 minutes); hyperbaric oxygen reduces it to about 20 minutes. ^[1][3]
• Give 100% oxygen for CO poisoning until symptoms resolve or carboxyhaemoglobin falls below 3%. ^[1]
• Hyperbaric oxygen is considered for selected high-risk patients (neurological deficits, cardiac injury, loss of consciousness, acidosis, pregnancy, very high carboxyhaemoglobin) but randomised trial evidence does not establish clear benefit; if used, start within 6 hours. ^[1][2][3]
• Hydroxocobalamin is the first-line antidote for confirmed cyanide poisoning: 5 g intravenously over 15 minutes in adults, with a possible further 5 g. ^[4][6]
• Sodium nitrite plus sodium thiosulfate is the older regimen: sodium nitrite 300 mg (10 mL) over 2.5 to 5 mL per minute then sodium thiosulfate 12.5 g (50 mL), with cautions in smoke inhalation and anemia. ^[5]
• Delayed neurological sequelae after CO poisoning should be anticipated, warned about and followed up. ^[1][2][3]
• Hydroxocobalamin is first-line for confirmed cyanide poisoning but its routine empiric use in unproven smoke inhalation is contested. ^[6]

Emergency medicine: smoke inhalation, burns, coma, seizures, metabolic acidosis. Respiratory: hypoxaemic respiratory failure, acute respiratory distress syndrome. Cardiology: arrhythmia, myocardial infarction. Critical care: shock, vasopressors. Neurology: delayed encephalopathy, dementia.