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Toxicology

Carbon Monoxide Poisoning

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CO

Definition:-Carbon monoxide is an asphyxiant gas capable of producing disease and death as a result of its ready capacity to combine with haemoglobin of RBC to form carboxyhemoglobin (COHb) and induce severe hypoxia
Character:- It is colourless, odourless, tasteless & non irritating toxic gas which is slightly lighter than air.

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Properties of CO (Cont.)

Average concentration of CO in air - 0.1 PPM / Atmospheric CO level stabilised by combining with ambient hydroxyl radicals to form CO₂
Sources CO:-

Natural- Atmospheric oxidation of methane, forest fires, terpene oxidation and the ocean- 90%
Human activity- 10% When ever incomplete combustion of organic matters (carbon containing compounds) occur
The automobile greatest source- 115 PPM in heavy traffic, 75 PPM on expressways & 23 PPM in residential areas, under ground garage 100 PPM
Smoking- 5.9% Median level of COHb

CO is the most abundant pollutant found in the lower atmosphere.In the ocean microorganisms produce CO The common name given to the atmospheric gases used in breathing and photosynthesis is air. By volume, dry air contains 78.09%nitrogen, 20.95% oxygen,^[1] 0.93% argon, 0.039% carbon dioxide, and small amounts of other gases. Air also contains a variable amount of water vapor, on average around 1% at sea level, and 0.4% over the entire atmosphere. Although air content and atmospheric pressure vary at different layers, air suitable for the survival of terrestrial plants and terrestrial animals currently is only known to be found in Earth's troposphere (0-12 Km of earth) and artificial atmospheres.

Atmospheric concentrations of carbon monoxide vary widely around the world and throughout the year, ranging from as low as 30 parts per billion up to around 200 parts per billion. Concentrations increased during the 20th century, but there are some signs that concentrations dropped slightly in the 1990s due to widespread use of catalytic convertors, with their lower carbon monoxide emissions, in cars.

Aside from man-made sources, a great deal of carbon monoxide comes from the chemical oxidation of methane and other hydrocarbons in our atmosphere. Additional natural sources include emission from vegetation and the world's oceans. By far the largest sink for carbon monoxide is its reaction with OH in the atmosphere, as noted previously. However, a small but significant amount is also lost from the atmosphere through deposition on the ground.

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Sources (cont.)

Home:- Faulty gas refrigerators, heaters fuelled by gas, coal, oil, or kerosene or petrol powered engines.
Industry:- Charcoal ovens, kilns, blast furnaces, blasting with high explosives, mine explosions, lot of CO gas is produced during fires.

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Etiopathology

One can breathe CO for 8 hrs if its concentration in inspired air does not exceed 0.01% or 100 PPM
0.1% (1000 PPM) will cause 50% Hb saturation
A concentration of 1% or 10000 PPM produces 50% saturation of blood in 15 mts 80% saturation in 23 mts which is fatal.
Factors reducing fatal concentration of gas

Bad health, extremes of age, Respiratory or circulatory deficiency, Anaemia, associated poisoning by depressants drugs like barbiturates, tranquillisers, alcohol etc.

Death may occur at as low as 30% saturation

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Etiopathology

Danger to life from CO as

220 times higher affinity of Hb for CO than O₂
saturation of blood depends on

Atmospheric concentration of CO
Rate of respiratory exchange

Fast respiratory rate due to Physical activity or Children

CO directly toxic by binding with cellular cytochromes
Oxyhaemoglobin dissociation curve shifted to left

Available O₂not released in tissue till tissue O₂ level falls to much lower level

Insidiousness with which high concentration of CO is reached without ringing the physiological alarm of dyspnea
Awareness gradually dulled by hypoxia leading to coma

Tissue most affected by CO are those most sensitive to Oxygen lack like Heart And brain. Lesions are predominently haemorrhagic- subendocardial infarction, cerebral oedema, and increased intracranial tension due to transudation across hypoxic capillaries

Danger to life because CO has 300 times higher affinity of Hb for CO than O₂and hence Hb not available for Oxygen. As both combine with same heme prosthetic groups in the tetrameric hemoglobin molecule.

Factors affecting rate of saturation of blood is Atmospheric concentration of CO and Rate of respiratory exchange

If Fast respiratory rate because of Physical activity or the patient is a child who as such has higher respiratory rate then saturation of Hb will be faster. Because of COHb theOxyhaemoglobin dissociation curve also shifted to left that is Available O₂not released in tissue till tissue O₂ level falls to much lower level

Toxicity of CO is not solely due to its interference with oxygen delivery to tissue. It also has direct toxic effect by binding to cellular cytochromes such as those contained in respiratory enzymes and myoglobin

Insidiousness with which high concentration of CO is reached without ringing the physiological alarm of dyspnea

Consciousness dulled by hypoxia

Available O₂not released in tissue till tissue O₂ level falls to much lower level

Insidiousness with which high concentration of CO is reached without ringing the physiological alarm of dyspnea

Consciousness dulled by hypoxia

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Pathology

Lesions are predominently haemorrhagic- subendocardial infarction, cerebral oedema & Increased intracranial tension
Complete neurological recovery if unconscious ness less that 21 hrs in persons below 48 yrs and 11 hrs in persons older
Complete recovery of mental functions does not take place if unconsciousness exceeds 15 hrs in older gr. Or 64 hrs in younger. Psychiatric abnormality like inappropriate euphoria, impaired judgement, concentration, & abstract thinking may develop late

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Clinical Manifestation

Severity of illness varies directly with the level of Carboxyhemoglobin. Clinical picture is that of oxygen lack Sign & Symptoms in declining order of frequency

Abnormal mental state

Irritability, emotional instability, disturbed judgement, defective memory, confusion, hallucination, coma

Neurologic abnormality

Dimness of vision, ataxia, convulsions, absent reflexes

Others :-Abnormal skin colour, Suffused mucus membrane, Abnormal chest signs, Vomiting, Headache, Skin lesions- Anoxic skin bullae, Excessive sweating, Palpable liver, Localised pain in chest & extremities, Localised oedema, Evidence of bleeding & pseudorecovery, Pulse, temp. and respiratory rate elevated

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Symptoms as per increasing level of COHb

0-10 % No symptoms

11-20% Tightness across forehead, possibly slight headache, dilation of cutaneous blood vessels

21-30% Headache, throbbing in temples

31-40% Severe headache, weakness, dizziness, dim vision, nausea, vomiting,

41-50% Heart rate & respiratory rate increased, May have syncope & collapse.

51-60% Faster Ht. Rate and resp. Mild coma with with Occasional convulsion

61`-70 % Coma, Convulsion, Cheyne-Stokes Resp.

71-80% Weak pulse, slow resp. may die

81% Death

The relationship is semiquantitave for relating exposure to effect. There may be some individual variation. Inhalation of high concentration may result in warning sign of transient weakness & dizziness before consciousness is lost but there may be no warning sign. COHb does not reduce the arterial Po₂ so carotid and aortic chemoreceptors are not activated so respiration rate does not increase but heart increases as there is peripheral vasodilatation due to hypoxia. Lactic acidosis results from tissue anoxia.

Protein, sugar, casts, and erythrocytes in urine

Leucocytosis,

if leucocytosis is associated with increase in neutrophils and decrease in lymphocytes then it is of grave prognosis

Similarly if temperature is elevated above 102⁰ F is of serious prognostic consequences.

Brain & Ht. Have highest O₂requirement because of highest metabolic rate and so their functioning is affected most by hypoxia

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Other findings –Pulse, temp. & resp. rate elevated

Temp. above 102⁰F of grave prognosis

Investigation:-

Urine- protein, sugar, casts & RBC

Leucocytosis- Increase in polymorphs & decrease in lymphocytes & eosinophils- grave prognosis

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Treatment

Remove the Pt. from the contaminated atmosphere
In mild cases where consciousness not lost

Fresh air and absolute rest for 4 hrs- half time 320 mts

Treatment in hospital required

If there is even transient loss of consciousness

Administer 100% Oxygen

Concentration of COHb halved in about 80 mts if ventilated with pure O₂

Therefore 100% O₂ therapy continuously for 2-3 hrs should suffice for control of anoxia

British Medical Research Council recommends 95% O₂ + 5% CO₂for CO poisoning cases

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Where respiration had stopped

Artificial respiration with 100% Oxygen
Rapid recovery from profound coma is reported if O₂therapy given in pressure chamber under 2 atmospheric pressure, half time may be less than 25 mts.
If temperature elevated above 102⁰ F or neurological disorder appears on the first day then induction of hypothermia should be considered
General management of a patient in coma

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Post-Mortem Finding

A cherry red discolouration of skin & mucus membrane specially in the area of hypostasis
Cherry red spots in retina, cherry red colour of blood, tissues and internal organs
Blood fluid, hyperaemia is general and serous effusion are common
Anoxic skin bullae and muscle necrosis common
Heart:- subendocardial infarction
Brain:- cerebral oedema,
Rapidly fatal cases:- Congestion & haemorrhages in all organs
Brochopneumonic consolidation in lungs may be present

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Post-Mortem Finding(Cont.)

Necrobiosis of heart muscle may be present
Pleural & pericardial anoxic haemorrhages are common
Bilateral symmetrical necrosis of the lenticular nuclei(Corpus striatum & Globus pallidus) and punctiform haemorrhages in the white matter of the brain with widespread oedema is seen in death due to CO poisoning

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M-L Aspects

Poisoning mostly accidental

The decrepit, diseased, drugged, drunk
In death due to fires Carboxyhaemoglobin level is usually above 50%
Most victims of closed space fire die from acute CO poisoning rather than from burns.

Exhibitionism & sexual deviation

To attract attention
To heighten sexual pleasure

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M-L Aspects(cont.)

Suicide

Very frequent in western countries
Readily available, Simple to administer, Action not violent, & death is Painless
Tube brought near mouth and whole head covered by coat etc.
Or a tube from exhaust of a car brought inside car and windows are closed
Or sleeping in a closed garage with car engine running

Homicide- Rare but cases reported
Putrefaction does not effect carboxyhaemoglobin which can be detected even after months

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Prolonged Low level Exposure to CO

At 6%-12% COHb

Metabolism shifts from aerobic to anaerobic
May facilitate development of atherosclerosis
Polycythaemia and other compensatory response by body to hypoxia - increased cardiac output and blood flow to critical organs. Old & diseased may not be able to compensate
Also affects behaviour

Performance on tests of vigilance impaired even at 2-5% COHb level (attained in smokers)

Effect on foetus:- Placental barrier crossed readily

Foetus extremely susceptible
Neurological sequelae/ gross damage to brain at high level
Even at low level of smokers CNS development may be affected

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Finger tip Carboxyhaemoglobin saturation monitor (SpCO%).

This is not the same as a pulse oximeter (SpO2%), although some models (such as this one) do measure both the oxygen and carbon monoxide saturation.

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Carbon monoxide detector inside buildings connected to a power outlet