Difference between revisions of "Carbon Monoxide Poisoning"
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==Introduction== | ==Introduction== | ||
Carbon monoxide (CO) is a '''colourless, odourless, poisonous gas''' weighing lighter than air, which is the result of the incomplete combustion of hydrocarbon fuels. It is produced in '''fires, from generators and from car exhaust systems'''. | Carbon monoxide (CO) is a '''colourless, odourless, poisonous gas''' weighing lighter than air, which is the result of the incomplete combustion of hydrocarbon fuels. It is produced in '''fires, from generators and from car exhaust systems'''. | ||
| − | When inhaled in high enough concentrations, CO leads to a '''fatal hypoxia'''. Cases in veterinary medicine usually follow '''house fires''' or are secondary to generator system | + | When inhaled in high enough concentrations, CO leads to a '''fatal hypoxia'''. |
| + | |||
| + | Cases in veterinary medicine usually follow '''house fires''' or are secondary to generator system disfunction. | ||
==Pathophysiology== | ==Pathophysiology== | ||
| − | Carbon monoxide has an affinity for haemoglobin that is '''240 times higher than that of oxygen''' and is readily absorbed across the alveolar membrane. When CO binds with haemoglobin it forms '''carboxyhaemoglobin''', which inhibits haemoglobin's ability to bind oxygen. It also causes the '''oxygen dissociation curve to shift to the left''', impairing oxygen release at tissue level. This results in hypoxia in the tissues of the body, most notably organs with a high oxygen demand such as the '''heart and brain'''. | + | Carbon monoxide has an affinity for haemoglobin that is '''240 times higher than that of oxygen''' and is readily absorbed across the alveolar membrane. |
| + | |||
| + | When CO binds with haemoglobin it forms '''carboxyhaemoglobin''', which inhibits haemoglobin's ability to bind oxygen. | ||
| + | |||
| + | It also causes the '''oxygen dissociation curve to shift to the left''', impairing oxygen release at tissue level. | ||
| + | |||
| + | This results in hypoxia in the tissues of the body, most notably organs with a high oxygen demand such as the '''heart and brain'''. | ||
'''Direct cytotoxicity''' occurs due to inactivation of intracellular respiratory enzymes by CO as it is delivered to the tissues. | '''Direct cytotoxicity''' occurs due to inactivation of intracellular respiratory enzymes by CO as it is delivered to the tissues. | ||
==Clinical Signs== | ==Clinical Signs== | ||
| − | The symptoms of CO poisoning depend on the percentage of carboxyhaemoglobin in the body | + | The symptoms of CO poisoning depend on the percentage of carboxyhaemoglobin in the body. |
| − | At '''10-20% carboxyhaemoglobin''' levels, clinical signs of '''mild dyspnoea, shortness of breath and confusion appear'''. The animal | + | Similar signs occur in most animals, and parallel the signs shown in humans. |
| + | |||
| + | At '''10-20% carboxyhaemoglobin''' levels, clinical signs of '''mild dyspnoea, shortness of breath and confusion appear'''. The animal become disorientated and loses the will and the capability to escape as levels of CO increase. | ||
'''Higher levels''' lead to irritability, '''nausea, vomiting, lack of coordination and convulsions'''. '''Blindness and deafness''' have also been reported. | '''Higher levels''' lead to irritability, '''nausea, vomiting, lack of coordination and convulsions'''. '''Blindness and deafness''' have also been reported. | ||
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'''Respiratory failure and death''' may occur at levels greater than 50-60%. | '''Respiratory failure and death''' may occur at levels greater than 50-60%. | ||
| − | Death | + | Death may also occur quickly if there are sudden high levels of CO, due to cardiac arrest. |
There is a '''bright cherry red or bright pink colouring to the mucous membranes''' and skin. | There is a '''bright cherry red or bright pink colouring to the mucous membranes''' and skin. | ||
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A '''blood carboxyhaemoglobin level''' should be obtained. Sampling should be done as soon as possible and it should be carried on ice to the laboratory. If the animal is breathing fresh air, carboxyhaemoglobin levels will return to normal within 3-4 hours. | A '''blood carboxyhaemoglobin level''' should be obtained. Sampling should be done as soon as possible and it should be carried on ice to the laboratory. If the animal is breathing fresh air, carboxyhaemoglobin levels will return to normal within 3-4 hours. | ||
| − | '''Haemoglobin saturation analysis''' will be impaired due to the presence of carboxyhaemoglobin displacing the oxygen. | + | '''Haemoglobin saturation analysis''' will be impaired due to the presence of carboxyhaemoglobin displacing the oxygen. Pulse oximetry will overestimate the amount of saturated haemoglobin, as the machine cannot differentiate between carboxyhaemoglobin and oxyhaemoglobin. |
| − | '''Arterial blood gas''' will measure the amount of dissolved oxygen in the blood ( | + | '''Arterial blood gas''' will measure the amount of dissolved oxygen in the blood (PaO2), but not the amount of usable oxygen as oxyhaemoglobin. |
| − | Smoke inhalation may have led to concurrent lung injury, and | + | Smoke inhalation may have led to concurrent lung injury, and PaO2 levels are therefore an important factor to evaluate. |
| − | '''Post-mortem findings''' include: dilated bronchi and distension of the major blood vessels. The ventricles of the heart may be dilated. The cherry red colour of the blood may or may not be present. Brain changes include: necrosis in the cortex and white matter of the cerebral hemispheres, globus pallidus and brainstem. | + | '''Post-mortem findings''' include: dilated bronchi and distension of the major blood vessels. The ventricles of the heart may be dilated. The cherry red colour of the blood may or may not be present. Brain changes include: necrosis in the cortex and white matter of the cerebral hemispheres, globus pallidus and brainstem. Oedema, demyelination and haemorrhage in the brain can also occur |
==Treatment== | ==Treatment== | ||
| − | '''Oxygen supplementation''' is the mainstay of therapy for CO poisoning. Carbon monoxide half-life is reduced to 30 minutes if '''100% FI oxygen''' is administered. Initial 100% | + | '''Oxygen supplementation''' is the mainstay of therapy for CO poisoning. Carbon monoxide half-life is reduced to 30 minutes if '''100% FI oxygen''' is administered. Initial 100% O2 therapy is recommended, but it should not be continued for more than 18 hours due to the risk of O2 toxicity. |
| − | Other '''supportive measures''' include: | + | Other '''supportive measures''' include: fluid therapy, monitoring of respiratory rate and effort (to monitor for secondary lung injury), evaluation of mentation and neurological signs. |
Patients with burns and other wounds should be treated accordingly. | Patients with burns and other wounds should be treated accordingly. | ||
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Merck, M. (2007) '''Veterinary forensics: animal cruelty investigations''' ''John Wiley and Sons'' | Merck, M. (2007) '''Veterinary forensics: animal cruelty investigations''' ''John Wiley and Sons'' | ||
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| − | + | [[Category:To Do - Review]] | |
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Revision as of 09:04, 22 August 2011
Introduction
Carbon monoxide (CO) is a colourless, odourless, poisonous gas weighing lighter than air, which is the result of the incomplete combustion of hydrocarbon fuels. It is produced in fires, from generators and from car exhaust systems.
When inhaled in high enough concentrations, CO leads to a fatal hypoxia.
Cases in veterinary medicine usually follow house fires or are secondary to generator system disfunction.
Pathophysiology
Carbon monoxide has an affinity for haemoglobin that is 240 times higher than that of oxygen and is readily absorbed across the alveolar membrane.
When CO binds with haemoglobin it forms carboxyhaemoglobin, which inhibits haemoglobin's ability to bind oxygen.
It also causes the oxygen dissociation curve to shift to the left, impairing oxygen release at tissue level.
This results in hypoxia in the tissues of the body, most notably organs with a high oxygen demand such as the heart and brain.
Direct cytotoxicity occurs due to inactivation of intracellular respiratory enzymes by CO as it is delivered to the tissues.
Clinical Signs
The symptoms of CO poisoning depend on the percentage of carboxyhaemoglobin in the body.
Similar signs occur in most animals, and parallel the signs shown in humans.
At 10-20% carboxyhaemoglobin levels, clinical signs of mild dyspnoea, shortness of breath and confusion appear. The animal become disorientated and loses the will and the capability to escape as levels of CO increase.
Higher levels lead to irritability, nausea, vomiting, lack of coordination and convulsions. Blindness and deafness have also been reported.
Respiratory failure and death may occur at levels greater than 50-60%.
Death may also occur quickly if there are sudden high levels of CO, due to cardiac arrest.
There is a bright cherry red or bright pink colouring to the mucous membranes and skin.
Diagnosis
Pets may smell of smoke and have concurrent signs of smoke or fire injury.
Haematology, biochemistry and urinalysis should be performed to monitor for organ damage and rule out other causes of neurological signs.
A blood carboxyhaemoglobin level should be obtained. Sampling should be done as soon as possible and it should be carried on ice to the laboratory. If the animal is breathing fresh air, carboxyhaemoglobin levels will return to normal within 3-4 hours.
Haemoglobin saturation analysis will be impaired due to the presence of carboxyhaemoglobin displacing the oxygen. Pulse oximetry will overestimate the amount of saturated haemoglobin, as the machine cannot differentiate between carboxyhaemoglobin and oxyhaemoglobin.
Arterial blood gas will measure the amount of dissolved oxygen in the blood (PaO2), but not the amount of usable oxygen as oxyhaemoglobin.
Smoke inhalation may have led to concurrent lung injury, and PaO2 levels are therefore an important factor to evaluate.
Post-mortem findings include: dilated bronchi and distension of the major blood vessels. The ventricles of the heart may be dilated. The cherry red colour of the blood may or may not be present. Brain changes include: necrosis in the cortex and white matter of the cerebral hemispheres, globus pallidus and brainstem. Oedema, demyelination and haemorrhage in the brain can also occur
Treatment
Oxygen supplementation is the mainstay of therapy for CO poisoning. Carbon monoxide half-life is reduced to 30 minutes if 100% FI oxygen is administered. Initial 100% O2 therapy is recommended, but it should not be continued for more than 18 hours due to the risk of O2 toxicity.
Other supportive measures include: fluid therapy, monitoring of respiratory rate and effort (to monitor for secondary lung injury), evaluation of mentation and neurological signs.
Patients with burns and other wounds should be treated accordingly.
Heat injuries to the airways can promote upper airway swelling and obstruction, and corticosteroids may be useful in those cases.
Prognosis
CO levels in the blood provide prognostic indicators.
Levels around 20-25% hold a good prognosis and animals should recover with intensive supportive care.
Delayed neurotoxicity may occur and neurological signs may reappear weeks after recovery. These signs usually resolve with supportive care.
If blood carboxyhaemoglobin levels are elevated and therapy is delayed, most patients will not survive.
Patients with additional lung injury due to smoke inhalation have a poorer prognosis.
| Carbon Monoxide Poisoning Learning Resources | |
|---|---|
 Test your knowledge using flashcard type questions |
Small Animal Emergency and Critical Care Medicine Q&A 07 |
References
Osweiler, G. (2010) Blackwell's Five-Minute veterinary consult clinical companion: small animal toxicology John Wiley and Sons
Merck, M. (2007) Veterinary forensics: animal cruelty investigations John Wiley and Sons