**16. Carbon monoxide poisoning**

Carbon monoxide (CO) is an odourless, tasteless, colourless and non-irritating gas.

Potential sources of Carbon monoxide (CO) are automotive exhaust, fuelled heaters, Woodor coal-burning stoves, Structure fires and gasoline-powered generators other than fires.

The incidence of co -poisoning increases during winter time because the use of space heaters, wood-burning stoves and charcoal burning for heat.

#### **16.1. Mechanism of action**

Carbon monoxide (CO) diffuses fast in the pulmonary capillary membrane and because of his rapid binding affinity (more than oxygen by 200 times), carbon monoxide bind to haemoglobin, that cause impaired releasing oxygen to tissue leading to shift the oxyhaemoglobin dissociation curve to the left [51].

#### **16.2. Clinical features**

Carbon monoxide poisoning have variable clinical picture depend on severity of exposure ranging from non-specific symptoms like headache, nausea and dizziness in mild to moderate cases to confusion, seizure and coma in severe cases patients may present with mild fever, tachycardia, tachypnoea and hypertension. Acute myocardial injury and life-threatening dysrhythmias are the most cardiovascular complications in case of severe Carbon monoxide poisoning. Delayed neuropsychiatric syndrome is long term neurological complication in severe cases characterized with different symptoms including cognitive deficiency, movement disorders and focal neurologic deficit. The standard pulse oximetry cannot differentiate carboxyhaemoglobin from oxyhaemoglobin, so it is unreliable in the diagnosis or screen carbon monoxide poisoning, so measuring carboxyhaemoglobin level in an arterial blood gas helps in diagnosis [52–55].

#### **16.3. Treatment**

**15.2. Clinical features**

264 Essentials of Accident and Emergency Medicine

**15.3. Treatment**

**16. Carbon monoxide poisoning**

**16.1. Mechanism of action**

**16.2. Clinical features**

dissociation curve to the left [51].

wood-burning stoves and charcoal burning for heat.

Cardiovascular system is the most affected system in CCBs toxicity. Patient present with hypotension and bradycardia or reflex tachycardia. Verapamil or diltiazem toxicity usually patients present with sinus bradycardia, on the hand dihydropyridine overdoses cause peripheral vasodilatation causing reflex tachycardia [55]. CCBs have not primary effect on pulmonary and CNS System; CNS symptoms (seizures, delirium, and coma) occur secondary to decrease organ perfusion. Cardiogenic pulmonary oedema and acute lung injury (non-

Decontamination can be done by oral activated charcoal if patient present within 1 h of ingestion also the whole-bowel irrigation is useful in case of extended-release CCBs. Hypotension treated with IV fluid, Calcium chloride or calcium gluconate, glucagon (3–10 mg), if not responding start Vasopressors (e.g., norepinephrine). If symptoms refractory to vasopressor therapy start, high dose Insulin -glucose. If patient still not responding, lipid emulsion can be started. Finally, circulatory support measures, such as the placement of intra-aortic balloon pumps may be used in case of sever toxicity not responding to standard therapy [49–51].

cardiogenic pulmonary oedema) have also been reported in severe toxicity [48].

First step in management is secure airway, stabilize ventilation and circulation.

Carbon monoxide (CO) is an odourless, tasteless, colourless and non-irritating gas.

Potential sources of Carbon monoxide (CO) are automotive exhaust, fuelled heaters, Woodor coal-burning stoves, Structure fires and gasoline-powered generators other than fires.

The incidence of co -poisoning increases during winter time because the use of space heaters,

Carbon monoxide (CO) diffuses fast in the pulmonary capillary membrane and because of his rapid binding affinity (more than oxygen by 200 times), carbon monoxide bind to haemoglobin, that cause impaired releasing oxygen to tissue leading to shift the oxyhaemoglobin

Carbon monoxide poisoning have variable clinical picture depend on severity of exposure ranging from non-specific symptoms like headache, nausea and dizziness in mild to moderate cases to confusion, seizure and coma in severe cases patients may present with mild fever, tachycardia, tachypnoea and hypertension. Acute myocardial injury and life-threatening dysrhythmias are the most cardiovascular complications in case of severe Carbon monoxide poisoning. Delayed neuropsychiatric syndrome is long term neurological complication in After securing the airway, the most important step in treatment is oxygen 100% via nonrebreathing mask or intubation and mechanically ventilation with 100% oxygen if the patient is comatose and cannot secure his air way, half-life of carboxyhaemoglobin in room air 250–320 min while via non-rebreathing with 100% oxygen decreased to 90 min. Hyperbaric oxygen therapy could be considered in certain cases, the indication for Hyperbaric oxygen includes Pregnancy with carboxyhaemoglobin level > 15%, Carboxyhaemoglobin >25%, evidence of acute myocardial ischemia, and severe metabolic acidosis [56].


**Histopathological Change of Esophagus Related to Dysphagia in Mixed Connective Tissue Disease**

Akihisa Kamataki, Miwa Uzuki and Takashi Sawai

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/60509