Section 1

Section 2

Section 3 

Section 4 

Section 5

Section 6

Section 7

Section 8

Section 9

Section 2c

DIAGNOSIS AND TREATMENT OF CARBON MONOXIDE and CYANIDE TOXICITY

Carbon monoxide toxicity is one of the leading causes of death associated with fires. As oxygen is being consumed in the process of combustion, CO is being released. Carbon monoxide is rapidly transported across the alveolar membrane and preferentially binds to hemoglobin in place of oxygen to form carboxyhemoglobin (COHb). In addition, CO causes the oxyhemoglobin dissociation curve to shift to the left, thereby impairing oxygen unloading at the tissue level; this shift results in a substantial reduction in oxygen delivery, given that 98 percent of the oxygen supplied to the tissues comes bound to hemoglobin.

Patients who were injured in a closed space or who have inhalation injuries should be suspected of inhaling CO. CO toxicity is determined by a high index of suspicion and by measuring the COHb level. Persistent metabolic acidosis in a patient with adequate volume resuscitation and adequate cardiac output suggests impairment of oxygen utilization by CO or by cyanide. The chemical alteration of hemoglobin or of the cytochrome system by CO will not affect the amount of oxygen dissolved in plasma, and arterial oxygen tension (PaOs) will thus remain relatively normal.

Initial symptoms of carbon monoxide toxicity are primarily neurological with coma present at CO-HGH levels above 50%.

Treatment of CO toxicity consists of promptly displacing CO from hemoglobin by administering 90-100 percent oxygen until the COHb level is less than seven percent.

The concentration of COHb is reduced by approximately 50 percent every 20-30 minutes if an oxygen concentration of 90-100 percent is used. Hyperbaric oxygen (w to 3 atm) yields even more rapid displacement, particularly from the cell cytochrome system, but is only required to treat CO exposure when there is a lack of response to 100% oxygen.

TOXIC ELEMENTS IN HOUSE FIRE SMOKE 

Hydrocyanide, the gaseous form of cyanide is a well-recognized cause of fire-associated morbidity and mortality, particularly when synthetics such as polyurethane are burned. Although cyanide can be absorbed through the GI tract or through skin, it is most dangerous when aerosolized and inhaled because it is absorbed especially rapidly through the respiratory tract. Once absorbed, cyanide binds to the cytochrome system, thereby inhibiting cell metabolism and ATP production.

The diagnosis of cyanide toxicity is made on the basis of the history and a high index of suspicion and is confirmed by the presence of elevated blood cyanide levels (normal, 0.1mg/L; values higher than 1mg/L are usually lethal). Sodium nitrite treatment begins with volume replenishment. 300mg IV is then given over a period of 10 minutes; methemoglobin is produced as the cyanide is detoxified. Finally, 50 ml of solution of sodium thiosulfate is given; this converts the cyanide to sodium thiocyanate, which is excreted in the urine.

Carbon Monoxide Toxicity Table

Respiratory excursion can be markedly impaired by a burn to the chest wall. The process is most evident with a circumferential third degree burn. The loss of elasticity in the chest wall due to the burn tissue will markedly increase the work of breathing required to maintain functional residual capacity and an adequate tidal volume. As more subeschar edema develops, compressing the chest wall, the end-expiratory intrathoracic volume begins to decrease. Full thickness burns produce a more severe limitation because tissue expansion is markedly impaired and intrathoracic volume becomes compressed. Maximum respiratory effort is frequently required just to maintain adequate gas exchange. Any process that compromises the necessary increase in inspiratory force and muscle activity, such as hypoxia, hypovolemia, pain, or sedation, will accentuate the severity of lung dysfunction.

Symptoms may not be clearly evident until edema formation peaks at about 10 to 12 hours. The first clinical evidence of the chest wall restrictive defect is often labored breathing followed by a rapid respiratory deterioration, particularly in the patient who is not receiving ventilator support. Clearance of secretions can be impaired due to the inability to generate a hyperinflation. In the combined chest burn and inhalation injury, it is very difficult to distinguish the degree of impairment in total lung compliance due to the increased airway edema and bronchospasm compared with that due to the impaired chest wall. The increasing airway pressure required to expand the stiff chest wall will lead to extension of the burn into fat.

Deep Chest Wall Burn
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Circumferential Third or Fourth Degree

Not Circumferential

- Perform chest wall escharotomy	- Closely monitor
- Elevate head, chest (if stable)	- Escharotomy with any symptoms of     restriction

 

Incision thru entire eschar

Completed Escharotomy