quiz treat the high carboxyhemoglobin level

[Admin]

A six-year old boy was trapped in the basement of a house fire. He was found conscious and breathing spontaneously. At the scene he was sleepy but arousable and followed some commands. In the emergency department pulse oximetry showed his oxygen saturation to be 98% but the carboxyhemoglobin level was noted to be 20%.

The next best step to treat the high carboxyhemoglobin level in this patient is

A normobaric oxygen therapy.

B sodium thiopental.

C hyperbaric oxygen therapy.

D hyperventilation.

E mannitol.

[Admin]

A

correct

Inhalation injury is the most frequent cause of death in burn patients. Although mortality from smoke inhalation alone is low (zero to 11%), smoke inhalation in combination with cutaneous burns is fatal in 30 to 90% of patients. The presence of inhalation injury increases burn mortality by 20%. The presence of inhalation injury results in both increased fluid requirements and increased risks of respiratory complications.

Carbon monoxide (CO) poisoning is a frequent finding in patients with inhalational injury.

CO decreases the oxygen carrying capacity of hemoglobin, decreases the uptake of oxygen by tissues and impairs the electron transport chain. The affinity of the heme molecule for CO is over two hundred times more than oxygen. Poisoning can be evaluated by measurement of serum carboxyhemoglobin levels. Hb-CO absorbs light almost identically as oxygenated hemoglobin and therefore pulse oximetry may not be useful to detect CO in the blood stream. CO oximetry measures the blood carboxyhemoglobin concentration. On average, exposures greater than 100 parts per million (ppm) (0.01%) causes a headache in two to three hours. At 800 ppm (0.08%) dizziness, nausea and seizures can occur within 45 minutes. At 1,600 ppm headache, tachycardia, dizziness and nausea occurs within 20 minutes of continuous exposure, with death occurring at about two hours.

The time from injury to carboxyhemoglobin measurement is important as it takes five hours for CO levels to fall by one half while the patient is breathing room air and less than one hour while breathing 100% oxygen.

In this patient, who is sleepy but conscious, breathing 100% oxygen is the best option for therapy. The use of hyperbaric oxygen (HBO) therapy has been advocated in patients with neurologic symptoms such as seizures, altered mental status, coma, abnormal mental status or a computerized tomography scan suggesting cerebral edema. The Cochrane Database of Systematic Reviews noted that existing data do not support the use of HBO to decrease neurologic sequelae. Although there are no universal criteria for the use of HBO, a survey of North American HBO facilities identified neurologic and cardiac symptoms as indications for HBO therapy. Delayed encephalopathy can be seen in patients after CO toxicity.

If there is concomitant acidosis that is not improving with oxygen therapy, cyanide poisoning should be suspected. Cyanide gas can be released with burning furniture. Cyanide toxicity is treated with sodium thiosulfate. If signs, symptoms or imaging studies suggest cerebral edema, hyperosmolar therapy with mannitol and hyperventilation may be helpful in treatment.

[Sharon]

A

[Admin]

A

correct

Inhalation injury is the most frequent cause of death in burn patients. Although mortality from smoke inhalation alone is low (zero to 11%), smoke inhalation in combination with cutaneous burns is fatal in 30 to 90% of patients. The presence of inhalation injury increases burn mortality by 20%. The presence of inhalation injury results in both increased fluid requirements and increased risks of respiratory complications.

Carbon monoxide (CO) poisoning is a frequent finding in patients with inhalational injury.

CO decreases the oxygen carrying capacity of hemoglobin, decreases the uptake of oxygen by tissues and impairs the electron transport chain. The affinity of the heme molecule for CO is over two hundred times more than oxygen. Poisoning can be evaluated by measurement of serum carboxyhemoglobin levels. Hb-CO absorbs light almost identically as oxygenated hemoglobin and therefore pulse oximetry may not be useful to detect CO in the blood stream. CO oximetry measures the blood carboxyhemoglobin concentration. On average, exposures greater than 100 parts per million (ppm) (0.01%) causes a headache in two to three hours. At 800 ppm (0.08%) dizziness, nausea and seizures can occur within 45 minutes. At 1,600 ppm headache, tachycardia, dizziness and nausea occurs within 20 minutes of continuous exposure, with death occurring at about two hours.

The time from injury to carboxyhemoglobin measurement is important as it takes five hours for CO levels to fall by one half while the patient is breathing room air and less than one hour while breathing 100% oxygen.

In this patient, who is sleepy but conscious, breathing 100% oxygen is the best option for therapy. The use of hyperbaric oxygen (HBO) therapy has been advocated in patients with neurologic symptoms such as seizures, altered mental status, coma, abnormal mental status or a computerized tomography scan suggesting cerebral edema. The Cochrane Database of Systematic Reviews noted that existing data do not support the use of HBO to decrease neurologic sequelae. Although there are no universal criteria for the use of HBO, a survey of North American HBO facilities identified neurologic and cardiac symptoms as indications for HBO therapy. Delayed encephalopathy can be seen in patients after CO toxicity.

If there is concomitant acidosis that is not improving with oxygen therapy, cyanide poisoning should be suspected. Cyanide gas can be released with burning furniture. Cyanide toxicity is treated with sodium thiosulfate. If signs, symptoms or imaging studies suggest cerebral edema, hyperosmolar therapy with mannitol and hyperventilation may be helpful in treatment.