Carbon Monoxide Toxicity Treatment & Management

Prehospital care for patients with carbon monoxide (CO) toxicity includes the following:

• Promptly remove the patient from continued exposure and immediately institute oxygen therapy with a nonrebreather mask.

• Perform intubation for the comatose patient or, if necessary for airway protection, and provide 100% oxygen therapy.

• Institute cardiac monitoring. Pulse oximetry, although not useful in detecting carboxyhemoglobin (HbCO), is still important because a low saturation causes even greater apprehension in this setting.

• Give notification to the emergency department for comatose or unstable patients because rapid or direct transfer to a hyperbaric center may be indicated.

• If possible, obtain ambient CO measurements from fire department or utility company personnel, when present.

• Early blood samples may provide much more accurate correlation between HbCO and clinical status; however, do not delay oxygen administration to acquire them.

• Obtain an estimate of exposure time, if possible.

• Avoid exertion to limit tissue oxygen demand.

Considerations in emergency department (ED) care include the following:

• Cardiac monitor: Sudden death has occurred in patients with severe atherosclerotic disease at HbCO levels of only 20%.

• Pulse oximetry: HbCO absorbs light almost identically to that of oxyhemoglobin. Although a linear drop in oxyhemoglobin occurs as HbCO level rises, pulse oximetry will not reflect it. Pulse oximetry gap, the difference between the saturation as measured by pulse oximetry and one measured directly, is equal to the HbCO level. ^[36] However, pulse CO-oximetry units are available that can screen for CO toxicity at the bedside.

Oxygen therapy is usually provided via a non-rebreather mask. However, Roth et al describe effective use of noninvasive continuous positive airway pressure (CPAP) ventilation using a tight mask and an inspired fraction of oxygen (FiO₂) of 100%. These authors provide case reports of simultaneous CO toxicity in a couple, in which HbCO levels fell from 21% at admission to 6% within 1 hour and 3% after 90 minutes in the patient treated with CPAP. In the spouse, who was treated with conventional oxygen therapy, reduction of HbCO from the admission level of 21% to 3% took 6 hours. ^[37]

Continue 100% oxygen therapy until the patient is asymptomatic and HbCO levels are below 10%. In patients with cardiovascular or pulmonary compromise, lower thresholds of 2% have been suggested. Calculate a gross estimate of the necessary duration of therapy using the initial level and half-life of 30-90 minutes at 100% oxygen.

In uncomplicated intoxications, venous HbCO levels and oxygen therapy are likely sufficient. Evaluate patients with significant cardiovascular disease and initial HbCO levels above 15% for myocardial ischemia and infarction.

Consider immediate transfer of patients with levels above 40% or cardiovascular or neurologic impairment to a hyperbaric facility, if feasible. Persistent impairment after 4 hours of normobaric oxygen therapy necessitates transfer to a hyperbaric center. Pregnant patients should be considered for hyperbaric treatment at lower HbCO levels (above 15%). Because fetal hemoglobin has a greater affinity for CO than hemoglobin in the mother's red blood cells, the fetus acts as a sink for the CO, so HbCO levels will be higher in the fetus than in the mother. ^[38]

Serial neurologic examinations, including funduscopy, CT scans, and, possibly, MRI, are important in detecting the development of cerebral edema. Cerebral edema requires intracranial pressure (ICP) and invasive blood pressure monitoring to further guide therapy. Head elevation, mannitol, and moderate hyperventilation to 28-30 mm Hg PCO₂ are indicated in the initial absence of ICP monitoring. Glucocorticoids have not been proven efficacious, yet the negative aspects of their use in severe cases are limited.

Do not aggressively treat acidosis with a pH above 7.15 because it results in a rightward shift in the oxyhemoglobin dissociation curve, increasing tissue oxygen availability. Acidosis generally improves with oxygen therapy.

In patients who fail to improve clinically, consider other toxic inhalants or thermal inhalation injury as contributing factors. Be aware that the nitrites used in cyanide kits cause methemoglobinemia, shifting the dissociation curve leftward and further inhibiting oxygen delivery at the tissue level. Combined intoxications of cyanide and CO may be treated with sodium thiosulfate 12.5 g intravenously to prevent the leftward shift.

Admit patients to a monitored setting and evaluate acid-base status if HbCO levels are 30-40% or above 25% with associated symptoms.  Admitted patients generally require monitored settings, telemetry beds, or cardiac care unit/medical intensive care unit (CCU/MICU) beds for more severe cases.

Patients with cerebral edema may be most appropriately treated in a neurosurgical ICU setting; this may dictate transfer to another facility. Admission or consult by toxicology service is helpful in these cases.

Locate the nearest hyperbaric oxygen center by contacting the Divers Alert Network (DAN) at Duke University at (919) 684-2948. However, note that a survey of hyperbaric programs in the United States found that only 43 of 361 centers (11.9%) had equipment, intravenous infusion pumps and ventilators, and staff necessary to treat high-acuity patients. ^[39]

Hyperbaric oxygen (HBO) therapy currently rests at the center of controversy surrounding management of CO poisoning. Increased elimination of HbCO clearly occurs. Certain studies proclaim major reductions in delayed neurologic sequelae, cerebral edema, pathologic central nervous system (CNS) changes, and reduced cytochrome oxidase impairment.

Despite these individual claims, systematic reviews have not revealed a clear reduction in neurologic sequelae with HBO. ^{[40, 41]} A 2017 clinical policy statement from the American College of Emergency Physicians (ACEP) concluded that it remains unclear whether HBO therapy is superior to normobaric oxygen therapy for improving long-term neurocognitive outcomes. ^[26]  

A study by Han et al, in which 224 patients with acute CO poisoning were followed for up to 6 months, found no difference in the incidence of delayed neuropsychiatric sequelae between patients receiving HBO (n=198) and those receiving normobaric oxygen (n=26). ^[42]  In contrast, a nationwide observational study from Japan reported that patients who received HBO therapy had significantly lower rates of depressed mental status and reduced activities of daily living at discharge compared with a control group. Similar benefits were seen in patients with non-severe CO poisoning. The study used one-to-one propensity score matching to pair 2034 patients who received HBO therapy within 1 day of admission with an equal number of patients who did not receive HBO. ^[43]

However, evidence of a mortality benefit with HBO therapy has emerged. A retrospective study by Rose et al that reviewed 1099 cases of CO poisoning in adults concluded that HBO therapy was associated with an absolute risk reduction of 2.1% in both inpatient and 1-year mortality. ^[44]  

Lower mortality with HBO therapy was also reported in a retrospective nationwide population-based cohort study from Taiwan that included 7,278 patients who received HBO and 18,459 patients who did not. Overall, the adjusted hazard ratio [AHR] for death in HBO-treated patients was 0.74 (95% CI, 0.67-0.81). In patients younger than 20 years, the AHR was 0.45 (95% CI, 0.26-0.80) and for those with acute respiratory failure, the AHR was 0.43 (95% CI, 0.35-0.53). The lower mortality rate was noted for a period of 4 years. ^[45]  

Presently, universal treatment criteria do not exist; however, a survey of directors of North American HBO facilities with 85% responding demonstrates some consensus. The most common selection criteria (regardless of HbCO level) include the following:

• Coma (98%)
• Transient loss of consciousness (77%)
• Ischemic ECG changes (91%)
• Focal neurologic deficits (94%)
• Abnormal neuropsychiatric test results (91%).

Ninety-two percent of HBO facility directors use HBO for headache, nausea, and HbCO levels above 40%; yet only 62% have a specific minimum HbCO level in asymptomatic patients. One half of the centers place a time limit on delay of treatment in patients with transient loss of consciousness alone.

Untreated pneumothorax is the only major contraindication for HBO therapy. ^[38]

HBO at 3 atm raises the amount of oxygen dissolved in the serum to 6.8%, enough to sustain cerebral metabolism. Elimination half-life is reduced to 15-23 minutes. Elimination half-life of CO from methylene chloride intoxication of 13 hours at room air temperature is reduced to 5.8 hours.

Chambers are small monoplace hulls, allowing space for a single patient in a supine position who can be viewed through a window at the head, or they are acrylic walled and allow full visualization. Many of these monoplace chambers allow for care of critically ill patients, including intravenous lines, arterial lines, and ventilator. Others are large multiplace chambers that permit ventilation equipment and allow medical teams to accompany the patient. A monoplace chamber is shown below.

Treatment regimens usually involve 100% oxygen at 2.4-3 atm for 90-120 minutes. Re-treatment, although controversial, may be performed for acutely and chronically persistent symptoms. One study suggests that degree of metabolic acidosis can predict the need for re-treatment. ^[46]

Complications of therapy include decompression sickness, sinus and middle ear barotrauma, seizure, progression of pneumothorax to tension pneumothorax, gas embolism, reversible visual refractive changes, and complications related to transport of unstable patients.

For treatment of complications from therapy, decongestants are useful, prophylactic myringotomy is common and a requirement for intubated patients, and chest tube placement is mandatory with pneumothorax. Exercise caution in patients who have experienced chest compressions, central venous catheterization, intubation, and positive pressure ventilation. Seizures are most often secondary to oxygen toxicity and do not mandate anticonvulsant therapy or discontinuation of HBO therapy.

In multiplace chambers, seizure therapy consists of removing the oxygen mask. In monoplace chambers, decompression lowers oxygen concentration. It is crucial not to do this during the tonic phase of the seizure because it may cause pulmonary barotrauma secondary to gas expansion in the lungs.

A 10-year retrospective study found that transfer to an HBO facility did not need to be delayed for concern of cardiac arrest, respiratory arrest, myocardial infarction, or worsening mental status if they had not occurred during initial resuscitation; however, hypotension, dysrhythmia, seizure, emesis, and agitation were of concern in transit as well as in initial resuscitation. ^[47]

Survivors of CO poisoning are at risk for a range of neurologic and psychiatric complications, including the following ^[48] :

• Impaired intellectual function
• Short-term memory loss
• Dementia
• Amnesia
• Psychosis
• Irritability
• Dysfunctional gait
• Speech disorders
• Parkinson disease ^[49]
• Cortical blindness
• Depression

Discuss the possibility of delayed neurologic complications, although they are much more common in patients with toxicity severe enough to require hospital admission.

Carbon monoxide (CO) detectors: Home CO detectors with audible alarms are available, and can limit CO toxicity. ^[50]  One study of 911 calls for suspected CO poisoning showed in 80% of calls for detector alarms, verifiable ambient CO levels were present in the home; the mean concentration of CO was 18.6 ppm in homes tested because of detector alarms but was 96.6 ppm in homes without alarms where calls were prompted by suspicious symptoms. ^[51]

 

For patient education information, see Carbon Monoxide Poisoning.

Asymptomatic patients with HbCO levels below 10% may be discharged. In cases of accidental CO poisoning, patients should be followed up in 4-6 weeks to screen for cognitive sequelae. With intentional poisoning, psychiatric follow-up is mandatory, given the high rate of subsequent completed suicide. ^[3]

A nationwide population-based study from Korea found that the risk of venous thromboembolism was significantly elevated in the first 90 days after CO poisoning (odds ratio [OR] 3.96; 95% confidence interval [CI] 2.50 to 6.25). Risk was especially high in the first 30 days for pulmonary embolism (OR 22.00; 95% CI 5.33 to 90.75) and deep venous thrombosis (OR 10.33; 95% CI 3.16 to 33.80). These researchers recommend monitoring patients for venous thromboembolism risk in the 3 months following CO poisoning. ^[52]