Carbon Monoxide Toxicity


Article Author:
Mary Hanley


Article Editor:
Pujan Patel


Editors In Chief:
Bette Bogdan
Lori Kerley
Robin Geiger


Managing Editors:
Frank Smeeks
Scott Dulebohn
Erin Hughes
Pritesh Sheth
Mark Pellegrini
James Hughes
Richard Ciresi
Phillip Hynes


Updated:
11/15/2018 10:11:01 PM

Introduction

Carbon monoxide (CO) is released into the environment by the incomplete combustion of carbonaceous materials. The sources of CO are plentiful, and except carbon dioxide (CO2), CO is the most abundant pollutant in the lower environment. It is tasteless, odorless, and colorless, and victims are usually rendered unconscious before they realize they are being poisoned. The effects of CO poisoning on humans are variable, and healthcare professionals are just beginning to understand these effects better.[1],[2],[3]

Etiology

The etiology of CO toxicity is due to its effect on oxygen binding to the hemoglobin molecule.  CO binds to hemoglobin forming carboxyhemoglobin (COHb) with a 220% greater affinity to hemoglobin than oxygen. This reduces the oxygen-carrying capacity of hemoglobin and leads to cellular hypoxia. Carboxyhemoglobin (COHb) increases the affinity of unbound hemoglobin for O2 thus causing a leftward shift in the oxyhemoglobin dissociation curve. Additionally, CO binds to the heme moiety of the cytochrome c oxidase in the electron transport chain and inhibits mitochondrial respiration. These effects cause a lower tissue and intracellular PO2 than would otherwise be expected for a given blood oxygen concentration. The hemoglobin concentration and the PO2 of blood may be normal, but the oxygen content of the blood is reduced significantly.[4],[5]

Epidemiology

Annually, there are over 40,000 cases of CO poisoning in the United States. There is a 0.5 to 1.0/1,000,000 person fatality rate. CO may be responsible for 50% of all fatal poisonings. CO poisoning is the major contributing cause of death in fire victims. Approximately 30% to 40% of CO-poisoning victims die before reaching the hospital. Of those hospitalized, approximately 2% die, 10% recover partially, and 23% to 47% suffer delayed neurologic sequelae.[6]

Pathophysiology

CO enters the body via the lungs. Direct interactions may damage the lung parenchyma without the need for delivery of blood-borne hemoglobin. Elsewhere in the body, CO is delivered by hemoglobin. The CO causes capillary leakage of macromolecules from the lungs and systemic vasculature, and this can occur in humans who have been exposed to relatively low concentrations of CO for prolonged periods. As carboxyhemoglobin (COHgb) levels rise, the cerebral blood vessels dilate, and both coronary blood flow and capillary density increases. If exposure continues, central respiratory depression develops which may result from cerebral hypoxia. Cardiac effects, especially ventricular arrhythmias occur. Ventricular arrhythmias are implicated as the cause of death most often in CO poisoning. There is evidence that myocardial impairment begins at the relatively low level of COHgb of 20%. The overall cause of death for most animals poisoned by CO is combined hypoxia and ischemia during the acute event.[7]

Toxicokinetics

HGB combines with CO 220 times more intensely than it does with oxygen. In the air in a standard room (21% O2), the half-life of CO is 320 minutes. In 100% O2, the half-life of CO is less than 90 minutes. With hyperbaric oxygen at a pressure of 3 ATA (atmospheres absolute), the half-life of CO is decreased to 23 minutes. The only adequate treatment for significant CO poisoning is hyperbaric oxygen therapy (HBOT).

History and Physical

The symptoms of CO poisoning can be variable which explains why only 5% to 6% of patients who present to the emergency department with CO poisoning receive HBOT.

Most commonly, patients will present with headache (more than 90%), dizziness, weakness, and nausea. Patients may be tachycardic and tachypneic. They may exhibit hypotension. Mental status changes such as confusion, altered level of consciousness, disorientation and memory loss may occur. Intraocular findings may include retinal hemorrhages, congestion with papilledema. The kidneys are susceptible to ischemic injury from CO poisoning. The classic symptoms of cherry red nail beds and mucous membranes are not "classic" and are usually post-mortem findings. Patients may also develop ataxia, apraxia, incontinence, and cortical blindness.

Evaluation

The standard ABCs (airway, breathing, and circulation) apply to CO-poisoned patients as well. Supplemental oxygen is the cornerstone of treatment. It is important to note that standard peripheral pulse oximeter devices cannot differentiate COHb from oxyhemoglobin and hence oxygen saturation (SpO2) will not show any abnormalities on the monitor.[7],[8]

Typically, an arterial blood gas sample with a co-oximetry analysis is the most useful initial step. The carboxyhemoglobin level is reported in this analysis. This number should not be the foundation upon which the treatment plan is built however because COHgB levels are loosely associated with symptoms, and there is no direct correlation between COHgb levels and the severity of the symptoms or the risk of mortality and morbidity. COHb levels above 3% to 4% in non-smokers and 10% in smokers are typically considered outside of normal limits. It is agreed that levels greater than 20 in adults indicate a significant poisoning, and levels greater than 15 in children are considered significant. The take-home point is to treat the patient, not the number.  

Other assessments such as a complete blood count (CBC), electrolytes, BUN, and creatinine levels and baseline troponin should be assessed. ECG should be checked for any signs of ischemia. New ischemia on ECG is indicative of severe CO poisoning. Chest radiographs should be ordered as well. CT of the head is not required; however, CO poisoning can manifest as global pallidus hemorrhage, therefore, it may be useful.

Treatment / Management

The cornerstone of treatment for CO poisoning is supplemental oxygen that should be initiated as soon as possible and continued throughout treatment. Patients with significant poisoning demonstrated by transient loss of consciousness, cardiac ischemia, mental status changes, tachycardia, and or hypotension, along with elevated carboxyhemoglobin levels should be treated emergently with hyperbaric oxygen. Although present in every state, only several hundred hyperbaric oxygen centers currently exist in the United States of America. The best outcomes occur when patients receive their first treatment within 6 hours of the poisoning event. Most hyperbaric physicians prescribe 3 treatments in the first 24 hours and then reassess the patient's symptoms and response before continuing daily treatments. Despite hyperbaric therapy, up to 40% of patients can still develop chronic, neurocognitive impairment and hence, patients should be scheduled for neuropsychological evaluation approximately 1 to 2 months after recovery.[9],[10],[11]

Alternate, more easily accessible, and useful therapies are still lacking. However, case reports and animal model studies are underway. These study therapies such as lung phototherapy.

Prognosis

The prognosis of patients with CO poisoning does vary on the severity, other comorbidities, and laboratory values. Individuals with documented abnormal MRI and CT findings usually have a poor prognosis. Any patient with a persistent neurological deficit also had a guarded prognosis.

Complications

  • Amnesia
  • Dementia
  • Irritability
  • Psychosis
  • Memory loss
  • Loss of executive function
  • Speech deficit
  • Parkinson disease
  • Depression
  • Cortical blindness

Postoperative and Rehabilitation Care

Only patients with HbCO levels should be discharged. After discharge, the patient should be followed within 4 to 8 weeks to screen for any neurological deficits. Those with intentional CO exposure should be referred to a psychiatrist prior to discharge.

Deterrence and Patient Education

Patients should be educated on the importance of home CO detector alarms.

Pearls and Other Issues

Carbon monoxide (CO) poisoning can be insidious or abrupt in onset. Symptoms can range from mildly bothersome to death. The clinician cannot make the diagnosis and treat the patient for this condition if he or she does not consider it when assessing a patient with multiple, vague complaints such as a headache and nausea or flu-like symptoms. Poisonings tend to be more common in winter months when improperly vented or poorly maintained heating units can poison entire households or apartment buildings. House fires and suicide attempts are also common causes of CO poisoning. CO can poison scuba divers if tanks are filled near a generator that is not adequately ventilated. Prompt treatment and referral for hyperbaric oxygen treatment is life-saving and reduces the morbidity and mortality associated with this, all too common, poisoning. Installing and maintaining CO detectors in homes and buildings saves lives.

Enhancing Healthcare Team Outcomes

Unintentional CO poisoning is a leading cause of preventable deaths in the United States. The majority of these patients present to the emergency room. If the diagnosis is delayed, the outcomes can be abysmal. An interprofessional team approach to CO poisoning is necessary to prevent the high morbidity. Once the diagnosis is made, it is necessary to consult with several health specialists including the physician in charge of the hyperbaric chamber. The key treatment is the administration of oxygen and close monitoring of the patient for mental status changes, arrhythmias, cardiac ischemia, and hypotension.[6],[12] [Level V]

Once the patient is treated, the nurse plays a vital role in educating the patient and the family about installing CO detectors in the home. If the poisoning was an attempt at suicide, a mental health consult should be obtained prior to discharge.

Outcomes

CO poisoning is very unpredictable in its outcomes. Even with prompt treatment, close to 40% of patients develop residual neurocognitive impairment. Patients need to be followed up for a few months to determine if a full recovery has occurred.[12],[13] [Level III]


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Carbon Monoxide Toxicity - Questions

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What treatment is indicated for significant poisoning with carbon monoxide?



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A female found unconscious near the scene of a fire is hypotensive and comatose. Her arterial pH is 7.0, with carboxyhemoglobin of 45%. Which treatment is not indicated emergently?



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A 17-year-old is found in his apartment after a fire. He says the fire started after he fell asleep while smoking. He is taken to the emergency department where he is evaluated for carbon monoxide poisoning. What is the most common symptom of carbon monoxide poisoning?



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A patient presents to the emergency department after being found confused and dyspneic at home. There was a power outage and she is using a gas stove to heat her home. Which of the following tests is most likely to yield the correct diagnosis?



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Which feature is not seen with carbon monoxide poisoning?



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What is the best treatment for patients with carbon monoxide poisoning?



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Which monitoring device is most suitable for the monitoring of a patient with carbon monoxide (CO) poisoning?



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Which of the following patient groups is most likely to present with carbon monoxide poisoning?



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A young male presents in November complaining of headaches and dizziness? What gas may he have inhaled?



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A 50 year old female presents with daily generalized headaches for a month. She reports the headaches are worst at night and in the morning before work. She recently separated from her husband of 25 years and moved into an older house. She admits she has been depressed and was started on an SSRI after her pet cat died in the basement. Her neurologist gave her sumatriptan for the headaches. The patient is brought to the emergency room by paramedics unresponsive and flushed. What is the diagnosis?



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A 50 year old female presents with daily generalized headaches for a month. She reports the headaches are worst at night and in the morning before work. She recently separated from her husband of 25 years into an older house. She admits she has been depressed and was started on an SSRI. The patient is found unresponsive in her home and brought to the emergency department. She is found to have carbon monoxide poisoning and treated with hyperbaric oxygen. After one week she is discharged home but complains of emotional problems. She is easily distracted, withdrawn, and depressed. What is the most likely diagnosis?



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When compared to oxygen, what is carbon monoxide's affinity for hemoglobin?



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At what percent should oxygen therapy, the primary treatment of carbon monoxide toxicity, should be administered?



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Which of the following is most useful during treatment of carbon monoxide poisoning?



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Which of the following groups is at lowest risk for carbon monoxide toxicity?



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Which is true of carbon monoxide?



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In the prehospital setting, which of the following is the preferred treatment for a spontaneously breathing individual with a decreased level of consciousness associated with carbon monoxide poisoning?



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Which of the following groups are at risk for carbon monoxide toxicity?



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A child rescued from a house fire is found to have elevated levels of carboxyhemoglobin consistent with carbon monoxide (CO) poisoning. Which of the following alterations would you expect to the hemoglobin dissociation curve?



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In the United States which of the following is the most common source of CO poisoning resulting in deaths?



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Which of the following is a sign of carbon monoxide toxicity?

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What is the mechanism of action in carbon monoxide poisoning?



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What area of the basal ganglia is damaged by carbon monoxide?



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During the winter, a patient presents with headache, nausea, vomiting, and dizziness. A medical history reveals that the patient is homebound and conserving money by using his fireplace to keep warm. An arterial blood gas reveals he has a decreased oxygen-carrying capacity and a normal arterial PO2. To which gas has the patient most likely been exposed?



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Which is an effective treatment for carbon monoxide poisoning?



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A 65-year-old female presents with a headache, dizziness, and confusion. She has no history of smoking and is taking no medication. On exam, she is tachycardic, hypotensive, confused, and agitated. Blood work reveals an elevated carboxyhemoglobin, which remains elevated with 100% oxygen therapy for 4 hours. What is the treatment of choice?



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What is the initial treatment in the field for a patient you suspect may have been poisoned by carbon monoxide?



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Carbon monoxide binds to hemoglobin molecules with a much greater affinity than oxygen. How does the presence of increased carboxyhemoglobin affect the accuracy of pulse oximetry readings?



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Carbon monoxide increases the affinity of unbound hemoglobin for oxygen thereby causing the oxyhemoglobin dissociation curve to shift toward:



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What is the main mechanism of carbon monoxide toxicity in humans?



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You receive a phone call from the wife of a young male patient who was treated with hyperbaric therapy for accidental carbon monoxide poisoning while working on his car in a poorly ventilated garage about 1 month ago. She is profoundly grateful to you and your staff for saving his life as he was comatose when found and required several treatments to awaken and recover. She tells you that the patient's personality is markedly changed and he is irritable and easily annoyed and distracted. Prior to the poisoning he was very affable and relaxed and had an outgoing pleasant disposition. She also notes that his gait is more like a shuffle and he falls easily. What should she be told?



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Which of the following patients should be treated with hyperbaric oxygen therapy?



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Cherry-red skin color in a comatose patient suggests the diagnosis of:



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A 50-year-old female presents with daily generalized headaches for a month. She reports the headaches are worst at night and in the morning before work. She recently separated from her husband of 25 years and moved into an older house. She admits she has been depressed and was started on an SSRI after her pet cat died in the basement. Her neurologist gave her sumatriptan for the headaches. The patient is brought to the emergency department by paramedics, unresponsive and flushed. What is the diagnosis?



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During mid-winter, a family is using a gas stove to heat their home. They do not have a smoke or carbon monoxide alarm in the home. Twelve hours later, the entire family presents to the emergency department with suspected carbon monoxide poisoning. What is one of the first symptoms of carbon monoxide poisoning?



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During mid-winter, a family is using a gas stove to heat the home. They do not have smoke or carbon monoxide alarm in the home. Twelve hours later the entire family presents to the emergency department with suspected carbon monoxide. Eye exam reveals papilledema and flamed shaped hemorrhages. What is the next step in this patient's management?



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Carbon Monoxide Toxicity - References

References

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