Carbon Monoxide Toxicity

Article Author:
Mary Hanley
Article Editor:
Pujan Patel
Updated:
11/15/2018 10:11:01 PM
PubMed Link:
Carbon Monoxide Toxicity

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]