Poisonings

Carbon Monoxide Poisoning

Introduction

Carbon monoxide is an odorless, colorless, tasteless gas produced from incomplete combustion of organic materials.  It is the most common gas exposure among the pediatric population.

 

Epidemiology

  • CO poisoning is responsible for up to 40,000 emergency department visits and 5000 to 6000 deaths per year.
  • Accidental exposure shows seasonal and regional variation. It most commonly occurs in cold climates during the winter.
  • Additionally, according to the Nelson Textbook of Pediatrics, CO exposure in recent years has been seen especially from sources such as malfunctioning portable generators in hurricane-related visits to healthcare facilities.
  • Other potential sources include: fuel powered ovens, gasoline-powered electrical generators, motor vehicles especially in poorly ventilated spaces, motorboat exhaust, household fires, and underground electrical cable fires.

 

Pathophysiology

  1. Carbon monoxide rapidly diffuses across the capillary membrane and binds to hemoglobin to form Carboxyhemoglobin.
  2. The plasma level of carboxyhemoglobin is normally quite low. At baseline, levels up to 3 percent may be seen in nonsmokers, while smokers may have levels up to 10-15 percent.
  3. When carboxyhemoglobin is formed it displaces oxygen from the hemoglobin molecule. The bond between CO and hemoglobin is roughly 230-240 times the strength of the bond between oxygen and hemoglobin.
  4. After CO binds to hemoglobin, an allosteric change occurs in the hemoglobin molecules. The ability of the hemoglobin molecule to off-load oxygen to the periphery from the 3 other binding sites is then decreased, causing a left-shift of the hemoglobin curve and decreased peripheral tissue delivery of oxygen.

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Carbon monoxide shifts the oxygen-dissociation curve to the left.  http://en.wikipedia.org/wiki/Carbon_monoxide_poisoning

  1. CO also interacts with other proteins. Cytochrome oxidase is a target of CO, the interaction of which results in decreased cellular respiration. Thus, not only is delivery of oxygen impaired, but so is utilization.
  2. CO also displaces NO from proteins. NO induced vasodilation may play a role in the headache, syncope, and hypotension that is clinically seen with CO poisoning. NO may also play a role in neurologic consequences of CO inhalation.

 

Clinical Presentation

symptoms_0.jpg
http://en.wikipedia.org/wiki/Carbon_monoxide_poisoning

A.) General

  • Signs and symptoms of CO poisoning are largely non-specific.
  • Headache is the most common symptom of CO poisoning.
  • Patients often present with constitutional symptoms including malaise, dizziness, nausea, and vomiting. These symptoms are often mistaken for viral illnesses or food poisoning initially.
  • According to sources, the classic sign of cherry red lips is very insensitive for CO poisoning.
  • At higher levels of exposure, patients may demonstrate mental status changes. These may include confusion and ataxia. A careful neurologic exam is thus warranted.
  • CO poisoning may also present with toxicity to the heart, skeletal muscle, kidney, and lungs, causing myocardial ischemia and arrythmias, rhabdomyolysis and ARF, and/or pulmonary edema. Lactic acidosis may also be present.
  • Coma, cardiovascular collapse, and death may follow severe poisoning.

B). Pediatric Specific

  • In the pediatric population, signs and symptoms may be even more non-specific than in the adult population.
  • Fussiness and difficulty feeding may be the only complaints in infants or toddlers.
  • Children may demonstrate affects of CO poisoning earlier than adults secondary to increased respiratory rate and oxygen utilization.

 

Diagnosis

  1. Based on history and physical
  2. Routine pulse oximetry does not differentiate between carboxyhemoglobin and oxyhemoglobin, thus it is not appropriate for use in detecting CO exposure.
  3. Measuring carboxyhemoglobin can confirm exposure, recalling that a certain baseline is normal among the population (See above).

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Finger tip carboxyhemoglobinsaturation monitor (SpCO%). Note: This is not the same as a pulse oximeter (SpO2%), although some models (such as this one) do measure both the oxygen and carbon monoxide saturation.
http://en.wikipedia.org/wiki/Carbon_monoxide_poisoning
                   

  1. UptoDate recommends ECG after a diagnosis of CO poisoning is confirmed. Evidence of myocardial ischemia on ECG should prompt cardiac biomarkers.

 

Treatment

  1. The most important treatment is removal from the source of CO and delivery of oxygen to competitively bind hemoglobin.
  2. In room air, the half-life of carboxyhemoglobin is 4-6 hours. This is reduced to 60-90 minutes when a patient is given 100% via a non-rebreather facemask.
  3. For patients presenting in a coma or with severe mental status changes, intubation is required plus delivery of 100% oxygen.
  4. Hyperbaric oxygen therapy may benefit severely poisoned patients. The half-life of carboxyhemoglobin is reduced to 20-30 minutes.
  5. Per UptoDate: criteria for treatment with HBO include: Carboxyhemogloobin levels >25%, evidence of ongoing end-organ ischemia (eg, profound metabolic acidosis (pH <7.1), myocardial ischemia), loss of consciousness, or in pregnant women a COHb >20 percent or evidence of fetal distress. However, the level of Carboxyhemoglobin at which hyperbaric oxygen therapy should be delivered is controversial is considered independently of clinical status.

 

Prevention

Prevention is key.  Routine car and furnace maintenance is crucial to ensuring levels of CO are acceptable.  Homes should have functioning carbon monoxide detectors installed and checked at least yearly as well.

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Carbon monoxide detectorhttp://www.cdc.gov/co/faqs.htm

The following list from the CDC on how to prevent CO poisoning is a helpful start, and click on the link below to access materials in other languages:

cdc_1.jpg

 

  • Install a battery-operated or battery back-up CO detector in your home and check or replace the battery when you change the time on your clocks each spring and fall.
  • Have your heating system, water heater, and any other gas, oil, or coal burning appliances serviced by a qualified technician every year.
  • Do not use portable flameless chemical heaters indoors.
  • If you smell an odor from your gas refrigerator have an expert service it. An odor from your gas refrigerator can mean it could be leaking CO.
  • When you buy gas equipment, buy only equipment carrying the seal of a national testing agency, such as Underwriters’ Laboratories.
  • Make sure your gas appliances are vented properly. Horizontal vent pipes for appliances, such as a water heater, should go up slightly as they go toward outdoors, as shown below. This prevents CO from leaking if the joints or pipes aren’t fitted tightly.
  • Have your chimney checked or cleaned every year. Chimneys can be blocked by debris. This can cause CO to build up inside your home or cabin.
  • Never patch a vent pipe with tape, gum, or something else. This kind of patch can make CO build up in your home, cabin, or camper.
  • Never use a gas range or oven for heating. Using a gas range or oven for heating can cause a build up of CO inside your home, cabin, or camper.
  • Never burn charcoal indoors. Burning charcoal - red, gray, black, or white - gives off CO.
  • Never use a portable gas camp stove indoors. Using a gas camp stove indoors can cause CO to build up inside your home, cabin, or camper.
  • Never use a generator inside your home, basement, or garage or less than 20 feet from any window, door, or vent.

 

References

  1. Behrman, Richard E., Robert Kliegman, and Hal B. Jenson. Nelson Textbook of Pediatrics. 17th / [edited by] Richard E. Behrman, Robert M. Kliegman, Hal B. Jenson. ed. Philadelphia, Pa.: Saunders, 2004. Print.
  2. Kao L., Nanagas K. Toxicity associated with carbon monoxide. Clinics in Laboratory Medicine. 2006 Mar;26(1):99-125.
  3. Cho C., Chiu N., Ho C., Peng C. Carbon monoxide poisoning in children. Pediatrics & Neonatology. 2008 Aug;49(4):121-5
  4. Hill, G. E., B. Ogunnaike, and D. Nasir. Patients Presenting with Acute Toxin Ingestion. Anesthesiology clinics 28.1 (2010): 117-37. Print.