Carbon Monoxide Poisoning – A Medical Student Clinical Pearl

Mitchell McDonough

DMNB, Class of 2022

Reviewed by Dr. Rachel Goss

Copyedited by Dr. Mandy Peach

Case

A 75 y/o male presented to the Emergency Department one afternoon via EMS with mild confusion and a headache. He recalled a sudden feeling of light-headedness while making breakfast in the morning, lowered himself to the floor, and then has very limited memory of events after this. He did not recall losing consciousness. Given his confusion, he was unable to provide an accurate recount of the events that had initially brought him to the ED and collateral history was required. EMS indicated that he was found by his upstairs neighbour after hearing him yelling. The patient noted that the power went out at his house early during the night, so he turned on his propane stovetop to provide some heat. He admitted to alcohol consumption the night prior but indicated he drinks frequently and that was unlikely to be the culprit of his current state. He had no other complaints at this time and a review of systems was unremarkable apart from a mild headache.

On general assessment the patient appeared well, vital signs were within normal limits. On physical exam he had normal strength in all four extremities. Neurologic, respiratory, cardiac and abdominal exams were unremarkable. The patient was slightly confused but it was difficult to ascertain if this was new or his normal baseline.

Differential for Confusion

Metabolic disorders
• Electrolyte abnormalities
• Endocrine disease
• Hypoglycemia
• Hypoxia

Stroke/CNS structural lesion/Head Injury

Infectious
• Systemic infection
• CNS infection (meningitis, encephalitis)

Intoxication/withdrawal
• Alcohol
• Drugs
• Carbon Monoxide

Investigations

Initial investigations included an ECG, which was normal with no evidence of an ischemic event, a toxicology panel which showed minimal blood alcohol remaining, and a blood gas sample with carboxyhemoglobin. While carbon monoxide poisoning was initially low on our differential, the carboxyhemoglobin level came back severely elevated, at 31%. Interestingly, PO2 from the ABG was within normal limits as the concentration of CO required to cause poisoning is sufficiently low that it does not significantly alter the quantity of oxygen dissolved in the plasma.

Pertinent Arterial Blood Gas Values for our patient:

pH 7.37 [7.35-7.45]
pCO2 36.2mmHg [35-45]
pO2 81.4 mmHg [75-105]
K+ 4.2mmol/L [3.7-4.7]
Na+ 139 mmol/L [136-146]
Ca2+ 1.27 mmol/L [1.15-1.30]
FCOHb 31.4% [0.3-1.8]
ctHb 132g/L [120-150]

 

Carbon Monoxide Poisoning Overview

Carbon monoxide is a gas formed by combustion of hydrocarbons. It is colourless, tasteless and odorless. Carbon monoxide binds to hemoglobin with approximately 200 times greater affinity than oxygen, forming carboxyhemoglobin which results in impaired utilization of oxygen by cells. The mechanism of impaired oxygen usage relates to CO binding cytochrome oxidase in peripheral tissues which prevents cells from using the reduced O2 received.

Potential sources of carbon monoxide include fires, heating systems, stoves, charcoal grills, generators and motor vehicles (1-3).

Figure 1: Oxygen dissociation curve demonstrating the left shift of carbon monoxide (13).

Clinical Presentation

The clinical presentations of carbon monoxide poisoning vary depending on the severity of intoxication and most findings are usually nonspecific (4,5). Patients may describe a general malaise, nausea, dizziness and headaches (6). Depending on the level of intoxication, patients may present with symptoms ranging from confusion to coma, seizures and myocardial ischemia.

Table 2: Symptoms at varying levels of carbon monoxide dissolved in blood. It should be noted that symptoms can vary substantially from individual to individual and that levels of CO do not correlate well with symptoms. For example, a typical cigarette smoker will have up to a 10% level of CO in their blood at baseline. (14).

 

Severe is classified as >30% and the following clinical signs:

• New neurologic findings
• Ischaemic ecg
• Clinically significant metabolic acidosis
• Requirement for ventilation.

Diagnosis

Diagnosis of carbon monoxide poisoning is based on history, physical exam and elevated carboxyhemoglobin on cooximetry of an arterial or venous blood gas. Due to their similar light absorbancy, standard pulse oximetry is not able to differentiate between carboxyhemoglobin and oxyhemoglobin, and therefore cannot screen for exposure to carbon monoxide (7,8). Because of the similar light absorbancy, SpO2 can also be falsely elevated. It is important to note that even with a normal SpO2 level that the patient is hypoxic.

A non-smoker may have up to 3% carboxyhemoglobin at baseline while a smoker may have 10-15%. Anything above these levels represents carbon monoxide poisoning.

Treatment

Treatment of patients with suspected carbon monoxide poisoning include:

• removal of the potential source
• administration of high-flow oxygen by face mask.
• IV mannitol for any potential cerebral edema.

Indications for treatment with hyperbaric oxygen vary from institution to institution and depend on factors such as symptoms, patient factors, length of exposure to carbon monoxide, as well as COHB levels.

In general, patients that should be considered for hyperbaric oxygen therapy include (4,9-12):

• carbon monoxide level >25% (>15% in pregnant women)
• neurosequelae
• loss of consciousness
• metabolic acidosis (pH < 7.1)
• evidence of end-organ ischemia

Case Conclusion

Given their severely elevated carboxyhemoglobin level and prolonged exposure, the patient was given 100% oxygen via a non-rebreather face mask until being transported to a hyperbaric oxygen chamber for further treatment.

This case highlights the importance of carbon monoxide poisoning as a potential diagnosis when a patient presents with a reduced level of consciousness or confusion, especially during the winter months when the risk of exposure is higher.

References

1. Thomassen Ø, Brattebø G, Rostrup M. Carbon monoxide poisoning while using a small cooking stove in a tent. Am J Emerg Med 2004; 22:204.
2. Centers for Disease Control and Prevention (CDC). Carbon monoxide poisoning from hurricane-associated use of portable generators–Florida, 2004. MMWR Morb Mortal Wkly Rep 2005; 54:697.
3. Hampson NB, Dunn SL. Carbon Monoxide Poisoning from Portable Electrical Generators. J Emerg Med 2015; 49:125.
4. Harper A, Croft-Baker J. Carbon monoxide poisoning: undetected by both patients and their doctors. Age Ageing 2004; 33:105
5. Kao LW, Nañagas KA. Carbon monoxide poisoning. Emerg Med Clin North Am 2004; 22:985.
6. Tomaszewski C. Carbon monoxide poisoning. Early awareness and intervention can save lives. Postgrad Med 1999; 105:39.
7. Bozeman WP, Myers RA, Barish RA. Confirmation of the pulse oximetry gap in carbon monoxide poisoning. Ann Emerg Med 1997; 30:608.
8. Tremper KK, Barker SJ. Pulse oximetry. Anesthesiology 1989; 70:98.
9. Ernst A, Zibrak JD. Carbon monoxide poisoning. N Engl J Med 1998; 339:1603.
10. Weaver LK. Carbon monoxide poisoning. Crit Care Clin 1999; 15:297.
11. Hampson NB, Dunford RG, Kramer CC, Norkool DM. Selection criteria utilized for hyperbaric oxygen treatment of carbon monoxide poisoning. J Emerg Med 1995; 13:227.
12. Huang CC, Ho CH, Chen YC, et al. Hyperbaric Oxygen Therapy Is Associated With Lower Short- and Long-Term Mortality in Patients With Carbon Monoxide Poisoning. Chest 2017; 152:943.
13. https://www.pulmonologyadvisor.com/home/decision-support-in-medicine/pulmonary-medicine/thermal-injury-and-smoke-inhalation/
14. https://www.cfinotebook.net/notebook/aeromedical-and-human-factors/carbon-monoxide-poisoning