CO Toxicity: A Potentially Elusive Diagnosis
- Apr 5th, 2017
Author: Patrick C. Ng, MD (EM Chief Resident, SAUSHEC Emergency Medicine Department) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)
It is flu season and the dead of winter, and temperatures are at a record low. You just get on shift and are trying to get warm after that brisk walk from the parking lot to the ED when you see two-family-members, an 89-year-old female and her 40-year-old daughter, pop up on the tracker board with a chief complaint of ‘flu like symptoms’. You get a sip of your lukewarm coffee in before you see those two new patients. Both have very similar HPIs: gradual onset of headache, nausea/vomiting, and body aches. They ask you how they could have possibly contracted the flu, as they have been inside their home by the heater for the past few days secondary to the cold.
As part of your work-up, you obtain a co-oximetry level to realize that both of their carboxyhemoglobin levels are abnormal. Your older patient has a level of 13% and is a nonsmoker, while her daughter has a level of 20%. Given that your younger patient is 38 weeks pregnant, you arrange for her to be transported to another facility to start hyperbaric oxygen therapy, while you order your elderly patient 100% oxygen and arrange for admission for carbon monoxide toxicity.
Carbon monoxide (CO) poisoning is an important topic for emergency physicians to understand. It is a common exposure and can lead to significant morbidity and mortality.1 According to the Centers for Disease Control and Prevention (CDC), more than 20,000 visits to the emergency department are related to carbon monoxide poisoning.2 CO poisoning has been associated with both intentional and accidental poisonings.3,4 Approximately 600 accidental deaths due to CO poisoning are reported annually.5
CO is produced by the burning of fuels/organic material and is produced in the human body in low amounts. A normal carboxyhemoglobin level in the body is <1.5%. This number can increase up to 15% in smokers.6 Carbon monoxide is also produced by the burning of fuels. Exposures to higher levels of carbon monoxide can occur in building fires, industrial plants, garages with engines running, or in the home with gas stoves/heating appliances. In these potential environments, associated exposures to cyanide, carbon dioxide, hydrogen sulfide, phosgene, and nitrogen dioxide have been reported.6-7
How does Carbon Monoxide Cause Toxicity?
Carbon monoxide interferes with oxygen transport and delivery to cells. It has greater affinity for hemoglobin when compared to oxygen, thus impairing oxygen transport and delivery in the blood stream leading to cellular hypoxia. Morbidity classically involves the cardiovascular and neurological systems.3-10
How does a patient exposed to carbon monoxide present?
Patients with carbon monoxide poisoning may present with a variety of non-specific symptoms. Headache is one of the most common symptoms reported. Other symptoms such as nausea, vomiting, dizziness, weakness, or confusion are also commonly reported.12-13 The table below demonstrates these findings. In severe toxicity, patients can present with syncope, altered mental status, myocardial ischemia, and even cardiac arrest.
|Presenting Symptom||% of Total Number of Patients Presenting with Elevated COHb levels (n=106)|
Table 1: Frequency of presenting symptoms in patients presenting with elevated COHb levels. From Deniz et al.
Due to the non-specific signs and symptoms of carbon monoxide poisoning, the diagnosis can be delayed and mistaken for other pathologies. By sign/symptoms, here are some conditions on the differential one should consider:14-30
|Headache||Influenza||Presentation: Headache, body ache, nausea, fever, potential history of exposure.
Evaluation: Can be evaluated with Rapid Influenza test, but typically a clinical diagnosis.
Management: Can be managed with supportive care and oseltamivir if within treatment window.
|Tick Borne Illness
|Presentation: Headache, body ache, nausea, fever, history of recent travel, hiking or camping trip. Presence of a rash may help distinguish from other illness (Erythema Migrans with Lyme, or centripetal rash of Rocky Mountain Spotted Fever)
Evaluation: Possible anemia, thrombocytopenia, electrolyte abnormalities on workup. Babesiosis (Peripheral blood smear with intraerythrocytic parasites). Consider antibody levels
Management: May be managed with supportive care and antibiotics depending on specific disease.
|Intracranial Infection||Presentation: Headache, nausea, fever, photophobia, seizure, nuchal rigidity, ophthalmoplegia, altered mental status, neurological deficit; recent instrumentation or recent sinus, URI, or middle ear infection can increase risk of intracranial infection.
Evaluation: Head jolt accentuation test, papilledema, focal neurological deficit on exam. Abnormal intracranial imaging. Abnormal lumbar puncture results.
Management: May be managed with supportive care and antibiotics and/or antivirals, and/or antifungal, and/or antiparasitic and in some cases neurosurgical intervention. Consider seizure prophylaxis.
Bacterial Meningitis: Ceftriaxone, Vancomycin, +/- Ampicillin, +/- Metronidazole
Viral Meningitis(HSV): Acyclovir, Valacyclovir
Fungal Meningitis: Amphotericin B
Toxoplasmosis: Pyrimethamine + sulfadiazine
Brain Abscess: Ceftriaxone and vancomycin OR cefotaxime and metronidazole
|Presentation: Headache, altered mental status, nausea, vomiting, focal neurological deficit
Evaluation: Coagulation studies, abnormal intracranial imaging
Management: Supportive, reversal of any coagulopathy, possible neurosurgical intervention
|Idiopathic intracranial hypertension
|Presentation: Classically, young, obese female with headache, nausea, vomiting, and possible visual complaints. History may reveal use of oral contraceptives or vitamin A supplementation
Evaluation: Papilledema, increased ICP on LP
Management: Supportive, acetazolamide, steroids, and serial lumbar punctures. Possible neurosurgical intervention
|Presentation: Classically, woman over the age of 50 years with head ache, eye discomfort, jaw claudication and vision changes
Evaluation: Tender temporal artery, possible APD, elevated ESR, elevated CRP, abnormal temporal artery biopsy
Management: Steroids, ophthalmology follow-up
|Acute Mountain Sickness/High altitude cerebral edema(HACE)
|Presentation: Classically, patient with recent altitude change, presents with headache, nausea, vomiting + cerebellar, CN deficit, and altered mental status in HACE
Evaluation: Tender temporal artery, possible APD, elevated ESR, elevated CRP, abnormal temporal artery biopsy
Management: Supportive, descent, supplemental oxygen, acetazolamide, steroids
|Cyanide, Hydrogen Sulfide poisoning||Presentation: Headache, syncope, nausea, vomiting, recent exposure (housefire, explosion, sewer), possible suicide attempt
Evaluation: Elevated lactic acid
Management: Supportive, hydroxocobalamin
|Presentation: Nausea, vomiting, inebriation, altered mental status, slurred speech, paresthesia (alcoholic with vitamin deficiency)
Visual changes (Methanol)
Evaluation: Blood alcohol level, elevated lactic acid, elevated anion gap/osmolal gap (ethylene glycol, methanol), oxalate crystals (ethylene glycol)
Ethylene glycol: Fomepizole, thiamine, pyridoxine, hemodialysis
Methanol: Fomepizole, folate, hemodialysis
|Presentation: Classically, nausea, vomiting, diarrhea and either intermittent or persistent crampy abdominal pain
Evaluation: BMP, stool culture, stool O and P (consider in patient with prolonged symptoms or history suggestive of giardia exposure)
Management: Mainly supportive;
Hospitalization if severe dehydration
Invasive Diarrhea: Ciprofloxacin
C. diff: Oral vancomycin
|Acute Coronary Syndrome||Presentation: Classically, chest pain, shortness of breath associated with nausea, vomiting
Evaluation: EKG, cardiac biomarkers, cardiac catheterization,
Management: Supportive, aspirin, anticoagulation, antiplatelet, thrombolytics vs. PCI
|DKA/HHS||Presentation: Classically, patient with recent infection or noncompliance of medication presents with nausea, vomiting, abdominal pain, possibly altered mental status
Evaluation: VBG, anion gap, osmolar gap, infectious workup, ketone levels, EKGManagement: Supportive care, IV fluids, insulin, dextrose, potassium, magnesium, and treatment of potential underlying precipitant
|Dyspnea/Fatigue/Syncope||Pneumonia||Presentation: Dyspnea, fatigue, productive cough, abdominal pain, chest pain, fever
Evaluation: Chest x-ray, chest CT
Management: Supportive, antibiotics
|Congestive Heart Failure||Presentation: Dyspnea, fatigue, orthopnea, cough, edema, chest pain
Evaluation: EKG, CXR, BNP, Echo, cardiac biomarkers
Management: Supportive, diuretics, non-invasive positive pressure ventilation
|Pulmonary Embolism||Presentation: Dyspnea, fatigue, hemoptysis, chest pain
Evaluation: EKG, echo with R heart strain, CTPA, V/Q scan, cardiac biomarkers
Management: Anticoagulation, thrombolytics (shock)
|Aortic Dissection||Presentation: Dyspnea, ripping/tearing chest pain, nausea, vomiting
Evaluation: EKG, chest x-ray, CT Aorta
Management: Supportive, heart rate and blood pressure control, surgical intervention
|Presentation: Recent URI, presents with chest pain, shortness of breath, fever, nausea
Evaluation: EKG, chest x ray, echo, cardiac biomarkers
Management: Supportive care, Chrono/inotropic medications, IVIG, may need pericardiocentesis
As seen, the differential is broad with the common signs and symptoms of carbon monoxide toxicity. The history and exam, along with several diagnostic tests, can assist.
In the ED, historical clues such as winter time, exposure to CO in a fire, gas appliances in the home, and multiple patients from the same household presenting with similar symptoms can help the emergency physician narrow the differential diagnosis down to carbon monoxide poisoning. Once suspected, as always, ABCs should be evaluated and supported.
CO-Oximetry should be obtained in CO toxicity is on the differential. Elevated carbon monoxide levels via CO-Oximetry can help make the diagnosis. Because pulse oximetry cannot distinguish between carboxyhemoglobin and oxyhemoglobin, pulse oximetry readings can be normal in carbon monoxide poisoning. Patients may also have a lactic acidosis, and a lactate level should be obtained. CBC, CMP, LFT, troponin, EKG, and targeted imaging such as a chest x-ray can also be considered depending on the clinical situation. Of note, troponin may be elevated.
Once the diagnosis of carbon monoxide poisoning is made, oxygen supplementation should be started. For mild to moderate toxicity, supplemental oxygen via non-rebreather can be considered. For more severe toxicity, or in select patient populations (pregnancy), hyperbaric oxygen can be considered.12-16,30
The diagnostic and therapeutic approach can be further reviewed at http://www.emdocs.net/carbon-monoxide-poisoning/.
Of note, ACEP recently published updated recommendations for CO toxicity evaluation and management.31 The clinical policy evaluates three questions:
1) In emergency department patients with suspected acute carbon monoxide poisoning, can noninvasive carboxyhemoglobin measurement be used to accurately diagnose carbon monoxide toxicity?
– With level B evidence, the ACEP clinical policy does not recommend the use of noninvasive COHb measurement to diagnose CO toxicity with suspected acute CO poisoning.
2) In emergency department patients diagnosed with acute carbon monoxide poisoning, does hyperbaric oxygen therapy as compared with normobaric oxygen therapy improve long-term neurocognitive outcomes?
– With Level B recommendations, the authors recommend that HBO2 therapy or high-flow normobaric therapy should be used by emergency physicians for acute CO-poisoned patients but that the effects of HBO2 versus normobaric therapy on long-term neurocognitive outcomes remain unclear.
3) In emergency department patients diagnosed with acute carbon monoxide poisoning, can cardiac testing be used to predict morbidity or mortality?
– With Level B recommendations, the authors recommend that an ECG and cardiac biomarker levels be obtained in ED patients with moderate to severe CO poisoning to identify acute myocardial injury.
-Carbon monoxide poisoning can be an elusive diagnosis.
–Headache, nausea, fatigue, and chest pain are non-specific, but common complaints in patients poisoned with CO.
-Historical clues such as high risk exposure environments (garages, heaters) and multiple family members with the same symptoms can narrow the differential to CO poisoning.
-Management can include supportive care, normobaric and hyperbaric oxygen.
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