Silent, Scentless and Deadly - The Emergency Medical Minute

Silent, Scentless and Deadly

Chief Complaint:

Headache


HPI:

A family consisting of a 22-year-old female, 27- year-old male and 10 month-old male presenting to the emergency department by EMS with family with concern for headache. Female is reporting around 1612 she came home from work and was doing her hair when she began experiencing a diffuse headache that was throbbing, squeezing and non-radiating with nausea and lightheadedness. Headache is worse when standing upright and ambulating. Patient denies any visual changes, sensory changes, neck pain, photophobia, trauma, fever, thunderclap onset and can recall having a worse headache in the past. When she left the house for a several minutes she noticed that her symptoms improved. Patient does report that she did hear an atypical beeping noise in the apartment building; she suspects it may have been an alarm of some sort. Patient denies prior HA history and has taken no medications for management of symptoms. No CO detector in her specific apartment. Patient does report improvement in symptoms after leaving house and being put on O2. Patient denies CP, SOB, cough, abdominal pain, vomiting and sensory changes.
Patient noting that her son was acting abnormally; not moving around as much as he usually does, acting more lethargic and irritable and laying his head on the ground. EMS reporting that patient did appear slightly lethargic and fussy on scene but upon removal from the house began to perk up. He has had no fevers, no cough, no pulling at ears, no vomiting, no diarrhea, no change in appetite, no decreased diaper output and is up-to-date on his vaccinations.
27-year-old male began experiencing diffuse posterior head pain and nausea a few hours prior to arrival to the emergency department with significant lightheadedness. Patient reports that he has been experiencing headache for the past week and a half after being involved in a car accident, but states this headache was different from prior. Patient reports constant throbbing discomfort to the posterior head that was worse with ambulation and standing upright. Patient notes worsening lightheadedness without dizziness, visual changes, photophobia, tinnitus or sensory changes. He began experiencing some shortness of breath without chest pain or palpitations but reports feeling better after leaving his home for a few moments. Upon arriving back into his house symptoms returned. There is no carbon monoxide detector in the home but was noted to hear an alarm going off somewhere in the apartment building. After patient was placed on oxygen by EMS symptoms began improving. Patient has taken no medications for management of symptoms but does report that after his car accident he had been taking ibuprofen, Tylenol and Aleve.

Pertinent Exam Findings:

No clinically significant abnormalities

Data Interpretation:

Labs
CBC, CMP, troponin, CK and lactic acid were unremarkable.
CO level 22.4 and repeat was 5.5 for the 27 year old.
CO level 18.4 and repeat was 3.2 for the 22 year old.
CO level 13.4 and repeat was 2.5 for the 10 month old.
EKGs were unremarkable.

ED Course:

Patient placed on a non-rebreather with 100% FiO2 oxygen and given symptomatic treatment for headache. Observed in the ED for 6 hours and were symptom free.


DISCUSSION:

Background:

Carbon monoxide (CO) is a gas formed through the combustion of hydrocarbon materials, which are used everyday for fuel and energy. Exposures to CO most commonly occur as a result of fire-related smoke inhalation, although exposures from dysfunctional heating systems, poorly ventilated generators or stoves, and motor vehicle exhaust are other common exposures. CO is particularly dangerous because it is odorless, colorless, tasteless, and does not cause irritation. In vivo, the gas has about 200 times greater affinity to hemoglobin than oxygen resulting in hypoxia and ischemic injury when inhaled in sufficient quantities. CO can also cause CNS lipid peroxidation leading to delayed neurological sequelae.

CO poisoning results in approximately 50,000 emergency department visits per year with unintentional non-fire related exposures contributing 21,000 visits and 2,300 hospitalizations. The winter months in areas with cold climates see the highest incidence of CO poisoning and higher rates of CO poisoning are usually seen in areas recently affected by a hurricane. This is thought to occur due to increased use of generators and alternative heating sources that utilize hydrocarbon fuel.

Prevention of CO poisoning is the most effective means of reducing morbidity and mortality associated with an exposure. CO monitors are required in some states to detect the gas, although studies suggest only 30% of households actually use alarms in the United States. Motor vehicle related exposures have decreased since the invention of the catalytic converter and the establishment of emission standards by the Clean Air Act of 1970.

Diagnosis:

The symptoms of CO poisoning vary widely and are non-specific. A detailed history can assist in assessing for acute CO poisoning, but detecting chronic exposure tends to be more difficult. Adult patients with mild to moderate exposure present with headache, malaise, nausea, and dizziness. Altered mental status and ataxia can occur, therefore a thorough neurologic examination can aid in diagnosis. While cherry-red lips are a classic finding purported in medical literature, this finding is not very sensitive leading to many false negatives. Those with severe poisoning can present with seizures, loss of consciousness, coma, lactic acidosis, myocardial ischemia, pulmonary edema, and arrhythmias. Symptoms tend to appear sooner in young pediatric patients and the symptoms are usually nonspecific (fussiness, lethargy, poor feeding).

A pulse oximeter reading (SpO2) is not helpful in detecting CO exposure as it cannot differentiate hemoglobin bound by oxygen from that bound by CO. Alongside a detailed history and physical exam, carboxyhemoglobin levels can be measured using co-oximetry of an arterial blood gas (ABG) or venous blood gas (VBG) in hemodynamically stable patients to diagnose CO toxicity. Over 3% carboxyhemoglobin in non-smokers and over 10% carboxyhemoglobin in smokers are consistent with CO poisoning.

Management in ED:

In the setting of suspected CO poisoning, the patient should be placed on high-flow oxygen via non-rebreather, assuming they are removed from further contamination by the source of CO. In patients with altered mentation or coma, intubation and mechanical ventilation should be prioritized to provide 100% oxygen. This increases the rate at which CO is removed via the lungs by competitive inhibition of oxygen to hemoglobin. A carboxyhemoglobin level should be obtained if available, although treatment should not be delayed if the ED does not have the capability of performing this test. If the facility cannot measure a carboxyhemoglobin level, transfer to another institution with this capability, intensive care, and hyperbaric oxygen treatment should be considered. The outcomes of hyperbaric oxygen therapy tend to improve with earlier initiation. Benefit has not been proven for patients who start hyperbaric treatment 12 hours after exposure.

Hyperbaric oxygen treatment should be started in patients with:

    • Carboxyhemoglobin level >25% (20% in pregnancy).
    • Loss of consciousness
    • Severe metabolic acidosis (pH <7.1)
    • Evidence of end-organ ischemia

Most patients will not require hyperbaric treatment and will have symptom improvement in the ED after oxygen therapy for 4-5 hours. These patients can be discharged when asymptomatic or when the carboxyhemoglobin level falls below 10%. If the patient’s CO poisoning is due to smoke-inhalation, consider evaluating for concomitant cyanide toxicity as well. Alongside managing the CO toxicity and possible cyanide toxicity, it is important to perform a psychiatric assessment of the patient to determine whether the exposure was intentional or unintentional. For more severe poisonings, consider obtaining an EKG and troponin to evaluate for myocardial ischemia.

Prognosis:

Prognosis of CO poisoning is generally thought to be correlated with the amount of CO to which the patient is exposed, the duration of the exposure, and their underlying risk factors. Poor outcomes are more common in those with long exposure times, advanced age, and loss of consciousness secondary to the exposure. Neurological sequelae, such as cognitive changes, psychosis, personality changes, incontinence, and Parkinsonism, occur in 10-32% of people recovering from CO exposure. These symptoms have been reported to manifest up to 240 days after initial exposure. Fortunately, 50-75% of patients recover fully within one year. One-third of cases in a retrospective study of patients with moderate to severe CO poisoning were found to have evidence of myocardial ischemia, which doubled the mortality in those with CO exposure.

Non-fire related CO poisoning is one of the leading causes of poisoning deaths in the United States and accounts for approximately 1,200 deaths per year. Of these, about 400 are unintentional and the rest are a result of intentional poisoning. The overall mortality of CO poisoning is between 1%-3%, with a higher mortality rate due to intentional exposure than unintentional exposure.

Differential Diagnoses:

    • Alcohol Intoxication
    • Acute Viral Syndrome
    • Depression, Suicidal Ideation
    • DKA
    • Encephalitis
    • Hypothyroidism
    • Meningitis
    • Migraine Headache
    • Opioid Intoxication
    • SAH
    • Tension Headache

Clinical Pearls:

    • If you suspect CO poisoning, start high-flow oxygen via non-rebreather and check a carboxyhemoglobin level.
    • Don’t be fooled by a normal pulse oximeter reading in patients with concern for CO poisoning.
    • Consider hyperbaric oxygen therapy in patients with significant acidosis, very elevated carboxyhemoglobin levels, loss of consciousness, and evidence of end-organ ischemia.
    • Remember to evaluate for psychiatric disorders and smoke inhalation injuries.

References:

  1. Blumenthal I. Carbon monoxide poisoning. J R Soc Med. 2001;94(6):270-272. doi:10.1177/014107680109400604
  2. Sircar K, Clower J, Shin MK, Bailey C, King M, Yip F. Carbon monoxide poisoning deaths in the United States, 1999 to 2012. Am J Emerg Med. 2015;33(9):1140-1145. doi:10.1016/j.ajem.2015.05.002
  3. Yoon SS, Macdonald SC, Parrish RG. Deaths from unintentional carbon monoxide poisoning and potential for prevention with carbon monoxide detectors. JAMA. 1998;279(9):685-687. doi:10.1001/jama.279.9.685
  4. Harper A, Croft-Baker J. Carbon monoxide poisoning: undetected by both patients and their doctors. Age Ageing. 2004;33(2):105-109. doi:10.1093/ageing/afh038
  5. Satran D, Henry CR, Adkinson C, Nicholson CI, Bracha Y, Henry TD. Cardiovascular manifestations of moderate to severe carbon monoxide poisoning. J Am Coll Cardiol. 2005;45(9):1513-1516. doi:10.1016/j.jacc.2005.01.044
  6. Touger M, Gallagher EJ, Tyrell J. Relationship between venous and arterial carboxyhemoglobin levels in patients with suspected carbon monoxide poisoning. Ann Emerg Med. 1995;25(4):481-483. doi:10.1016/s0196-0644(95)70262-8
  7. Hampson NB. U.S. Mortality Due to Carbon Monoxide Poisoning, 1999-2014. Accidental and Intentional Deaths. Ann Am Thorac Soc. 2016;13(10):1768-1774. doi:10.1513/AnnalsATS.201604-318OC
  8. Tibbles PM, Perrotta PL. Treatment of carbon monoxide poisoning: a critical review of human outcome studies comparing normobaric oxygen with hyperbaric oxygen. Ann Emerg Med. 1994 Aug;24(2):269-76. doi: 10.1016/s0196-0644(94)70141-5. PMID: 8037395.
  9. Olson K, Smollin C. Carbon monoxide poisoning (acute). BMJ Clin Evid. 2008;2008:2103. Published 2008 Jul 23.

Authors

Aaron Wolfe, DO, FACEP

Jackson Roos, MSIV

John Spartz, MSIII

 

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