A 44-year-old previously healthy man is brought to the emergency department in early December by his girlfriend due to confusion. When the girlfriend went to the patient's mobile home yesterday, she found him feeling unwell with headache, nausea, and dizziness. The patient did not seek medical care because he began feeling better after they went out later in the day. This morning when the girlfriend went back, the patient was confused and disoriented on the bed. He had also urinated on himself. Temperature is 36.8 C (98.2 F), blood pressure is 140/84 mm Hg, pulse is 92/min, and respirations are 20/min. Oxygen saturation is 96% on room air. On physical examination, the patient is somnolent but rouses to voice. Pupils are equal and briskly reactive. There is no facial droop, but a small laceration on the lateral border of the tongue is present. The lungs are clear on auscultation and heart sounds are normal. The abdomen is nondistended, soft, and nontender. Extremities are without edema or cyanosis. Muscle strength and deep tendon reflexes are normal throughout and there is no neck stiffness. Fingerstick blood glucose is 118 mg/dL and non-contrast CT scan of the head is normal. What is the best next step in management?
Carbon monoxide poisoning | |
Epidemiology |
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Manifestations | Mild-moderate
Severe
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Diagnosis |
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Treatment |
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ABG = arterial blood gas. | |
This patient likely has acute carbon monoxide (CO) poisoning. Unintentional CO poisonings most commonly result from smoke inhalation (eg, house fires) or from faulty indoor heating systems during the winter months. Following inhalation, CO binds to hemoglobin with great affinity, readily displacing oxygen (O2) to create carboxyhemoglobin. This both reduces O2-carrying capacity and causes a left shift in the hemoglobin dissociation curve to decrease O2 unloading in the tissues. CO also impairs O2 utilization via disruption of mitochondrial oxidative phosphorylation.
Accordingly, patients with excessive CO exposure develop manifestations of cerebral hypoxia, including headache, nausea, dizziness, and confusion. Severe intoxication can cause myocardial ischemia, seizure (evidenced by urinary incontinence and lateral tongue biting in this patient), coma, and death. Patients sometimes have "cherry red" mucous membranes caused by high carboxyhemoglobin levels.
Pulse oximetry shows normal O2 saturation because it cannot differentiate between oxyhemoglobin and carboxyhemoglobin. Diagnosis is best confirmed via co-oximetry of arterial blood gas showing elevated carboxyhemoglobin levels (>3% for nonsmokers, >10% for smokers) in a symptomatic patient. Initial treatment with 100% O2 by nonrebreather facemask increases blood O2 level and enhances the rate of CO removal via the lungs.
(Choice B) This patient's seizure (eg, tongue laceration, urinary incontinence) was likely due to CO poisoning. Electroencephalogram findings in CO poisoning are nonspecific and would not help make the diagnosis or change management.
(Choice C) Lumbar puncture is used to evaluate for encephalitis or meningitis, which can cause headache, seizure, and confusion but are unlikely in the absence of fever (encephalitis, meningitis) or neck rigidity (meningitis). Furthermore, the patient's symptoms would not have improved when he left the mobile home for a walk (unlike symptoms of CO poisoning).
(Choice D) MRI is more sensitive than CT scan for detecting early acute stroke; however, stroke is less likely in this patient with confusion in the absence of focal neurologic findings (eg, focal weakness, abnormal reflexes).
(Choice E) Hepatic encephalopathy can cause somnolence but is less likely in this patient with no hyperreflexia (eg, asterixis) or findings of advanced liver disease (eg, abdominal distension, peripheral edema). Also, due to significant variability in levels, serum ammonia testing should not be used to diagnose hepatic encephalopathy.
Educational objective:
Carbon monoxide poisoning can occur due to faulty indoor heating systems during the winter months. Both oxygen delivery and usage are disrupted, causing clinical manifestations of cerebral hypoxia (eg, headache, confusion, seizure, coma, death). Diagnosis is made by co-oximetry of arterial blood gas showing an elevated carboxyhemoglobin level, and treatment is with 100% oxygen.