Carbon Monoxide Poisoning
A 72-year-old man was brought to the ED by paramedics with inability to move his left leg and difficulty speaking. The patient had been heating his home with a generator placed inside the house during an ice storm, and paramedics reported a strong smell of gas inside the house.
The patient was unable to describe the time of onset of his symptoms. He complained of headache, slurred speech, and inability to move his left leg. He also said he felt the urge to urinate, but was unable to do so. He denied chest pain or shortness of breath. His medical history was significant only for hypertension, which was controlled with hydrochlorothiazide and lisinopril. He admitted to smoking a few cigarettes daily, but denied any alcohol use.
On physical examination, the patient’s vital signs were: blood pressure (BP) 162/98 mm Hg; heart rate (HR), 110 beats/minute; respiratory rate (RR), 20 breaths/minute; and temperature (T), 98.6˚F. The patient had 100% oxygen (O2) saturation on 4L O2 via nasal cannula. The head, eyes, ears, nose, and throat examination was normal. There was no facial droop; his speech was slurred, but he was easily understandable. The cardiopulmonary examination revealed tachycardia without murmurs, rubs, or gallop; the lungs were clear to auscultation bilaterally. The neurological examination revealed 5/5 motor strength in the upper extremities and symmetrical; there was no pronator drift. The left leg had 2/5 motor strength compared to 5/5 in the right lower extremity. There was also fullness and tenderness over his suprapubic region.
The emergency physician (EP) ordered a complete blood count, basic metabolic profile, carboxyhemoglobin (COHb) test, electrocardiogram (ECG), portable chest X-ray (CXR), and a noncontrast computed tomography (CT) scan of the head. Since the history and physical examination suggested urinary retention, a Foley catheter was placed; a total of 1,200 cc of clear urine was obtained, after which the patient expressed a feeling of relief.
The patient’s COHb level was 8.5%. The portable CXR and CT scan of the head were both reported as normal by the radiologist. Likewise, the results of the rest of the laboratory evaluation were normal. The ECG revealed sinus tachycardia without evidence of strain or injury.
The EP diagnosed an acute cerebrovascular accident (CVA) and admitted the patient to the hospital. He did not feel that carbon monoxide (CO) contributed to the event given the low level in a cigarette smoker. After an uneventful hospital stay, the patient was transferred to a physical rehabilitation unit. He was ultimately discharged with a neurogenic bladder and weak left leg.
The patient sued the EP for negligence in the failure to diagnose CO poisoning and prompt initiation of 100% O2 therapy. The EP argued that CO poisoning had been properly ruled out and that the diagnosis of CVA was correct. The defense also claimed that even if the patient had suffered CO poisoning, the length of the exposure would have led to the same outcome. A defense verdict was returned.
Carbon monoxide poisoning is one of the leading causes of poisoning morbidity and mortality in the United States. This is in part due to the fact that CO is a colorless, odorless, and tasteless gas. The peak incidence for CO poisoning is in the fall and winter, when people are more likely to use space heaters, wood burning stoves, or portable generators inside without adequate ventilation.
The clinical presentation of CO poisoning can range from mild (eg, headache, flu-like symptoms) to devastating (eg, coma, death). The central nervous system is the organ system that is most sensitive to CO poisoning. Symptoms can range from a dull frontal headache, dizziness, and ataxia, to syncope, seizures, focal neurological deficit, and coma. In fact, the most serious complication of CO poisoning may be persistent or delayed neurological or neurocognitive sequelae, which can occur in up to 50% of patients with symptomatic acute poisoning.1 Unfortunately, COHb levels and symptoms do not always correlate well. In fact, particular COHb levels are not predictive of symptoms or outcome.1
The treatment for CO poisoning consists of administering 100% O2 as soon as the diagnosis is considered. If 100% O2 is administered, the half-life of COHb can be reduced from 5 hours (room air) to approximately 1 hour.1 While some argue that treatment with hyperbaric O2 (HBO) therapy should be considered standard of care, it has not yet been determined which patient population benefits from HBO therapy; moreover, there is currently no established optimum timing of therapy. Regardless, the jury came to the correct decision in this case as it is impossible to determine, with any degree of medical certainty, if the patient’s neurological deficits were due to the natural course of an ischemic stroke, or if CO contributed to or was the sole cause of the CVA.