A 6-month-old boy was brought to the emergency department by his parents for seizure activity just prior to arrival. They reported that the baby had been feverish for two days, and was evaluated in a different ED. He was given Tylenol there.
The growth plate in rickets is thickened and disorganized, with a large zone of hypertrophic cartilage cells. An irregular perforation of the cartilage plate by osteoclasts appears because there is little calcified cartilage. The woven bone on the surface of some of the primary trabeculae is unmineralized and will be easily fractured. Such microfractures often lead to hemorrhage at the interface between the plate and the metaphysis.
Dr. Park (pictured) is an assistant professor of emergency medicine at the University of Kansas Medical Center. Dr. Hunter is a third-year emergency medicine resident there.
By Punam Patel, DO, & Steven Sattler, DO
A 62-year-old Caucasian woman presented to the emergency department with palpitations that had started that morning. She had no history of similar symptoms and denied medications, allergies, and alcohol or drug use. She had quit smoking cigarettes 13 years earlier.
She initially denied all other symptoms, but staff overheard the patient and spouse complaining of headaches. They reported that they had been awakening with headaches and fatigue since moving into a new home a week earlier.
Vital signs upon arrival were respiration, 20 breaths per minute; heart rate, 156 beats per minute; blood pressure, 113/78 mm Hg, and temperature 97F orally. Physical exam showed a well-appearing woman in no acute distress with a rapid irregularly irregular heartbeat. The rest of the physical exam was normal.
An electrocardiogram showed AF with rapid ventricular response, a PVC, and a prolonged QTc. (Figure 1.) Laboratory results including complete blood count, basic metabolic panel, cardiac enzymes, and TSH were unremarkable. The COHb level was 22.2% of total hemoglobin. A chest radiograph was normal. The patient was started on high-flow oxygen therapy. The heart rate was controlled with Diltiazem 15 mg IVP followed by Diltiazem 90 mg PO.
The patient’s symptoms resolved with a repeat electrocardiogram that displayed normal sinus rhythm. (Figure 2.) A hyperbaric therapy-equipped institution was consulted, but we decided not to transfer her because her symptoms had resolved. The fire department was notified of the case to ensure a safe return home.
Cardiology was consulted, and an echocardiogram was normal. The patient was monitored in a telemetry unit overnight with no further episodes of AF. The patient was discharged on Diltiazem CD 120 mg PO daily and scheduled to follow up with her cardiologist. Diltiazem was discontinued shortly after discharge with no recurrence of AF. No signs of delayed neurological sequelae were reported, and the CO culprit was a faulty furnace.
Carbon monoxide intoxication is the leading cause of unintentional poisoning deaths in the United States. CO is a colorless, odorless, tasteless but highly toxic gas byproduct from incomplete combustion of hydrocarbon fuels. (J Neurol Sci 2007;262:122.) Lacking a unique clinical vignette, CO poisoning is a challenging diagnosis that is often missed.
CO when inhaled is readily absorbed from the lungs to the bloodstream forming a tight but slowly reversible complex with hemoglobin (Hb) known as carboxyhemoglobin (COHb). (Toxicology 2000;145:1.) CO easily displaces oxygen because the affinity of hemoglobin for CO is 210 times its affinity for oxygen. The reduced oxygen-carrying capacity results in tissue hypoxia and impaired cellular oxidative metabolism. The organs with the highest demand for oxygen such as the brain and the heart are more vulnerable to injury.
Clinical manifestations of CO poisoning range from mild to severe. Early symptoms include fatigue, headache, dizziness, confusion, nausea, and vomiting. Moderate symptoms include ataxia, tachypnea, palpitations, and chest pain. Hypotension, cardiac arrhythmias, myocardial ischemia, respiratory depression, seizures, and coma indicate severe intoxication.
The clinical symptoms of CO poisoning are often nonspecific, and can mimic a variety of common disorders. The severity ranges from mild flu-like symptoms to coma and death. (J Neurol Sci 2007;262:122.) A high index of suspicion and detailed history are essential to make this diagnosis. A delayed or incorrect diagnosis can mean poor outcomes for the patient and cohabitants.
The clinical spectrum of cardiac involvement in patients with carbon monoxide intoxication is broad, and may encompass cardiomyopathy, unstable angina, myocardial infarction, arrhythmias, heart failure, myocardial stunning, cardiogenic shock, and sudden death. (Clin Biochem 2012;45[16-17]:1278.) Chronic exposure to CO can induce myocardial injury and fibrosis while acute exposure is associated with arrhythmias that may lead to sudden death. (J Mol Cell Cardiol 2012;52:359.)
Myocardial injury is attributed to tissue hypoxia from hemoglobin’s extremely high affinity for CO, but this does not explain the cause of arrhythmias because COHb levels do not correlate to electrocardiogram changes. (J Mol Cell Cardiol 2012;52:359.) QT dispersion and variability, which reflect ventricular repolarization, and P-wave dispersion as a marker of sinoatrial conduction, are pathologically increased with CO exposure. (Respir Physiol Neurobiol 2012;184:204.) These electrocardiographic disturbances are directly linked to increased susceptibility of AF, premature ventricular contractions, and lower threshold for developing ventricular fibrillation observed after CO poisoning. (Respir Physiol Neurobiol 2012;184:204.) A detailed investigation of the effects of CO on ion channel activity is needed. (J Mol Cell Cardiol 2012;52:359.)
Carbon monoxide is eliminated through the lungs; its typical half-life is three to four hours. High-flow 100% oxygen therapy reduces the half-life to 30 to 60 minutes and hyperbaric oxygen therapy at 2.5 atm to 15 to 23 minutes. (Clin Biochem 2012;45[16-17]:1278.) The initial mainstay treatment for carbon monoxide toxicity is 100% oxygen at normal barometric pressure. HBO is recommended for severe poisoning regardless of CO level.
The specific requirements for normobaric versus hyperbaric treatment and their outcomes is a continued topic of debate. (Toxicology 2000;145:1.) A clinical policy statement by the American College of Emergency Physicians concluded that HBO is a treatment option but cannot be mandated; they failed to identify clinical variables where HBO would prove beneficial or harmful. (Ann Emerg Med 2008;51:138.) A Cochrane review concluded that existing evidence does not show that HBO decreases the incidence of adverse neurological sequelae. (Cochrane Database Syst Rev 2011 Apr 13:CD002041.) Pregnancy was an exclusion criterion in most randomized trials, but should always be considered because of potential benefit for mother and fetus. (Crit Care Clin 2012;28:537.)
This case illustrates the high index of suspicion required to link a new arrhythmia to CO poisoning. The complaint that led to the diagnosis of CO poisoning was initially missed in our case, and it could have easily resulted in misdiagnosis. Arrhythmias are commonly referred to as an effect of CO, but reports of CO-induced AF with resolution after oxygen therapy are limited.
Dr. Patel is a second-year emergency medicine resident, and Dr. Sattler is an emergency physician and the associate research director at Good Samaritan Hospital Medical Center, West Islip, NY.
Figure 1. Electrocardiogram showing atrial fibrillation on presentation to the ED.
Figure 2. Electrocardiogram showing normal sinus rhythm 22 hours after first presentation.
Emergency Medicine Residency Program. Dr. Khan is
a clinical instructor in emergency medicine at Stanford
Elevated acute phase reactants (ESR, CRP)
Prolonged PR interval
Positive throat culture of rapid streptococcal antigen test
Elevated or rising streptococcal antibody titer