Author Credentials and Financial Disclosure: Daniel K. Mullin, MD, is a Clinical Instructor of Emergency Medicine at Drexel University College of Medicine in Philadelphia.
Dr. Mullin has disclosed that he has no financial interests in or relationships with any commercial companies pertaining to this educational activity.
Learning Objectives: After reading this article, the physician should be able to:
1. Summarize the common causes of pneumonia in children based on their age and the recommended appropriate empiric treatment plans.
2. Describe the typical electrocardiographic patterns seen in acute ST-segment elevation myocardial infarctions and recognize the common arrhythmias and conduction diseases associated with acute myocardial infarctions.
3. Discuss the typical presentation of a gamma hydroxybutyric acid intoxication and the treatment approach.
Release Date: August 2007
Community-Acquired Pneumonia in Children
N Engl J Med
Community-acquired pneumonia is a common and potentially serious infection in children. For the purposes of this review, pneumonia is defined as the presence of fever, acute respiratory symptoms, or both, plus evidence of parenchymal infiltrates on chest x-ray. This definition differs from that of the World Health Organization which defines it solely on the basis of clinical findings.
The exact microbiologic cause for most cases of pneumonia has been difficult to decipher. That said, studies appear to demonstrate that they're usually caused by respiratory viruses (respiratory syncytial virus, influenza A or B, parainfluenza, adenovirus, and rhinovirus), Mycoplasma pneumoniae, Chlamydia pneumonia, Streptococcus pneumoniae, or Haemophilus influenza. The role of S. pneumoniae in causing pneumonia in children appears to be more important than previously thought. This has been demonstrated by a 35 percent reduction in incidence of the disease with the recent introduction of the pneumococcal conjugate vaccine now given to all children in Europe and the United States.
The diagnosis of pneumonia can be made by clinical features such as fever, cough, and tachypnea, with or occasionally without an infiltrate seen on chest radiograph. Studies have repeatedly demonstrated the challenge in differentiating viral from bacterial pneumonias in children, even based on clinical features and chest radiographs. Two studies found, however, that wheezing occurs more often in viral pneumonia. Other studies have shown that the finding of an alveolar (lobar) infiltrate on chest x-ray is a specific but insensitive indication of a bacterial infection.
Treatment decisions should be based on diagnostic algorithms that begin with the age of the child, then consider clinical and epidemiologic factors, and finally take into account the results of chest radiography.
Pneumonia during the first three weeks of life is uncommon, but when it occurs is usually related to perinatally associated infections (Group B streptococci, gram-negative enteric bacteria, and L. monocytogenes). Children should be admitted and started on ampicillin and gentamicin, with or without cefotaxime. Between 3 weeks and 3 months, pneumonia is usually caused by respiratory syncytial virus, but also can be caused by C. trachomatis, S. pneumoniae, and occasionally B. pertussis. Treatment consists of a macrolide (erythromycin or azithromycin), with the addition of cefotaxime if the child is ill or has a lobar infiltrate on chest radiograph.
From 4 months to 4 years of age, the viruses are the most common cause of pneumonia, but S. pneumoniae causes the majority of bacterial cases, especially when there is a lobar infiltrate on the chest x-ray. If treated as an outpatient, high-dose amoxicillin (80–100 mg/kg/day) is appropriate. If treated as an inpatient, treatment should consist of IV ampicillin or a third-generation cephalosporin. For children in the 5- to 15-year age group, M. pneumoniae is the most likely etiologic agent, however C. pneumoniae and S. pneumoniae also appear to cause disease. Treatment should consist of a macrolide or doxycycline (if over age 8), with the addition of either ampicillin or a third-generation cephalosporin if admitted.
Use of the Electrocardiogram in Acute Myocardial Infarction
Zimetbaum PJ, Josephson ME
N Engl J Med
The electrocardiogram plays a crucial role in diagnosing and managing patients presenting with acute myocardial infarction (AMI). More specifically, patients presenting with specific patterns of ST-segment elevation on their ECGs in the correct scenario require rapid reperfusion therapy with either intravenous thrombolysis or through percutaneous intervention. Additionally, electrocardiographic signs of reperfusion represent an important marker of microvascular blood flow and prognosis. The ECG also is crucial for identifying new conduction disturbances and arrhythmias that influence short- and long-term outcomes.
The culprit vessel in inferior myocardial infarction may be either the right coronary artery (in 80 percent of cases) or the left circumflex artery. Greater ST-segment elevation in lead III than in lead II and ST-segment depression in leads I and aVL suggest involvement of the right coronary artery. ST-elevation that is greater in lead II than lead III and ST-segment depression in leads V1 and V2 (posterior MI) suggest involvement of the left circumflex artery, but the posterior MI pattern also may be seen with sudden occlusion of a dominant right coronary artery. A right ventricular MI is always associated with occlusion of the proximal segment of the right coronary artery. The most sensitive ECG finding for this is ST-segment elevation of more than 1 mm in lead V4R with an upright T wave in the same lead. In an anterior wall MI, ST-segment elevation in leads V1-V3 indicate occlusion of the left anterior descending artery.
When there is a spontaneous left bundle branch block or one induced by a right ventricular paced rhythm, the normal ECG changes that occur during an AMI are obscured. Because of this, patients with new left bundle branch blocks and symptoms consistent with an AMI are treated as if they have an ST-segment elevation MI. Another important indicator of myocardial infarction in the presence of a previously known left bundle branch block is primary ST change. That means physicians should look for ST-segment deviation in the same (concordant) direction as the major QRS vector. This should be rather apparent to the astute physician because the ST-segments tend to be obviously discordant when a left bundle branch pattern is present. Extremely discordant ST deviation (> 5 mm) is also suggestive of myocardial infarction in the presence of left bundle branch block.
After reperfusion therapy is performed, resolution of ST-segment elevation is believed to be an excellent marker of tissue perfusion. The absence of tissue perfusion is the most important predictor of impaired ventricular function and the risk of death after an AMI. The assessment of ST-segment resolution also is useful for guiding reperfusion therapy, and the absence of ST-segment resolution during the first 90 minutes after the administration of thrombolytics should prompt consideration for rescue angioplasty. A reduction of more than 70 percent in ST-segment elevation is associated with the most favorable outcomes. Other ECG markers of reperfusion include T-wave inversion within four hours of the AMI. T-wave inversion that develops after four hours is part of the normal ECG progression of MI. An accelerated idioventricular rhythm (defined as a heart rate of 60 to 120 beats per minute initiated by late, coupled ventricular premature depolarization) is a highly specific marker of reperfusion. It is also a benign rhythm, and should not be suppressed.
Conduction abnormalities during AMI are common, but less so now in the era of early revascularization. Conduction abnormalities in association with inferior MI can occur immediately or hours to days after the infarct. Sinus bradycardia or varying degrees of heart block (including complete) usually occur due to heightened vagal tone. These conditions often resolve and are very responsive to atropine.
Complete atrioventricular block is generally associated with a narrow complex escape rhythm between 40 to 60 beats per minute. It is generally transient and usually resolves within five to seven days. Conduction disease associated with an anterior MI is not related to heightened vagal tone but rather to necrosis of the intramyocardial conduction system. This occurs almost exclusively in the presence of proximal occlusion of the left anterior descending artery and usually portends a worse prognosis.
Finally, ventricular premature depolarizations are common during AMI, but do not predict the subsequent development of sustained ventricular arrhythmias. Anti-arrhythmics should not be given in an attempt to suppress these premature ventricular contractions.
Gamma Hydroxybutyric Acid (GHB) Intoxication
Mason PE, Kerns WP
Acad Emerg Med
GHB is a naturally occurring analog of gamma-aminobutyric acid (GABA). In the 1960s and 1970s, GHB was used as a general anesthetic agent, but fell out of favor due to abnormal EEG patterns that developed. Now the only FDA-approved indication for GHB is for treating narcolepsy. Over the past decade or so, GHB became very popular as a dietary supplement and recreational drug.
GHB is naturally found in the brain, but after typical doses, its levels increase by 100- to 500-fold. The principal clinical effect of GHB is CNS depression. This neurodepressant effect appears to be mediated by several mechanisms including binding to a specific GHB receptor, binding to GABA receptors, and modulating GABA levels. Peak blood levels after oral administration occur in 15 to 45 minutes with a peak clinical effect at 30 to 60 minutes post-ingestion.
GHB was touted for years as a bodybuilding supplement, and it became popular among bodybuilders. The recreational use of GHB started to rise in the 1990s, especially in the underground parties know as raves. It became popular because it induced a euphoric state that is not associated with any residual hangover effects. Additionally, because of its short-lived hypnotic effects, relative safety, and fact that it cannot be detected on routine drug screens, it became a means of assault, particularly in date rape. In March 2000, GHB was added to the list of Schedule I substances by the DEA.
The primary clinical manifestations of GHB intoxication are CNS and respiratory depression. One feature of GHB intoxication is the almost universal presence of co-intoxicants, often multiple, that cloud the clinical picture. The typical GHB patient is a white man in his mid- to late 20s with a clear history of ingestion. Minor effects include ataxia, nystagmus, somnolence, and aggression. The cardinal manifestation of GHB intoxication is CNS depression, often presenting as coma. A resolution of symptoms occurs abruptly, with patients going from unresponsive to agitated and combative over very short periods of time.
Many times, the CNS depression and respiratory depression are so bad that the patients require intubation. Several case series have demonstrated an intubation rate of up to 50 percent, with mean intubation time of about three hours. Because of GHB's short half-life, many patients can be extubated and discharged from the emergency department. Patients who do not recover in six hours are atypical of GHB intoxication, and an alternative diagnosis should be sought. The outcome in GHB overdose is typically good, provided the patient doesn't die before receiving medical care.
Although rare, GHB withdrawal can be extremely serious with symptoms similar to ethanol and benzodiazepine withdrawal. Benzodiazepines are the mainstay of therapy and often require exceptionally large doses. Symptoms may start within several hours of cessation and last for five to 15 days.
About the LLSA
As part of its continuous certification program, the American Board of Emergency Medicine has developed the Lifelong Learning and Self-Assessment (LLSA) program to promote continuous education of diplomates. Each year, beginning in 2004, 16 to 20 articles are chosen based on the Emergency Medicine Model. A list of these articles can be found on the ABEM web site, www.abem.org.
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CME Participation Instructions
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