Practice Guidelines

Joint Guideline Released for Atrial Fibrillation

AMBER HUNTZINGER

Atrial fibrillation is the most common arrhythmia in clinical practice and causes substantial morbidity and mortality. The prevalence of the condition is estimated to be 0.4 to 1 percent, and atrial fibrillation hospitalizations have increased by more than 60 percent over the past two decades. The condition is associated with increased risk of stroke, heart failure, and all-cause mortality. Although atrial fibrillation is commonly associated with structural heart disease, many patients have no detectable heart disease. This guideline assists physicians in clinical decision making by describing options for the diagnosis and management of atrial fibrillation.

Evaluation

The clinical evaluation of patients with suspected atrial fibrillation (Table 1) includes characterizing the arrhythmia pattern as paroxysmal or persistent, determining its cause, and defining associated cardiac and extracardiac factors. The evaluation usually can be completed in one outpatient visit, unless the rhythm pattern cannot be specifically documented and additional monitoring is needed.

Table 1. Clinical Evaluation in Patients with Atrial Fibrillation

Minimal evaluation History and physical examination to define: Presence and nature of symptoms associated with atrial fibrillation Clinical type of atrial fibrillation (e.g., first episode, paroxysmal, persistent, permanent) Onset of the first symptomatic attack or date of discovery of atrial fibrillation Frequency, duration, precipitating factors, and modes of termination of atrial fibrillation Response to pharmacologic agents that have been administered Presence of underlying heart disease or other reversible factors (e.g., hyperthyroidism, alcohol consumption) Electrocardiography To identify: Rhythm (verify atrial fibrillation) Left ventricular hypertrophy P-wave duration and morphology or fibrillatory waves Preexcitation Bundle branch block Prior myocardial infarction Other atrial arrhythmias To measure R-R, QRS, and Q-T intervals in conjunction with antiarrhythmic drug therapy Transthoracic echocardiography to identify: Valvular heart disease Left and right atrial size Left ventricular size and function Peak right ventricular pressure (pulmonary hypertension) Left ventricular hypertrophy Left atrial thrombus (low sensitivity) Pericardial disease Blood tests (for a first episode of atrial fibrillation, when the ventricular rate is difficult to control) to evaluate thyroid, renal, and hepatic function Additional testing (one or several tests may be necessary) Six-minute walk test (if the adequacy of rate control is in question) Exercise test (if the adequacy of rate control is in question [permanent atrial fibrillation]) To reproduce exercise-induced atrial fibrillation To exclude ischemia before treatment of selected patients with a type IC* antiarrhythmic drug Holter monitor test or event recording (if diagnosis of the type of arrhythmia is in question) to evaluate rate control Transesophageal echocardiography To identify left atrial thrombus (in the left atrial appendage) To guide cardioversion Electrophysiologic study To clarify the mechanism of wide-QRS-complex tachycardia To identify a predisposing arrhythmia (e.g., atrial flutter, paroxysmal supraventricular tachycardia) To seek sites for curative ablation or atrioventricular conduction block/modification Chest radiography to evaluate lung parenchyma and pulmonary vasculature, when clinical findings suggest an abnormality

*-Type IC refers to the Vaughan Williams classification of antiarrhythmic drugs. Source: American Heart Association.

Physical examination findings suggestive of atrial fibrillation include irregular pulse, irregular jugular venous pulsations, variations in the intensity of the first heart sound, or absence of a fourth heart sound heard previously during sinus rhythm. A diagnosis must be confirmed with electrocardiography (ECG). Patients diagnosed with atrial fibrillation should receive two-dimensional Doppler echocardiography to assess left atrial and ventricular dimensions and left ventricular wall thickness and function and to exclude valvular heart disease and pericardial disease. Thyroid, renal, and hepatic functions should be measured during the evaluation.

If necessary, additional testing may include exercise or walking tests, a Holter monitor test or event recording, transesophageal echocardiography, and chest radiography.

Prevention of Thromboembolism

Antithrombotic therapy to prevent thromboembolism is recommended for patients with atrial fibrillation unless the patient does not have heart disease or has contraindications to antithrombotic therapy. ECG may detect risk factors; however, the test's value for stratifying risk is limited because it is unclear whether the absence of abnormalities suggests low risk. Table 2 is a guideline for determining antithrombotic therapy in patients with atrial fibrillation. It is reasonable to regularly reevaluate the need for anticoagulation.

Table 2. Antithrombotic Therapy for Patients with Atrial Fibrillation
Risk factors
Weaker (or less validated) 65 to 74 years of age Coronary artery disease Female sex Thyrotoxicosis	Moderate 75 years or older Diabetes Hypertension Heart failure Left ventricular ejection fraction of 35 percent or less	High Mitral stenosis Previous stroke, transient ischemic attack, or embolism Prosthetic heart valve*
Risk category		Recommended therapy
No risk factors		Aspirin (81 to 325 mg daily)
One moderate risk factor		Aspirin (81 to 325 mg daily) or warfarin (Coumadin; INR 2.0 to 3.0, target 2.5)*
Any high risk factor or more than one moderate risk factor		Warfarin (INR 2.0 to 3.0, target 2.5)*
INR = International Normalized Ratio. *-If patient has a mechanical valve, target INR is greater than 2.5. Source: American Heart Association.

anticoagulation agents

Therapy should be based on the patient's risk of stroke and bleeding. Patients with atrial fibrillation and a high risk of stroke who do not have a mechanical heart valve should receive a vitamin K antagonist. Aspirin is an alternative to a vitamin K antagonist in low-risk patients or in those who have contraindications to vitamin K antagonists.

The intensity of anticoagulation should be based on prevention of ischemic stroke versus avoidance of hemorrhagic complications. The recommended target is an International Normalized Ratio (INR) of between 2.0 and 3.0. INR should be measured at least weekly during therapy and monthly when anticoagulation is stable. Minimizing the risk of bleeding is particularly important in older patients.

interruption of anticoagulation

If anticoagulation is interrupted for more than one week because of surgery in high-risk patients, unfractionated or low-molecular-weight heparin may be administered to prevent thrombosis, although the effectiveness of these therapies has not been evaluated in controlled trials.

In patients undergoing percutaneous coronary intervention, anticoagulation may be interrupted to prevent bleeding; however, vitamin K anticoagulation should be reinstated as soon as possible after the procedure. Platelet-inhibitor drugs are valuable for preventing recurrent myocardial ischemia in patients undergoing percutaneous coronary intervention. Although aspirin may be given during the hiatus, maintenance therapy should consist of clopidogrel (Plavix) and warfarin (Coumadin); warfarin may be continued as monotherapy after nine to 12 months if no coronary events occur.

Cardioversion

Cardioversion (via drugs or electric shock) may be used to restore sinus rhythm in patients with persistent atrial fibrillation; however, there is a risk of thromboembolism unless anticoagulation is initiated before the procedure. Cardioversion is recommended for hemodynamically stable patients with atrial fibrillation symptoms that the patient feels are unacceptable (Figure 1). Recommended agents for pharmacologic cardioversion of atrial fibrillation are flecainide (Tambocor), dofetilide (Tikosyn), propafenone (Rythmol), and ibutilide (Corvert). Direct-current cardioversion is recommended if rapid ventricular response does not occur with pharmacologic cardioversion in patients with ongoing myocardial ischemia, symptomatic hypotension, angina, or heart failure.

AAN Releases Recommendations for the Diagnostic Evaluation of the Child with Status Epilepticus

LISA GRAHAM

Status epilepticus is a life-threatening condition that requires timely recognition and immediate treatment in children and adults. There are many definitions of status epilepticus, but the one most commonly accepted is 30 minutes of continuous seizures or two or more seizures in a row without full recovery of consciousness between seizures. Status epilepticus can be categorized based on the type and etiology of the seizure (Table 1), with type being determined by the origin of epileptic discharge (i.e., focal or generalized); however, if there is insufficient information available, the seizure is indeterminate or unclassifiable.

Table 1. Classification of Status Epilepticus
Type*	Definition	Examples
Remote symptomatic (33%)	SE occurring without an acute provocation in a patient with a history of CNS insult (e.g., chronic encephalopathy)	CNS malformation, previous traumatic brain injury or insult, chromosomal disorder
Acute symptomatic (26%)	SE occurring during an acute illness (e.g., acute CNS insult, acute encephalopathy)	Meningitis, encephalitis, electrolyte disturbance, hypoxia, intoxication, sepsis, trauma
Febrile (22%)	SE occurring when the only provocation is a febrile illness, after excluding a direct CNS infection such as meningitis or encephalitis	Upper respiratory infection, sinusitis, sepsis
Cryptogenic† (15%)	SE occurring in the absence of an acute precipitating CNS insult, systemic metabolic disturbance, or both	No definable cause
Progressive encephalopathy (3%)	SE occurring with an underlying, progressive CNS disorder	Amino or organic acidopathies, CNS lipid storage diseases, mitochondrial disorders
Remote symptomatic with an acute precipitant (1%)	SE occurring with a chronic encephalopathy, but with an acute provocation	CNS malformation or previous CNS insult with concurrent infection, hypoglycemia, hypocalcemia, or intoxication
SE = status epilepticus; CNS = central nervous system. *- Percentages represent the number of patients out of 2,093 children from 20 different class III studies whose SE was attributed to each type. †- The category cryptogenic is now used instead of idiopathic, which had been used in the original classification. Adapted with permission from Riviello JJ Jr, Ashwal S, Hirtz D, Glauser T, Ballaban-Gil K, Kelley K, et al. Practice parameter: diagnostic assessment of the child with status epilepticus (an evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society. Neurology 2006;67:1543.

Studies have shown that symptomatic status epilepticus is common in younger children and infants. In one study of almost 400 children one month to 16 years of age, more than 80 percent of those younger than two years had acute symptomatic or febrile status epilepticus or a progressive encephalopathy. The incidence of status epilepticus in children one to 19 years of age is 10 to 58 per 100,000 children per year. Infants younger than one year have a higher incidence, with approximately 135 to 156 per 100,000 infants affected per year. Status epilepticus is common in children with epilepsy (occurring at a rate of 9.1 to 27.0 percent), and it may be a presenting sign of epilepsy.

Children may develop status epilepticus for many different reasons. Infectious or inflammatory illnesses may cause seizures by affecting the brain or through involvement of the central nervous system (CNS). Drug abuse or ingestion of a toxin also could be to blame. If the child is taking antiepileptic drugs, a low drug level from inadequate dosing, noncompliance, or discontinuation of treatment may cause the status epilepticus. Inborn errors of metabolism (e.g., amino acid, ammonia, or organic acid disorders), as well as specific chromosomal and genetic disorders, can cause neurologic dysfunction and epilepsy. In some children, seizures may get worse because of metabolic stress or during an intercurrent illness.

Drug treatment guidelines for status epilepticus in children are already available; however, there are no guidelines on diagnostic evaluation that are specific to children or that are evidence based. The American Academy of Neurology (AAN) and the Child Neurology Society reviewed the available evidence on children with status epilepticus and created recommendations for diagnostic laboratory testing.

Evidence and Recommendations

blood cultures

In six studies (n = 357) that reported on sepsis, a minimal diagnostic yield of a positive blood culture was found in 2.5 percent of children with status epilepticus. This minimal diagnostic yield was based on the assumption that blood cultures were obtained in all patients in the studies, whether or not sepsis was suspected.

The evidence is insufficient to support or refute whether blood cultures should be obtained routinely in children with no clinical suspicion of infection. None of the studies indicated that blood cultures were obtained routinely in all children with status epilepticus; it was either stated or presumed that testing was done selectively.

lumbar puncture

Data from 18 studies (n = 1,859) showed that the diagnosed CNS infection rate was 12.8 percent. According to the results of one study involving 49 children with convulsive status epilepticus, 24 children (49 percent) had a fever, and 17 percent of those had bacterial meningitis; none of the children without fever had meningitis. In three studies involving 185 children, lumbar puncture was used to diagnose and confirm the following illnesses: meningitis (14 percent of children), encephalitis (11 percent), and leukemic meningitis (1 percent). Vasculitis and shunted hydrocephalus each occurred in less than 1 percent of the children.

The evidence is insufficient to support or refute whether lumbar puncture should be performed routinely in children with no clinical suspicion of CNS infection. As with blood culture, there was no indication to show that lumbar puncture was performed routinely in these studies.

antiepileptic drug levels

Data on antiepileptic drug levels were available in nine studies (n = 528), with low levels reported in 32 percent of children. Reasons for the low drug levels included discontinuation of treatment (9 percent) and noncompliance (0.2 percent). However, it was not assumed that the low levels of antiepileptic drugs were the cause of status epilepticus in the children studied.

Antiepileptic drug levels should be considered when a child with epilepsy on antiepileptic prophylaxis develops status epilepticus.

toxicology testing

In 11 studies (n = 1,221), toxic ingestion was found in 3.6 percent of children. Specific toxins included theophylline, lindane, carbamazepine (Tegretol), and chemotherapy. It is unknown whether toxicology testing was performed on the patients based on history or physical examination findings, or because initial laboratory studies were unable to find other causes of the children's status epilepticus.

Because ingestion was found to be the cause of status epilepticus in 3.6 percent of children, toxicology testing can be considered if no apparent cause is immediately found. A specific serum toxicology test is required when identifying specific ingestion, which may be suspected because of the patient's clinical history.

metabolic and genetic testing

Nine studies (n = 735) showed that an inborn error of metabolism was the diagnosis in 4.2 percent of children. More specifically, pyridoxine (vitamin B6) dependency, Leigh disease, neuronal ceroid-lipofuscinosis, and mitochondrial disorders were each found in 0.3 percent of the children, and Alper's disease, methylmalonicacidemia, and carnitine deficiency were each found in 0.2 percent. Separate information on genetic or chromosomal disorders was unavailable.

Studies for inborn errors of metabolism can be considered if initial evaluation finds no etiology, especially if the patient has a history suggestive of a metabolic disorder. The type of study that should be done depends on the patient history and clinical examination; however, there are insufficient data to support or refute their routine use. There also are insufficient data to support or refute routine use of genetic testing (e.g., chromosomal, molecular).

eeg

Six studies that included 413 electroencephalography (EEG) findings in 358 children found that 89 percent of the findings could be categorized as abnormal. Generalized or focal epileptiform activity was observed in 43.1 percent of the children. One study (n = 407) that looked at the prognosis of those with a first unprovoked seizure reviewed the EEG findings in 46 of the children with status epilepticus. Sixty-two percent of the EEG findings in children with status epilepticus were considered abnormal compared with 41 percent in children who only had seizures lasting less than 30 minutes.

Nonconvulsive status epilepticus and pseudostatus epilepticus (a nonepileptic event that imitates status epilepticus) also may occur. One study (n = 29) of children with convulsive status epilepticus found that 21 percent had pseudoseizures. No data are available on the prevalence of nonconvulsive status epilepticus in children after convulsive status epilepticus is controlled; however, one study showed that among adults, nonconvulsive status epilepticus is present in 14 percent of patients in whom impaired consciousness remains after convulsive status epilepticus is controlled.

EEG may be considered in children presenting with new-onset status epilepticus because it can help to determine whether there are focal or generalized abnormalities, which can influence diagnosis and treatment (Table 2). Although nonconvulsive status epilepticus does occur, the evidence is insufficient to support or refute recommendations regarding the use of EEG to confirm this diagnosis. EEG may be considered if a diagnosis of pseudostatus epilepticus is suspected.

Table 2. EEG Findings in 358 Children with Status Epilepticus
EEG findings	Number of patients	Percentage	Range ( %)
Electrocerebral inactivity	8	1.9	0 to 3.9
Epileptiform features
Focal only	66	16.0	0 to 47
Generalized only	33	8.0	0 to 19
Generalized and focal	79	19.1	0 to 42
Focal slowing	26	6.3	0 to 23
Generalized slowing	169	41.0	26 to 93
Normal	32	7.7	0 to 34
Total*	413
EEG = electroencephalography. *-Refers to 413 EEG abnormalities reported in 358 patients from six class III studies. Adapted with permission from Riviello JJ Jr, Ashwal S, Hirtz D, Glauser T, Ballaban-Gil K, Kelley K, et al. Practice parameter: diagnostic assessment of the child with status epilepticus (an evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society. Neurology 2006;67:1547.

neuroimaging

Information from 20 studies (n = 1,951) found that lesions were detected by neuroimaging in 7.8 percent of patients. Specific lesions included CNS malformation in 1.7 percent, trauma in 1.6 percent, stroke/hemorrhage in 0.9 percent, tumor in 0.8 percent, infarction in 0.6 percent, hemorrhage in 0.4 percent, and abscess/cerebritis in 0.4 percent.

In five studies reporting on computed tomography (CT) results, a mean of 49 percent of CT findings were categorized as abnormal (e.g., presence of cerebral edema, atrophy, infection). In one small study, magnetic resonance imaging was performed in nine of 24 children. The findings were classified as normal in two of the children and abnormal in seven.

Neuroimaging may be considered if clinically indicated or if the etiology of status epilepticus is unknown. It should be used only after the seizures are under control and the patient is stabilized. The data are insufficient to support or refute routine use of neuroimaging. Neuroimaging can identify structural causes of status epilepticus and eliminate the need for neurosurgical interventions in children with new-onset status epilepticus and no history of epilepsy, or in those in whom status epilepticus persists despite treatment.

Future Research

Research is still needed to help define what precipitates status epilepticus in children, as well as to determine the frequency, etiology, and prognostic significance of nonconvulsive status epilepticus in children whose convulsive status epilepticus has already been adequately controlled. Controlled prospective trials should be conducted to determine the role of routine or selective laboratory testing, to define the setting and timing of EEG, and to examine the yield of routine or selective neuroimaging in the evaluation of children with status epilepticus.

Practice Guideline Briefs

AHA Diet and Lifestyle Recommendations

Guideline source: American Heart Association

Literature search described? No

Evidence rating system used? No

Published source: Circulation, July 4, 2006

Available at: http://circ.ahajournals.org/cgi/content/full/114/1/82

Improving dietary and lifestyle habits is a critical part of any strategy for cardiovascular risk reduction. The American Heart Association (AHA) recently revised its diet and lifestyle recommendations to reflect new evidence.

Goals

There are seven lifestyle goals to help in the prevention of cardiovascular disease. These goals are intended for patients older than two years.

• Consume an overall healthy diet. Persons should aim to improve their diet as a whole by eating a variety of fruits, vegetables, and grains (especially whole grains) as opposed to focusing on a single nutrient or food. The AHA also recommends that persons eat legumes, poultry, lean meats, fish, and low-fat and fat-free dairy products.

• Aim for a healthy body weight. A heathy body weight is defined as a body mass index (BMI) of 18.5 to 24.9 kg per m2. A BMI of
25 to 29.9 kg per m2 is considered overweight, and a BMI of 30 kg per m2 or higher is considered obese.

• Aim for a desirable lipid profile. An optimal low-density lipoprotein (LDL) cholesterol level is a measurement lower than 100 mg per dL (2.60 mmol per L). A measurement of 100 to 129 mg per dL (3.34 mmol per L) is near optimal; 130 to 159 mg per dL (3.36 to 4.12 mmol per L) is borderline high; 160 to 189 mg per dL (4.14 to 4.90 mmol per L) is high; and 190 mg per dL (4.92 mmol per L) or higher is very high. Saturated fats and trans fats are the greatest dietary causes of elevated LDL cholesterol levels.

Although the AHA does not recommend specific goals for high-density lipoprotein cholesterol, levels lower than 40 mg per dL (1.04 mmol per L) for men and lower than 50 mg per dL (1.30 mmol per L) for women are criteria for metabolic syndrome.[correction] There also are no triglyceride goals, but a level higher than 150 mg per dL (1.70 mmol per L) is a criterion for metabolic syndrome.

• Aim for normal blood pressure. Normal blood pressure is a systolic measurement of less than 120 mm Hg and a diastolic measurement of less than 80 mm Hg. Elevated blood pressure is caused by environmental factors, genetic factors, and the interaction of these factors. The largest environmental cause is diet. Dietary modifications that lower blood pressure include reducing salt intake, creating a caloric deficit (to induce weight loss), moderating alcohol consumption in persons who consume alcohol, increasing potassium intake, and consuming an overall heathy diet.

• Aim for a normal blood glucose level. A normal fasting glucose level is 100 mg per dL (5.55 mmol per L) or less. A fasting glucose level of 126 mg per dL (7.00 mmol per L) or higher is classified as diabetes. Type 2 diabetes is the most common form of diabetes, and reduced caloric intake and increased physical activity can decrease insulin resistance and improve glucose control.

• Be physically active. Regular physical activity improves blood pressure, lipid profiles, and blood sugar levels. It also can lower the risk of developing type 2 diabetes, osteoporosis, obesity, depression, and cancers of the breast and colon.

• Avoid the use of and exposure to tobacco products.

Recommendations

There are nine diet and lifestyle recommendations intended to reduce cardiovascular disease risk.

• Balance caloric intake and physical activity to achieve or maintain a healthy body weight. To control caloric intake, persons should be aware of the calorie content in foods and beverages and control portion size. A physically active lifestyle is recommended for all persons, even those at a healthy weight. The AHA recommends that all adults exercise for at least 30 minutes on most days (60 minutes for adults trying to lose weight and for children).

• Consume a diet rich in vegetables and fruits. Vegetables and fruits have been proven to lower blood pressure. Deeply colored vegetables and fruits (e.g., spinach, carrots, peaches, berries) should be emphasized because of their high nutrient content.

• Choose whole-grain, high-fiber foods. Diets high in whole-grain products and fiber are associated with a decreased risk of cardiovascular disease.

• Consume fish, especially oily fish, at least twice a week. Consuming 8 oz of fish high in very long-chain omega-3 polyunsaturated fatty acids per week reduces the risk of sudden death and death from coronary artery disease. Because of possible methyl mercury contamination, children and pregnant women are advised to avoid eating shark, swordfish, king mackerel, or tilefish. For older men and postmenopausal women, the benefits of fish consumption outweigh the risks.

• Limit intake of saturated and trans fat and cholesterol. The AHA recommends that persons consume less than 7 percent of calories as saturated fat and less than 1 percent as trans fat, and consume less than 300 mg of cholesterol per day. The major dietary sources of saturated fats and cholesterol are of animal origin (e.g., meat, eggs, dairy), and the major sources of trans fats are partially hydrogenated oils used to prepare commercially fried and baked products.

• Minimize intake of beverages and foods with added sugars. Persons who consume beverages with added sugars usually consume more calories per day and gain weight.

• Choose and prepare foods with little or no salt. The AHA recommends a daily sodium intake of no more than 2.3 g. Blood pressure tends to increase with salt intake. Reduced sodium intake is associated with slowed age-related increase in blood pressure and reduced risk of atherosclerotic cardiovascular events and congestive heart failure.

• Consume alcohol in moderation, if at all. It is recommended that men consume no more than two drinks per day, and women consume no more than one. Alcoholic drinks should be consumed with meals.

• Follow the AHA 2006 diet and lifestyle recommendations when eating food that is prepared outside the home.

LAURA COUGHLIN

This is a corrected version of the item that appeared in print.

Answers to This Issue's Clinical Quiz Q1. D Q2. B Q3. C Q4. E Q5. B Q6. C Q7. A, C, D Q8. B, C Q9. A, C, D Q10. A, B, C

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