Atrial fibrillation (AF)—the most common supraventricular tachycardia—affects as many as 6.1 million adults in the United States.¹ It is associated with a 5-fold increased risk of stroke,² a 3-fold increased risk of heart failure (HF),³ and about a 2-fold increased risk of dementia⁴ and mortality.² The prevalence of AF increases with maturity, from 2% in people <65 years of age to 9% in those ≥65 years,⁵ and that prevalence is expected to double over the next 25 years as the population ages.¹

The primary goals of treatment are to alleviate symptoms and prevent thromboembolism. Strokes related to AF are more likely to result in severe disability or death when compared with those unrelated to AF.⁶ And yet anticoagulation remains underutilized.⁷

The net clinical benefit of oral anticoagulation appears to be greatest in patients with the highest risk of bleeding, since these patients are also at the highest risk for stroke.⁸ Patients at increased risk of stroke are more likely to receive oral anticoagulation; however, for unknown reasons, more than half of people with the highest risk of stroke are not prescribed these important anti-blood-clotting medications.⁷ One theory is that physicians may be relying on their gut rather than objective risk scores, and underuse of validated schemata leads to poor estimation of risk.

IMAGE: © ALICIA BUELO

For example, results from the ORBIT-AF (Outcomes Registry for Better Informed Treatment of Atrial Fibrillation) trial, which involved over 10,000 people with AF, found that although 72% (n=7251) had high-risk CHADS₂ scores (≥2), only 16% were assessed as having a high risk of stroke by physicians.⁹ Along the same lines, a recent study of Canadian primary care physicians showed that stroke risk and bleeding risk were not evaluated with validated tools in 58% and 81% of patients, respectively, leading to both significant underestimation and overestimation of risk.¹⁰

This review provides the tools to identify when anticoagulation is indicated, reports the advantages and disadvantages of the currently available anticoagulants, and discusses the selection and implementation of rate- vs rhythm-control strategies. But first, a word about the etiology, classification, and diagnosis of AF.

AF: The result of any number of cardiac and non-cardiac causes

AF is characterized by uncoordinated activation of the atria, which results in ineffective atrial contractions and an irregular, often rapid, ventricular response. It is the ultimate clinical manifestation of multiple diseases that alter atrial tissue through inflammation, fibrosis, or hypertrophy.⁵ The most common causes are hypertension, coronary artery disease, HF, cardiomyopathies, and valvular heart disease, all of which stimulate the renin-angiotensin-aldosterone system, leading to increased susceptibility to arrhythmia.⁵ Atrial ectopic tachycardia, Wolff-Parkinson-White (WPW) syndrome, and atrioventricular (AV) nodal reentrant tachycardia also may precipitate AF.⁵ In these cases, AF usually resolves after catheter ablation (CA) of the primary arrhythmia.¹¹ Unrecognized AF may trigger atrial flutter, and more than 80% of patients who undergo radiofrequency ablation for atrial flutter experience AF at some point in the subsequent 5 years.¹²

Strokes related to atrial fibrillation are more likely to result in severe disability or death when compared with those unrelated to AF. And yet anticoagulation remains underutilized.

Non-cardiac causes of AF include sleep apnea, obesity, hyperthyroidism, drugs, electrocution, pneumonia, and pulmonary embolism.⁵ An association between binge drinking and AF (“holiday heart syndrome”) has long been recognized. The evidence now suggests that alcohol increases the risk of AF in a dose-dependent manner with intakes of ≥1 drink per day (12 g per drink).¹³

Classification schema no longer includes “lone AF”

AF is classified in terms of the duration of episodes:⁵

• Paroxysmal AF is characterized by brief episodes that terminate spontaneously or with intervention within 7 days of onset. These episodes recur with variable frequency.
• Persistent AF refers to AF that is continuously sustained for more than 7 days.
• Longstanding persistent AF refers to continuous AF that lasts longer than 12 months.
• Permanent AF is not an inherent pathophysiologic attribute of AF, but rather an acceptance of AF where the patient and physician abandon further efforts to restore and/or maintain sinus rhythm.
• Nonvalvular AF occurs in the absence of a valve replacement (mechanical or bioprosthetic), rheumatic mitral stenosis, or mitral valve repair.

Although paroxysmal and persistent AF may occur in the same individual, the distinction is still clinically relevant, as outcomes of certain therapies, such as CA, are superior in patients with paroxysmal AF.¹⁴ With a more complete understanding of AF pathophysiology, guidelines now discourage use of the potentially confusing term “lone AF,” which has historically been applied to younger patients with no known clinical risk factors or echocardiographic abnormalities. As a result, therapeutic decisions are no longer based on this nomenclature, according to the 2014 AF practice guideline from the American College of Cardiology (ACC)/American Heart Association (AHA)/Heart Rhythm Society (HRS).⁵

Patient complaints—or incidental findings—can prompt a Dx

Fatigue is the most common symptom of AF. Other signs and symptoms include palpitations, dyspnea, HF, hypotension, syncope, chest pain, and stroke. Some patients are asymptomatic, and AF is an incidental finding when an irregular pulse is discovered during a physical examination. The diagnosis is confirmed by electrocardiogram (EKG), telemetry, Holter monitor, event recorder, or an implanted electrocardiographic recording device. A chest x-ray, serum electrolyte levels, a complete blood count, thyroid testing, and renal and hepatic function testing are recommended. Transthoracic echocardiography to measure cardiac function, detect underlying structural heart disease, and evaluate atrial size is essential.⁵

Warfarin remains the only recommended anticoagulation strategy for patients with severe renal impairment or valvular atrial fibrillation.

An electrophysiologic (EP) study may be needed for diagnosis or treatment if another arrhythmia is present. Aberrant conduction may cause AF to present as a wide complex tachycardia and be mislabeled as ventricular tachycardia. The presence of delta waves is an indication for an EP study targeting the WPW accessory pathway. Transesophageal echocardiography (TEE) is the most sensitive and specific test for left atrial thrombi. If you are considering a TEE for a patient with AF of unknown, or >48 hours’, duration who has not been anticoagulated in the preceding 3 weeks, obtain it before performing cardioversion because of the risk of embolism.⁵

Stroke prevention

The ACC/AHA/HRS AF guideline recommends basing anticoagulation decisions on thromboembolic risk, regardless of AF pattern (paroxysmal, persistent, or permanent) (Class I recommendation).⁵ For patients with nonvalvular AF and atrial flutter, the guideline recommends using the Birmingham 2009 schema (CHA₂DS₂-VASc score) (TABLE 1^15-18) to estimate thromboembolic risk.^5,15 CHA₂DS₂-VASc improves on the older CHADS₂ score by significantly reducing the number of patients categorized as having intermediate risk and better identifying truly low-risk patients who are unlikely to benefit from anticoagulation.^16,17,19

Men with a CHA₂DS₂-VASc score of zero and women with a score of one do not need anticoagulation.^5,20 Discuss the risks and benefits of oral anticoagulation with men who have a score of one. In these intermediate-risk men, antiplatelet therapy with aspirin and/or clopidogrel may be reasonable, especially if there is an indication other than stroke prevention (eg, post-myocardial infarction). Oral anticoagulation is strongly recommended for all patients with a CHA₂DS₂-VASc score of 2 or higher.^5,18,21,22

Anticoagulant considerations: Warfarin vs DOACs

Warfarin was the gold standard for stroke prevention in nonvalvular AF until the direct oral anticoagulants (DOACs) became available in 2010. Guidelines in the United States and the United Kingdom recommend shared decision-making to help patients with AF who do not have a specific indication for warfarin choose between warfarin and the DOACs.^5,21 Canadian and European guidelines recommend DOACs as the first-line option for anticoagulation and reserve warfarin for patients who have contraindications to, or are unable to afford, DOACs.^18,22 All current guidelines recommend continuing warfarin in patients who are stable, well controlled, and satisfied with warfarin therapy and the monitoring and dietary restrictions it entails.

DOACs are as effective as warfarin. All of the DOACs are approved for stroke prevention based on individual phase III non-inferiority trials in which they were compared to warfarin.^23-26 In addition, a meta-analysis of these 4 trials involving a total of 71,683 patients (mean age 70-73 years; median follow-up, 1.8-2.8 years) evaluated the benefits and risks of the 4 DOACs against the former gold standard.²⁷

Higher doses of the DOACs (dabigatran 150 mg BID, rivaroxaban 20 mg/d, edoxaban 60 mg/d, and apixaban 5 mg BID) reduced the rates of stroke or systemic embolism (relative risk [RR]=0.81; 95% confidence interval [CI], 0.73-0.91; P<.0001; number needed to treat [NNT]=147), hemorrhagic stroke (RR=0.49; 95% CI, 0.38-0.64; P<.0001; NNT=219), and all-cause mortality (RR=0.90; 95% CI, 0.85-0.95; P=.0003; NNT=128), compared with warfarin.²⁷ It is important to note that while lower doses of some DOACs (dabigatran 110 mg BID and edoxaban 30 mg/d) were not as effective at preventing ischemic stroke when compared with warfarin (RR=1.3; 95% CI, 1-1.6; P=.045), they still significantly reduced hemorrhagic stroke (RR=0.33; 95% CI, 0.23-0.46; P<.0001) and all-cause mortality (RR=0.89; 95% CI, 0.83-0.96; P=.003).

Of course, the biggest concern is bleeding. In that same meta-analysis, the difference in major bleeding events with DOACs vs warfarin was not statistically significant (RR=0.86; 95% CI, 0.73-1; P=.06). While DOACs likely lower rates of intracranial hemorrhage (RR=0.48; 95% CI, 0.39-0.59; P<.0001; NNT=132), they seem to increase the risk of gastrointestinal (GI) bleeding (RR=1.3; 95% CI, 1-1.6; P=.043; number needed to harm [NNH]=185).²⁷

Without head-to-head trials, it is impossible to know if one direct oral anticoagulant is superior to another.

There was significant heterogeneity in the GI bleeding outcome, however. When compared with warfarin, GI bleeding was increased by dabigatran 150 mg BID (RR=1.5; 95% CI, 1.2-1.9; P<.001) and edoxaban 60 mg/d (HR=1.2; 95% CI, 1.02-1.5; P=.03), but there were no significant differences for dabigatran 110 mg BID or apixaban 5 mg BID.^23,25,26

On the other hand, edoxaban 30 mg/d had a lower risk of GI bleeding when compared with warfarin (HR=0.67; 95% CI, 0.53-0.83; P<.001).²⁵ Without head-to-head trials, it is impossible to know if one DOAC is superior to another. Apixaban 5 mg BID appears to offer the best overall balance between efficacy and safety. Other DOACs may be better options for patients who have specific concerns regarding efficacy or safety.^28,29

Convenience, interactions, and cost may be the deciding factors. Since all DOACs are fairly comparable in efficacy and safety, other factors such as convenience, interactions with other medications, and cost should be considered when deciding on a medication for an individual patient (TABLE 2^30,31). The DOACs require no lab monitoring or dose titration, and all 4 have fewer potential drug interactions than warfarin.³⁰ Due to their relatively short half-lives, strict adherence is critical; DOACs are not suitable for patients who frequently miss doses.⁵ (For more information on starting or switching to DOACs, see, “Is a novel anticoagulant right for your patient?” J Fam Pract. 2014;63:22-28.)

A word about DOACs and renal impairment. Another concern with DOACs is their reliance on renal metabolism and excretion. A meta-analysis of the 4 phase III trials of the DOACs, this time involving 58,338 patients, evaluated DOAC efficacy and safety compared to warfarin in the presence of kidney dysfunction.³² Renal function was categorized as normal (estimated glomerular filtration rate [eGFR] >80 mL/min/1.73 m²), mildly impaired (eGFR 50-80 mL/min/1.73 m²), or moderately impaired (eGFR <50 mL/min/1.73m²). Compared with warfarin, DOACs lowered stroke risk in patients with mild (RR=0.71; 95% CI, 0.62-0.81) or moderate (RR=0.79; 95% CI, 0.66-0.94) renal impairment. DOACs also reduced major bleeding compared to warfarin in patients with mild (RR=0.88; 95% CI, 0.80-0.97) or moderate (RR=0.80; 95% CI, 0.66-0.94) renal impairment. How the DOACs fare in patients with severe renal dysfunction could not be determined because such patients were excluded from the trials.

Keep in mind that the DOACs require dose adjustment at different levels of renal impairment (TABLE 2^30,31), and warfarin remains the only recommended treatment for patients with severe renal impairment, according to both AHA/ACC/HRS and European Society of Cardiology guidelines.^5,18

Tools to help assess patients’ bleeding risk

Of the available scoring mechanisms to identify risk factors for bleeding, 3 have been specifically validated in AF populations (ie, ATRIA,³³ HEMORR₂HAGES,³⁴ and HAS-BLED³⁵). Of the 3, HAS-BLED is superior,³⁶ the most practical, and recommended by expert guidelines.^18,21,22 Additionally, HAS-BLED has good correlation with intracranial hemorrhage risk. The HAS-BLED score ranges from 0 to 9 points with one point assigned for each of the following:³⁵

• Hypertension–uncontrolled with systolic BP >160 mm Hg
• Abnormal liver function–cirrhosis, bilirubin >2× normal, or liver enzymes >3× normal
• Abnormal renal function–dialysis, transplant, or serum creatinine >2.26 mg/dL
• Stroke history–including lacunar infarcts
• Bleeding predisposition–history of major bleeding due to any cause
• Labile international normalized ratio (INR)–time in therapeutic range <60%
• Elderly–age >65 years
• Drug–antiplatelet agents, including nonsteroidal anti-inflammatory drugs
• Alcohol usage–>8 drinks per week.

Patients with a HAS-BLED score ≥3 warrant additional monitoring and attempts to reduce bleeding risk by addressing modifiable risk factors. Bleeding risk scores should not be used to exclude patients from anticoagulation therapy.⁵ In fact, the British National Institute for Health and Clinical Excellence (NICE) guidelines state that anticoagulation should not be withheld solely due to fall risk.²¹

Also, anticoagulation with warfarin should not be permanently discontinued because of a single GI bleed, since restarting warfarin is associated with decreased risks of thromboembolism and mortality and a statistically insignificant increase in recurrent GI bleeding.³⁷ Restarting DOAC therapy following a GI bleed has not been evaluated in clinical trials; however, it may be reasonable to use one of the DOAC doses with a lower risk of GI bleeding (dabigatran 110 mg BID, apixaban 5 mg BID, or edoxaban 30 mg/d) in patients who have experienced a GI bleed on warfarin or another DOAC.^18,22

An online calculator is available that uses CHA₂DS₂-VASc and HAS-BLED scores to determine an individual’s risk/benefit profile with the various anticoagulation strategies available (http://www.sparctool.com). Consider percutaneous left atrial appendage occlusion if the risks of anticoagulation truly exceed the benefits.³⁸

Rate control vs rhythm control

Most patients who present with AF require immediate ventricular rate control to reduce symptoms. In the acute setting, this can be accomplished with intravenous (IV) beta-blockers or IV calcium channel antagonists.^5,39 If the patient is hemodynamically unstable, urgent direct-current cardioversion is the preferred treatment strategy and should not be delayed pending anticoagulation. IV amiodarone can be used in the ICU patient who does not require cardioversion, but is unable to tolerate beta-blockers or calcium channel antagonists.⁴⁰ Once the patient is stable, long-term treatment focuses on ventricular rate control or restoration and maintenance of sinus rhythm.

Direct oral anticoagulants are not suitable for patients who frequently miss doses.

The AFFIRM (Atrial Fibrillation Follow-up Investigation of Rhythm Management) trial enrolled 4060 patients (mean age 70 years, mean follow-up 3.5 years) with paroxysmal and persistent AF and randomized them to either pharmacologic rate control or rhythm control.⁴¹ No significant differences were found in all-cause mortality or in the composite secondary endpoint of death, ischemic stroke, anoxic encephalopathy, major bleeding, or cardiac arrest. In addition, no significant differences emerged in quality of life or global functional status. The number of patients requiring hospitalization during follow-up was significantly lower in the rate-control group vs the rhythm-control group (73% vs 80%; P<.001). Anticoagulation was encouraged but not mandated in the rhythm-control group after 4 weeks in sinus rhythm, and there was a trend toward higher mortality in the rhythm-control group (27% vs 26%; P=.08).

Patients <65 years were excluded from the AFFIRM trial. When younger patients experience significant symptoms, early referral to Cardiology should be considered to discuss the long-term benefits and risks of a rhythm-control strategy. Regardless of age, when patients remain symptomatic despite rate- or rhythm-control management, the strategy should be changed.⁵

Rate-control targets and options

Target heart rates should be individualized. The 2014 ACC/AHA/HRS guideline recommends a resting target heart rate <80 beats per minute (bpm) in symptomatic patients.⁵ In patients with permanent AF who remain asymptomatic at higher resting heart rates, a more lenient rate-control strategy (resting heart rate <110 bpm) has demonstrated outcomes equivalent to those of a more strict approach (resting heart rate <80 bpm and heart rate during moderate exercise <110 bpm).⁴² Pharmacologic rate-control options include beta-blockers, non-dihydropyridine calcium channel antagonists, and digoxin (TABLE 3⁵). Digoxin is associated with increased all-cause mortality in patients with AF regardless of HF status (HR=1.4; 95% CI, 1.2-1.6, P=.0001).⁴³ Digoxin should be reserved for patients who are sedentary or have inadequate control with first-line medications.⁵

Indications for rhythm control

The NICE guidelines, which are consistent with the ACC/AHA/HRS guidelines, recommend rate control as the first-line strategy for AF management, except in people:²¹

• whose AF has a reversible cause
• who have HF believed to be primarily caused by AF
• with new-onset AF
• with atrial flutter that is considered suitable for an ablation strategy to restore sinus rhythm
• for whom a rhythm-control strategy would be more suitable based on clinical judgment.

In addition, patients who continue to experience symptomatic AF despite an adequate trial of rate control should be offered rhythm control.⁵

Pharmacologic rhythm-control strategies. Antiarrhythmic drugs can be used for chemical cardioversion, reduction of paroxysms, and long-term maintenance of sinus rhythm. The most commonly used antiarrhythmic drugs are Class IC and Class III agents (TABLE 3).⁵ Tailored drug selection for each patient is key. Patients with left atrial diameters >4.5 cm are less likely to remain in sinus rhythm, and patients with left ventricular hypertrophy are at increased risk for proarrhythmic adverse effects.⁴⁴ Patients with paroxysmal AF may be candidates for a “pill-in-the-pocket” strategy using propafenone or flecainide.⁵

AF frequently progresses from paroxysmal to persistent and can subsequently result in electrical and structural remodeling that becomes irreversible over time.⁴⁵ The patient with uncontrolled symptoms despite attempts at rate control and rhythm control should be promptly referred to an electrophysiologist.

Surgical interventions for rate or rhythm control

Electrophysiology interventions include AV nodal ablation with pacemaker placement for rate control, or catheter-directed ablation (radiofrequency or cryotherapy) for rhythm control. CA appears to be more effective than pharmacologic rhythm control.^46,47 Treatment with CA is indicated for symptomatic paroxysmal AF when a rhythm-control strategy is desired and the AF is refractory to, or the patient is intolerant of, at least one class I or III antiarrhythmic medication.⁵ With these same caveats, CA is a reasonable strategy for symptomatic persistent AF.

Consider more invasive interventions, such as an atrial maze procedure, when patients require cardiac surgery for another indication. Patients with an increased risk of thromboembolism (based on CHA₂DS₂-VASc) remain at high risk even after successful ablation.⁴⁸ As a result, some guidelines recommend continued long-term anticoagulation following CA.^18,22

CORRESPONDENCE
Philip Dooley, MD, University of Kansas School of Medicine–Wichita Family Medicine Residency at Via Christi, 707 North Emporia, Wichita, KS 67207; [email protected].

ACKNOWLEDGMENTS
We thank Professor Anne Walling, MB, ChB, FFPHM, Department of Family and Community Medicine, University of Kansas School of Medicine–Wichita for her suggestions and critical review of an earlier version of this manuscript.

Atrial fibrillation (AF)—the most common supraventricular tachycardia—affects as many as 6.1 million adults in the United States.¹ It is associated with a 5-fold increased risk of stroke,² a 3-fold increased risk of heart failure (HF),³ and about a 2-fold increased risk of dementia⁴ and mortality.² The prevalence of AF increases with maturity, from 2% in people <65 years of age to 9% in those ≥65 years,⁵ and that prevalence is expected to double over the next 25 years as the population ages.¹

The primary goals of treatment are to alleviate symptoms and prevent thromboembolism. Strokes related to AF are more likely to result in severe disability or death when compared with those unrelated to AF.⁶ And yet anticoagulation remains underutilized.⁷

The net clinical benefit of oral anticoagulation appears to be greatest in patients with the highest risk of bleeding, since these patients are also at the highest risk for stroke.⁸ Patients at increased risk of stroke are more likely to receive oral anticoagulation; however, for unknown reasons, more than half of people with the highest risk of stroke are not prescribed these important anti-blood-clotting medications.⁷ One theory is that physicians may be relying on their gut rather than objective risk scores, and underuse of validated schemata leads to poor estimation of risk.

IMAGE: © ALICIA BUELO

For example, results from the ORBIT-AF (Outcomes Registry for Better Informed Treatment of Atrial Fibrillation) trial, which involved over 10,000 people with AF, found that although 72% (n=7251) had high-risk CHADS₂ scores (≥2), only 16% were assessed as having a high risk of stroke by physicians.⁹ Along the same lines, a recent study of Canadian primary care physicians showed that stroke risk and bleeding risk were not evaluated with validated tools in 58% and 81% of patients, respectively, leading to both significant underestimation and overestimation of risk.¹⁰

This review provides the tools to identify when anticoagulation is indicated, reports the advantages and disadvantages of the currently available anticoagulants, and discusses the selection and implementation of rate- vs rhythm-control strategies. But first, a word about the etiology, classification, and diagnosis of AF.

AF: The result of any number of cardiac and non-cardiac causes

AF is characterized by uncoordinated activation of the atria, which results in ineffective atrial contractions and an irregular, often rapid, ventricular response. It is the ultimate clinical manifestation of multiple diseases that alter atrial tissue through inflammation, fibrosis, or hypertrophy.⁵ The most common causes are hypertension, coronary artery disease, HF, cardiomyopathies, and valvular heart disease, all of which stimulate the renin-angiotensin-aldosterone system, leading to increased susceptibility to arrhythmia.⁵ Atrial ectopic tachycardia, Wolff-Parkinson-White (WPW) syndrome, and atrioventricular (AV) nodal reentrant tachycardia also may precipitate AF.⁵ In these cases, AF usually resolves after catheter ablation (CA) of the primary arrhythmia.¹¹ Unrecognized AF may trigger atrial flutter, and more than 80% of patients who undergo radiofrequency ablation for atrial flutter experience AF at some point in the subsequent 5 years.¹²

Strokes related to atrial fibrillation are more likely to result in severe disability or death when compared with those unrelated to AF. And yet anticoagulation remains underutilized.

Non-cardiac causes of AF include sleep apnea, obesity, hyperthyroidism, drugs, electrocution, pneumonia, and pulmonary embolism.⁵ An association between binge drinking and AF (“holiday heart syndrome”) has long been recognized. The evidence now suggests that alcohol increases the risk of AF in a dose-dependent manner with intakes of ≥1 drink per day (12 g per drink).¹³

Classification schema no longer includes “lone AF”

AF is classified in terms of the duration of episodes:⁵

• Paroxysmal AF is characterized by brief episodes that terminate spontaneously or with intervention within 7 days of onset. These episodes recur with variable frequency.
• Persistent AF refers to AF that is continuously sustained for more than 7 days.
• Longstanding persistent AF refers to continuous AF that lasts longer than 12 months.
• Permanent AF is not an inherent pathophysiologic attribute of AF, but rather an acceptance of AF where the patient and physician abandon further efforts to restore and/or maintain sinus rhythm.
• Nonvalvular AF occurs in the absence of a valve replacement (mechanical or bioprosthetic), rheumatic mitral stenosis, or mitral valve repair.

Although paroxysmal and persistent AF may occur in the same individual, the distinction is still clinically relevant, as outcomes of certain therapies, such as CA, are superior in patients with paroxysmal AF.¹⁴ With a more complete understanding of AF pathophysiology, guidelines now discourage use of the potentially confusing term “lone AF,” which has historically been applied to younger patients with no known clinical risk factors or echocardiographic abnormalities. As a result, therapeutic decisions are no longer based on this nomenclature, according to the 2014 AF practice guideline from the American College of Cardiology (ACC)/American Heart Association (AHA)/Heart Rhythm Society (HRS).⁵

Patient complaints—or incidental findings—can prompt a Dx

Fatigue is the most common symptom of AF. Other signs and symptoms include palpitations, dyspnea, HF, hypotension, syncope, chest pain, and stroke. Some patients are asymptomatic, and AF is an incidental finding when an irregular pulse is discovered during a physical examination. The diagnosis is confirmed by electrocardiogram (EKG), telemetry, Holter monitor, event recorder, or an implanted electrocardiographic recording device. A chest x-ray, serum electrolyte levels, a complete blood count, thyroid testing, and renal and hepatic function testing are recommended. Transthoracic echocardiography to measure cardiac function, detect underlying structural heart disease, and evaluate atrial size is essential.⁵

Warfarin remains the only recommended anticoagulation strategy for patients with severe renal impairment or valvular atrial fibrillation.

An electrophysiologic (EP) study may be needed for diagnosis or treatment if another arrhythmia is present. Aberrant conduction may cause AF to present as a wide complex tachycardia and be mislabeled as ventricular tachycardia. The presence of delta waves is an indication for an EP study targeting the WPW accessory pathway. Transesophageal echocardiography (TEE) is the most sensitive and specific test for left atrial thrombi. If you are considering a TEE for a patient with AF of unknown, or >48 hours’, duration who has not been anticoagulated in the preceding 3 weeks, obtain it before performing cardioversion because of the risk of embolism.⁵

Stroke prevention

The ACC/AHA/HRS AF guideline recommends basing anticoagulation decisions on thromboembolic risk, regardless of AF pattern (paroxysmal, persistent, or permanent) (Class I recommendation).⁵ For patients with nonvalvular AF and atrial flutter, the guideline recommends using the Birmingham 2009 schema (CHA₂DS₂-VASc score) (TABLE 1^15-18) to estimate thromboembolic risk.^5,15 CHA₂DS₂-VASc improves on the older CHADS₂ score by significantly reducing the number of patients categorized as having intermediate risk and better identifying truly low-risk patients who are unlikely to benefit from anticoagulation.^16,17,19

Men with a CHA₂DS₂-VASc score of zero and women with a score of one do not need anticoagulation.^5,20 Discuss the risks and benefits of oral anticoagulation with men who have a score of one. In these intermediate-risk men, antiplatelet therapy with aspirin and/or clopidogrel may be reasonable, especially if there is an indication other than stroke prevention (eg, post-myocardial infarction). Oral anticoagulation is strongly recommended for all patients with a CHA₂DS₂-VASc score of 2 or higher.^5,18,21,22

Anticoagulant considerations: Warfarin vs DOACs

Warfarin was the gold standard for stroke prevention in nonvalvular AF until the direct oral anticoagulants (DOACs) became available in 2010. Guidelines in the United States and the United Kingdom recommend shared decision-making to help patients with AF who do not have a specific indication for warfarin choose between warfarin and the DOACs.^5,21 Canadian and European guidelines recommend DOACs as the first-line option for anticoagulation and reserve warfarin for patients who have contraindications to, or are unable to afford, DOACs.^18,22 All current guidelines recommend continuing warfarin in patients who are stable, well controlled, and satisfied with warfarin therapy and the monitoring and dietary restrictions it entails.

DOACs are as effective as warfarin. All of the DOACs are approved for stroke prevention based on individual phase III non-inferiority trials in which they were compared to warfarin.^23-26 In addition, a meta-analysis of these 4 trials involving a total of 71,683 patients (mean age 70-73 years; median follow-up, 1.8-2.8 years) evaluated the benefits and risks of the 4 DOACs against the former gold standard.²⁷

Higher doses of the DOACs (dabigatran 150 mg BID, rivaroxaban 20 mg/d, edoxaban 60 mg/d, and apixaban 5 mg BID) reduced the rates of stroke or systemic embolism (relative risk [RR]=0.81; 95% confidence interval [CI], 0.73-0.91; P<.0001; number needed to treat [NNT]=147), hemorrhagic stroke (RR=0.49; 95% CI, 0.38-0.64; P<.0001; NNT=219), and all-cause mortality (RR=0.90; 95% CI, 0.85-0.95; P=.0003; NNT=128), compared with warfarin.²⁷ It is important to note that while lower doses of some DOACs (dabigatran 110 mg BID and edoxaban 30 mg/d) were not as effective at preventing ischemic stroke when compared with warfarin (RR=1.3; 95% CI, 1-1.6; P=.045), they still significantly reduced hemorrhagic stroke (RR=0.33; 95% CI, 0.23-0.46; P<.0001) and all-cause mortality (RR=0.89; 95% CI, 0.83-0.96; P=.003).

Of course, the biggest concern is bleeding. In that same meta-analysis, the difference in major bleeding events with DOACs vs warfarin was not statistically significant (RR=0.86; 95% CI, 0.73-1; P=.06). While DOACs likely lower rates of intracranial hemorrhage (RR=0.48; 95% CI, 0.39-0.59; P<.0001; NNT=132), they seem to increase the risk of gastrointestinal (GI) bleeding (RR=1.3; 95% CI, 1-1.6; P=.043; number needed to harm [NNH]=185).²⁷

Without head-to-head trials, it is impossible to know if one direct oral anticoagulant is superior to another.

There was significant heterogeneity in the GI bleeding outcome, however. When compared with warfarin, GI bleeding was increased by dabigatran 150 mg BID (RR=1.5; 95% CI, 1.2-1.9; P<.001) and edoxaban 60 mg/d (HR=1.2; 95% CI, 1.02-1.5; P=.03), but there were no significant differences for dabigatran 110 mg BID or apixaban 5 mg BID.^23,25,26

On the other hand, edoxaban 30 mg/d had a lower risk of GI bleeding when compared with warfarin (HR=0.67; 95% CI, 0.53-0.83; P<.001).²⁵ Without head-to-head trials, it is impossible to know if one DOAC is superior to another. Apixaban 5 mg BID appears to offer the best overall balance between efficacy and safety. Other DOACs may be better options for patients who have specific concerns regarding efficacy or safety.^28,29

Convenience, interactions, and cost may be the deciding factors. Since all DOACs are fairly comparable in efficacy and safety, other factors such as convenience, interactions with other medications, and cost should be considered when deciding on a medication for an individual patient (TABLE 2^30,31). The DOACs require no lab monitoring or dose titration, and all 4 have fewer potential drug interactions than warfarin.³⁰ Due to their relatively short half-lives, strict adherence is critical; DOACs are not suitable for patients who frequently miss doses.⁵ (For more information on starting or switching to DOACs, see, “Is a novel anticoagulant right for your patient?” J Fam Pract. 2014;63:22-28.)

A word about DOACs and renal impairment. Another concern with DOACs is their reliance on renal metabolism and excretion. A meta-analysis of the 4 phase III trials of the DOACs, this time involving 58,338 patients, evaluated DOAC efficacy and safety compared to warfarin in the presence of kidney dysfunction.³² Renal function was categorized as normal (estimated glomerular filtration rate [eGFR] >80 mL/min/1.73 m²), mildly impaired (eGFR 50-80 mL/min/1.73 m²), or moderately impaired (eGFR <50 mL/min/1.73m²). Compared with warfarin, DOACs lowered stroke risk in patients with mild (RR=0.71; 95% CI, 0.62-0.81) or moderate (RR=0.79; 95% CI, 0.66-0.94) renal impairment. DOACs also reduced major bleeding compared to warfarin in patients with mild (RR=0.88; 95% CI, 0.80-0.97) or moderate (RR=0.80; 95% CI, 0.66-0.94) renal impairment. How the DOACs fare in patients with severe renal dysfunction could not be determined because such patients were excluded from the trials.

Keep in mind that the DOACs require dose adjustment at different levels of renal impairment (TABLE 2^30,31), and warfarin remains the only recommended treatment for patients with severe renal impairment, according to both AHA/ACC/HRS and European Society of Cardiology guidelines.^5,18

Tools to help assess patients’ bleeding risk

Of the available scoring mechanisms to identify risk factors for bleeding, 3 have been specifically validated in AF populations (ie, ATRIA,³³ HEMORR₂HAGES,³⁴ and HAS-BLED³⁵). Of the 3, HAS-BLED is superior,³⁶ the most practical, and recommended by expert guidelines.^18,21,22 Additionally, HAS-BLED has good correlation with intracranial hemorrhage risk. The HAS-BLED score ranges from 0 to 9 points with one point assigned for each of the following:³⁵

• Hypertension–uncontrolled with systolic BP >160 mm Hg
• Abnormal liver function–cirrhosis, bilirubin >2× normal, or liver enzymes >3× normal
• Abnormal renal function–dialysis, transplant, or serum creatinine >2.26 mg/dL
• Stroke history–including lacunar infarcts
• Bleeding predisposition–history of major bleeding due to any cause
• Labile international normalized ratio (INR)–time in therapeutic range <60%
• Elderly–age >65 years
• Drug–antiplatelet agents, including nonsteroidal anti-inflammatory drugs
• Alcohol usage–>8 drinks per week.

Patients with a HAS-BLED score ≥3 warrant additional monitoring and attempts to reduce bleeding risk by addressing modifiable risk factors. Bleeding risk scores should not be used to exclude patients from anticoagulation therapy.⁵ In fact, the British National Institute for Health and Clinical Excellence (NICE) guidelines state that anticoagulation should not be withheld solely due to fall risk.²¹

Also, anticoagulation with warfarin should not be permanently discontinued because of a single GI bleed, since restarting warfarin is associated with decreased risks of thromboembolism and mortality and a statistically insignificant increase in recurrent GI bleeding.³⁷ Restarting DOAC therapy following a GI bleed has not been evaluated in clinical trials; however, it may be reasonable to use one of the DOAC doses with a lower risk of GI bleeding (dabigatran 110 mg BID, apixaban 5 mg BID, or edoxaban 30 mg/d) in patients who have experienced a GI bleed on warfarin or another DOAC.^18,22

An online calculator is available that uses CHA₂DS₂-VASc and HAS-BLED scores to determine an individual’s risk/benefit profile with the various anticoagulation strategies available (http://www.sparctool.com). Consider percutaneous left atrial appendage occlusion if the risks of anticoagulation truly exceed the benefits.³⁸

Rate control vs rhythm control

Most patients who present with AF require immediate ventricular rate control to reduce symptoms. In the acute setting, this can be accomplished with intravenous (IV) beta-blockers or IV calcium channel antagonists.^5,39 If the patient is hemodynamically unstable, urgent direct-current cardioversion is the preferred treatment strategy and should not be delayed pending anticoagulation. IV amiodarone can be used in the ICU patient who does not require cardioversion, but is unable to tolerate beta-blockers or calcium channel antagonists.⁴⁰ Once the patient is stable, long-term treatment focuses on ventricular rate control or restoration and maintenance of sinus rhythm.

Direct oral anticoagulants are not suitable for patients who frequently miss doses.

The AFFIRM (Atrial Fibrillation Follow-up Investigation of Rhythm Management) trial enrolled 4060 patients (mean age 70 years, mean follow-up 3.5 years) with paroxysmal and persistent AF and randomized them to either pharmacologic rate control or rhythm control.⁴¹ No significant differences were found in all-cause mortality or in the composite secondary endpoint of death, ischemic stroke, anoxic encephalopathy, major bleeding, or cardiac arrest. In addition, no significant differences emerged in quality of life or global functional status. The number of patients requiring hospitalization during follow-up was significantly lower in the rate-control group vs the rhythm-control group (73% vs 80%; P<.001). Anticoagulation was encouraged but not mandated in the rhythm-control group after 4 weeks in sinus rhythm, and there was a trend toward higher mortality in the rhythm-control group (27% vs 26%; P=.08).

Patients <65 years were excluded from the AFFIRM trial. When younger patients experience significant symptoms, early referral to Cardiology should be considered to discuss the long-term benefits and risks of a rhythm-control strategy. Regardless of age, when patients remain symptomatic despite rate- or rhythm-control management, the strategy should be changed.⁵

Rate-control targets and options

Target heart rates should be individualized. The 2014 ACC/AHA/HRS guideline recommends a resting target heart rate <80 beats per minute (bpm) in symptomatic patients.⁵ In patients with permanent AF who remain asymptomatic at higher resting heart rates, a more lenient rate-control strategy (resting heart rate <110 bpm) has demonstrated outcomes equivalent to those of a more strict approach (resting heart rate <80 bpm and heart rate during moderate exercise <110 bpm).⁴² Pharmacologic rate-control options include beta-blockers, non-dihydropyridine calcium channel antagonists, and digoxin (TABLE 3⁵). Digoxin is associated with increased all-cause mortality in patients with AF regardless of HF status (HR=1.4; 95% CI, 1.2-1.6, P=.0001).⁴³ Digoxin should be reserved for patients who are sedentary or have inadequate control with first-line medications.⁵

Indications for rhythm control

The NICE guidelines, which are consistent with the ACC/AHA/HRS guidelines, recommend rate control as the first-line strategy for AF management, except in people:²¹

• whose AF has a reversible cause
• who have HF believed to be primarily caused by AF
• with new-onset AF
• with atrial flutter that is considered suitable for an ablation strategy to restore sinus rhythm
• for whom a rhythm-control strategy would be more suitable based on clinical judgment.

In addition, patients who continue to experience symptomatic AF despite an adequate trial of rate control should be offered rhythm control.⁵

Pharmacologic rhythm-control strategies. Antiarrhythmic drugs can be used for chemical cardioversion, reduction of paroxysms, and long-term maintenance of sinus rhythm. The most commonly used antiarrhythmic drugs are Class IC and Class III agents (TABLE 3).⁵ Tailored drug selection for each patient is key. Patients with left atrial diameters >4.5 cm are less likely to remain in sinus rhythm, and patients with left ventricular hypertrophy are at increased risk for proarrhythmic adverse effects.⁴⁴ Patients with paroxysmal AF may be candidates for a “pill-in-the-pocket” strategy using propafenone or flecainide.⁵

AF frequently progresses from paroxysmal to persistent and can subsequently result in electrical and structural remodeling that becomes irreversible over time.⁴⁵ The patient with uncontrolled symptoms despite attempts at rate control and rhythm control should be promptly referred to an electrophysiologist.

Surgical interventions for rate or rhythm control

Electrophysiology interventions include AV nodal ablation with pacemaker placement for rate control, or catheter-directed ablation (radiofrequency or cryotherapy) for rhythm control. CA appears to be more effective than pharmacologic rhythm control.^46,47 Treatment with CA is indicated for symptomatic paroxysmal AF when a rhythm-control strategy is desired and the AF is refractory to, or the patient is intolerant of, at least one class I or III antiarrhythmic medication.⁵ With these same caveats, CA is a reasonable strategy for symptomatic persistent AF.

Consider more invasive interventions, such as an atrial maze procedure, when patients require cardiac surgery for another indication. Patients with an increased risk of thromboembolism (based on CHA₂DS₂-VASc) remain at high risk even after successful ablation.⁴⁸ As a result, some guidelines recommend continued long-term anticoagulation following CA.^18,22

CORRESPONDENCE
Philip Dooley, MD, University of Kansas School of Medicine–Wichita Family Medicine Residency at Via Christi, 707 North Emporia, Wichita, KS 67207; [email protected].

ACKNOWLEDGMENTS
We thank Professor Anne Walling, MB, ChB, FFPHM, Department of Family and Community Medicine, University of Kansas School of Medicine–Wichita for her suggestions and critical review of an earlier version of this manuscript.

Atrial fibrillation (AF)—the most common supraventricular tachycardia—affects as many as 6.1 million adults in the United States.¹ It is associated with a 5-fold increased risk of stroke,² a 3-fold increased risk of heart failure (HF),³ and about a 2-fold increased risk of dementia⁴ and mortality.² The prevalence of AF increases with maturity, from 2% in people <65 years of age to 9% in those ≥65 years,⁵ and that prevalence is expected to double over the next 25 years as the population ages.¹

The primary goals of treatment are to alleviate symptoms and prevent thromboembolism. Strokes related to AF are more likely to result in severe disability or death when compared with those unrelated to AF.⁶ And yet anticoagulation remains underutilized.⁷

The net clinical benefit of oral anticoagulation appears to be greatest in patients with the highest risk of bleeding, since these patients are also at the highest risk for stroke.⁸ Patients at increased risk of stroke are more likely to receive oral anticoagulation; however, for unknown reasons, more than half of people with the highest risk of stroke are not prescribed these important anti-blood-clotting medications.⁷ One theory is that physicians may be relying on their gut rather than objective risk scores, and underuse of validated schemata leads to poor estimation of risk.

IMAGE: © ALICIA BUELO

For example, results from the ORBIT-AF (Outcomes Registry for Better Informed Treatment of Atrial Fibrillation) trial, which involved over 10,000 people with AF, found that although 72% (n=7251) had high-risk CHADS₂ scores (≥2), only 16% were assessed as having a high risk of stroke by physicians.⁹ Along the same lines, a recent study of Canadian primary care physicians showed that stroke risk and bleeding risk were not evaluated with validated tools in 58% and 81% of patients, respectively, leading to both significant underestimation and overestimation of risk.¹⁰

This review provides the tools to identify when anticoagulation is indicated, reports the advantages and disadvantages of the currently available anticoagulants, and discusses the selection and implementation of rate- vs rhythm-control strategies. But first, a word about the etiology, classification, and diagnosis of AF.

AF: The result of any number of cardiac and non-cardiac causes

AF is characterized by uncoordinated activation of the atria, which results in ineffective atrial contractions and an irregular, often rapid, ventricular response. It is the ultimate clinical manifestation of multiple diseases that alter atrial tissue through inflammation, fibrosis, or hypertrophy.⁵ The most common causes are hypertension, coronary artery disease, HF, cardiomyopathies, and valvular heart disease, all of which stimulate the renin-angiotensin-aldosterone system, leading to increased susceptibility to arrhythmia.⁵ Atrial ectopic tachycardia, Wolff-Parkinson-White (WPW) syndrome, and atrioventricular (AV) nodal reentrant tachycardia also may precipitate AF.⁵ In these cases, AF usually resolves after catheter ablation (CA) of the primary arrhythmia.¹¹ Unrecognized AF may trigger atrial flutter, and more than 80% of patients who undergo radiofrequency ablation for atrial flutter experience AF at some point in the subsequent 5 years.¹²

Strokes related to atrial fibrillation are more likely to result in severe disability or death when compared with those unrelated to AF. And yet anticoagulation remains underutilized.

Non-cardiac causes of AF include sleep apnea, obesity, hyperthyroidism, drugs, electrocution, pneumonia, and pulmonary embolism.⁵ An association between binge drinking and AF (“holiday heart syndrome”) has long been recognized. The evidence now suggests that alcohol increases the risk of AF in a dose-dependent manner with intakes of ≥1 drink per day (12 g per drink).¹³

Classification schema no longer includes “lone AF”

AF is classified in terms of the duration of episodes:⁵

• Paroxysmal AF is characterized by brief episodes that terminate spontaneously or with intervention within 7 days of onset. These episodes recur with variable frequency.
• Persistent AF refers to AF that is continuously sustained for more than 7 days.
• Longstanding persistent AF refers to continuous AF that lasts longer than 12 months.
• Permanent AF is not an inherent pathophysiologic attribute of AF, but rather an acceptance of AF where the patient and physician abandon further efforts to restore and/or maintain sinus rhythm.
• Nonvalvular AF occurs in the absence of a valve replacement (mechanical or bioprosthetic), rheumatic mitral stenosis, or mitral valve repair.

Although paroxysmal and persistent AF may occur in the same individual, the distinction is still clinically relevant, as outcomes of certain therapies, such as CA, are superior in patients with paroxysmal AF.¹⁴ With a more complete understanding of AF pathophysiology, guidelines now discourage use of the potentially confusing term “lone AF,” which has historically been applied to younger patients with no known clinical risk factors or echocardiographic abnormalities. As a result, therapeutic decisions are no longer based on this nomenclature, according to the 2014 AF practice guideline from the American College of Cardiology (ACC)/American Heart Association (AHA)/Heart Rhythm Society (HRS).⁵

Patient complaints—or incidental findings—can prompt a Dx

Fatigue is the most common symptom of AF. Other signs and symptoms include palpitations, dyspnea, HF, hypotension, syncope, chest pain, and stroke. Some patients are asymptomatic, and AF is an incidental finding when an irregular pulse is discovered during a physical examination. The diagnosis is confirmed by electrocardiogram (EKG), telemetry, Holter monitor, event recorder, or an implanted electrocardiographic recording device. A chest x-ray, serum electrolyte levels, a complete blood count, thyroid testing, and renal and hepatic function testing are recommended. Transthoracic echocardiography to measure cardiac function, detect underlying structural heart disease, and evaluate atrial size is essential.⁵

Warfarin remains the only recommended anticoagulation strategy for patients with severe renal impairment or valvular atrial fibrillation.

An electrophysiologic (EP) study may be needed for diagnosis or treatment if another arrhythmia is present. Aberrant conduction may cause AF to present as a wide complex tachycardia and be mislabeled as ventricular tachycardia. The presence of delta waves is an indication for an EP study targeting the WPW accessory pathway. Transesophageal echocardiography (TEE) is the most sensitive and specific test for left atrial thrombi. If you are considering a TEE for a patient with AF of unknown, or >48 hours’, duration who has not been anticoagulated in the preceding 3 weeks, obtain it before performing cardioversion because of the risk of embolism.⁵

Stroke prevention

The ACC/AHA/HRS AF guideline recommends basing anticoagulation decisions on thromboembolic risk, regardless of AF pattern (paroxysmal, persistent, or permanent) (Class I recommendation).⁵ For patients with nonvalvular AF and atrial flutter, the guideline recommends using the Birmingham 2009 schema (CHA₂DS₂-VASc score) (TABLE 1^15-18) to estimate thromboembolic risk.^5,15 CHA₂DS₂-VASc improves on the older CHADS₂ score by significantly reducing the number of patients categorized as having intermediate risk and better identifying truly low-risk patients who are unlikely to benefit from anticoagulation.^16,17,19

Men with a CHA₂DS₂-VASc score of zero and women with a score of one do not need anticoagulation.^5,20 Discuss the risks and benefits of oral anticoagulation with men who have a score of one. In these intermediate-risk men, antiplatelet therapy with aspirin and/or clopidogrel may be reasonable, especially if there is an indication other than stroke prevention (eg, post-myocardial infarction). Oral anticoagulation is strongly recommended for all patients with a CHA₂DS₂-VASc score of 2 or higher.^5,18,21,22

Anticoagulant considerations: Warfarin vs DOACs

Warfarin was the gold standard for stroke prevention in nonvalvular AF until the direct oral anticoagulants (DOACs) became available in 2010. Guidelines in the United States and the United Kingdom recommend shared decision-making to help patients with AF who do not have a specific indication for warfarin choose between warfarin and the DOACs.^5,21 Canadian and European guidelines recommend DOACs as the first-line option for anticoagulation and reserve warfarin for patients who have contraindications to, or are unable to afford, DOACs.^18,22 All current guidelines recommend continuing warfarin in patients who are stable, well controlled, and satisfied with warfarin therapy and the monitoring and dietary restrictions it entails.

DOACs are as effective as warfarin. All of the DOACs are approved for stroke prevention based on individual phase III non-inferiority trials in which they were compared to warfarin.^23-26 In addition, a meta-analysis of these 4 trials involving a total of 71,683 patients (mean age 70-73 years; median follow-up, 1.8-2.8 years) evaluated the benefits and risks of the 4 DOACs against the former gold standard.²⁷

Higher doses of the DOACs (dabigatran 150 mg BID, rivaroxaban 20 mg/d, edoxaban 60 mg/d, and apixaban 5 mg BID) reduced the rates of stroke or systemic embolism (relative risk [RR]=0.81; 95% confidence interval [CI], 0.73-0.91; P<.0001; number needed to treat [NNT]=147), hemorrhagic stroke (RR=0.49; 95% CI, 0.38-0.64; P<.0001; NNT=219), and all-cause mortality (RR=0.90; 95% CI, 0.85-0.95; P=.0003; NNT=128), compared with warfarin.²⁷ It is important to note that while lower doses of some DOACs (dabigatran 110 mg BID and edoxaban 30 mg/d) were not as effective at preventing ischemic stroke when compared with warfarin (RR=1.3; 95% CI, 1-1.6; P=.045), they still significantly reduced hemorrhagic stroke (RR=0.33; 95% CI, 0.23-0.46; P<.0001) and all-cause mortality (RR=0.89; 95% CI, 0.83-0.96; P=.003).

Of course, the biggest concern is bleeding. In that same meta-analysis, the difference in major bleeding events with DOACs vs warfarin was not statistically significant (RR=0.86; 95% CI, 0.73-1; P=.06). While DOACs likely lower rates of intracranial hemorrhage (RR=0.48; 95% CI, 0.39-0.59; P<.0001; NNT=132), they seem to increase the risk of gastrointestinal (GI) bleeding (RR=1.3; 95% CI, 1-1.6; P=.043; number needed to harm [NNH]=185).²⁷

Without head-to-head trials, it is impossible to know if one direct oral anticoagulant is superior to another.

There was significant heterogeneity in the GI bleeding outcome, however. When compared with warfarin, GI bleeding was increased by dabigatran 150 mg BID (RR=1.5; 95% CI, 1.2-1.9; P<.001) and edoxaban 60 mg/d (HR=1.2; 95% CI, 1.02-1.5; P=.03), but there were no significant differences for dabigatran 110 mg BID or apixaban 5 mg BID.^23,25,26

On the other hand, edoxaban 30 mg/d had a lower risk of GI bleeding when compared with warfarin (HR=0.67; 95% CI, 0.53-0.83; P<.001).²⁵ Without head-to-head trials, it is impossible to know if one DOAC is superior to another. Apixaban 5 mg BID appears to offer the best overall balance between efficacy and safety. Other DOACs may be better options for patients who have specific concerns regarding efficacy or safety.^28,29

Convenience, interactions, and cost may be the deciding factors. Since all DOACs are fairly comparable in efficacy and safety, other factors such as convenience, interactions with other medications, and cost should be considered when deciding on a medication for an individual patient (TABLE 2^30,31). The DOACs require no lab monitoring or dose titration, and all 4 have fewer potential drug interactions than warfarin.³⁰ Due to their relatively short half-lives, strict adherence is critical; DOACs are not suitable for patients who frequently miss doses.⁵ (For more information on starting or switching to DOACs, see, “Is a novel anticoagulant right for your patient?” J Fam Pract. 2014;63:22-28.)

A word about DOACs and renal impairment. Another concern with DOACs is their reliance on renal metabolism and excretion. A meta-analysis of the 4 phase III trials of the DOACs, this time involving 58,338 patients, evaluated DOAC efficacy and safety compared to warfarin in the presence of kidney dysfunction.³² Renal function was categorized as normal (estimated glomerular filtration rate [eGFR] >80 mL/min/1.73 m²), mildly impaired (eGFR 50-80 mL/min/1.73 m²), or moderately impaired (eGFR <50 mL/min/1.73m²). Compared with warfarin, DOACs lowered stroke risk in patients with mild (RR=0.71; 95% CI, 0.62-0.81) or moderate (RR=0.79; 95% CI, 0.66-0.94) renal impairment. DOACs also reduced major bleeding compared to warfarin in patients with mild (RR=0.88; 95% CI, 0.80-0.97) or moderate (RR=0.80; 95% CI, 0.66-0.94) renal impairment. How the DOACs fare in patients with severe renal dysfunction could not be determined because such patients were excluded from the trials.

Keep in mind that the DOACs require dose adjustment at different levels of renal impairment (TABLE 2^30,31), and warfarin remains the only recommended treatment for patients with severe renal impairment, according to both AHA/ACC/HRS and European Society of Cardiology guidelines.^5,18

Tools to help assess patients’ bleeding risk

Of the available scoring mechanisms to identify risk factors for bleeding, 3 have been specifically validated in AF populations (ie, ATRIA,³³ HEMORR₂HAGES,³⁴ and HAS-BLED³⁵). Of the 3, HAS-BLED is superior,³⁶ the most practical, and recommended by expert guidelines.^18,21,22 Additionally, HAS-BLED has good correlation with intracranial hemorrhage risk. The HAS-BLED score ranges from 0 to 9 points with one point assigned for each of the following:³⁵

• Hypertension–uncontrolled with systolic BP >160 mm Hg
• Abnormal liver function–cirrhosis, bilirubin >2× normal, or liver enzymes >3× normal
• Abnormal renal function–dialysis, transplant, or serum creatinine >2.26 mg/dL
• Stroke history–including lacunar infarcts
• Bleeding predisposition–history of major bleeding due to any cause
• Labile international normalized ratio (INR)–time in therapeutic range <60%
• Elderly–age >65 years
• Drug–antiplatelet agents, including nonsteroidal anti-inflammatory drugs
• Alcohol usage–>8 drinks per week.

Patients with a HAS-BLED score ≥3 warrant additional monitoring and attempts to reduce bleeding risk by addressing modifiable risk factors. Bleeding risk scores should not be used to exclude patients from anticoagulation therapy.⁵ In fact, the British National Institute for Health and Clinical Excellence (NICE) guidelines state that anticoagulation should not be withheld solely due to fall risk.²¹

Also, anticoagulation with warfarin should not be permanently discontinued because of a single GI bleed, since restarting warfarin is associated with decreased risks of thromboembolism and mortality and a statistically insignificant increase in recurrent GI bleeding.³⁷ Restarting DOAC therapy following a GI bleed has not been evaluated in clinical trials; however, it may be reasonable to use one of the DOAC doses with a lower risk of GI bleeding (dabigatran 110 mg BID, apixaban 5 mg BID, or edoxaban 30 mg/d) in patients who have experienced a GI bleed on warfarin or another DOAC.^18,22

An online calculator is available that uses CHA₂DS₂-VASc and HAS-BLED scores to determine an individual’s risk/benefit profile with the various anticoagulation strategies available (http://www.sparctool.com). Consider percutaneous left atrial appendage occlusion if the risks of anticoagulation truly exceed the benefits.³⁸

Rate control vs rhythm control

Most patients who present with AF require immediate ventricular rate control to reduce symptoms. In the acute setting, this can be accomplished with intravenous (IV) beta-blockers or IV calcium channel antagonists.^5,39 If the patient is hemodynamically unstable, urgent direct-current cardioversion is the preferred treatment strategy and should not be delayed pending anticoagulation. IV amiodarone can be used in the ICU patient who does not require cardioversion, but is unable to tolerate beta-blockers or calcium channel antagonists.⁴⁰ Once the patient is stable, long-term treatment focuses on ventricular rate control or restoration and maintenance of sinus rhythm.

Direct oral anticoagulants are not suitable for patients who frequently miss doses.

The AFFIRM (Atrial Fibrillation Follow-up Investigation of Rhythm Management) trial enrolled 4060 patients (mean age 70 years, mean follow-up 3.5 years) with paroxysmal and persistent AF and randomized them to either pharmacologic rate control or rhythm control.⁴¹ No significant differences were found in all-cause mortality or in the composite secondary endpoint of death, ischemic stroke, anoxic encephalopathy, major bleeding, or cardiac arrest. In addition, no significant differences emerged in quality of life or global functional status. The number of patients requiring hospitalization during follow-up was significantly lower in the rate-control group vs the rhythm-control group (73% vs 80%; P<.001). Anticoagulation was encouraged but not mandated in the rhythm-control group after 4 weeks in sinus rhythm, and there was a trend toward higher mortality in the rhythm-control group (27% vs 26%; P=.08).

Patients <65 years were excluded from the AFFIRM trial. When younger patients experience significant symptoms, early referral to Cardiology should be considered to discuss the long-term benefits and risks of a rhythm-control strategy. Regardless of age, when patients remain symptomatic despite rate- or rhythm-control management, the strategy should be changed.⁵

Rate-control targets and options

Target heart rates should be individualized. The 2014 ACC/AHA/HRS guideline recommends a resting target heart rate <80 beats per minute (bpm) in symptomatic patients.⁵ In patients with permanent AF who remain asymptomatic at higher resting heart rates, a more lenient rate-control strategy (resting heart rate <110 bpm) has demonstrated outcomes equivalent to those of a more strict approach (resting heart rate <80 bpm and heart rate during moderate exercise <110 bpm).⁴² Pharmacologic rate-control options include beta-blockers, non-dihydropyridine calcium channel antagonists, and digoxin (TABLE 3⁵). Digoxin is associated with increased all-cause mortality in patients with AF regardless of HF status (HR=1.4; 95% CI, 1.2-1.6, P=.0001).⁴³ Digoxin should be reserved for patients who are sedentary or have inadequate control with first-line medications.⁵

Indications for rhythm control

The NICE guidelines, which are consistent with the ACC/AHA/HRS guidelines, recommend rate control as the first-line strategy for AF management, except in people:²¹

• whose AF has a reversible cause
• who have HF believed to be primarily caused by AF
• with new-onset AF
• with atrial flutter that is considered suitable for an ablation strategy to restore sinus rhythm
• for whom a rhythm-control strategy would be more suitable based on clinical judgment.

In addition, patients who continue to experience symptomatic AF despite an adequate trial of rate control should be offered rhythm control.⁵

Pharmacologic rhythm-control strategies. Antiarrhythmic drugs can be used for chemical cardioversion, reduction of paroxysms, and long-term maintenance of sinus rhythm. The most commonly used antiarrhythmic drugs are Class IC and Class III agents (TABLE 3).⁵ Tailored drug selection for each patient is key. Patients with left atrial diameters >4.5 cm are less likely to remain in sinus rhythm, and patients with left ventricular hypertrophy are at increased risk for proarrhythmic adverse effects.⁴⁴ Patients with paroxysmal AF may be candidates for a “pill-in-the-pocket” strategy using propafenone or flecainide.⁵

AF frequently progresses from paroxysmal to persistent and can subsequently result in electrical and structural remodeling that becomes irreversible over time.⁴⁵ The patient with uncontrolled symptoms despite attempts at rate control and rhythm control should be promptly referred to an electrophysiologist.

Surgical interventions for rate or rhythm control

Electrophysiology interventions include AV nodal ablation with pacemaker placement for rate control, or catheter-directed ablation (radiofrequency or cryotherapy) for rhythm control. CA appears to be more effective than pharmacologic rhythm control.^46,47 Treatment with CA is indicated for symptomatic paroxysmal AF when a rhythm-control strategy is desired and the AF is refractory to, or the patient is intolerant of, at least one class I or III antiarrhythmic medication.⁵ With these same caveats, CA is a reasonable strategy for symptomatic persistent AF.

Consider more invasive interventions, such as an atrial maze procedure, when patients require cardiac surgery for another indication. Patients with an increased risk of thromboembolism (based on CHA₂DS₂-VASc) remain at high risk even after successful ablation.⁴⁸ As a result, some guidelines recommend continued long-term anticoagulation following CA.^18,22

CORRESPONDENCE
Philip Dooley, MD, University of Kansas School of Medicine–Wichita Family Medicine Residency at Via Christi, 707 North Emporia, Wichita, KS 67207; [email protected].

ACKNOWLEDGMENTS
We thank Professor Anne Walling, MB, ChB, FFPHM, Department of Family and Community Medicine, University of Kansas School of Medicine–Wichita for her suggestions and critical review of an earlier version of this manuscript.

Drug release in a cancer cell

Image courtesy of PNAS

A diabetes medication and an antihypertensive drug may prove effective in the treatment of hematologic malignancies and other cancers, according to preclinical research published in Science Advances.

Past research has shown that metformin, a drug used to treat type 2 diabetes, has anticancer properties.

However, the usual therapeutic dose is too low to effectively fight cancer, and higher doses of metformin could be too toxic.

With the current study, researchers found that the antihypertensive drug syrosingopine enhances the anticancer efficacy of metformin without harming normal blood cells.

The team screened over a thousand drugs to find one that could boost metformin’s efficacy against cancers.

They identified syrosingopine and tested it in combination with metformin—at concentrations substantially below the drugs’ therapeutic thresholds—on a range of cancer cell lines and in mouse models of liver cancer.

Thirty-five of the 43 cell lines tested were susceptible to both syrosingopine and metformin. This included leukemia, lymphoma, and multiple myeloma cell lines.

In addition, the mice given a short course of syrosingopine and metformin experienced a reduction in the number of visible liver tumors.

The researchers also tested syrosingopine and metformin in peripheral blasts from 12 patients with acute myeloid leukemia and a patient with blast crisis chronic myeloid leukemia. All 13 samples responded to the treatment.

On the other hand, syrosingopine and metformin did not affect peripheral blood cells from healthy subjects.

“[A]lmost all tumor cells were killed by this cocktail and at doses that are actually not toxic to normal cells,” said study author Don Benjamin, of the University of Basel in Switzerland.

“And the effect was exclusively confined to cancer cells, as the blood cells from healthy donors were insensitive to the treatment.”

The researchers believe metformin functions by lowering blood glucose levels for cancer cells, starving them of essential nutrients needed for their survival. However, it is not clear how syrosingopine works in conjunction with metformin.

The team emphasized the need for more research evaluating the drugs in combination.

“We have been able to show that the 2 known drugs lead to more profound effects on cancer cell proliferation than each drug alone,” Dr Benjamin said. “The data from this study support the development of combination approaches for the treatment of cancer patients.”

Drug release in a cancer cell

Image courtesy of PNAS

A diabetes medication and an antihypertensive drug may prove effective in the treatment of hematologic malignancies and other cancers, according to preclinical research published in Science Advances.

Past research has shown that metformin, a drug used to treat type 2 diabetes, has anticancer properties.

However, the usual therapeutic dose is too low to effectively fight cancer, and higher doses of metformin could be too toxic.

With the current study, researchers found that the antihypertensive drug syrosingopine enhances the anticancer efficacy of metformin without harming normal blood cells.

The team screened over a thousand drugs to find one that could boost metformin’s efficacy against cancers.

They identified syrosingopine and tested it in combination with metformin—at concentrations substantially below the drugs’ therapeutic thresholds—on a range of cancer cell lines and in mouse models of liver cancer.

Thirty-five of the 43 cell lines tested were susceptible to both syrosingopine and metformin. This included leukemia, lymphoma, and multiple myeloma cell lines.

In addition, the mice given a short course of syrosingopine and metformin experienced a reduction in the number of visible liver tumors.

The researchers also tested syrosingopine and metformin in peripheral blasts from 12 patients with acute myeloid leukemia and a patient with blast crisis chronic myeloid leukemia. All 13 samples responded to the treatment.

On the other hand, syrosingopine and metformin did not affect peripheral blood cells from healthy subjects.

“[A]lmost all tumor cells were killed by this cocktail and at doses that are actually not toxic to normal cells,” said study author Don Benjamin, of the University of Basel in Switzerland.

“And the effect was exclusively confined to cancer cells, as the blood cells from healthy donors were insensitive to the treatment.”

The researchers believe metformin functions by lowering blood glucose levels for cancer cells, starving them of essential nutrients needed for their survival. However, it is not clear how syrosingopine works in conjunction with metformin.

The team emphasized the need for more research evaluating the drugs in combination.

“We have been able to show that the 2 known drugs lead to more profound effects on cancer cell proliferation than each drug alone,” Dr Benjamin said. “The data from this study support the development of combination approaches for the treatment of cancer patients.”

Drug release in a cancer cell

Image courtesy of PNAS

A diabetes medication and an antihypertensive drug may prove effective in the treatment of hematologic malignancies and other cancers, according to preclinical research published in Science Advances.

Past research has shown that metformin, a drug used to treat type 2 diabetes, has anticancer properties.

However, the usual therapeutic dose is too low to effectively fight cancer, and higher doses of metformin could be too toxic.

With the current study, researchers found that the antihypertensive drug syrosingopine enhances the anticancer efficacy of metformin without harming normal blood cells.

The team screened over a thousand drugs to find one that could boost metformin’s efficacy against cancers.

They identified syrosingopine and tested it in combination with metformin—at concentrations substantially below the drugs’ therapeutic thresholds—on a range of cancer cell lines and in mouse models of liver cancer.

Thirty-five of the 43 cell lines tested were susceptible to both syrosingopine and metformin. This included leukemia, lymphoma, and multiple myeloma cell lines.

In addition, the mice given a short course of syrosingopine and metformin experienced a reduction in the number of visible liver tumors.

The researchers also tested syrosingopine and metformin in peripheral blasts from 12 patients with acute myeloid leukemia and a patient with blast crisis chronic myeloid leukemia. All 13 samples responded to the treatment.

On the other hand, syrosingopine and metformin did not affect peripheral blood cells from healthy subjects.

“[A]lmost all tumor cells were killed by this cocktail and at doses that are actually not toxic to normal cells,” said study author Don Benjamin, of the University of Basel in Switzerland.

“And the effect was exclusively confined to cancer cells, as the blood cells from healthy donors were insensitive to the treatment.”

The researchers believe metformin functions by lowering blood glucose levels for cancer cells, starving them of essential nutrients needed for their survival. However, it is not clear how syrosingopine works in conjunction with metformin.

The team emphasized the need for more research evaluating the drugs in combination.

“We have been able to show that the 2 known drugs lead to more profound effects on cancer cell proliferation than each drug alone,” Dr Benjamin said. “The data from this study support the development of combination approaches for the treatment of cancer patients.”

IN THIS ARTICLE

• Types of shoulder dislocations
• Schematics of the shoulder with three types of dislocations
• Association with seizures

CASE  A 59-year-old man with a remote history of seizures is transported to the emergency department (ED) by ambulance after a witnessed tonic-clonic seizure. At the time of arrival he is postictal and confused, but his vital signs are stable. A left eyebrow laceration indicating a possible fall is observed on physical exam, as is a left shoulder displacement with no obvious signs of neurovascular compromise. The patient is not currently taking anticonvulsant medication, stating that he has been “seizure free” for five years, and therefore chose to discontinue taking phenytoin against medical advice.

An anteroposterior (AP) bilateral shoulder x-ray is obtained in the ED (see Figures 1a and 1b). The image shows the humeral head to be anteriorly dislocated and reveals a large impaction fracture of the posterior superior humeral head. For a more detailed view of the fracture and to further assess any associated deformities, CT of the left shoulder is performed. The fracture has a depth of 11.6 mm and a length of 24.1 mm, with no additional pathology noted (see Figure 1c).

The shoulder is a large joint capable of moving in many directions and therefore is inherently unstable. The glenoid fossa is shallow, and stability of the joint is provided by both the fibrocartilaginous labrum and varying muscles of the rotator cuff. Because the shoulder joint is poorly supported, dislocations are not uncommon (see the illustrations). 

The first step in evaluating a suspected shoulder dislocation is to order an AP radiographic view of the shoulder (known as the Grashey view). A transcapular view (known as the scapular “Y” view) is also sufficient.¹ While diagnostic studies, such as CT or MRI arthrography, are excellent for evaluating the glenohumeral ligaments and labrum, they generally are not done in an acute setting.¹ For patients who present to the ED, some would recommend taking a CT scan, especially if a posterior dislocation is suspected.²

The three types of shoulder dislocations include anterior, posterior, and inferior.

ANTERIOR

Anterior dislocations account for 95% of all presented cases of shoulder dislocation, making them the most common type.³ They may be caused by a fall on an outstretched arm, trauma to the posterior humerus, or—more frequently—trauma to the arm while it is extended, externally rotated, and abducted (eg, blocking a shot in basketball).

A patient with an anterior dislocation will enter the ED with a slightly abducted and externally rotated arm (see illustration) and will resist any movement by the examiner. Typically, the shoulder loses its rounded appearance, and in thin individuals, the acromion may be prominent. A detailed neurovascular examination of the arm must be performed. 

Dislocation of the humerus in any direction may compromise the axillary nerve, artery, or both. The axillary nerve and artery run parallel to each other, beneath and in close proximity to the humeral head. The axillary artery is located upstream from the radial artery; compression of the artery may lead to a diminution or complete absence of the radial pulse and/or coolness of the hand.⁴ The axillary nerve is both a sensory and motor nerve. If injured, a 2- to 3-cm area over the lateral deltoid may have complete sensory loss, which can be tested for with a light touch and pinprick.⁵ The patient may also have difficulty abducting the arm, but limitations of movement are difficult to measure with a new dislocation and a patient in pain.⁴

Any patient presenting with an anterior shoulder dislocation should also be screened for two other potential abnormalities. Hill-Sachs lesion, which occurs in up to 40% of anterior dislocations and 90% of all dislocations, is a cortical depression occurring in the humeral head. Bankart lesions, which occur in less than 5% of all dislocations, are avulsed bone fragments that occur when there is a glenoid labrum disruption.⁶ Both can be seen on plain films, although Bankart lesions are best seen on CT.⁴

The combination of an anterior dislocation and a humeral fracture, as seen in this case, is rare.⁷

POSTERIOR 

Posterior shoulder dislocations occur far less frequently than anterior dislocations, representing 2% to 5% of all shoulder dislocations.² They often result from blows to the anterior portion of the shoulder (ie, motor vehicle accidents or sports-related collisions) or violent muscle contractions (eg, electrocution, electroconvulsive therapy, or seizures). 

Unable to externally rotate the shoulder, patients with posterior dislocations present with the arm in adduction and internal rotation, making the coracoid process prominent (see illustration).⁸ This position is sometimes misdiagnosed as a “frozen shoulder.”²

INFERIOR

Inferior dislocation of the shoulder is the rarest type, accounting for only 0.5% of all cases of shoulder dislocation. The mechanism of injury is forceful hyperabduction and extension of the shoulder during a fall. 

Patients present with the affected arm hyperadducted, flexed at the elbow, with the hand positioned above or behind the head in fixed abduction:  a “hands up” position of the affected arm (see illustration). These dislocations are best identified via the transcapular “Y” radiographs. Inferior dislocations are often associated with neurovascular compromise, and there are often related tears of the infraspinatus, supraspinatus, and teres minor muscles.⁹

ASSOCIATION WITH SEIZURES

Any patient who has had a seizure is subject to a variety of injuries, including lacerations, contusions, long bone and skull fractures, and dislocations. Seizures with a fall are associated with a 20% chance of injury.¹⁰

Shaw et al were the first to note that, during an active convulsion, the patient’s shoulder is in adduction, internal rotation, and flexion. This positioning predisposes to injury: With sustained contraction of the surrounding shoulder girdle muscles, the humeral head is forced superiorly and posteriorly against the acromion andmedially against the glenoid fossa. The glenoid fossa is shallow; therefore, the humeral head is forced posteriorly and dislocates.¹¹

Researchers at the Mayo Clinic followed 247 patients who were diagnosed with seizures over nine years; 16% of the cohort experienced seizure-related injuries. Of the seizures recorded, 82% were tonic-clonic seizures. The singular predictive factor for injury was seizure frequency: Patients who had more seizures were more susceptible to injury.¹²

In an evaluation of outpatients with epilepsy, 25% of recorded seizures involved a fall. Among those who sustained an orthopedic injury, one injury occurred for every 178.6 generalized tonic-clonic seizures (0.6%)—a number that doubled for generalized tonic-clonic seizure associated with a fall (1.2%).¹⁰

The collective evidence from these and other studies suggests that patients who have poorly controlled tonic-clonic seizures have a higher incidence of seizures and, therefore, falls and injuries.^10,12 In the absence of known trauma, a posterior shoulder dislocation is almost pathognomonic of a seizure. In high-risk populations (ie, individuals who have poorly controlled diabetes or who are experiencing alcohol or drug withdrawal), suspicion for posterior shoulder dislocation should be elevated.⁸

After evaluation in the ED, the patient immediately underwent a nonsurgical closed reduction of the shoulder and suturing of the laceration. He was admitted overnight for further evaluation and was started on an anticonvulsant (levetiracetam). An orthopedic consult was obtained; the dislocation/fracture was managed conservatively with a sling for immobilization. No surgical intervention was recommended, since the patient had a manageable fracture without neurovascular compromise. He was discharged home within 36 hours and scheduled for follow-up appointments with both the neurologist and orthopedic surgeon. 

CONCLUSION

This patient had a seizure with an associated fall; both the laceration and the anterior shoulder dislocation with a humeral fracture were associated with the fall and not with tonic-clonic activity from the seizure. Because injuries vary widely from soft tissue to joint dislocations, with possible axillary nerve and/or artery damage, clinicians must do a comprehensive examination of patients entering the ED who have had seizures. Each injury must be addressed individually.

IN THIS ARTICLE

• Types of shoulder dislocations
• Schematics of the shoulder with three types of dislocations
• Association with seizures

CASE  A 59-year-old man with a remote history of seizures is transported to the emergency department (ED) by ambulance after a witnessed tonic-clonic seizure. At the time of arrival he is postictal and confused, but his vital signs are stable. A left eyebrow laceration indicating a possible fall is observed on physical exam, as is a left shoulder displacement with no obvious signs of neurovascular compromise. The patient is not currently taking anticonvulsant medication, stating that he has been “seizure free” for five years, and therefore chose to discontinue taking phenytoin against medical advice.

An anteroposterior (AP) bilateral shoulder x-ray is obtained in the ED (see Figures 1a and 1b). The image shows the humeral head to be anteriorly dislocated and reveals a large impaction fracture of the posterior superior humeral head. For a more detailed view of the fracture and to further assess any associated deformities, CT of the left shoulder is performed. The fracture has a depth of 11.6 mm and a length of 24.1 mm, with no additional pathology noted (see Figure 1c).

The shoulder is a large joint capable of moving in many directions and therefore is inherently unstable. The glenoid fossa is shallow, and stability of the joint is provided by both the fibrocartilaginous labrum and varying muscles of the rotator cuff. Because the shoulder joint is poorly supported, dislocations are not uncommon (see the illustrations). 

The first step in evaluating a suspected shoulder dislocation is to order an AP radiographic view of the shoulder (known as the Grashey view). A transcapular view (known as the scapular “Y” view) is also sufficient.¹ While diagnostic studies, such as CT or MRI arthrography, are excellent for evaluating the glenohumeral ligaments and labrum, they generally are not done in an acute setting.¹ For patients who present to the ED, some would recommend taking a CT scan, especially if a posterior dislocation is suspected.²

The three types of shoulder dislocations include anterior, posterior, and inferior.

ANTERIOR

Anterior dislocations account for 95% of all presented cases of shoulder dislocation, making them the most common type.³ They may be caused by a fall on an outstretched arm, trauma to the posterior humerus, or—more frequently—trauma to the arm while it is extended, externally rotated, and abducted (eg, blocking a shot in basketball).

A patient with an anterior dislocation will enter the ED with a slightly abducted and externally rotated arm (see illustration) and will resist any movement by the examiner. Typically, the shoulder loses its rounded appearance, and in thin individuals, the acromion may be prominent. A detailed neurovascular examination of the arm must be performed. 

Dislocation of the humerus in any direction may compromise the axillary nerve, artery, or both. The axillary nerve and artery run parallel to each other, beneath and in close proximity to the humeral head. The axillary artery is located upstream from the radial artery; compression of the artery may lead to a diminution or complete absence of the radial pulse and/or coolness of the hand.⁴ The axillary nerve is both a sensory and motor nerve. If injured, a 2- to 3-cm area over the lateral deltoid may have complete sensory loss, which can be tested for with a light touch and pinprick.⁵ The patient may also have difficulty abducting the arm, but limitations of movement are difficult to measure with a new dislocation and a patient in pain.⁴

Any patient presenting with an anterior shoulder dislocation should also be screened for two other potential abnormalities. Hill-Sachs lesion, which occurs in up to 40% of anterior dislocations and 90% of all dislocations, is a cortical depression occurring in the humeral head. Bankart lesions, which occur in less than 5% of all dislocations, are avulsed bone fragments that occur when there is a glenoid labrum disruption.⁶ Both can be seen on plain films, although Bankart lesions are best seen on CT.⁴

The combination of an anterior dislocation and a humeral fracture, as seen in this case, is rare.⁷

POSTERIOR 

Posterior shoulder dislocations occur far less frequently than anterior dislocations, representing 2% to 5% of all shoulder dislocations.² They often result from blows to the anterior portion of the shoulder (ie, motor vehicle accidents or sports-related collisions) or violent muscle contractions (eg, electrocution, electroconvulsive therapy, or seizures). 

Unable to externally rotate the shoulder, patients with posterior dislocations present with the arm in adduction and internal rotation, making the coracoid process prominent (see illustration).⁸ This position is sometimes misdiagnosed as a “frozen shoulder.”²

INFERIOR

Inferior dislocation of the shoulder is the rarest type, accounting for only 0.5% of all cases of shoulder dislocation. The mechanism of injury is forceful hyperabduction and extension of the shoulder during a fall. 

Patients present with the affected arm hyperadducted, flexed at the elbow, with the hand positioned above or behind the head in fixed abduction:  a “hands up” position of the affected arm (see illustration). These dislocations are best identified via the transcapular “Y” radiographs. Inferior dislocations are often associated with neurovascular compromise, and there are often related tears of the infraspinatus, supraspinatus, and teres minor muscles.⁹

ASSOCIATION WITH SEIZURES

Any patient who has had a seizure is subject to a variety of injuries, including lacerations, contusions, long bone and skull fractures, and dislocations. Seizures with a fall are associated with a 20% chance of injury.¹⁰

Shaw et al were the first to note that, during an active convulsion, the patient’s shoulder is in adduction, internal rotation, and flexion. This positioning predisposes to injury: With sustained contraction of the surrounding shoulder girdle muscles, the humeral head is forced superiorly and posteriorly against the acromion andmedially against the glenoid fossa. The glenoid fossa is shallow; therefore, the humeral head is forced posteriorly and dislocates.¹¹

Researchers at the Mayo Clinic followed 247 patients who were diagnosed with seizures over nine years; 16% of the cohort experienced seizure-related injuries. Of the seizures recorded, 82% were tonic-clonic seizures. The singular predictive factor for injury was seizure frequency: Patients who had more seizures were more susceptible to injury.¹²

In an evaluation of outpatients with epilepsy, 25% of recorded seizures involved a fall. Among those who sustained an orthopedic injury, one injury occurred for every 178.6 generalized tonic-clonic seizures (0.6%)—a number that doubled for generalized tonic-clonic seizure associated with a fall (1.2%).¹⁰

The collective evidence from these and other studies suggests that patients who have poorly controlled tonic-clonic seizures have a higher incidence of seizures and, therefore, falls and injuries.^10,12 In the absence of known trauma, a posterior shoulder dislocation is almost pathognomonic of a seizure. In high-risk populations (ie, individuals who have poorly controlled diabetes or who are experiencing alcohol or drug withdrawal), suspicion for posterior shoulder dislocation should be elevated.⁸

After evaluation in the ED, the patient immediately underwent a nonsurgical closed reduction of the shoulder and suturing of the laceration. He was admitted overnight for further evaluation and was started on an anticonvulsant (levetiracetam). An orthopedic consult was obtained; the dislocation/fracture was managed conservatively with a sling for immobilization. No surgical intervention was recommended, since the patient had a manageable fracture without neurovascular compromise. He was discharged home within 36 hours and scheduled for follow-up appointments with both the neurologist and orthopedic surgeon. 

CONCLUSION

This patient had a seizure with an associated fall; both the laceration and the anterior shoulder dislocation with a humeral fracture were associated with the fall and not with tonic-clonic activity from the seizure. Because injuries vary widely from soft tissue to joint dislocations, with possible axillary nerve and/or artery damage, clinicians must do a comprehensive examination of patients entering the ED who have had seizures. Each injury must be addressed individually.

IN THIS ARTICLE

• Types of shoulder dislocations
• Schematics of the shoulder with three types of dislocations
• Association with seizures

CASE  A 59-year-old man with a remote history of seizures is transported to the emergency department (ED) by ambulance after a witnessed tonic-clonic seizure. At the time of arrival he is postictal and confused, but his vital signs are stable. A left eyebrow laceration indicating a possible fall is observed on physical exam, as is a left shoulder displacement with no obvious signs of neurovascular compromise. The patient is not currently taking anticonvulsant medication, stating that he has been “seizure free” for five years, and therefore chose to discontinue taking phenytoin against medical advice.

An anteroposterior (AP) bilateral shoulder x-ray is obtained in the ED (see Figures 1a and 1b). The image shows the humeral head to be anteriorly dislocated and reveals a large impaction fracture of the posterior superior humeral head. For a more detailed view of the fracture and to further assess any associated deformities, CT of the left shoulder is performed. The fracture has a depth of 11.6 mm and a length of 24.1 mm, with no additional pathology noted (see Figure 1c).

The shoulder is a large joint capable of moving in many directions and therefore is inherently unstable. The glenoid fossa is shallow, and stability of the joint is provided by both the fibrocartilaginous labrum and varying muscles of the rotator cuff. Because the shoulder joint is poorly supported, dislocations are not uncommon (see the illustrations). 

The first step in evaluating a suspected shoulder dislocation is to order an AP radiographic view of the shoulder (known as the Grashey view). A transcapular view (known as the scapular “Y” view) is also sufficient.¹ While diagnostic studies, such as CT or MRI arthrography, are excellent for evaluating the glenohumeral ligaments and labrum, they generally are not done in an acute setting.¹ For patients who present to the ED, some would recommend taking a CT scan, especially if a posterior dislocation is suspected.²

The three types of shoulder dislocations include anterior, posterior, and inferior.

ANTERIOR

Anterior dislocations account for 95% of all presented cases of shoulder dislocation, making them the most common type.³ They may be caused by a fall on an outstretched arm, trauma to the posterior humerus, or—more frequently—trauma to the arm while it is extended, externally rotated, and abducted (eg, blocking a shot in basketball).

A patient with an anterior dislocation will enter the ED with a slightly abducted and externally rotated arm (see illustration) and will resist any movement by the examiner. Typically, the shoulder loses its rounded appearance, and in thin individuals, the acromion may be prominent. A detailed neurovascular examination of the arm must be performed. 

Dislocation of the humerus in any direction may compromise the axillary nerve, artery, or both. The axillary nerve and artery run parallel to each other, beneath and in close proximity to the humeral head. The axillary artery is located upstream from the radial artery; compression of the artery may lead to a diminution or complete absence of the radial pulse and/or coolness of the hand.⁴ The axillary nerve is both a sensory and motor nerve. If injured, a 2- to 3-cm area over the lateral deltoid may have complete sensory loss, which can be tested for with a light touch and pinprick.⁵ The patient may also have difficulty abducting the arm, but limitations of movement are difficult to measure with a new dislocation and a patient in pain.⁴

Any patient presenting with an anterior shoulder dislocation should also be screened for two other potential abnormalities. Hill-Sachs lesion, which occurs in up to 40% of anterior dislocations and 90% of all dislocations, is a cortical depression occurring in the humeral head. Bankart lesions, which occur in less than 5% of all dislocations, are avulsed bone fragments that occur when there is a glenoid labrum disruption.⁶ Both can be seen on plain films, although Bankart lesions are best seen on CT.⁴

The combination of an anterior dislocation and a humeral fracture, as seen in this case, is rare.⁷

POSTERIOR 

Posterior shoulder dislocations occur far less frequently than anterior dislocations, representing 2% to 5% of all shoulder dislocations.² They often result from blows to the anterior portion of the shoulder (ie, motor vehicle accidents or sports-related collisions) or violent muscle contractions (eg, electrocution, electroconvulsive therapy, or seizures). 

Unable to externally rotate the shoulder, patients with posterior dislocations present with the arm in adduction and internal rotation, making the coracoid process prominent (see illustration).⁸ This position is sometimes misdiagnosed as a “frozen shoulder.”²

INFERIOR

Inferior dislocation of the shoulder is the rarest type, accounting for only 0.5% of all cases of shoulder dislocation. The mechanism of injury is forceful hyperabduction and extension of the shoulder during a fall. 

Patients present with the affected arm hyperadducted, flexed at the elbow, with the hand positioned above or behind the head in fixed abduction:  a “hands up” position of the affected arm (see illustration). These dislocations are best identified via the transcapular “Y” radiographs. Inferior dislocations are often associated with neurovascular compromise, and there are often related tears of the infraspinatus, supraspinatus, and teres minor muscles.⁹

ASSOCIATION WITH SEIZURES

Any patient who has had a seizure is subject to a variety of injuries, including lacerations, contusions, long bone and skull fractures, and dislocations. Seizures with a fall are associated with a 20% chance of injury.¹⁰

Shaw et al were the first to note that, during an active convulsion, the patient’s shoulder is in adduction, internal rotation, and flexion. This positioning predisposes to injury: With sustained contraction of the surrounding shoulder girdle muscles, the humeral head is forced superiorly and posteriorly against the acromion andmedially against the glenoid fossa. The glenoid fossa is shallow; therefore, the humeral head is forced posteriorly and dislocates.¹¹

Researchers at the Mayo Clinic followed 247 patients who were diagnosed with seizures over nine years; 16% of the cohort experienced seizure-related injuries. Of the seizures recorded, 82% were tonic-clonic seizures. The singular predictive factor for injury was seizure frequency: Patients who had more seizures were more susceptible to injury.¹²

In an evaluation of outpatients with epilepsy, 25% of recorded seizures involved a fall. Among those who sustained an orthopedic injury, one injury occurred for every 178.6 generalized tonic-clonic seizures (0.6%)—a number that doubled for generalized tonic-clonic seizure associated with a fall (1.2%).¹⁰

The collective evidence from these and other studies suggests that patients who have poorly controlled tonic-clonic seizures have a higher incidence of seizures and, therefore, falls and injuries.^10,12 In the absence of known trauma, a posterior shoulder dislocation is almost pathognomonic of a seizure. In high-risk populations (ie, individuals who have poorly controlled diabetes or who are experiencing alcohol or drug withdrawal), suspicion for posterior shoulder dislocation should be elevated.⁸

After evaluation in the ED, the patient immediately underwent a nonsurgical closed reduction of the shoulder and suturing of the laceration. He was admitted overnight for further evaluation and was started on an anticonvulsant (levetiracetam). An orthopedic consult was obtained; the dislocation/fracture was managed conservatively with a sling for immobilization. No surgical intervention was recommended, since the patient had a manageable fracture without neurovascular compromise. He was discharged home within 36 hours and scheduled for follow-up appointments with both the neurologist and orthopedic surgeon. 

CONCLUSION

This patient had a seizure with an associated fall; both the laceration and the anterior shoulder dislocation with a humeral fracture were associated with the fall and not with tonic-clonic activity from the seizure. Because injuries vary widely from soft tissue to joint dislocations, with possible axillary nerve and/or artery damage, clinicians must do a comprehensive examination of patients entering the ED who have had seizures. Each injury must be addressed individually.

Clinical question: Does pulse variability on plethysmography, or the Pleth Variability Index (PVI), correlate with disease severity in obstructive airway disease in children?

Background: Asthma is the most common reason for hospitalization in the United S. for children 3-12 years old. Asthma accounts for a quarter of ED visits for children aged 1-9 years old.¹ Although systems have been developed to assess asthma exacerbation severity and the need for hospitalization, many of these depend on reassessments over time or have been proven to be invalid in larger studies.^2,3,4 Pulsus paradoxus (PP), which is defined as a drop in systolic blood pressure greater than 10 mm Hg, correlates with the severity of obstruction in asthma exacerbations, but it is not practical in the children being evaluated in the ED or hospital.^5,6 PP measurement using plethysmography has been found to correlate with measurement by sphygmomanometry.⁷ Furthermore, PVI, which is derived from amplitude variability in the pulse oximeter waveform, has been found to correlate with fluid responsiveness in mechanically ventilated patients. To this date, no study has assessed the correlation between PVI and exacerbation severity in asthma.

A printout of the first ED pulse oximetry reading was used to obtain the PImax and PImin as below:

Researchers followed patients after the initial evaluation to determine disposition from the ED, which included either discharge to home, admission to a general pediatrics floor, or admission to the PICU. The hospital utilized specific criteria for disposition from the ED (see Table 1).

References

1. Care of children and adolescents in U.S. hospitals. Agency for Healthcare Research and Quality website. Available at: https://archive.ahrq.gov/data/hcup/factbk4/factbk4.htm. Accessed Nov. 18, 2016.

2. Kelly AM, Kerr D, Powell C. Is severity assessment after one hour of treatment better for predicting the need for admission in acute asthma? Respir Med. 2004;98(8):777-781.

3. Keogh KA, Macarthur C, Parkin PC, et al. Predictors of hospitalization in children with acute asthma. J Pediatr. 2001;139(2):273-277.

4. Keahey L, Bulloch B, Becker AB, et al. Initial oxygen saturation as a predictor of admission in children presenting to the emergency department with acute asthma. Ann Emerg Med. 2002;40(3):300-307.

5. Guntheroth WG, Morgan BC, Mullins GL. Effect of respiration on venous return and stroke volume in cardiac tamponade. Mechanism of pulsus paradoxus. Circ Res. 1967;20(4):381-390.

6. Frey B, Freezer N. Diagnostic value and pathophysiologic basis of pulsus paradoxus in infants and children with respiratory disease. Pediatr Pulmonol. 2001;31(2):138-143.

7. Clark JA, Lieh-Lai M, Thomas R, Raghavan K, Sarnaik AP. Comparison of traditional and plethysmographic methods for measuring pulsus paradoxus. Arch Pediatr Adolesc Med. 2004;158(1):48-51.
 

Clinical question: Does pulse variability on plethysmography, or the Pleth Variability Index (PVI), correlate with disease severity in obstructive airway disease in children?

Background: Asthma is the most common reason for hospitalization in the United S. for children 3-12 years old. Asthma accounts for a quarter of ED visits for children aged 1-9 years old.¹ Although systems have been developed to assess asthma exacerbation severity and the need for hospitalization, many of these depend on reassessments over time or have been proven to be invalid in larger studies.^2,3,4 Pulsus paradoxus (PP), which is defined as a drop in systolic blood pressure greater than 10 mm Hg, correlates with the severity of obstruction in asthma exacerbations, but it is not practical in the children being evaluated in the ED or hospital.^5,6 PP measurement using plethysmography has been found to correlate with measurement by sphygmomanometry.⁷ Furthermore, PVI, which is derived from amplitude variability in the pulse oximeter waveform, has been found to correlate with fluid responsiveness in mechanically ventilated patients. To this date, no study has assessed the correlation between PVI and exacerbation severity in asthma.

A printout of the first ED pulse oximetry reading was used to obtain the PImax and PImin as below:

Researchers followed patients after the initial evaluation to determine disposition from the ED, which included either discharge to home, admission to a general pediatrics floor, or admission to the PICU. The hospital utilized specific criteria for disposition from the ED (see Table 1).

References

1. Care of children and adolescents in U.S. hospitals. Agency for Healthcare Research and Quality website. Available at: https://archive.ahrq.gov/data/hcup/factbk4/factbk4.htm. Accessed Nov. 18, 2016.

2. Kelly AM, Kerr D, Powell C. Is severity assessment after one hour of treatment better for predicting the need for admission in acute asthma? Respir Med. 2004;98(8):777-781.

3. Keogh KA, Macarthur C, Parkin PC, et al. Predictors of hospitalization in children with acute asthma. J Pediatr. 2001;139(2):273-277.

4. Keahey L, Bulloch B, Becker AB, et al. Initial oxygen saturation as a predictor of admission in children presenting to the emergency department with acute asthma. Ann Emerg Med. 2002;40(3):300-307.

5. Guntheroth WG, Morgan BC, Mullins GL. Effect of respiration on venous return and stroke volume in cardiac tamponade. Mechanism of pulsus paradoxus. Circ Res. 1967;20(4):381-390.

6. Frey B, Freezer N. Diagnostic value and pathophysiologic basis of pulsus paradoxus in infants and children with respiratory disease. Pediatr Pulmonol. 2001;31(2):138-143.

7. Clark JA, Lieh-Lai M, Thomas R, Raghavan K, Sarnaik AP. Comparison of traditional and plethysmographic methods for measuring pulsus paradoxus. Arch Pediatr Adolesc Med. 2004;158(1):48-51.
 

Clinical question: Does pulse variability on plethysmography, or the Pleth Variability Index (PVI), correlate with disease severity in obstructive airway disease in children?

Background: Asthma is the most common reason for hospitalization in the United S. for children 3-12 years old. Asthma accounts for a quarter of ED visits for children aged 1-9 years old.¹ Although systems have been developed to assess asthma exacerbation severity and the need for hospitalization, many of these depend on reassessments over time or have been proven to be invalid in larger studies.^2,3,4 Pulsus paradoxus (PP), which is defined as a drop in systolic blood pressure greater than 10 mm Hg, correlates with the severity of obstruction in asthma exacerbations, but it is not practical in the children being evaluated in the ED or hospital.^5,6 PP measurement using plethysmography has been found to correlate with measurement by sphygmomanometry.⁷ Furthermore, PVI, which is derived from amplitude variability in the pulse oximeter waveform, has been found to correlate with fluid responsiveness in mechanically ventilated patients. To this date, no study has assessed the correlation between PVI and exacerbation severity in asthma.

A printout of the first ED pulse oximetry reading was used to obtain the PImax and PImin as below:

Researchers followed patients after the initial evaluation to determine disposition from the ED, which included either discharge to home, admission to a general pediatrics floor, or admission to the PICU. The hospital utilized specific criteria for disposition from the ED (see Table 1).

References

1. Care of children and adolescents in U.S. hospitals. Agency for Healthcare Research and Quality website. Available at: https://archive.ahrq.gov/data/hcup/factbk4/factbk4.htm. Accessed Nov. 18, 2016.

2. Kelly AM, Kerr D, Powell C. Is severity assessment after one hour of treatment better for predicting the need for admission in acute asthma? Respir Med. 2004;98(8):777-781.

3. Keogh KA, Macarthur C, Parkin PC, et al. Predictors of hospitalization in children with acute asthma. J Pediatr. 2001;139(2):273-277.

4. Keahey L, Bulloch B, Becker AB, et al. Initial oxygen saturation as a predictor of admission in children presenting to the emergency department with acute asthma. Ann Emerg Med. 2002;40(3):300-307.

5. Guntheroth WG, Morgan BC, Mullins GL. Effect of respiration on venous return and stroke volume in cardiac tamponade. Mechanism of pulsus paradoxus. Circ Res. 1967;20(4):381-390.

6. Frey B, Freezer N. Diagnostic value and pathophysiologic basis of pulsus paradoxus in infants and children with respiratory disease. Pediatr Pulmonol. 2001;31(2):138-143.

7. Clark JA, Lieh-Lai M, Thomas R, Raghavan K, Sarnaik AP. Comparison of traditional and plethysmographic methods for measuring pulsus paradoxus. Arch Pediatr Adolesc Med. 2004;158(1):48-51.
 

We work in complex environments and in a flawed and rapidly changing health care system. Caregivers, patients, and communities will be led through this complexity by those who embrace change. Last October, I had the privilege of attending and facilitating the SHM Leadership Academy in Orlando, which allowed me the opportunity to meet a group of people who embrace change, including the benefits and challenges that often accompany it.

SHM board member Jeff Glasheen, MD, SFHM, taught one of the first lessons at Leadership Academy, focusing on the importance of meaningful, difficult change. With comparisons to companies that have embraced change, like Apple, and some that have not, like Sears, Jeff summed up how complacency with “good” and a reluctance to tackle the difficulty of change keeps organizations – and people – from becoming great.

“Good is the enemy of great,” Jeff preached.

He largely focused on hospitalists leading organizational change, but the concepts can apply to personal change, too. He explained that “people generally want things to be different, but they don’t want to change.”

Leaders in training

Ten emerging hospitalist leaders sat at my table, soaking in the message. Several of them, like me 8 years ago, had the responsibilities of leadership unexpectedly thrust upon them. Some carried with them the heavy expectations of their colleagues or hospital administration (or both) that by being elevated into a role such as medical director, they would abruptly be able to make improvements in patient care and hospital operations. They had accepted the challenge to change – to move out of purely clinical roles and take on new ones in leadership despite having little or no experience. Doing so, they gingerly but willingly were following in the footsteps of leaders before them, growing their skills, improving their hospitals, and laying a path for future leaders to follow.

A few weeks prior, I had taken a new leadership position myself. The Cleveland Clinic recently acquired a hospital and health system in Akron, Ohio, about 40 miles away from the city. I assumed the role of president of this acquisition, embracing the complex challenge of leading the process of integrating two health systems. After 3 years overseeing a different hospital in the health system, I finally felt I had developed the people, processes, and culture that I had been striving to build. But like the young leaders at Leadership Academy, I had the opportunity to change, grow, develop, take on new risk, and become a stronger leader in this new role. A significant part of the experience of the Leadership Academy involves table exercises. For the first few exercises, the group was quiet, uncertain, tentative. I was struck both by how early these individuals were in their development and by how so much of what is happening today in hospitals and health care is dependent upon the development and success of individuals like these who are enthusiastic and talented but young and overwhelmed.

I believe that successful hospitalists are, through experience, training, and nature, rapid assimilators into their environments. By the third day, the dynamic at my table had gone from tentative and uncertain to much more confident and assertive. To experience this transformation in person at SHM’s Leadership Academy, we welcome you to Scottsdale, Ariz., later this year. Learn more about the program at www.shmleadershipacademy.org.

At Leadership Academy and beyond, I implore hospitalists to look for opportunities to change during this time of New Year’s resolutions and to take the opposite posture and want to change – change how we think, act, and respond; change our roles to take on new, uncomfortable responsibilities; and change how we view change itself.

We will be better for it both personally and professionally, and we will stand out as role models for our colleagues, coworkers, and hospitalists who follow in our footsteps.

Dr. Harte is a practicing hospitalist, president of the Society of Hospital Medicine, and president of Hillcrest Hospital in Mayfield Heights, Ohio, part of the Cleveland Clinic Health System. He is associate professor of medicine at the Cleveland Clinic, Lerner College of Medicine in Cleveland.

We work in complex environments and in a flawed and rapidly changing health care system. Caregivers, patients, and communities will be led through this complexity by those who embrace change. Last October, I had the privilege of attending and facilitating the SHM Leadership Academy in Orlando, which allowed me the opportunity to meet a group of people who embrace change, including the benefits and challenges that often accompany it.

SHM board member Jeff Glasheen, MD, SFHM, taught one of the first lessons at Leadership Academy, focusing on the importance of meaningful, difficult change. With comparisons to companies that have embraced change, like Apple, and some that have not, like Sears, Jeff summed up how complacency with “good” and a reluctance to tackle the difficulty of change keeps organizations – and people – from becoming great.

“Good is the enemy of great,” Jeff preached.

He largely focused on hospitalists leading organizational change, but the concepts can apply to personal change, too. He explained that “people generally want things to be different, but they don’t want to change.”

Leaders in training

Ten emerging hospitalist leaders sat at my table, soaking in the message. Several of them, like me 8 years ago, had the responsibilities of leadership unexpectedly thrust upon them. Some carried with them the heavy expectations of their colleagues or hospital administration (or both) that by being elevated into a role such as medical director, they would abruptly be able to make improvements in patient care and hospital operations. They had accepted the challenge to change – to move out of purely clinical roles and take on new ones in leadership despite having little or no experience. Doing so, they gingerly but willingly were following in the footsteps of leaders before them, growing their skills, improving their hospitals, and laying a path for future leaders to follow.

A few weeks prior, I had taken a new leadership position myself. The Cleveland Clinic recently acquired a hospital and health system in Akron, Ohio, about 40 miles away from the city. I assumed the role of president of this acquisition, embracing the complex challenge of leading the process of integrating two health systems. After 3 years overseeing a different hospital in the health system, I finally felt I had developed the people, processes, and culture that I had been striving to build. But like the young leaders at Leadership Academy, I had the opportunity to change, grow, develop, take on new risk, and become a stronger leader in this new role. A significant part of the experience of the Leadership Academy involves table exercises. For the first few exercises, the group was quiet, uncertain, tentative. I was struck both by how early these individuals were in their development and by how so much of what is happening today in hospitals and health care is dependent upon the development and success of individuals like these who are enthusiastic and talented but young and overwhelmed.

I believe that successful hospitalists are, through experience, training, and nature, rapid assimilators into their environments. By the third day, the dynamic at my table had gone from tentative and uncertain to much more confident and assertive. To experience this transformation in person at SHM’s Leadership Academy, we welcome you to Scottsdale, Ariz., later this year. Learn more about the program at www.shmleadershipacademy.org.

At Leadership Academy and beyond, I implore hospitalists to look for opportunities to change during this time of New Year’s resolutions and to take the opposite posture and want to change – change how we think, act, and respond; change our roles to take on new, uncomfortable responsibilities; and change how we view change itself.

We will be better for it both personally and professionally, and we will stand out as role models for our colleagues, coworkers, and hospitalists who follow in our footsteps.

Dr. Harte is a practicing hospitalist, president of the Society of Hospital Medicine, and president of Hillcrest Hospital in Mayfield Heights, Ohio, part of the Cleveland Clinic Health System. He is associate professor of medicine at the Cleveland Clinic, Lerner College of Medicine in Cleveland.

We work in complex environments and in a flawed and rapidly changing health care system. Caregivers, patients, and communities will be led through this complexity by those who embrace change. Last October, I had the privilege of attending and facilitating the SHM Leadership Academy in Orlando, which allowed me the opportunity to meet a group of people who embrace change, including the benefits and challenges that often accompany it.

SHM board member Jeff Glasheen, MD, SFHM, taught one of the first lessons at Leadership Academy, focusing on the importance of meaningful, difficult change. With comparisons to companies that have embraced change, like Apple, and some that have not, like Sears, Jeff summed up how complacency with “good” and a reluctance to tackle the difficulty of change keeps organizations – and people – from becoming great.

“Good is the enemy of great,” Jeff preached.

He largely focused on hospitalists leading organizational change, but the concepts can apply to personal change, too. He explained that “people generally want things to be different, but they don’t want to change.”

Leaders in training

Ten emerging hospitalist leaders sat at my table, soaking in the message. Several of them, like me 8 years ago, had the responsibilities of leadership unexpectedly thrust upon them. Some carried with them the heavy expectations of their colleagues or hospital administration (or both) that by being elevated into a role such as medical director, they would abruptly be able to make improvements in patient care and hospital operations. They had accepted the challenge to change – to move out of purely clinical roles and take on new ones in leadership despite having little or no experience. Doing so, they gingerly but willingly were following in the footsteps of leaders before them, growing their skills, improving their hospitals, and laying a path for future leaders to follow.

A few weeks prior, I had taken a new leadership position myself. The Cleveland Clinic recently acquired a hospital and health system in Akron, Ohio, about 40 miles away from the city. I assumed the role of president of this acquisition, embracing the complex challenge of leading the process of integrating two health systems. After 3 years overseeing a different hospital in the health system, I finally felt I had developed the people, processes, and culture that I had been striving to build. But like the young leaders at Leadership Academy, I had the opportunity to change, grow, develop, take on new risk, and become a stronger leader in this new role. A significant part of the experience of the Leadership Academy involves table exercises. For the first few exercises, the group was quiet, uncertain, tentative. I was struck both by how early these individuals were in their development and by how so much of what is happening today in hospitals and health care is dependent upon the development and success of individuals like these who are enthusiastic and talented but young and overwhelmed.

I believe that successful hospitalists are, through experience, training, and nature, rapid assimilators into their environments. By the third day, the dynamic at my table had gone from tentative and uncertain to much more confident and assertive. To experience this transformation in person at SHM’s Leadership Academy, we welcome you to Scottsdale, Ariz., later this year. Learn more about the program at www.shmleadershipacademy.org.

At Leadership Academy and beyond, I implore hospitalists to look for opportunities to change during this time of New Year’s resolutions and to take the opposite posture and want to change – change how we think, act, and respond; change our roles to take on new, uncomfortable responsibilities; and change how we view change itself.

We will be better for it both personally and professionally, and we will stand out as role models for our colleagues, coworkers, and hospitalists who follow in our footsteps.

Dr. Harte is a practicing hospitalist, president of the Society of Hospital Medicine, and president of Hillcrest Hospital in Mayfield Heights, Ohio, part of the Cleveland Clinic Health System. He is associate professor of medicine at the Cleveland Clinic, Lerner College of Medicine in Cleveland.

Unveiling the hospitalist specialty code

The Centers for Medicare & Medicaid Services announced in November the official implementation date for the Medicare physician specialty code for hospitalists. On April 3, “hospitalist” will be an official specialty designation under Medicare; the code will be C6. Starting on that date, hospitalists can change their specialty designation on the Medicare enrollment application (Form CMS-855I) or through CMS’ online portal (Provider Enrollment, Chain, and Ownership System, or PECOS).

Appropriate use of specialty codes helps distinguish differences among providers and improves the quality of utilization data. SHM applied for a specialty code for hospitalists nearly 3 years ago, and CMS approved the application in February 2016.

Stand with your fellow hospitalists and make sure to declare, “I’m a C6.”
 

Develop curricula to educate, engage medical students and residents

The ACGME requirements for training in quality and safety are changing – it is no longer an elective. As sponsoring institutions’ residency and fellowship programs mobilize to meet these requirements, leaders may find few faculty members are comfortable enough with the material to teach and create educational content for trainees. These faculty need further development.

Sponsored by SHM, the Quality and Safety Educators Academy (QSEA) responds to that demand by providing medical educators with the knowledge and tools to integrate quality improvement and safety concepts into their curricula. The 2017 meeting is Feb. 26-28 at the Tempe Mission Palms Hotel in Arizona.

This 2½ day meeting aims to fill the current gaps for faculty by offering basic concepts and educational tools in quality improvement and patient safety. Material is presented in an interactive way, providing guidance on career and curriculum development and establishing a national network of quality and safety educators.

For more information and to register, visit www.shmqsea.org.
 

EHRs: blessing or curse?

SHM’s Health Information Technology (HIT) Committee invited you to participate in a brief survey to inform your experiences with inpatient electronic health record (EHR) systems. The results will serve as a foundation for a white paper to be written by the HIT Committee addressing hospitalists’ attitudes toward EHR systems. It will be released next month, so stay tuned then to view the final paper.

SHM chapters: Your connection to local education, networking, leadership opportunities

SHM offers various opportunities to grow professionally, expand your CV, and engage with other hospitalists. With more than 50 chapters across the country, you can network, learn, teach, and continue to improve patient care at a local level. Find a chapter in your area or start a chapter today by visiting www.hospitalmedicine.org/chapters.

Enhance opioid safety for inpatients

SHM enrolled 10 hospitals into a second mentored implementation cohort around Reducing Adverse Drug Events Related to Opioids (RADEO). The program is now in its second month as the sites work with their mentors to enhance safety for patients in the hospital who are prescribed opioid medications by:

• Developing a needs assessment.
• Putting in place formal selections of data collection measures.
• Beginning to take outcomes and process data collection on intervention units.
• Starting to design and implement key interventions.

Even if you’re not in this mentored implementation cohort, visit www.hospitalmedicine.org/RADEO and view the online toolkit or download the implementation guide.
 

Earn recognition for your research with SHM’s Junior Investigator Award

The SHM Junior Investigator Award was created for junior/early-stage investigators, defined as faculty in the first 5 years of their most recent position/appointment. Applicants must be a hospitalist or clinician-investigators whose research interests focus on the care of hospitalized patients, the organization of hospitals, or the practice of hospitalists. Applicants must be members of SHM in good standing. Nominations from mentors and self-nominations are both welcome.

The winner will be invited to receive the award during SHM’s annual meeting, HM17, May 1-4, at Mandalay Bay Resort and Casino in Las Vegas. The winner will receive complimentary registration for this meeting as well as a complimentary 1-year membership to SHM.

For more information on the application process, visit www.hospitalmedicine.org/juniorinvestigator.
 

Unveiling the hospitalist specialty code

The Centers for Medicare & Medicaid Services announced in November the official implementation date for the Medicare physician specialty code for hospitalists. On April 3, “hospitalist” will be an official specialty designation under Medicare; the code will be C6. Starting on that date, hospitalists can change their specialty designation on the Medicare enrollment application (Form CMS-855I) or through CMS’ online portal (Provider Enrollment, Chain, and Ownership System, or PECOS).

Appropriate use of specialty codes helps distinguish differences among providers and improves the quality of utilization data. SHM applied for a specialty code for hospitalists nearly 3 years ago, and CMS approved the application in February 2016.

Stand with your fellow hospitalists and make sure to declare, “I’m a C6.”
 

Develop curricula to educate, engage medical students and residents

The ACGME requirements for training in quality and safety are changing – it is no longer an elective. As sponsoring institutions’ residency and fellowship programs mobilize to meet these requirements, leaders may find few faculty members are comfortable enough with the material to teach and create educational content for trainees. These faculty need further development.

Sponsored by SHM, the Quality and Safety Educators Academy (QSEA) responds to that demand by providing medical educators with the knowledge and tools to integrate quality improvement and safety concepts into their curricula. The 2017 meeting is Feb. 26-28 at the Tempe Mission Palms Hotel in Arizona.

This 2½ day meeting aims to fill the current gaps for faculty by offering basic concepts and educational tools in quality improvement and patient safety. Material is presented in an interactive way, providing guidance on career and curriculum development and establishing a national network of quality and safety educators.

For more information and to register, visit www.shmqsea.org.
 

EHRs: blessing or curse?

SHM’s Health Information Technology (HIT) Committee invited you to participate in a brief survey to inform your experiences with inpatient electronic health record (EHR) systems. The results will serve as a foundation for a white paper to be written by the HIT Committee addressing hospitalists’ attitudes toward EHR systems. It will be released next month, so stay tuned then to view the final paper.

SHM chapters: Your connection to local education, networking, leadership opportunities

SHM offers various opportunities to grow professionally, expand your CV, and engage with other hospitalists. With more than 50 chapters across the country, you can network, learn, teach, and continue to improve patient care at a local level. Find a chapter in your area or start a chapter today by visiting www.hospitalmedicine.org/chapters.

Enhance opioid safety for inpatients

SHM enrolled 10 hospitals into a second mentored implementation cohort around Reducing Adverse Drug Events Related to Opioids (RADEO). The program is now in its second month as the sites work with their mentors to enhance safety for patients in the hospital who are prescribed opioid medications by:

• Developing a needs assessment.
• Putting in place formal selections of data collection measures.
• Beginning to take outcomes and process data collection on intervention units.
• Starting to design and implement key interventions.

Even if you’re not in this mentored implementation cohort, visit www.hospitalmedicine.org/RADEO and view the online toolkit or download the implementation guide.
 

Earn recognition for your research with SHM’s Junior Investigator Award

The SHM Junior Investigator Award was created for junior/early-stage investigators, defined as faculty in the first 5 years of their most recent position/appointment. Applicants must be a hospitalist or clinician-investigators whose research interests focus on the care of hospitalized patients, the organization of hospitals, or the practice of hospitalists. Applicants must be members of SHM in good standing. Nominations from mentors and self-nominations are both welcome.

The winner will be invited to receive the award during SHM’s annual meeting, HM17, May 1-4, at Mandalay Bay Resort and Casino in Las Vegas. The winner will receive complimentary registration for this meeting as well as a complimentary 1-year membership to SHM.

For more information on the application process, visit www.hospitalmedicine.org/juniorinvestigator.
 

Unveiling the hospitalist specialty code

The Centers for Medicare & Medicaid Services announced in November the official implementation date for the Medicare physician specialty code for hospitalists. On April 3, “hospitalist” will be an official specialty designation under Medicare; the code will be C6. Starting on that date, hospitalists can change their specialty designation on the Medicare enrollment application (Form CMS-855I) or through CMS’ online portal (Provider Enrollment, Chain, and Ownership System, or PECOS).

Appropriate use of specialty codes helps distinguish differences among providers and improves the quality of utilization data. SHM applied for a specialty code for hospitalists nearly 3 years ago, and CMS approved the application in February 2016.

Stand with your fellow hospitalists and make sure to declare, “I’m a C6.”
 

Develop curricula to educate, engage medical students and residents

The ACGME requirements for training in quality and safety are changing – it is no longer an elective. As sponsoring institutions’ residency and fellowship programs mobilize to meet these requirements, leaders may find few faculty members are comfortable enough with the material to teach and create educational content for trainees. These faculty need further development.

Sponsored by SHM, the Quality and Safety Educators Academy (QSEA) responds to that demand by providing medical educators with the knowledge and tools to integrate quality improvement and safety concepts into their curricula. The 2017 meeting is Feb. 26-28 at the Tempe Mission Palms Hotel in Arizona.

This 2½ day meeting aims to fill the current gaps for faculty by offering basic concepts and educational tools in quality improvement and patient safety. Material is presented in an interactive way, providing guidance on career and curriculum development and establishing a national network of quality and safety educators.

For more information and to register, visit www.shmqsea.org.
 

EHRs: blessing or curse?

SHM’s Health Information Technology (HIT) Committee invited you to participate in a brief survey to inform your experiences with inpatient electronic health record (EHR) systems. The results will serve as a foundation for a white paper to be written by the HIT Committee addressing hospitalists’ attitudes toward EHR systems. It will be released next month, so stay tuned then to view the final paper.

SHM chapters: Your connection to local education, networking, leadership opportunities

SHM offers various opportunities to grow professionally, expand your CV, and engage with other hospitalists. With more than 50 chapters across the country, you can network, learn, teach, and continue to improve patient care at a local level. Find a chapter in your area or start a chapter today by visiting www.hospitalmedicine.org/chapters.

Enhance opioid safety for inpatients

SHM enrolled 10 hospitals into a second mentored implementation cohort around Reducing Adverse Drug Events Related to Opioids (RADEO). The program is now in its second month as the sites work with their mentors to enhance safety for patients in the hospital who are prescribed opioid medications by:

• Developing a needs assessment.
• Putting in place formal selections of data collection measures.
• Beginning to take outcomes and process data collection on intervention units.
• Starting to design and implement key interventions.

Even if you’re not in this mentored implementation cohort, visit www.hospitalmedicine.org/RADEO and view the online toolkit or download the implementation guide.
 

Earn recognition for your research with SHM’s Junior Investigator Award

The SHM Junior Investigator Award was created for junior/early-stage investigators, defined as faculty in the first 5 years of their most recent position/appointment. Applicants must be a hospitalist or clinician-investigators whose research interests focus on the care of hospitalized patients, the organization of hospitals, or the practice of hospitalists. Applicants must be members of SHM in good standing. Nominations from mentors and self-nominations are both welcome.

The winner will be invited to receive the award during SHM’s annual meeting, HM17, May 1-4, at Mandalay Bay Resort and Casino in Las Vegas. The winner will receive complimentary registration for this meeting as well as a complimentary 1-year membership to SHM.

For more information on the application process, visit www.hospitalmedicine.org/juniorinvestigator.
 

Here are 5 articles in the January issue of Clinician Reviews (individual articles are valid for one year from date of publication—expiration dates below):

1. Gluten-free Adherence Triples While Celiac Disease Prevalence Remains Stable

To take the posttest, go to: http://bit.ly/2h2LFDu
Expires September 6, 2017

2. Fluoxetine Appears Safer  for Bone Health in At-risk Older Patients

To take the posttest, go to: http://bit.ly/2he1FTD
Expires September 15, 2017

3. High Free T4 Levels Linked to Sudden Cardiac Death

To take the posttest, go to: http://bit.ly/2gMJqUz
Expires September 16, 2017

4. Morning Sickness Linked to Lower Risk for Pregnancy Loss

To take the posttest, go to: http://bit.ly/2uaWMkH
Expires September 26, 2017

5. Anxiety, Depression May Precede Parkinson's by 25 Years

To take the posttest, go to: http://bit.ly/2gMFQtr
Expires September 27, 2017

Here are 5 articles in the January issue of Clinician Reviews (individual articles are valid for one year from date of publication—expiration dates below):

1. Gluten-free Adherence Triples While Celiac Disease Prevalence Remains Stable

To take the posttest, go to: http://bit.ly/2h2LFDu
Expires September 6, 2017

2. Fluoxetine Appears Safer  for Bone Health in At-risk Older Patients

To take the posttest, go to: http://bit.ly/2he1FTD
Expires September 15, 2017

3. High Free T4 Levels Linked to Sudden Cardiac Death

To take the posttest, go to: http://bit.ly/2gMJqUz
Expires September 16, 2017

4. Morning Sickness Linked to Lower Risk for Pregnancy Loss

To take the posttest, go to: http://bit.ly/2uaWMkH
Expires September 26, 2017

5. Anxiety, Depression May Precede Parkinson's by 25 Years

To take the posttest, go to: http://bit.ly/2gMFQtr
Expires September 27, 2017

Here are 5 articles in the January issue of Clinician Reviews (individual articles are valid for one year from date of publication—expiration dates below):

1. Gluten-free Adherence Triples While Celiac Disease Prevalence Remains Stable

To take the posttest, go to: http://bit.ly/2h2LFDu
Expires September 6, 2017

2. Fluoxetine Appears Safer  for Bone Health in At-risk Older Patients

To take the posttest, go to: http://bit.ly/2he1FTD
Expires September 15, 2017

3. High Free T4 Levels Linked to Sudden Cardiac Death

To take the posttest, go to: http://bit.ly/2gMJqUz
Expires September 16, 2017

4. Morning Sickness Linked to Lower Risk for Pregnancy Loss

To take the posttest, go to: http://bit.ly/2uaWMkH
Expires September 26, 2017

5. Anxiety, Depression May Precede Parkinson's by 25 Years

To take the posttest, go to: http://bit.ly/2gMFQtr
Expires September 27, 2017

Did mother’s allergic reaction cause fetal injury?

When a mother was admitted to the labor and delivery unit, she had strep throat; ampicillin was administered. She experienced anaphylactic symptoms that were attended to. The baby, delivered vaginally 3 hours later, was severely distressed and showed signs of asphyxia. He was found to have a permanent brain injury.

PARENTS’ CLAIM:

The ObGyn and hospital nurses failed to properly manage the mother’s anaphylactic reaction to ampicillin. Fetal heart-rate tracings indicated fetal distress. Standard of care required prompt intervention with epinephrine and/or emergency cesarean delivery. Brain injury occurred because these procedures were not performed.

DEFENDANTS’ DEFENSE:

The nurses denied fault and explained that they appropriately and immediately responded to mild anaphylactic symptoms in the mother. They could not administer epinephrine because the ObGyn did not order it.

The ObGyn denied violating the standard of care that included minimizing the mother’s allergic reaction. Because the mother didn’t have a rash, it was not necessary to order epinephrine. The baby sustained an unknown injury earlier in the pregnancy that was unrelated to labor.

VERDICT:

A Tennessee defense verdict was returned.

Resident blamed for shoulder dystocia

A mother presented to a federally funded health center in labor. A first-year resident managed labor and delivery under the supervision of the attending physician. Shoulder dystocia was encountered and the baby suffered a permanent brachial plexus injury.

PARENTS’ CLAIM:

Negligence occurred when the resident used excessive force by pulling on the infant’s neck during delivery. The resident, who had just received his medical license, was poorly supervised by the attending physician.

DEFENDANTS’ DEFENSE:

Suit was brought against the resident, the attending physician, the federal government, and the hospital’s residency program. The resident denied using excessive force. As soon as delivery became complex, the attending physician completed the delivery. The baby’s injuries were unpredictable and unavoidable.

VERDICT:

A $290,000 settlement with the federal government was reached before trial. A Pennsylvania defense verdict was returned for the other parties.

Related Article:
Tackle the challenging shoulder dystocia emergency by practicing delivery of the posterior arm

What caused brachial plexus injury?

An experienced midwife delivered a baby who sustained a brachial plexus injury resulting in flail arm syndrome.

PARENTS’ CLAIM:

The midwife mismanaged the delivery causing permanent injury. The child has gained little improvement with surgery and physical therapy.

DEFENDANTS’ DEFENSE:

The injury was caused by the natural forces of labor. The midwife used appropriate techniques during the birth.

VERDICT:

A Washington defense verdict was returned.

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Did mother’s allergic reaction cause fetal injury?

When a mother was admitted to the labor and delivery unit, she had strep throat; ampicillin was administered. She experienced anaphylactic symptoms that were attended to. The baby, delivered vaginally 3 hours later, was severely distressed and showed signs of asphyxia. He was found to have a permanent brain injury.

PARENTS’ CLAIM:

The ObGyn and hospital nurses failed to properly manage the mother’s anaphylactic reaction to ampicillin. Fetal heart-rate tracings indicated fetal distress. Standard of care required prompt intervention with epinephrine and/or emergency cesarean delivery. Brain injury occurred because these procedures were not performed.

DEFENDANTS’ DEFENSE:

The nurses denied fault and explained that they appropriately and immediately responded to mild anaphylactic symptoms in the mother. They could not administer epinephrine because the ObGyn did not order it.

The ObGyn denied violating the standard of care that included minimizing the mother’s allergic reaction. Because the mother didn’t have a rash, it was not necessary to order epinephrine. The baby sustained an unknown injury earlier in the pregnancy that was unrelated to labor.

VERDICT:

A Tennessee defense verdict was returned.

Resident blamed for shoulder dystocia

A mother presented to a federally funded health center in labor. A first-year resident managed labor and delivery under the supervision of the attending physician. Shoulder dystocia was encountered and the baby suffered a permanent brachial plexus injury.

PARENTS’ CLAIM:

Negligence occurred when the resident used excessive force by pulling on the infant’s neck during delivery. The resident, who had just received his medical license, was poorly supervised by the attending physician.

DEFENDANTS’ DEFENSE:

Suit was brought against the resident, the attending physician, the federal government, and the hospital’s residency program. The resident denied using excessive force. As soon as delivery became complex, the attending physician completed the delivery. The baby’s injuries were unpredictable and unavoidable.

VERDICT:

A $290,000 settlement with the federal government was reached before trial. A Pennsylvania defense verdict was returned for the other parties.

Related Article:
Tackle the challenging shoulder dystocia emergency by practicing delivery of the posterior arm

What caused brachial plexus injury?

An experienced midwife delivered a baby who sustained a brachial plexus injury resulting in flail arm syndrome.

PARENTS’ CLAIM:

The midwife mismanaged the delivery causing permanent injury. The child has gained little improvement with surgery and physical therapy.

DEFENDANTS’ DEFENSE:

The injury was caused by the natural forces of labor. The midwife used appropriate techniques during the birth.

VERDICT:

A Washington defense verdict was returned.

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Did mother’s allergic reaction cause fetal injury?

When a mother was admitted to the labor and delivery unit, she had strep throat; ampicillin was administered. She experienced anaphylactic symptoms that were attended to. The baby, delivered vaginally 3 hours later, was severely distressed and showed signs of asphyxia. He was found to have a permanent brain injury.

PARENTS’ CLAIM:

The ObGyn and hospital nurses failed to properly manage the mother’s anaphylactic reaction to ampicillin. Fetal heart-rate tracings indicated fetal distress. Standard of care required prompt intervention with epinephrine and/or emergency cesarean delivery. Brain injury occurred because these procedures were not performed.

DEFENDANTS’ DEFENSE:

The nurses denied fault and explained that they appropriately and immediately responded to mild anaphylactic symptoms in the mother. They could not administer epinephrine because the ObGyn did not order it.

The ObGyn denied violating the standard of care that included minimizing the mother’s allergic reaction. Because the mother didn’t have a rash, it was not necessary to order epinephrine. The baby sustained an unknown injury earlier in the pregnancy that was unrelated to labor.

VERDICT:

A Tennessee defense verdict was returned.

Resident blamed for shoulder dystocia

A mother presented to a federally funded health center in labor. A first-year resident managed labor and delivery under the supervision of the attending physician. Shoulder dystocia was encountered and the baby suffered a permanent brachial plexus injury.

PARENTS’ CLAIM:

Negligence occurred when the resident used excessive force by pulling on the infant’s neck during delivery. The resident, who had just received his medical license, was poorly supervised by the attending physician.

DEFENDANTS’ DEFENSE:

Suit was brought against the resident, the attending physician, the federal government, and the hospital’s residency program. The resident denied using excessive force. As soon as delivery became complex, the attending physician completed the delivery. The baby’s injuries were unpredictable and unavoidable.

VERDICT:

A $290,000 settlement with the federal government was reached before trial. A Pennsylvania defense verdict was returned for the other parties.

Related Article:
Tackle the challenging shoulder dystocia emergency by practicing delivery of the posterior arm

What caused brachial plexus injury?

An experienced midwife delivered a baby who sustained a brachial plexus injury resulting in flail arm syndrome.

PARENTS’ CLAIM:

The midwife mismanaged the delivery causing permanent injury. The child has gained little improvement with surgery and physical therapy.

DEFENDANTS’ DEFENSE:

The injury was caused by the natural forces of labor. The midwife used appropriate techniques during the birth.

VERDICT:

A Washington defense verdict was returned.

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Removal of wrong ovary?

Several years earlier, a patient had undergone a hysterectomy but retained her ovaries and fallopian tubes. She reported recurrent pelvic pain, especially on the left side, to a gynecologic surgeon. Ultrasonography (US) results showed a small follicular cyst on the right ovary and a simple cyst on the left ovary. The patient consented to diagnostic laparoscopy with possible left salpingo-oophorectomy. During the procedure, the surgeon removed the right fallopian tube and ovary. After recovery, the patient continued to have left-sided pelvic pain. When she saw another surgeon a year later, US results showed that the left ovary and tube were still intact. The patient underwent left salpingo-oophorectomy.

PATIENT’S CLAIM:

The surgeon removed the wrong ovary and tube, a breach of the standard of care, and didn’t adequately explain his surgical actions.

DEFENDANTS’ DEFENSE:

Standard of care was maintained. During surgery, the surgeon encountered severe adhesions on the patient’s left side and was unable to visualize her left ovary. He decided that what had appeared to be an ovary on US most likely was a fluid collection, and that the patient’s left ovary must have been removed at hysterectomy. The surgeon concluded that the hemorrhagic cyst on the right ovary and adhesions were causing the patient’s pain, and removed them. The patient had given him permission to perform laparoscopic surgery, but he did not have her consent to convert to laparotomy, which would have been necessary to confirm the absence of her left ovary.

VERDICT:

An Alabama defense verdict was returned.

Related Article:
Medical errors: Meeting ethical obligations and reducing liability with proper communication

Was wrong hysterectomy procedure chosen?

After being treated by her ObGyn for postmenopausal bleeding with medication and dilation and curettage, a 50-year-old woman underwent total abdominal hysterectomy (TAH). At an office visit 3 weeks postsurgery, she reported uncontrollable urination. The patient was admitted to a hospital, where cystogram results showed a vesico-vaginal fistula (VVF). She was treated with catheter drainage and referred to a urologist. The patient underwent 2 unsuccessful repair operations. A third repair, performed 10 months after the TAH, was successful.

PATIENT’S CLAIM:

The ObGyn should have performed laparoscopic supracervical hysterectomy (LSH) instead of TAH because the patient’s cervix would have remained intact and VVF would not have developed. Medical bills totaled $194,000.

PHYSICIAN’S DEFENSE:

The standard of care did not require LSH. Had the ObGyn left the cervix intact, the patient could have continued bleeding with increased risk of cervical cancer. A bladder injury is a known complication of hysterectomy.

VERDICT:

A Mississippi defense verdict was returned.

Woman dies after uterine fibroid removal

A 39-year-old woman with a history of hypertension, diabetes, moderate obesity, and end-stage renal disease underwent myomectomy. A first-year resident assisted the attending anesthesiologist during the procedure. While the patient was under general anesthesia, her blood pressure (BP) dropped rapidly and remained at an abnormally low level for 45 minutes. Then the patient’s heart rate dropped to around 30 bpm and remained at that level for 15 minutes before her BP and heart rate were finally restored. The patient never regained consciousness and remained in an irreversible coma until she died 6 days later.

ESTATE’S CLAIM:

The anesthesiologist and resident negligently allowed the patient’s BP and heart rate to fall to dangerously low levels. Because the patient had hypertension, diabetes, and obesity, she required a higher BP to maintain adequate cerebral perfusion. The physicians precipitated the patient’s hypotension by giving her an excessive dose of morphine and bupivacaine via epidural catheter prior to induction of general anesthesia, and then failed to give her sufficient doses of vasopressors to increase her BP to safe levels. They failed to properly treat the condition in a timely manner, causing brain damage, and ultimately, death.

DEFENDANTS’ DEFENSE:

The case was settled during mediation.

VERDICT:

A $900,000 Massachusetts settlement was reached.

Related Article:
Total abdominal hysterectomy the Mayo Clinic way

Ureter injured during hysterectomy

A 47-year-old woman’s right ureter was damaged during laparoscopic hysterectomy. During surgery, the gynecologist called in a urologist to repair the injury. The patient reported postsurgical complications including renal function impairment. A computed tomography scan showed a right ureter obstruction. When surgery confirmed complete obstruction of the ureter, she had a temporary nephrostomy drain placed. After 4 weeks, the patient returned to the operating room to have the right ureter implanted into the bladder. The patient reported occasional painful urination with increased urinary frequency and decreased right kidney size.

PATIENT’S CLAIM:

The gynecologist lacerated the ureter because he did not adequately identify and protect the ureter; this error represented a departure from the standard of care. The urologist failed to properly repair the injury. The patient sought recovery of $990,000 for past and future pain and suffering.

DEFENDANTS’ CLAIM:

The suit against the urologist and hospital was dropped, but continued against the gynecologist. The gynecologist claimed that the patient’s injury was a thermal burn, and is a known complication of the procedure.

VERDICT:

A $500,000 New York verdict was returned.

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Removal of wrong ovary?

Several years earlier, a patient had undergone a hysterectomy but retained her ovaries and fallopian tubes. She reported recurrent pelvic pain, especially on the left side, to a gynecologic surgeon. Ultrasonography (US) results showed a small follicular cyst on the right ovary and a simple cyst on the left ovary. The patient consented to diagnostic laparoscopy with possible left salpingo-oophorectomy. During the procedure, the surgeon removed the right fallopian tube and ovary. After recovery, the patient continued to have left-sided pelvic pain. When she saw another surgeon a year later, US results showed that the left ovary and tube were still intact. The patient underwent left salpingo-oophorectomy.

PATIENT’S CLAIM:

The surgeon removed the wrong ovary and tube, a breach of the standard of care, and didn’t adequately explain his surgical actions.

DEFENDANTS’ DEFENSE:

Standard of care was maintained. During surgery, the surgeon encountered severe adhesions on the patient’s left side and was unable to visualize her left ovary. He decided that what had appeared to be an ovary on US most likely was a fluid collection, and that the patient’s left ovary must have been removed at hysterectomy. The surgeon concluded that the hemorrhagic cyst on the right ovary and adhesions were causing the patient’s pain, and removed them. The patient had given him permission to perform laparoscopic surgery, but he did not have her consent to convert to laparotomy, which would have been necessary to confirm the absence of her left ovary.

VERDICT:

An Alabama defense verdict was returned.

Related Article:
Medical errors: Meeting ethical obligations and reducing liability with proper communication

Was wrong hysterectomy procedure chosen?

After being treated by her ObGyn for postmenopausal bleeding with medication and dilation and curettage, a 50-year-old woman underwent total abdominal hysterectomy (TAH). At an office visit 3 weeks postsurgery, she reported uncontrollable urination. The patient was admitted to a hospital, where cystogram results showed a vesico-vaginal fistula (VVF). She was treated with catheter drainage and referred to a urologist. The patient underwent 2 unsuccessful repair operations. A third repair, performed 10 months after the TAH, was successful.

PATIENT’S CLAIM:

The ObGyn should have performed laparoscopic supracervical hysterectomy (LSH) instead of TAH because the patient’s cervix would have remained intact and VVF would not have developed. Medical bills totaled $194,000.

PHYSICIAN’S DEFENSE:

The standard of care did not require LSH. Had the ObGyn left the cervix intact, the patient could have continued bleeding with increased risk of cervical cancer. A bladder injury is a known complication of hysterectomy.

VERDICT:

A Mississippi defense verdict was returned.

Woman dies after uterine fibroid removal

A 39-year-old woman with a history of hypertension, diabetes, moderate obesity, and end-stage renal disease underwent myomectomy. A first-year resident assisted the attending anesthesiologist during the procedure. While the patient was under general anesthesia, her blood pressure (BP) dropped rapidly and remained at an abnormally low level for 45 minutes. Then the patient’s heart rate dropped to around 30 bpm and remained at that level for 15 minutes before her BP and heart rate were finally restored. The patient never regained consciousness and remained in an irreversible coma until she died 6 days later.

ESTATE’S CLAIM:

The anesthesiologist and resident negligently allowed the patient’s BP and heart rate to fall to dangerously low levels. Because the patient had hypertension, diabetes, and obesity, she required a higher BP to maintain adequate cerebral perfusion. The physicians precipitated the patient’s hypotension by giving her an excessive dose of morphine and bupivacaine via epidural catheter prior to induction of general anesthesia, and then failed to give her sufficient doses of vasopressors to increase her BP to safe levels. They failed to properly treat the condition in a timely manner, causing brain damage, and ultimately, death.

DEFENDANTS’ DEFENSE:

The case was settled during mediation.

VERDICT:

A $900,000 Massachusetts settlement was reached.

Related Article:
Total abdominal hysterectomy the Mayo Clinic way

Ureter injured during hysterectomy

A 47-year-old woman’s right ureter was damaged during laparoscopic hysterectomy. During surgery, the gynecologist called in a urologist to repair the injury. The patient reported postsurgical complications including renal function impairment. A computed tomography scan showed a right ureter obstruction. When surgery confirmed complete obstruction of the ureter, she had a temporary nephrostomy drain placed. After 4 weeks, the patient returned to the operating room to have the right ureter implanted into the bladder. The patient reported occasional painful urination with increased urinary frequency and decreased right kidney size.

PATIENT’S CLAIM:

The gynecologist lacerated the ureter because he did not adequately identify and protect the ureter; this error represented a departure from the standard of care. The urologist failed to properly repair the injury. The patient sought recovery of $990,000 for past and future pain and suffering.

DEFENDANTS’ CLAIM:

The suit against the urologist and hospital was dropped, but continued against the gynecologist. The gynecologist claimed that the patient’s injury was a thermal burn, and is a known complication of the procedure.

VERDICT:

A $500,000 New York verdict was returned.

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Removal of wrong ovary?

Several years earlier, a patient had undergone a hysterectomy but retained her ovaries and fallopian tubes. She reported recurrent pelvic pain, especially on the left side, to a gynecologic surgeon. Ultrasonography (US) results showed a small follicular cyst on the right ovary and a simple cyst on the left ovary. The patient consented to diagnostic laparoscopy with possible left salpingo-oophorectomy. During the procedure, the surgeon removed the right fallopian tube and ovary. After recovery, the patient continued to have left-sided pelvic pain. When she saw another surgeon a year later, US results showed that the left ovary and tube were still intact. The patient underwent left salpingo-oophorectomy.

PATIENT’S CLAIM:

The surgeon removed the wrong ovary and tube, a breach of the standard of care, and didn’t adequately explain his surgical actions.

DEFENDANTS’ DEFENSE:

Standard of care was maintained. During surgery, the surgeon encountered severe adhesions on the patient’s left side and was unable to visualize her left ovary. He decided that what had appeared to be an ovary on US most likely was a fluid collection, and that the patient’s left ovary must have been removed at hysterectomy. The surgeon concluded that the hemorrhagic cyst on the right ovary and adhesions were causing the patient’s pain, and removed them. The patient had given him permission to perform laparoscopic surgery, but he did not have her consent to convert to laparotomy, which would have been necessary to confirm the absence of her left ovary.

VERDICT:

An Alabama defense verdict was returned.

Related Article:
Medical errors: Meeting ethical obligations and reducing liability with proper communication

Was wrong hysterectomy procedure chosen?

After being treated by her ObGyn for postmenopausal bleeding with medication and dilation and curettage, a 50-year-old woman underwent total abdominal hysterectomy (TAH). At an office visit 3 weeks postsurgery, she reported uncontrollable urination. The patient was admitted to a hospital, where cystogram results showed a vesico-vaginal fistula (VVF). She was treated with catheter drainage and referred to a urologist. The patient underwent 2 unsuccessful repair operations. A third repair, performed 10 months after the TAH, was successful.

PATIENT’S CLAIM:

The ObGyn should have performed laparoscopic supracervical hysterectomy (LSH) instead of TAH because the patient’s cervix would have remained intact and VVF would not have developed. Medical bills totaled $194,000.

PHYSICIAN’S DEFENSE:

The standard of care did not require LSH. Had the ObGyn left the cervix intact, the patient could have continued bleeding with increased risk of cervical cancer. A bladder injury is a known complication of hysterectomy.

VERDICT:

A Mississippi defense verdict was returned.

Woman dies after uterine fibroid removal

A 39-year-old woman with a history of hypertension, diabetes, moderate obesity, and end-stage renal disease underwent myomectomy. A first-year resident assisted the attending anesthesiologist during the procedure. While the patient was under general anesthesia, her blood pressure (BP) dropped rapidly and remained at an abnormally low level for 45 minutes. Then the patient’s heart rate dropped to around 30 bpm and remained at that level for 15 minutes before her BP and heart rate were finally restored. The patient never regained consciousness and remained in an irreversible coma until she died 6 days later.

ESTATE’S CLAIM:

The anesthesiologist and resident negligently allowed the patient’s BP and heart rate to fall to dangerously low levels. Because the patient had hypertension, diabetes, and obesity, she required a higher BP to maintain adequate cerebral perfusion. The physicians precipitated the patient’s hypotension by giving her an excessive dose of morphine and bupivacaine via epidural catheter prior to induction of general anesthesia, and then failed to give her sufficient doses of vasopressors to increase her BP to safe levels. They failed to properly treat the condition in a timely manner, causing brain damage, and ultimately, death.

DEFENDANTS’ DEFENSE:

The case was settled during mediation.

VERDICT:

A $900,000 Massachusetts settlement was reached.

Related Article:
Total abdominal hysterectomy the Mayo Clinic way

Ureter injured during hysterectomy

A 47-year-old woman’s right ureter was damaged during laparoscopic hysterectomy. During surgery, the gynecologist called in a urologist to repair the injury. The patient reported postsurgical complications including renal function impairment. A computed tomography scan showed a right ureter obstruction. When surgery confirmed complete obstruction of the ureter, she had a temporary nephrostomy drain placed. After 4 weeks, the patient returned to the operating room to have the right ureter implanted into the bladder. The patient reported occasional painful urination with increased urinary frequency and decreased right kidney size.

PATIENT’S CLAIM:

The gynecologist lacerated the ureter because he did not adequately identify and protect the ureter; this error represented a departure from the standard of care. The urologist failed to properly repair the injury. The patient sought recovery of $990,000 for past and future pain and suffering.

DEFENDANTS’ CLAIM:

The suit against the urologist and hospital was dropped, but continued against the gynecologist. The gynecologist claimed that the patient’s injury was a thermal burn, and is a known complication of the procedure.

VERDICT:

A $500,000 New York verdict was returned.

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.