Applied Evidence

One of the most concerning and challenging patient complaints presented to physicians is chest pain. Chest pain is a ubiquitous complaint in primary care settings and in the emergency department (ED), accounting for 8 million ED visits and 0.4% of all primary care visits in North America annually.^1,2

Acute coronary syndrome is the cause of chest pain in 5.1% of patients with chest pain who present to the ED, compared with 1.5% to 3.1% of chestpain patients seen in ambulatory care.

Despite the great number of chest-pain encounters, early identification of life-threatening causes and prompt treatment remain a challenge. In this article, we examine how the approach to a complaint of chest pain in a primary care practice (and, likewise, in the ED) must first, rest on the clinical evaluation and second, employ risk-stratification tools to aid in evaluation, appropriate diagnosis, triage, and treatment.

Chest pain by the numbers

Acute coronary syndrome (ACS) is the cause of chest pain in 5.1% of patients with chest pain who present to the ED, compared with 1.5% to 3.1% of chest-pain patients seen in ambulatory care.^1,3 “Nonspecific chest pain” is the most frequent diagnosis of chest pain in the ED for all age groups (47.5% to 55.8%).³ In contrast, the most common cause of chest pain in primary care is musculoskeletal (36%), followed by gastrointestinal disease (18% to 19%); serious cardiac causes (15%), including ACS (1.5%); nonspecific causes (16%); psychiatric causes (8%); and pulmonary causes (5% to 10%).⁴ Among patients seen in the ED because of chest pain, 57.4% are discharged, 30.6% are admitted for further evaluation, and 0.4% die in the ED or after admission.³

IMAGE: © KIMBERLY MARTENS-KIEFER

First challenge: The scale of the differential Dx

The differential diagnosis of chest pain is broad. It includes life-threatening causes, such as ACS (from ST-segment elevation myocardial infarction [STEMI], Type 1 non-STEMI, and unstable angina), acute aortic dissection, pulmonary embolism (PE), esophageal rupture, and tension pneumothorax, as well as non-life-threatening causes (TABLE 1).

History and physical exam guide early decisions

Triage assessment of the patient with chest pain, including vital signs, general appearance, and basic symptom questions, can guide you as to whether they require transfer to a higher level of care. Although an individual’s findings cannot, alone, accurately exclude or diagnose ACS, the findings can be used in combination in clinical decision tools to distinguish noncardiac chest pain from ACS.

History. Features in the history (TABLE 2^5-9) that are most helpful at increasing the probability (ie, a positive likelihood ratio [LR] ≥ 2) of chest pain being caused by ACS are:

• pain radiating to both arms or the right arm
• pain that is worse upon exertion
• a history of peripheral artery disease or coronary artery disease (CAD)
• a previously abnormal stress test.

The presence of any prior normal stress test is unhelpful: Such patients have a similar risk of a 30-day adverse cardiac event as a patient who has never had a stress test.⁵

Continue to: A history of tobacco use...

 

A history of tobacco use, hyperlipidemia, hypertension, obesity, acute myocardial infarction (AMI), coronary artery bypass grafting, or a family history of CAD does not significantly increase the risk of ACS.⁶ However, exploring each of these risk factors further is important, because genetic links between these risk factors can lead to an increased risk of CAD (eg, familial hypercholesterolemia).⁷

A history of normal or near-normal coronary angiography (< 25% stenosis) is associated with a lower likelihood of ACS, because 98% of such patients are free of AMI and 90% are without single-vessel coronary disease nearly 10 years out.⁶ A history of coronary artery bypass grafting is not necessarily predictive of ACS (LR = 1-3).^5,6

Historical features classically associated with ACS, but that have an LR < 2, are pain radiating to the neck or jaw, nausea or vomiting, dyspnea, and pain that is relieved with nitroglycerin.^5,6 Pain described as pleuritic, sharp, positional, or reproduced with palpation is less likely due to AMI.⁵

Physical exam findings are not independently diagnostic when evaluating chest pain. However, a third heart sound is the most likely finding associated with AMI and hypotension is the clinical sign most likely associated with ACS.⁵

Consider the diagnosis of PE in all patients with chest pain. In PE, chest pain might be associated with dyspnea, presyncope, syncope, or hemoptysis.⁸ On examination, 40% of patients have tachycardia.⁸ If PE is suspected; the patient should be risk-stratified using a validated prediction rule (see the discussion of PE that follows).

Continue to: Other historical features...

 

Other historical features or physical exam findings correlate with aortic dissection, pneumonia, and psychiatric causes of chest pain (TABLE 2^5-9).

Useful EKG findings

Among patients in whom ACS or PE is suspected, 12-lead electrocardiography (EKG) should be performed.

AMI. EKG findings most predictive of AMI are new ST-segment elevation or depression > 1 mm (LR = 6-54), new left bundle branch block (LR = 6.3), Q wave (positive LR = 3.9), and prominent, wide-based (hyperacute) T wave (LR = 3.1).¹⁰

ACS. Useful EKG findings to predict ACS are ST-segment depression (LR = 5.3 [95% CI, 2.1-8.6]) and any evidence of ischemia, defined as ST-segment depression, T-wave inversion, or Q wave (LR = 3.6 [95% CI, 1.6-5.7]).¹⁰

PE. The most common abnormal finding on EKG in the setting of PE is sinus tachycardia.

Continue to: Right ventricular strain

 

Right ventricular strain. Other findings that reflect right ventricular strain, but are much less common, are complete or incomplete right bundle branch block, prominent S wave in lead I, Q wave in lead III, and T-wave inversion in lead III (S1Q3T3; the ­McGinn-White sign) and in leads V₁-V₄.⁸

The utility of troponin and high-sensitivity troponin testing

Clinical evaluation and EKG findings are unable to diagnose or exclude ACS without the use of the cardiac biomarker troponin. In the past decade, high-sensitivity troponin assays have been used to stratify patients at risk of ACS.^11,12 Many protocols now exist using short interval (2-3 hours), high-sensitivity troponin testing to identify patients at low risk of myocardial infarction who can be safely discharged from the ED after 2 normal tests of the troponin level.^13-16

An elevated troponin value alone, however, is not a specific indicator of ACS; troponin can be elevated in the settings of myocardial ischemia related to increased oxygen demand (Type 2 non-STEMI) and decreased renal clearance. Consideration of the rate of rising and falling levels of troponin, its absolute value > 99th percentile, and other findings is critical to interpreting an elevated troponin level.¹⁷ Studies in which the HEART score (History, Electrocardiography, Age, Risk factors, Troponin) was combined with high-sensitivity troponin measurement show that this pairing is promising in reducing unnecessary admissions for chest pain.¹⁸ (For a description of this tool, see the discussion of the HEART score that follows.) Carlton and colleagues¹⁸ showed that a HEART score ≤ 3 and a negative high-sensitivity troponin I level had a negative predictive value of ≥ 99.5% for AMI.

Clinical decision tools: Who needs care? Who can go home?

Given the varied presentations of patients with life-threatening causes of chest pain, it is challenging to confidently determine who is safe to send home after initial assessment. Guidance in 2014 from the American Heart Association and American College of Cardiology recommends risk-stratifying patients for ACS using clinical decision tools to help guide management.^19,20 The American College of Physicians, in its 2015 guidelines, also recommends using a clinical decision tool to assess patients when there is suspicion of PE.²¹ Clinical application of these tools identifies patients at low risk of life-threatening conditions and can help avoid unnecessary intervention and a higher level of care. 

Tools for investigating ACS

The Marburg Heart Score²² assesses the likelihood of CAD in ambulatory settings while the HEART score assesses the risk of major adverse cardiac events in ED patients.²³ The Diamond Forrester criteria can be used to assess the pretest probability of CAD in both settings.²⁴

Continue to: Marburg Heart Score

 

Marburg Heart Score. Validated in patients older than 35 years of age in 2 different outpatient populations in 2010²² and 2012,²⁵ the Marburg score is determined by answering 5 questions:

• Female ≥ 65 years? Or male ≥ 55 years of age? (No, 0; Yes, +1)
• Known CAD, cerebrovascular disease, or peripheral vascular disease? (No, 0; Yes, +1)
• Is pain worse with exercise? (No, 0; Yes, +1)
• Is pain reproducible with palpation? (No, +1, Yes, 0)
• Does the patient assume that the pain is cardiac in nature? (No, 0; Yes, +1)

A Marburg Heart Score of 0 or 1 means CAD is highly unlikely in a patient with chest pain (negative predictive value = 99%-100%; positive predictive value = 0.6%)⁴ (TABLE 3^4,26-28). A score of ≤ 2 has a negative predictive value of 98%. A Marburg Heart Score of 4 or 5 has a relatively low positive predictive value (63%).⁴

The most common causes of chest pain in primary care? In descending order, musculoskeletal, GI, serious cardiac, nonspecific, psychiatric, and pulmonary causes.

This tool does not accurately diagnose acute MI, but it does help identify patients at low risk of ACS, thus reducing unnecessary subsequent testing. Although no clinical decision tool can rule out AMI with absolute certainty, the Marburg Heart Score is considered one of the most extensively tested and sensitive tools to predict low risk of CAD in outpatient primary care.²⁹

INTERCHEST rule (in outpatient primary care) is a newer prediction rule using data from 5 primary care–based studies of chest pain.³⁰ For a score ≤ 2, the negative predictive value for CAD causing chest pain is 97% to 98% and the positive predictive value is 43%. INTERCHEST incorporates studies used to validate the Marburg Heart Score, but has not been validated beyond initial pooled studies. Concerns have been raised about the quality of these pooled studies, however, and this rule has not been widely accepted for clinical use at this time.²⁹

The HEART score has been validated in patients older than 12 years in multiple institutions and across multiple ED populations.^23,31,32 It is widely used in the ED to assess a patient’s risk of major adverse cardiac events (MACE) over the next 6 weeks. MACE is defined as AMI, percutaneous coronary intervention, coronary artery bypass grafting, or death.

Continue to: The HEART score...

 

The HEART score is calculated based on 5 components:

• History of chest pain (slightly [0], moderately [+1], or highly [+2]) suspicious for ACS)
• EKG (normal [0], nonspecific ST changes [+1], significant ST deviations [+2])
• Age (< 45 y [0], 45-64 y [+1], ≥ 65 y [+2])
• Risk factors (none [0], 1 or 2 [+1], ≥ 3 or a history of atherosclerotic disease [+2]) ^a
• Initial troponin assay, standard sensitivity (≤ normal [0], 1-3× normal [+1], > 3× normal [+2]).

For patients with a HEART score of 0-3 (ie, at low risk), the pooled positive predictive value of a MACE was determined to be 0.19 (95% CI, 0.14-0.24), and the negative predictive value was 0.99 (95% CI, 0.98-0.99)—making it an effective tool to rule out a MACE over the short term²⁶ (TABLE 3^4,26-28).

Because the HEART Score was published in 2008, multiple systematic reviews and meta-analyses have compared it to the TIMI (Thrombolysis in Myocardial Infarction) and GRACE (Global Registry of Acute Coronary Events) scores for predicting short-term (30-day to 6-week) MACE in ED patients.^27,28,33,34 These studies have all shown that the HEART score is relatively superior to the TIMI and GRACE tools.

Characteristics of these tools are summarized in TABLE 3.^4,26-28

Diamond Forrester classification (in ED and outpatient settings). This tool uses 3 criteria—substernal chest pain, pain that increases upon exertion or with stress, and pain relieved by nitroglycerin or rest—to classify chest pain as typical angina (all 3 criteria), atypical angina (2 criteria), or noncardiac chest pain (0 criteria or 1 criterion).²⁴ Pretest probability (ie, the likelihood of an outcome before noninvasive testing) of the pain being due to CAD can then be determined from the type of chest pain and the patient’s gender and age¹⁹ (TABLE 4¹⁹). Recent studies have found that the Diamond Forrester criteria might overestimate the probability of CAD.³⁵

Continue to: Noninvasive imaging-based diagnostic methods

 

 

Noninvasive imaging-based diagnostic methods 

Positron-emission tomography stress testing, stress echocardiography, myocardial perfusion scanning, exercise treadmill testing. The first 3 of these imaging tests have a sensitivity and specificity ranging from 74% to 87%³⁶; exercise treadmill testing is less sensitive (68%) and specific (77%).³⁷

In a patient with a very low (< 5%) probability of CAD, a positive stress test (of any modality) is likely to be a false-positive; conversely, in a patient with a very high (> 90%) probability of CAD, a negative stress test is likely to be a false-negative.¹⁹ The American Heart Association, therefore, does not recommend any of these modalities for patients who have a < 5% or > 90% probability of CAD.¹⁹

Triage assessment of the chestpain patient, including vital signs, general appearance, and basic symptom questions, can clarify whether they need transfer to a higher level of care.

Noninvasive testing to rule out ACS in low- and intermediate-risk patients who present to the ED with chest pain provides no clinical benefit over clinical evaluation alone.³⁸ Therefore, these tests are rarely used in the initial evaluation of chest pain in an acute setting.

Coronary artery calcium score (CACS), coronary computed tomography angiography (CCTA). These tests have demonstrated promise in the risk stratification of chest pain, given their high sensitivity and negative predictive value in low- and intermediate-risk patients.^39,40 However, their application remains unclear in the evaluation of acute chest pain: Appropriate-use criteria do not favor CACS or CCTA alone to evaluate acute chest pain when there is suspicion of ACS.⁴¹ The Choosing Wisely initiative (for “avoiding unnecessary medical tests, treatments, and procedures”; www.choosingwisely.org) recommends against CCTA for high-risk patients presenting to the ED with acute chest pain.⁴²

Cardiac magnetic resonance imaging does not have an established role in the evaluation of patients with suspected ACS.⁴³

Continue to: Tools for investigating PE

 

 

Tools for investigating PE

Three clinical decision tools have been validated to predict the risk of PE: the Wells score, the Geneva score, and Pulmonary Embolism Rule Out Criteria (PERC).^44,45

Wells score is more sensitive than the Geneva score and has been validated in ambulatory¹ and ED^46-48 settings. Based on Wells criteria, high-risk patients need further evaluation with imaging. In low-risk patients, a normal D-dimer level effectively excludes PE, with a < 1% risk of subsequent thromboembolism in the following 3 months. Positive predictive value of the Wells decision tool is low because it is intended to rule out, not confirm, PE.

PERC can be used in a low-probability setting (defined as the treating physician arriving at the conclusion that PE is not the most likely diagnosis and can be excluded with a negative D-dimer test). In that setting, if the patient meets the 8 clinical variables in PERC, the diagnosis of PE is, effectively, ruled out.⁴⁸

Summing up: Evaluation of chest pain guided by risk of CAD

Patients who present in an outpatient setting with a potentially life-threatening cause of chest pain (TABLE 1) and patients with unstable vital signs should be sent to the ED for urgent evaluation. In the remaining outpatients, use the Marburg Heart Score or Diamond Forrester classification to assess the likelihood that pain is due to CAD (in the ED, the HEART score can be used for this purpose) (FIGURE).

When the risk is low. No further cardiac testing is indicated in patients with a risk of CAD < 5%, based on a Marburg score of 0 or 1, or on Diamond Forrester criteria; an abnormal stress test is likely to be a false-positive.¹⁹

Continue to: Moderate risk

 

Moderate risk. However, further testing is indicated, with a stress test (with or without myocardial imaging), in patients whose risk of CAD is 5% to 70%, based on the Diamond Forrester classification or an intermediate Marburg Heart Score (ie, a score of 2 or 3 but a normal EKG). This further testing can be performed urgently in patients who have multiple other risk factors that are not assessed by the Marburg Heart Score.

High risk. In patients whose risk is > 70%, invasive testing with angiography should be considered.^35,49

EKG abnormalities. Patients with a Marburg Score of 2 or 3 and an abnormal EKG should be sent to the ED (FIGURE). There, patients with a HEART score < 4 and a negative 2-3–hour troponin test have a < 1% chance of ACS and can be safely discharged.³¹

CORRESPONDENCE
Anne Mounsey, MD, UNC Family Medicine, 590 Manning Drive, Chapel Hill, NC 27599; [email protected]

One of the most concerning and challenging patient complaints presented to physicians is chest pain. Chest pain is a ubiquitous complaint in primary care settings and in the emergency department (ED), accounting for 8 million ED visits and 0.4% of all primary care visits in North America annually.^1,2

Acute coronary syndrome is the cause of chest pain in 5.1% of patients with chest pain who present to the ED, compared with 1.5% to 3.1% of chestpain patients seen in ambulatory care.

Despite the great number of chest-pain encounters, early identification of life-threatening causes and prompt treatment remain a challenge. In this article, we examine how the approach to a complaint of chest pain in a primary care practice (and, likewise, in the ED) must first, rest on the clinical evaluation and second, employ risk-stratification tools to aid in evaluation, appropriate diagnosis, triage, and treatment.

Chest pain by the numbers

Acute coronary syndrome (ACS) is the cause of chest pain in 5.1% of patients with chest pain who present to the ED, compared with 1.5% to 3.1% of chest-pain patients seen in ambulatory care.^1,3 “Nonspecific chest pain” is the most frequent diagnosis of chest pain in the ED for all age groups (47.5% to 55.8%).³ In contrast, the most common cause of chest pain in primary care is musculoskeletal (36%), followed by gastrointestinal disease (18% to 19%); serious cardiac causes (15%), including ACS (1.5%); nonspecific causes (16%); psychiatric causes (8%); and pulmonary causes (5% to 10%).⁴ Among patients seen in the ED because of chest pain, 57.4% are discharged, 30.6% are admitted for further evaluation, and 0.4% die in the ED or after admission.³

IMAGE: © KIMBERLY MARTENS-KIEFER

First challenge: The scale of the differential Dx

The differential diagnosis of chest pain is broad. It includes life-threatening causes, such as ACS (from ST-segment elevation myocardial infarction [STEMI], Type 1 non-STEMI, and unstable angina), acute aortic dissection, pulmonary embolism (PE), esophageal rupture, and tension pneumothorax, as well as non-life-threatening causes (TABLE 1).

History and physical exam guide early decisions

Triage assessment of the patient with chest pain, including vital signs, general appearance, and basic symptom questions, can guide you as to whether they require transfer to a higher level of care. Although an individual’s findings cannot, alone, accurately exclude or diagnose ACS, the findings can be used in combination in clinical decision tools to distinguish noncardiac chest pain from ACS.

History. Features in the history (TABLE 2^5-9) that are most helpful at increasing the probability (ie, a positive likelihood ratio [LR] ≥ 2) of chest pain being caused by ACS are:

• pain radiating to both arms or the right arm
• pain that is worse upon exertion
• a history of peripheral artery disease or coronary artery disease (CAD)
• a previously abnormal stress test.

The presence of any prior normal stress test is unhelpful: Such patients have a similar risk of a 30-day adverse cardiac event as a patient who has never had a stress test.⁵

Continue to: A history of tobacco use...

 

A history of tobacco use, hyperlipidemia, hypertension, obesity, acute myocardial infarction (AMI), coronary artery bypass grafting, or a family history of CAD does not significantly increase the risk of ACS.⁶ However, exploring each of these risk factors further is important, because genetic links between these risk factors can lead to an increased risk of CAD (eg, familial hypercholesterolemia).⁷

A history of normal or near-normal coronary angiography (< 25% stenosis) is associated with a lower likelihood of ACS, because 98% of such patients are free of AMI and 90% are without single-vessel coronary disease nearly 10 years out.⁶ A history of coronary artery bypass grafting is not necessarily predictive of ACS (LR = 1-3).^5,6

Historical features classically associated with ACS, but that have an LR < 2, are pain radiating to the neck or jaw, nausea or vomiting, dyspnea, and pain that is relieved with nitroglycerin.^5,6 Pain described as pleuritic, sharp, positional, or reproduced with palpation is less likely due to AMI.⁵

Physical exam findings are not independently diagnostic when evaluating chest pain. However, a third heart sound is the most likely finding associated with AMI and hypotension is the clinical sign most likely associated with ACS.⁵

Consider the diagnosis of PE in all patients with chest pain. In PE, chest pain might be associated with dyspnea, presyncope, syncope, or hemoptysis.⁸ On examination, 40% of patients have tachycardia.⁸ If PE is suspected; the patient should be risk-stratified using a validated prediction rule (see the discussion of PE that follows).

Continue to: Other historical features...

 

Other historical features or physical exam findings correlate with aortic dissection, pneumonia, and psychiatric causes of chest pain (TABLE 2^5-9).

Useful EKG findings

Among patients in whom ACS or PE is suspected, 12-lead electrocardiography (EKG) should be performed.

AMI. EKG findings most predictive of AMI are new ST-segment elevation or depression > 1 mm (LR = 6-54), new left bundle branch block (LR = 6.3), Q wave (positive LR = 3.9), and prominent, wide-based (hyperacute) T wave (LR = 3.1).¹⁰

ACS. Useful EKG findings to predict ACS are ST-segment depression (LR = 5.3 [95% CI, 2.1-8.6]) and any evidence of ischemia, defined as ST-segment depression, T-wave inversion, or Q wave (LR = 3.6 [95% CI, 1.6-5.7]).¹⁰

PE. The most common abnormal finding on EKG in the setting of PE is sinus tachycardia.

Continue to: Right ventricular strain

 

Right ventricular strain. Other findings that reflect right ventricular strain, but are much less common, are complete or incomplete right bundle branch block, prominent S wave in lead I, Q wave in lead III, and T-wave inversion in lead III (S1Q3T3; the ­McGinn-White sign) and in leads V₁-V₄.⁸

The utility of troponin and high-sensitivity troponin testing

Clinical evaluation and EKG findings are unable to diagnose or exclude ACS without the use of the cardiac biomarker troponin. In the past decade, high-sensitivity troponin assays have been used to stratify patients at risk of ACS.^11,12 Many protocols now exist using short interval (2-3 hours), high-sensitivity troponin testing to identify patients at low risk of myocardial infarction who can be safely discharged from the ED after 2 normal tests of the troponin level.^13-16

An elevated troponin value alone, however, is not a specific indicator of ACS; troponin can be elevated in the settings of myocardial ischemia related to increased oxygen demand (Type 2 non-STEMI) and decreased renal clearance. Consideration of the rate of rising and falling levels of troponin, its absolute value > 99th percentile, and other findings is critical to interpreting an elevated troponin level.¹⁷ Studies in which the HEART score (History, Electrocardiography, Age, Risk factors, Troponin) was combined with high-sensitivity troponin measurement show that this pairing is promising in reducing unnecessary admissions for chest pain.¹⁸ (For a description of this tool, see the discussion of the HEART score that follows.) Carlton and colleagues¹⁸ showed that a HEART score ≤ 3 and a negative high-sensitivity troponin I level had a negative predictive value of ≥ 99.5% for AMI.

Clinical decision tools: Who needs care? Who can go home?

Given the varied presentations of patients with life-threatening causes of chest pain, it is challenging to confidently determine who is safe to send home after initial assessment. Guidance in 2014 from the American Heart Association and American College of Cardiology recommends risk-stratifying patients for ACS using clinical decision tools to help guide management.^19,20 The American College of Physicians, in its 2015 guidelines, also recommends using a clinical decision tool to assess patients when there is suspicion of PE.²¹ Clinical application of these tools identifies patients at low risk of life-threatening conditions and can help avoid unnecessary intervention and a higher level of care. 

Tools for investigating ACS

The Marburg Heart Score²² assesses the likelihood of CAD in ambulatory settings while the HEART score assesses the risk of major adverse cardiac events in ED patients.²³ The Diamond Forrester criteria can be used to assess the pretest probability of CAD in both settings.²⁴

Continue to: Marburg Heart Score

 

Marburg Heart Score. Validated in patients older than 35 years of age in 2 different outpatient populations in 2010²² and 2012,²⁵ the Marburg score is determined by answering 5 questions:

• Female ≥ 65 years? Or male ≥ 55 years of age? (No, 0; Yes, +1)
• Known CAD, cerebrovascular disease, or peripheral vascular disease? (No, 0; Yes, +1)
• Is pain worse with exercise? (No, 0; Yes, +1)
• Is pain reproducible with palpation? (No, +1, Yes, 0)
• Does the patient assume that the pain is cardiac in nature? (No, 0; Yes, +1)

A Marburg Heart Score of 0 or 1 means CAD is highly unlikely in a patient with chest pain (negative predictive value = 99%-100%; positive predictive value = 0.6%)⁴ (TABLE 3^4,26-28). A score of ≤ 2 has a negative predictive value of 98%. A Marburg Heart Score of 4 or 5 has a relatively low positive predictive value (63%).⁴

The most common causes of chest pain in primary care? In descending order, musculoskeletal, GI, serious cardiac, nonspecific, psychiatric, and pulmonary causes.

This tool does not accurately diagnose acute MI, but it does help identify patients at low risk of ACS, thus reducing unnecessary subsequent testing. Although no clinical decision tool can rule out AMI with absolute certainty, the Marburg Heart Score is considered one of the most extensively tested and sensitive tools to predict low risk of CAD in outpatient primary care.²⁹

INTERCHEST rule (in outpatient primary care) is a newer prediction rule using data from 5 primary care–based studies of chest pain.³⁰ For a score ≤ 2, the negative predictive value for CAD causing chest pain is 97% to 98% and the positive predictive value is 43%. INTERCHEST incorporates studies used to validate the Marburg Heart Score, but has not been validated beyond initial pooled studies. Concerns have been raised about the quality of these pooled studies, however, and this rule has not been widely accepted for clinical use at this time.²⁹

The HEART score has been validated in patients older than 12 years in multiple institutions and across multiple ED populations.^23,31,32 It is widely used in the ED to assess a patient’s risk of major adverse cardiac events (MACE) over the next 6 weeks. MACE is defined as AMI, percutaneous coronary intervention, coronary artery bypass grafting, or death.

Continue to: The HEART score...

 

The HEART score is calculated based on 5 components:

• History of chest pain (slightly [0], moderately [+1], or highly [+2]) suspicious for ACS)
• EKG (normal [0], nonspecific ST changes [+1], significant ST deviations [+2])
• Age (< 45 y [0], 45-64 y [+1], ≥ 65 y [+2])
• Risk factors (none [0], 1 or 2 [+1], ≥ 3 or a history of atherosclerotic disease [+2]) ^a
• Initial troponin assay, standard sensitivity (≤ normal [0], 1-3× normal [+1], > 3× normal [+2]).

For patients with a HEART score of 0-3 (ie, at low risk), the pooled positive predictive value of a MACE was determined to be 0.19 (95% CI, 0.14-0.24), and the negative predictive value was 0.99 (95% CI, 0.98-0.99)—making it an effective tool to rule out a MACE over the short term²⁶ (TABLE 3^4,26-28).

Because the HEART Score was published in 2008, multiple systematic reviews and meta-analyses have compared it to the TIMI (Thrombolysis in Myocardial Infarction) and GRACE (Global Registry of Acute Coronary Events) scores for predicting short-term (30-day to 6-week) MACE in ED patients.^27,28,33,34 These studies have all shown that the HEART score is relatively superior to the TIMI and GRACE tools.

Characteristics of these tools are summarized in TABLE 3.^4,26-28

Diamond Forrester classification (in ED and outpatient settings). This tool uses 3 criteria—substernal chest pain, pain that increases upon exertion or with stress, and pain relieved by nitroglycerin or rest—to classify chest pain as typical angina (all 3 criteria), atypical angina (2 criteria), or noncardiac chest pain (0 criteria or 1 criterion).²⁴ Pretest probability (ie, the likelihood of an outcome before noninvasive testing) of the pain being due to CAD can then be determined from the type of chest pain and the patient’s gender and age¹⁹ (TABLE 4¹⁹). Recent studies have found that the Diamond Forrester criteria might overestimate the probability of CAD.³⁵

Continue to: Noninvasive imaging-based diagnostic methods

 

 

Noninvasive imaging-based diagnostic methods 

Positron-emission tomography stress testing, stress echocardiography, myocardial perfusion scanning, exercise treadmill testing. The first 3 of these imaging tests have a sensitivity and specificity ranging from 74% to 87%³⁶; exercise treadmill testing is less sensitive (68%) and specific (77%).³⁷

In a patient with a very low (< 5%) probability of CAD, a positive stress test (of any modality) is likely to be a false-positive; conversely, in a patient with a very high (> 90%) probability of CAD, a negative stress test is likely to be a false-negative.¹⁹ The American Heart Association, therefore, does not recommend any of these modalities for patients who have a < 5% or > 90% probability of CAD.¹⁹

Triage assessment of the chestpain patient, including vital signs, general appearance, and basic symptom questions, can clarify whether they need transfer to a higher level of care.

Noninvasive testing to rule out ACS in low- and intermediate-risk patients who present to the ED with chest pain provides no clinical benefit over clinical evaluation alone.³⁸ Therefore, these tests are rarely used in the initial evaluation of chest pain in an acute setting.

Coronary artery calcium score (CACS), coronary computed tomography angiography (CCTA). These tests have demonstrated promise in the risk stratification of chest pain, given their high sensitivity and negative predictive value in low- and intermediate-risk patients.^39,40 However, their application remains unclear in the evaluation of acute chest pain: Appropriate-use criteria do not favor CACS or CCTA alone to evaluate acute chest pain when there is suspicion of ACS.⁴¹ The Choosing Wisely initiative (for “avoiding unnecessary medical tests, treatments, and procedures”; www.choosingwisely.org) recommends against CCTA for high-risk patients presenting to the ED with acute chest pain.⁴²

Cardiac magnetic resonance imaging does not have an established role in the evaluation of patients with suspected ACS.⁴³

Continue to: Tools for investigating PE

 

 

Tools for investigating PE

Three clinical decision tools have been validated to predict the risk of PE: the Wells score, the Geneva score, and Pulmonary Embolism Rule Out Criteria (PERC).^44,45

Wells score is more sensitive than the Geneva score and has been validated in ambulatory¹ and ED^46-48 settings. Based on Wells criteria, high-risk patients need further evaluation with imaging. In low-risk patients, a normal D-dimer level effectively excludes PE, with a < 1% risk of subsequent thromboembolism in the following 3 months. Positive predictive value of the Wells decision tool is low because it is intended to rule out, not confirm, PE.

PERC can be used in a low-probability setting (defined as the treating physician arriving at the conclusion that PE is not the most likely diagnosis and can be excluded with a negative D-dimer test). In that setting, if the patient meets the 8 clinical variables in PERC, the diagnosis of PE is, effectively, ruled out.⁴⁸

Summing up: Evaluation of chest pain guided by risk of CAD

Patients who present in an outpatient setting with a potentially life-threatening cause of chest pain (TABLE 1) and patients with unstable vital signs should be sent to the ED for urgent evaluation. In the remaining outpatients, use the Marburg Heart Score or Diamond Forrester classification to assess the likelihood that pain is due to CAD (in the ED, the HEART score can be used for this purpose) (FIGURE).

When the risk is low. No further cardiac testing is indicated in patients with a risk of CAD < 5%, based on a Marburg score of 0 or 1, or on Diamond Forrester criteria; an abnormal stress test is likely to be a false-positive.¹⁹

Continue to: Moderate risk

 

Moderate risk. However, further testing is indicated, with a stress test (with or without myocardial imaging), in patients whose risk of CAD is 5% to 70%, based on the Diamond Forrester classification or an intermediate Marburg Heart Score (ie, a score of 2 or 3 but a normal EKG). This further testing can be performed urgently in patients who have multiple other risk factors that are not assessed by the Marburg Heart Score.

High risk. In patients whose risk is > 70%, invasive testing with angiography should be considered.^35,49

EKG abnormalities. Patients with a Marburg Score of 2 or 3 and an abnormal EKG should be sent to the ED (FIGURE). There, patients with a HEART score < 4 and a negative 2-3–hour troponin test have a < 1% chance of ACS and can be safely discharged.³¹

CORRESPONDENCE
Anne Mounsey, MD, UNC Family Medicine, 590 Manning Drive, Chapel Hill, NC 27599; [email protected]

One of the most concerning and challenging patient complaints presented to physicians is chest pain. Chest pain is a ubiquitous complaint in primary care settings and in the emergency department (ED), accounting for 8 million ED visits and 0.4% of all primary care visits in North America annually.^1,2

Acute coronary syndrome is the cause of chest pain in 5.1% of patients with chest pain who present to the ED, compared with 1.5% to 3.1% of chestpain patients seen in ambulatory care.

Despite the great number of chest-pain encounters, early identification of life-threatening causes and prompt treatment remain a challenge. In this article, we examine how the approach to a complaint of chest pain in a primary care practice (and, likewise, in the ED) must first, rest on the clinical evaluation and second, employ risk-stratification tools to aid in evaluation, appropriate diagnosis, triage, and treatment.

Chest pain by the numbers

Acute coronary syndrome (ACS) is the cause of chest pain in 5.1% of patients with chest pain who present to the ED, compared with 1.5% to 3.1% of chest-pain patients seen in ambulatory care.^1,3 “Nonspecific chest pain” is the most frequent diagnosis of chest pain in the ED for all age groups (47.5% to 55.8%).³ In contrast, the most common cause of chest pain in primary care is musculoskeletal (36%), followed by gastrointestinal disease (18% to 19%); serious cardiac causes (15%), including ACS (1.5%); nonspecific causes (16%); psychiatric causes (8%); and pulmonary causes (5% to 10%).⁴ Among patients seen in the ED because of chest pain, 57.4% are discharged, 30.6% are admitted for further evaluation, and 0.4% die in the ED or after admission.³

IMAGE: © KIMBERLY MARTENS-KIEFER

First challenge: The scale of the differential Dx

The differential diagnosis of chest pain is broad. It includes life-threatening causes, such as ACS (from ST-segment elevation myocardial infarction [STEMI], Type 1 non-STEMI, and unstable angina), acute aortic dissection, pulmonary embolism (PE), esophageal rupture, and tension pneumothorax, as well as non-life-threatening causes (TABLE 1).

History and physical exam guide early decisions

Triage assessment of the patient with chest pain, including vital signs, general appearance, and basic symptom questions, can guide you as to whether they require transfer to a higher level of care. Although an individual’s findings cannot, alone, accurately exclude or diagnose ACS, the findings can be used in combination in clinical decision tools to distinguish noncardiac chest pain from ACS.

History. Features in the history (TABLE 2^5-9) that are most helpful at increasing the probability (ie, a positive likelihood ratio [LR] ≥ 2) of chest pain being caused by ACS are:

• pain radiating to both arms or the right arm
• pain that is worse upon exertion
• a history of peripheral artery disease or coronary artery disease (CAD)
• a previously abnormal stress test.

The presence of any prior normal stress test is unhelpful: Such patients have a similar risk of a 30-day adverse cardiac event as a patient who has never had a stress test.⁵

Continue to: A history of tobacco use...

 

A history of tobacco use, hyperlipidemia, hypertension, obesity, acute myocardial infarction (AMI), coronary artery bypass grafting, or a family history of CAD does not significantly increase the risk of ACS.⁶ However, exploring each of these risk factors further is important, because genetic links between these risk factors can lead to an increased risk of CAD (eg, familial hypercholesterolemia).⁷

A history of normal or near-normal coronary angiography (< 25% stenosis) is associated with a lower likelihood of ACS, because 98% of such patients are free of AMI and 90% are without single-vessel coronary disease nearly 10 years out.⁶ A history of coronary artery bypass grafting is not necessarily predictive of ACS (LR = 1-3).^5,6

Historical features classically associated with ACS, but that have an LR < 2, are pain radiating to the neck or jaw, nausea or vomiting, dyspnea, and pain that is relieved with nitroglycerin.^5,6 Pain described as pleuritic, sharp, positional, or reproduced with palpation is less likely due to AMI.⁵

Physical exam findings are not independently diagnostic when evaluating chest pain. However, a third heart sound is the most likely finding associated with AMI and hypotension is the clinical sign most likely associated with ACS.⁵

Consider the diagnosis of PE in all patients with chest pain. In PE, chest pain might be associated with dyspnea, presyncope, syncope, or hemoptysis.⁸ On examination, 40% of patients have tachycardia.⁸ If PE is suspected; the patient should be risk-stratified using a validated prediction rule (see the discussion of PE that follows).

Continue to: Other historical features...

 

Other historical features or physical exam findings correlate with aortic dissection, pneumonia, and psychiatric causes of chest pain (TABLE 2^5-9).

Useful EKG findings

Among patients in whom ACS or PE is suspected, 12-lead electrocardiography (EKG) should be performed.

AMI. EKG findings most predictive of AMI are new ST-segment elevation or depression > 1 mm (LR = 6-54), new left bundle branch block (LR = 6.3), Q wave (positive LR = 3.9), and prominent, wide-based (hyperacute) T wave (LR = 3.1).¹⁰

ACS. Useful EKG findings to predict ACS are ST-segment depression (LR = 5.3 [95% CI, 2.1-8.6]) and any evidence of ischemia, defined as ST-segment depression, T-wave inversion, or Q wave (LR = 3.6 [95% CI, 1.6-5.7]).¹⁰

PE. The most common abnormal finding on EKG in the setting of PE is sinus tachycardia.

Continue to: Right ventricular strain

 

Right ventricular strain. Other findings that reflect right ventricular strain, but are much less common, are complete or incomplete right bundle branch block, prominent S wave in lead I, Q wave in lead III, and T-wave inversion in lead III (S1Q3T3; the ­McGinn-White sign) and in leads V₁-V₄.⁸

The utility of troponin and high-sensitivity troponin testing

Clinical evaluation and EKG findings are unable to diagnose or exclude ACS without the use of the cardiac biomarker troponin. In the past decade, high-sensitivity troponin assays have been used to stratify patients at risk of ACS.^11,12 Many protocols now exist using short interval (2-3 hours), high-sensitivity troponin testing to identify patients at low risk of myocardial infarction who can be safely discharged from the ED after 2 normal tests of the troponin level.^13-16

An elevated troponin value alone, however, is not a specific indicator of ACS; troponin can be elevated in the settings of myocardial ischemia related to increased oxygen demand (Type 2 non-STEMI) and decreased renal clearance. Consideration of the rate of rising and falling levels of troponin, its absolute value > 99th percentile, and other findings is critical to interpreting an elevated troponin level.¹⁷ Studies in which the HEART score (History, Electrocardiography, Age, Risk factors, Troponin) was combined with high-sensitivity troponin measurement show that this pairing is promising in reducing unnecessary admissions for chest pain.¹⁸ (For a description of this tool, see the discussion of the HEART score that follows.) Carlton and colleagues¹⁸ showed that a HEART score ≤ 3 and a negative high-sensitivity troponin I level had a negative predictive value of ≥ 99.5% for AMI.

Clinical decision tools: Who needs care? Who can go home?

Given the varied presentations of patients with life-threatening causes of chest pain, it is challenging to confidently determine who is safe to send home after initial assessment. Guidance in 2014 from the American Heart Association and American College of Cardiology recommends risk-stratifying patients for ACS using clinical decision tools to help guide management.^19,20 The American College of Physicians, in its 2015 guidelines, also recommends using a clinical decision tool to assess patients when there is suspicion of PE.²¹ Clinical application of these tools identifies patients at low risk of life-threatening conditions and can help avoid unnecessary intervention and a higher level of care. 

Tools for investigating ACS

The Marburg Heart Score²² assesses the likelihood of CAD in ambulatory settings while the HEART score assesses the risk of major adverse cardiac events in ED patients.²³ The Diamond Forrester criteria can be used to assess the pretest probability of CAD in both settings.²⁴

Continue to: Marburg Heart Score

 

Marburg Heart Score. Validated in patients older than 35 years of age in 2 different outpatient populations in 2010²² and 2012,²⁵ the Marburg score is determined by answering 5 questions:

• Female ≥ 65 years? Or male ≥ 55 years of age? (No, 0; Yes, +1)
• Known CAD, cerebrovascular disease, or peripheral vascular disease? (No, 0; Yes, +1)
• Is pain worse with exercise? (No, 0; Yes, +1)
• Is pain reproducible with palpation? (No, +1, Yes, 0)
• Does the patient assume that the pain is cardiac in nature? (No, 0; Yes, +1)

A Marburg Heart Score of 0 or 1 means CAD is highly unlikely in a patient with chest pain (negative predictive value = 99%-100%; positive predictive value = 0.6%)⁴ (TABLE 3^4,26-28). A score of ≤ 2 has a negative predictive value of 98%. A Marburg Heart Score of 4 or 5 has a relatively low positive predictive value (63%).⁴

The most common causes of chest pain in primary care? In descending order, musculoskeletal, GI, serious cardiac, nonspecific, psychiatric, and pulmonary causes.

This tool does not accurately diagnose acute MI, but it does help identify patients at low risk of ACS, thus reducing unnecessary subsequent testing. Although no clinical decision tool can rule out AMI with absolute certainty, the Marburg Heart Score is considered one of the most extensively tested and sensitive tools to predict low risk of CAD in outpatient primary care.²⁹

INTERCHEST rule (in outpatient primary care) is a newer prediction rule using data from 5 primary care–based studies of chest pain.³⁰ For a score ≤ 2, the negative predictive value for CAD causing chest pain is 97% to 98% and the positive predictive value is 43%. INTERCHEST incorporates studies used to validate the Marburg Heart Score, but has not been validated beyond initial pooled studies. Concerns have been raised about the quality of these pooled studies, however, and this rule has not been widely accepted for clinical use at this time.²⁹

The HEART score has been validated in patients older than 12 years in multiple institutions and across multiple ED populations.^23,31,32 It is widely used in the ED to assess a patient’s risk of major adverse cardiac events (MACE) over the next 6 weeks. MACE is defined as AMI, percutaneous coronary intervention, coronary artery bypass grafting, or death.

Continue to: The HEART score...

 

The HEART score is calculated based on 5 components:

• History of chest pain (slightly [0], moderately [+1], or highly [+2]) suspicious for ACS)
• EKG (normal [0], nonspecific ST changes [+1], significant ST deviations [+2])
• Age (< 45 y [0], 45-64 y [+1], ≥ 65 y [+2])
• Risk factors (none [0], 1 or 2 [+1], ≥ 3 or a history of atherosclerotic disease [+2]) ^a
• Initial troponin assay, standard sensitivity (≤ normal [0], 1-3× normal [+1], > 3× normal [+2]).

For patients with a HEART score of 0-3 (ie, at low risk), the pooled positive predictive value of a MACE was determined to be 0.19 (95% CI, 0.14-0.24), and the negative predictive value was 0.99 (95% CI, 0.98-0.99)—making it an effective tool to rule out a MACE over the short term²⁶ (TABLE 3^4,26-28).

Because the HEART Score was published in 2008, multiple systematic reviews and meta-analyses have compared it to the TIMI (Thrombolysis in Myocardial Infarction) and GRACE (Global Registry of Acute Coronary Events) scores for predicting short-term (30-day to 6-week) MACE in ED patients.^27,28,33,34 These studies have all shown that the HEART score is relatively superior to the TIMI and GRACE tools.

Characteristics of these tools are summarized in TABLE 3.^4,26-28

Diamond Forrester classification (in ED and outpatient settings). This tool uses 3 criteria—substernal chest pain, pain that increases upon exertion or with stress, and pain relieved by nitroglycerin or rest—to classify chest pain as typical angina (all 3 criteria), atypical angina (2 criteria), or noncardiac chest pain (0 criteria or 1 criterion).²⁴ Pretest probability (ie, the likelihood of an outcome before noninvasive testing) of the pain being due to CAD can then be determined from the type of chest pain and the patient’s gender and age¹⁹ (TABLE 4¹⁹). Recent studies have found that the Diamond Forrester criteria might overestimate the probability of CAD.³⁵

Continue to: Noninvasive imaging-based diagnostic methods

 

 

Noninvasive imaging-based diagnostic methods 

Positron-emission tomography stress testing, stress echocardiography, myocardial perfusion scanning, exercise treadmill testing. The first 3 of these imaging tests have a sensitivity and specificity ranging from 74% to 87%³⁶; exercise treadmill testing is less sensitive (68%) and specific (77%).³⁷

In a patient with a very low (< 5%) probability of CAD, a positive stress test (of any modality) is likely to be a false-positive; conversely, in a patient with a very high (> 90%) probability of CAD, a negative stress test is likely to be a false-negative.¹⁹ The American Heart Association, therefore, does not recommend any of these modalities for patients who have a < 5% or > 90% probability of CAD.¹⁹

Triage assessment of the chestpain patient, including vital signs, general appearance, and basic symptom questions, can clarify whether they need transfer to a higher level of care.

Noninvasive testing to rule out ACS in low- and intermediate-risk patients who present to the ED with chest pain provides no clinical benefit over clinical evaluation alone.³⁸ Therefore, these tests are rarely used in the initial evaluation of chest pain in an acute setting.

Coronary artery calcium score (CACS), coronary computed tomography angiography (CCTA). These tests have demonstrated promise in the risk stratification of chest pain, given their high sensitivity and negative predictive value in low- and intermediate-risk patients.^39,40 However, their application remains unclear in the evaluation of acute chest pain: Appropriate-use criteria do not favor CACS or CCTA alone to evaluate acute chest pain when there is suspicion of ACS.⁴¹ The Choosing Wisely initiative (for “avoiding unnecessary medical tests, treatments, and procedures”; www.choosingwisely.org) recommends against CCTA for high-risk patients presenting to the ED with acute chest pain.⁴²

Cardiac magnetic resonance imaging does not have an established role in the evaluation of patients with suspected ACS.⁴³

Continue to: Tools for investigating PE

 

 

Tools for investigating PE

Three clinical decision tools have been validated to predict the risk of PE: the Wells score, the Geneva score, and Pulmonary Embolism Rule Out Criteria (PERC).^44,45

Wells score is more sensitive than the Geneva score and has been validated in ambulatory¹ and ED^46-48 settings. Based on Wells criteria, high-risk patients need further evaluation with imaging. In low-risk patients, a normal D-dimer level effectively excludes PE, with a < 1% risk of subsequent thromboembolism in the following 3 months. Positive predictive value of the Wells decision tool is low because it is intended to rule out, not confirm, PE.

PERC can be used in a low-probability setting (defined as the treating physician arriving at the conclusion that PE is not the most likely diagnosis and can be excluded with a negative D-dimer test). In that setting, if the patient meets the 8 clinical variables in PERC, the diagnosis of PE is, effectively, ruled out.⁴⁸

Summing up: Evaluation of chest pain guided by risk of CAD

Patients who present in an outpatient setting with a potentially life-threatening cause of chest pain (TABLE 1) and patients with unstable vital signs should be sent to the ED for urgent evaluation. In the remaining outpatients, use the Marburg Heart Score or Diamond Forrester classification to assess the likelihood that pain is due to CAD (in the ED, the HEART score can be used for this purpose) (FIGURE).

When the risk is low. No further cardiac testing is indicated in patients with a risk of CAD < 5%, based on a Marburg score of 0 or 1, or on Diamond Forrester criteria; an abnormal stress test is likely to be a false-positive.¹⁹

Continue to: Moderate risk

 

Moderate risk. However, further testing is indicated, with a stress test (with or without myocardial imaging), in patients whose risk of CAD is 5% to 70%, based on the Diamond Forrester classification or an intermediate Marburg Heart Score (ie, a score of 2 or 3 but a normal EKG). This further testing can be performed urgently in patients who have multiple other risk factors that are not assessed by the Marburg Heart Score.

High risk. In patients whose risk is > 70%, invasive testing with angiography should be considered.^35,49

EKG abnormalities. Patients with a Marburg Score of 2 or 3 and an abnormal EKG should be sent to the ED (FIGURE). There, patients with a HEART score < 4 and a negative 2-3–hour troponin test have a < 1% chance of ACS and can be safely discharged.³¹

CORRESPONDENCE
Anne Mounsey, MD, UNC Family Medicine, 590 Manning Drive, Chapel Hill, NC 27599; [email protected]

Since their discovery in the early 1900s as the treatment for life-threatening deficiency syndromes, vitamins have been touted as panaceas for numerous ailments. While observational data have suggested potential correlations between vitamin status and every imaginable disease, randomized controlled trials (RCTs) have generally failed to find benefits from supplementation. Despite this lack of proven efficacy, more than half of older adults reported taking vitamins regularly.¹

While most clinicians consider vitamins to be, at worst, expensive placebos, the potential for harm and dangerous interactions exists. Unlike pharmaceuticals, vitamins are generally unregulated, and the true content of many dietary supplements is often difficult to elucidate. Understanding the physiologic role, foundational evidence, and specific indications for the various vitamins is key to providing the best recommendations to patients.

Vitamins are essential organic nutrients, required in small quantities for normal metabolism. Since they are not synthesized endogenously, they must be ingested via food intake. In the developed world, vitamin deficiency syndromes are rare, thanks to sufficiently balanced diets and availability of fortified foods. The focus of this article will be on vitamin supplementation in healthy patients with well-balanced diets. TABLE W1² (available at mdedge.com/familymedicine) lists the 13 recognized vitamins, their recommended dietary allowances, and any known toxicity risks. TABLE 2² outlines elements of the history to consider when evaluating for deficiency. A summary of the most clinically significant evidence for vitamin supplementation follows; a more comprehensive review can be found in TABLE 3.^3-96

B COMPLEX VITAMINS

Vitamin B1

Vitamers: Thiamine (thiamin)

Physiologic role: Critical in carbohydrate and amino-acid catabolism and energy metabolism

Dietary sources: Whole grains, meat, fish, fortified cereals, and breads

Thiamine serves as an essential cofactor in energy metabolism.² Thiamine deficiency is responsible for beriberi syndrome (rare in the developed world) and Wernicke-Korsakoff syndrome, the latter of which is a relatively common complication of chronic alcohol dependence. Although thiamine’s administration in these conditions can be curative, evidence is lacking to support its use preventively in patients with alcoholism.³ Thiamine has additionally been theorized to play a role in cardiac and cognitive function, but RCT data has not shown consistent patient-oriented benefits.^4,5

The takeaway: Given the lack of evidence, supplementation in the general population is not recommended.

Vitamin B2

Vitamers: Riboflavin

Physiologic role: Essential component of cellular function and growth, energy production, and metabolism of fats and drugs

Dietary sources: Eggs, organ meats, lean meats, milk, green vegetables, fortified cereals and grains

Riboflavin is essential to energy production, cellular growth, and metabolism.²

The takeaway: Its use as migraine prophylaxis has limited data,⁹⁷ but there is otherwise no evidence to support health benefits of riboflavin supplementation.

Vitamin B3

Vitamers: Nicotinic acid (niacin); nicotinamide (niacinamide); nicotinamide riboside

Physiologic role: Converted to nicotinamide adenine dinucleotide (NAD), which is widely required in most cellular metabolic redox processes. Crucial to the synthesis and metabolism of carbohydrates, fatty acids, and proteins

Dietary sources: Poultry, beef, fish, nuts, legumes, grains. (Tryptophan can also be converted to NAD.)

Niacin is readily converted to NAD, an essential coenzyme for multiple catalytic processes in the body. While niacin at doses more than 100 times the recommended dietary allowance (RDA; 1-3 g/d) has been extensively studied for its role in dyslipidemias,² pharmacologic dosing is beyond the scope of this article.

The takeaway: There is no evidence supporting a clinical benefit from niacin supplementation.

Vitamin B5

Vitamers: Pantothenic acid; pantethine

Physiologic role: Required for synthesis of coenzyme A (CoA) and acyl carrier protein, both essential in fatty acid and other anabolic/catabolic processes

Dietary sources: Almost all plant/animal-based foods. Richest sources include beef, chicken, organ meats, whole grains, and some vegetables

Pantothenic acid is essential to multiple metabolic processes and readily available in sufficient amounts in most foods.² Although limited RCT data suggest pantethine may improve lipid measures,^12,98,99 pantothenic acid itself does not seem to share this effect.

The takeaway: There is no data that supplementation of any form of vitamin B5 has any patient-oriented clinical benefits.

Continue to: Vitamin B6

 

 

Vitamin B6

Vitamers: Pyridoxine; pyridoxamine; pyridoxal

Physiologic role: Widely involved coenzyme for cognitive development, neurotransmitter biosynthesis, homocysteine and glucose metabolism, immune function, and hemoglobin formation

Dietary sources: Fish, organ meats, potatoes/starchy vegetables, fruit (other than citrus), and fortified cereals

Pyridoxine is required for numerous enzymatic processes in the body, including biosynthesis of neurotransmitters and homeostasis of the amino acid homocysteine.² While overt deficiency is rare, marginal insufficiency may become clinically apparent and has been associated with malabsorption, malignancies, pregnancy, heart disease, alcoholism, and use of drugs such as isoniazid, hydralazine, and levodopa/carbidopa.² Vitamin B6 supplementation is known to decrease plasma homocysteine levels, a theorized intermediary for cardiovascular disease; however, studies have failed to consistently demonstrate patient-­oriented benefits.^100-102 While observational data has suggested a correlation between vitamin B6 status and cancer risk, RCTs have not supported benefit from supplementation.^14-16 Potential effects of vitamin B6 supplementation on cognitive function have also been studied without observed benefit.^17,18

The takeaway: Vitamin B6 is recommended as a potential treatment option for nausea in pregnancy.¹⁹ Otherwise, vitamin B6 is readily available in food, deficiency is rare, and no patient-oriented evidence supports supplementation in the general population.

Vitamin B7

Vitamers: Biotin

Physiologic role: Cofactor in the metabolism of fatty acids, glucose, and amino acids. Also plays key role in histone modifications, gene regulation, and cell signaling

Dietary sources: Widely available; most prevalent in organ meats, fish, meat, seeds, nuts, and vegetables (eg, sweet potatoes). Whole cooked eggs are a major source, but raw eggs contain avidin, which blocks absorption

Biotin serves a key role in metabolism, gene regulation, and cell signaling.² Biotin is known to interfere with laboratory assays— including cardiac enzymes, thyroid studies, and hormone studies—at normal supplementation doses, resulting in both false-positive and false-negative results.¹⁰³

The takeaway: No evidence supports the health benefits of biotin supplementation.

Vitamin B9

Vitamers: Folates; folic acid

Physiologic role: Functions as a coenzyme in the synthesis of DNA/RNA and metabolism of amino acids

Dietary sources: Highest content in spinach, liver, asparagus, and brussels sprouts. Generally found in green leafy vegetables, fruits, nuts, beans, peas, seafood, eggs, dairy, meat, poultry, grains, and fortified cereals.

Continue to: Vitamin B12

 

 

Vitamin B12

Vitamers: Cyanocobalamin; hydroxocobalamin; methylcobalamin; adenosylcobalamin

Physiologic role: Required for red blood cell formation, neurologic function, and DNA synthesis

Dietary sources: Only in animal products: fish, poultry, meat, eggs, and milk/dairy products. Not present in plant foods. Fortified cereals, nutritional yeast are sources for vegans/vegetarians.

Given their linked physiologic roles, vitamins B9 and B12 are frequently studied together. Folate and cobalamins play key roles in nucleic acid synthesis and amino acid metabolism, with their most clinically significant role in hematopoiesis. Vitamin B12 is also essential to normal neurologic function.²

The US Preventive Services Task Force (USPSTF) recommends preconceptual folate supplementation of 0.4-0.8 mg/d in women of childbearing age to decrease the risk of fetal neural tube defects (grade A).²¹ This is supported by high-quality RCT evidence demonstrating a protective effect of daily folate supplementation in preventing neural tube defects.²² Folate supplementation’s effect on other fetal birth defects has been investigated, but no benefit has been demonstrated. While observational studies have suggested an inverse relationship with folate status and fetal autism spectrum disorder,^23-25 the RCT data is mixed.²⁶

A potential role for folate in cancer prevention has been extensively investigated. An expert panel of the National Toxicology Program (NTP) concluded that folate supplementation does not reduce cancer risk in people with adequate baseline folate status based on high-quality meta-analysis data.^27,104 Conversely, long-term follow-up from RCTs demonstrated an increased risk of colorectal adenomas and cancers,^28,29 leading the NTP panel to conclude there is sufficient concern for adverse effects of folate on cancer growth to justify further research.¹⁰⁴

While observational studies have found a correlation of increased risk for disease with lower antioxidant serum levels, RCTs have not demonstrated a reduction in disease risk with supplementation.

Given folate and vitamin B12’s ­homocysteine-reducing effects, it has been theorized that supplementation may protect from cardiovascular disease. However, despite extensive research, there remains no consistent patient-oriented outcomes data to support such a benefit.^31,32,105

The evidence is mixed but generally has found no benefit of folate or vitamin B12 supplementation on cognitive function.^18,33-35 Finally, RCT data has failed to demonstrate a reduction in fracture risk with supplementation.^36,106

The takeaway: High-quality RCT evidence demonstrates a protective effect of preconceptual daily folate supplementation in preventing neural tube defects.²² The USPSTF recommends preconceptual folate supplementation of 0.4-0.8 mg/d in women of childbearing age to decrease the risk of fetal neural tube defects.

Continue to: ANTIOXIDANTS

 

 

ANTIOXIDANTS

In addition to their individual roles, vitamins A, E, and C are antioxidants, functioning to protect cells from oxidative damage by free radical species.² Due to this shared role, these vitamins are commonly studied together. Antioxidants are hypothesized to protect from various diseases, including cancer, cardiovascular disease, dementia, autoimmune disorders, depression, cataracts, and age-related vision decline.^2,37,107-112

Though observational studies have found a correlation of increased risk for disease with lower antioxidant serum levels, RCTs have not demonstrated a reduction in disease risk with supplementation and, in some cases, have found an increased risk of mortality. While several studies have found potential benefit of antioxidant use in reducing colon and breast cancer risk,^38,113-115 vitamins A and E have been associated with increased risk of lung and prostate cancer, respectively.^47,110 Cardiovascular disease and antioxidant vitamin supplementation has similar inconsistent data, ranging from slight benefit to harm.^2,116 After a large Cochrane review in 2012 found a significant increase in all-cause mortality associated with vitamin E and ­beta-carotene,¹¹⁷ the USPSTF made a specific recommendation against supplementation of these vitamins for the prevention of cardiovascular disease or cancer (grade D).¹¹⁸ Given its limited risk for harm, vitamin C was excluded from this recommendation.

Vitamin A

Vitamers: Retinol; retinal; retinyl esters; provitamin A carotenoids (beta-carotene, alpha-carotene, beta-cryptoxanthin)

Physiologic role: Essential for vision and corneal development. Also involved in general cell differentiation and immune function

Dietary sources: Liver, fish oil, dairy, and fortified cereals. Provitamin A sources: leafy green vegetables, orange/yellow vegetables, tomato products, fruits, and vegetable oils

Retinoids and their precursors, carotenoids, serve a critical function in vision, as well as regulating cell differentiation and proliferation throughout the body.² While evidence suggests mortality benefit of supplementation in populations at risk of deficiency,⁴⁵ wide-ranging studies have found either inconsistent benefit or outright harms in the developed world.

The takeaway: Given the USPSTF grade “D” recommendation and concern for potential harms, supplementation is not recommended in healthy patients without risk factors for deficiency.²

Vitamin E

Vitamers: Tocopherols (alpha-, beta-, ­gamma-, delta-); tocotrienol (alpha-, beta-, gamma-, delta-)

Physiologic role: Antioxidant; protects polyunsaturated fats from free radical oxidative damage. Involved in immune function, cell signaling, and regulation of gene expression

Dietary sources: Nuts, seeds, vegetable oil, green leafy vegetables, and fortified cereals

Vitamin E is the collective name of 8 compounds; alpha-tocopherol is the physiologically active form. Vitamin E is involved with cell proliferation as well as endothelial and platelet function.²

The takeaway: Vitamin E supplementation’s effects on cancer, cardiovascular disease, ophthalmologic disorders, and cognition have been investigated; data is either lacking to support a benefit or demonstrates harms as outlined above. Given this and the USPSTF grade “D” recommendation, supplementation is not recommended in healthy patients.²

Vitamin C

Vitamers: Ascorbic acid

Physiologic role: Required for synthesis of collagen, L-carnitine, and some neurotransmitters. Also involved in protein metabolism

Dietary sources: Primarily in fruits and vegetables: citrus, tomato, potatoes, red/green peppers, kiwi fruit, broccoli, strawberries, brussels sprouts, cantaloupe, and fortified cereals

Vitamin C supplementation at the onset of illness does not seem to have benefit.

Ascorbic acid is a required cofactor for biosynthesis of collagen, neurotransmitters, and protein metabolism.² In addition to the shared hypothesized benefits of antioxidants, vitamin C supplementation has undergone extensive research into its potential role in augmenting the immune system and preventing the common cold. Systematic reviews have found daily vitamin C supplementation of at least 200 mg did not affect the incidence of the common cold in healthy adults but may shorten duration and could be of benefit in those exposed to extreme physical exercise or cold.⁴⁸ Vitamin C supplementation at the onset of illness does not seem to have benefit.⁴⁸ Data is insufficient to draw conclusions about a potential effect on pneumonia incidence or severity.^119,120

The takeaway: Overall, data remain inconclusive as to potential benefits of vitamin C supplementation, although risks of potential harms are likely low.

Continue to: Vitamin D

 

 

Vitamin D

Vitamers: Cholecalciferol (D3); ergocalciferol (D2)

Physiologic role: Hydroxylation in liver and kidney required to activate. Promotes dietary calcium absorption, enables normal bone mineralization. Also involved in modulation of cell growth, and neuromuscular and immune function

Dietary sources: Few natural dietary sources, which include fatty fish, fish liver oils; small amount in beef liver, cheese, egg yolks. Primary sources include fortified milk and endogenous synthesis in skin with UV exposure

Calciferol is a fat-soluble vitamin required for calcium and bone homeostasis. It is not naturally available in many foods but is primarily produced endogenously in the skin with ultraviolet light exposure.²

The AAP recommends supplementing exclusively breastfed infants with 400 IU/d of vitamin D to prevent rickets.

Bone density and fracture risk reduction are the most often cited benefits of vitamin D supplementation, but this has not been demonstrated consistently in RCTs. Multiple systematic reviews showing inconsistent benefit of vitamin D (with or without calcium) on fracture risk led the USPSTF to conclude that there is insufficient evidence (grade I) to issue a recommendation on vitamin D and calcium supplementation for primary prevention of fractures in postmenopausal women.^49-51 Despite some initial evidence suggesting a benefit of vitamin D supplementation on falls reduction, 3 recent systematic reviews did not demonstrate this in community-dwelling elders,^54-56 although a separate Cochrane review did suggest a reduction in rate of falls among institutionalized elders.⁵⁷

The takeaway: Given these findings, the USPSTF has recommended against (grade D) vitamin D supplementation to prevent falls in community-dwelling elders.⁵⁵

Beyond falls. While the vitamin D receptor is expressed throughout the body and observational studies have suggested a correlation between vitamin D status and many outcomes, extensive RCT data has generally failed to demonstrate extraskeletal benefits from supplementation. Meta-analysis data have demonstrated potential reductions in acute respiratory infection rates and asthma exacerbations with vitamin D supplementation. There is also limited evidence suggesting a reduction in preeclampsia and low-birthweight infant risk with vitamin D supplementation in pregnancy. However, several large meta-analyses and systematic reviews have investigated vitamin D supplementation’s effect on all-cause mortality and found no consistent data to support an association.^41,58-62

Multiple systematic reviews have investigated and found high-quality evidence demonstrating no association between vitamin D supplementation and cancer^41,63-66,121 or cardiovascular disease risk.^41,70,71 There is high-quality data showing no benefit of vitamin D supplementation for multiple additional diseases, including diabetes, cognitive decline, depression, pain, obesity, and liver disease.^{43,72-75,85-90,122}

The takeaway: Due to poor availability in breastmilk, the American Academy of Pediatrics (AAP) recommends supplementing exclusively breastfed infants with 400 IU/d of vitamin D to prevent rickets.¹²³ RCT data support high-dose supplementation of lactating women (6400 IU/d) as an alternative strategy to supplementation of the infant.¹²⁴ The AAP recommends that all nonbreastfeeding infants and older children ingesting < 1000 mL/d of vitamin D–fortified formula or milk should also be supplemented with 400 IU/d of vitamin D.¹²³ Despite these universal recommendations for supplementation, evidence is mixed on the effect of vitamin D supplementation on bone health in children.^52,53

Although concerns about vitamin D supplementation and increased risk of urolithiasis and hypercalcemia have been raised,^51,62,121 systematic reviews have not demonstrated significant, clinically relevant risks, even with high-dose supplementation (> 2800 IU/d).^125,126

Vitamin K

Vitamers: Phylloquinone (K1); menaquinones (K2)

Physiologic role: Coenzyme for synthesis of proteins involved in hemostasis and bone metabolism

Dietary sources: Phylloquinone is found in green leafy vegetables, vegetable oils, some fruits, meat, dairy, and eggs. Menaquinone is produced by gut bacteria and present in fermented foods

Vitamin K includes 2 groups of similar compounds: phylloquinone and menaquinones. Unlike other fat-soluble vitamins, vitamin K is rapidly metabolized and has low tissue storage.²

Children taking multivitamins were often found to have excess levels of potentially harmful nutrients, such as retinol, zinc, and folic acid.

Administration of vitamin K 0.5 to 1 mg intramuscularly (IM) to newborns is standard of care for the prevention of vitamin K deficiency bleeding (VKDB). This is supported by RCT data demonstrating a reduction in classic VKDB (occurring within 7 days)⁹¹ and epidemiologic data from various countries showing a reduction in late-onset VKDB with vitamin K prophylaxis programs.¹²⁷ Oral dosing appears to reduce the risk of VKDB in the setting of parental refusal but is less effective than IM dosing.^128,129

Vitamin K’s effects on bone density and fracture risk have also been investigated. Systematic reviews have demonstrated a reduction in fracture risk with vitamin K supplementation,^92,93 and European and Asian regulatory bodies have recognized a potential benefit on bone health.² The FDA considers the evidence insufficient at this time to support such a claim.² Higher dietary vitamin K consumption has been associated with lower risk of cardiovascular disease in observational studies⁹⁴ and supplementation was associated with improved disease measures,¹³⁰ but no patient-oriented outcomes have been demonstrated.¹³¹

The takeaway: The administration of vitamin K 0.5 to 1 mg intramuscularly (IM) to newborns is standard of care for the prevention of VKDB. Vitamin K may lead to a reduction in fracture risk, but the FDA considers the evidence insufficient. Vitamin K’s potential link to a lowered risk of cardiovascular disease has not been demonstrated with patient-­oriented outcomes. Vitamin K has low potential for toxicity, although its interaction with vitamin K antagonists (ie, warfarin) is clinically relevant.

Continue to: MULTIVITAMINS

 

 

MULTIVITAMINS

Multivitamins are often defined as a supplement containing 3 or more vitamins and minerals but without herbs, hormones, or drugs.¹³² Many multivitamins do contain additional substances, and some include levels of vitamins that exceed the RDA or even the established tolerable upper intake level.¹³³

Safe medication storage should be practiced, as multivitamins with iron are a leading cause of poisoning in children.

A 2013 systematic review found limited evidence to support any benefit from multivitamin supplementation.⁴¹ Two included RCTs demonstrated a narrowly significant decrease in cancer rates among men, but saw no effect in women or the combined population.^134,135 This benefit appears to disappear at 5 years of follow-up.¹³⁶ RCT data have shown no benefit of multivitamin use on cognitive function,⁹⁵ and high-quality data suggest there is no effect on all-cause mortality.¹³⁷ Given this lack of supporting evidence, the USPSTF has concluded that there is insufficient evidence (grade I) to recommend vitamin supplementation in general to prevent cardiovascular disease or cancer.⁴¹

The use of prenatal multivitamins is generally recommended in the pregnancy and preconception period and has been associated with reduced risk of autism spectrum disorders, pediatric cancer rates, small-for-gestational-age infants, and multiple birth defects in offspring; however, studies have not examined if this benefit exceeds that of folate supplementation alone.^138-140 AAP does not recommend multivitamins for children with a well-balanced diet.¹⁴¹ Of concern, children taking multivitamins were often found to have excess levels of potentially harmful nutrients such as retinol, zinc, and folic acid.¹⁴²

The takeaway: There is limited evidence to support any benefit from multivitamin supplementation. Prenatal multivitamins are generally recommended in the pregnancy and preconception period. Overall, the risks of multivitamins are minimal, although that risk is dependent on the multivitamin’s constituent components.¹⁴³ Components such as vitamin K may interact with a patient’s medications, and multivitamins have been shown to reduce the circulating levels of antiretrovirals.¹⁴⁴ Specifically, multivitamins with iron should be avoided in men and postmenopausal women, and safe medication storage should be practiced as multivitamins with iron are a leading cause of poisoning in children.²

SUMMARY

Vitamin supplementation in the developed world remains common despite a paucity of RCT data supporting it. Supplementation of folate in women planning to conceive, vitamin D in breastfeeding infants, and vitamin K in newborns are well supported by clinical evidence. Otherwise, there is limited evidence supporting clinically significant benefit from supplementation in healthy patients with well-balanced diets—and in the case of vitamins A and E, there may be outright harms.

CORRESPONDENCE
Joel Herness, MD, 4700 North Las Vegas Boulevard, Nellis AFB, NV 89191; [email protected]

Since their discovery in the early 1900s as the treatment for life-threatening deficiency syndromes, vitamins have been touted as panaceas for numerous ailments. While observational data have suggested potential correlations between vitamin status and every imaginable disease, randomized controlled trials (RCTs) have generally failed to find benefits from supplementation. Despite this lack of proven efficacy, more than half of older adults reported taking vitamins regularly.¹

While most clinicians consider vitamins to be, at worst, expensive placebos, the potential for harm and dangerous interactions exists. Unlike pharmaceuticals, vitamins are generally unregulated, and the true content of many dietary supplements is often difficult to elucidate. Understanding the physiologic role, foundational evidence, and specific indications for the various vitamins is key to providing the best recommendations to patients.

Vitamins are essential organic nutrients, required in small quantities for normal metabolism. Since they are not synthesized endogenously, they must be ingested via food intake. In the developed world, vitamin deficiency syndromes are rare, thanks to sufficiently balanced diets and availability of fortified foods. The focus of this article will be on vitamin supplementation in healthy patients with well-balanced diets. TABLE W1² (available at mdedge.com/familymedicine) lists the 13 recognized vitamins, their recommended dietary allowances, and any known toxicity risks. TABLE 2² outlines elements of the history to consider when evaluating for deficiency. A summary of the most clinically significant evidence for vitamin supplementation follows; a more comprehensive review can be found in TABLE 3.^3-96

B COMPLEX VITAMINS

Vitamin B1

Vitamers: Thiamine (thiamin)

Physiologic role: Critical in carbohydrate and amino-acid catabolism and energy metabolism

Dietary sources: Whole grains, meat, fish, fortified cereals, and breads

Thiamine serves as an essential cofactor in energy metabolism.² Thiamine deficiency is responsible for beriberi syndrome (rare in the developed world) and Wernicke-Korsakoff syndrome, the latter of which is a relatively common complication of chronic alcohol dependence. Although thiamine’s administration in these conditions can be curative, evidence is lacking to support its use preventively in patients with alcoholism.³ Thiamine has additionally been theorized to play a role in cardiac and cognitive function, but RCT data has not shown consistent patient-oriented benefits.^4,5

The takeaway: Given the lack of evidence, supplementation in the general population is not recommended.

Vitamin B2

Vitamers: Riboflavin

Physiologic role: Essential component of cellular function and growth, energy production, and metabolism of fats and drugs

Dietary sources: Eggs, organ meats, lean meats, milk, green vegetables, fortified cereals and grains

Riboflavin is essential to energy production, cellular growth, and metabolism.²

The takeaway: Its use as migraine prophylaxis has limited data,⁹⁷ but there is otherwise no evidence to support health benefits of riboflavin supplementation.

Vitamin B3

Vitamers: Nicotinic acid (niacin); nicotinamide (niacinamide); nicotinamide riboside

Physiologic role: Converted to nicotinamide adenine dinucleotide (NAD), which is widely required in most cellular metabolic redox processes. Crucial to the synthesis and metabolism of carbohydrates, fatty acids, and proteins

Dietary sources: Poultry, beef, fish, nuts, legumes, grains. (Tryptophan can also be converted to NAD.)

Niacin is readily converted to NAD, an essential coenzyme for multiple catalytic processes in the body. While niacin at doses more than 100 times the recommended dietary allowance (RDA; 1-3 g/d) has been extensively studied for its role in dyslipidemias,² pharmacologic dosing is beyond the scope of this article.

The takeaway: There is no evidence supporting a clinical benefit from niacin supplementation.

Vitamin B5

Vitamers: Pantothenic acid; pantethine

Physiologic role: Required for synthesis of coenzyme A (CoA) and acyl carrier protein, both essential in fatty acid and other anabolic/catabolic processes

Dietary sources: Almost all plant/animal-based foods. Richest sources include beef, chicken, organ meats, whole grains, and some vegetables

Pantothenic acid is essential to multiple metabolic processes and readily available in sufficient amounts in most foods.² Although limited RCT data suggest pantethine may improve lipid measures,^12,98,99 pantothenic acid itself does not seem to share this effect.

The takeaway: There is no data that supplementation of any form of vitamin B5 has any patient-oriented clinical benefits.

Continue to: Vitamin B6

 

 

Vitamin B6

Vitamers: Pyridoxine; pyridoxamine; pyridoxal

Physiologic role: Widely involved coenzyme for cognitive development, neurotransmitter biosynthesis, homocysteine and glucose metabolism, immune function, and hemoglobin formation

Dietary sources: Fish, organ meats, potatoes/starchy vegetables, fruit (other than citrus), and fortified cereals

Pyridoxine is required for numerous enzymatic processes in the body, including biosynthesis of neurotransmitters and homeostasis of the amino acid homocysteine.² While overt deficiency is rare, marginal insufficiency may become clinically apparent and has been associated with malabsorption, malignancies, pregnancy, heart disease, alcoholism, and use of drugs such as isoniazid, hydralazine, and levodopa/carbidopa.² Vitamin B6 supplementation is known to decrease plasma homocysteine levels, a theorized intermediary for cardiovascular disease; however, studies have failed to consistently demonstrate patient-­oriented benefits.^100-102 While observational data has suggested a correlation between vitamin B6 status and cancer risk, RCTs have not supported benefit from supplementation.^14-16 Potential effects of vitamin B6 supplementation on cognitive function have also been studied without observed benefit.^17,18

The takeaway: Vitamin B6 is recommended as a potential treatment option for nausea in pregnancy.¹⁹ Otherwise, vitamin B6 is readily available in food, deficiency is rare, and no patient-oriented evidence supports supplementation in the general population.

Vitamin B7

Vitamers: Biotin

Physiologic role: Cofactor in the metabolism of fatty acids, glucose, and amino acids. Also plays key role in histone modifications, gene regulation, and cell signaling

Dietary sources: Widely available; most prevalent in organ meats, fish, meat, seeds, nuts, and vegetables (eg, sweet potatoes). Whole cooked eggs are a major source, but raw eggs contain avidin, which blocks absorption

Biotin serves a key role in metabolism, gene regulation, and cell signaling.² Biotin is known to interfere with laboratory assays— including cardiac enzymes, thyroid studies, and hormone studies—at normal supplementation doses, resulting in both false-positive and false-negative results.¹⁰³

The takeaway: No evidence supports the health benefits of biotin supplementation.

Vitamin B9

Vitamers: Folates; folic acid

Physiologic role: Functions as a coenzyme in the synthesis of DNA/RNA and metabolism of amino acids

Dietary sources: Highest content in spinach, liver, asparagus, and brussels sprouts. Generally found in green leafy vegetables, fruits, nuts, beans, peas, seafood, eggs, dairy, meat, poultry, grains, and fortified cereals.

Continue to: Vitamin B12

 

 

Vitamin B12

Vitamers: Cyanocobalamin; hydroxocobalamin; methylcobalamin; adenosylcobalamin

Physiologic role: Required for red blood cell formation, neurologic function, and DNA synthesis

Dietary sources: Only in animal products: fish, poultry, meat, eggs, and milk/dairy products. Not present in plant foods. Fortified cereals, nutritional yeast are sources for vegans/vegetarians.

Given their linked physiologic roles, vitamins B9 and B12 are frequently studied together. Folate and cobalamins play key roles in nucleic acid synthesis and amino acid metabolism, with their most clinically significant role in hematopoiesis. Vitamin B12 is also essential to normal neurologic function.²

The US Preventive Services Task Force (USPSTF) recommends preconceptual folate supplementation of 0.4-0.8 mg/d in women of childbearing age to decrease the risk of fetal neural tube defects (grade A).²¹ This is supported by high-quality RCT evidence demonstrating a protective effect of daily folate supplementation in preventing neural tube defects.²² Folate supplementation’s effect on other fetal birth defects has been investigated, but no benefit has been demonstrated. While observational studies have suggested an inverse relationship with folate status and fetal autism spectrum disorder,^23-25 the RCT data is mixed.²⁶

A potential role for folate in cancer prevention has been extensively investigated. An expert panel of the National Toxicology Program (NTP) concluded that folate supplementation does not reduce cancer risk in people with adequate baseline folate status based on high-quality meta-analysis data.^27,104 Conversely, long-term follow-up from RCTs demonstrated an increased risk of colorectal adenomas and cancers,^28,29 leading the NTP panel to conclude there is sufficient concern for adverse effects of folate on cancer growth to justify further research.¹⁰⁴

While observational studies have found a correlation of increased risk for disease with lower antioxidant serum levels, RCTs have not demonstrated a reduction in disease risk with supplementation.

Given folate and vitamin B12’s ­homocysteine-reducing effects, it has been theorized that supplementation may protect from cardiovascular disease. However, despite extensive research, there remains no consistent patient-oriented outcomes data to support such a benefit.^31,32,105

The evidence is mixed but generally has found no benefit of folate or vitamin B12 supplementation on cognitive function.^18,33-35 Finally, RCT data has failed to demonstrate a reduction in fracture risk with supplementation.^36,106

The takeaway: High-quality RCT evidence demonstrates a protective effect of preconceptual daily folate supplementation in preventing neural tube defects.²² The USPSTF recommends preconceptual folate supplementation of 0.4-0.8 mg/d in women of childbearing age to decrease the risk of fetal neural tube defects.

Continue to: ANTIOXIDANTS

 

 

ANTIOXIDANTS

In addition to their individual roles, vitamins A, E, and C are antioxidants, functioning to protect cells from oxidative damage by free radical species.² Due to this shared role, these vitamins are commonly studied together. Antioxidants are hypothesized to protect from various diseases, including cancer, cardiovascular disease, dementia, autoimmune disorders, depression, cataracts, and age-related vision decline.^2,37,107-112

Though observational studies have found a correlation of increased risk for disease with lower antioxidant serum levels, RCTs have not demonstrated a reduction in disease risk with supplementation and, in some cases, have found an increased risk of mortality. While several studies have found potential benefit of antioxidant use in reducing colon and breast cancer risk,^38,113-115 vitamins A and E have been associated with increased risk of lung and prostate cancer, respectively.^47,110 Cardiovascular disease and antioxidant vitamin supplementation has similar inconsistent data, ranging from slight benefit to harm.^2,116 After a large Cochrane review in 2012 found a significant increase in all-cause mortality associated with vitamin E and ­beta-carotene,¹¹⁷ the USPSTF made a specific recommendation against supplementation of these vitamins for the prevention of cardiovascular disease or cancer (grade D).¹¹⁸ Given its limited risk for harm, vitamin C was excluded from this recommendation.

Vitamin A

Vitamers: Retinol; retinal; retinyl esters; provitamin A carotenoids (beta-carotene, alpha-carotene, beta-cryptoxanthin)

Physiologic role: Essential for vision and corneal development. Also involved in general cell differentiation and immune function

Dietary sources: Liver, fish oil, dairy, and fortified cereals. Provitamin A sources: leafy green vegetables, orange/yellow vegetables, tomato products, fruits, and vegetable oils

Retinoids and their precursors, carotenoids, serve a critical function in vision, as well as regulating cell differentiation and proliferation throughout the body.² While evidence suggests mortality benefit of supplementation in populations at risk of deficiency,⁴⁵ wide-ranging studies have found either inconsistent benefit or outright harms in the developed world.

The takeaway: Given the USPSTF grade “D” recommendation and concern for potential harms, supplementation is not recommended in healthy patients without risk factors for deficiency.²

Vitamin E

Vitamers: Tocopherols (alpha-, beta-, ­gamma-, delta-); tocotrienol (alpha-, beta-, gamma-, delta-)

Physiologic role: Antioxidant; protects polyunsaturated fats from free radical oxidative damage. Involved in immune function, cell signaling, and regulation of gene expression

Dietary sources: Nuts, seeds, vegetable oil, green leafy vegetables, and fortified cereals

Vitamin E is the collective name of 8 compounds; alpha-tocopherol is the physiologically active form. Vitamin E is involved with cell proliferation as well as endothelial and platelet function.²

The takeaway: Vitamin E supplementation’s effects on cancer, cardiovascular disease, ophthalmologic disorders, and cognition have been investigated; data is either lacking to support a benefit or demonstrates harms as outlined above. Given this and the USPSTF grade “D” recommendation, supplementation is not recommended in healthy patients.²

Vitamin C

Vitamers: Ascorbic acid

Physiologic role: Required for synthesis of collagen, L-carnitine, and some neurotransmitters. Also involved in protein metabolism

Dietary sources: Primarily in fruits and vegetables: citrus, tomato, potatoes, red/green peppers, kiwi fruit, broccoli, strawberries, brussels sprouts, cantaloupe, and fortified cereals

Vitamin C supplementation at the onset of illness does not seem to have benefit.

Ascorbic acid is a required cofactor for biosynthesis of collagen, neurotransmitters, and protein metabolism.² In addition to the shared hypothesized benefits of antioxidants, vitamin C supplementation has undergone extensive research into its potential role in augmenting the immune system and preventing the common cold. Systematic reviews have found daily vitamin C supplementation of at least 200 mg did not affect the incidence of the common cold in healthy adults but may shorten duration and could be of benefit in those exposed to extreme physical exercise or cold.⁴⁸ Vitamin C supplementation at the onset of illness does not seem to have benefit.⁴⁸ Data is insufficient to draw conclusions about a potential effect on pneumonia incidence or severity.^119,120

The takeaway: Overall, data remain inconclusive as to potential benefits of vitamin C supplementation, although risks of potential harms are likely low.

Continue to: Vitamin D

 

 

Vitamin D

Vitamers: Cholecalciferol (D3); ergocalciferol (D2)

Physiologic role: Hydroxylation in liver and kidney required to activate. Promotes dietary calcium absorption, enables normal bone mineralization. Also involved in modulation of cell growth, and neuromuscular and immune function

Dietary sources: Few natural dietary sources, which include fatty fish, fish liver oils; small amount in beef liver, cheese, egg yolks. Primary sources include fortified milk and endogenous synthesis in skin with UV exposure

Calciferol is a fat-soluble vitamin required for calcium and bone homeostasis. It is not naturally available in many foods but is primarily produced endogenously in the skin with ultraviolet light exposure.²

The AAP recommends supplementing exclusively breastfed infants with 400 IU/d of vitamin D to prevent rickets.

Bone density and fracture risk reduction are the most often cited benefits of vitamin D supplementation, but this has not been demonstrated consistently in RCTs. Multiple systematic reviews showing inconsistent benefit of vitamin D (with or without calcium) on fracture risk led the USPSTF to conclude that there is insufficient evidence (grade I) to issue a recommendation on vitamin D and calcium supplementation for primary prevention of fractures in postmenopausal women.^49-51 Despite some initial evidence suggesting a benefit of vitamin D supplementation on falls reduction, 3 recent systematic reviews did not demonstrate this in community-dwelling elders,^54-56 although a separate Cochrane review did suggest a reduction in rate of falls among institutionalized elders.⁵⁷

The takeaway: Given these findings, the USPSTF has recommended against (grade D) vitamin D supplementation to prevent falls in community-dwelling elders.⁵⁵

Beyond falls. While the vitamin D receptor is expressed throughout the body and observational studies have suggested a correlation between vitamin D status and many outcomes, extensive RCT data has generally failed to demonstrate extraskeletal benefits from supplementation. Meta-analysis data have demonstrated potential reductions in acute respiratory infection rates and asthma exacerbations with vitamin D supplementation. There is also limited evidence suggesting a reduction in preeclampsia and low-birthweight infant risk with vitamin D supplementation in pregnancy. However, several large meta-analyses and systematic reviews have investigated vitamin D supplementation’s effect on all-cause mortality and found no consistent data to support an association.^41,58-62

Multiple systematic reviews have investigated and found high-quality evidence demonstrating no association between vitamin D supplementation and cancer^41,63-66,121 or cardiovascular disease risk.^41,70,71 There is high-quality data showing no benefit of vitamin D supplementation for multiple additional diseases, including diabetes, cognitive decline, depression, pain, obesity, and liver disease.^{43,72-75,85-90,122}

The takeaway: Due to poor availability in breastmilk, the American Academy of Pediatrics (AAP) recommends supplementing exclusively breastfed infants with 400 IU/d of vitamin D to prevent rickets.¹²³ RCT data support high-dose supplementation of lactating women (6400 IU/d) as an alternative strategy to supplementation of the infant.¹²⁴ The AAP recommends that all nonbreastfeeding infants and older children ingesting < 1000 mL/d of vitamin D–fortified formula or milk should also be supplemented with 400 IU/d of vitamin D.¹²³ Despite these universal recommendations for supplementation, evidence is mixed on the effect of vitamin D supplementation on bone health in children.^52,53

Although concerns about vitamin D supplementation and increased risk of urolithiasis and hypercalcemia have been raised,^51,62,121 systematic reviews have not demonstrated significant, clinically relevant risks, even with high-dose supplementation (> 2800 IU/d).^125,126

Vitamin K

Vitamers: Phylloquinone (K1); menaquinones (K2)

Physiologic role: Coenzyme for synthesis of proteins involved in hemostasis and bone metabolism

Dietary sources: Phylloquinone is found in green leafy vegetables, vegetable oils, some fruits, meat, dairy, and eggs. Menaquinone is produced by gut bacteria and present in fermented foods

Vitamin K includes 2 groups of similar compounds: phylloquinone and menaquinones. Unlike other fat-soluble vitamins, vitamin K is rapidly metabolized and has low tissue storage.²

Children taking multivitamins were often found to have excess levels of potentially harmful nutrients, such as retinol, zinc, and folic acid.

Administration of vitamin K 0.5 to 1 mg intramuscularly (IM) to newborns is standard of care for the prevention of vitamin K deficiency bleeding (VKDB). This is supported by RCT data demonstrating a reduction in classic VKDB (occurring within 7 days)⁹¹ and epidemiologic data from various countries showing a reduction in late-onset VKDB with vitamin K prophylaxis programs.¹²⁷ Oral dosing appears to reduce the risk of VKDB in the setting of parental refusal but is less effective than IM dosing.^128,129

Vitamin K’s effects on bone density and fracture risk have also been investigated. Systematic reviews have demonstrated a reduction in fracture risk with vitamin K supplementation,^92,93 and European and Asian regulatory bodies have recognized a potential benefit on bone health.² The FDA considers the evidence insufficient at this time to support such a claim.² Higher dietary vitamin K consumption has been associated with lower risk of cardiovascular disease in observational studies⁹⁴ and supplementation was associated with improved disease measures,¹³⁰ but no patient-oriented outcomes have been demonstrated.¹³¹

The takeaway: The administration of vitamin K 0.5 to 1 mg intramuscularly (IM) to newborns is standard of care for the prevention of VKDB. Vitamin K may lead to a reduction in fracture risk, but the FDA considers the evidence insufficient. Vitamin K’s potential link to a lowered risk of cardiovascular disease has not been demonstrated with patient-­oriented outcomes. Vitamin K has low potential for toxicity, although its interaction with vitamin K antagonists (ie, warfarin) is clinically relevant.

Continue to: MULTIVITAMINS

 

 

MULTIVITAMINS

Multivitamins are often defined as a supplement containing 3 or more vitamins and minerals but without herbs, hormones, or drugs.¹³² Many multivitamins do contain additional substances, and some include levels of vitamins that exceed the RDA or even the established tolerable upper intake level.¹³³

Safe medication storage should be practiced, as multivitamins with iron are a leading cause of poisoning in children.

A 2013 systematic review found limited evidence to support any benefit from multivitamin supplementation.⁴¹ Two included RCTs demonstrated a narrowly significant decrease in cancer rates among men, but saw no effect in women or the combined population.^134,135 This benefit appears to disappear at 5 years of follow-up.¹³⁶ RCT data have shown no benefit of multivitamin use on cognitive function,⁹⁵ and high-quality data suggest there is no effect on all-cause mortality.¹³⁷ Given this lack of supporting evidence, the USPSTF has concluded that there is insufficient evidence (grade I) to recommend vitamin supplementation in general to prevent cardiovascular disease or cancer.⁴¹

The use of prenatal multivitamins is generally recommended in the pregnancy and preconception period and has been associated with reduced risk of autism spectrum disorders, pediatric cancer rates, small-for-gestational-age infants, and multiple birth defects in offspring; however, studies have not examined if this benefit exceeds that of folate supplementation alone.^138-140 AAP does not recommend multivitamins for children with a well-balanced diet.¹⁴¹ Of concern, children taking multivitamins were often found to have excess levels of potentially harmful nutrients such as retinol, zinc, and folic acid.¹⁴²

The takeaway: There is limited evidence to support any benefit from multivitamin supplementation. Prenatal multivitamins are generally recommended in the pregnancy and preconception period. Overall, the risks of multivitamins are minimal, although that risk is dependent on the multivitamin’s constituent components.¹⁴³ Components such as vitamin K may interact with a patient’s medications, and multivitamins have been shown to reduce the circulating levels of antiretrovirals.¹⁴⁴ Specifically, multivitamins with iron should be avoided in men and postmenopausal women, and safe medication storage should be practiced as multivitamins with iron are a leading cause of poisoning in children.²

SUMMARY

Vitamin supplementation in the developed world remains common despite a paucity of RCT data supporting it. Supplementation of folate in women planning to conceive, vitamin D in breastfeeding infants, and vitamin K in newborns are well supported by clinical evidence. Otherwise, there is limited evidence supporting clinically significant benefit from supplementation in healthy patients with well-balanced diets—and in the case of vitamins A and E, there may be outright harms.

CORRESPONDENCE
Joel Herness, MD, 4700 North Las Vegas Boulevard, Nellis AFB, NV 89191; [email protected]

Since their discovery in the early 1900s as the treatment for life-threatening deficiency syndromes, vitamins have been touted as panaceas for numerous ailments. While observational data have suggested potential correlations between vitamin status and every imaginable disease, randomized controlled trials (RCTs) have generally failed to find benefits from supplementation. Despite this lack of proven efficacy, more than half of older adults reported taking vitamins regularly.¹

While most clinicians consider vitamins to be, at worst, expensive placebos, the potential for harm and dangerous interactions exists. Unlike pharmaceuticals, vitamins are generally unregulated, and the true content of many dietary supplements is often difficult to elucidate. Understanding the physiologic role, foundational evidence, and specific indications for the various vitamins is key to providing the best recommendations to patients.

Vitamins are essential organic nutrients, required in small quantities for normal metabolism. Since they are not synthesized endogenously, they must be ingested via food intake. In the developed world, vitamin deficiency syndromes are rare, thanks to sufficiently balanced diets and availability of fortified foods. The focus of this article will be on vitamin supplementation in healthy patients with well-balanced diets. TABLE W1² (available at mdedge.com/familymedicine) lists the 13 recognized vitamins, their recommended dietary allowances, and any known toxicity risks. TABLE 2² outlines elements of the history to consider when evaluating for deficiency. A summary of the most clinically significant evidence for vitamin supplementation follows; a more comprehensive review can be found in TABLE 3.^3-96

B COMPLEX VITAMINS

Vitamin B1

Vitamers: Thiamine (thiamin)

Physiologic role: Critical in carbohydrate and amino-acid catabolism and energy metabolism

Dietary sources: Whole grains, meat, fish, fortified cereals, and breads

Thiamine serves as an essential cofactor in energy metabolism.² Thiamine deficiency is responsible for beriberi syndrome (rare in the developed world) and Wernicke-Korsakoff syndrome, the latter of which is a relatively common complication of chronic alcohol dependence. Although thiamine’s administration in these conditions can be curative, evidence is lacking to support its use preventively in patients with alcoholism.³ Thiamine has additionally been theorized to play a role in cardiac and cognitive function, but RCT data has not shown consistent patient-oriented benefits.^4,5

The takeaway: Given the lack of evidence, supplementation in the general population is not recommended.

Vitamin B2

Vitamers: Riboflavin

Physiologic role: Essential component of cellular function and growth, energy production, and metabolism of fats and drugs

Dietary sources: Eggs, organ meats, lean meats, milk, green vegetables, fortified cereals and grains

Riboflavin is essential to energy production, cellular growth, and metabolism.²

The takeaway: Its use as migraine prophylaxis has limited data,⁹⁷ but there is otherwise no evidence to support health benefits of riboflavin supplementation.

Vitamin B3

Vitamers: Nicotinic acid (niacin); nicotinamide (niacinamide); nicotinamide riboside

Physiologic role: Converted to nicotinamide adenine dinucleotide (NAD), which is widely required in most cellular metabolic redox processes. Crucial to the synthesis and metabolism of carbohydrates, fatty acids, and proteins

Dietary sources: Poultry, beef, fish, nuts, legumes, grains. (Tryptophan can also be converted to NAD.)

Niacin is readily converted to NAD, an essential coenzyme for multiple catalytic processes in the body. While niacin at doses more than 100 times the recommended dietary allowance (RDA; 1-3 g/d) has been extensively studied for its role in dyslipidemias,² pharmacologic dosing is beyond the scope of this article.

The takeaway: There is no evidence supporting a clinical benefit from niacin supplementation.

Vitamin B5

Vitamers: Pantothenic acid; pantethine

Physiologic role: Required for synthesis of coenzyme A (CoA) and acyl carrier protein, both essential in fatty acid and other anabolic/catabolic processes

Dietary sources: Almost all plant/animal-based foods. Richest sources include beef, chicken, organ meats, whole grains, and some vegetables

Pantothenic acid is essential to multiple metabolic processes and readily available in sufficient amounts in most foods.² Although limited RCT data suggest pantethine may improve lipid measures,^12,98,99 pantothenic acid itself does not seem to share this effect.

The takeaway: There is no data that supplementation of any form of vitamin B5 has any patient-oriented clinical benefits.

Continue to: Vitamin B6

 

 

Vitamin B6

Vitamers: Pyridoxine; pyridoxamine; pyridoxal

Physiologic role: Widely involved coenzyme for cognitive development, neurotransmitter biosynthesis, homocysteine and glucose metabolism, immune function, and hemoglobin formation

Dietary sources: Fish, organ meats, potatoes/starchy vegetables, fruit (other than citrus), and fortified cereals

Pyridoxine is required for numerous enzymatic processes in the body, including biosynthesis of neurotransmitters and homeostasis of the amino acid homocysteine.² While overt deficiency is rare, marginal insufficiency may become clinically apparent and has been associated with malabsorption, malignancies, pregnancy, heart disease, alcoholism, and use of drugs such as isoniazid, hydralazine, and levodopa/carbidopa.² Vitamin B6 supplementation is known to decrease plasma homocysteine levels, a theorized intermediary for cardiovascular disease; however, studies have failed to consistently demonstrate patient-­oriented benefits.^100-102 While observational data has suggested a correlation between vitamin B6 status and cancer risk, RCTs have not supported benefit from supplementation.^14-16 Potential effects of vitamin B6 supplementation on cognitive function have also been studied without observed benefit.^17,18

The takeaway: Vitamin B6 is recommended as a potential treatment option for nausea in pregnancy.¹⁹ Otherwise, vitamin B6 is readily available in food, deficiency is rare, and no patient-oriented evidence supports supplementation in the general population.

Vitamin B7

Vitamers: Biotin

Physiologic role: Cofactor in the metabolism of fatty acids, glucose, and amino acids. Also plays key role in histone modifications, gene regulation, and cell signaling

Dietary sources: Widely available; most prevalent in organ meats, fish, meat, seeds, nuts, and vegetables (eg, sweet potatoes). Whole cooked eggs are a major source, but raw eggs contain avidin, which blocks absorption

Biotin serves a key role in metabolism, gene regulation, and cell signaling.² Biotin is known to interfere with laboratory assays— including cardiac enzymes, thyroid studies, and hormone studies—at normal supplementation doses, resulting in both false-positive and false-negative results.¹⁰³

The takeaway: No evidence supports the health benefits of biotin supplementation.

Vitamin B9

Vitamers: Folates; folic acid

Physiologic role: Functions as a coenzyme in the synthesis of DNA/RNA and metabolism of amino acids

Dietary sources: Highest content in spinach, liver, asparagus, and brussels sprouts. Generally found in green leafy vegetables, fruits, nuts, beans, peas, seafood, eggs, dairy, meat, poultry, grains, and fortified cereals.

Continue to: Vitamin B12

 

 

Vitamin B12

Vitamers: Cyanocobalamin; hydroxocobalamin; methylcobalamin; adenosylcobalamin

Physiologic role: Required for red blood cell formation, neurologic function, and DNA synthesis

Dietary sources: Only in animal products: fish, poultry, meat, eggs, and milk/dairy products. Not present in plant foods. Fortified cereals, nutritional yeast are sources for vegans/vegetarians.

Given their linked physiologic roles, vitamins B9 and B12 are frequently studied together. Folate and cobalamins play key roles in nucleic acid synthesis and amino acid metabolism, with their most clinically significant role in hematopoiesis. Vitamin B12 is also essential to normal neurologic function.²

The US Preventive Services Task Force (USPSTF) recommends preconceptual folate supplementation of 0.4-0.8 mg/d in women of childbearing age to decrease the risk of fetal neural tube defects (grade A).²¹ This is supported by high-quality RCT evidence demonstrating a protective effect of daily folate supplementation in preventing neural tube defects.²² Folate supplementation’s effect on other fetal birth defects has been investigated, but no benefit has been demonstrated. While observational studies have suggested an inverse relationship with folate status and fetal autism spectrum disorder,^23-25 the RCT data is mixed.²⁶

A potential role for folate in cancer prevention has been extensively investigated. An expert panel of the National Toxicology Program (NTP) concluded that folate supplementation does not reduce cancer risk in people with adequate baseline folate status based on high-quality meta-analysis data.^27,104 Conversely, long-term follow-up from RCTs demonstrated an increased risk of colorectal adenomas and cancers,^28,29 leading the NTP panel to conclude there is sufficient concern for adverse effects of folate on cancer growth to justify further research.¹⁰⁴

While observational studies have found a correlation of increased risk for disease with lower antioxidant serum levels, RCTs have not demonstrated a reduction in disease risk with supplementation.

Given folate and vitamin B12’s ­homocysteine-reducing effects, it has been theorized that supplementation may protect from cardiovascular disease. However, despite extensive research, there remains no consistent patient-oriented outcomes data to support such a benefit.^31,32,105

The evidence is mixed but generally has found no benefit of folate or vitamin B12 supplementation on cognitive function.^18,33-35 Finally, RCT data has failed to demonstrate a reduction in fracture risk with supplementation.^36,106

The takeaway: High-quality RCT evidence demonstrates a protective effect of preconceptual daily folate supplementation in preventing neural tube defects.²² The USPSTF recommends preconceptual folate supplementation of 0.4-0.8 mg/d in women of childbearing age to decrease the risk of fetal neural tube defects.

Continue to: ANTIOXIDANTS

 

 

ANTIOXIDANTS

In addition to their individual roles, vitamins A, E, and C are antioxidants, functioning to protect cells from oxidative damage by free radical species.² Due to this shared role, these vitamins are commonly studied together. Antioxidants are hypothesized to protect from various diseases, including cancer, cardiovascular disease, dementia, autoimmune disorders, depression, cataracts, and age-related vision decline.^2,37,107-112

Though observational studies have found a correlation of increased risk for disease with lower antioxidant serum levels, RCTs have not demonstrated a reduction in disease risk with supplementation and, in some cases, have found an increased risk of mortality. While several studies have found potential benefit of antioxidant use in reducing colon and breast cancer risk,^38,113-115 vitamins A and E have been associated with increased risk of lung and prostate cancer, respectively.^47,110 Cardiovascular disease and antioxidant vitamin supplementation has similar inconsistent data, ranging from slight benefit to harm.^2,116 After a large Cochrane review in 2012 found a significant increase in all-cause mortality associated with vitamin E and ­beta-carotene,¹¹⁷ the USPSTF made a specific recommendation against supplementation of these vitamins for the prevention of cardiovascular disease or cancer (grade D).¹¹⁸ Given its limited risk for harm, vitamin C was excluded from this recommendation.

Vitamin A

Vitamers: Retinol; retinal; retinyl esters; provitamin A carotenoids (beta-carotene, alpha-carotene, beta-cryptoxanthin)

Physiologic role: Essential for vision and corneal development. Also involved in general cell differentiation and immune function

Dietary sources: Liver, fish oil, dairy, and fortified cereals. Provitamin A sources: leafy green vegetables, orange/yellow vegetables, tomato products, fruits, and vegetable oils

Retinoids and their precursors, carotenoids, serve a critical function in vision, as well as regulating cell differentiation and proliferation throughout the body.² While evidence suggests mortality benefit of supplementation in populations at risk of deficiency,⁴⁵ wide-ranging studies have found either inconsistent benefit or outright harms in the developed world.

The takeaway: Given the USPSTF grade “D” recommendation and concern for potential harms, supplementation is not recommended in healthy patients without risk factors for deficiency.²

Vitamin E

Vitamers: Tocopherols (alpha-, beta-, ­gamma-, delta-); tocotrienol (alpha-, beta-, gamma-, delta-)

Physiologic role: Antioxidant; protects polyunsaturated fats from free radical oxidative damage. Involved in immune function, cell signaling, and regulation of gene expression

Dietary sources: Nuts, seeds, vegetable oil, green leafy vegetables, and fortified cereals

Vitamin E is the collective name of 8 compounds; alpha-tocopherol is the physiologically active form. Vitamin E is involved with cell proliferation as well as endothelial and platelet function.²

The takeaway: Vitamin E supplementation’s effects on cancer, cardiovascular disease, ophthalmologic disorders, and cognition have been investigated; data is either lacking to support a benefit or demonstrates harms as outlined above. Given this and the USPSTF grade “D” recommendation, supplementation is not recommended in healthy patients.²

Vitamin C

Vitamers: Ascorbic acid

Physiologic role: Required for synthesis of collagen, L-carnitine, and some neurotransmitters. Also involved in protein metabolism

Dietary sources: Primarily in fruits and vegetables: citrus, tomato, potatoes, red/green peppers, kiwi fruit, broccoli, strawberries, brussels sprouts, cantaloupe, and fortified cereals

Vitamin C supplementation at the onset of illness does not seem to have benefit.

Ascorbic acid is a required cofactor for biosynthesis of collagen, neurotransmitters, and protein metabolism.² In addition to the shared hypothesized benefits of antioxidants, vitamin C supplementation has undergone extensive research into its potential role in augmenting the immune system and preventing the common cold. Systematic reviews have found daily vitamin C supplementation of at least 200 mg did not affect the incidence of the common cold in healthy adults but may shorten duration and could be of benefit in those exposed to extreme physical exercise or cold.⁴⁸ Vitamin C supplementation at the onset of illness does not seem to have benefit.⁴⁸ Data is insufficient to draw conclusions about a potential effect on pneumonia incidence or severity.^119,120

The takeaway: Overall, data remain inconclusive as to potential benefits of vitamin C supplementation, although risks of potential harms are likely low.

Continue to: Vitamin D

 

 

Vitamin D

Vitamers: Cholecalciferol (D3); ergocalciferol (D2)

Physiologic role: Hydroxylation in liver and kidney required to activate. Promotes dietary calcium absorption, enables normal bone mineralization. Also involved in modulation of cell growth, and neuromuscular and immune function

Dietary sources: Few natural dietary sources, which include fatty fish, fish liver oils; small amount in beef liver, cheese, egg yolks. Primary sources include fortified milk and endogenous synthesis in skin with UV exposure

Calciferol is a fat-soluble vitamin required for calcium and bone homeostasis. It is not naturally available in many foods but is primarily produced endogenously in the skin with ultraviolet light exposure.²

The AAP recommends supplementing exclusively breastfed infants with 400 IU/d of vitamin D to prevent rickets.

Bone density and fracture risk reduction are the most often cited benefits of vitamin D supplementation, but this has not been demonstrated consistently in RCTs. Multiple systematic reviews showing inconsistent benefit of vitamin D (with or without calcium) on fracture risk led the USPSTF to conclude that there is insufficient evidence (grade I) to issue a recommendation on vitamin D and calcium supplementation for primary prevention of fractures in postmenopausal women.^49-51 Despite some initial evidence suggesting a benefit of vitamin D supplementation on falls reduction, 3 recent systematic reviews did not demonstrate this in community-dwelling elders,^54-56 although a separate Cochrane review did suggest a reduction in rate of falls among institutionalized elders.⁵⁷

The takeaway: Given these findings, the USPSTF has recommended against (grade D) vitamin D supplementation to prevent falls in community-dwelling elders.⁵⁵

Beyond falls. While the vitamin D receptor is expressed throughout the body and observational studies have suggested a correlation between vitamin D status and many outcomes, extensive RCT data has generally failed to demonstrate extraskeletal benefits from supplementation. Meta-analysis data have demonstrated potential reductions in acute respiratory infection rates and asthma exacerbations with vitamin D supplementation. There is also limited evidence suggesting a reduction in preeclampsia and low-birthweight infant risk with vitamin D supplementation in pregnancy. However, several large meta-analyses and systematic reviews have investigated vitamin D supplementation’s effect on all-cause mortality and found no consistent data to support an association.^41,58-62

Multiple systematic reviews have investigated and found high-quality evidence demonstrating no association between vitamin D supplementation and cancer^41,63-66,121 or cardiovascular disease risk.^41,70,71 There is high-quality data showing no benefit of vitamin D supplementation for multiple additional diseases, including diabetes, cognitive decline, depression, pain, obesity, and liver disease.^{43,72-75,85-90,122}

The takeaway: Due to poor availability in breastmilk, the American Academy of Pediatrics (AAP) recommends supplementing exclusively breastfed infants with 400 IU/d of vitamin D to prevent rickets.¹²³ RCT data support high-dose supplementation of lactating women (6400 IU/d) as an alternative strategy to supplementation of the infant.¹²⁴ The AAP recommends that all nonbreastfeeding infants and older children ingesting < 1000 mL/d of vitamin D–fortified formula or milk should also be supplemented with 400 IU/d of vitamin D.¹²³ Despite these universal recommendations for supplementation, evidence is mixed on the effect of vitamin D supplementation on bone health in children.^52,53

Although concerns about vitamin D supplementation and increased risk of urolithiasis and hypercalcemia have been raised,^51,62,121 systematic reviews have not demonstrated significant, clinically relevant risks, even with high-dose supplementation (> 2800 IU/d).^125,126

Vitamin K

Vitamers: Phylloquinone (K1); menaquinones (K2)

Physiologic role: Coenzyme for synthesis of proteins involved in hemostasis and bone metabolism

Dietary sources: Phylloquinone is found in green leafy vegetables, vegetable oils, some fruits, meat, dairy, and eggs. Menaquinone is produced by gut bacteria and present in fermented foods

Vitamin K includes 2 groups of similar compounds: phylloquinone and menaquinones. Unlike other fat-soluble vitamins, vitamin K is rapidly metabolized and has low tissue storage.²

Children taking multivitamins were often found to have excess levels of potentially harmful nutrients, such as retinol, zinc, and folic acid.

Administration of vitamin K 0.5 to 1 mg intramuscularly (IM) to newborns is standard of care for the prevention of vitamin K deficiency bleeding (VKDB). This is supported by RCT data demonstrating a reduction in classic VKDB (occurring within 7 days)⁹¹ and epidemiologic data from various countries showing a reduction in late-onset VKDB with vitamin K prophylaxis programs.¹²⁷ Oral dosing appears to reduce the risk of VKDB in the setting of parental refusal but is less effective than IM dosing.^128,129

Vitamin K’s effects on bone density and fracture risk have also been investigated. Systematic reviews have demonstrated a reduction in fracture risk with vitamin K supplementation,^92,93 and European and Asian regulatory bodies have recognized a potential benefit on bone health.² The FDA considers the evidence insufficient at this time to support such a claim.² Higher dietary vitamin K consumption has been associated with lower risk of cardiovascular disease in observational studies⁹⁴ and supplementation was associated with improved disease measures,¹³⁰ but no patient-oriented outcomes have been demonstrated.¹³¹

The takeaway: The administration of vitamin K 0.5 to 1 mg intramuscularly (IM) to newborns is standard of care for the prevention of VKDB. Vitamin K may lead to a reduction in fracture risk, but the FDA considers the evidence insufficient. Vitamin K’s potential link to a lowered risk of cardiovascular disease has not been demonstrated with patient-­oriented outcomes. Vitamin K has low potential for toxicity, although its interaction with vitamin K antagonists (ie, warfarin) is clinically relevant.

Continue to: MULTIVITAMINS

 

 

MULTIVITAMINS

Multivitamins are often defined as a supplement containing 3 or more vitamins and minerals but without herbs, hormones, or drugs.¹³² Many multivitamins do contain additional substances, and some include levels of vitamins that exceed the RDA or even the established tolerable upper intake level.¹³³

Safe medication storage should be practiced, as multivitamins with iron are a leading cause of poisoning in children.

A 2013 systematic review found limited evidence to support any benefit from multivitamin supplementation.⁴¹ Two included RCTs demonstrated a narrowly significant decrease in cancer rates among men, but saw no effect in women or the combined population.^134,135 This benefit appears to disappear at 5 years of follow-up.¹³⁶ RCT data have shown no benefit of multivitamin use on cognitive function,⁹⁵ and high-quality data suggest there is no effect on all-cause mortality.¹³⁷ Given this lack of supporting evidence, the USPSTF has concluded that there is insufficient evidence (grade I) to recommend vitamin supplementation in general to prevent cardiovascular disease or cancer.⁴¹

The use of prenatal multivitamins is generally recommended in the pregnancy and preconception period and has been associated with reduced risk of autism spectrum disorders, pediatric cancer rates, small-for-gestational-age infants, and multiple birth defects in offspring; however, studies have not examined if this benefit exceeds that of folate supplementation alone.^138-140 AAP does not recommend multivitamins for children with a well-balanced diet.¹⁴¹ Of concern, children taking multivitamins were often found to have excess levels of potentially harmful nutrients such as retinol, zinc, and folic acid.¹⁴²

The takeaway: There is limited evidence to support any benefit from multivitamin supplementation. Prenatal multivitamins are generally recommended in the pregnancy and preconception period. Overall, the risks of multivitamins are minimal, although that risk is dependent on the multivitamin’s constituent components.¹⁴³ Components such as vitamin K may interact with a patient’s medications, and multivitamins have been shown to reduce the circulating levels of antiretrovirals.¹⁴⁴ Specifically, multivitamins with iron should be avoided in men and postmenopausal women, and safe medication storage should be practiced as multivitamins with iron are a leading cause of poisoning in children.²

SUMMARY

Vitamin supplementation in the developed world remains common despite a paucity of RCT data supporting it. Supplementation of folate in women planning to conceive, vitamin D in breastfeeding infants, and vitamin K in newborns are well supported by clinical evidence. Otherwise, there is limited evidence supporting clinically significant benefit from supplementation in healthy patients with well-balanced diets—and in the case of vitamins A and E, there may be outright harms.

CORRESPONDENCE
Joel Herness, MD, 4700 North Las Vegas Boulevard, Nellis AFB, NV 89191; [email protected]

The architecture of the glenohumeral joint makes it the most common large joint to become dislocated, accounting for approximately 45% of all dislocations. Anterior dislocation constitutes more than 95% of glenohumeral joint dislocations; posterior dislocation, only 2% to 5%.^1,2

For the family physician, determining appropriate follow-up after emergent reduction depends on several distinct variables, which we review here; subsequent treatment might involve, as we outline, physical therapy, immobilization, surgical intervention, or a combination of several modalities. Treatment decisions can make the difference between successful rehabilitation and potential disability, particularly in typically young and active patients.

Numerous mechanisms of injury

Anterior shoulder dislocations typically occur with the affected shoulder in a position of abduction and external rotation; 90% of patients are 21 to 30 years of age, and men are affected 3 times more often than women.² Unsurprisingly, athletes are affected most frequently, with the common sports-related mechanism of injury being either sudden pressure exerted on the abducted and externally rotated arm or a fall onto an outstretched hand with the arm elevated. Repetitive microtrauma from such sports as swimming, baseball, and volleyball can also lead to instability.

Bankart lesion. This tear of the anterior or inferior section of the labrum is the most characteristic lesion noted in anterior dislocations, found in 73% of first-time dislocations and 100% of recurrent dislocations.^3,4

Hills-Sachs lesion is often associated with a Bankart lesion. The Hills-Sachs lesion is an impaction fracture of the posterolateral aspect of the humeral head resulting from its displacement over the anterior lip of the glenoid. Hill-Sachs lesions are seen in 71% of first-time and recurrent dislocations.³

Less common concomitant injuries during anterior shoulder dislocation include rupture of the rotator-cuff tendons (particularly in patients older than 40 years), glenoid and proximal humerus fractures, a tear of the superior labrum (known as a “SLAP lesion”), cartilage injury, and neurovascular injury.

Posterior instability typically occurs as a result of a strong muscle contraction, as seen in electrocution or seizure; however, it can be caused by athletic trauma, particularly in football.⁵ Repetitive forces exerted on the forward-flexed and internally rotated shoulder position during blocking puts football players at increased risk of posterior instability.⁵

Continue to: Multidirectional instability

 

Multidirectional instability is more frequently attributable to congenital hyperlaxity of the glenohumeral joint capsule, rather than to acute injury. However, athletes can also develop capsular laxity from repetitive microtrauma to the shoulder.⁵

Emergent reduction: Prompt action needed

Acute dislocation of the shoulder should be reduced as soon as possible to minimize neurovascular injury and patient discomfort. (Typically, but not always, this is done in the emergency department.) It is crucial to have effective muscle relaxation before any attempt at reduction, to minimize the risk of iatrogenic injury to bone, cartilage, tendons, and neurovascular structures.

Muscle relaxation can be facilitated with intravenous midazolam or other agents, as specified by institutional protocol. Intra-articular lidocaine injection or intravenous fentanyl is often utilized in conjunction with the sedating agent to reduce pain and further accommodate relaxation.

Anterior reduction. Any one of several techniques can be used to perform emergent reduction of anterior shoulder dislocations, all of which have demonstrated success. The Milch technique is among the least traumatic for effective reduction.⁶ In this technique (FIGURE 1), the patient is supine; gentle but firm downward traction is applied to the humerus at the elbow of the affected arm while the arm is in abduction and external rotation. The provider can manipulate the humeral head at that point by placing a thumb in the patient’s axilla; the arm can also be further internally rotated and adducted until reduction is achieved.

Posterior reduction of a dislocation is performed while the patient is supine, with the body stabilized. Traction is applied on the adducted and internally rotated arm in conjunction with direct pressure on the posterior aspect of the humeral head (FIGURE 2).

Continue to: Follow-up actions

 

Follow-up actions. Before discharging the patient after reduction of a dislocation, it is essential to:

• perform post-reduction evaluation of shoulder stability at different levels of abduction
• perform a thorough neurovascular assessment
• obtain an anteroposterior (AP) radiograph to ensure proper positioning of the glenohumeral joint.

The reduced shoulder should be immobilized in a sling. The discharge plan should include pain management for several days and a follow-up appointment in 5 to 8 days with the primary care provider² (FIGURE 3).

Follow-up evaluation by the primary care provider

History. Prior to the initial examination at follow-up, obtain a comprehensive history that includes the nature of the injury and the direction of force that was placed on the shoulder. Determine whether the shoulder was reduced spontaneously or required manual reduction in the field or an emergency department. Note any associated injury sustained concurrently and the presence (or absence) of neck pain, numbness, tingling, or weakness in the affected arm.

Physical exam starts with thorough inspection of the affected shoulder, with comparison to the contralateral side, at rest and during shoulder motion. Palpation to reveal points of tenderness should include the anterior joint line, acromioclavicular joint, bicipital groove, subacromial space, acromion, and greater tuberosity.

Acute dislocation of the shoulder should be reduced as soon as possible to minimize neurovascular injury and patient discomfort.

Following inspection and palpation, assess active and passive range of motion in forward elevation, abduction, internal and external rotation at the side of the body, and internal and external rotation in shoulder abduction. Assessment might be limited by pain and apprehension, and should be performed within the patient’s comfortable range of motion.

Continue to: Once range of motion...

 

Once range of motion is determined, assess⁷:

• muscle power of the rotator cuff in abduction (for the supraspinatus muscle)
• resisted external rotation at the side of the body (the infraspinatus)
• resisted external rotation in abduction > 60° (the teres minor)
• resisted internal rotation (the subscapularis).

Specific tests for shoulder laxity and stability

It is important during the primary care follow-up examination to differentiate true instability and shoulder hyperlaxity, particularly in young, flexible patients (TABLE). Many of these patients present with painless hypermobility of the shoulder without true injury to the labrum or ligamentous structures. It might appear to the patient, or to family, that the shoulder is subluxating; however, the humeral head returns to a centered position on the glenoid in a hypermobile state—typically, without pain. Actual shoulder instability is defined as loss of the ability of the humeral head to re-center, accompanied by pain—pathology that is frequently associated with damage to the capsulolabral complex.

The load and shift test is used to assess anterior and posterior laxity. The patient is seated, and the forearm is allowed to rest on the thigh. Examination is performed using 1 hand to press anteriorly or posteriorly on the humeral head; the other hand is simultaneously positioned on the joint line to feel movement of the humeral head in relation to the glenoid (FIGURE 4).

The apprehension test is a common maneuver used to assess anterior shoulder instability. It is performed by positioning the affected arm to 90° external rotation and then elevating it to 90° abduction. Although this maneuver can be performed with the patient upright, it is beneficial to have them supine, to more easily control the arm (FIGURE 5). A positive test is noted when the patient reports a sensation of impending instability (apprehension), rather than pain alone.

Relocation test. When the apprehension test is positive, the supine position can be exploited to further perform the relocation test, in 2 stages (FIGURE 6):

• Apply a posteriorly directed force on the humeral head, which stabilizes the shoulder and typically alleviates symptoms.
• Release pressure quickly from the humeral head to assess recurrence of pain and apprehension as the humeral head snaps back against the anterior labrum.

Continue to: Combined, apprehension and relocation...

 

Combined, apprehension and relocation tests to identify anterior shoulder instability have been shown to significantly improve specificity while maintaining sensitivity.⁸

The posterior apprehension test is used to assess posterior instability. The patient is supine; the affected arm is placed in flexion, adduction, and internal rotation; and posterior pressure is applied (FIGURE 7). A positive test is noted when pain is reported at the posterior aspect of the shoulder. Clicking might be noted as the humeral head dislocates rearward.¹

Sulcus sign. Multidirectional instability is elicited using the sulcus sign. While the patient is seated upright, arms resting at their sides, a direct downward pull at elbow level will, when positive, reveal a depression (sulcus) at the lateral aspect of the affected shoulder as the humeral head translates inferiorly (FIGURE 8). A positive sulcus sign is documented in 3 grades, according to the amount of translation¹:

• Grade I: < 1 cm
• Grade II: 1-2 cm
• Grade III: > 2 cm.

Neurovascular status should be verified at every physical evaluation, with motor and sensory function tested in the axillary, musculocutaneous, median, radial, and ulnar nerve distributions. If nerve injury is suspected, electromyography and nerve-conduction testing is indicated.^9-13 Vascular compromise is much less common but equally important to assess.¹¹

Use of imaging

Post-reduction radiographs, including internal and external AP—and especially axillary—views are invaluable. Not only do they help to ensure reduction, but they also help to assess for fracture. A magnetic resonance imaging (MRI) arthrogram is the preferred imaging modality if a labral tear is suspected (FIGURE 9). Other concomitant shoulder injuries, such as subtle bone fracture, rotator cuff tear, and biceps pathology can also be reliably diagnosed with noncontrast MRI.

Continue to: Roadmap for treatment

 

 

Roadmap for treatment

The rate of recurrence after a first anterior shoulder dislocation is strongly associated with a person’s age and level of activity. Active patients younger than 20 years have a 92% to 96% recurrence rate¹⁴; patients 20 to 40 years, 25% to 48%; and patients older than 40 years, < 10%.¹⁵

Young, athletic patients who are treated nonoperatively are left at an unacceptably high risk of recurrence, leading to progressive damage to bony and soft-tissue structures.^16,17 Surgical labral repair after a first-time anterior dislocation produced improved outcomes in terms of recurrent dislocation (7.9%), compared to outcomes after nonsurgical treatment (52.9%),¹⁴ and has been associated with a lower incidence of future glenohumeral osteoarthritis.¹⁸ For those reasons, we recommend referral to an orthopedic surgeon for all patients younger than 20 years who sustain an anterior shoulder dislocation.

Patients older than 20 years who do not have concomitant shoulder injury, and who demonstrate full strength in abduction, external rotation, and internal rotation of the shoulder on clinical examination, have a low probability of associated rotator-cuff tear. They can be immobilized in a sling for 1 to 3 weeks, followed by a 6 to 12–week regimen of physical therapy.

Concomitant tear of the rotator cuff. Weakness on examination requires MRI or a magnetic resonance arthrogram for evaluation of associated rotator-cuff tear. A tear identified on MRI should be referred to an orthopedic surgeon because timely repair can be crucial to attaining best outcomes. Conservative treatment of traumatic full-­tendon rotator-cuff tear is associated with poor results, progression in the size of the tear, and advancement of muscle atrophy.^19,20 For patients younger than 40 years, arthroscopic rotator-cuff repair, with or without labral repair, produces excellent clinical outcomes, carries a low risk of complications, and results in a > 95% rate of return to a preoperative level of recreational and job activities.²¹

Patients who demonstrate weakness of the rotator-cuff muscles on examination, but who do not have a tear noted on MRI, should be evaluated by electromyography and nerve-conduction testing to assess nerve injury as an alternative cause of weakness.^10,11 If a neurologic deficit is found on nerve-conduction testing, the patient should be referred for neurologic evaluation.¹⁰

Continue to: Patients with negative findings...

 

Patients with negative findings on MRI and nerve-conduction studies should be offered physical therapy. Patients with recurrent anterior shoulder dislocation should be referred to an orthopedic surgeon for surgical repair. Frequently, improper or delayed treatment with chronic instability results in degenerative arthropathy of the joint²² (FIGURE 10).

Posterior and multidirectional instability can typically be treated conservatively; however, whereas posterior dislocation typically must be immobilized for 3 to 6 weeks post reduction, multidirectional instability does not require immobilization. Instead, physical therapy should start as soon as possible. In these cases, recurrent dislocation or subluxation that persists after conservative treatment should be referred for possible surgical intervention.⁵

Instability with associated fracture

Fracture concomitant with dislocation most commonly involves the humeral neck, humeral head, greater tuberosity, or the glenoid itself.² Clinical variables that predict a fracture associated with shoulder dislocation include²³:

• first episode of dislocation
• age ≥ 40 years
• fall from higher than 1 flight of stairs
• fight or assault
• motor vehicle crash.

A computed tomography scan with 3-dimensional reconstruction can help characterize associated fracture accurately—including location, size, and displacement—and can play an important role in treatment planning and prognosis in these complicated injuries. Displaced fracture should be referred to an orthopedic surgeon. Nondisplaced fracture of the humeral head or greater tuberosity (FIGURE 11) poses less risk of complications and can be treated conservatively with 6 weeks in an arm sling, followed by physical therapy.²⁴

Summing up

Management of shoulder dislocation must, first, be tailored to the individual and, second, account for several interactive factors—including age, direction of instability, functional demands, risk of recurrence, and associated injuries. In many patients, conservative treatment produces a favorable long-term outcome. Particularly in young, active patients with anterior shoulder instability, most surgeons consider open or arthroscopic reconstruction to be the treatment of choice.^2,18

Continue to: Pre-reduction and post-reduction...

 

Pre-reduction and post-reduction imaging should be carefully examined for the presence of concomitant injury, which might change the preferred treatment modality appreciably.

Last, communication among emergency department providers, the primary care provider, orthopedist, radiologist, and neurologist is crucial for determining an appropriate patient-centered approach to initial and long-term management.

CORRESPONDENCE
Nata Parnes, MD, Carthage Area Hospital, 3 Bridge Street, Carthage, NY; [email protected]

The architecture of the glenohumeral joint makes it the most common large joint to become dislocated, accounting for approximately 45% of all dislocations. Anterior dislocation constitutes more than 95% of glenohumeral joint dislocations; posterior dislocation, only 2% to 5%.^1,2

For the family physician, determining appropriate follow-up after emergent reduction depends on several distinct variables, which we review here; subsequent treatment might involve, as we outline, physical therapy, immobilization, surgical intervention, or a combination of several modalities. Treatment decisions can make the difference between successful rehabilitation and potential disability, particularly in typically young and active patients.

Numerous mechanisms of injury

Anterior shoulder dislocations typically occur with the affected shoulder in a position of abduction and external rotation; 90% of patients are 21 to 30 years of age, and men are affected 3 times more often than women.² Unsurprisingly, athletes are affected most frequently, with the common sports-related mechanism of injury being either sudden pressure exerted on the abducted and externally rotated arm or a fall onto an outstretched hand with the arm elevated. Repetitive microtrauma from such sports as swimming, baseball, and volleyball can also lead to instability.

Bankart lesion. This tear of the anterior or inferior section of the labrum is the most characteristic lesion noted in anterior dislocations, found in 73% of first-time dislocations and 100% of recurrent dislocations.^3,4

Hills-Sachs lesion is often associated with a Bankart lesion. The Hills-Sachs lesion is an impaction fracture of the posterolateral aspect of the humeral head resulting from its displacement over the anterior lip of the glenoid. Hill-Sachs lesions are seen in 71% of first-time and recurrent dislocations.³

Less common concomitant injuries during anterior shoulder dislocation include rupture of the rotator-cuff tendons (particularly in patients older than 40 years), glenoid and proximal humerus fractures, a tear of the superior labrum (known as a “SLAP lesion”), cartilage injury, and neurovascular injury.

Posterior instability typically occurs as a result of a strong muscle contraction, as seen in electrocution or seizure; however, it can be caused by athletic trauma, particularly in football.⁵ Repetitive forces exerted on the forward-flexed and internally rotated shoulder position during blocking puts football players at increased risk of posterior instability.⁵

Continue to: Multidirectional instability

 

Multidirectional instability is more frequently attributable to congenital hyperlaxity of the glenohumeral joint capsule, rather than to acute injury. However, athletes can also develop capsular laxity from repetitive microtrauma to the shoulder.⁵

Emergent reduction: Prompt action needed

Acute dislocation of the shoulder should be reduced as soon as possible to minimize neurovascular injury and patient discomfort. (Typically, but not always, this is done in the emergency department.) It is crucial to have effective muscle relaxation before any attempt at reduction, to minimize the risk of iatrogenic injury to bone, cartilage, tendons, and neurovascular structures.

Muscle relaxation can be facilitated with intravenous midazolam or other agents, as specified by institutional protocol. Intra-articular lidocaine injection or intravenous fentanyl is often utilized in conjunction with the sedating agent to reduce pain and further accommodate relaxation.

Anterior reduction. Any one of several techniques can be used to perform emergent reduction of anterior shoulder dislocations, all of which have demonstrated success. The Milch technique is among the least traumatic for effective reduction.⁶ In this technique (FIGURE 1), the patient is supine; gentle but firm downward traction is applied to the humerus at the elbow of the affected arm while the arm is in abduction and external rotation. The provider can manipulate the humeral head at that point by placing a thumb in the patient’s axilla; the arm can also be further internally rotated and adducted until reduction is achieved.

Posterior reduction of a dislocation is performed while the patient is supine, with the body stabilized. Traction is applied on the adducted and internally rotated arm in conjunction with direct pressure on the posterior aspect of the humeral head (FIGURE 2).

Continue to: Follow-up actions

 

Follow-up actions. Before discharging the patient after reduction of a dislocation, it is essential to:

• perform post-reduction evaluation of shoulder stability at different levels of abduction
• perform a thorough neurovascular assessment
• obtain an anteroposterior (AP) radiograph to ensure proper positioning of the glenohumeral joint.

The reduced shoulder should be immobilized in a sling. The discharge plan should include pain management for several days and a follow-up appointment in 5 to 8 days with the primary care provider² (FIGURE 3).

Follow-up evaluation by the primary care provider

History. Prior to the initial examination at follow-up, obtain a comprehensive history that includes the nature of the injury and the direction of force that was placed on the shoulder. Determine whether the shoulder was reduced spontaneously or required manual reduction in the field or an emergency department. Note any associated injury sustained concurrently and the presence (or absence) of neck pain, numbness, tingling, or weakness in the affected arm.

Physical exam starts with thorough inspection of the affected shoulder, with comparison to the contralateral side, at rest and during shoulder motion. Palpation to reveal points of tenderness should include the anterior joint line, acromioclavicular joint, bicipital groove, subacromial space, acromion, and greater tuberosity.

Acute dislocation of the shoulder should be reduced as soon as possible to minimize neurovascular injury and patient discomfort.

Following inspection and palpation, assess active and passive range of motion in forward elevation, abduction, internal and external rotation at the side of the body, and internal and external rotation in shoulder abduction. Assessment might be limited by pain and apprehension, and should be performed within the patient’s comfortable range of motion.

Continue to: Once range of motion...

 

Once range of motion is determined, assess⁷:

• muscle power of the rotator cuff in abduction (for the supraspinatus muscle)
• resisted external rotation at the side of the body (the infraspinatus)
• resisted external rotation in abduction > 60° (the teres minor)
• resisted internal rotation (the subscapularis).

Specific tests for shoulder laxity and stability

It is important during the primary care follow-up examination to differentiate true instability and shoulder hyperlaxity, particularly in young, flexible patients (TABLE). Many of these patients present with painless hypermobility of the shoulder without true injury to the labrum or ligamentous structures. It might appear to the patient, or to family, that the shoulder is subluxating; however, the humeral head returns to a centered position on the glenoid in a hypermobile state—typically, without pain. Actual shoulder instability is defined as loss of the ability of the humeral head to re-center, accompanied by pain—pathology that is frequently associated with damage to the capsulolabral complex.

The load and shift test is used to assess anterior and posterior laxity. The patient is seated, and the forearm is allowed to rest on the thigh. Examination is performed using 1 hand to press anteriorly or posteriorly on the humeral head; the other hand is simultaneously positioned on the joint line to feel movement of the humeral head in relation to the glenoid (FIGURE 4).

The apprehension test is a common maneuver used to assess anterior shoulder instability. It is performed by positioning the affected arm to 90° external rotation and then elevating it to 90° abduction. Although this maneuver can be performed with the patient upright, it is beneficial to have them supine, to more easily control the arm (FIGURE 5). A positive test is noted when the patient reports a sensation of impending instability (apprehension), rather than pain alone.

Relocation test. When the apprehension test is positive, the supine position can be exploited to further perform the relocation test, in 2 stages (FIGURE 6):

• Apply a posteriorly directed force on the humeral head, which stabilizes the shoulder and typically alleviates symptoms.
• Release pressure quickly from the humeral head to assess recurrence of pain and apprehension as the humeral head snaps back against the anterior labrum.

Continue to: Combined, apprehension and relocation...

 

Combined, apprehension and relocation tests to identify anterior shoulder instability have been shown to significantly improve specificity while maintaining sensitivity.⁸

The posterior apprehension test is used to assess posterior instability. The patient is supine; the affected arm is placed in flexion, adduction, and internal rotation; and posterior pressure is applied (FIGURE 7). A positive test is noted when pain is reported at the posterior aspect of the shoulder. Clicking might be noted as the humeral head dislocates rearward.¹

Sulcus sign. Multidirectional instability is elicited using the sulcus sign. While the patient is seated upright, arms resting at their sides, a direct downward pull at elbow level will, when positive, reveal a depression (sulcus) at the lateral aspect of the affected shoulder as the humeral head translates inferiorly (FIGURE 8). A positive sulcus sign is documented in 3 grades, according to the amount of translation¹:

• Grade I: < 1 cm
• Grade II: 1-2 cm
• Grade III: > 2 cm.

Neurovascular status should be verified at every physical evaluation, with motor and sensory function tested in the axillary, musculocutaneous, median, radial, and ulnar nerve distributions. If nerve injury is suspected, electromyography and nerve-conduction testing is indicated.^9-13 Vascular compromise is much less common but equally important to assess.¹¹

Use of imaging

Post-reduction radiographs, including internal and external AP—and especially axillary—views are invaluable. Not only do they help to ensure reduction, but they also help to assess for fracture. A magnetic resonance imaging (MRI) arthrogram is the preferred imaging modality if a labral tear is suspected (FIGURE 9). Other concomitant shoulder injuries, such as subtle bone fracture, rotator cuff tear, and biceps pathology can also be reliably diagnosed with noncontrast MRI.

Continue to: Roadmap for treatment

 

 

Roadmap for treatment

The rate of recurrence after a first anterior shoulder dislocation is strongly associated with a person’s age and level of activity. Active patients younger than 20 years have a 92% to 96% recurrence rate¹⁴; patients 20 to 40 years, 25% to 48%; and patients older than 40 years, < 10%.¹⁵

Young, athletic patients who are treated nonoperatively are left at an unacceptably high risk of recurrence, leading to progressive damage to bony and soft-tissue structures.^16,17 Surgical labral repair after a first-time anterior dislocation produced improved outcomes in terms of recurrent dislocation (7.9%), compared to outcomes after nonsurgical treatment (52.9%),¹⁴ and has been associated with a lower incidence of future glenohumeral osteoarthritis.¹⁸ For those reasons, we recommend referral to an orthopedic surgeon for all patients younger than 20 years who sustain an anterior shoulder dislocation.

Patients older than 20 years who do not have concomitant shoulder injury, and who demonstrate full strength in abduction, external rotation, and internal rotation of the shoulder on clinical examination, have a low probability of associated rotator-cuff tear. They can be immobilized in a sling for 1 to 3 weeks, followed by a 6 to 12–week regimen of physical therapy.

Concomitant tear of the rotator cuff. Weakness on examination requires MRI or a magnetic resonance arthrogram for evaluation of associated rotator-cuff tear. A tear identified on MRI should be referred to an orthopedic surgeon because timely repair can be crucial to attaining best outcomes. Conservative treatment of traumatic full-­tendon rotator-cuff tear is associated with poor results, progression in the size of the tear, and advancement of muscle atrophy.^19,20 For patients younger than 40 years, arthroscopic rotator-cuff repair, with or without labral repair, produces excellent clinical outcomes, carries a low risk of complications, and results in a > 95% rate of return to a preoperative level of recreational and job activities.²¹

Patients who demonstrate weakness of the rotator-cuff muscles on examination, but who do not have a tear noted on MRI, should be evaluated by electromyography and nerve-conduction testing to assess nerve injury as an alternative cause of weakness.^10,11 If a neurologic deficit is found on nerve-conduction testing, the patient should be referred for neurologic evaluation.¹⁰

Continue to: Patients with negative findings...

 

Patients with negative findings on MRI and nerve-conduction studies should be offered physical therapy. Patients with recurrent anterior shoulder dislocation should be referred to an orthopedic surgeon for surgical repair. Frequently, improper or delayed treatment with chronic instability results in degenerative arthropathy of the joint²² (FIGURE 10).

Posterior and multidirectional instability can typically be treated conservatively; however, whereas posterior dislocation typically must be immobilized for 3 to 6 weeks post reduction, multidirectional instability does not require immobilization. Instead, physical therapy should start as soon as possible. In these cases, recurrent dislocation or subluxation that persists after conservative treatment should be referred for possible surgical intervention.⁵

Instability with associated fracture

Fracture concomitant with dislocation most commonly involves the humeral neck, humeral head, greater tuberosity, or the glenoid itself.² Clinical variables that predict a fracture associated with shoulder dislocation include²³:

• first episode of dislocation
• age ≥ 40 years
• fall from higher than 1 flight of stairs
• fight or assault
• motor vehicle crash.

A computed tomography scan with 3-dimensional reconstruction can help characterize associated fracture accurately—including location, size, and displacement—and can play an important role in treatment planning and prognosis in these complicated injuries. Displaced fracture should be referred to an orthopedic surgeon. Nondisplaced fracture of the humeral head or greater tuberosity (FIGURE 11) poses less risk of complications and can be treated conservatively with 6 weeks in an arm sling, followed by physical therapy.²⁴

Summing up

Management of shoulder dislocation must, first, be tailored to the individual and, second, account for several interactive factors—including age, direction of instability, functional demands, risk of recurrence, and associated injuries. In many patients, conservative treatment produces a favorable long-term outcome. Particularly in young, active patients with anterior shoulder instability, most surgeons consider open or arthroscopic reconstruction to be the treatment of choice.^2,18

Continue to: Pre-reduction and post-reduction...

 

Pre-reduction and post-reduction imaging should be carefully examined for the presence of concomitant injury, which might change the preferred treatment modality appreciably.

Last, communication among emergency department providers, the primary care provider, orthopedist, radiologist, and neurologist is crucial for determining an appropriate patient-centered approach to initial and long-term management.

CORRESPONDENCE
Nata Parnes, MD, Carthage Area Hospital, 3 Bridge Street, Carthage, NY; [email protected]

The architecture of the glenohumeral joint makes it the most common large joint to become dislocated, accounting for approximately 45% of all dislocations. Anterior dislocation constitutes more than 95% of glenohumeral joint dislocations; posterior dislocation, only 2% to 5%.^1,2

For the family physician, determining appropriate follow-up after emergent reduction depends on several distinct variables, which we review here; subsequent treatment might involve, as we outline, physical therapy, immobilization, surgical intervention, or a combination of several modalities. Treatment decisions can make the difference between successful rehabilitation and potential disability, particularly in typically young and active patients.

Numerous mechanisms of injury

Anterior shoulder dislocations typically occur with the affected shoulder in a position of abduction and external rotation; 90% of patients are 21 to 30 years of age, and men are affected 3 times more often than women.² Unsurprisingly, athletes are affected most frequently, with the common sports-related mechanism of injury being either sudden pressure exerted on the abducted and externally rotated arm or a fall onto an outstretched hand with the arm elevated. Repetitive microtrauma from such sports as swimming, baseball, and volleyball can also lead to instability.

Bankart lesion. This tear of the anterior or inferior section of the labrum is the most characteristic lesion noted in anterior dislocations, found in 73% of first-time dislocations and 100% of recurrent dislocations.^3,4

Hills-Sachs lesion is often associated with a Bankart lesion. The Hills-Sachs lesion is an impaction fracture of the posterolateral aspect of the humeral head resulting from its displacement over the anterior lip of the glenoid. Hill-Sachs lesions are seen in 71% of first-time and recurrent dislocations.³

Less common concomitant injuries during anterior shoulder dislocation include rupture of the rotator-cuff tendons (particularly in patients older than 40 years), glenoid and proximal humerus fractures, a tear of the superior labrum (known as a “SLAP lesion”), cartilage injury, and neurovascular injury.

Posterior instability typically occurs as a result of a strong muscle contraction, as seen in electrocution or seizure; however, it can be caused by athletic trauma, particularly in football.⁵ Repetitive forces exerted on the forward-flexed and internally rotated shoulder position during blocking puts football players at increased risk of posterior instability.⁵

Continue to: Multidirectional instability

 

Multidirectional instability is more frequently attributable to congenital hyperlaxity of the glenohumeral joint capsule, rather than to acute injury. However, athletes can also develop capsular laxity from repetitive microtrauma to the shoulder.⁵

Emergent reduction: Prompt action needed

Acute dislocation of the shoulder should be reduced as soon as possible to minimize neurovascular injury and patient discomfort. (Typically, but not always, this is done in the emergency department.) It is crucial to have effective muscle relaxation before any attempt at reduction, to minimize the risk of iatrogenic injury to bone, cartilage, tendons, and neurovascular structures.

Muscle relaxation can be facilitated with intravenous midazolam or other agents, as specified by institutional protocol. Intra-articular lidocaine injection or intravenous fentanyl is often utilized in conjunction with the sedating agent to reduce pain and further accommodate relaxation.

Anterior reduction. Any one of several techniques can be used to perform emergent reduction of anterior shoulder dislocations, all of which have demonstrated success. The Milch technique is among the least traumatic for effective reduction.⁶ In this technique (FIGURE 1), the patient is supine; gentle but firm downward traction is applied to the humerus at the elbow of the affected arm while the arm is in abduction and external rotation. The provider can manipulate the humeral head at that point by placing a thumb in the patient’s axilla; the arm can also be further internally rotated and adducted until reduction is achieved.

Posterior reduction of a dislocation is performed while the patient is supine, with the body stabilized. Traction is applied on the adducted and internally rotated arm in conjunction with direct pressure on the posterior aspect of the humeral head (FIGURE 2).

Continue to: Follow-up actions

 

Follow-up actions. Before discharging the patient after reduction of a dislocation, it is essential to:

• perform post-reduction evaluation of shoulder stability at different levels of abduction
• perform a thorough neurovascular assessment
• obtain an anteroposterior (AP) radiograph to ensure proper positioning of the glenohumeral joint.

The reduced shoulder should be immobilized in a sling. The discharge plan should include pain management for several days and a follow-up appointment in 5 to 8 days with the primary care provider² (FIGURE 3).

Follow-up evaluation by the primary care provider

History. Prior to the initial examination at follow-up, obtain a comprehensive history that includes the nature of the injury and the direction of force that was placed on the shoulder. Determine whether the shoulder was reduced spontaneously or required manual reduction in the field or an emergency department. Note any associated injury sustained concurrently and the presence (or absence) of neck pain, numbness, tingling, or weakness in the affected arm.

Physical exam starts with thorough inspection of the affected shoulder, with comparison to the contralateral side, at rest and during shoulder motion. Palpation to reveal points of tenderness should include the anterior joint line, acromioclavicular joint, bicipital groove, subacromial space, acromion, and greater tuberosity.

Acute dislocation of the shoulder should be reduced as soon as possible to minimize neurovascular injury and patient discomfort.

Following inspection and palpation, assess active and passive range of motion in forward elevation, abduction, internal and external rotation at the side of the body, and internal and external rotation in shoulder abduction. Assessment might be limited by pain and apprehension, and should be performed within the patient’s comfortable range of motion.

Continue to: Once range of motion...

 

Once range of motion is determined, assess⁷:

• muscle power of the rotator cuff in abduction (for the supraspinatus muscle)
• resisted external rotation at the side of the body (the infraspinatus)
• resisted external rotation in abduction > 60° (the teres minor)
• resisted internal rotation (the subscapularis).

Specific tests for shoulder laxity and stability

It is important during the primary care follow-up examination to differentiate true instability and shoulder hyperlaxity, particularly in young, flexible patients (TABLE). Many of these patients present with painless hypermobility of the shoulder without true injury to the labrum or ligamentous structures. It might appear to the patient, or to family, that the shoulder is subluxating; however, the humeral head returns to a centered position on the glenoid in a hypermobile state—typically, without pain. Actual shoulder instability is defined as loss of the ability of the humeral head to re-center, accompanied by pain—pathology that is frequently associated with damage to the capsulolabral complex.

The load and shift test is used to assess anterior and posterior laxity. The patient is seated, and the forearm is allowed to rest on the thigh. Examination is performed using 1 hand to press anteriorly or posteriorly on the humeral head; the other hand is simultaneously positioned on the joint line to feel movement of the humeral head in relation to the glenoid (FIGURE 4).

The apprehension test is a common maneuver used to assess anterior shoulder instability. It is performed by positioning the affected arm to 90° external rotation and then elevating it to 90° abduction. Although this maneuver can be performed with the patient upright, it is beneficial to have them supine, to more easily control the arm (FIGURE 5). A positive test is noted when the patient reports a sensation of impending instability (apprehension), rather than pain alone.

Relocation test. When the apprehension test is positive, the supine position can be exploited to further perform the relocation test, in 2 stages (FIGURE 6):

• Apply a posteriorly directed force on the humeral head, which stabilizes the shoulder and typically alleviates symptoms.
• Release pressure quickly from the humeral head to assess recurrence of pain and apprehension as the humeral head snaps back against the anterior labrum.

Continue to: Combined, apprehension and relocation...

 

Combined, apprehension and relocation tests to identify anterior shoulder instability have been shown to significantly improve specificity while maintaining sensitivity.⁸

The posterior apprehension test is used to assess posterior instability. The patient is supine; the affected arm is placed in flexion, adduction, and internal rotation; and posterior pressure is applied (FIGURE 7). A positive test is noted when pain is reported at the posterior aspect of the shoulder. Clicking might be noted as the humeral head dislocates rearward.¹

Sulcus sign. Multidirectional instability is elicited using the sulcus sign. While the patient is seated upright, arms resting at their sides, a direct downward pull at elbow level will, when positive, reveal a depression (sulcus) at the lateral aspect of the affected shoulder as the humeral head translates inferiorly (FIGURE 8). A positive sulcus sign is documented in 3 grades, according to the amount of translation¹:

• Grade I: < 1 cm
• Grade II: 1-2 cm
• Grade III: > 2 cm.

Neurovascular status should be verified at every physical evaluation, with motor and sensory function tested in the axillary, musculocutaneous, median, radial, and ulnar nerve distributions. If nerve injury is suspected, electromyography and nerve-conduction testing is indicated.^9-13 Vascular compromise is much less common but equally important to assess.¹¹

Use of imaging

Post-reduction radiographs, including internal and external AP—and especially axillary—views are invaluable. Not only do they help to ensure reduction, but they also help to assess for fracture. A magnetic resonance imaging (MRI) arthrogram is the preferred imaging modality if a labral tear is suspected (FIGURE 9). Other concomitant shoulder injuries, such as subtle bone fracture, rotator cuff tear, and biceps pathology can also be reliably diagnosed with noncontrast MRI.

Continue to: Roadmap for treatment

 

 

Roadmap for treatment

The rate of recurrence after a first anterior shoulder dislocation is strongly associated with a person’s age and level of activity. Active patients younger than 20 years have a 92% to 96% recurrence rate¹⁴; patients 20 to 40 years, 25% to 48%; and patients older than 40 years, < 10%.¹⁵

Young, athletic patients who are treated nonoperatively are left at an unacceptably high risk of recurrence, leading to progressive damage to bony and soft-tissue structures.^16,17 Surgical labral repair after a first-time anterior dislocation produced improved outcomes in terms of recurrent dislocation (7.9%), compared to outcomes after nonsurgical treatment (52.9%),¹⁴ and has been associated with a lower incidence of future glenohumeral osteoarthritis.¹⁸ For those reasons, we recommend referral to an orthopedic surgeon for all patients younger than 20 years who sustain an anterior shoulder dislocation.

Patients older than 20 years who do not have concomitant shoulder injury, and who demonstrate full strength in abduction, external rotation, and internal rotation of the shoulder on clinical examination, have a low probability of associated rotator-cuff tear. They can be immobilized in a sling for 1 to 3 weeks, followed by a 6 to 12–week regimen of physical therapy.

Concomitant tear of the rotator cuff. Weakness on examination requires MRI or a magnetic resonance arthrogram for evaluation of associated rotator-cuff tear. A tear identified on MRI should be referred to an orthopedic surgeon because timely repair can be crucial to attaining best outcomes. Conservative treatment of traumatic full-­tendon rotator-cuff tear is associated with poor results, progression in the size of the tear, and advancement of muscle atrophy.^19,20 For patients younger than 40 years, arthroscopic rotator-cuff repair, with or without labral repair, produces excellent clinical outcomes, carries a low risk of complications, and results in a > 95% rate of return to a preoperative level of recreational and job activities.²¹

Patients who demonstrate weakness of the rotator-cuff muscles on examination, but who do not have a tear noted on MRI, should be evaluated by electromyography and nerve-conduction testing to assess nerve injury as an alternative cause of weakness.^10,11 If a neurologic deficit is found on nerve-conduction testing, the patient should be referred for neurologic evaluation.¹⁰

Continue to: Patients with negative findings...

 

Patients with negative findings on MRI and nerve-conduction studies should be offered physical therapy. Patients with recurrent anterior shoulder dislocation should be referred to an orthopedic surgeon for surgical repair. Frequently, improper or delayed treatment with chronic instability results in degenerative arthropathy of the joint²² (FIGURE 10).

Posterior and multidirectional instability can typically be treated conservatively; however, whereas posterior dislocation typically must be immobilized for 3 to 6 weeks post reduction, multidirectional instability does not require immobilization. Instead, physical therapy should start as soon as possible. In these cases, recurrent dislocation or subluxation that persists after conservative treatment should be referred for possible surgical intervention.⁵

Instability with associated fracture

Fracture concomitant with dislocation most commonly involves the humeral neck, humeral head, greater tuberosity, or the glenoid itself.² Clinical variables that predict a fracture associated with shoulder dislocation include²³:

• first episode of dislocation
• age ≥ 40 years
• fall from higher than 1 flight of stairs
• fight or assault
• motor vehicle crash.

A computed tomography scan with 3-dimensional reconstruction can help characterize associated fracture accurately—including location, size, and displacement—and can play an important role in treatment planning and prognosis in these complicated injuries. Displaced fracture should be referred to an orthopedic surgeon. Nondisplaced fracture of the humeral head or greater tuberosity (FIGURE 11) poses less risk of complications and can be treated conservatively with 6 weeks in an arm sling, followed by physical therapy.²⁴

Summing up

Management of shoulder dislocation must, first, be tailored to the individual and, second, account for several interactive factors—including age, direction of instability, functional demands, risk of recurrence, and associated injuries. In many patients, conservative treatment produces a favorable long-term outcome. Particularly in young, active patients with anterior shoulder instability, most surgeons consider open or arthroscopic reconstruction to be the treatment of choice.^2,18

Continue to: Pre-reduction and post-reduction...

 

Pre-reduction and post-reduction imaging should be carefully examined for the presence of concomitant injury, which might change the preferred treatment modality appreciably.

Last, communication among emergency department providers, the primary care provider, orthopedist, radiologist, and neurologist is crucial for determining an appropriate patient-centered approach to initial and long-term management.

CORRESPONDENCE
Nata Parnes, MD, Carthage Area Hospital, 3 Bridge Street, Carthage, NY; [email protected]

Our approach to caring for the growing number of community-dwelling US adults ages ≥ 65 years has shifted. Although we continue to manage disease and disability, there is an increasing emphasis on the promotion of healthy aging by optimizing health care needs and quality of life (QOL).

The American Geriatric Society (AGS) uses the term “healthy aging” to reflect a dedication to improving the health, independence, and QOL of older people.¹ The World Health Organization (WHO) defines healthy aging as “the process of developing and maintaining the functional ability that enables well-being in older age.”² Functional ability encompasses capabilities that align with a person’s values, including meeting basic needs; learning, growing, and making independent decisions; being mobile; building and maintaining healthy relationships; and contributing to society.² Similarly, the US Department of Health and Human Services has adopted a multidimensional approach to support people in creating “a productive and meaningful life” as they grow older.³

Numerous theoretical models have emerged from research on aging as a multidimensional construct, as evidenced by a 2016 citation analysis that identified 1755 articles written between 1902 and 2015 relating to “successful aging.”⁴ The analysis revealed 609 definitions operationalized by researchers’ measurement tools (mostly focused on physical function and other health metrics) and 1146 descriptions created by older adults, many emphasizing psychosocial strategies and cultural factors as key to successful aging.⁴

One approach that is likely to be useful for family physicians is the Age-Friendly Health System. This is an initiative of The John A. Hartford Foundation and the Institute for Healthcare Improvement that uses a multidisciplinary approach to create environments that foster inclusivity and address the needs of older people.⁵ Following this guidance, primary care providers use evidence-informed strategies that promote safety and address what matters most to older adults and their family caregivers.

Medicare annual wellness visits provide an opportunity to assess current health status as well as discuss behavior-change and risk-reduction strategies with patients.

The Age-Friendly Health System, as well as AGS and WHO, recognize that there are multiple aspects to well-being as one grows older. By using focused, evidence-based screening, assessments, and interventions, family physicians can best support aging patients in living their most fulfilling lives.

Here we present a review of evidence-based strategies that promote safety and address what matters most to older adults and their family caregivers using a 4-pronged framework, in the style of the Age-Friendly Health System model. However, the literature on healthy aging includes important messages about patient context and lifelong health behaviors, which we capture in an expanded set of thematic guidance. As such, we encourage family physicians to approach healthy aging as follows: (1) monitor health (screening and prevention), (2) promote mobility (physical function), (3) manage mentation (emotional health and cognitive function), and (4) encourage maintenance of social connections (social networks and QOL).

Monitoring health

Leverage Medicare annual wellness visits. A systematic approach is needed to prevent frailty and functional decline, and thus increase the QOL of older adults. To do this, it is important to focus on health promotion and disease prevention, while addressing existing ailments. One method is to leverage the Medicare annual wellness visit (AWV), which provides an opportunity to assess current health status as well as discuss behavior-change and risk-reduction strategies with patients.

Continue to: Although AWVs...

 

Although AWVs are an opportunity to improve patient outcomes, we are not taking full advantage of them.⁶ While AWVs have gained traction since their introduction in 2011, usage rates among ethnoracial minority groups has lagged behind.⁶ A 2018 cohort study examined reasons for disparate utilization rates among individuals ages ≥ 66 years (N = 14,687).⁷ Researchers found that differences in utilization between ethnoracial groups were explained by socioeconomic factors. Lower education and lower income, as well as rural living, were associated with lower rates of AWV completion.⁷ In addition, having a usual, nonemergent place to obtain medical care served as a powerful predictor of AWV utilization for all groups.⁷

Strategies to increase AWV completion rates among all eligible adults include increasing staff awareness of health literacy challenges and ensuring communication strategies are inclusive by providing printed materials in multiple languages, Braille, or larger typefaces; using accessible vocabulary that does not include medical jargon; and making medical interpreters accessible. In addition, training clinicians about unconscious bias and cultural humility can help foster empathy and awareness of differences in health beliefs and behaviors within diverse patient populations.

A 2019 scoping review of 11 studies (N > 60 million) focused on outcomes from Medicare AWVs for patients ages ≥ 65 years.⁸ This included uptake of preventive services, such as vaccinations or cancer screenings; advice, education, or referrals offered during the AWV; medication use; and hospitalization rates. Overall findings showed that older adults who received a Medicare AWV were more likely to receive referrals for preventive screenings and follow-through on these recommendations compared with those who did not undergo an AWV.⁸

The approach to caring for individuals later in life has shifted from management of disease and disability to promotion of healthy aging by optimizing health care needs and QOL.

Completion rates for vaccines, while remaining low overall, were higher among those who completed an AWV. Additionally, these studies showed improved completion of screenings for breast cancer, bone density, and colon cancer. Several studies in the scoping review supported the use of AWVs as an effective means by which to offer health education and advice related to health promotion and risk reduction, such as diet and lifestyle modifications.⁸ Little evidence exists on long-term outcomes related to AWV completion.⁸

Utilize shared decision-making to determine whether preventive screening makes sense for your patient. Although cancer remains the second leading cause of death among Americans ages ≥ 65 years,⁹ clear screening guidelines for this age group remain elusive.¹⁰ Physicians and patients often are reluctant to stop cancer screening despite lower life expectancy and fewer potential benefits of diagnosis in this population.⁹ Some recent studies reinforce the heterogeneity of the older adult population and further underscore the importance of individual-level decision-making.^11-14 It is important to let older adult patients and their caregivers know about the potential risks of screening tests, especially the possibility that incidental findings may lead to unwarranted additional care or monitoring.⁹

Continue to: Avoid these screening conversation missteps

 

Avoid these screening conversation missteps. A 2017 qualitative study asked 40 community-dwelling older adults (mean age = 76 years) about their preferences for discussing screening cessation with their physicians.¹³ Three themes emerged.First, they were open to stopping their screenings, especially when suggested by a trusted physician. Second, health status and physical function made sense as decision points, but life expectancy did not. Finally, lengthy discussions with expanded details about risks and benefits were not appreciated, especially if coupled with comments on the limited benefits for those nearing the end of life. When discussing life expectancy, patients preferred phrasing that focused on how the screening was unnecessary because it would not help them live longer.¹³

Ensure that your message is understood—and culturally relevant. Recent studies on lower health literacy among older adults^15,16 and ethnic and racial minorities^17-21—as revealed in the 2003 National Assessment of Adult Literacy²²—might offer clues to patient receptivity to discussions about preventive screening and other health decisions.

One study found a significant correlation between higher self-rated health literacy and higher engagement in health behaviors such as mammography screening, moderate physical activity, and tobacco avoidance.¹⁶ Perceptions of personal control over health status, as well as perceived social standing, also correlated with health literacy score levels.¹⁶ Another study concluded that lower health literacy combined with lower self-­efficacy, cultural beliefs about health topics (eg, diet and exercise), and distrust in the health care system contributed to lower rates of preventive care utilization among ethnocultural minority older adults in Canada, the United Kingdom, the United States, and Australia.¹⁸

Ensuring that easy-to-understand information is equitably shared with older adults of all races and ethnicities is critical. A 2018 study showed that distrust of the health system and cultural issues contributed to the lower incidence of colorectal cancer screenings in Hispanic and Asian American patients ages 50 to 75 years.²¹ Patients whose physicians engaged in “health literate practices” (eg, offering clear explanations of diagnostic plans and asking patients to describe what they understood) were more likely to obtain recommended breast and colorectal cancer screenings.²⁰ In particular, researchers found that non-Hispanic Blacks were nearly twice as likely to follow through on colorectal cancer screening if their physicians engaged in health literate practices.²⁰ In addition, receiving clear instructions from physicians increased the odds of completing breast cancer screening among Hispanic and non-­Hispanic White women.²⁰

Overall, screening information and recommendations should be standardized for all patients. This is particularly important in light of research that found that older non-Hispanic Black patients were less likely than their non-Hispanic White counterparts to receive information from their physicians about colorectal cancer screening.²⁰

Continue to: Mobility

 

Mobility

Encourage physical activity. Frequent exercise and other forms of physical activity are associated with healthy aging, as shown in a 2017 systematic review and meta-analysis of 23 studies (N = 174,114).²³ Despite considerable heterogeneity between studies in how researchers defined healthy aging and physical activity, they found that adults who incorporate regular movement and exercise into daily life are likely to continue to benefit from it into older age.²³ In addition, a 2016 secondary analysis of data from the InCHIANTI longitudinal aging study concluded that adults ages ≥ 65 years (N = 1149) who had maintained higher physical activity levels throughout adulthood had less physical function decline and reduced rates of mobility disability and premature death compared with those who reported being less active.²⁴

Preserve gait speed (and bolster health) with these activities. Walking speed, or gait, measured on a level surface has been used as a predictor for various aspects of well-being in older age, such as daily function, mobility, independence, falls, mortality, and hospitalization risk.²⁵ Reduced gait speed is also one of the key indicators of functional impairment in older adults.

A 2015 systematic review sought to determine which type of exercise intervention (resistance, coordination, or multimodal training) would be most effective in preserving gait speed in healthy older adults (N = 2495; mean age = 74.2 years).²⁵ While the 42 included studies were deemed to be fairly low quality, the review revealed (with large effect size [0.84]) that a number of exercise modalities might stave off loss of gait speed in older adults. Patients in the resistance training group had the greatest improvement in gait speed (0.11 m/s), followed by those in the coordination training group (0.09 m/s) and the multimodal training group (0.05 m/s).²⁵

Individuals who had maintained higher physical activity levels throughout adulthood had less physical functional decline and reduced rates of mobility disability and premature death.

Finally, muscle mass and strength offer a measure of physical performance and functionality. A 2020 systematic review of 83 studies (N = 108,428) showed that low muscle mass and strength, reduced handgrip strength, and lower physical performance were predictive of reduced capacities in activities of daily living and instrumental activities of daily living.²⁶ It is important to counsel adults to remain active throughout their lives and to include resistance training to maintain muscle mass and strength to preserve their motor function, mobility, independence, and QOL.

Use 1 of these scales to identify frailty. Frailty is a distinct clinical syndrome, in which an individual has low reserves and is highly vulnerable to internal and external stressors. It affects many community-­dwelling older adults. Within the literature, there has been ongoing discussion regarding the definition of frailty²⁷ (TABLE 1^28-31).

Continue to: The Fried Frailty Index...

 

The Fried Frailty Index defines frailty as a purely physical condition; patients need to exhibit 3 of 5 components (ie, weight loss, exhaustion, weakness, slowness, and low physical activity) to be deemed frail.³¹ The Edmonton Frail Scale is commonly used in geriatric assessments and counts impairments across several domains including physical activity, mood, cognition, and incontinence.^30,32,33 Physicians need to complete a training course prior to its use. Finally, the definition of frailty used by Rockwood et al^{28, 29} was used to develop the Clinical Frailty Scale, which relies on broader criteria that include social and psychological elements in addition to physical elements.The Clinical Frailty Scale uses clinician judgment to evaluate patient-specific domains (eg, comorbidities, functionality, and cognition) and to generate a score ranging from 1 (very fit) to 9 (terminally ill).²⁹ This scale is accessible and easy to implement. As a result, use of this scale has increased during the COVID-19 pandemic. All definitions include a pre-frail state, indicating the dynamic nature of frailty over time.

It is important to identify pre-frail and frail older adults using 1 of these screening tools. Interventions to reverse frailty that can be initiated in the primary care setting include identifying treatable medical conditions, assessing medication appropriateness, providing nutritional advice, and developing an exercise plan.³⁴

Conduct a nutritional assessment; consider this diet. Studies show that nutritional status can predict physical function and frailty risk in older adults. A 2017 systematic review of 19 studies (N = 22,270) of frail adults ages ≥ 65 years found associations related to specific dietary constructs (ie, micronutrients, macronutrients, antioxidants, overall diet quality, and timing of consumption).³⁵ Plant-based diets with higher levels of micronutrients, such as vitamins C and E and beta-carotene, or diets with more protein or macronutrients, regardless of source foods, all resulted in inverse associations with frailty syndrome.³⁵

A 2017 study showed that physical exercise and maintaining good nutritional status may be effective for preventing frailty in ­community-dwelling pre-frail older individuals.³⁶ A 2019 study showed that a combination of muscle strength training and protein supplementation was the most effective intervention to delay or reverse frailty and was easiest to implement in primary care.³⁷ A 2020 meta-analysis of 31 studies (N = 4794) addressing frailty among primary care patients > 60 years showed that interventions using predominantly resistance-based exercise and nutrition supplementation improved frailty status over the control.³⁸ Researchers also found that a comprehensive geriatric assessment or exercise—alone or in combination with nutrition education—reduced physical frailty.

Mentation

Screen and treat cognitive impairments. Cognitive function and autonomy in ­decision-making are important factors in healthy aging. Aspects of mental health (eg, depression and anxiety), sensory impairment (eg, visual and auditory impairment), and mentation issues (eg, delirium, dementia, and related conditions), as well as diet, physical exercise, and mobility, can all impede cognitive functionality. The long-term effects of depression, anxiety,³⁹ sensory deficits,⁴⁰ mobility,⁴¹ diet,⁴² and, ultimately, aging may impact Alzheimer disease (AD). The risk of an AD diagnosis increases with age.³⁹

Continue to: A 2018 prospective cohort study...

 

A 2018 prospective cohort study using data from the National Alzheimer’s Coordinating Center followed individuals (N = 12,053) who were cognitively asymptomatic at their initial visits to determine who developed clinical signs of AD.³⁹ Survival analysis showed several psychosocial factors—anxiety, sleep disturbances, and depressive episodes of any type (occurring within the past 2 years, clinician verified, lifetime report)—were significantly associated with an eventual AD diagnosis and increased the risk of AD.³⁹ More research is needed to verify the impact of early intervention for these conditions on neurodegenerative disease; however, screening and treating psychosocial factors such as anxiety and depression should be maintained.

For patients ages ≥ 65 years, it is recommended that eye examinations occur every 1 to 2 years.

Researchers evaluated the impact of a dual sensory impairment (DSI) on dementia risk using data from 2051 participants in the Ginkgo Evaluation of Memory Study.⁴⁰ Hearing and visual impairments (defined as DSI when these conditions coexist) or visual impairment alone were significantly associated with increased risk of dementia in older adults. The researchers reported that DSI was significantly associated with a higher risk of all-cause dementia (hazard ratio [HR] = 1.86; 95% CI, 1.25-2.76) and AD (HR = 2.12; 95% CI, 1.34-3.36).⁴⁰ Visual impairment alone was associated with an increased risk of all-cause dementia (HR = 1.32; 95% CI, 1.02-1.71).⁴⁰ These results suggest that screening of DSI or visual impairment earlier in the patient’s lifespan may identify those at high risk of dementia in older adulthood.

The American Academy of Ophthalmology recommends patients with healthy eyes be screened once during their 20s and twice in their 30s; a full examination is recommended by age 40. For patients ages ≥ 65 years, it is recommended that eye examinations occur every 1 to 2 years.⁴³

Diet and mobility play a big role in cognition. Diet⁴³ and exercise^41,42,44 are believed to have an impact on mentation, and recent studies show memory and global cognition could be malleable later in life. A 2015 meta-analysis of 490 treatment arms of 24 randomized controlled studies showed improvement in global cognition with consumption of a Mediterranean diet plus olive oil (effect size [ES] standardized mean difference [SMD] = 0.22; 95% CI, 0.16-0.27) and tai chi exercises (ES SMD = 0.18; 95% CI, 0.06-0.29).⁴² The analysis also found improved memory among participants who consumed the Mediterranean diet/olive oil combination (ES SMD = 0.22; 95% CI, 0.12-0.32) and soy isoflavone supplements (ES SMD = 0.11; 95% CI, 0.04-0.17). Although the ESs are small, they are significant and offer promising evidence that individual choices related to nutrition or exercise may influence cognition and memory.

A 2018 systematic review found that all domains of cognition showed improvement with 45 to 60 minutes of moderate-to-vigorous physical exercise.⁴⁴ Attention, executive function, memory, and working memory showed significant increases, whereas global cognition improvements were not statistically significant.⁴⁴ A 2016 meta-analysis of 26 studies (N = 26,355) found a positive association between an objective mobility measure (gait, lower-extremity function, and balance) and cognitive function (global, executive function, memory, and processing speed) in older adults.⁴¹ These results highlight that diet, mobility, and physical exercise impact cognitive functioning.

Continue to: Maintaining social connections

 

Maintaining social connections

Social isolation and loneliness—compounded by a pandemic. The US Department of Health and Human Services notes that “community connections” are among the key factors required for healthy aging.³ Similarly, the WHO definition of healthy aging considers whether individuals can build and sustain relationships with other people and find ways to engender their personal values through these connections.²

Prioritizing interventions that identify and connect isolated older adults to social support may increase survivability.

As people age, their social connections often decrease due to the death of friends and family, shifts in living arrangements, loss of mobility or eyesight (and thus self-­transport), and the onset or increased acuity of illness or chronic conditions.⁴⁵ This has been exacerbated by the COVID-19 pandemic, which has spurred shelter-in-place and stay-at-home orders along with recommendations for physical distancing (also known as social distancing), especially for older adults who are at higher risk.⁴⁶ Smith et al⁴⁷ calls this the COVID-19 Social Connectivity Paradox, in which older adults limit their interactions with others to protect their physical health and reduce their risk of contracting the virus, but as a result they may undermine their psychosocial health by placing themselves at risk of social isolation and loneliness.⁴⁷

The double threat. Social isolation and loneliness have been shown to negatively impact physical health and well-being, resulting in an increased risk of early death^48-50; higher likelihood of specific diagnoses, including dementia and cardiovascular conditions^48,50; and more frequent use of health care services.⁵⁰ These concepts, while related, represent different mechanisms for negative health outcomes. Social isolation is an objective condition when one has a lack of opportunities for interaction with other people; loneliness refers to the emotional disconnect one feels when separated from others. Few studies have compared outcomes between these concepts, but in those that have, social isolation appears to be more strongly associated with early death.^48-50

A 2013 observational study using data from the English Longitudinal Study on Aging found that both social isolation and loneliness were associated with increased mortality among men and women ages ≥ 52 years (N = 6500).⁴⁸ However, when studied independently, loneliness was not found to be a significant risk factor. In contrast, social isolation significantly impacted mortality risk, even after adjusting for demographic factors and baseline health status.⁴⁸ These findings are supported by a 2018 cohort study of individuals (N = 479,054) with a history of an acute cardiovascular event that concluded social isolation was a predictor of mortality, whereas loneliness was not.⁵⁰

A large 2015 meta-analysis (70 studies, N = 3,407,134) of mortality causes among community-dwelling older adults (average age, 66) confirmed that both objective measures of isolation, as well as subjective measures (such as feelings of loneliness or living alone), have a significant predictive effect in longer-term studies. Each measure shows an approximately 30% increase in the likelihood of death after an average of 7 years.⁴⁹

Continue to: Health care remains a connection point

 

Health care remains a connection point. Even when life course events and conditions (eg, death of loved ones, loss of transportation or financial resources, or disengagement from community activities) reduce social connections, most older adults engage in some way with the health care system. A 2020 consensus report by the National Academies of Sciences, Engineering, and Medicine suggests health care professionals capitalize on these connection points with adults ages ≥ 50 years by periodically screening for social isolation and loneliness, documenting social status updates in medical records, and piloting and evaluating interventions in the clinical setting.⁵¹

The report offered information about potential avenues for intervention by primary care professionals beyond screening, such as participating in research studies that investigate screening tools and multisystem interventions; social prescribing (linking patients to embedded social work services or ­community-based organizations); referring patients to support groups; initiating ­cognitive-based therapy or other behavioral health interventions; or recommending mindfulness practices.⁵¹ However, most of the cited intervention studies were not specific to primary care settings and contained poor-quality evidence related to efficacy.

Isolation creates a greater reliance on health services due to a lack of a social support system, while a feeling of emotional disconnection (loneliness) seems to be a barrier to accessing care. A 2017 cohort study linking data from the Health and Retirement Study and Medicare claims revealed that social isolation predicts higher annual health expenditures (> $1600 per beneficiary) driven by hospitalization and skilled nursing facility usage, along with greater mortality, whereas individuals who are lonely result in reduced costs (a reduction of $770 annually) due to lower usage of inpatient and outpatient services.⁵² Prioritizing interventions that identify and connect isolated older adults to social support, therefore, may increase survivability by ensuring they have access to resources and health care interventions when needed.

Assessing and treating vision and hearing impairments and mental health issues may guard against losses in cognition.

In addition, these findings underscore the importance of looking at quality—not just quantity—of older adults’ social connections. A number of validated screening tools exist for social isolation and loneliness (TABLE 2^53-59); however, concerns exist about assessing risk using a unidimensional tool for a complex concern,⁴⁷ as well as identifying a problem without having evidence-based interventions to offer as solutions.^47,51 Until future studies resolve these concerns, leveraging the physician-patient relationship to broach these difficult subjects may help normalize the issues and create safe spaces to identify individuals who are at risk.

QOL is key to healthy aging. As Kusumastuti et al⁴ state, “successful ageing lies in the eyes of the beholder.” A 2019 systematic review of 48 qualitative studies revealed that community-dwelling older adults ages ≥ 50 years in 11 countries (N > 4175) perceive well-being by considering QOL within 9 domains: health perception, autonomy, role and activity, relationships, emotional comfort, attitude and adaptation, spirituality, financial security, and home and neighborhood.⁶⁰ Researchers found that as engagement in any one of these domains declines, older adults may shift their definition of health toward their remaining abilities.⁶⁰ This offers an explanation as to why patients might rate their health status much higher than their physicians do: older adults tend to have a more holistic concept of health.

Continue to: Take a multidimensional approach to healthy aging

 

Take a multidimensional approach to healthy aging

Although we have separately examined each of the 4 components of managing healthy aging in a community-dwelling adult, applying a multidimensional approach is most effective. Increasing use of the Medicare AWV provides an opportunity to assess patient health status, determine care preferences, and improve follow-through on preventive screening. It is also important to encourage older adults to engage in regular physical activity—especially muscle-strengthening exercises—and to discuss nutrition and caloric intake to prevent frailty and functional decline.

Assessing and treating vision and hearing impairments and mental health issues, including anxiety and depression, may guard against losses in cognition. When speaking with older adult patients about their social connections, consider asking not only about frequency of contact and access to resources such as food and transportation, but also about whether they are finding ways to bring their own values into those relationships to bolster their QOL. This guidance also may be useful for primary care practices and health care networks when planning future quality-improvement initiatives.

Additional research is needed to support the evidence base for aligning older adult preferences in health care interventions, such as preventive screenings. Also, clinical decision-making requires more clarity about the efficacy of specific diet and exercise interventions for older adults; the impact of early intervention for depression, anxiety, and sleep disorders on neurodegenerative disease; whether loneliness predicts mortality; and how health care delivery systems can be effective at building social connectivity.

Initiating health education, screening, and prevention throughout the patient’s lifespan can promote healthy aging outcomes later in life.

For now, it is essential to recognize that initiating health education, screening, and prevention throughout the patient’s lifespan can promote healthy aging outcomes. As family physicians, it is important to capitalize on longitudinal relationships with patients and begin educating younger patients using this multidimensional framework to promote living “a productive and meaningful life”at any age.³

CORRESPONDENCE

Lynn M. Wilson, DO, 707 Hamilton Street, 8th floor, Department of Family Medicine, Lehigh Valley Health Network, Allentown, PA 18101; [email protected]

Our approach to caring for the growing number of community-dwelling US adults ages ≥ 65 years has shifted. Although we continue to manage disease and disability, there is an increasing emphasis on the promotion of healthy aging by optimizing health care needs and quality of life (QOL).

The American Geriatric Society (AGS) uses the term “healthy aging” to reflect a dedication to improving the health, independence, and QOL of older people.¹ The World Health Organization (WHO) defines healthy aging as “the process of developing and maintaining the functional ability that enables well-being in older age.”² Functional ability encompasses capabilities that align with a person’s values, including meeting basic needs; learning, growing, and making independent decisions; being mobile; building and maintaining healthy relationships; and contributing to society.² Similarly, the US Department of Health and Human Services has adopted a multidimensional approach to support people in creating “a productive and meaningful life” as they grow older.³

Numerous theoretical models have emerged from research on aging as a multidimensional construct, as evidenced by a 2016 citation analysis that identified 1755 articles written between 1902 and 2015 relating to “successful aging.”⁴ The analysis revealed 609 definitions operationalized by researchers’ measurement tools (mostly focused on physical function and other health metrics) and 1146 descriptions created by older adults, many emphasizing psychosocial strategies and cultural factors as key to successful aging.⁴

One approach that is likely to be useful for family physicians is the Age-Friendly Health System. This is an initiative of The John A. Hartford Foundation and the Institute for Healthcare Improvement that uses a multidisciplinary approach to create environments that foster inclusivity and address the needs of older people.⁵ Following this guidance, primary care providers use evidence-informed strategies that promote safety and address what matters most to older adults and their family caregivers.

Medicare annual wellness visits provide an opportunity to assess current health status as well as discuss behavior-change and risk-reduction strategies with patients.

The Age-Friendly Health System, as well as AGS and WHO, recognize that there are multiple aspects to well-being as one grows older. By using focused, evidence-based screening, assessments, and interventions, family physicians can best support aging patients in living their most fulfilling lives.

Here we present a review of evidence-based strategies that promote safety and address what matters most to older adults and their family caregivers using a 4-pronged framework, in the style of the Age-Friendly Health System model. However, the literature on healthy aging includes important messages about patient context and lifelong health behaviors, which we capture in an expanded set of thematic guidance. As such, we encourage family physicians to approach healthy aging as follows: (1) monitor health (screening and prevention), (2) promote mobility (physical function), (3) manage mentation (emotional health and cognitive function), and (4) encourage maintenance of social connections (social networks and QOL).

Monitoring health

Leverage Medicare annual wellness visits. A systematic approach is needed to prevent frailty and functional decline, and thus increase the QOL of older adults. To do this, it is important to focus on health promotion and disease prevention, while addressing existing ailments. One method is to leverage the Medicare annual wellness visit (AWV), which provides an opportunity to assess current health status as well as discuss behavior-change and risk-reduction strategies with patients.

Continue to: Although AWVs...

 

Although AWVs are an opportunity to improve patient outcomes, we are not taking full advantage of them.⁶ While AWVs have gained traction since their introduction in 2011, usage rates among ethnoracial minority groups has lagged behind.⁶ A 2018 cohort study examined reasons for disparate utilization rates among individuals ages ≥ 66 years (N = 14,687).⁷ Researchers found that differences in utilization between ethnoracial groups were explained by socioeconomic factors. Lower education and lower income, as well as rural living, were associated with lower rates of AWV completion.⁷ In addition, having a usual, nonemergent place to obtain medical care served as a powerful predictor of AWV utilization for all groups.⁷

Strategies to increase AWV completion rates among all eligible adults include increasing staff awareness of health literacy challenges and ensuring communication strategies are inclusive by providing printed materials in multiple languages, Braille, or larger typefaces; using accessible vocabulary that does not include medical jargon; and making medical interpreters accessible. In addition, training clinicians about unconscious bias and cultural humility can help foster empathy and awareness of differences in health beliefs and behaviors within diverse patient populations.

A 2019 scoping review of 11 studies (N > 60 million) focused on outcomes from Medicare AWVs for patients ages ≥ 65 years.⁸ This included uptake of preventive services, such as vaccinations or cancer screenings; advice, education, or referrals offered during the AWV; medication use; and hospitalization rates. Overall findings showed that older adults who received a Medicare AWV were more likely to receive referrals for preventive screenings and follow-through on these recommendations compared with those who did not undergo an AWV.⁸

The approach to caring for individuals later in life has shifted from management of disease and disability to promotion of healthy aging by optimizing health care needs and QOL.

Completion rates for vaccines, while remaining low overall, were higher among those who completed an AWV. Additionally, these studies showed improved completion of screenings for breast cancer, bone density, and colon cancer. Several studies in the scoping review supported the use of AWVs as an effective means by which to offer health education and advice related to health promotion and risk reduction, such as diet and lifestyle modifications.⁸ Little evidence exists on long-term outcomes related to AWV completion.⁸

Utilize shared decision-making to determine whether preventive screening makes sense for your patient. Although cancer remains the second leading cause of death among Americans ages ≥ 65 years,⁹ clear screening guidelines for this age group remain elusive.¹⁰ Physicians and patients often are reluctant to stop cancer screening despite lower life expectancy and fewer potential benefits of diagnosis in this population.⁹ Some recent studies reinforce the heterogeneity of the older adult population and further underscore the importance of individual-level decision-making.^11-14 It is important to let older adult patients and their caregivers know about the potential risks of screening tests, especially the possibility that incidental findings may lead to unwarranted additional care or monitoring.⁹

Continue to: Avoid these screening conversation missteps

 

Avoid these screening conversation missteps. A 2017 qualitative study asked 40 community-dwelling older adults (mean age = 76 years) about their preferences for discussing screening cessation with their physicians.¹³ Three themes emerged.First, they were open to stopping their screenings, especially when suggested by a trusted physician. Second, health status and physical function made sense as decision points, but life expectancy did not. Finally, lengthy discussions with expanded details about risks and benefits were not appreciated, especially if coupled with comments on the limited benefits for those nearing the end of life. When discussing life expectancy, patients preferred phrasing that focused on how the screening was unnecessary because it would not help them live longer.¹³

Ensure that your message is understood—and culturally relevant. Recent studies on lower health literacy among older adults^15,16 and ethnic and racial minorities^17-21—as revealed in the 2003 National Assessment of Adult Literacy²²—might offer clues to patient receptivity to discussions about preventive screening and other health decisions.

One study found a significant correlation between higher self-rated health literacy and higher engagement in health behaviors such as mammography screening, moderate physical activity, and tobacco avoidance.¹⁶ Perceptions of personal control over health status, as well as perceived social standing, also correlated with health literacy score levels.¹⁶ Another study concluded that lower health literacy combined with lower self-­efficacy, cultural beliefs about health topics (eg, diet and exercise), and distrust in the health care system contributed to lower rates of preventive care utilization among ethnocultural minority older adults in Canada, the United Kingdom, the United States, and Australia.¹⁸

Ensuring that easy-to-understand information is equitably shared with older adults of all races and ethnicities is critical. A 2018 study showed that distrust of the health system and cultural issues contributed to the lower incidence of colorectal cancer screenings in Hispanic and Asian American patients ages 50 to 75 years.²¹ Patients whose physicians engaged in “health literate practices” (eg, offering clear explanations of diagnostic plans and asking patients to describe what they understood) were more likely to obtain recommended breast and colorectal cancer screenings.²⁰ In particular, researchers found that non-Hispanic Blacks were nearly twice as likely to follow through on colorectal cancer screening if their physicians engaged in health literate practices.²⁰ In addition, receiving clear instructions from physicians increased the odds of completing breast cancer screening among Hispanic and non-­Hispanic White women.²⁰

Overall, screening information and recommendations should be standardized for all patients. This is particularly important in light of research that found that older non-Hispanic Black patients were less likely than their non-Hispanic White counterparts to receive information from their physicians about colorectal cancer screening.²⁰

Continue to: Mobility

 

Mobility

Encourage physical activity. Frequent exercise and other forms of physical activity are associated with healthy aging, as shown in a 2017 systematic review and meta-analysis of 23 studies (N = 174,114).²³ Despite considerable heterogeneity between studies in how researchers defined healthy aging and physical activity, they found that adults who incorporate regular movement and exercise into daily life are likely to continue to benefit from it into older age.²³ In addition, a 2016 secondary analysis of data from the InCHIANTI longitudinal aging study concluded that adults ages ≥ 65 years (N = 1149) who had maintained higher physical activity levels throughout adulthood had less physical function decline and reduced rates of mobility disability and premature death compared with those who reported being less active.²⁴

Preserve gait speed (and bolster health) with these activities. Walking speed, or gait, measured on a level surface has been used as a predictor for various aspects of well-being in older age, such as daily function, mobility, independence, falls, mortality, and hospitalization risk.²⁵ Reduced gait speed is also one of the key indicators of functional impairment in older adults.

A 2015 systematic review sought to determine which type of exercise intervention (resistance, coordination, or multimodal training) would be most effective in preserving gait speed in healthy older adults (N = 2495; mean age = 74.2 years).²⁵ While the 42 included studies were deemed to be fairly low quality, the review revealed (with large effect size [0.84]) that a number of exercise modalities might stave off loss of gait speed in older adults. Patients in the resistance training group had the greatest improvement in gait speed (0.11 m/s), followed by those in the coordination training group (0.09 m/s) and the multimodal training group (0.05 m/s).²⁵

Individuals who had maintained higher physical activity levels throughout adulthood had less physical functional decline and reduced rates of mobility disability and premature death.

Finally, muscle mass and strength offer a measure of physical performance and functionality. A 2020 systematic review of 83 studies (N = 108,428) showed that low muscle mass and strength, reduced handgrip strength, and lower physical performance were predictive of reduced capacities in activities of daily living and instrumental activities of daily living.²⁶ It is important to counsel adults to remain active throughout their lives and to include resistance training to maintain muscle mass and strength to preserve their motor function, mobility, independence, and QOL.

Use 1 of these scales to identify frailty. Frailty is a distinct clinical syndrome, in which an individual has low reserves and is highly vulnerable to internal and external stressors. It affects many community-­dwelling older adults. Within the literature, there has been ongoing discussion regarding the definition of frailty²⁷ (TABLE 1^28-31).

Continue to: The Fried Frailty Index...

 

The Fried Frailty Index defines frailty as a purely physical condition; patients need to exhibit 3 of 5 components (ie, weight loss, exhaustion, weakness, slowness, and low physical activity) to be deemed frail.³¹ The Edmonton Frail Scale is commonly used in geriatric assessments and counts impairments across several domains including physical activity, mood, cognition, and incontinence.^30,32,33 Physicians need to complete a training course prior to its use. Finally, the definition of frailty used by Rockwood et al^{28, 29} was used to develop the Clinical Frailty Scale, which relies on broader criteria that include social and psychological elements in addition to physical elements.The Clinical Frailty Scale uses clinician judgment to evaluate patient-specific domains (eg, comorbidities, functionality, and cognition) and to generate a score ranging from 1 (very fit) to 9 (terminally ill).²⁹ This scale is accessible and easy to implement. As a result, use of this scale has increased during the COVID-19 pandemic. All definitions include a pre-frail state, indicating the dynamic nature of frailty over time.

It is important to identify pre-frail and frail older adults using 1 of these screening tools. Interventions to reverse frailty that can be initiated in the primary care setting include identifying treatable medical conditions, assessing medication appropriateness, providing nutritional advice, and developing an exercise plan.³⁴

Conduct a nutritional assessment; consider this diet. Studies show that nutritional status can predict physical function and frailty risk in older adults. A 2017 systematic review of 19 studies (N = 22,270) of frail adults ages ≥ 65 years found associations related to specific dietary constructs (ie, micronutrients, macronutrients, antioxidants, overall diet quality, and timing of consumption).³⁵ Plant-based diets with higher levels of micronutrients, such as vitamins C and E and beta-carotene, or diets with more protein or macronutrients, regardless of source foods, all resulted in inverse associations with frailty syndrome.³⁵

A 2017 study showed that physical exercise and maintaining good nutritional status may be effective for preventing frailty in ­community-dwelling pre-frail older individuals.³⁶ A 2019 study showed that a combination of muscle strength training and protein supplementation was the most effective intervention to delay or reverse frailty and was easiest to implement in primary care.³⁷ A 2020 meta-analysis of 31 studies (N = 4794) addressing frailty among primary care patients > 60 years showed that interventions using predominantly resistance-based exercise and nutrition supplementation improved frailty status over the control.³⁸ Researchers also found that a comprehensive geriatric assessment or exercise—alone or in combination with nutrition education—reduced physical frailty.

Mentation

Screen and treat cognitive impairments. Cognitive function and autonomy in ­decision-making are important factors in healthy aging. Aspects of mental health (eg, depression and anxiety), sensory impairment (eg, visual and auditory impairment), and mentation issues (eg, delirium, dementia, and related conditions), as well as diet, physical exercise, and mobility, can all impede cognitive functionality. The long-term effects of depression, anxiety,³⁹ sensory deficits,⁴⁰ mobility,⁴¹ diet,⁴² and, ultimately, aging may impact Alzheimer disease (AD). The risk of an AD diagnosis increases with age.³⁹

Continue to: A 2018 prospective cohort study...

 

A 2018 prospective cohort study using data from the National Alzheimer’s Coordinating Center followed individuals (N = 12,053) who were cognitively asymptomatic at their initial visits to determine who developed clinical signs of AD.³⁹ Survival analysis showed several psychosocial factors—anxiety, sleep disturbances, and depressive episodes of any type (occurring within the past 2 years, clinician verified, lifetime report)—were significantly associated with an eventual AD diagnosis and increased the risk of AD.³⁹ More research is needed to verify the impact of early intervention for these conditions on neurodegenerative disease; however, screening and treating psychosocial factors such as anxiety and depression should be maintained.

For patients ages ≥ 65 years, it is recommended that eye examinations occur every 1 to 2 years.

Researchers evaluated the impact of a dual sensory impairment (DSI) on dementia risk using data from 2051 participants in the Ginkgo Evaluation of Memory Study.⁴⁰ Hearing and visual impairments (defined as DSI when these conditions coexist) or visual impairment alone were significantly associated with increased risk of dementia in older adults. The researchers reported that DSI was significantly associated with a higher risk of all-cause dementia (hazard ratio [HR] = 1.86; 95% CI, 1.25-2.76) and AD (HR = 2.12; 95% CI, 1.34-3.36).⁴⁰ Visual impairment alone was associated with an increased risk of all-cause dementia (HR = 1.32; 95% CI, 1.02-1.71).⁴⁰ These results suggest that screening of DSI or visual impairment earlier in the patient’s lifespan may identify those at high risk of dementia in older adulthood.

The American Academy of Ophthalmology recommends patients with healthy eyes be screened once during their 20s and twice in their 30s; a full examination is recommended by age 40. For patients ages ≥ 65 years, it is recommended that eye examinations occur every 1 to 2 years.⁴³

Diet and mobility play a big role in cognition. Diet⁴³ and exercise^41,42,44 are believed to have an impact on mentation, and recent studies show memory and global cognition could be malleable later in life. A 2015 meta-analysis of 490 treatment arms of 24 randomized controlled studies showed improvement in global cognition with consumption of a Mediterranean diet plus olive oil (effect size [ES] standardized mean difference [SMD] = 0.22; 95% CI, 0.16-0.27) and tai chi exercises (ES SMD = 0.18; 95% CI, 0.06-0.29).⁴² The analysis also found improved memory among participants who consumed the Mediterranean diet/olive oil combination (ES SMD = 0.22; 95% CI, 0.12-0.32) and soy isoflavone supplements (ES SMD = 0.11; 95% CI, 0.04-0.17). Although the ESs are small, they are significant and offer promising evidence that individual choices related to nutrition or exercise may influence cognition and memory.

A 2018 systematic review found that all domains of cognition showed improvement with 45 to 60 minutes of moderate-to-vigorous physical exercise.⁴⁴ Attention, executive function, memory, and working memory showed significant increases, whereas global cognition improvements were not statistically significant.⁴⁴ A 2016 meta-analysis of 26 studies (N = 26,355) found a positive association between an objective mobility measure (gait, lower-extremity function, and balance) and cognitive function (global, executive function, memory, and processing speed) in older adults.⁴¹ These results highlight that diet, mobility, and physical exercise impact cognitive functioning.

Continue to: Maintaining social connections

 

Maintaining social connections

Social isolation and loneliness—compounded by a pandemic. The US Department of Health and Human Services notes that “community connections” are among the key factors required for healthy aging.³ Similarly, the WHO definition of healthy aging considers whether individuals can build and sustain relationships with other people and find ways to engender their personal values through these connections.²

Prioritizing interventions that identify and connect isolated older adults to social support may increase survivability.

As people age, their social connections often decrease due to the death of friends and family, shifts in living arrangements, loss of mobility or eyesight (and thus self-­transport), and the onset or increased acuity of illness or chronic conditions.⁴⁵ This has been exacerbated by the COVID-19 pandemic, which has spurred shelter-in-place and stay-at-home orders along with recommendations for physical distancing (also known as social distancing), especially for older adults who are at higher risk.⁴⁶ Smith et al⁴⁷ calls this the COVID-19 Social Connectivity Paradox, in which older adults limit their interactions with others to protect their physical health and reduce their risk of contracting the virus, but as a result they may undermine their psychosocial health by placing themselves at risk of social isolation and loneliness.⁴⁷

The double threat. Social isolation and loneliness have been shown to negatively impact physical health and well-being, resulting in an increased risk of early death^48-50; higher likelihood of specific diagnoses, including dementia and cardiovascular conditions^48,50; and more frequent use of health care services.⁵⁰ These concepts, while related, represent different mechanisms for negative health outcomes. Social isolation is an objective condition when one has a lack of opportunities for interaction with other people; loneliness refers to the emotional disconnect one feels when separated from others. Few studies have compared outcomes between these concepts, but in those that have, social isolation appears to be more strongly associated with early death.^48-50

A 2013 observational study using data from the English Longitudinal Study on Aging found that both social isolation and loneliness were associated with increased mortality among men and women ages ≥ 52 years (N = 6500).⁴⁸ However, when studied independently, loneliness was not found to be a significant risk factor. In contrast, social isolation significantly impacted mortality risk, even after adjusting for demographic factors and baseline health status.⁴⁸ These findings are supported by a 2018 cohort study of individuals (N = 479,054) with a history of an acute cardiovascular event that concluded social isolation was a predictor of mortality, whereas loneliness was not.⁵⁰

A large 2015 meta-analysis (70 studies, N = 3,407,134) of mortality causes among community-dwelling older adults (average age, 66) confirmed that both objective measures of isolation, as well as subjective measures (such as feelings of loneliness or living alone), have a significant predictive effect in longer-term studies. Each measure shows an approximately 30% increase in the likelihood of death after an average of 7 years.⁴⁹

Continue to: Health care remains a connection point

 

Health care remains a connection point. Even when life course events and conditions (eg, death of loved ones, loss of transportation or financial resources, or disengagement from community activities) reduce social connections, most older adults engage in some way with the health care system. A 2020 consensus report by the National Academies of Sciences, Engineering, and Medicine suggests health care professionals capitalize on these connection points with adults ages ≥ 50 years by periodically screening for social isolation and loneliness, documenting social status updates in medical records, and piloting and evaluating interventions in the clinical setting.⁵¹

The report offered information about potential avenues for intervention by primary care professionals beyond screening, such as participating in research studies that investigate screening tools and multisystem interventions; social prescribing (linking patients to embedded social work services or ­community-based organizations); referring patients to support groups; initiating ­cognitive-based therapy or other behavioral health interventions; or recommending mindfulness practices.⁵¹ However, most of the cited intervention studies were not specific to primary care settings and contained poor-quality evidence related to efficacy.

Isolation creates a greater reliance on health services due to a lack of a social support system, while a feeling of emotional disconnection (loneliness) seems to be a barrier to accessing care. A 2017 cohort study linking data from the Health and Retirement Study and Medicare claims revealed that social isolation predicts higher annual health expenditures (> $1600 per beneficiary) driven by hospitalization and skilled nursing facility usage, along with greater mortality, whereas individuals who are lonely result in reduced costs (a reduction of $770 annually) due to lower usage of inpatient and outpatient services.⁵² Prioritizing interventions that identify and connect isolated older adults to social support, therefore, may increase survivability by ensuring they have access to resources and health care interventions when needed.

Assessing and treating vision and hearing impairments and mental health issues may guard against losses in cognition.

In addition, these findings underscore the importance of looking at quality—not just quantity—of older adults’ social connections. A number of validated screening tools exist for social isolation and loneliness (TABLE 2^53-59); however, concerns exist about assessing risk using a unidimensional tool for a complex concern,⁴⁷ as well as identifying a problem without having evidence-based interventions to offer as solutions.^47,51 Until future studies resolve these concerns, leveraging the physician-patient relationship to broach these difficult subjects may help normalize the issues and create safe spaces to identify individuals who are at risk.

QOL is key to healthy aging. As Kusumastuti et al⁴ state, “successful ageing lies in the eyes of the beholder.” A 2019 systematic review of 48 qualitative studies revealed that community-dwelling older adults ages ≥ 50 years in 11 countries (N > 4175) perceive well-being by considering QOL within 9 domains: health perception, autonomy, role and activity, relationships, emotional comfort, attitude and adaptation, spirituality, financial security, and home and neighborhood.⁶⁰ Researchers found that as engagement in any one of these domains declines, older adults may shift their definition of health toward their remaining abilities.⁶⁰ This offers an explanation as to why patients might rate their health status much higher than their physicians do: older adults tend to have a more holistic concept of health.

Continue to: Take a multidimensional approach to healthy aging

 

Take a multidimensional approach to healthy aging

Although we have separately examined each of the 4 components of managing healthy aging in a community-dwelling adult, applying a multidimensional approach is most effective. Increasing use of the Medicare AWV provides an opportunity to assess patient health status, determine care preferences, and improve follow-through on preventive screening. It is also important to encourage older adults to engage in regular physical activity—especially muscle-strengthening exercises—and to discuss nutrition and caloric intake to prevent frailty and functional decline.

Assessing and treating vision and hearing impairments and mental health issues, including anxiety and depression, may guard against losses in cognition. When speaking with older adult patients about their social connections, consider asking not only about frequency of contact and access to resources such as food and transportation, but also about whether they are finding ways to bring their own values into those relationships to bolster their QOL. This guidance also may be useful for primary care practices and health care networks when planning future quality-improvement initiatives.

Additional research is needed to support the evidence base for aligning older adult preferences in health care interventions, such as preventive screenings. Also, clinical decision-making requires more clarity about the efficacy of specific diet and exercise interventions for older adults; the impact of early intervention for depression, anxiety, and sleep disorders on neurodegenerative disease; whether loneliness predicts mortality; and how health care delivery systems can be effective at building social connectivity.

Initiating health education, screening, and prevention throughout the patient’s lifespan can promote healthy aging outcomes later in life.

For now, it is essential to recognize that initiating health education, screening, and prevention throughout the patient’s lifespan can promote healthy aging outcomes. As family physicians, it is important to capitalize on longitudinal relationships with patients and begin educating younger patients using this multidimensional framework to promote living “a productive and meaningful life”at any age.³

CORRESPONDENCE

Lynn M. Wilson, DO, 707 Hamilton Street, 8th floor, Department of Family Medicine, Lehigh Valley Health Network, Allentown, PA 18101; [email protected]

Our approach to caring for the growing number of community-dwelling US adults ages ≥ 65 years has shifted. Although we continue to manage disease and disability, there is an increasing emphasis on the promotion of healthy aging by optimizing health care needs and quality of life (QOL).

The American Geriatric Society (AGS) uses the term “healthy aging” to reflect a dedication to improving the health, independence, and QOL of older people.¹ The World Health Organization (WHO) defines healthy aging as “the process of developing and maintaining the functional ability that enables well-being in older age.”² Functional ability encompasses capabilities that align with a person’s values, including meeting basic needs; learning, growing, and making independent decisions; being mobile; building and maintaining healthy relationships; and contributing to society.² Similarly, the US Department of Health and Human Services has adopted a multidimensional approach to support people in creating “a productive and meaningful life” as they grow older.³

Numerous theoretical models have emerged from research on aging as a multidimensional construct, as evidenced by a 2016 citation analysis that identified 1755 articles written between 1902 and 2015 relating to “successful aging.”⁴ The analysis revealed 609 definitions operationalized by researchers’ measurement tools (mostly focused on physical function and other health metrics) and 1146 descriptions created by older adults, many emphasizing psychosocial strategies and cultural factors as key to successful aging.⁴

One approach that is likely to be useful for family physicians is the Age-Friendly Health System. This is an initiative of The John A. Hartford Foundation and the Institute for Healthcare Improvement that uses a multidisciplinary approach to create environments that foster inclusivity and address the needs of older people.⁵ Following this guidance, primary care providers use evidence-informed strategies that promote safety and address what matters most to older adults and their family caregivers.

Medicare annual wellness visits provide an opportunity to assess current health status as well as discuss behavior-change and risk-reduction strategies with patients.

The Age-Friendly Health System, as well as AGS and WHO, recognize that there are multiple aspects to well-being as one grows older. By using focused, evidence-based screening, assessments, and interventions, family physicians can best support aging patients in living their most fulfilling lives.

Here we present a review of evidence-based strategies that promote safety and address what matters most to older adults and their family caregivers using a 4-pronged framework, in the style of the Age-Friendly Health System model. However, the literature on healthy aging includes important messages about patient context and lifelong health behaviors, which we capture in an expanded set of thematic guidance. As such, we encourage family physicians to approach healthy aging as follows: (1) monitor health (screening and prevention), (2) promote mobility (physical function), (3) manage mentation (emotional health and cognitive function), and (4) encourage maintenance of social connections (social networks and QOL).

Monitoring health

Leverage Medicare annual wellness visits. A systematic approach is needed to prevent frailty and functional decline, and thus increase the QOL of older adults. To do this, it is important to focus on health promotion and disease prevention, while addressing existing ailments. One method is to leverage the Medicare annual wellness visit (AWV), which provides an opportunity to assess current health status as well as discuss behavior-change and risk-reduction strategies with patients.

Continue to: Although AWVs...

 

Although AWVs are an opportunity to improve patient outcomes, we are not taking full advantage of them.⁶ While AWVs have gained traction since their introduction in 2011, usage rates among ethnoracial minority groups has lagged behind.⁶ A 2018 cohort study examined reasons for disparate utilization rates among individuals ages ≥ 66 years (N = 14,687).⁷ Researchers found that differences in utilization between ethnoracial groups were explained by socioeconomic factors. Lower education and lower income, as well as rural living, were associated with lower rates of AWV completion.⁷ In addition, having a usual, nonemergent place to obtain medical care served as a powerful predictor of AWV utilization for all groups.⁷

Strategies to increase AWV completion rates among all eligible adults include increasing staff awareness of health literacy challenges and ensuring communication strategies are inclusive by providing printed materials in multiple languages, Braille, or larger typefaces; using accessible vocabulary that does not include medical jargon; and making medical interpreters accessible. In addition, training clinicians about unconscious bias and cultural humility can help foster empathy and awareness of differences in health beliefs and behaviors within diverse patient populations.

A 2019 scoping review of 11 studies (N > 60 million) focused on outcomes from Medicare AWVs for patients ages ≥ 65 years.⁸ This included uptake of preventive services, such as vaccinations or cancer screenings; advice, education, or referrals offered during the AWV; medication use; and hospitalization rates. Overall findings showed that older adults who received a Medicare AWV were more likely to receive referrals for preventive screenings and follow-through on these recommendations compared with those who did not undergo an AWV.⁸

The approach to caring for individuals later in life has shifted from management of disease and disability to promotion of healthy aging by optimizing health care needs and QOL.

Completion rates for vaccines, while remaining low overall, were higher among those who completed an AWV. Additionally, these studies showed improved completion of screenings for breast cancer, bone density, and colon cancer. Several studies in the scoping review supported the use of AWVs as an effective means by which to offer health education and advice related to health promotion and risk reduction, such as diet and lifestyle modifications.⁸ Little evidence exists on long-term outcomes related to AWV completion.⁸

Utilize shared decision-making to determine whether preventive screening makes sense for your patient. Although cancer remains the second leading cause of death among Americans ages ≥ 65 years,⁹ clear screening guidelines for this age group remain elusive.¹⁰ Physicians and patients often are reluctant to stop cancer screening despite lower life expectancy and fewer potential benefits of diagnosis in this population.⁹ Some recent studies reinforce the heterogeneity of the older adult population and further underscore the importance of individual-level decision-making.^11-14 It is important to let older adult patients and their caregivers know about the potential risks of screening tests, especially the possibility that incidental findings may lead to unwarranted additional care or monitoring.⁹

Continue to: Avoid these screening conversation missteps

 

Avoid these screening conversation missteps. A 2017 qualitative study asked 40 community-dwelling older adults (mean age = 76 years) about their preferences for discussing screening cessation with their physicians.¹³ Three themes emerged.First, they were open to stopping their screenings, especially when suggested by a trusted physician. Second, health status and physical function made sense as decision points, but life expectancy did not. Finally, lengthy discussions with expanded details about risks and benefits were not appreciated, especially if coupled with comments on the limited benefits for those nearing the end of life. When discussing life expectancy, patients preferred phrasing that focused on how the screening was unnecessary because it would not help them live longer.¹³

Ensure that your message is understood—and culturally relevant. Recent studies on lower health literacy among older adults^15,16 and ethnic and racial minorities^17-21—as revealed in the 2003 National Assessment of Adult Literacy²²—might offer clues to patient receptivity to discussions about preventive screening and other health decisions.

One study found a significant correlation between higher self-rated health literacy and higher engagement in health behaviors such as mammography screening, moderate physical activity, and tobacco avoidance.¹⁶ Perceptions of personal control over health status, as well as perceived social standing, also correlated with health literacy score levels.¹⁶ Another study concluded that lower health literacy combined with lower self-­efficacy, cultural beliefs about health topics (eg, diet and exercise), and distrust in the health care system contributed to lower rates of preventive care utilization among ethnocultural minority older adults in Canada, the United Kingdom, the United States, and Australia.¹⁸

Ensuring that easy-to-understand information is equitably shared with older adults of all races and ethnicities is critical. A 2018 study showed that distrust of the health system and cultural issues contributed to the lower incidence of colorectal cancer screenings in Hispanic and Asian American patients ages 50 to 75 years.²¹ Patients whose physicians engaged in “health literate practices” (eg, offering clear explanations of diagnostic plans and asking patients to describe what they understood) were more likely to obtain recommended breast and colorectal cancer screenings.²⁰ In particular, researchers found that non-Hispanic Blacks were nearly twice as likely to follow through on colorectal cancer screening if their physicians engaged in health literate practices.²⁰ In addition, receiving clear instructions from physicians increased the odds of completing breast cancer screening among Hispanic and non-­Hispanic White women.²⁰

Overall, screening information and recommendations should be standardized for all patients. This is particularly important in light of research that found that older non-Hispanic Black patients were less likely than their non-Hispanic White counterparts to receive information from their physicians about colorectal cancer screening.²⁰

Continue to: Mobility

 

Mobility

Encourage physical activity. Frequent exercise and other forms of physical activity are associated with healthy aging, as shown in a 2017 systematic review and meta-analysis of 23 studies (N = 174,114).²³ Despite considerable heterogeneity between studies in how researchers defined healthy aging and physical activity, they found that adults who incorporate regular movement and exercise into daily life are likely to continue to benefit from it into older age.²³ In addition, a 2016 secondary analysis of data from the InCHIANTI longitudinal aging study concluded that adults ages ≥ 65 years (N = 1149) who had maintained higher physical activity levels throughout adulthood had less physical function decline and reduced rates of mobility disability and premature death compared with those who reported being less active.²⁴

Preserve gait speed (and bolster health) with these activities. Walking speed, or gait, measured on a level surface has been used as a predictor for various aspects of well-being in older age, such as daily function, mobility, independence, falls, mortality, and hospitalization risk.²⁵ Reduced gait speed is also one of the key indicators of functional impairment in older adults.

A 2015 systematic review sought to determine which type of exercise intervention (resistance, coordination, or multimodal training) would be most effective in preserving gait speed in healthy older adults (N = 2495; mean age = 74.2 years).²⁵ While the 42 included studies were deemed to be fairly low quality, the review revealed (with large effect size [0.84]) that a number of exercise modalities might stave off loss of gait speed in older adults. Patients in the resistance training group had the greatest improvement in gait speed (0.11 m/s), followed by those in the coordination training group (0.09 m/s) and the multimodal training group (0.05 m/s).²⁵

Individuals who had maintained higher physical activity levels throughout adulthood had less physical functional decline and reduced rates of mobility disability and premature death.

Finally, muscle mass and strength offer a measure of physical performance and functionality. A 2020 systematic review of 83 studies (N = 108,428) showed that low muscle mass and strength, reduced handgrip strength, and lower physical performance were predictive of reduced capacities in activities of daily living and instrumental activities of daily living.²⁶ It is important to counsel adults to remain active throughout their lives and to include resistance training to maintain muscle mass and strength to preserve their motor function, mobility, independence, and QOL.

Use 1 of these scales to identify frailty. Frailty is a distinct clinical syndrome, in which an individual has low reserves and is highly vulnerable to internal and external stressors. It affects many community-­dwelling older adults. Within the literature, there has been ongoing discussion regarding the definition of frailty²⁷ (TABLE 1^28-31).

Continue to: The Fried Frailty Index...

 

The Fried Frailty Index defines frailty as a purely physical condition; patients need to exhibit 3 of 5 components (ie, weight loss, exhaustion, weakness, slowness, and low physical activity) to be deemed frail.³¹ The Edmonton Frail Scale is commonly used in geriatric assessments and counts impairments across several domains including physical activity, mood, cognition, and incontinence.^30,32,33 Physicians need to complete a training course prior to its use. Finally, the definition of frailty used by Rockwood et al^{28, 29} was used to develop the Clinical Frailty Scale, which relies on broader criteria that include social and psychological elements in addition to physical elements.The Clinical Frailty Scale uses clinician judgment to evaluate patient-specific domains (eg, comorbidities, functionality, and cognition) and to generate a score ranging from 1 (very fit) to 9 (terminally ill).²⁹ This scale is accessible and easy to implement. As a result, use of this scale has increased during the COVID-19 pandemic. All definitions include a pre-frail state, indicating the dynamic nature of frailty over time.

It is important to identify pre-frail and frail older adults using 1 of these screening tools. Interventions to reverse frailty that can be initiated in the primary care setting include identifying treatable medical conditions, assessing medication appropriateness, providing nutritional advice, and developing an exercise plan.³⁴

Conduct a nutritional assessment; consider this diet. Studies show that nutritional status can predict physical function and frailty risk in older adults. A 2017 systematic review of 19 studies (N = 22,270) of frail adults ages ≥ 65 years found associations related to specific dietary constructs (ie, micronutrients, macronutrients, antioxidants, overall diet quality, and timing of consumption).³⁵ Plant-based diets with higher levels of micronutrients, such as vitamins C and E and beta-carotene, or diets with more protein or macronutrients, regardless of source foods, all resulted in inverse associations with frailty syndrome.³⁵

A 2017 study showed that physical exercise and maintaining good nutritional status may be effective for preventing frailty in ­community-dwelling pre-frail older individuals.³⁶ A 2019 study showed that a combination of muscle strength training and protein supplementation was the most effective intervention to delay or reverse frailty and was easiest to implement in primary care.³⁷ A 2020 meta-analysis of 31 studies (N = 4794) addressing frailty among primary care patients > 60 years showed that interventions using predominantly resistance-based exercise and nutrition supplementation improved frailty status over the control.³⁸ Researchers also found that a comprehensive geriatric assessment or exercise—alone or in combination with nutrition education—reduced physical frailty.

Mentation

Screen and treat cognitive impairments. Cognitive function and autonomy in ­decision-making are important factors in healthy aging. Aspects of mental health (eg, depression and anxiety), sensory impairment (eg, visual and auditory impairment), and mentation issues (eg, delirium, dementia, and related conditions), as well as diet, physical exercise, and mobility, can all impede cognitive functionality. The long-term effects of depression, anxiety,³⁹ sensory deficits,⁴⁰ mobility,⁴¹ diet,⁴² and, ultimately, aging may impact Alzheimer disease (AD). The risk of an AD diagnosis increases with age.³⁹

Continue to: A 2018 prospective cohort study...

 

A 2018 prospective cohort study using data from the National Alzheimer’s Coordinating Center followed individuals (N = 12,053) who were cognitively asymptomatic at their initial visits to determine who developed clinical signs of AD.³⁹ Survival analysis showed several psychosocial factors—anxiety, sleep disturbances, and depressive episodes of any type (occurring within the past 2 years, clinician verified, lifetime report)—were significantly associated with an eventual AD diagnosis and increased the risk of AD.³⁹ More research is needed to verify the impact of early intervention for these conditions on neurodegenerative disease; however, screening and treating psychosocial factors such as anxiety and depression should be maintained.

For patients ages ≥ 65 years, it is recommended that eye examinations occur every 1 to 2 years.

Researchers evaluated the impact of a dual sensory impairment (DSI) on dementia risk using data from 2051 participants in the Ginkgo Evaluation of Memory Study.⁴⁰ Hearing and visual impairments (defined as DSI when these conditions coexist) or visual impairment alone were significantly associated with increased risk of dementia in older adults. The researchers reported that DSI was significantly associated with a higher risk of all-cause dementia (hazard ratio [HR] = 1.86; 95% CI, 1.25-2.76) and AD (HR = 2.12; 95% CI, 1.34-3.36).⁴⁰ Visual impairment alone was associated with an increased risk of all-cause dementia (HR = 1.32; 95% CI, 1.02-1.71).⁴⁰ These results suggest that screening of DSI or visual impairment earlier in the patient’s lifespan may identify those at high risk of dementia in older adulthood.

The American Academy of Ophthalmology recommends patients with healthy eyes be screened once during their 20s and twice in their 30s; a full examination is recommended by age 40. For patients ages ≥ 65 years, it is recommended that eye examinations occur every 1 to 2 years.⁴³

Diet and mobility play a big role in cognition. Diet⁴³ and exercise^41,42,44 are believed to have an impact on mentation, and recent studies show memory and global cognition could be malleable later in life. A 2015 meta-analysis of 490 treatment arms of 24 randomized controlled studies showed improvement in global cognition with consumption of a Mediterranean diet plus olive oil (effect size [ES] standardized mean difference [SMD] = 0.22; 95% CI, 0.16-0.27) and tai chi exercises (ES SMD = 0.18; 95% CI, 0.06-0.29).⁴² The analysis also found improved memory among participants who consumed the Mediterranean diet/olive oil combination (ES SMD = 0.22; 95% CI, 0.12-0.32) and soy isoflavone supplements (ES SMD = 0.11; 95% CI, 0.04-0.17). Although the ESs are small, they are significant and offer promising evidence that individual choices related to nutrition or exercise may influence cognition and memory.

A 2018 systematic review found that all domains of cognition showed improvement with 45 to 60 minutes of moderate-to-vigorous physical exercise.⁴⁴ Attention, executive function, memory, and working memory showed significant increases, whereas global cognition improvements were not statistically significant.⁴⁴ A 2016 meta-analysis of 26 studies (N = 26,355) found a positive association between an objective mobility measure (gait, lower-extremity function, and balance) and cognitive function (global, executive function, memory, and processing speed) in older adults.⁴¹ These results highlight that diet, mobility, and physical exercise impact cognitive functioning.

Continue to: Maintaining social connections

 

Maintaining social connections

Social isolation and loneliness—compounded by a pandemic. The US Department of Health and Human Services notes that “community connections” are among the key factors required for healthy aging.³ Similarly, the WHO definition of healthy aging considers whether individuals can build and sustain relationships with other people and find ways to engender their personal values through these connections.²

Prioritizing interventions that identify and connect isolated older adults to social support may increase survivability.

As people age, their social connections often decrease due to the death of friends and family, shifts in living arrangements, loss of mobility or eyesight (and thus self-­transport), and the onset or increased acuity of illness or chronic conditions.⁴⁵ This has been exacerbated by the COVID-19 pandemic, which has spurred shelter-in-place and stay-at-home orders along with recommendations for physical distancing (also known as social distancing), especially for older adults who are at higher risk.⁴⁶ Smith et al⁴⁷ calls this the COVID-19 Social Connectivity Paradox, in which older adults limit their interactions with others to protect their physical health and reduce their risk of contracting the virus, but as a result they may undermine their psychosocial health by placing themselves at risk of social isolation and loneliness.⁴⁷

The double threat. Social isolation and loneliness have been shown to negatively impact physical health and well-being, resulting in an increased risk of early death^48-50; higher likelihood of specific diagnoses, including dementia and cardiovascular conditions^48,50; and more frequent use of health care services.⁵⁰ These concepts, while related, represent different mechanisms for negative health outcomes. Social isolation is an objective condition when one has a lack of opportunities for interaction with other people; loneliness refers to the emotional disconnect one feels when separated from others. Few studies have compared outcomes between these concepts, but in those that have, social isolation appears to be more strongly associated with early death.^48-50

A 2013 observational study using data from the English Longitudinal Study on Aging found that both social isolation and loneliness were associated with increased mortality among men and women ages ≥ 52 years (N = 6500).⁴⁸ However, when studied independently, loneliness was not found to be a significant risk factor. In contrast, social isolation significantly impacted mortality risk, even after adjusting for demographic factors and baseline health status.⁴⁸ These findings are supported by a 2018 cohort study of individuals (N = 479,054) with a history of an acute cardiovascular event that concluded social isolation was a predictor of mortality, whereas loneliness was not.⁵⁰

A large 2015 meta-analysis (70 studies, N = 3,407,134) of mortality causes among community-dwelling older adults (average age, 66) confirmed that both objective measures of isolation, as well as subjective measures (such as feelings of loneliness or living alone), have a significant predictive effect in longer-term studies. Each measure shows an approximately 30% increase in the likelihood of death after an average of 7 years.⁴⁹

Continue to: Health care remains a connection point

 

Health care remains a connection point. Even when life course events and conditions (eg, death of loved ones, loss of transportation or financial resources, or disengagement from community activities) reduce social connections, most older adults engage in some way with the health care system. A 2020 consensus report by the National Academies of Sciences, Engineering, and Medicine suggests health care professionals capitalize on these connection points with adults ages ≥ 50 years by periodically screening for social isolation and loneliness, documenting social status updates in medical records, and piloting and evaluating interventions in the clinical setting.⁵¹

The report offered information about potential avenues for intervention by primary care professionals beyond screening, such as participating in research studies that investigate screening tools and multisystem interventions; social prescribing (linking patients to embedded social work services or ­community-based organizations); referring patients to support groups; initiating ­cognitive-based therapy or other behavioral health interventions; or recommending mindfulness practices.⁵¹ However, most of the cited intervention studies were not specific to primary care settings and contained poor-quality evidence related to efficacy.

Isolation creates a greater reliance on health services due to a lack of a social support system, while a feeling of emotional disconnection (loneliness) seems to be a barrier to accessing care. A 2017 cohort study linking data from the Health and Retirement Study and Medicare claims revealed that social isolation predicts higher annual health expenditures (> $1600 per beneficiary) driven by hospitalization and skilled nursing facility usage, along with greater mortality, whereas individuals who are lonely result in reduced costs (a reduction of $770 annually) due to lower usage of inpatient and outpatient services.⁵² Prioritizing interventions that identify and connect isolated older adults to social support, therefore, may increase survivability by ensuring they have access to resources and health care interventions when needed.

Assessing and treating vision and hearing impairments and mental health issues may guard against losses in cognition.

In addition, these findings underscore the importance of looking at quality—not just quantity—of older adults’ social connections. A number of validated screening tools exist for social isolation and loneliness (TABLE 2^53-59); however, concerns exist about assessing risk using a unidimensional tool for a complex concern,⁴⁷ as well as identifying a problem without having evidence-based interventions to offer as solutions.^47,51 Until future studies resolve these concerns, leveraging the physician-patient relationship to broach these difficult subjects may help normalize the issues and create safe spaces to identify individuals who are at risk.

QOL is key to healthy aging. As Kusumastuti et al⁴ state, “successful ageing lies in the eyes of the beholder.” A 2019 systematic review of 48 qualitative studies revealed that community-dwelling older adults ages ≥ 50 years in 11 countries (N > 4175) perceive well-being by considering QOL within 9 domains: health perception, autonomy, role and activity, relationships, emotional comfort, attitude and adaptation, spirituality, financial security, and home and neighborhood.⁶⁰ Researchers found that as engagement in any one of these domains declines, older adults may shift their definition of health toward their remaining abilities.⁶⁰ This offers an explanation as to why patients might rate their health status much higher than their physicians do: older adults tend to have a more holistic concept of health.

Continue to: Take a multidimensional approach to healthy aging

 

Take a multidimensional approach to healthy aging

Although we have separately examined each of the 4 components of managing healthy aging in a community-dwelling adult, applying a multidimensional approach is most effective. Increasing use of the Medicare AWV provides an opportunity to assess patient health status, determine care preferences, and improve follow-through on preventive screening. It is also important to encourage older adults to engage in regular physical activity—especially muscle-strengthening exercises—and to discuss nutrition and caloric intake to prevent frailty and functional decline.

Assessing and treating vision and hearing impairments and mental health issues, including anxiety and depression, may guard against losses in cognition. When speaking with older adult patients about their social connections, consider asking not only about frequency of contact and access to resources such as food and transportation, but also about whether they are finding ways to bring their own values into those relationships to bolster their QOL. This guidance also may be useful for primary care practices and health care networks when planning future quality-improvement initiatives.

Additional research is needed to support the evidence base for aligning older adult preferences in health care interventions, such as preventive screenings. Also, clinical decision-making requires more clarity about the efficacy of specific diet and exercise interventions for older adults; the impact of early intervention for depression, anxiety, and sleep disorders on neurodegenerative disease; whether loneliness predicts mortality; and how health care delivery systems can be effective at building social connectivity.

Initiating health education, screening, and prevention throughout the patient’s lifespan can promote healthy aging outcomes later in life.

For now, it is essential to recognize that initiating health education, screening, and prevention throughout the patient’s lifespan can promote healthy aging outcomes. As family physicians, it is important to capitalize on longitudinal relationships with patients and begin educating younger patients using this multidimensional framework to promote living “a productive and meaningful life”at any age.³

CORRESPONDENCE

Lynn M. Wilson, DO, 707 Hamilton Street, 8th floor, Department of Family Medicine, Lehigh Valley Health Network, Allentown, PA 18101; [email protected]

CASE

A 55-year-old right-hand-dominant woman presented to the clinic with a chief complaint of right ring finger pain and stiffness. There was no history of trauma or prior surgery. She had no tingling or numbness. She had a history of type 2 diabetes that was well controlled. She worked as a clerk for a government office for many years, and her painful, limited finger motion interfered with keyboarding and picking up items. Physical examination revealed tenderness to palpation over the palmar aspect of the metacarpophalangeal joint (MCPJ) of the ring finger with no other joint tenderness or swelling. When she made a fist, her ring finger MCPJ, proximal interphalangeal joint (PIPJ), and distal interphalangeal joint (DIPJ) locked in a flexed position that required manipulation to extend the finger. A firm mass was palpated in the palm with finger flexion that moved into the finger with extension.

Stenosing tenosynovitis, also known as trigger finger (TF), is an inflammatory condition that causes pain in the distal palm and proximal digit with associated limited motion. The most commonly affected digits are the middle and ring fingers of the dominant hand.¹ The disorder is particularly noticeable when it inhibits day-to-day functioning.

TF affects 2% to 3% of the general population and up to 20% of patients with diabetes.^2,3 Patient age and duration of diabetes are commonly cited as contributing factors, although the effect of well-controlled blood glucose and A1C on the frequency and cure rate of TF has not been established.^3,4 TF is most commonly seen in individuals ages 40 to 60 years, with a 6 times’ greater frequency in females than males.⁵

In the United States, there are an estimated 200,000 cases of TF each year, with initial presentation typically being to a primary care physician.⁶ For this reason, it is essential for primary care physicians to recognize this common pathology and treat symptoms early to prevent progression and the need for surgical intervention.

An impaired gliding motion of the flexor tendons

In each finger, a tendon sheath, consisting of 5 annular pulleys and 3 cruciate pulleys, forms a tunnel around the flexor digitorum profundus (FDP) and flexor digitorum superficialis (FDS). The tendon sheath allows for maximum force by eliminating bowstringing of the tendons when the digit is flexed. Deep to the tendons and surrounding the tendons is a synovial membrane that provides nutrition and reduces friction between the tendons and the tendon sheath.⁷

Trigger finger affects 2% to 3% of the general population and up to 20% of patients with diabetes.

The FDP is longer and assists in flexion of the MCPJ and the PIPJ. It is the sole flexor of the DIPJ. The shorter FDS assists in flexion of the MCPJ and is the primary flexor of the PIPJ. The bifurcation of the shorter FDS tendon allows the longer FDP tendon to pass through to continue to its insertion on the distal phalanx.

In the thumb, the flexor pollicis longus (FPL) is the only flexor within its tendon sheath. The FPL assists in flexion of the MCPJ and flexes the thumb interphalangeal joint (IPJ). The intrinsic muscles (lumbricals and interossei) do not extend into the tendon sheath and do not contribute to TF.

Continue to: TF occurs when

 

TF occurs when the tendon sheath, most commonly at the first annular pulley (A1), or the flexor tendons thicken due to fibrocartilaginous metaplasia. This results in impaired gliding motion of the flexor tendons.⁸ The stenosed A1 pulley can lead to pinching of the flexor tendons and cause the formation of a nodule on the FDS tendon at its bifurcation.⁹ The nodule of the FDS bifurcation moves proximal to the A1 pulley when the finger is flexed. Upon extension, the tendon nodule may get caught on the A1 pulley. This prevents smooth extension and is the source of pain and triggering (FIGURE 1). In a similar manner, thumb triggering is the result of a stenosed A1 pulley creating a nodule on the FPL tendon, which prevents smooth gliding of the FPL.

What you’ll see

TF is characterized by locking, popping, or clicking at the base of the finger or thumb.^7,10 A small nodule may be palpated on the palmar aspect of the MCPJ when the finger is flexed. This nodule will then move distally when the finger is extended. Patients will present with the affected digit in a flexed position and will have difficulty extending the digit. In some cases, the patient may have to use the other hand to straighten the affected digit. In more severe cases, the digit may be fixed in a position of flexion or extension. The severity of triggering is commonly graded by the Green’s classification system (see TABLE¹¹).

Is it Dupuytren contracture, trigger finger, or something else?

The differential diagnosis for TF includes Dupuytren contracture, MCPJ sprain, calcific peritendinitis, flexor tenosynovitis, diabetic cheiroarthropathy (DCA), rheumatoid arthritis (RA), osteoarthritis (OA), and crystalline arthropathy (gout).⁵

Dupuytren contracture is usually nonpainful and manifests with a palpable cord in the palm and a fixed flexion contracture that has progressed over time, with no history of catching.

MCPJ sprain is diagnosed with tenderness of the MCPJ and a history of trauma.

Continue to: Calcific peritendinitis

 

Calcific peritendinitis is characterized by pain, tenderness, and edema near a joint with calcified deposits seen on radiographs.

Flexor tenosynovitis manifests with fusiform swelling of the digit, tenderness over the flexor tendon sheath, and pain with passive extension of the digit; it is more commonly associated with RA.

DCA, RA, OA, and gout usually affect more than 1 digit. DCA is associated with both type 1 and type 2 diabetes and is characterized by thickened, waxy skin and painless, limited extension of the digits. RA and OA are diagnosed by medical history, lab work, and radiographs. Gout is diagnosed with lab work and aspiration of joint fluid.

Trigger finger occurs when the tendon sheath or the flexor tendons thicken due to fibrocartilaginous metaplasia.

A thorough history, physical exam, and review of radiographs must be performed to rule out these other disorders. Once the diagnosis of TF is made, available treatment options should be pursued.

Treatment: A conservative or surgical approach?

Current treatment options include both nonsurgical (conservative) and surgical interventions. Nonsurgical interventions include activity modification, splinting, and corticosteroid injections. While nonsteroidal anti-inflammatory drugs are commonly recommended to resolve the local inflammation secondary to triggering, there is no scientific evidence to support their use at this time.⁷ Surgical interventions, utilized in more severe cases or after conservative treatment has failed, include percutaneous and open release of the tendon sheath.^2,7

Continue to: Conservative treatments

 

 

Conservative treatments

Splinting is only an option for digits that retain flexibility (Green’s classification grades I, II, and III). The goal of splinting is to keep the affected digit in extension to avoid repeated friction between the tendon and the tendon sheath.¹² This ideally allows any cartilaginous metaplasia or inflammation to resolve, subsequently alleviating symptoms. The recommended length of treatment with splinting ranges from 3 to 12 weeks, with an average of 6 weeks.¹

Multiple studies have shown long-term alleviation of symptoms with the use of orthotic devices. A retrospective analysis found that 87% of patients who wore their PIPJ orthotic device both day and night for a minimum of 6 weeks required no further treatment at 1-year follow-up.¹³ In contrast, MCPJ splinting only at night has been shown to resolve symptoms in just 55% of patients after 6 weeks.¹⁴ From a practical standpoint, however, patients are more likely to be compliant with night-only splinting, making it a reasonable option. Splinting does remain efficacious for patients even after 6 months of symptomatology.¹⁵

Day and night splinting for approximately 8 weeks using a PIPJ orthotic could be considered as an effective first-line intervention.¹⁶ Notably, PIPJ splinting is more functional, as it allows motion of the MCPJ and DIPJ. There are several options available for PIPJ splints, including a stiff cushioned sleeve, a prefabricated plastic splint, and a large adhesive bandage.

An adjunct treatment to splinting is tendon-gliding exercises, including passive IPJ flexion, full finger flexion and extension, and hooking.¹³ Patients may remove the orthotic device to perform these exercises 3 times a day for 5 repetitions, as well as for activities that are not conducive to splinting.¹³

Corticosteroid injections. Injections of a corticosteroid and 1% lidocaine in a 1:1 mixture for a total volume of 1 cc can be inserted into the tendon sheath, A1 pulley, or adjacent tissue.¹⁷ Steroid injections help to decrease inflammation and pain in the affected area, giving symptom relief lasting a few months in as many as 57% to 87% of patients.¹⁸

Continue to: While the location of the injection...

 

While the location of the injection has been debated, recent literature suggests that symptoms can be effectively alleviated regardless of the specific anatomic injection site, such as intra-sheath or extra-sheath (FIGURE 2).¹⁹ This allows flexibility for the clinician, as the injection does not have to be placed within the tendon sheath. Corticosteroids should not be injected into the tendon itself, and the needle tip should be slightly withdrawn if there is resistance while injecting. Patients who are averse to injections have been shown to benefit from needle-free jet lidocaine (J-tip) administration prior to the actual steroid injection.²⁰

A randomized controlled trial comparing dexamethasone to triamcinolone injections found no difference in outcome at the 3-month follow-up (n = 84).¹⁷ This may suggest that the choice of corticosteroid is at the clinician’s discretion. In terms of long-term efficacy of steroid injections, it has been shown that 70% of trigger digits had complete resolution of symptoms at a mean follow-up of 8 years after just 1 injection (n = 43).²¹

Some patients, though, may require additional corticosteroid injections to maintain symptom control. If multiple injections are performed, they should not be given in intervals shorter than 4 months between treatments.⁵ Furthermore, steroids can be administered safely up to 3 times in the same digit before surgery is recommended.²²

A patient’s options should be reconsidered if efficacy is not demonstrated with prior injections. Notably, a lower success rate has been shown in patients with type 2 diabetes (66%) compared to those without diabetes (90%).^4,23 This difference in success rates is not well understood, as there is no causal relationship between well-controlled diabetes and TF.⁴ Complications of corticosteroid injections include local pain, fat atrophy, and hypopigmentation at the site of the injection, as well as short-term elevations in blood glucose levels in patients with diabetes.^5,24

Surgical correction (to be discussed) remains superior to steroid injections in terms of cure rate and resolution of symptoms. A randomized controlled trial (n = 165) found that an injection-only group reported 86% and 49% success at 3-month and 12-month follow-up, respectively, compared to 99% success at both 3- and 12-month follow-up for the surgical group. Further, at 12-month follow-up, the median pain scores were significantly higher in the injection group (3; range, 1-9) than in the surgery group (1; range, 1-7).²⁵ If conservative treatment modalities lead to unresolved symptoms or recurrence, referral to a hand specialist for surgery is recommended.

Continue to: Surgical treatments in an office setting

 

Surgical treatments in an office setting

Procedures for TF can be safely performed under conscious sedation or local anesthesia, with or without a tourniquet.²⁶ Wide-awake procedures with local anesthesia and no tourniquet (WALANT) can be performed in an office-based procedure room rather than the operating room. This increases efficiency for the surgeon, reduces the amount of preparation and recovery time for the patient, and helps to keep costs down.

Percutaneous release involves the insertion of a 16-gauge hypodermic needle into the affected A1 pulley. The needle is used to fray and disrupt the pulley by moving the needle tip over the fibrotic A1 pulley.

While NSAIDs are commonly recommended to resolve the local inflammation secondary to triggering, there is no scientific evidence to support their use.

However, it is not without possible complications.²⁷ Inadvertent A2 pulley damage is particularly troublesome, as it leads to “bowstringing” or protrusion of the flexor tendon into the palm upon flexion. This can cause pain and failure to fully extend or flex the finger.¹⁰ Because the anatomy is not well visualized during the percutaneous approach, incomplete release, neurovascular injury, and iatrogenic injury to the A2 pulley or deep tendon may occur.²⁸ Ultrasound-guided percutaneous release techniques have shown effective clinical outcomes with minimal complications compared to nonguided percutaneous release techniques.^29,30

Open release is the gold standard surgical treatment for trigger finger (FIGURE 3). A small incision (1-2 cm) is made directly over or proximal to the A1 pulley in the distal palmar crease at the base of the affected digit. After blunt dissection through the subcutaneous tissue, the A1 pulley is sharply incised. An open approach has the clear benefit of avoiding the digital neurovascular bundles, as well as visualizing the resolution of triggering upon flexion and extension prior to closure. The WALANT procedure has the advantage of allowing the awake patient to actively flex and extend the digit to determine if the A1 release has been successful prior to closure of the incision.

Outcomes and complications of surgery. A recent systematic review and meta-analysis has shown percutaneous techniques to be successful in 94% of cases.²⁷ The success rate of open surgery has been reported at 99% to 100% at varying follow-up intervals up to 1 year.^25,30,31 The complication rate for percutaneous release (guided and nonguided) was calculated at 2.2% (n = 2114).²⁷ In another study, the overall complication rate of open releases was calculated at 1% (n = 999).³² When comparing percutaneous release (guided and nonguided) and open release, a meta-analysis found no significant difference in complication rate (RR = 0.84) or failure rate (RR = 0.94).³²

Continue to: Several risk factors...

 

Several risk factors have been associated with postoperative surgical infection, including recent steroid injection (< 80 d), smoking status, increasing age, and pre-operative use of lidocaine with epinephrine.³³ Open release has been shown to be an effective and safe treatment modality for patients with and without diabetes alike.³⁴ Overall, definitive surgical correction has been demonstrated to be superior to conservative measures due to a significantly lower rate of recurrence.³⁵

CASE

Given the patient’s presentation with triggering of the digit, tenderness over the A1 pulley, and lack of trauma history, we diagnosed trigger finger in this patient. Potential treatments included splinting, corticosteroid injections, and surgery. After discussion of the risks and benefits of each treatment option, the patient elected to undergo a corticosteroid injection. She was also given a neoprene finger sleeve to wear every night, and in the daytime when possible.

At 12-week follow-up, she noted early improvement in her triggering, which had since recurred. Due to her history of diabetes, the patient was then referred for surgery. She had an open release under local anesthesia. The surgery was uncomplicated, and the abnormality was corrected. At the patient’s 1-year postoperative follow-up visit, there was no evidence of recurrence, and she had regained full active and passive range of motion of her finger.

Acknowledgements
The authors wish to thank Jose Borrero, MD, for contributing his time and creative talents to produce the illustrations in this article.

CORRESPONDENCE
Evan P. Johnson, MD; 506 South Greer Street, Memphis, TN 38111; [email protected]

CASE

A 55-year-old right-hand-dominant woman presented to the clinic with a chief complaint of right ring finger pain and stiffness. There was no history of trauma or prior surgery. She had no tingling or numbness. She had a history of type 2 diabetes that was well controlled. She worked as a clerk for a government office for many years, and her painful, limited finger motion interfered with keyboarding and picking up items. Physical examination revealed tenderness to palpation over the palmar aspect of the metacarpophalangeal joint (MCPJ) of the ring finger with no other joint tenderness or swelling. When she made a fist, her ring finger MCPJ, proximal interphalangeal joint (PIPJ), and distal interphalangeal joint (DIPJ) locked in a flexed position that required manipulation to extend the finger. A firm mass was palpated in the palm with finger flexion that moved into the finger with extension.

Stenosing tenosynovitis, also known as trigger finger (TF), is an inflammatory condition that causes pain in the distal palm and proximal digit with associated limited motion. The most commonly affected digits are the middle and ring fingers of the dominant hand.¹ The disorder is particularly noticeable when it inhibits day-to-day functioning.

TF affects 2% to 3% of the general population and up to 20% of patients with diabetes.^2,3 Patient age and duration of diabetes are commonly cited as contributing factors, although the effect of well-controlled blood glucose and A1C on the frequency and cure rate of TF has not been established.^3,4 TF is most commonly seen in individuals ages 40 to 60 years, with a 6 times’ greater frequency in females than males.⁵

In the United States, there are an estimated 200,000 cases of TF each year, with initial presentation typically being to a primary care physician.⁶ For this reason, it is essential for primary care physicians to recognize this common pathology and treat symptoms early to prevent progression and the need for surgical intervention.

An impaired gliding motion of the flexor tendons

In each finger, a tendon sheath, consisting of 5 annular pulleys and 3 cruciate pulleys, forms a tunnel around the flexor digitorum profundus (FDP) and flexor digitorum superficialis (FDS). The tendon sheath allows for maximum force by eliminating bowstringing of the tendons when the digit is flexed. Deep to the tendons and surrounding the tendons is a synovial membrane that provides nutrition and reduces friction between the tendons and the tendon sheath.⁷

Trigger finger affects 2% to 3% of the general population and up to 20% of patients with diabetes.

The FDP is longer and assists in flexion of the MCPJ and the PIPJ. It is the sole flexor of the DIPJ. The shorter FDS assists in flexion of the MCPJ and is the primary flexor of the PIPJ. The bifurcation of the shorter FDS tendon allows the longer FDP tendon to pass through to continue to its insertion on the distal phalanx.

In the thumb, the flexor pollicis longus (FPL) is the only flexor within its tendon sheath. The FPL assists in flexion of the MCPJ and flexes the thumb interphalangeal joint (IPJ). The intrinsic muscles (lumbricals and interossei) do not extend into the tendon sheath and do not contribute to TF.

Continue to: TF occurs when

 

TF occurs when the tendon sheath, most commonly at the first annular pulley (A1), or the flexor tendons thicken due to fibrocartilaginous metaplasia. This results in impaired gliding motion of the flexor tendons.⁸ The stenosed A1 pulley can lead to pinching of the flexor tendons and cause the formation of a nodule on the FDS tendon at its bifurcation.⁹ The nodule of the FDS bifurcation moves proximal to the A1 pulley when the finger is flexed. Upon extension, the tendon nodule may get caught on the A1 pulley. This prevents smooth extension and is the source of pain and triggering (FIGURE 1). In a similar manner, thumb triggering is the result of a stenosed A1 pulley creating a nodule on the FPL tendon, which prevents smooth gliding of the FPL.

What you’ll see

TF is characterized by locking, popping, or clicking at the base of the finger or thumb.^7,10 A small nodule may be palpated on the palmar aspect of the MCPJ when the finger is flexed. This nodule will then move distally when the finger is extended. Patients will present with the affected digit in a flexed position and will have difficulty extending the digit. In some cases, the patient may have to use the other hand to straighten the affected digit. In more severe cases, the digit may be fixed in a position of flexion or extension. The severity of triggering is commonly graded by the Green’s classification system (see TABLE¹¹).

Is it Dupuytren contracture, trigger finger, or something else?

The differential diagnosis for TF includes Dupuytren contracture, MCPJ sprain, calcific peritendinitis, flexor tenosynovitis, diabetic cheiroarthropathy (DCA), rheumatoid arthritis (RA), osteoarthritis (OA), and crystalline arthropathy (gout).⁵

Dupuytren contracture is usually nonpainful and manifests with a palpable cord in the palm and a fixed flexion contracture that has progressed over time, with no history of catching.

MCPJ sprain is diagnosed with tenderness of the MCPJ and a history of trauma.

Continue to: Calcific peritendinitis

 

Calcific peritendinitis is characterized by pain, tenderness, and edema near a joint with calcified deposits seen on radiographs.

Flexor tenosynovitis manifests with fusiform swelling of the digit, tenderness over the flexor tendon sheath, and pain with passive extension of the digit; it is more commonly associated with RA.

DCA, RA, OA, and gout usually affect more than 1 digit. DCA is associated with both type 1 and type 2 diabetes and is characterized by thickened, waxy skin and painless, limited extension of the digits. RA and OA are diagnosed by medical history, lab work, and radiographs. Gout is diagnosed with lab work and aspiration of joint fluid.

Trigger finger occurs when the tendon sheath or the flexor tendons thicken due to fibrocartilaginous metaplasia.

A thorough history, physical exam, and review of radiographs must be performed to rule out these other disorders. Once the diagnosis of TF is made, available treatment options should be pursued.

Treatment: A conservative or surgical approach?

Current treatment options include both nonsurgical (conservative) and surgical interventions. Nonsurgical interventions include activity modification, splinting, and corticosteroid injections. While nonsteroidal anti-inflammatory drugs are commonly recommended to resolve the local inflammation secondary to triggering, there is no scientific evidence to support their use at this time.⁷ Surgical interventions, utilized in more severe cases or after conservative treatment has failed, include percutaneous and open release of the tendon sheath.^2,7

Continue to: Conservative treatments

 

 

Conservative treatments

Splinting is only an option for digits that retain flexibility (Green’s classification grades I, II, and III). The goal of splinting is to keep the affected digit in extension to avoid repeated friction between the tendon and the tendon sheath.¹² This ideally allows any cartilaginous metaplasia or inflammation to resolve, subsequently alleviating symptoms. The recommended length of treatment with splinting ranges from 3 to 12 weeks, with an average of 6 weeks.¹

Multiple studies have shown long-term alleviation of symptoms with the use of orthotic devices. A retrospective analysis found that 87% of patients who wore their PIPJ orthotic device both day and night for a minimum of 6 weeks required no further treatment at 1-year follow-up.¹³ In contrast, MCPJ splinting only at night has been shown to resolve symptoms in just 55% of patients after 6 weeks.¹⁴ From a practical standpoint, however, patients are more likely to be compliant with night-only splinting, making it a reasonable option. Splinting does remain efficacious for patients even after 6 months of symptomatology.¹⁵

Day and night splinting for approximately 8 weeks using a PIPJ orthotic could be considered as an effective first-line intervention.¹⁶ Notably, PIPJ splinting is more functional, as it allows motion of the MCPJ and DIPJ. There are several options available for PIPJ splints, including a stiff cushioned sleeve, a prefabricated plastic splint, and a large adhesive bandage.

An adjunct treatment to splinting is tendon-gliding exercises, including passive IPJ flexion, full finger flexion and extension, and hooking.¹³ Patients may remove the orthotic device to perform these exercises 3 times a day for 5 repetitions, as well as for activities that are not conducive to splinting.¹³

Corticosteroid injections. Injections of a corticosteroid and 1% lidocaine in a 1:1 mixture for a total volume of 1 cc can be inserted into the tendon sheath, A1 pulley, or adjacent tissue.¹⁷ Steroid injections help to decrease inflammation and pain in the affected area, giving symptom relief lasting a few months in as many as 57% to 87% of patients.¹⁸

Continue to: While the location of the injection...

 

While the location of the injection has been debated, recent literature suggests that symptoms can be effectively alleviated regardless of the specific anatomic injection site, such as intra-sheath or extra-sheath (FIGURE 2).¹⁹ This allows flexibility for the clinician, as the injection does not have to be placed within the tendon sheath. Corticosteroids should not be injected into the tendon itself, and the needle tip should be slightly withdrawn if there is resistance while injecting. Patients who are averse to injections have been shown to benefit from needle-free jet lidocaine (J-tip) administration prior to the actual steroid injection.²⁰

A randomized controlled trial comparing dexamethasone to triamcinolone injections found no difference in outcome at the 3-month follow-up (n = 84).¹⁷ This may suggest that the choice of corticosteroid is at the clinician’s discretion. In terms of long-term efficacy of steroid injections, it has been shown that 70% of trigger digits had complete resolution of symptoms at a mean follow-up of 8 years after just 1 injection (n = 43).²¹

Some patients, though, may require additional corticosteroid injections to maintain symptom control. If multiple injections are performed, they should not be given in intervals shorter than 4 months between treatments.⁵ Furthermore, steroids can be administered safely up to 3 times in the same digit before surgery is recommended.²²

A patient’s options should be reconsidered if efficacy is not demonstrated with prior injections. Notably, a lower success rate has been shown in patients with type 2 diabetes (66%) compared to those without diabetes (90%).^4,23 This difference in success rates is not well understood, as there is no causal relationship between well-controlled diabetes and TF.⁴ Complications of corticosteroid injections include local pain, fat atrophy, and hypopigmentation at the site of the injection, as well as short-term elevations in blood glucose levels in patients with diabetes.^5,24

Surgical correction (to be discussed) remains superior to steroid injections in terms of cure rate and resolution of symptoms. A randomized controlled trial (n = 165) found that an injection-only group reported 86% and 49% success at 3-month and 12-month follow-up, respectively, compared to 99% success at both 3- and 12-month follow-up for the surgical group. Further, at 12-month follow-up, the median pain scores were significantly higher in the injection group (3; range, 1-9) than in the surgery group (1; range, 1-7).²⁵ If conservative treatment modalities lead to unresolved symptoms or recurrence, referral to a hand specialist for surgery is recommended.

Continue to: Surgical treatments in an office setting

 

Surgical treatments in an office setting

Procedures for TF can be safely performed under conscious sedation or local anesthesia, with or without a tourniquet.²⁶ Wide-awake procedures with local anesthesia and no tourniquet (WALANT) can be performed in an office-based procedure room rather than the operating room. This increases efficiency for the surgeon, reduces the amount of preparation and recovery time for the patient, and helps to keep costs down.

Percutaneous release involves the insertion of a 16-gauge hypodermic needle into the affected A1 pulley. The needle is used to fray and disrupt the pulley by moving the needle tip over the fibrotic A1 pulley.

While NSAIDs are commonly recommended to resolve the local inflammation secondary to triggering, there is no scientific evidence to support their use.

However, it is not without possible complications.²⁷ Inadvertent A2 pulley damage is particularly troublesome, as it leads to “bowstringing” or protrusion of the flexor tendon into the palm upon flexion. This can cause pain and failure to fully extend or flex the finger.¹⁰ Because the anatomy is not well visualized during the percutaneous approach, incomplete release, neurovascular injury, and iatrogenic injury to the A2 pulley or deep tendon may occur.²⁸ Ultrasound-guided percutaneous release techniques have shown effective clinical outcomes with minimal complications compared to nonguided percutaneous release techniques.^29,30

Open release is the gold standard surgical treatment for trigger finger (FIGURE 3). A small incision (1-2 cm) is made directly over or proximal to the A1 pulley in the distal palmar crease at the base of the affected digit. After blunt dissection through the subcutaneous tissue, the A1 pulley is sharply incised. An open approach has the clear benefit of avoiding the digital neurovascular bundles, as well as visualizing the resolution of triggering upon flexion and extension prior to closure. The WALANT procedure has the advantage of allowing the awake patient to actively flex and extend the digit to determine if the A1 release has been successful prior to closure of the incision.

Outcomes and complications of surgery. A recent systematic review and meta-analysis has shown percutaneous techniques to be successful in 94% of cases.²⁷ The success rate of open surgery has been reported at 99% to 100% at varying follow-up intervals up to 1 year.^25,30,31 The complication rate for percutaneous release (guided and nonguided) was calculated at 2.2% (n = 2114).²⁷ In another study, the overall complication rate of open releases was calculated at 1% (n = 999).³² When comparing percutaneous release (guided and nonguided) and open release, a meta-analysis found no significant difference in complication rate (RR = 0.84) or failure rate (RR = 0.94).³²

Continue to: Several risk factors...

 

Several risk factors have been associated with postoperative surgical infection, including recent steroid injection (< 80 d), smoking status, increasing age, and pre-operative use of lidocaine with epinephrine.³³ Open release has been shown to be an effective and safe treatment modality for patients with and without diabetes alike.³⁴ Overall, definitive surgical correction has been demonstrated to be superior to conservative measures due to a significantly lower rate of recurrence.³⁵

CASE

Given the patient’s presentation with triggering of the digit, tenderness over the A1 pulley, and lack of trauma history, we diagnosed trigger finger in this patient. Potential treatments included splinting, corticosteroid injections, and surgery. After discussion of the risks and benefits of each treatment option, the patient elected to undergo a corticosteroid injection. She was also given a neoprene finger sleeve to wear every night, and in the daytime when possible.

At 12-week follow-up, she noted early improvement in her triggering, which had since recurred. Due to her history of diabetes, the patient was then referred for surgery. She had an open release under local anesthesia. The surgery was uncomplicated, and the abnormality was corrected. At the patient’s 1-year postoperative follow-up visit, there was no evidence of recurrence, and she had regained full active and passive range of motion of her finger.

Acknowledgements
The authors wish to thank Jose Borrero, MD, for contributing his time and creative talents to produce the illustrations in this article.

CORRESPONDENCE
Evan P. Johnson, MD; 506 South Greer Street, Memphis, TN 38111; [email protected]

CASE

A 55-year-old right-hand-dominant woman presented to the clinic with a chief complaint of right ring finger pain and stiffness. There was no history of trauma or prior surgery. She had no tingling or numbness. She had a history of type 2 diabetes that was well controlled. She worked as a clerk for a government office for many years, and her painful, limited finger motion interfered with keyboarding and picking up items. Physical examination revealed tenderness to palpation over the palmar aspect of the metacarpophalangeal joint (MCPJ) of the ring finger with no other joint tenderness or swelling. When she made a fist, her ring finger MCPJ, proximal interphalangeal joint (PIPJ), and distal interphalangeal joint (DIPJ) locked in a flexed position that required manipulation to extend the finger. A firm mass was palpated in the palm with finger flexion that moved into the finger with extension.

Stenosing tenosynovitis, also known as trigger finger (TF), is an inflammatory condition that causes pain in the distal palm and proximal digit with associated limited motion. The most commonly affected digits are the middle and ring fingers of the dominant hand.¹ The disorder is particularly noticeable when it inhibits day-to-day functioning.

TF affects 2% to 3% of the general population and up to 20% of patients with diabetes.^2,3 Patient age and duration of diabetes are commonly cited as contributing factors, although the effect of well-controlled blood glucose and A1C on the frequency and cure rate of TF has not been established.^3,4 TF is most commonly seen in individuals ages 40 to 60 years, with a 6 times’ greater frequency in females than males.⁵

In the United States, there are an estimated 200,000 cases of TF each year, with initial presentation typically being to a primary care physician.⁶ For this reason, it is essential for primary care physicians to recognize this common pathology and treat symptoms early to prevent progression and the need for surgical intervention.

An impaired gliding motion of the flexor tendons

In each finger, a tendon sheath, consisting of 5 annular pulleys and 3 cruciate pulleys, forms a tunnel around the flexor digitorum profundus (FDP) and flexor digitorum superficialis (FDS). The tendon sheath allows for maximum force by eliminating bowstringing of the tendons when the digit is flexed. Deep to the tendons and surrounding the tendons is a synovial membrane that provides nutrition and reduces friction between the tendons and the tendon sheath.⁷

Trigger finger affects 2% to 3% of the general population and up to 20% of patients with diabetes.

The FDP is longer and assists in flexion of the MCPJ and the PIPJ. It is the sole flexor of the DIPJ. The shorter FDS assists in flexion of the MCPJ and is the primary flexor of the PIPJ. The bifurcation of the shorter FDS tendon allows the longer FDP tendon to pass through to continue to its insertion on the distal phalanx.

In the thumb, the flexor pollicis longus (FPL) is the only flexor within its tendon sheath. The FPL assists in flexion of the MCPJ and flexes the thumb interphalangeal joint (IPJ). The intrinsic muscles (lumbricals and interossei) do not extend into the tendon sheath and do not contribute to TF.

Continue to: TF occurs when

 

TF occurs when the tendon sheath, most commonly at the first annular pulley (A1), or the flexor tendons thicken due to fibrocartilaginous metaplasia. This results in impaired gliding motion of the flexor tendons.⁸ The stenosed A1 pulley can lead to pinching of the flexor tendons and cause the formation of a nodule on the FDS tendon at its bifurcation.⁹ The nodule of the FDS bifurcation moves proximal to the A1 pulley when the finger is flexed. Upon extension, the tendon nodule may get caught on the A1 pulley. This prevents smooth extension and is the source of pain and triggering (FIGURE 1). In a similar manner, thumb triggering is the result of a stenosed A1 pulley creating a nodule on the FPL tendon, which prevents smooth gliding of the FPL.

What you’ll see

TF is characterized by locking, popping, or clicking at the base of the finger or thumb.^7,10 A small nodule may be palpated on the palmar aspect of the MCPJ when the finger is flexed. This nodule will then move distally when the finger is extended. Patients will present with the affected digit in a flexed position and will have difficulty extending the digit. In some cases, the patient may have to use the other hand to straighten the affected digit. In more severe cases, the digit may be fixed in a position of flexion or extension. The severity of triggering is commonly graded by the Green’s classification system (see TABLE¹¹).

Is it Dupuytren contracture, trigger finger, or something else?

The differential diagnosis for TF includes Dupuytren contracture, MCPJ sprain, calcific peritendinitis, flexor tenosynovitis, diabetic cheiroarthropathy (DCA), rheumatoid arthritis (RA), osteoarthritis (OA), and crystalline arthropathy (gout).⁵

Dupuytren contracture is usually nonpainful and manifests with a palpable cord in the palm and a fixed flexion contracture that has progressed over time, with no history of catching.

MCPJ sprain is diagnosed with tenderness of the MCPJ and a history of trauma.

Continue to: Calcific peritendinitis

 

Calcific peritendinitis is characterized by pain, tenderness, and edema near a joint with calcified deposits seen on radiographs.

Flexor tenosynovitis manifests with fusiform swelling of the digit, tenderness over the flexor tendon sheath, and pain with passive extension of the digit; it is more commonly associated with RA.

DCA, RA, OA, and gout usually affect more than 1 digit. DCA is associated with both type 1 and type 2 diabetes and is characterized by thickened, waxy skin and painless, limited extension of the digits. RA and OA are diagnosed by medical history, lab work, and radiographs. Gout is diagnosed with lab work and aspiration of joint fluid.

Trigger finger occurs when the tendon sheath or the flexor tendons thicken due to fibrocartilaginous metaplasia.

A thorough history, physical exam, and review of radiographs must be performed to rule out these other disorders. Once the diagnosis of TF is made, available treatment options should be pursued.

Treatment: A conservative or surgical approach?

Current treatment options include both nonsurgical (conservative) and surgical interventions. Nonsurgical interventions include activity modification, splinting, and corticosteroid injections. While nonsteroidal anti-inflammatory drugs are commonly recommended to resolve the local inflammation secondary to triggering, there is no scientific evidence to support their use at this time.⁷ Surgical interventions, utilized in more severe cases or after conservative treatment has failed, include percutaneous and open release of the tendon sheath.^2,7

Continue to: Conservative treatments

 

 

Conservative treatments

Splinting is only an option for digits that retain flexibility (Green’s classification grades I, II, and III). The goal of splinting is to keep the affected digit in extension to avoid repeated friction between the tendon and the tendon sheath.¹² This ideally allows any cartilaginous metaplasia or inflammation to resolve, subsequently alleviating symptoms. The recommended length of treatment with splinting ranges from 3 to 12 weeks, with an average of 6 weeks.¹

Multiple studies have shown long-term alleviation of symptoms with the use of orthotic devices. A retrospective analysis found that 87% of patients who wore their PIPJ orthotic device both day and night for a minimum of 6 weeks required no further treatment at 1-year follow-up.¹³ In contrast, MCPJ splinting only at night has been shown to resolve symptoms in just 55% of patients after 6 weeks.¹⁴ From a practical standpoint, however, patients are more likely to be compliant with night-only splinting, making it a reasonable option. Splinting does remain efficacious for patients even after 6 months of symptomatology.¹⁵

Day and night splinting for approximately 8 weeks using a PIPJ orthotic could be considered as an effective first-line intervention.¹⁶ Notably, PIPJ splinting is more functional, as it allows motion of the MCPJ and DIPJ. There are several options available for PIPJ splints, including a stiff cushioned sleeve, a prefabricated plastic splint, and a large adhesive bandage.

An adjunct treatment to splinting is tendon-gliding exercises, including passive IPJ flexion, full finger flexion and extension, and hooking.¹³ Patients may remove the orthotic device to perform these exercises 3 times a day for 5 repetitions, as well as for activities that are not conducive to splinting.¹³

Corticosteroid injections. Injections of a corticosteroid and 1% lidocaine in a 1:1 mixture for a total volume of 1 cc can be inserted into the tendon sheath, A1 pulley, or adjacent tissue.¹⁷ Steroid injections help to decrease inflammation and pain in the affected area, giving symptom relief lasting a few months in as many as 57% to 87% of patients.¹⁸

Continue to: While the location of the injection...

 

While the location of the injection has been debated, recent literature suggests that symptoms can be effectively alleviated regardless of the specific anatomic injection site, such as intra-sheath or extra-sheath (FIGURE 2).¹⁹ This allows flexibility for the clinician, as the injection does not have to be placed within the tendon sheath. Corticosteroids should not be injected into the tendon itself, and the needle tip should be slightly withdrawn if there is resistance while injecting. Patients who are averse to injections have been shown to benefit from needle-free jet lidocaine (J-tip) administration prior to the actual steroid injection.²⁰

A randomized controlled trial comparing dexamethasone to triamcinolone injections found no difference in outcome at the 3-month follow-up (n = 84).¹⁷ This may suggest that the choice of corticosteroid is at the clinician’s discretion. In terms of long-term efficacy of steroid injections, it has been shown that 70% of trigger digits had complete resolution of symptoms at a mean follow-up of 8 years after just 1 injection (n = 43).²¹

Some patients, though, may require additional corticosteroid injections to maintain symptom control. If multiple injections are performed, they should not be given in intervals shorter than 4 months between treatments.⁵ Furthermore, steroids can be administered safely up to 3 times in the same digit before surgery is recommended.²²

A patient’s options should be reconsidered if efficacy is not demonstrated with prior injections. Notably, a lower success rate has been shown in patients with type 2 diabetes (66%) compared to those without diabetes (90%).^4,23 This difference in success rates is not well understood, as there is no causal relationship between well-controlled diabetes and TF.⁴ Complications of corticosteroid injections include local pain, fat atrophy, and hypopigmentation at the site of the injection, as well as short-term elevations in blood glucose levels in patients with diabetes.^5,24

Surgical correction (to be discussed) remains superior to steroid injections in terms of cure rate and resolution of symptoms. A randomized controlled trial (n = 165) found that an injection-only group reported 86% and 49% success at 3-month and 12-month follow-up, respectively, compared to 99% success at both 3- and 12-month follow-up for the surgical group. Further, at 12-month follow-up, the median pain scores were significantly higher in the injection group (3; range, 1-9) than in the surgery group (1; range, 1-7).²⁵ If conservative treatment modalities lead to unresolved symptoms or recurrence, referral to a hand specialist for surgery is recommended.

Continue to: Surgical treatments in an office setting

 

Surgical treatments in an office setting

Procedures for TF can be safely performed under conscious sedation or local anesthesia, with or without a tourniquet.²⁶ Wide-awake procedures with local anesthesia and no tourniquet (WALANT) can be performed in an office-based procedure room rather than the operating room. This increases efficiency for the surgeon, reduces the amount of preparation and recovery time for the patient, and helps to keep costs down.

Percutaneous release involves the insertion of a 16-gauge hypodermic needle into the affected A1 pulley. The needle is used to fray and disrupt the pulley by moving the needle tip over the fibrotic A1 pulley.

While NSAIDs are commonly recommended to resolve the local inflammation secondary to triggering, there is no scientific evidence to support their use.

However, it is not without possible complications.²⁷ Inadvertent A2 pulley damage is particularly troublesome, as it leads to “bowstringing” or protrusion of the flexor tendon into the palm upon flexion. This can cause pain and failure to fully extend or flex the finger.¹⁰ Because the anatomy is not well visualized during the percutaneous approach, incomplete release, neurovascular injury, and iatrogenic injury to the A2 pulley or deep tendon may occur.²⁸ Ultrasound-guided percutaneous release techniques have shown effective clinical outcomes with minimal complications compared to nonguided percutaneous release techniques.^29,30

Open release is the gold standard surgical treatment for trigger finger (FIGURE 3). A small incision (1-2 cm) is made directly over or proximal to the A1 pulley in the distal palmar crease at the base of the affected digit. After blunt dissection through the subcutaneous tissue, the A1 pulley is sharply incised. An open approach has the clear benefit of avoiding the digital neurovascular bundles, as well as visualizing the resolution of triggering upon flexion and extension prior to closure. The WALANT procedure has the advantage of allowing the awake patient to actively flex and extend the digit to determine if the A1 release has been successful prior to closure of the incision.

Outcomes and complications of surgery. A recent systematic review and meta-analysis has shown percutaneous techniques to be successful in 94% of cases.²⁷ The success rate of open surgery has been reported at 99% to 100% at varying follow-up intervals up to 1 year.^25,30,31 The complication rate for percutaneous release (guided and nonguided) was calculated at 2.2% (n = 2114).²⁷ In another study, the overall complication rate of open releases was calculated at 1% (n = 999).³² When comparing percutaneous release (guided and nonguided) and open release, a meta-analysis found no significant difference in complication rate (RR = 0.84) or failure rate (RR = 0.94).³²

Continue to: Several risk factors...

 

Several risk factors have been associated with postoperative surgical infection, including recent steroid injection (< 80 d), smoking status, increasing age, and pre-operative use of lidocaine with epinephrine.³³ Open release has been shown to be an effective and safe treatment modality for patients with and without diabetes alike.³⁴ Overall, definitive surgical correction has been demonstrated to be superior to conservative measures due to a significantly lower rate of recurrence.³⁵

CASE

Given the patient’s presentation with triggering of the digit, tenderness over the A1 pulley, and lack of trauma history, we diagnosed trigger finger in this patient. Potential treatments included splinting, corticosteroid injections, and surgery. After discussion of the risks and benefits of each treatment option, the patient elected to undergo a corticosteroid injection. She was also given a neoprene finger sleeve to wear every night, and in the daytime when possible.

At 12-week follow-up, she noted early improvement in her triggering, which had since recurred. Due to her history of diabetes, the patient was then referred for surgery. She had an open release under local anesthesia. The surgery was uncomplicated, and the abnormality was corrected. At the patient’s 1-year postoperative follow-up visit, there was no evidence of recurrence, and she had regained full active and passive range of motion of her finger.

Acknowledgements
The authors wish to thank Jose Borrero, MD, for contributing his time and creative talents to produce the illustrations in this article.

CORRESPONDENCE
Evan P. Johnson, MD; 506 South Greer Street, Memphis, TN 38111; [email protected]