Clinical Review

From the California State University, Long Beach, School of Nursing, Long Beach, CA (Dr. McGuire, Ms. Ahearn), and the University of California, Los Angeles, School of Nursing, Los Angeles, CA (Dr. Doering).

Abstract

• Objective: To review the current literature regarding psychological distress in patients with cardiovascular disease (CVD).
• Methods: Relevant and current (2005–2015) studies were retrieved by a series of searches conducted in the PubMed and PsychINFO databases using Boolean terms/phrases along with manual extraction from the reference lists of pertinent studies. Narrative and tabular summaries of the findings are reported.
• Results: There is a vast literature on psychological distress and CVD. Depression is the most common disorder studied followed by anxiety and post-traumatic stress disorder. Physiologic mechanisms linking psychological distress to CVD are well theorized. Screening for psychological distress in CVD is recommended. Referral and treatment issues need further exploration. Pharmacologic treatment of psychological distress in CVD remains equivocal; however, promising data exists for other therapies such as cognitive behavioral therapy and social support strategies.
• Conclusion: Psychological distress has a significant negative impact on patients with CVD and is underrecognized by health care providers. Primary care providers and cardiovascular specialty providers are called upon to improve their recognition of psychological distress in their patients and assure referrals are made to collaborative care teams for proper diagnosis and treatment.

The association between the heart and the mind has been proposed by scientists since the 17th century. However, it was not until the 1970s that the relationship between cardiovascular disease (CVD) and psychological states came into scientific focus. The study of heart-psyche interactions began with investigations of cardiovascular risk and “type A” personality behaviors (aggressiveness, impatience, a sense of time-urgency, intense achievement drive, seeking recognition) [1,2]. Hundreds of studies generated over the last 10 years have yielded an extensive body of literature regarding this complex interaction.

CVD continues to be the leading cause of death globally. Worldwide and in the United States, CVD accounts for 30% of deaths and more than 2000 deaths per day, respectively [3,4]. Psychological distress (specifically depression) has been reported by the World Health Organization (WHO) as the leading cause of disability in the world [4]. Taken together, CVD and depression constitute an immense health burden and result in poor health status, increased care giver burden [5], increased readmission rates to hospitals, increased utilization of primary care services, poor health compliance [6], decreased health related quality of life [7], and a greater than 2 times increase in mortality [8,9].

Despite its devastating consequences, comorbid CVD and psychological distress remains poorly recognized and treated. In this paper, we present a review of the evidence related to key aspects of psychological distress and CVD (for the purposes of this paper, defined as ischemic heart disease and stroke), and provide information to help improve identification among health care providers. Relevant and current (2005-2015) studies for this review were retrieved by a series of searches conducted in the PubMed and PsychINFO databases using Boolean terms/phrases, along with manual extraction from the reference lists of pertinent studies. Due to the breadth and extent of the literature, a comprehensive review of the literature is beyond the scope of this article. However, the reader will be directed to current systematic reviews, meta-analyses, and recent select research studies sourced for this summary and presented in tabular form.

Mechanisms of Psychological Distress

Psychological Distress Disorders Related to CVD

Depression, anxiety, and post-traumatic stress disorder (PTSD) are the 3 most common psychological distress disorders related to CVD [20]. Cardiac disease and depression has been most commonly studied. In stroke, the science is not as well evolved due to greater heterogeneity of study samples and outcome measures.

Depression

Dysphoria (feeling blue), anhedonia (inability to experience joy in otherwise enjoyable activities), insomnia or hypersomnia, fatigue or loss of energy, increased guilt or worthlessness, decreased concentration, appetite change with significant weight loss or gain, psychomotor retardation or agitation, and suicidal ideation are the symptoms of depression [21]. These symptoms exist on a continuum, ranging from mild symptoms with short duration and limited functional impairment to major depression. Importantly, among otherwise healthy individuals, even minor depressive symptoms have been significantly associated with increased incidence of coronary disease [22].

Screening Issues

In recognition of the high prevalence of depression in patients with CHD, an American Heart Association (AHA) science advisory in 2008 recommended routine screening for depression in patients with CHD, with follow-up evaluation for diagnosis and treatment of depression by qualified professionals for positive cases [26]. In 2014, an AHA scientific statement recommended elevating depression to the level of a risk factor in ACS patients [27]. The recommendation for screening was initially met with some concern as being premature [28], when past supporters spoke out against the routine screening of depression in cardiac patients [29]. The dissenting authors claimed that there was a lack of scientific evidence supporting the efficacy of treatment for depression in cardiac patients, and that potential negative effects of routine screening and follow-up treatment were unknown. They argued the following: limited data from randomized controlled trials and/or evidenced-based reviews exist demonstrating improved outcomes in cardiac patients based on screening and referral [30]; antidepressants are not yet recognized to be effective in cardiac populations and there is a lack of evidence related to potential harms [28]; concerns exist about the potential for mass screening to increase health care resource use at the expense of other health care needs [29]; and routine screening may cause unnecessary negative social stigma related to false-positive findings [31].

Although clinical trials of depression treatment in cardiac patients have not demonstrated an increase in survival, treatment has been shown to be effective in reducing depression symptoms, improving patient satisfaction with depression care and improving health related quality of life [32–34]. Further, recent studies described the AHA recommendation as well accepted by cardiac unit staff, not heavily resource intensive, feasible, and accurate [35,36]. Bigger and Glassman [37] published a recent analytical review of the AHA advisory and concluded that the advisory is supported by the literature. A salient point regarding the depression screening debate is that screening without proper follow-up for further diagnosis and potential treatment may be harmful [28,29,31]. Despite concerns of the potential negative impact of depression screening in cardiac patients raised in the literature, the preponderance of the literature indicates that its benefits are likely to outweigh its risks [32,34,36,38–40].

Outcomes of Depression Treatment

Answers to questions about improvement in cardiovascular and all-cause mortality outcomes with depression treatment remain elusive in the literature. However, data show an improvement in depressive symptoms and quality of life for depressed patients receiving some types of treatment [33,41–45]. The Enhancing Recovery in Coronary Heart Disease Patients (ENRICHD) study was a landmark study of MI patients with a 6-month treatment intervention of cognitive behavioral therapy (CBT) plus pharmacologic intervention if indicated for depression [33]. Patients were followed for an average of 29 months post-MI. A significant improvement was seen in depressive symptoms and social isolation in the treatment group; however, there was no improvement in event-free survival [33]. When outcome measures are restricted to mortality alone, subsequent trials of antidepressant medications for treatment of depression in cardiac patients have shown them to be ineffective [46]. However, CBT and other supportive stress management strategies are effective in decreasing depressive symptoms and improving the quality of life in patients suffering with depression and CVD [46].

Promising results are emerging in the literature as researchers refocus their analysis on subgroups of depressed cardiac patients. In one large study of 442 depressed and 325 non-depressed patients, the number of depressive symptoms after an MI irrespective of the pre-MI depression status was associated with worse cardiac outcomes [47]. For every 1 additional depressive symptom reported 1 year post-MI, patients had a 15% increased risk for a new cardiac event in the next 2.5 years [47]. Another study demonstrated an improvement in depressive symptoms by 75.3% in in post-cardiac surgery patients with low ejection fraction (< 40%) after 8 weeks of nurse-guided CBT and worsening in depressive symptoms by 26.8% in usual care patients. More moderate findings were seen in the those with higher ejection fraction receiving the same CBT intervention for depression [45]. A treatment-resistant depression subgroup analyzed in a recent secondary analysis of the ENRICHD trial showed a twofold increase in mortality when compared to those in the non–treatment-resistant depression group [48]. Since treatment does not work for all patients with depression, including depressed post-MI patients, further evaluation with a focus on those who respond to treatment is needed.

Depression in Stroke

Issues related to treatment of stroke patients parallel those of depressed patients with cardiac disease, as the effect on mortality and survival is unknown. Depression has been reported to go untreated in up to 67.9% of depressed post-stroke patients [54]. In addition, mismatches between antidepressant prescription and those with depression suggested that some patients without depression were being treated for depression while some patients with depression were not being treated [54].

Anxiety

Anxiety disorders create behavioral disturbances of fear and avoidance related to an individual’s propensity to overestimate dangers [21]. Though a number of anxiety disorders are described in the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5), anxiety as a general constellation of symptoms (afraid, inability to relax, worry about everyday problems, feelings of panic) is described in most of the literature related to CVD [55–57]. To a lesser extent, generalized anxiety disorder (GAD), defined as anxiety symptoms on more days than not and lasting more than 6 months [58,59] has also been studied. Because anxiety can be a component of depression, the 2 are often discussed together. Taken together, in the context of CHD, individuals with both anxiety and depression are at significantly greater risk for death (odds ratio 2.35, 95% confidence interval 1.23-4.47, P =0.01), compared with those without symptoms [60].

Post-Traumatic Stress Disorder

PTSD presents with a heterogeneous cluster of symptoms that are generally described as avoidance, re-experiencing, arousal, and negative cognitions and mood [21]. Previously classified as a anxiety disorder in DSM-IV, PTSD is in a new category of trauma and stress or related disorders in the revised DSM-V [21]. In addition, the temporal component of the symptoms has been changed to a disturbance lasting more than 1 month, without reference to acuity or chronicity.

Implications for Clinical Practice

Despite the extensive body of literature regarding the negative association of psychological distress to health outcomes in CVD patients, there remains a significant practice gap related to screening, referral, and treatment of psychological distress in CVD patients [30,36,66]. Busy clinical practices focused on physical symptoms (which may not be recognized as mental health–related), along with a health system that has historically regarded mental health issues as the sole domain of mental health professionals creates barriers that need to be overcome. Many health care providers are not proactive in screening patients for psychological distress [11]. Additionally, psychological distress is often perceived as a metaphysical, inexact phenomenon, and is not regarded with the same import as physiological indices, such blood pressure and lipid levels [13]. Another significant barrier may be that the importance of psychological distress, especially depression, has been minimized by some investigators and clinicians because of the lack of data that show improvement with treatment of “hard” outcomes, such as mortality. Lastly, no studies have conclusively demonstrated that treating depression in the general population would lower subsequent cardiovascular clinical events, adding to the minimization of the importance of screening, referral, and treatment of psychological distress among clinicians.

The challenges associated with psychological distress and CVD are centered on the perceived role of the health care provider and role of the patient [11,67]. To date, identification of patients with psychological distress in CVD populations has not been considered a part of routine practice, and only a small percent of those identified with psychological distress are treated. In one study, 17.6% of 1181 patients had moderate to severe depression and of those, only 24.5% were recognized as depressed by their health care providers [68]. In a smaller study of 35 patients with depression after an acute MI, only 10% received treatment with antidepressants [66]. Similarly poor treatment rates were seen in a recent study of antidepressant use after stroke and transient ischemic attack (TIA), with 67.9% of stroke patients and 70.0% of TIA patients with persistent depression going untreated [54].

Stress, depression, anxiety, and PTSD are often not self-contained or experienced in isolation. Rather, some or all of these conditions may present as an interconnected phenomenon [69,70]. There are several reasons for this. First, symptom identification relies on self-report and/or observation of the symptoms, which may confound validity and reliability of diagnosis [70]. Second, the conditions share some symptoms, which may complicate diagnosis of a primary condition. In addition, the overlap of somatic, cognitive, and affective symptoms [71] may deter health care providers from using screening tools that have physical symptoms as part of the screening process. In a recent study of depressed cardiac patients, investigators clustered symptoms and demonstrated that cognitive affective symptoms of depression predict depression in patients with heart disease [72]. Certain events, such as stroke, may make screening especially difficult due to the presence of neurological changes that may complicate the screening process [73]. These issues highlight the need for formalized depression screening tools such as the Patient Health Questionnaire 2-item screening tool (PHQ-2) and/or Patient Health Questionnaire nine-item screening tool (PHQ-9) (Appendix), as recommended by the AHA. The PHQs have been validated in stroke patients and cardiac patients and have been found to be accurate, easy to use, and feasible [35,36,73].

Patients look to their providers for information and security during vulnerable times in their life. In a 2014 study regarding the perceptions of psychosocial consequences and access to support after MI, patients reported a high sense of security regarding being able to contact their providers [74]. Providers in both the primary and acute care settings should use these opportunities to assess for psychological distress. Many inpatient health care providers assume that it is the primary care providers’ responsibility to screen for depression [75]; however, screening should be done in all practice settings caring for patients with CVD. Clinical practice environments should develop policies and procedures to define who, when, and how screening for psychological distress is accomplished using currently available brief screening tools.

A plan for insuring that proper referrals are made following screening to ensure accurate diagnosis, effective treatment, and follow-up should be in place. To date, there is ample evidence that patients benefit from screening in the context of an interdisciplinary treatment approach [34]. Collaborative care, utilizing a team of health professionals (physician, case manager trained in working with patients with psychological distress, and mental health specialist) working with the patient, is an ideal model to improve outcomes [44]. A Cochrane review of 79 RCTs with over 24,000 participants compared utilization of a collaborative team with routine care and found decreased depression and anxiety symptoms in patients receiving team care for up 2 years, along with improved medication adherence, improved quality of life, and improved patient satisfaction with care [39].

Conclusion

Psychological distress remains underrecognized in CVD patients. Brief screening tools such as the PHQ-2 and PHQ-9 are available, easy to use, and reliable for use by clinicians to improve case finding. Primary care providers and cardiovascular specialty providers are called upon to improve the recognition of psychological distress in their patients and assure referrals are made to collaborative care teams for proper diagnosis and treatment of mental health issues. Longitudinal studies focused on the impact of primary/secondary/tertiary psychological distress prevention strategies in the general population, as well as those with CVD, are needed to bring the state of the science forward and provide evidence to enhance the care of those with psychological distress and CVD.

Corresponding author: Anthony McGuire, RN, PhD, ACNP-BC, CSULB, School of Nursing, #2 1250 Bellflower Blvd., Long Beach, CA 90804, [email protected].

Financial disclosures: None

Author contributions: conception and design, AWM, EA, LVD; drafting of article, AWM, EA, LVD; critical revision of the article, AWM, EA, LVD; collection and assembly of data, AWM, EA, LVD.

From the California State University, Long Beach, School of Nursing, Long Beach, CA (Dr. McGuire, Ms. Ahearn), and the University of California, Los Angeles, School of Nursing, Los Angeles, CA (Dr. Doering).

Abstract

• Objective: To review the current literature regarding psychological distress in patients with cardiovascular disease (CVD).
• Methods: Relevant and current (2005–2015) studies were retrieved by a series of searches conducted in the PubMed and PsychINFO databases using Boolean terms/phrases along with manual extraction from the reference lists of pertinent studies. Narrative and tabular summaries of the findings are reported.
• Results: There is a vast literature on psychological distress and CVD. Depression is the most common disorder studied followed by anxiety and post-traumatic stress disorder. Physiologic mechanisms linking psychological distress to CVD are well theorized. Screening for psychological distress in CVD is recommended. Referral and treatment issues need further exploration. Pharmacologic treatment of psychological distress in CVD remains equivocal; however, promising data exists for other therapies such as cognitive behavioral therapy and social support strategies.
• Conclusion: Psychological distress has a significant negative impact on patients with CVD and is underrecognized by health care providers. Primary care providers and cardiovascular specialty providers are called upon to improve their recognition of psychological distress in their patients and assure referrals are made to collaborative care teams for proper diagnosis and treatment.

The association between the heart and the mind has been proposed by scientists since the 17th century. However, it was not until the 1970s that the relationship between cardiovascular disease (CVD) and psychological states came into scientific focus. The study of heart-psyche interactions began with investigations of cardiovascular risk and “type A” personality behaviors (aggressiveness, impatience, a sense of time-urgency, intense achievement drive, seeking recognition) [1,2]. Hundreds of studies generated over the last 10 years have yielded an extensive body of literature regarding this complex interaction.

CVD continues to be the leading cause of death globally. Worldwide and in the United States, CVD accounts for 30% of deaths and more than 2000 deaths per day, respectively [3,4]. Psychological distress (specifically depression) has been reported by the World Health Organization (WHO) as the leading cause of disability in the world [4]. Taken together, CVD and depression constitute an immense health burden and result in poor health status, increased care giver burden [5], increased readmission rates to hospitals, increased utilization of primary care services, poor health compliance [6], decreased health related quality of life [7], and a greater than 2 times increase in mortality [8,9].

Despite its devastating consequences, comorbid CVD and psychological distress remains poorly recognized and treated. In this paper, we present a review of the evidence related to key aspects of psychological distress and CVD (for the purposes of this paper, defined as ischemic heart disease and stroke), and provide information to help improve identification among health care providers. Relevant and current (2005-2015) studies for this review were retrieved by a series of searches conducted in the PubMed and PsychINFO databases using Boolean terms/phrases, along with manual extraction from the reference lists of pertinent studies. Due to the breadth and extent of the literature, a comprehensive review of the literature is beyond the scope of this article. However, the reader will be directed to current systematic reviews, meta-analyses, and recent select research studies sourced for this summary and presented in tabular form.

Mechanisms of Psychological Distress

Psychological Distress Disorders Related to CVD

Depression, anxiety, and post-traumatic stress disorder (PTSD) are the 3 most common psychological distress disorders related to CVD [20]. Cardiac disease and depression has been most commonly studied. In stroke, the science is not as well evolved due to greater heterogeneity of study samples and outcome measures.

Depression

Dysphoria (feeling blue), anhedonia (inability to experience joy in otherwise enjoyable activities), insomnia or hypersomnia, fatigue or loss of energy, increased guilt or worthlessness, decreased concentration, appetite change with significant weight loss or gain, psychomotor retardation or agitation, and suicidal ideation are the symptoms of depression [21]. These symptoms exist on a continuum, ranging from mild symptoms with short duration and limited functional impairment to major depression. Importantly, among otherwise healthy individuals, even minor depressive symptoms have been significantly associated with increased incidence of coronary disease [22].

Screening Issues

In recognition of the high prevalence of depression in patients with CHD, an American Heart Association (AHA) science advisory in 2008 recommended routine screening for depression in patients with CHD, with follow-up evaluation for diagnosis and treatment of depression by qualified professionals for positive cases [26]. In 2014, an AHA scientific statement recommended elevating depression to the level of a risk factor in ACS patients [27]. The recommendation for screening was initially met with some concern as being premature [28], when past supporters spoke out against the routine screening of depression in cardiac patients [29]. The dissenting authors claimed that there was a lack of scientific evidence supporting the efficacy of treatment for depression in cardiac patients, and that potential negative effects of routine screening and follow-up treatment were unknown. They argued the following: limited data from randomized controlled trials and/or evidenced-based reviews exist demonstrating improved outcomes in cardiac patients based on screening and referral [30]; antidepressants are not yet recognized to be effective in cardiac populations and there is a lack of evidence related to potential harms [28]; concerns exist about the potential for mass screening to increase health care resource use at the expense of other health care needs [29]; and routine screening may cause unnecessary negative social stigma related to false-positive findings [31].

Although clinical trials of depression treatment in cardiac patients have not demonstrated an increase in survival, treatment has been shown to be effective in reducing depression symptoms, improving patient satisfaction with depression care and improving health related quality of life [32–34]. Further, recent studies described the AHA recommendation as well accepted by cardiac unit staff, not heavily resource intensive, feasible, and accurate [35,36]. Bigger and Glassman [37] published a recent analytical review of the AHA advisory and concluded that the advisory is supported by the literature. A salient point regarding the depression screening debate is that screening without proper follow-up for further diagnosis and potential treatment may be harmful [28,29,31]. Despite concerns of the potential negative impact of depression screening in cardiac patients raised in the literature, the preponderance of the literature indicates that its benefits are likely to outweigh its risks [32,34,36,38–40].

Outcomes of Depression Treatment

Answers to questions about improvement in cardiovascular and all-cause mortality outcomes with depression treatment remain elusive in the literature. However, data show an improvement in depressive symptoms and quality of life for depressed patients receiving some types of treatment [33,41–45]. The Enhancing Recovery in Coronary Heart Disease Patients (ENRICHD) study was a landmark study of MI patients with a 6-month treatment intervention of cognitive behavioral therapy (CBT) plus pharmacologic intervention if indicated for depression [33]. Patients were followed for an average of 29 months post-MI. A significant improvement was seen in depressive symptoms and social isolation in the treatment group; however, there was no improvement in event-free survival [33]. When outcome measures are restricted to mortality alone, subsequent trials of antidepressant medications for treatment of depression in cardiac patients have shown them to be ineffective [46]. However, CBT and other supportive stress management strategies are effective in decreasing depressive symptoms and improving the quality of life in patients suffering with depression and CVD [46].

Promising results are emerging in the literature as researchers refocus their analysis on subgroups of depressed cardiac patients. In one large study of 442 depressed and 325 non-depressed patients, the number of depressive symptoms after an MI irrespective of the pre-MI depression status was associated with worse cardiac outcomes [47]. For every 1 additional depressive symptom reported 1 year post-MI, patients had a 15% increased risk for a new cardiac event in the next 2.5 years [47]. Another study demonstrated an improvement in depressive symptoms by 75.3% in in post-cardiac surgery patients with low ejection fraction (< 40%) after 8 weeks of nurse-guided CBT and worsening in depressive symptoms by 26.8% in usual care patients. More moderate findings were seen in the those with higher ejection fraction receiving the same CBT intervention for depression [45]. A treatment-resistant depression subgroup analyzed in a recent secondary analysis of the ENRICHD trial showed a twofold increase in mortality when compared to those in the non–treatment-resistant depression group [48]. Since treatment does not work for all patients with depression, including depressed post-MI patients, further evaluation with a focus on those who respond to treatment is needed.

Depression in Stroke

Issues related to treatment of stroke patients parallel those of depressed patients with cardiac disease, as the effect on mortality and survival is unknown. Depression has been reported to go untreated in up to 67.9% of depressed post-stroke patients [54]. In addition, mismatches between antidepressant prescription and those with depression suggested that some patients without depression were being treated for depression while some patients with depression were not being treated [54].

Anxiety

Anxiety disorders create behavioral disturbances of fear and avoidance related to an individual’s propensity to overestimate dangers [21]. Though a number of anxiety disorders are described in the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5), anxiety as a general constellation of symptoms (afraid, inability to relax, worry about everyday problems, feelings of panic) is described in most of the literature related to CVD [55–57]. To a lesser extent, generalized anxiety disorder (GAD), defined as anxiety symptoms on more days than not and lasting more than 6 months [58,59] has also been studied. Because anxiety can be a component of depression, the 2 are often discussed together. Taken together, in the context of CHD, individuals with both anxiety and depression are at significantly greater risk for death (odds ratio 2.35, 95% confidence interval 1.23-4.47, P =0.01), compared with those without symptoms [60].

Post-Traumatic Stress Disorder

PTSD presents with a heterogeneous cluster of symptoms that are generally described as avoidance, re-experiencing, arousal, and negative cognitions and mood [21]. Previously classified as a anxiety disorder in DSM-IV, PTSD is in a new category of trauma and stress or related disorders in the revised DSM-V [21]. In addition, the temporal component of the symptoms has been changed to a disturbance lasting more than 1 month, without reference to acuity or chronicity.

Implications for Clinical Practice

Despite the extensive body of literature regarding the negative association of psychological distress to health outcomes in CVD patients, there remains a significant practice gap related to screening, referral, and treatment of psychological distress in CVD patients [30,36,66]. Busy clinical practices focused on physical symptoms (which may not be recognized as mental health–related), along with a health system that has historically regarded mental health issues as the sole domain of mental health professionals creates barriers that need to be overcome. Many health care providers are not proactive in screening patients for psychological distress [11]. Additionally, psychological distress is often perceived as a metaphysical, inexact phenomenon, and is not regarded with the same import as physiological indices, such blood pressure and lipid levels [13]. Another significant barrier may be that the importance of psychological distress, especially depression, has been minimized by some investigators and clinicians because of the lack of data that show improvement with treatment of “hard” outcomes, such as mortality. Lastly, no studies have conclusively demonstrated that treating depression in the general population would lower subsequent cardiovascular clinical events, adding to the minimization of the importance of screening, referral, and treatment of psychological distress among clinicians.

The challenges associated with psychological distress and CVD are centered on the perceived role of the health care provider and role of the patient [11,67]. To date, identification of patients with psychological distress in CVD populations has not been considered a part of routine practice, and only a small percent of those identified with psychological distress are treated. In one study, 17.6% of 1181 patients had moderate to severe depression and of those, only 24.5% were recognized as depressed by their health care providers [68]. In a smaller study of 35 patients with depression after an acute MI, only 10% received treatment with antidepressants [66]. Similarly poor treatment rates were seen in a recent study of antidepressant use after stroke and transient ischemic attack (TIA), with 67.9% of stroke patients and 70.0% of TIA patients with persistent depression going untreated [54].

Stress, depression, anxiety, and PTSD are often not self-contained or experienced in isolation. Rather, some or all of these conditions may present as an interconnected phenomenon [69,70]. There are several reasons for this. First, symptom identification relies on self-report and/or observation of the symptoms, which may confound validity and reliability of diagnosis [70]. Second, the conditions share some symptoms, which may complicate diagnosis of a primary condition. In addition, the overlap of somatic, cognitive, and affective symptoms [71] may deter health care providers from using screening tools that have physical symptoms as part of the screening process. In a recent study of depressed cardiac patients, investigators clustered symptoms and demonstrated that cognitive affective symptoms of depression predict depression in patients with heart disease [72]. Certain events, such as stroke, may make screening especially difficult due to the presence of neurological changes that may complicate the screening process [73]. These issues highlight the need for formalized depression screening tools such as the Patient Health Questionnaire 2-item screening tool (PHQ-2) and/or Patient Health Questionnaire nine-item screening tool (PHQ-9) (Appendix), as recommended by the AHA. The PHQs have been validated in stroke patients and cardiac patients and have been found to be accurate, easy to use, and feasible [35,36,73].

Patients look to their providers for information and security during vulnerable times in their life. In a 2014 study regarding the perceptions of psychosocial consequences and access to support after MI, patients reported a high sense of security regarding being able to contact their providers [74]. Providers in both the primary and acute care settings should use these opportunities to assess for psychological distress. Many inpatient health care providers assume that it is the primary care providers’ responsibility to screen for depression [75]; however, screening should be done in all practice settings caring for patients with CVD. Clinical practice environments should develop policies and procedures to define who, when, and how screening for psychological distress is accomplished using currently available brief screening tools.

A plan for insuring that proper referrals are made following screening to ensure accurate diagnosis, effective treatment, and follow-up should be in place. To date, there is ample evidence that patients benefit from screening in the context of an interdisciplinary treatment approach [34]. Collaborative care, utilizing a team of health professionals (physician, case manager trained in working with patients with psychological distress, and mental health specialist) working with the patient, is an ideal model to improve outcomes [44]. A Cochrane review of 79 RCTs with over 24,000 participants compared utilization of a collaborative team with routine care and found decreased depression and anxiety symptoms in patients receiving team care for up 2 years, along with improved medication adherence, improved quality of life, and improved patient satisfaction with care [39].

Conclusion

Psychological distress remains underrecognized in CVD patients. Brief screening tools such as the PHQ-2 and PHQ-9 are available, easy to use, and reliable for use by clinicians to improve case finding. Primary care providers and cardiovascular specialty providers are called upon to improve the recognition of psychological distress in their patients and assure referrals are made to collaborative care teams for proper diagnosis and treatment of mental health issues. Longitudinal studies focused on the impact of primary/secondary/tertiary psychological distress prevention strategies in the general population, as well as those with CVD, are needed to bring the state of the science forward and provide evidence to enhance the care of those with psychological distress and CVD.

Corresponding author: Anthony McGuire, RN, PhD, ACNP-BC, CSULB, School of Nursing, #2 1250 Bellflower Blvd., Long Beach, CA 90804, [email protected].

Financial disclosures: None

Author contributions: conception and design, AWM, EA, LVD; drafting of article, AWM, EA, LVD; critical revision of the article, AWM, EA, LVD; collection and assembly of data, AWM, EA, LVD.

From the California State University, Long Beach, School of Nursing, Long Beach, CA (Dr. McGuire, Ms. Ahearn), and the University of California, Los Angeles, School of Nursing, Los Angeles, CA (Dr. Doering).

Abstract

• Objective: To review the current literature regarding psychological distress in patients with cardiovascular disease (CVD).
• Methods: Relevant and current (2005–2015) studies were retrieved by a series of searches conducted in the PubMed and PsychINFO databases using Boolean terms/phrases along with manual extraction from the reference lists of pertinent studies. Narrative and tabular summaries of the findings are reported.
• Results: There is a vast literature on psychological distress and CVD. Depression is the most common disorder studied followed by anxiety and post-traumatic stress disorder. Physiologic mechanisms linking psychological distress to CVD are well theorized. Screening for psychological distress in CVD is recommended. Referral and treatment issues need further exploration. Pharmacologic treatment of psychological distress in CVD remains equivocal; however, promising data exists for other therapies such as cognitive behavioral therapy and social support strategies.
• Conclusion: Psychological distress has a significant negative impact on patients with CVD and is underrecognized by health care providers. Primary care providers and cardiovascular specialty providers are called upon to improve their recognition of psychological distress in their patients and assure referrals are made to collaborative care teams for proper diagnosis and treatment.

The association between the heart and the mind has been proposed by scientists since the 17th century. However, it was not until the 1970s that the relationship between cardiovascular disease (CVD) and psychological states came into scientific focus. The study of heart-psyche interactions began with investigations of cardiovascular risk and “type A” personality behaviors (aggressiveness, impatience, a sense of time-urgency, intense achievement drive, seeking recognition) [1,2]. Hundreds of studies generated over the last 10 years have yielded an extensive body of literature regarding this complex interaction.

CVD continues to be the leading cause of death globally. Worldwide and in the United States, CVD accounts for 30% of deaths and more than 2000 deaths per day, respectively [3,4]. Psychological distress (specifically depression) has been reported by the World Health Organization (WHO) as the leading cause of disability in the world [4]. Taken together, CVD and depression constitute an immense health burden and result in poor health status, increased care giver burden [5], increased readmission rates to hospitals, increased utilization of primary care services, poor health compliance [6], decreased health related quality of life [7], and a greater than 2 times increase in mortality [8,9].

Despite its devastating consequences, comorbid CVD and psychological distress remains poorly recognized and treated. In this paper, we present a review of the evidence related to key aspects of psychological distress and CVD (for the purposes of this paper, defined as ischemic heart disease and stroke), and provide information to help improve identification among health care providers. Relevant and current (2005-2015) studies for this review were retrieved by a series of searches conducted in the PubMed and PsychINFO databases using Boolean terms/phrases, along with manual extraction from the reference lists of pertinent studies. Due to the breadth and extent of the literature, a comprehensive review of the literature is beyond the scope of this article. However, the reader will be directed to current systematic reviews, meta-analyses, and recent select research studies sourced for this summary and presented in tabular form.

Mechanisms of Psychological Distress

Psychological Distress Disorders Related to CVD

Depression, anxiety, and post-traumatic stress disorder (PTSD) are the 3 most common psychological distress disorders related to CVD [20]. Cardiac disease and depression has been most commonly studied. In stroke, the science is not as well evolved due to greater heterogeneity of study samples and outcome measures.

Depression

Dysphoria (feeling blue), anhedonia (inability to experience joy in otherwise enjoyable activities), insomnia or hypersomnia, fatigue or loss of energy, increased guilt or worthlessness, decreased concentration, appetite change with significant weight loss or gain, psychomotor retardation or agitation, and suicidal ideation are the symptoms of depression [21]. These symptoms exist on a continuum, ranging from mild symptoms with short duration and limited functional impairment to major depression. Importantly, among otherwise healthy individuals, even minor depressive symptoms have been significantly associated with increased incidence of coronary disease [22].

Screening Issues

In recognition of the high prevalence of depression in patients with CHD, an American Heart Association (AHA) science advisory in 2008 recommended routine screening for depression in patients with CHD, with follow-up evaluation for diagnosis and treatment of depression by qualified professionals for positive cases [26]. In 2014, an AHA scientific statement recommended elevating depression to the level of a risk factor in ACS patients [27]. The recommendation for screening was initially met with some concern as being premature [28], when past supporters spoke out against the routine screening of depression in cardiac patients [29]. The dissenting authors claimed that there was a lack of scientific evidence supporting the efficacy of treatment for depression in cardiac patients, and that potential negative effects of routine screening and follow-up treatment were unknown. They argued the following: limited data from randomized controlled trials and/or evidenced-based reviews exist demonstrating improved outcomes in cardiac patients based on screening and referral [30]; antidepressants are not yet recognized to be effective in cardiac populations and there is a lack of evidence related to potential harms [28]; concerns exist about the potential for mass screening to increase health care resource use at the expense of other health care needs [29]; and routine screening may cause unnecessary negative social stigma related to false-positive findings [31].

Although clinical trials of depression treatment in cardiac patients have not demonstrated an increase in survival, treatment has been shown to be effective in reducing depression symptoms, improving patient satisfaction with depression care and improving health related quality of life [32–34]. Further, recent studies described the AHA recommendation as well accepted by cardiac unit staff, not heavily resource intensive, feasible, and accurate [35,36]. Bigger and Glassman [37] published a recent analytical review of the AHA advisory and concluded that the advisory is supported by the literature. A salient point regarding the depression screening debate is that screening without proper follow-up for further diagnosis and potential treatment may be harmful [28,29,31]. Despite concerns of the potential negative impact of depression screening in cardiac patients raised in the literature, the preponderance of the literature indicates that its benefits are likely to outweigh its risks [32,34,36,38–40].

Outcomes of Depression Treatment

Answers to questions about improvement in cardiovascular and all-cause mortality outcomes with depression treatment remain elusive in the literature. However, data show an improvement in depressive symptoms and quality of life for depressed patients receiving some types of treatment [33,41–45]. The Enhancing Recovery in Coronary Heart Disease Patients (ENRICHD) study was a landmark study of MI patients with a 6-month treatment intervention of cognitive behavioral therapy (CBT) plus pharmacologic intervention if indicated for depression [33]. Patients were followed for an average of 29 months post-MI. A significant improvement was seen in depressive symptoms and social isolation in the treatment group; however, there was no improvement in event-free survival [33]. When outcome measures are restricted to mortality alone, subsequent trials of antidepressant medications for treatment of depression in cardiac patients have shown them to be ineffective [46]. However, CBT and other supportive stress management strategies are effective in decreasing depressive symptoms and improving the quality of life in patients suffering with depression and CVD [46].

Promising results are emerging in the literature as researchers refocus their analysis on subgroups of depressed cardiac patients. In one large study of 442 depressed and 325 non-depressed patients, the number of depressive symptoms after an MI irrespective of the pre-MI depression status was associated with worse cardiac outcomes [47]. For every 1 additional depressive symptom reported 1 year post-MI, patients had a 15% increased risk for a new cardiac event in the next 2.5 years [47]. Another study demonstrated an improvement in depressive symptoms by 75.3% in in post-cardiac surgery patients with low ejection fraction (< 40%) after 8 weeks of nurse-guided CBT and worsening in depressive symptoms by 26.8% in usual care patients. More moderate findings were seen in the those with higher ejection fraction receiving the same CBT intervention for depression [45]. A treatment-resistant depression subgroup analyzed in a recent secondary analysis of the ENRICHD trial showed a twofold increase in mortality when compared to those in the non–treatment-resistant depression group [48]. Since treatment does not work for all patients with depression, including depressed post-MI patients, further evaluation with a focus on those who respond to treatment is needed.

Depression in Stroke

Issues related to treatment of stroke patients parallel those of depressed patients with cardiac disease, as the effect on mortality and survival is unknown. Depression has been reported to go untreated in up to 67.9% of depressed post-stroke patients [54]. In addition, mismatches between antidepressant prescription and those with depression suggested that some patients without depression were being treated for depression while some patients with depression were not being treated [54].

Anxiety

Anxiety disorders create behavioral disturbances of fear and avoidance related to an individual’s propensity to overestimate dangers [21]. Though a number of anxiety disorders are described in the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5), anxiety as a general constellation of symptoms (afraid, inability to relax, worry about everyday problems, feelings of panic) is described in most of the literature related to CVD [55–57]. To a lesser extent, generalized anxiety disorder (GAD), defined as anxiety symptoms on more days than not and lasting more than 6 months [58,59] has also been studied. Because anxiety can be a component of depression, the 2 are often discussed together. Taken together, in the context of CHD, individuals with both anxiety and depression are at significantly greater risk for death (odds ratio 2.35, 95% confidence interval 1.23-4.47, P =0.01), compared with those without symptoms [60].

Post-Traumatic Stress Disorder

PTSD presents with a heterogeneous cluster of symptoms that are generally described as avoidance, re-experiencing, arousal, and negative cognitions and mood [21]. Previously classified as a anxiety disorder in DSM-IV, PTSD is in a new category of trauma and stress or related disorders in the revised DSM-V [21]. In addition, the temporal component of the symptoms has been changed to a disturbance lasting more than 1 month, without reference to acuity or chronicity.

Implications for Clinical Practice

Despite the extensive body of literature regarding the negative association of psychological distress to health outcomes in CVD patients, there remains a significant practice gap related to screening, referral, and treatment of psychological distress in CVD patients [30,36,66]. Busy clinical practices focused on physical symptoms (which may not be recognized as mental health–related), along with a health system that has historically regarded mental health issues as the sole domain of mental health professionals creates barriers that need to be overcome. Many health care providers are not proactive in screening patients for psychological distress [11]. Additionally, psychological distress is often perceived as a metaphysical, inexact phenomenon, and is not regarded with the same import as physiological indices, such blood pressure and lipid levels [13]. Another significant barrier may be that the importance of psychological distress, especially depression, has been minimized by some investigators and clinicians because of the lack of data that show improvement with treatment of “hard” outcomes, such as mortality. Lastly, no studies have conclusively demonstrated that treating depression in the general population would lower subsequent cardiovascular clinical events, adding to the minimization of the importance of screening, referral, and treatment of psychological distress among clinicians.

The challenges associated with psychological distress and CVD are centered on the perceived role of the health care provider and role of the patient [11,67]. To date, identification of patients with psychological distress in CVD populations has not been considered a part of routine practice, and only a small percent of those identified with psychological distress are treated. In one study, 17.6% of 1181 patients had moderate to severe depression and of those, only 24.5% were recognized as depressed by their health care providers [68]. In a smaller study of 35 patients with depression after an acute MI, only 10% received treatment with antidepressants [66]. Similarly poor treatment rates were seen in a recent study of antidepressant use after stroke and transient ischemic attack (TIA), with 67.9% of stroke patients and 70.0% of TIA patients with persistent depression going untreated [54].

Stress, depression, anxiety, and PTSD are often not self-contained or experienced in isolation. Rather, some or all of these conditions may present as an interconnected phenomenon [69,70]. There are several reasons for this. First, symptom identification relies on self-report and/or observation of the symptoms, which may confound validity and reliability of diagnosis [70]. Second, the conditions share some symptoms, which may complicate diagnosis of a primary condition. In addition, the overlap of somatic, cognitive, and affective symptoms [71] may deter health care providers from using screening tools that have physical symptoms as part of the screening process. In a recent study of depressed cardiac patients, investigators clustered symptoms and demonstrated that cognitive affective symptoms of depression predict depression in patients with heart disease [72]. Certain events, such as stroke, may make screening especially difficult due to the presence of neurological changes that may complicate the screening process [73]. These issues highlight the need for formalized depression screening tools such as the Patient Health Questionnaire 2-item screening tool (PHQ-2) and/or Patient Health Questionnaire nine-item screening tool (PHQ-9) (Appendix), as recommended by the AHA. The PHQs have been validated in stroke patients and cardiac patients and have been found to be accurate, easy to use, and feasible [35,36,73].

Patients look to their providers for information and security during vulnerable times in their life. In a 2014 study regarding the perceptions of psychosocial consequences and access to support after MI, patients reported a high sense of security regarding being able to contact their providers [74]. Providers in both the primary and acute care settings should use these opportunities to assess for psychological distress. Many inpatient health care providers assume that it is the primary care providers’ responsibility to screen for depression [75]; however, screening should be done in all practice settings caring for patients with CVD. Clinical practice environments should develop policies and procedures to define who, when, and how screening for psychological distress is accomplished using currently available brief screening tools.

A plan for insuring that proper referrals are made following screening to ensure accurate diagnosis, effective treatment, and follow-up should be in place. To date, there is ample evidence that patients benefit from screening in the context of an interdisciplinary treatment approach [34]. Collaborative care, utilizing a team of health professionals (physician, case manager trained in working with patients with psychological distress, and mental health specialist) working with the patient, is an ideal model to improve outcomes [44]. A Cochrane review of 79 RCTs with over 24,000 participants compared utilization of a collaborative team with routine care and found decreased depression and anxiety symptoms in patients receiving team care for up 2 years, along with improved medication adherence, improved quality of life, and improved patient satisfaction with care [39].

Conclusion

Psychological distress remains underrecognized in CVD patients. Brief screening tools such as the PHQ-2 and PHQ-9 are available, easy to use, and reliable for use by clinicians to improve case finding. Primary care providers and cardiovascular specialty providers are called upon to improve the recognition of psychological distress in their patients and assure referrals are made to collaborative care teams for proper diagnosis and treatment of mental health issues. Longitudinal studies focused on the impact of primary/secondary/tertiary psychological distress prevention strategies in the general population, as well as those with CVD, are needed to bring the state of the science forward and provide evidence to enhance the care of those with psychological distress and CVD.

Corresponding author: Anthony McGuire, RN, PhD, ACNP-BC, CSULB, School of Nursing, #2 1250 Bellflower Blvd., Long Beach, CA 90804, [email protected].

Financial disclosures: None

Author contributions: conception and design, AWM, EA, LVD; drafting of article, AWM, EA, LVD; critical revision of the article, AWM, EA, LVD; collection and assembly of data, AWM, EA, LVD.

Fracture of the distal radius is the wrist injury most often encountered by orthopedic and hand surgeons.¹ The number of fractures of the distal radius in the United States was estimated to be 640,000 in 2001, and the incidence is increasing.^2,3 Recent evidence has shown a substantial increase in treating these fractures with internal rather than closed fixation, even in the elderly.⁴

Treatment of complex intra-articular fractures of the distal radius requires an accurate diagnosis of the fracture pattern and a thoughtful approach to fixation. Although a majority of the fractures that meet the operative criteria are now treated with various anterior locked-plating techniques with good results, a subset requires more technically demanding fixation approaches, including fragment-specific approaches, dorsal and palmar plating, and combined internal and external fixation.

The sustentaculum lunatum, as we have named the palmar lunate facet, deserves specific attention because of its importance in load transmission across the radiocarpal joint and its key role in restoring the anatomy of the palmar distal radial metaphysis during internal fixation. This fragment in comminuted fractures was first ascribed special importance by Melone⁵ in his description of common fracture patterns. In the present article, we describe the anatomical characteristics of the sustentaculum lunatum and the clinical relevance of this fragment to management of fractures of the distal radius.

Classification

A variety of classification systems have been proposed to characterize and guide treatment of fractures of the distal radius. The earliest descriptions of fracture patterns were presented by Castaing⁶ and Frykman⁷ in the 1960s. The Frykman classification historically has been popular but is limited in accuracy in its characterization of fragments and their displacement and is limited in its ability to guide treatment. The classification system proposed by Melone and colleagues^5,8-10 was the first to truly describe fracture of the distal radius fragments in a relevant manner, including their characteristic “4 parts” (Figure 1). The authors emphasized the importance of the “medial complex” as the cornerstone of the radiocarpal and radioulnar joints.

The classification system developed by Müller and colleagues,¹¹ which was adopted by the AO (Arbeitsgemeinschaft für Osteosynthesefragen), might be the most descriptive and informative system, and it is widely used to conduct research and direct treatment. This system classifies fractures into A (extra-articular), B (partial articular), and C (complete articular) types and subclassifies them according to fracture location and comminution. These classifications, along with a conceptualization of the distal forearm as a 3-column structure involving the radial, ulnar, and intermediate columns (including the lunate facet), as proposed by Peine and colleagues,¹² gave us a framework for approaching fixation of fractures of the distal radius.

Etymology and Definition

Sustentaculum, from the Latin sustinere, “to support, check, or put off,” and taculum, “receptacle or holding space,” is a fitting description of the most distal portion of the palmar lunate facet, as it supports and holds the carpus, and specifically the lunate, on the radial articular surface. This portion is analogous to the sustentaculum tali, the named portion of the calcaneus that supports and articulates with the middle calcaneal articular surface of the talus¹³ and provides a reliable fragment for internal fixation of the calcaneus.

Anatomical and Biomechanical Considerations

The distal radial articular surface is composed of distinct scaphoid and lunate facets that articulate with their respective carpal bones. Several studies have characterized the anatomy of the distal radius.^14-17 Linscheid¹⁴ found that the lunate and scaphoid facets account for 46% and 43% of the contact area across the radiocarpal joint, respectively; this has been corroborated by others.¹⁵ A biomechanical study by Genda and Horii¹⁸ showed that the majority of stress across the wrist joint was concentrated at the palmar side of the distal radius in the neutral position. Although it is recognized that the scaphoid facet bears most of the load across the wrist in the neutral wrist position, most activities of daily living place the wrist in a slightly extended and ulnarly deviated position. This position results in a shift of the majority of load to the radiolunar articulation, constituting 53% of total force transmission.¹⁸ Subchondral bone density analyses have supported this lunate-predominant loading pattern across the radiocarpal articulation in most people.¹⁹ This loading pattern is also supported by the observation that failure of fixation and carpal subluxation generally occurs at the radiolunate articulation.

The palmar lip of the distal radius traditionally has been depicted and conceptualized as a flat extension of the metaphysis, leading to the development of implants that are not ideally designed for capturing this area in the fracture setting. A 3-dimensional (3-D) computed tomography (CT) study of the distal radii of healthy volunteers, conducted by Andermahr and colleagues,²⁰ showed that the contour of the palmar lunate facet projects from the palmar cortex of the radius by 3 mm on average and is about 19 mm in width (radial to ulnar dimension) (Figures 2A-2C). In the axial plane, the anterior cortex of the distal radius slopes in a palmar direction, from radial to ulnar. This presents a challenge in attempts to support the entire surface (scaphoid and lunate facets) with a single palmar implant.^20-25

A study conducted by Harness and colleagues²⁴ showed that the majority of palmar shear fractures are composed of multiple fragments of the lunar articular facet. Anatomical studies of the distal radiocarpal articulation have also described the ligamentous attachments to the sustentaculum lunatum.²⁶ The short radiolunate ligament, which originates from this fragment and inserts onto the lunate, provides stability to the carpus and, if not adequately fixed, leads to an incompetent restraint to palmar carpal translation. Isolated injuries of the short radiolunate ligament or fractures of the palmar lunate facet have been shown to result in palmar carpal translation.^27,28 In addition, attachments of the palmar radioulnar ligament and other more ulnar radiocarpal ligaments act as deforming forces on the palmar lunate facet.^24,26

Fracture Pattern Recognition

Although the AO type B palmar shear fracture pattern, also known as the Barton fracture, has classically been recognized as the fracture involving the palmar lunate facet and requiring special attention, many complete articular fractures feature involvement and fragmentation of this portion of the distal radius (Figures 3A-3F).²⁹ In highly comminuted complete articular and palmar shear fracture patterns, the morphology of the sustentaculum lunatum should be appreciated, and its adequate fixation to the radial metaphysis ensured, to prevent loss of reduction.

Visualization of the palmar lunate facet as a distinct fragment might be difficult in cases of highly comminuted fracture patterns. Standard CT or more recently described 3-D CT techniques with subtraction of the carpus might facilitate appreciation of this fragment for preoperative planning of approach and fixation.^29,30 Our institutional protocol involves obtaining preoperative traction radiographs of every fracture of the distal radius. These radiographs have reduced the need for CT in understanding the fracture pattern and aid in decision making.³¹

Besides appreciating the existence of the sustentaculum lunatum fragment, we should recognize that some injury patterns that split the lunate facet into unstable dorsal and palmar fragments might necessitate a separate dorsal approach to reduce and fix the dorsal lunate fragment. Traction radiographs can be especially useful in recognizing these patterns (a V sign is present) (Figures 4A, 4B).

Open Fractures

Highly comminuted fractures of the distal radius presenting with displaced lunate facet fragments can have high-energy mechanisms of injury. Although open fractures of the distal radius are associated with lower risk for infection (compared with open fractures of other long bones), they deserve special attention because of associated tendon and neurovascular injuries. Few studies have specifically assessed open fractures of the distal radius.^32-35 Only the study by Rozental and Blazar³⁴ listed associated injuries at the wrist level. The authors identified 4 patients (out of 18) with concomitant flexor tendon or neurovascular injuries that included radial or ulnar artery injury. In our experience, many open fractures of the distal radius are caused by an inside-out mechanism and present with an open wound either over the ulnar styloid or in the area of the ulnar side of the palmar radial metaphysis corresponding to the metaphyseal spike that mates with the sustentaculum lunatum (Figures 5A, 5B). Given these findings, we approach this intermediate column with particular care in cases of open fracture, paying attention to important structures (flexors, neurovascular) and looking for contamination from the environment into the fracture.

Fixation Techniques

The approach to fixation of partial articular palmar shear fractures is fairly straightforward. Buttress plate fixation has been well described and has had reliably good results.³⁶ However, in very distal fracture patterns and in cases in which the palmar lunate facet is fragmented as part of a complete articular fracture, a fragment-specific approach to fixation with or without spanning external fixation often is necessary.³⁷ The unrecognized sustentaculum lunatum fragment in comminuted complete articular fractures can lead to inadequate fixation constructs, resulting in loss of reduction and carpal subluxation in a palmar direction.^24,34,38

Our surgical approach uses the standard anterior interval between the radial artery and the flexor carpi radialis, as described by Henry.³⁹ The flexor pollicis longus is retracted ulnarly, revealing the pronator quadratus. We then reflect the pronator quadratus from the distal radial metaphysis until the most proximal and ulnar extent of the fracture is easily visualized. The palmar ulnar metaphyseal cortex that mates with the displaced sustentaculum lunatum is, in our experience, often the least comminuted portion of the metaphysis, thus providing a cortical key for restoration of height and alignment (Figures 5A, 5B). At our institution, fixation typically is achieved by contouring miniplates (1.3 or 1.5 mm) to capture and buttress the sustentaculum lunatum (Figures 6A, 6B). In our experience, the screw lengths in the most distal fixed-angle constructs at the palmar lip are limited to 6 mm or less to avoid penetration of the articular surface, though this has not been previously reported in the literature. After restoring the length and tilt of this intermediate column of the distal radius, we proceed with “rebuilding” the remainder of the fragments to our stabilized initial construct.

Various authors^40-43 have described alternative fixation methods for the palmar lunate facet fragment. Jupiter and Marent-Huber⁴² described 2.4-mm locked-plate fixation with either a standard palmar plate or T- or L-plates for cases in which the palmar lip fragment is very distal and small. In fact, some newer anatomical distal radius implants include features designed to target these fragments (Figures 7A, 7B). An alternative fixation method involves use of a 26-gauge stainless steel wire passed through drill holes in the metaphysis 1 cm proximal to the fracture and then passed through the palmar capsule just distal to the fragment and secured in figure-8 fashion while the fragment is manually held reduced.⁴¹ Still others have recommended limited internal fixation of the sustentaculum lunatum through an ulna-sided palmar approach to the distal radius (between the ulnar neurovascular bundle and the flexor tendons) combined with external fixation to restore length and palmar tilt in highly comminuted fractures.^40,43

A method involving arthroscopically assisted reduction and fixation of the lunate facet has also been described, though this procedure is technically demanding and has limited indications.⁴⁴ It uses a Freer elevator passed through the standard 3-4 portal after initial visualization and evacuation of hematoma. The Freer elevator is used to disimpact the sustentaculum lunatum and to elevate it from its depressed position. With the dorsal lunate facet left displaced to facilitate access to the palmar fragment, a nerve hook retractor is used to reduce the palmar facet to the radial styloid, and Kirschner wires are used to achieve interfragmentary fixation. The dorsal lunate fragment is then pieced back to the articular segment, and the entire construct is fixed to the radial metaphysis with additional Kirschner wires.

Discussion

Given the increasing incidence of fractures of the distal radius, internal fixation of these injuries will continue to be relevant. American Academy of Orthopaedic Surgeons guidelines recommend operative fixation for fractures with postreduction radial shortening of more than 3 mm, dorsal tilt of more than 10°, or intra-articular displacement or step-off of more than 2 mm.⁴⁵ Dr. Eglseder and Dr. Pensy indicate operative treatment of any incongruity of more than 2 mm in a young, active adult with a fracture of the distal radius. For the multifragmentary distal radius being treated operatively, attempts are made to achieve reduction more accurate than this, but formal dorsal exposure or direct visualization of the joint surface via dorsal capsulotomy is carefully chosen based on age, activity level, and bone quality. Recent high-level evidence⁴⁶ showed that closed treatment of unstable fractures of the distal radius results in good outcomes in the elderly. However, it is important to note that fractures displaced in a palmar direction and palmar shear patterns were excluded from that work. It is widely accepted that palmar carpal translation should be addressed with internal fixation, and specific attention must therefore be paid to the lunate facet as the cornerstone of the distal radius. Furthermore, high-energy comminuted fractures in young patients still necessitate internal fixation of fragments to restore alignment and articular congruity.

Conclusion

The importance of the palmar lunate facet in providing support and restraint to palmar carpal translation and the key role of this facet in restoring the anatomy of the distal radius have been known. This fragment deserves special attention because failure to adequately stabilize it results in loss of fixation and carpal subluxation. Various approaches and fixation techniques have been recommended, including the method we prefer and have described here. Our newly proposed term, sustentaculum lunatum, our review of its structure and function, and our descriptions of fixation techniques are intended to promote awareness of this fragment in the treatment of fractures of the distal radius.

Fracture of the distal radius is the wrist injury most often encountered by orthopedic and hand surgeons.¹ The number of fractures of the distal radius in the United States was estimated to be 640,000 in 2001, and the incidence is increasing.^2,3 Recent evidence has shown a substantial increase in treating these fractures with internal rather than closed fixation, even in the elderly.⁴

Treatment of complex intra-articular fractures of the distal radius requires an accurate diagnosis of the fracture pattern and a thoughtful approach to fixation. Although a majority of the fractures that meet the operative criteria are now treated with various anterior locked-plating techniques with good results, a subset requires more technically demanding fixation approaches, including fragment-specific approaches, dorsal and palmar plating, and combined internal and external fixation.

The sustentaculum lunatum, as we have named the palmar lunate facet, deserves specific attention because of its importance in load transmission across the radiocarpal joint and its key role in restoring the anatomy of the palmar distal radial metaphysis during internal fixation. This fragment in comminuted fractures was first ascribed special importance by Melone⁵ in his description of common fracture patterns. In the present article, we describe the anatomical characteristics of the sustentaculum lunatum and the clinical relevance of this fragment to management of fractures of the distal radius.

Classification

A variety of classification systems have been proposed to characterize and guide treatment of fractures of the distal radius. The earliest descriptions of fracture patterns were presented by Castaing⁶ and Frykman⁷ in the 1960s. The Frykman classification historically has been popular but is limited in accuracy in its characterization of fragments and their displacement and is limited in its ability to guide treatment. The classification system proposed by Melone and colleagues^5,8-10 was the first to truly describe fracture of the distal radius fragments in a relevant manner, including their characteristic “4 parts” (Figure 1). The authors emphasized the importance of the “medial complex” as the cornerstone of the radiocarpal and radioulnar joints.

The classification system developed by Müller and colleagues,¹¹ which was adopted by the AO (Arbeitsgemeinschaft für Osteosynthesefragen), might be the most descriptive and informative system, and it is widely used to conduct research and direct treatment. This system classifies fractures into A (extra-articular), B (partial articular), and C (complete articular) types and subclassifies them according to fracture location and comminution. These classifications, along with a conceptualization of the distal forearm as a 3-column structure involving the radial, ulnar, and intermediate columns (including the lunate facet), as proposed by Peine and colleagues,¹² gave us a framework for approaching fixation of fractures of the distal radius.

Etymology and Definition

Sustentaculum, from the Latin sustinere, “to support, check, or put off,” and taculum, “receptacle or holding space,” is a fitting description of the most distal portion of the palmar lunate facet, as it supports and holds the carpus, and specifically the lunate, on the radial articular surface. This portion is analogous to the sustentaculum tali, the named portion of the calcaneus that supports and articulates with the middle calcaneal articular surface of the talus¹³ and provides a reliable fragment for internal fixation of the calcaneus.

Anatomical and Biomechanical Considerations

The distal radial articular surface is composed of distinct scaphoid and lunate facets that articulate with their respective carpal bones. Several studies have characterized the anatomy of the distal radius.^14-17 Linscheid¹⁴ found that the lunate and scaphoid facets account for 46% and 43% of the contact area across the radiocarpal joint, respectively; this has been corroborated by others.¹⁵ A biomechanical study by Genda and Horii¹⁸ showed that the majority of stress across the wrist joint was concentrated at the palmar side of the distal radius in the neutral position. Although it is recognized that the scaphoid facet bears most of the load across the wrist in the neutral wrist position, most activities of daily living place the wrist in a slightly extended and ulnarly deviated position. This position results in a shift of the majority of load to the radiolunar articulation, constituting 53% of total force transmission.¹⁸ Subchondral bone density analyses have supported this lunate-predominant loading pattern across the radiocarpal articulation in most people.¹⁹ This loading pattern is also supported by the observation that failure of fixation and carpal subluxation generally occurs at the radiolunate articulation.

The palmar lip of the distal radius traditionally has been depicted and conceptualized as a flat extension of the metaphysis, leading to the development of implants that are not ideally designed for capturing this area in the fracture setting. A 3-dimensional (3-D) computed tomography (CT) study of the distal radii of healthy volunteers, conducted by Andermahr and colleagues,²⁰ showed that the contour of the palmar lunate facet projects from the palmar cortex of the radius by 3 mm on average and is about 19 mm in width (radial to ulnar dimension) (Figures 2A-2C). In the axial plane, the anterior cortex of the distal radius slopes in a palmar direction, from radial to ulnar. This presents a challenge in attempts to support the entire surface (scaphoid and lunate facets) with a single palmar implant.^20-25

A study conducted by Harness and colleagues²⁴ showed that the majority of palmar shear fractures are composed of multiple fragments of the lunar articular facet. Anatomical studies of the distal radiocarpal articulation have also described the ligamentous attachments to the sustentaculum lunatum.²⁶ The short radiolunate ligament, which originates from this fragment and inserts onto the lunate, provides stability to the carpus and, if not adequately fixed, leads to an incompetent restraint to palmar carpal translation. Isolated injuries of the short radiolunate ligament or fractures of the palmar lunate facet have been shown to result in palmar carpal translation.^27,28 In addition, attachments of the palmar radioulnar ligament and other more ulnar radiocarpal ligaments act as deforming forces on the palmar lunate facet.^24,26

Fracture Pattern Recognition

Although the AO type B palmar shear fracture pattern, also known as the Barton fracture, has classically been recognized as the fracture involving the palmar lunate facet and requiring special attention, many complete articular fractures feature involvement and fragmentation of this portion of the distal radius (Figures 3A-3F).²⁹ In highly comminuted complete articular and palmar shear fracture patterns, the morphology of the sustentaculum lunatum should be appreciated, and its adequate fixation to the radial metaphysis ensured, to prevent loss of reduction.

Visualization of the palmar lunate facet as a distinct fragment might be difficult in cases of highly comminuted fracture patterns. Standard CT or more recently described 3-D CT techniques with subtraction of the carpus might facilitate appreciation of this fragment for preoperative planning of approach and fixation.^29,30 Our institutional protocol involves obtaining preoperative traction radiographs of every fracture of the distal radius. These radiographs have reduced the need for CT in understanding the fracture pattern and aid in decision making.³¹

Besides appreciating the existence of the sustentaculum lunatum fragment, we should recognize that some injury patterns that split the lunate facet into unstable dorsal and palmar fragments might necessitate a separate dorsal approach to reduce and fix the dorsal lunate fragment. Traction radiographs can be especially useful in recognizing these patterns (a V sign is present) (Figures 4A, 4B).

Open Fractures

Highly comminuted fractures of the distal radius presenting with displaced lunate facet fragments can have high-energy mechanisms of injury. Although open fractures of the distal radius are associated with lower risk for infection (compared with open fractures of other long bones), they deserve special attention because of associated tendon and neurovascular injuries. Few studies have specifically assessed open fractures of the distal radius.^32-35 Only the study by Rozental and Blazar³⁴ listed associated injuries at the wrist level. The authors identified 4 patients (out of 18) with concomitant flexor tendon or neurovascular injuries that included radial or ulnar artery injury. In our experience, many open fractures of the distal radius are caused by an inside-out mechanism and present with an open wound either over the ulnar styloid or in the area of the ulnar side of the palmar radial metaphysis corresponding to the metaphyseal spike that mates with the sustentaculum lunatum (Figures 5A, 5B). Given these findings, we approach this intermediate column with particular care in cases of open fracture, paying attention to important structures (flexors, neurovascular) and looking for contamination from the environment into the fracture.

Fixation Techniques

The approach to fixation of partial articular palmar shear fractures is fairly straightforward. Buttress plate fixation has been well described and has had reliably good results.³⁶ However, in very distal fracture patterns and in cases in which the palmar lunate facet is fragmented as part of a complete articular fracture, a fragment-specific approach to fixation with or without spanning external fixation often is necessary.³⁷ The unrecognized sustentaculum lunatum fragment in comminuted complete articular fractures can lead to inadequate fixation constructs, resulting in loss of reduction and carpal subluxation in a palmar direction.^24,34,38

Our surgical approach uses the standard anterior interval between the radial artery and the flexor carpi radialis, as described by Henry.³⁹ The flexor pollicis longus is retracted ulnarly, revealing the pronator quadratus. We then reflect the pronator quadratus from the distal radial metaphysis until the most proximal and ulnar extent of the fracture is easily visualized. The palmar ulnar metaphyseal cortex that mates with the displaced sustentaculum lunatum is, in our experience, often the least comminuted portion of the metaphysis, thus providing a cortical key for restoration of height and alignment (Figures 5A, 5B). At our institution, fixation typically is achieved by contouring miniplates (1.3 or 1.5 mm) to capture and buttress the sustentaculum lunatum (Figures 6A, 6B). In our experience, the screw lengths in the most distal fixed-angle constructs at the palmar lip are limited to 6 mm or less to avoid penetration of the articular surface, though this has not been previously reported in the literature. After restoring the length and tilt of this intermediate column of the distal radius, we proceed with “rebuilding” the remainder of the fragments to our stabilized initial construct.

Various authors^40-43 have described alternative fixation methods for the palmar lunate facet fragment. Jupiter and Marent-Huber⁴² described 2.4-mm locked-plate fixation with either a standard palmar plate or T- or L-plates for cases in which the palmar lip fragment is very distal and small. In fact, some newer anatomical distal radius implants include features designed to target these fragments (Figures 7A, 7B). An alternative fixation method involves use of a 26-gauge stainless steel wire passed through drill holes in the metaphysis 1 cm proximal to the fracture and then passed through the palmar capsule just distal to the fragment and secured in figure-8 fashion while the fragment is manually held reduced.⁴¹ Still others have recommended limited internal fixation of the sustentaculum lunatum through an ulna-sided palmar approach to the distal radius (between the ulnar neurovascular bundle and the flexor tendons) combined with external fixation to restore length and palmar tilt in highly comminuted fractures.^40,43

A method involving arthroscopically assisted reduction and fixation of the lunate facet has also been described, though this procedure is technically demanding and has limited indications.⁴⁴ It uses a Freer elevator passed through the standard 3-4 portal after initial visualization and evacuation of hematoma. The Freer elevator is used to disimpact the sustentaculum lunatum and to elevate it from its depressed position. With the dorsal lunate facet left displaced to facilitate access to the palmar fragment, a nerve hook retractor is used to reduce the palmar facet to the radial styloid, and Kirschner wires are used to achieve interfragmentary fixation. The dorsal lunate fragment is then pieced back to the articular segment, and the entire construct is fixed to the radial metaphysis with additional Kirschner wires.

Discussion

Given the increasing incidence of fractures of the distal radius, internal fixation of these injuries will continue to be relevant. American Academy of Orthopaedic Surgeons guidelines recommend operative fixation for fractures with postreduction radial shortening of more than 3 mm, dorsal tilt of more than 10°, or intra-articular displacement or step-off of more than 2 mm.⁴⁵ Dr. Eglseder and Dr. Pensy indicate operative treatment of any incongruity of more than 2 mm in a young, active adult with a fracture of the distal radius. For the multifragmentary distal radius being treated operatively, attempts are made to achieve reduction more accurate than this, but formal dorsal exposure or direct visualization of the joint surface via dorsal capsulotomy is carefully chosen based on age, activity level, and bone quality. Recent high-level evidence⁴⁶ showed that closed treatment of unstable fractures of the distal radius results in good outcomes in the elderly. However, it is important to note that fractures displaced in a palmar direction and palmar shear patterns were excluded from that work. It is widely accepted that palmar carpal translation should be addressed with internal fixation, and specific attention must therefore be paid to the lunate facet as the cornerstone of the distal radius. Furthermore, high-energy comminuted fractures in young patients still necessitate internal fixation of fragments to restore alignment and articular congruity.

Conclusion

The importance of the palmar lunate facet in providing support and restraint to palmar carpal translation and the key role of this facet in restoring the anatomy of the distal radius have been known. This fragment deserves special attention because failure to adequately stabilize it results in loss of fixation and carpal subluxation. Various approaches and fixation techniques have been recommended, including the method we prefer and have described here. Our newly proposed term, sustentaculum lunatum, our review of its structure and function, and our descriptions of fixation techniques are intended to promote awareness of this fragment in the treatment of fractures of the distal radius.

Fracture of the distal radius is the wrist injury most often encountered by orthopedic and hand surgeons.¹ The number of fractures of the distal radius in the United States was estimated to be 640,000 in 2001, and the incidence is increasing.^2,3 Recent evidence has shown a substantial increase in treating these fractures with internal rather than closed fixation, even in the elderly.⁴

Treatment of complex intra-articular fractures of the distal radius requires an accurate diagnosis of the fracture pattern and a thoughtful approach to fixation. Although a majority of the fractures that meet the operative criteria are now treated with various anterior locked-plating techniques with good results, a subset requires more technically demanding fixation approaches, including fragment-specific approaches, dorsal and palmar plating, and combined internal and external fixation.

The sustentaculum lunatum, as we have named the palmar lunate facet, deserves specific attention because of its importance in load transmission across the radiocarpal joint and its key role in restoring the anatomy of the palmar distal radial metaphysis during internal fixation. This fragment in comminuted fractures was first ascribed special importance by Melone⁵ in his description of common fracture patterns. In the present article, we describe the anatomical characteristics of the sustentaculum lunatum and the clinical relevance of this fragment to management of fractures of the distal radius.

Classification

A variety of classification systems have been proposed to characterize and guide treatment of fractures of the distal radius. The earliest descriptions of fracture patterns were presented by Castaing⁶ and Frykman⁷ in the 1960s. The Frykman classification historically has been popular but is limited in accuracy in its characterization of fragments and their displacement and is limited in its ability to guide treatment. The classification system proposed by Melone and colleagues^5,8-10 was the first to truly describe fracture of the distal radius fragments in a relevant manner, including their characteristic “4 parts” (Figure 1). The authors emphasized the importance of the “medial complex” as the cornerstone of the radiocarpal and radioulnar joints.

The classification system developed by Müller and colleagues,¹¹ which was adopted by the AO (Arbeitsgemeinschaft für Osteosynthesefragen), might be the most descriptive and informative system, and it is widely used to conduct research and direct treatment. This system classifies fractures into A (extra-articular), B (partial articular), and C (complete articular) types and subclassifies them according to fracture location and comminution. These classifications, along with a conceptualization of the distal forearm as a 3-column structure involving the radial, ulnar, and intermediate columns (including the lunate facet), as proposed by Peine and colleagues,¹² gave us a framework for approaching fixation of fractures of the distal radius.

Etymology and Definition

Sustentaculum, from the Latin sustinere, “to support, check, or put off,” and taculum, “receptacle or holding space,” is a fitting description of the most distal portion of the palmar lunate facet, as it supports and holds the carpus, and specifically the lunate, on the radial articular surface. This portion is analogous to the sustentaculum tali, the named portion of the calcaneus that supports and articulates with the middle calcaneal articular surface of the talus¹³ and provides a reliable fragment for internal fixation of the calcaneus.

Anatomical and Biomechanical Considerations

The distal radial articular surface is composed of distinct scaphoid and lunate facets that articulate with their respective carpal bones. Several studies have characterized the anatomy of the distal radius.^14-17 Linscheid¹⁴ found that the lunate and scaphoid facets account for 46% and 43% of the contact area across the radiocarpal joint, respectively; this has been corroborated by others.¹⁵ A biomechanical study by Genda and Horii¹⁸ showed that the majority of stress across the wrist joint was concentrated at the palmar side of the distal radius in the neutral position. Although it is recognized that the scaphoid facet bears most of the load across the wrist in the neutral wrist position, most activities of daily living place the wrist in a slightly extended and ulnarly deviated position. This position results in a shift of the majority of load to the radiolunar articulation, constituting 53% of total force transmission.¹⁸ Subchondral bone density analyses have supported this lunate-predominant loading pattern across the radiocarpal articulation in most people.¹⁹ This loading pattern is also supported by the observation that failure of fixation and carpal subluxation generally occurs at the radiolunate articulation.

The palmar lip of the distal radius traditionally has been depicted and conceptualized as a flat extension of the metaphysis, leading to the development of implants that are not ideally designed for capturing this area in the fracture setting. A 3-dimensional (3-D) computed tomography (CT) study of the distal radii of healthy volunteers, conducted by Andermahr and colleagues,²⁰ showed that the contour of the palmar lunate facet projects from the palmar cortex of the radius by 3 mm on average and is about 19 mm in width (radial to ulnar dimension) (Figures 2A-2C). In the axial plane, the anterior cortex of the distal radius slopes in a palmar direction, from radial to ulnar. This presents a challenge in attempts to support the entire surface (scaphoid and lunate facets) with a single palmar implant.^20-25

A study conducted by Harness and colleagues²⁴ showed that the majority of palmar shear fractures are composed of multiple fragments of the lunar articular facet. Anatomical studies of the distal radiocarpal articulation have also described the ligamentous attachments to the sustentaculum lunatum.²⁶ The short radiolunate ligament, which originates from this fragment and inserts onto the lunate, provides stability to the carpus and, if not adequately fixed, leads to an incompetent restraint to palmar carpal translation. Isolated injuries of the short radiolunate ligament or fractures of the palmar lunate facet have been shown to result in palmar carpal translation.^27,28 In addition, attachments of the palmar radioulnar ligament and other more ulnar radiocarpal ligaments act as deforming forces on the palmar lunate facet.^24,26

Fracture Pattern Recognition

Although the AO type B palmar shear fracture pattern, also known as the Barton fracture, has classically been recognized as the fracture involving the palmar lunate facet and requiring special attention, many complete articular fractures feature involvement and fragmentation of this portion of the distal radius (Figures 3A-3F).²⁹ In highly comminuted complete articular and palmar shear fracture patterns, the morphology of the sustentaculum lunatum should be appreciated, and its adequate fixation to the radial metaphysis ensured, to prevent loss of reduction.

Visualization of the palmar lunate facet as a distinct fragment might be difficult in cases of highly comminuted fracture patterns. Standard CT or more recently described 3-D CT techniques with subtraction of the carpus might facilitate appreciation of this fragment for preoperative planning of approach and fixation.^29,30 Our institutional protocol involves obtaining preoperative traction radiographs of every fracture of the distal radius. These radiographs have reduced the need for CT in understanding the fracture pattern and aid in decision making.³¹

Besides appreciating the existence of the sustentaculum lunatum fragment, we should recognize that some injury patterns that split the lunate facet into unstable dorsal and palmar fragments might necessitate a separate dorsal approach to reduce and fix the dorsal lunate fragment. Traction radiographs can be especially useful in recognizing these patterns (a V sign is present) (Figures 4A, 4B).

Open Fractures

Highly comminuted fractures of the distal radius presenting with displaced lunate facet fragments can have high-energy mechanisms of injury. Although open fractures of the distal radius are associated with lower risk for infection (compared with open fractures of other long bones), they deserve special attention because of associated tendon and neurovascular injuries. Few studies have specifically assessed open fractures of the distal radius.^32-35 Only the study by Rozental and Blazar³⁴ listed associated injuries at the wrist level. The authors identified 4 patients (out of 18) with concomitant flexor tendon or neurovascular injuries that included radial or ulnar artery injury. In our experience, many open fractures of the distal radius are caused by an inside-out mechanism and present with an open wound either over the ulnar styloid or in the area of the ulnar side of the palmar radial metaphysis corresponding to the metaphyseal spike that mates with the sustentaculum lunatum (Figures 5A, 5B). Given these findings, we approach this intermediate column with particular care in cases of open fracture, paying attention to important structures (flexors, neurovascular) and looking for contamination from the environment into the fracture.

Fixation Techniques

The approach to fixation of partial articular palmar shear fractures is fairly straightforward. Buttress plate fixation has been well described and has had reliably good results.³⁶ However, in very distal fracture patterns and in cases in which the palmar lunate facet is fragmented as part of a complete articular fracture, a fragment-specific approach to fixation with or without spanning external fixation often is necessary.³⁷ The unrecognized sustentaculum lunatum fragment in comminuted complete articular fractures can lead to inadequate fixation constructs, resulting in loss of reduction and carpal subluxation in a palmar direction.^24,34,38

Our surgical approach uses the standard anterior interval between the radial artery and the flexor carpi radialis, as described by Henry.³⁹ The flexor pollicis longus is retracted ulnarly, revealing the pronator quadratus. We then reflect the pronator quadratus from the distal radial metaphysis until the most proximal and ulnar extent of the fracture is easily visualized. The palmar ulnar metaphyseal cortex that mates with the displaced sustentaculum lunatum is, in our experience, often the least comminuted portion of the metaphysis, thus providing a cortical key for restoration of height and alignment (Figures 5A, 5B). At our institution, fixation typically is achieved by contouring miniplates (1.3 or 1.5 mm) to capture and buttress the sustentaculum lunatum (Figures 6A, 6B). In our experience, the screw lengths in the most distal fixed-angle constructs at the palmar lip are limited to 6 mm or less to avoid penetration of the articular surface, though this has not been previously reported in the literature. After restoring the length and tilt of this intermediate column of the distal radius, we proceed with “rebuilding” the remainder of the fragments to our stabilized initial construct.

Various authors^40-43 have described alternative fixation methods for the palmar lunate facet fragment. Jupiter and Marent-Huber⁴² described 2.4-mm locked-plate fixation with either a standard palmar plate or T- or L-plates for cases in which the palmar lip fragment is very distal and small. In fact, some newer anatomical distal radius implants include features designed to target these fragments (Figures 7A, 7B). An alternative fixation method involves use of a 26-gauge stainless steel wire passed through drill holes in the metaphysis 1 cm proximal to the fracture and then passed through the palmar capsule just distal to the fragment and secured in figure-8 fashion while the fragment is manually held reduced.⁴¹ Still others have recommended limited internal fixation of the sustentaculum lunatum through an ulna-sided palmar approach to the distal radius (between the ulnar neurovascular bundle and the flexor tendons) combined with external fixation to restore length and palmar tilt in highly comminuted fractures.^40,43

A method involving arthroscopically assisted reduction and fixation of the lunate facet has also been described, though this procedure is technically demanding and has limited indications.⁴⁴ It uses a Freer elevator passed through the standard 3-4 portal after initial visualization and evacuation of hematoma. The Freer elevator is used to disimpact the sustentaculum lunatum and to elevate it from its depressed position. With the dorsal lunate facet left displaced to facilitate access to the palmar fragment, a nerve hook retractor is used to reduce the palmar facet to the radial styloid, and Kirschner wires are used to achieve interfragmentary fixation. The dorsal lunate fragment is then pieced back to the articular segment, and the entire construct is fixed to the radial metaphysis with additional Kirschner wires.

Discussion

Given the increasing incidence of fractures of the distal radius, internal fixation of these injuries will continue to be relevant. American Academy of Orthopaedic Surgeons guidelines recommend operative fixation for fractures with postreduction radial shortening of more than 3 mm, dorsal tilt of more than 10°, or intra-articular displacement or step-off of more than 2 mm.⁴⁵ Dr. Eglseder and Dr. Pensy indicate operative treatment of any incongruity of more than 2 mm in a young, active adult with a fracture of the distal radius. For the multifragmentary distal radius being treated operatively, attempts are made to achieve reduction more accurate than this, but formal dorsal exposure or direct visualization of the joint surface via dorsal capsulotomy is carefully chosen based on age, activity level, and bone quality. Recent high-level evidence⁴⁶ showed that closed treatment of unstable fractures of the distal radius results in good outcomes in the elderly. However, it is important to note that fractures displaced in a palmar direction and palmar shear patterns were excluded from that work. It is widely accepted that palmar carpal translation should be addressed with internal fixation, and specific attention must therefore be paid to the lunate facet as the cornerstone of the distal radius. Furthermore, high-energy comminuted fractures in young patients still necessitate internal fixation of fragments to restore alignment and articular congruity.

Conclusion

The importance of the palmar lunate facet in providing support and restraint to palmar carpal translation and the key role of this facet in restoring the anatomy of the distal radius have been known. This fragment deserves special attention because failure to adequately stabilize it results in loss of fixation and carpal subluxation. Various approaches and fixation techniques have been recommended, including the method we prefer and have described here. Our newly proposed term, sustentaculum lunatum, our review of its structure and function, and our descriptions of fixation techniques are intended to promote awareness of this fragment in the treatment of fractures of the distal radius.

Perilunate injuries typically stem from a high-energy insult to the carpus. Because of their relative infrequency and often subtle radiographic and physical examination findings, these injuries are often undetected in the emergency department setting.¹ Early anatomic reduction of any carpal malalignment is essential. Even with optimal treatment, complications such as generalized wrist stiffness, diminished grip strength, and posttraumatic arthritis, commonly develop; however, recent studies suggest these issues are often well tolerated.^1-5 In this article, the diagnosis, treatment, and outcomes after perilunate injuries are examined. 

History and Physical Examination

Perilunate injuries result from high-energy trauma to the carpus. Patients with these injuries often present with vague wrist pain and loss of wrist motion. Their fingers are frequently held in slight flexion. The patient may complain of numbness and tingling in the median nerve distribution. An acute carpal tunnel syndrome can rapidly develop. The general belief is that acute carpal tunnel syndrome occurs more commonly in pure volar lunate dislocations than in dorsal perilunate dislocations. However, no studies compare the incidence of acute carpal tunnel syndrome in lunate versus perilunate dislocations.

Radiographic Evaluation

Standard radiographic evaluation of a potential perilunate injury includes posteroanterior (PA), lateral, and oblique views of the wrist (Figure 1). A scaphoid view (ie, PA view with the wrist in ulnar deviation) may also be helpful. The PA view is particularly helpful because it enables assessment of Gilula lines, which are imaginary lines drawn across the proximal and distal aspects of the proximal carpal row and the proximal aspect of the distal carpal row. These lines should appear as 3 smooth arcs running nearly parallel to each other.⁶ Any disruption in these lines suggests carpal incongruity. It may be possible to note a triangular-shaped lunate on the PA view, which is a sign of lunate dislocation.⁷ 

While the PA view is certainly useful, the lateral view is the most important in diagnosing a perilunate injury. The lateral view allows assessment of the collinearity of radius, lunate, and capitate. Any disruption in this collinearity strongly suggests a perilunate dislocation.^7,8 

Classification

Mayfield and colleagues^9,10 described 4 stages of perilunate instability proceeding from a radial to an ulnar direction around the lunate. Stage I involves disruption of the scapholunate joint, while stage II involves both the scapholunate and capitolunate joints. In stage III, the scapholunate, capitolunate, and lunotriquetral ligaments are disrupted, and the result is a perilunate dislocation, usually dorsal. Finally, in stage IV, all the ligaments surrounding the lunate are disrupted and the lunate dislocates, most often volarly.

Lastly, perilunate injuries can be classified as greater-arc injuries if concomitant fracture of the carpus occurs, lesser-arc injuries if the injury is purely ligamentous, or inferior-arc injuries if there is an associated fracture of the volar rim of the distal radius.⁸

Treatment

Closed Reduction

All acute perilunate dislocations should be managed initially with an attempted closed reduction.¹¹ If the injury is older than 72 hours, such an attempt may be futile. For any closed reduction performed in the emergency department setting, intravenous sedation is generally advised for muscle relaxation. Gentle traction with finger traps can also be used prior to the reduction attempt. For a dorsal perilunate dislocation, longitudinal traction followed by volar flexion of the wrist with volar pressure on the lunate and dorsal pressure on the capitate (ie, Tavernier’s maneuver) is required. Once reduction is complete, PA and lateral views of the wrist should be obtained to assess carpal alignment. If closed reduction is unsuccessful, an open reduction is required, although the timing of said procedure is an area of debate, which we will discuss later.^1,3 Restoration of anatomic carpal alignment is essential to optimizing outcome, although it does not guarantee a good overall result.

Open Reduction

If successful closed reduction is achieved, the patient can be immobilized temporarily in a short-arm plaster splint. However, open reduction and either pinning or internal fixation will be required to maintain this alignment. The exact timing of open reduction and fixation is debatable and often dictated by the absence or presence of median nerve symptoms.^1,3 If a patient with no median nerve symptoms undergoes a successful closed reduction, he or she may be stabilized surgically within 3 to 5 days (or longer) with either pins or headless screws. If closed reduction is unsuccessful, an open reduction should be done within 2 to 3 days. However, if the patient has progressive numbness in the median nerve distribution upon presentation that fails to improve or worsens despite a successful closed reduction, an urgent open reduction (within 24 hours) and carpal tunnel release should be performed to prevent permanent damage to the median nerve.

Once open reduction is undertaken, a dorsal, volar, and combined approach can be used.^2-4 In most cases the dorsal approach is selected first. A longitudinal incision is made over the dorsum of the wrist, centered on the Lister tubercle. Dissection occurs between the third and fourth dorsal compartments. After the capsule is exposed, reduction of the lunate to the capitate is confirmed. If any fractures are present in the carpus (eg, scaphoid), they are internally fixed. The scapholunate articulation is then addressed. In general, the scapholunate ligament is not disrupted with a transscaphoid perilunate dislocation. However, if the scapholunate ligament is disrupted, the joint should be reduced and pinned. Repair or reconstruction of the scapholunate ligament is performed. Finally, the lunotriquetral articulation is reduced and stabilized with pins. There are no studies that specifically suggest direct repair of the lunotriquetral ligament versus pinning of the lunotriquetral articulation, but the lunotriquetral ligament could be repaired in similar fashion to the scapholunate ligament at the surgeon’s discretion.

As an alternative to percutaneous pinning, intercarpal screw fixation can be used to stabilize the carpus. A 2007 study by Souer and colleagues¹² showed no substantial difference in outcome between the 2 methods of fixation. However, a second procedure is required to remove the screws.

The volar approach, if selected, is typically done second and performed via an extended carpal tunnel incision. It allows decompression of the carpal tunnel and enables repair of volar capsular ligaments (ie, long and short radiolunate ligaments, volar scapholunate ligament, and volar lunotriquetral ligament), which increases overall carpal stability. Currently, many surgeons favor a combined dorsal-volar approach for its efficacy.^2,3 Some use a dorsal approach in all patients and perform a volar procedure only if the patient has median nerve symptoms.⁴ However, Başar and colleagues¹³ report use of only the volar approach for treatment of perilunate injuries. The authors repaired the long and short radiolunate ligaments, volar scapholunate ligament, and volar lunotriquetral ligament. They reported reasonably good outcomes, which are equivalent to those reported in similar studies using dorsal or combined dorsal-volar approaches. However, no studies in the literature directly compare any of the different approaches with each other.

Postoperatively, patients are placed in a long-arm thumb-spica cast for 4 weeks, and then in a short-arm cast for 4 to 8 weeks (Figure 2). If present, pins are removed in 3 to 12 weeks, with most authors recommending removal at 8 weeks.^2,14

Lastly, carpal tunnel symptoms can develop late and even after a successful reduction and surgical stabilization. One theory is that a significant perilunate injury can create slightly higher baseline carpal tunnel pressures, which can compromise the blood flow to the median nerve and cause carpal tunnel symptoms. Additionally, it is possible that direct median nerve contusion and/or traction injury via a displaced lunate can also cause these symptoms. Whatever the inciting cause of median-nerve irritation, a delayed carpal tunnel release is sometimes required.

Conclusion

Outcomes after either perilunate or lunate dislocation are fair to good at best but can be optimized with prompt, appropriate treatment. Closed reduction and casting as definitive treatment has been abandoned because of frequent loss of reduction.¹² Early open reduction (ie, less than 3 days after injury) has been shown to be beneficial.^1,2 However, even those treated early and with anatomic restoration of carpal alignment can expect a loss of grip strength and a range of motion of approximately 70% compared with the contralateral side.^2-5 A recent study has suggested that lesser-arc injures generally have a poorer overall outcome than their greater-arc counterparts.¹⁵

More than half of all patients with perilunate injuries will develop radiographic signs of osteoarthritis, and some will require additional salvage procedures.3-5 Kremer and colleagues4 showed that overall results after perilunate injuries deteriorate with time. However, according to a paper by Forli and colleagues5 in which patients were followed a minimum of 10 years after their injuries, the authors found that, despite radiographic progression of arthritis, most patients maintained reasonable hand function.

Perilunate injuries typically stem from a high-energy insult to the carpus. Because of their relative infrequency and often subtle radiographic and physical examination findings, these injuries are often undetected in the emergency department setting.¹ Early anatomic reduction of any carpal malalignment is essential. Even with optimal treatment, complications such as generalized wrist stiffness, diminished grip strength, and posttraumatic arthritis, commonly develop; however, recent studies suggest these issues are often well tolerated.^1-5 In this article, the diagnosis, treatment, and outcomes after perilunate injuries are examined. 

History and Physical Examination

Perilunate injuries result from high-energy trauma to the carpus. Patients with these injuries often present with vague wrist pain and loss of wrist motion. Their fingers are frequently held in slight flexion. The patient may complain of numbness and tingling in the median nerve distribution. An acute carpal tunnel syndrome can rapidly develop. The general belief is that acute carpal tunnel syndrome occurs more commonly in pure volar lunate dislocations than in dorsal perilunate dislocations. However, no studies compare the incidence of acute carpal tunnel syndrome in lunate versus perilunate dislocations.

Radiographic Evaluation

Standard radiographic evaluation of a potential perilunate injury includes posteroanterior (PA), lateral, and oblique views of the wrist (Figure 1). A scaphoid view (ie, PA view with the wrist in ulnar deviation) may also be helpful. The PA view is particularly helpful because it enables assessment of Gilula lines, which are imaginary lines drawn across the proximal and distal aspects of the proximal carpal row and the proximal aspect of the distal carpal row. These lines should appear as 3 smooth arcs running nearly parallel to each other.⁶ Any disruption in these lines suggests carpal incongruity. It may be possible to note a triangular-shaped lunate on the PA view, which is a sign of lunate dislocation.⁷ 

While the PA view is certainly useful, the lateral view is the most important in diagnosing a perilunate injury. The lateral view allows assessment of the collinearity of radius, lunate, and capitate. Any disruption in this collinearity strongly suggests a perilunate dislocation.^7,8 

Classification

Mayfield and colleagues^9,10 described 4 stages of perilunate instability proceeding from a radial to an ulnar direction around the lunate. Stage I involves disruption of the scapholunate joint, while stage II involves both the scapholunate and capitolunate joints. In stage III, the scapholunate, capitolunate, and lunotriquetral ligaments are disrupted, and the result is a perilunate dislocation, usually dorsal. Finally, in stage IV, all the ligaments surrounding the lunate are disrupted and the lunate dislocates, most often volarly.

Lastly, perilunate injuries can be classified as greater-arc injuries if concomitant fracture of the carpus occurs, lesser-arc injuries if the injury is purely ligamentous, or inferior-arc injuries if there is an associated fracture of the volar rim of the distal radius.⁸

Treatment

Closed Reduction

All acute perilunate dislocations should be managed initially with an attempted closed reduction.¹¹ If the injury is older than 72 hours, such an attempt may be futile. For any closed reduction performed in the emergency department setting, intravenous sedation is generally advised for muscle relaxation. Gentle traction with finger traps can also be used prior to the reduction attempt. For a dorsal perilunate dislocation, longitudinal traction followed by volar flexion of the wrist with volar pressure on the lunate and dorsal pressure on the capitate (ie, Tavernier’s maneuver) is required. Once reduction is complete, PA and lateral views of the wrist should be obtained to assess carpal alignment. If closed reduction is unsuccessful, an open reduction is required, although the timing of said procedure is an area of debate, which we will discuss later.^1,3 Restoration of anatomic carpal alignment is essential to optimizing outcome, although it does not guarantee a good overall result.

Open Reduction

If successful closed reduction is achieved, the patient can be immobilized temporarily in a short-arm plaster splint. However, open reduction and either pinning or internal fixation will be required to maintain this alignment. The exact timing of open reduction and fixation is debatable and often dictated by the absence or presence of median nerve symptoms.^1,3 If a patient with no median nerve symptoms undergoes a successful closed reduction, he or she may be stabilized surgically within 3 to 5 days (or longer) with either pins or headless screws. If closed reduction is unsuccessful, an open reduction should be done within 2 to 3 days. However, if the patient has progressive numbness in the median nerve distribution upon presentation that fails to improve or worsens despite a successful closed reduction, an urgent open reduction (within 24 hours) and carpal tunnel release should be performed to prevent permanent damage to the median nerve.

Once open reduction is undertaken, a dorsal, volar, and combined approach can be used.^2-4 In most cases the dorsal approach is selected first. A longitudinal incision is made over the dorsum of the wrist, centered on the Lister tubercle. Dissection occurs between the third and fourth dorsal compartments. After the capsule is exposed, reduction of the lunate to the capitate is confirmed. If any fractures are present in the carpus (eg, scaphoid), they are internally fixed. The scapholunate articulation is then addressed. In general, the scapholunate ligament is not disrupted with a transscaphoid perilunate dislocation. However, if the scapholunate ligament is disrupted, the joint should be reduced and pinned. Repair or reconstruction of the scapholunate ligament is performed. Finally, the lunotriquetral articulation is reduced and stabilized with pins. There are no studies that specifically suggest direct repair of the lunotriquetral ligament versus pinning of the lunotriquetral articulation, but the lunotriquetral ligament could be repaired in similar fashion to the scapholunate ligament at the surgeon’s discretion.

As an alternative to percutaneous pinning, intercarpal screw fixation can be used to stabilize the carpus. A 2007 study by Souer and colleagues¹² showed no substantial difference in outcome between the 2 methods of fixation. However, a second procedure is required to remove the screws.

The volar approach, if selected, is typically done second and performed via an extended carpal tunnel incision. It allows decompression of the carpal tunnel and enables repair of volar capsular ligaments (ie, long and short radiolunate ligaments, volar scapholunate ligament, and volar lunotriquetral ligament), which increases overall carpal stability. Currently, many surgeons favor a combined dorsal-volar approach for its efficacy.^2,3 Some use a dorsal approach in all patients and perform a volar procedure only if the patient has median nerve symptoms.⁴ However, Başar and colleagues¹³ report use of only the volar approach for treatment of perilunate injuries. The authors repaired the long and short radiolunate ligaments, volar scapholunate ligament, and volar lunotriquetral ligament. They reported reasonably good outcomes, which are equivalent to those reported in similar studies using dorsal or combined dorsal-volar approaches. However, no studies in the literature directly compare any of the different approaches with each other.

Postoperatively, patients are placed in a long-arm thumb-spica cast for 4 weeks, and then in a short-arm cast for 4 to 8 weeks (Figure 2). If present, pins are removed in 3 to 12 weeks, with most authors recommending removal at 8 weeks.^2,14

Lastly, carpal tunnel symptoms can develop late and even after a successful reduction and surgical stabilization. One theory is that a significant perilunate injury can create slightly higher baseline carpal tunnel pressures, which can compromise the blood flow to the median nerve and cause carpal tunnel symptoms. Additionally, it is possible that direct median nerve contusion and/or traction injury via a displaced lunate can also cause these symptoms. Whatever the inciting cause of median-nerve irritation, a delayed carpal tunnel release is sometimes required.

Conclusion

Outcomes after either perilunate or lunate dislocation are fair to good at best but can be optimized with prompt, appropriate treatment. Closed reduction and casting as definitive treatment has been abandoned because of frequent loss of reduction.¹² Early open reduction (ie, less than 3 days after injury) has been shown to be beneficial.^1,2 However, even those treated early and with anatomic restoration of carpal alignment can expect a loss of grip strength and a range of motion of approximately 70% compared with the contralateral side.^2-5 A recent study has suggested that lesser-arc injures generally have a poorer overall outcome than their greater-arc counterparts.¹⁵

More than half of all patients with perilunate injuries will develop radiographic signs of osteoarthritis, and some will require additional salvage procedures.3-5 Kremer and colleagues4 showed that overall results after perilunate injuries deteriorate with time. However, according to a paper by Forli and colleagues5 in which patients were followed a minimum of 10 years after their injuries, the authors found that, despite radiographic progression of arthritis, most patients maintained reasonable hand function.

Perilunate injuries typically stem from a high-energy insult to the carpus. Because of their relative infrequency and often subtle radiographic and physical examination findings, these injuries are often undetected in the emergency department setting.¹ Early anatomic reduction of any carpal malalignment is essential. Even with optimal treatment, complications such as generalized wrist stiffness, diminished grip strength, and posttraumatic arthritis, commonly develop; however, recent studies suggest these issues are often well tolerated.^1-5 In this article, the diagnosis, treatment, and outcomes after perilunate injuries are examined. 

History and Physical Examination

Perilunate injuries result from high-energy trauma to the carpus. Patients with these injuries often present with vague wrist pain and loss of wrist motion. Their fingers are frequently held in slight flexion. The patient may complain of numbness and tingling in the median nerve distribution. An acute carpal tunnel syndrome can rapidly develop. The general belief is that acute carpal tunnel syndrome occurs more commonly in pure volar lunate dislocations than in dorsal perilunate dislocations. However, no studies compare the incidence of acute carpal tunnel syndrome in lunate versus perilunate dislocations.

Radiographic Evaluation

Standard radiographic evaluation of a potential perilunate injury includes posteroanterior (PA), lateral, and oblique views of the wrist (Figure 1). A scaphoid view (ie, PA view with the wrist in ulnar deviation) may also be helpful. The PA view is particularly helpful because it enables assessment of Gilula lines, which are imaginary lines drawn across the proximal and distal aspects of the proximal carpal row and the proximal aspect of the distal carpal row. These lines should appear as 3 smooth arcs running nearly parallel to each other.⁶ Any disruption in these lines suggests carpal incongruity. It may be possible to note a triangular-shaped lunate on the PA view, which is a sign of lunate dislocation.⁷ 

While the PA view is certainly useful, the lateral view is the most important in diagnosing a perilunate injury. The lateral view allows assessment of the collinearity of radius, lunate, and capitate. Any disruption in this collinearity strongly suggests a perilunate dislocation.^7,8 

Classification

Mayfield and colleagues^9,10 described 4 stages of perilunate instability proceeding from a radial to an ulnar direction around the lunate. Stage I involves disruption of the scapholunate joint, while stage II involves both the scapholunate and capitolunate joints. In stage III, the scapholunate, capitolunate, and lunotriquetral ligaments are disrupted, and the result is a perilunate dislocation, usually dorsal. Finally, in stage IV, all the ligaments surrounding the lunate are disrupted and the lunate dislocates, most often volarly.

Lastly, perilunate injuries can be classified as greater-arc injuries if concomitant fracture of the carpus occurs, lesser-arc injuries if the injury is purely ligamentous, or inferior-arc injuries if there is an associated fracture of the volar rim of the distal radius.⁸

Treatment

Closed Reduction

All acute perilunate dislocations should be managed initially with an attempted closed reduction.¹¹ If the injury is older than 72 hours, such an attempt may be futile. For any closed reduction performed in the emergency department setting, intravenous sedation is generally advised for muscle relaxation. Gentle traction with finger traps can also be used prior to the reduction attempt. For a dorsal perilunate dislocation, longitudinal traction followed by volar flexion of the wrist with volar pressure on the lunate and dorsal pressure on the capitate (ie, Tavernier’s maneuver) is required. Once reduction is complete, PA and lateral views of the wrist should be obtained to assess carpal alignment. If closed reduction is unsuccessful, an open reduction is required, although the timing of said procedure is an area of debate, which we will discuss later.^1,3 Restoration of anatomic carpal alignment is essential to optimizing outcome, although it does not guarantee a good overall result.

Open Reduction

If successful closed reduction is achieved, the patient can be immobilized temporarily in a short-arm plaster splint. However, open reduction and either pinning or internal fixation will be required to maintain this alignment. The exact timing of open reduction and fixation is debatable and often dictated by the absence or presence of median nerve symptoms.^1,3 If a patient with no median nerve symptoms undergoes a successful closed reduction, he or she may be stabilized surgically within 3 to 5 days (or longer) with either pins or headless screws. If closed reduction is unsuccessful, an open reduction should be done within 2 to 3 days. However, if the patient has progressive numbness in the median nerve distribution upon presentation that fails to improve or worsens despite a successful closed reduction, an urgent open reduction (within 24 hours) and carpal tunnel release should be performed to prevent permanent damage to the median nerve.

Once open reduction is undertaken, a dorsal, volar, and combined approach can be used.^2-4 In most cases the dorsal approach is selected first. A longitudinal incision is made over the dorsum of the wrist, centered on the Lister tubercle. Dissection occurs between the third and fourth dorsal compartments. After the capsule is exposed, reduction of the lunate to the capitate is confirmed. If any fractures are present in the carpus (eg, scaphoid), they are internally fixed. The scapholunate articulation is then addressed. In general, the scapholunate ligament is not disrupted with a transscaphoid perilunate dislocation. However, if the scapholunate ligament is disrupted, the joint should be reduced and pinned. Repair or reconstruction of the scapholunate ligament is performed. Finally, the lunotriquetral articulation is reduced and stabilized with pins. There are no studies that specifically suggest direct repair of the lunotriquetral ligament versus pinning of the lunotriquetral articulation, but the lunotriquetral ligament could be repaired in similar fashion to the scapholunate ligament at the surgeon’s discretion.

As an alternative to percutaneous pinning, intercarpal screw fixation can be used to stabilize the carpus. A 2007 study by Souer and colleagues¹² showed no substantial difference in outcome between the 2 methods of fixation. However, a second procedure is required to remove the screws.

The volar approach, if selected, is typically done second and performed via an extended carpal tunnel incision. It allows decompression of the carpal tunnel and enables repair of volar capsular ligaments (ie, long and short radiolunate ligaments, volar scapholunate ligament, and volar lunotriquetral ligament), which increases overall carpal stability. Currently, many surgeons favor a combined dorsal-volar approach for its efficacy.^2,3 Some use a dorsal approach in all patients and perform a volar procedure only if the patient has median nerve symptoms.⁴ However, Başar and colleagues¹³ report use of only the volar approach for treatment of perilunate injuries. The authors repaired the long and short radiolunate ligaments, volar scapholunate ligament, and volar lunotriquetral ligament. They reported reasonably good outcomes, which are equivalent to those reported in similar studies using dorsal or combined dorsal-volar approaches. However, no studies in the literature directly compare any of the different approaches with each other.

Postoperatively, patients are placed in a long-arm thumb-spica cast for 4 weeks, and then in a short-arm cast for 4 to 8 weeks (Figure 2). If present, pins are removed in 3 to 12 weeks, with most authors recommending removal at 8 weeks.^2,14

Lastly, carpal tunnel symptoms can develop late and even after a successful reduction and surgical stabilization. One theory is that a significant perilunate injury can create slightly higher baseline carpal tunnel pressures, which can compromise the blood flow to the median nerve and cause carpal tunnel symptoms. Additionally, it is possible that direct median nerve contusion and/or traction injury via a displaced lunate can also cause these symptoms. Whatever the inciting cause of median-nerve irritation, a delayed carpal tunnel release is sometimes required.

Conclusion

Outcomes after either perilunate or lunate dislocation are fair to good at best but can be optimized with prompt, appropriate treatment. Closed reduction and casting as definitive treatment has been abandoned because of frequent loss of reduction.¹² Early open reduction (ie, less than 3 days after injury) has been shown to be beneficial.^1,2 However, even those treated early and with anatomic restoration of carpal alignment can expect a loss of grip strength and a range of motion of approximately 70% compared with the contralateral side.^2-5 A recent study has suggested that lesser-arc injures generally have a poorer overall outcome than their greater-arc counterparts.¹⁵

More than half of all patients with perilunate injuries will develop radiographic signs of osteoarthritis, and some will require additional salvage procedures.3-5 Kremer and colleagues4 showed that overall results after perilunate injuries deteriorate with time. However, according to a paper by Forli and colleagues5 in which patients were followed a minimum of 10 years after their injuries, the authors found that, despite radiographic progression of arthritis, most patients maintained reasonable hand function.

With older women in the United States about 4 times more likely than their male counterparts to develop osteoporosis,^1,2 physicians often fail to screen for—or to treat—low bone mass in men. There are plenty of reasons why they should.

First and foremost: Osteoporosis is a leading cause of morbidity and mortality in the elderly.³ An estimated 8.8 million American men suffer from osteoporosis or osteopenia.³ And, although only about 20% of osteoporosis patients are male, men sustain between 30% and 40% of osteoporotic fractures.^1,2 What’s more, hip fracture in men has a mortality rate of up to 37.5%—2 to 3 times higher than that of women with hip fracture.^4,5

Clearly, then, it is crucial to be aware of the risks of osteoporosis faced by both men and women as they age. Here’s a look at what to consider, when to screen, and how to treat male patients who have, or are at risk for, osteoporosis.

Which men are at risk? 

The incidence of fractures secondary to osteoporosis varies with race/ethnicity and geography. The highest rates worldwide occur in Scandinavia and among Caucasians in the United States; black, Asian, and Hispanic populations have the lowest rates.^6,7 As with women, the risk of osteoporotic fracture in men increases with age. However, the peak incidence of fracture occurs about 10 years later in men than in women, starting at about age 70.⁸ Approximately 13% of white men older than 50 years will experience at least one osteoporotic fracture.⁹

There are 2 main types of osteoporosis: primary and secondary. Up to 40% of osteoporosis in men is primary,⁴ with bone loss due either to age (senile osteoporosis) or to an unknown cause (idiopathic osteoporosis).¹⁰ For men 70 years or older, osteoporosis is assumed to be age related. Idiopathic osteoporosis is diagnosed only in men younger than 70 who have no obvious secondary cause.¹⁰ There are numerous secondary causes, however, and most men with bone loss have at least one.⁴

Common secondary causes: Lifestyle, medical conditions, and meds

The most common causes of secondary osteoporosis in men are exposure to glucocorticoids, primary or secondary hypogonadism (low testosterone), diabetes, alcohol abuse, smoking, gastrointestinal (GI) disease, hypercalciuria, low body weight (body mass index <20 kg/m2), and immobility (TABLE 1).^4,5,8,10

Chronic use of corticosteroids, often used to treat chronic obstructive pulmonary disease (COPD), asthma, and rheumatoid arthritis, directly affects the bone, decreasing skeletal muscle, increasing immobility, and reducing intestinal absorption of calcium as well as serum testosterone levels.¹⁰ Men with androgen deficiency (which may be due to androgen deprivation therapy to treat prostate cancer) or chronic use of opioids are also at increased risk.^4,5,10-12

Diagnostic screening and criteria

The World Health Organization has established diagnostic criteria for osteoporosis using bone mineral density (BMD), reported as both T-scores and Z-scores as measured on dual-energy x-ray absorptiometry (DEXA) scan.¹³ The T-score represents the number of standard deviations above or below the mean BMD for young adults, matched for sex and race, but not age. It classifies individuals into 3 categories: normal; low (osteopenia), with a T-score between -1 and -2.5; and osteoporosis (T-score ≤-2.5).^4,14 The Z-score indicates the number of standard deviations above or below the mean for age, as well as sex and race. A Z-score of ≤-2.0 is below the expected range, indicating an increased likelihood of a secondary form of osteoporosis.¹⁴

Which men to screen?

The US Preventive Services Task Force has concluded that evidence is insufficient to assess the balance of benefits and harms of screening for osteoporosis in men. It therefore makes no recommendation to screen men who don't have evidence of previous fractures or secondary causes of osteoporosis.¹⁵

Other organizations agree that there is insufficient evidence to recommend routine screening for men without known osteoporotic fractures or secondary causes for osteoporosis. There are, however, some guidelines that are useful in clinical practice.

The most common causes of secondary osteoporosis in men include exposure to glucocorticoids, primary or secondary hypogonadism, diabetes, alcohol abuse, and smoking.

The Endocrine Society, American College of Physicians (ACP), and National Osteoporosis Foundation (NOF) recommend screening men ages 70 years or older, and men ages 50 to 69 who have risk factors for fracture and/or a history of fracture sustained after age 50.^5,16,17 (See “Did you know?”)^{1,2,4,5,9-12,16,17} Prior to screening, it is important to do a complete medical history and physical examination.

Screening considerations. The Endocrine Society, ACP, and NOF recommend a DEXA scan of the spine and hip for men who are at increased risk for osteoporosis and have no contraindications to drug therapy.^5,16,17 In patients who have degenerative changes of the spine and hip that would likely obscure DEXA outcomes, a scan of the radius may provide a more accurate assessment of bone status. Men receiving androgen deprivation therapy for prostate cancer will have a greater decline of bone density in the radius than in the hip or spine and are therefore ideal candidates for DEXA of the forearm, as well.^5,11 Keep in mind, however, that no studies have looked at how well, or whether, men with osteoporosis measured only in the radius respond to treatment.⁵

A DEXA scan is not always widely available, nor is it a perfect predictor of fracture risk. In addition, it is not always cost effective. For some patients, the use of a validated clinical predictive tool is preferable as an initial option.

The Male Osteoporosis Risk Estimation Score (MORES) uses age, weight, and history of COPD to identify men 60 years or older who are at risk for osteoporosis (TABLE 2).¹⁸ The score can be easily calculated during a clinical encounter and is beneficial for identifying men who should be referred for DEXA scan. A score of ≥6 has been found to yield an overall sensitivity of 0.93 (95% confidence interval [CI], 0.85-0.97) and a specificity of 0.59 (95% CI, 0.56-0.62), with a number needed to screen to prevent one additional hip fracture of 279.¹⁸

The Osteoporosis Self-assessment Tool (OST) (http://depts.washington.edu/osteoed/tools.php?type=ost) is a calculated value that uses age and weight to determine an individual’s risk for osteoporosis (risk score=weight [in kg] – age [in years]/5).^16,19 Although there is not a defined value to determine a positive OST risk score, scores of -1 to 3 have been used in a variety of studies.¹⁶ In a study of 181 American men, the OST predicted osteoporosis with a sensitivity of 93% and a specificity of 66% when using a cutoff score of 3.²⁰

Treating men at risk

Pharmacologic therapy is recommended for men at an increased risk for fracture. This includes men who have had a hip or vertebral fracture without major trauma, as well as those who have not had such a fracture but have a BMD of the spine, femoral neck, and/or total hip of ≤-2.5.^5,17 This standard also applies to the radius when used as an alternative site.

Several organizations recommend screening men ages ≥70 years and those ages 50 to 69 who have risk factors for fractures or who sustained a fracture after age 50.

The International Society for Clinical Densitometry and International Osteoporosis Foundation endorse the use of the Fracture Risk Assessment Tool (FRAX). Available at http://shef.ac.uk/FRAX/tool.aspx?country=9, FRAX is a computer-based calculator that uses risk factors and BMD of the femoral neck to estimate an individual’s 10-year fracture probability.²¹ Men who are 50 years or older, have a T-score between -1.0 and -2.5 in the spine, femoral neck, or total hip, and a 10-year risk of ≥20% of developing any fracture or ≥3% of developing a hip fracture based on FRAX, should be offered pharmacotherapy.^5,17

Bisphosphonates are first-line therapy

Although oral bisphosphonates are first-line therapy for men who meet these criteria,⁴ pharmacotherapy should be individualized based on factors such as fracture history, severity of osteoporosis, comorbidities (eg, peptic ulcer disease, malignancy, renal disease, or malabsorption), and cost (TABLE 3).^22,23

Alendronate once weekly has been proven to increase BMD and to reduce the risk of fracture in men.^24,25 A randomized, placebo-controlled trial of 241 men with osteoporosis found that alendronate increased BMD by 7.1% (±0.3) at the lumbar spine, 2.5% (±0.4) at the femoral neck, and 2% (±0.2) for the total body. Those in the placebo group had a 1.8% (±0.5) increase in BMD of the lumbar spine, with no significant change in femoral neck or total-body BMD—and a higher incidence of vertebral fractures (7.1% vs. 0.8% for those on alendronate; P=.02).²⁴

Risedronate once daily has also been proven to increase BMD in the lumbar spine and hip, with a reduction in vertebral fractures.²⁶ Another investigation—a 2-year, multicenter double-blind placebo-controlled study of 284 men with osteoporosis—found that risedronate given once a week increased BMD in the spine and hip, but did not reduce the incidence of either vertebral or nonvertebral fractures.²⁷

Because a DEXA scan is not always available or cost effective, a validated clinical predictive tool is preferred as an intial screening option.

Both alendronate and risedronate are effective for secondary causes of bone loss, such as corticosteroid use, androgen deprivation therapy/hypogonadism, and rheumatologic conditions.²⁸ Oral bisphosphonates may cause GI irritation, however. Abdominal pain associated with alendronate use is between 1% and 7%, vs 2% to 12% for risedronate.²³ Neither medication is recommended for use in patients with an estimated glomerular filtration rate <35 mL/min.²³ There is no clearly established duration of therapy for men.

Zoledronic acid infusions, given intravenously (IV) once a year, are available for men who cannot tolerate oral bisphosphonates. In a multicenter double-blind, placebocontrolled trial, zoledronic acid was found to reduce the risk of vertebral fractures in men with primary or hypogonadism-associated osteoporosis by 67% (1.6% vertebral fractures in the treatment group after 24 months vs 4.9% with placebo).²⁹ Given within 90 days of a hip fracture repair, zoledronic acid was associated with both a reduction in the rate of new fractures and an increased survival rate.³⁰

Adverse effects of zoledronic acid include diffuse bone pain (3%-9%), fever (9%-22%) and flu-like symptoms (1%-11%). Osteonecrosis of the jaw has been reported in <1% of patients.²³

Recombinant human parathyroid hormone stimulates bone growth

Pharmacotherapy should be individualized based on factors such as fracture history, severity of osteoporosis, comorbidities (eg, peptic ulcer disease, malignancy), and cost.

Teriparatide, administered subcutaneously (SC) once a day, directly stimulates bone formation. In a randomized placebo controlled trial of 437 men with a T-score of -2, teriparatide was found to increase BMD at the spine and femoral neck. Participants were randomized to receive teriparatide (20 or 40 mcg/d) or placebo. Those who received teriparatide had a doserelated increase in BMD from baseline at the spine (5.9% with 20 mcg and 9% with 40 mcg) and femoral neck (1.5% and 2.9%, respectively) compared with the placebo group.³¹ Teriparatide was shown to reduce vertebral fractures by 51% compared with placebo in a randomized study of 355 men with osteoporosis.³²

Teriparatide is indicated for men with severe osteoporosis and those for whom bisphosphonate treatment has been unsuccessful. Its use is limited to 2 years due to a dose-dependent risk of osteosarcoma. Teriparatide is contraindicated in patients with skeletal metastasis and has been associated with transient hypercalcemia 4 to 6 hours after administration.²³ Its use in combination with bisphosphonates is not recommended due to the lack of proven benefit, risk of adverse effects, and associated cost.⁵

Testosterone boosts bone density

Testosterone therapy is recommended for men with low levels of testosterone (<200 ng/dL), high risk for fracture, and contraindications to pharmacologic agents approved for the treatment of osteoporosis.⁵ Supplementation of testosterone to restore correct physiologic levels will decrease bone turnover and increase bone density.³³ In a meta-analysis of 8 trials with a total of 365 participants, testosterone administered intramuscularly was found to increase lumbar BMD by 8% compared with placebo. The effect on fractures is not known.¹²

Monoclonal antibody reduces fracture risk

Denosumab, a monoclonal antibody that prevents osteoclast formation leading to decreased bone resorption, is administered SC every 6 months.²³ In a placebo-controlled trial of 242 men with low bone mass, denosumab increased BMD at the lumbar spine (5.7%), total hip (2.4%), femoral neck (2.1%), trochanter (3.1%), and one-third radius (0.6%) compared with placebo after one year.³⁴ In men receiving androgen deprivation therapy for nonmetastatic prostate cancer, denosumab has been shown to increase BMD and reduce the incidence of vertebral fractures.³⁵

Adverse effects include hypocalcemia, hypophosphatemia, fatigue, and back pain.²³ No data exist on the ability of denosumab to reduce fracture risk in men without androgen deprivation.

Calcium and vitamin D for men at risk

Men who are at risk for or have osteoporosis should consume 1000 mg to 1200 mg of calcium per day. Ideally, this should come through dietary sources, but calcium supplementation may be added when diet is inadequate.⁵ The Institute of Medicine recommends a calcium intake of 1000 mg/d for men ages 51 to 70 years and 1200 mg/d for men ages 70 and older.³⁶

Supplementation of testosterone to restore correct physiologic levels in men with low testosterone will decrease bone turnover and increase bone density.

Men with vitamin D levels below 30 ng/mL should receive vitamin D supplementation to attain blood 25(OH) D levels of at least 30 ng/mL.⁵ The Institute of Medicine recommends a daily intake of 600 international units (IU) of vitamin D for men ages 51 to 70 and 800 IU for men 70 and older.³⁶ A recent Cochrane review on vitamin D and vitamin D analogues concluded that vitamin D alone was unlikely to prevent fractures in older people; when taken with calcium, however, it may have a preventive effect.³⁷

Counseling and follow-up

Lifestyle modification is an important means of primary prevention for osteoporosis. Advise men at risk for osteoporosis to limit alcohol consumption to 2 drinks daily.^4,5,8,10 Tell those who smoke that doing so increases their risk for osteoporotic fracture and refer them for smoking cessation counseling. Emphasize that weight-bearing exercise can improve BMD and should be done at least 3 days per week.^4,5,8,10 It is important, too, to do a medication review to look for drug-drug interactions and to discuss fall prevention strategies, such as gait training and an environmental assessment and removal of fall hazards.

A Cochrane review concluded that vitamin D alone was unlikely to prevent fractures in older people; when taken with calcium, however, it may have a preventive effect.

The evidence for monitoring treatment using BMD is not very strong.^5,14 However, the Endocrine Society recommends that response to treatment be monitored using DEXA scans every one to 2 years, with reduced frequency once the BMD has stabilized.⁵ Any patient found to have a decrease in BMD after treatment is initiated should undergo further evaluation to determine the cause of the decline.

CORRESPONDENCE
Bryan Farford, DO, Mayo Clinic Division of Regional Medicine, 742 Marsh Landing Parkway, Jacksonville Beach, FL 32250; [email protected]

With older women in the United States about 4 times more likely than their male counterparts to develop osteoporosis,^1,2 physicians often fail to screen for—or to treat—low bone mass in men. There are plenty of reasons why they should.

First and foremost: Osteoporosis is a leading cause of morbidity and mortality in the elderly.³ An estimated 8.8 million American men suffer from osteoporosis or osteopenia.³ And, although only about 20% of osteoporosis patients are male, men sustain between 30% and 40% of osteoporotic fractures.^1,2 What’s more, hip fracture in men has a mortality rate of up to 37.5%—2 to 3 times higher than that of women with hip fracture.^4,5

Clearly, then, it is crucial to be aware of the risks of osteoporosis faced by both men and women as they age. Here’s a look at what to consider, when to screen, and how to treat male patients who have, or are at risk for, osteoporosis.

Which men are at risk? 

The incidence of fractures secondary to osteoporosis varies with race/ethnicity and geography. The highest rates worldwide occur in Scandinavia and among Caucasians in the United States; black, Asian, and Hispanic populations have the lowest rates.^6,7 As with women, the risk of osteoporotic fracture in men increases with age. However, the peak incidence of fracture occurs about 10 years later in men than in women, starting at about age 70.⁸ Approximately 13% of white men older than 50 years will experience at least one osteoporotic fracture.⁹

There are 2 main types of osteoporosis: primary and secondary. Up to 40% of osteoporosis in men is primary,⁴ with bone loss due either to age (senile osteoporosis) or to an unknown cause (idiopathic osteoporosis).¹⁰ For men 70 years or older, osteoporosis is assumed to be age related. Idiopathic osteoporosis is diagnosed only in men younger than 70 who have no obvious secondary cause.¹⁰ There are numerous secondary causes, however, and most men with bone loss have at least one.⁴

Common secondary causes: Lifestyle, medical conditions, and meds

The most common causes of secondary osteoporosis in men are exposure to glucocorticoids, primary or secondary hypogonadism (low testosterone), diabetes, alcohol abuse, smoking, gastrointestinal (GI) disease, hypercalciuria, low body weight (body mass index <20 kg/m2), and immobility (TABLE 1).^4,5,8,10

Chronic use of corticosteroids, often used to treat chronic obstructive pulmonary disease (COPD), asthma, and rheumatoid arthritis, directly affects the bone, decreasing skeletal muscle, increasing immobility, and reducing intestinal absorption of calcium as well as serum testosterone levels.¹⁰ Men with androgen deficiency (which may be due to androgen deprivation therapy to treat prostate cancer) or chronic use of opioids are also at increased risk.^4,5,10-12

Diagnostic screening and criteria

The World Health Organization has established diagnostic criteria for osteoporosis using bone mineral density (BMD), reported as both T-scores and Z-scores as measured on dual-energy x-ray absorptiometry (DEXA) scan.¹³ The T-score represents the number of standard deviations above or below the mean BMD for young adults, matched for sex and race, but not age. It classifies individuals into 3 categories: normal; low (osteopenia), with a T-score between -1 and -2.5; and osteoporosis (T-score ≤-2.5).^4,14 The Z-score indicates the number of standard deviations above or below the mean for age, as well as sex and race. A Z-score of ≤-2.0 is below the expected range, indicating an increased likelihood of a secondary form of osteoporosis.¹⁴

Which men to screen?

The US Preventive Services Task Force has concluded that evidence is insufficient to assess the balance of benefits and harms of screening for osteoporosis in men. It therefore makes no recommendation to screen men who don't have evidence of previous fractures or secondary causes of osteoporosis.¹⁵

Other organizations agree that there is insufficient evidence to recommend routine screening for men without known osteoporotic fractures or secondary causes for osteoporosis. There are, however, some guidelines that are useful in clinical practice.

The most common causes of secondary osteoporosis in men include exposure to glucocorticoids, primary or secondary hypogonadism, diabetes, alcohol abuse, and smoking.

The Endocrine Society, American College of Physicians (ACP), and National Osteoporosis Foundation (NOF) recommend screening men ages 70 years or older, and men ages 50 to 69 who have risk factors for fracture and/or a history of fracture sustained after age 50.^5,16,17 (See “Did you know?”)^{1,2,4,5,9-12,16,17} Prior to screening, it is important to do a complete medical history and physical examination.

Screening considerations. The Endocrine Society, ACP, and NOF recommend a DEXA scan of the spine and hip for men who are at increased risk for osteoporosis and have no contraindications to drug therapy.^5,16,17 In patients who have degenerative changes of the spine and hip that would likely obscure DEXA outcomes, a scan of the radius may provide a more accurate assessment of bone status. Men receiving androgen deprivation therapy for prostate cancer will have a greater decline of bone density in the radius than in the hip or spine and are therefore ideal candidates for DEXA of the forearm, as well.^5,11 Keep in mind, however, that no studies have looked at how well, or whether, men with osteoporosis measured only in the radius respond to treatment.⁵

A DEXA scan is not always widely available, nor is it a perfect predictor of fracture risk. In addition, it is not always cost effective. For some patients, the use of a validated clinical predictive tool is preferable as an initial option.

The Male Osteoporosis Risk Estimation Score (MORES) uses age, weight, and history of COPD to identify men 60 years or older who are at risk for osteoporosis (TABLE 2).¹⁸ The score can be easily calculated during a clinical encounter and is beneficial for identifying men who should be referred for DEXA scan. A score of ≥6 has been found to yield an overall sensitivity of 0.93 (95% confidence interval [CI], 0.85-0.97) and a specificity of 0.59 (95% CI, 0.56-0.62), with a number needed to screen to prevent one additional hip fracture of 279.¹⁸

The Osteoporosis Self-assessment Tool (OST) (http://depts.washington.edu/osteoed/tools.php?type=ost) is a calculated value that uses age and weight to determine an individual’s risk for osteoporosis (risk score=weight [in kg] – age [in years]/5).^16,19 Although there is not a defined value to determine a positive OST risk score, scores of -1 to 3 have been used in a variety of studies.¹⁶ In a study of 181 American men, the OST predicted osteoporosis with a sensitivity of 93% and a specificity of 66% when using a cutoff score of 3.²⁰

Treating men at risk

Pharmacologic therapy is recommended for men at an increased risk for fracture. This includes men who have had a hip or vertebral fracture without major trauma, as well as those who have not had such a fracture but have a BMD of the spine, femoral neck, and/or total hip of ≤-2.5.^5,17 This standard also applies to the radius when used as an alternative site.

Several organizations recommend screening men ages ≥70 years and those ages 50 to 69 who have risk factors for fractures or who sustained a fracture after age 50.

The International Society for Clinical Densitometry and International Osteoporosis Foundation endorse the use of the Fracture Risk Assessment Tool (FRAX). Available at http://shef.ac.uk/FRAX/tool.aspx?country=9, FRAX is a computer-based calculator that uses risk factors and BMD of the femoral neck to estimate an individual’s 10-year fracture probability.²¹ Men who are 50 years or older, have a T-score between -1.0 and -2.5 in the spine, femoral neck, or total hip, and a 10-year risk of ≥20% of developing any fracture or ≥3% of developing a hip fracture based on FRAX, should be offered pharmacotherapy.^5,17

Bisphosphonates are first-line therapy

Although oral bisphosphonates are first-line therapy for men who meet these criteria,⁴ pharmacotherapy should be individualized based on factors such as fracture history, severity of osteoporosis, comorbidities (eg, peptic ulcer disease, malignancy, renal disease, or malabsorption), and cost (TABLE 3).^22,23

Alendronate once weekly has been proven to increase BMD and to reduce the risk of fracture in men.^24,25 A randomized, placebo-controlled trial of 241 men with osteoporosis found that alendronate increased BMD by 7.1% (±0.3) at the lumbar spine, 2.5% (±0.4) at the femoral neck, and 2% (±0.2) for the total body. Those in the placebo group had a 1.8% (±0.5) increase in BMD of the lumbar spine, with no significant change in femoral neck or total-body BMD—and a higher incidence of vertebral fractures (7.1% vs. 0.8% for those on alendronate; P=.02).²⁴

Risedronate once daily has also been proven to increase BMD in the lumbar spine and hip, with a reduction in vertebral fractures.²⁶ Another investigation—a 2-year, multicenter double-blind placebo-controlled study of 284 men with osteoporosis—found that risedronate given once a week increased BMD in the spine and hip, but did not reduce the incidence of either vertebral or nonvertebral fractures.²⁷

Because a DEXA scan is not always available or cost effective, a validated clinical predictive tool is preferred as an intial screening option.

Both alendronate and risedronate are effective for secondary causes of bone loss, such as corticosteroid use, androgen deprivation therapy/hypogonadism, and rheumatologic conditions.²⁸ Oral bisphosphonates may cause GI irritation, however. Abdominal pain associated with alendronate use is between 1% and 7%, vs 2% to 12% for risedronate.²³ Neither medication is recommended for use in patients with an estimated glomerular filtration rate <35 mL/min.²³ There is no clearly established duration of therapy for men.

Zoledronic acid infusions, given intravenously (IV) once a year, are available for men who cannot tolerate oral bisphosphonates. In a multicenter double-blind, placebocontrolled trial, zoledronic acid was found to reduce the risk of vertebral fractures in men with primary or hypogonadism-associated osteoporosis by 67% (1.6% vertebral fractures in the treatment group after 24 months vs 4.9% with placebo).²⁹ Given within 90 days of a hip fracture repair, zoledronic acid was associated with both a reduction in the rate of new fractures and an increased survival rate.³⁰

Adverse effects of zoledronic acid include diffuse bone pain (3%-9%), fever (9%-22%) and flu-like symptoms (1%-11%). Osteonecrosis of the jaw has been reported in <1% of patients.²³

Recombinant human parathyroid hormone stimulates bone growth

Pharmacotherapy should be individualized based on factors such as fracture history, severity of osteoporosis, comorbidities (eg, peptic ulcer disease, malignancy), and cost.

Teriparatide, administered subcutaneously (SC) once a day, directly stimulates bone formation. In a randomized placebo controlled trial of 437 men with a T-score of -2, teriparatide was found to increase BMD at the spine and femoral neck. Participants were randomized to receive teriparatide (20 or 40 mcg/d) or placebo. Those who received teriparatide had a doserelated increase in BMD from baseline at the spine (5.9% with 20 mcg and 9% with 40 mcg) and femoral neck (1.5% and 2.9%, respectively) compared with the placebo group.³¹ Teriparatide was shown to reduce vertebral fractures by 51% compared with placebo in a randomized study of 355 men with osteoporosis.³²

Teriparatide is indicated for men with severe osteoporosis and those for whom bisphosphonate treatment has been unsuccessful. Its use is limited to 2 years due to a dose-dependent risk of osteosarcoma. Teriparatide is contraindicated in patients with skeletal metastasis and has been associated with transient hypercalcemia 4 to 6 hours after administration.²³ Its use in combination with bisphosphonates is not recommended due to the lack of proven benefit, risk of adverse effects, and associated cost.⁵

Testosterone boosts bone density

Testosterone therapy is recommended for men with low levels of testosterone (<200 ng/dL), high risk for fracture, and contraindications to pharmacologic agents approved for the treatment of osteoporosis.⁵ Supplementation of testosterone to restore correct physiologic levels will decrease bone turnover and increase bone density.³³ In a meta-analysis of 8 trials with a total of 365 participants, testosterone administered intramuscularly was found to increase lumbar BMD by 8% compared with placebo. The effect on fractures is not known.¹²

Monoclonal antibody reduces fracture risk

Denosumab, a monoclonal antibody that prevents osteoclast formation leading to decreased bone resorption, is administered SC every 6 months.²³ In a placebo-controlled trial of 242 men with low bone mass, denosumab increased BMD at the lumbar spine (5.7%), total hip (2.4%), femoral neck (2.1%), trochanter (3.1%), and one-third radius (0.6%) compared with placebo after one year.³⁴ In men receiving androgen deprivation therapy for nonmetastatic prostate cancer, denosumab has been shown to increase BMD and reduce the incidence of vertebral fractures.³⁵

Adverse effects include hypocalcemia, hypophosphatemia, fatigue, and back pain.²³ No data exist on the ability of denosumab to reduce fracture risk in men without androgen deprivation.

Calcium and vitamin D for men at risk

Men who are at risk for or have osteoporosis should consume 1000 mg to 1200 mg of calcium per day. Ideally, this should come through dietary sources, but calcium supplementation may be added when diet is inadequate.⁵ The Institute of Medicine recommends a calcium intake of 1000 mg/d for men ages 51 to 70 years and 1200 mg/d for men ages 70 and older.³⁶

Supplementation of testosterone to restore correct physiologic levels in men with low testosterone will decrease bone turnover and increase bone density.

Men with vitamin D levels below 30 ng/mL should receive vitamin D supplementation to attain blood 25(OH) D levels of at least 30 ng/mL.⁵ The Institute of Medicine recommends a daily intake of 600 international units (IU) of vitamin D for men ages 51 to 70 and 800 IU for men 70 and older.³⁶ A recent Cochrane review on vitamin D and vitamin D analogues concluded that vitamin D alone was unlikely to prevent fractures in older people; when taken with calcium, however, it may have a preventive effect.³⁷

Counseling and follow-up

Lifestyle modification is an important means of primary prevention for osteoporosis. Advise men at risk for osteoporosis to limit alcohol consumption to 2 drinks daily.^4,5,8,10 Tell those who smoke that doing so increases their risk for osteoporotic fracture and refer them for smoking cessation counseling. Emphasize that weight-bearing exercise can improve BMD and should be done at least 3 days per week.^4,5,8,10 It is important, too, to do a medication review to look for drug-drug interactions and to discuss fall prevention strategies, such as gait training and an environmental assessment and removal of fall hazards.

A Cochrane review concluded that vitamin D alone was unlikely to prevent fractures in older people; when taken with calcium, however, it may have a preventive effect.

The evidence for monitoring treatment using BMD is not very strong.^5,14 However, the Endocrine Society recommends that response to treatment be monitored using DEXA scans every one to 2 years, with reduced frequency once the BMD has stabilized.⁵ Any patient found to have a decrease in BMD after treatment is initiated should undergo further evaluation to determine the cause of the decline.

CORRESPONDENCE
Bryan Farford, DO, Mayo Clinic Division of Regional Medicine, 742 Marsh Landing Parkway, Jacksonville Beach, FL 32250; [email protected]

With older women in the United States about 4 times more likely than their male counterparts to develop osteoporosis,^1,2 physicians often fail to screen for—or to treat—low bone mass in men. There are plenty of reasons why they should.

First and foremost: Osteoporosis is a leading cause of morbidity and mortality in the elderly.³ An estimated 8.8 million American men suffer from osteoporosis or osteopenia.³ And, although only about 20% of osteoporosis patients are male, men sustain between 30% and 40% of osteoporotic fractures.^1,2 What’s more, hip fracture in men has a mortality rate of up to 37.5%—2 to 3 times higher than that of women with hip fracture.^4,5

Clearly, then, it is crucial to be aware of the risks of osteoporosis faced by both men and women as they age. Here’s a look at what to consider, when to screen, and how to treat male patients who have, or are at risk for, osteoporosis.

Which men are at risk? 

The incidence of fractures secondary to osteoporosis varies with race/ethnicity and geography. The highest rates worldwide occur in Scandinavia and among Caucasians in the United States; black, Asian, and Hispanic populations have the lowest rates.^6,7 As with women, the risk of osteoporotic fracture in men increases with age. However, the peak incidence of fracture occurs about 10 years later in men than in women, starting at about age 70.⁸ Approximately 13% of white men older than 50 years will experience at least one osteoporotic fracture.⁹

There are 2 main types of osteoporosis: primary and secondary. Up to 40% of osteoporosis in men is primary,⁴ with bone loss due either to age (senile osteoporosis) or to an unknown cause (idiopathic osteoporosis).¹⁰ For men 70 years or older, osteoporosis is assumed to be age related. Idiopathic osteoporosis is diagnosed only in men younger than 70 who have no obvious secondary cause.¹⁰ There are numerous secondary causes, however, and most men with bone loss have at least one.⁴

Common secondary causes: Lifestyle, medical conditions, and meds

The most common causes of secondary osteoporosis in men are exposure to glucocorticoids, primary or secondary hypogonadism (low testosterone), diabetes, alcohol abuse, smoking, gastrointestinal (GI) disease, hypercalciuria, low body weight (body mass index <20 kg/m2), and immobility (TABLE 1).^4,5,8,10

Chronic use of corticosteroids, often used to treat chronic obstructive pulmonary disease (COPD), asthma, and rheumatoid arthritis, directly affects the bone, decreasing skeletal muscle, increasing immobility, and reducing intestinal absorption of calcium as well as serum testosterone levels.¹⁰ Men with androgen deficiency (which may be due to androgen deprivation therapy to treat prostate cancer) or chronic use of opioids are also at increased risk.^4,5,10-12

Diagnostic screening and criteria

The World Health Organization has established diagnostic criteria for osteoporosis using bone mineral density (BMD), reported as both T-scores and Z-scores as measured on dual-energy x-ray absorptiometry (DEXA) scan.¹³ The T-score represents the number of standard deviations above or below the mean BMD for young adults, matched for sex and race, but not age. It classifies individuals into 3 categories: normal; low (osteopenia), with a T-score between -1 and -2.5; and osteoporosis (T-score ≤-2.5).^4,14 The Z-score indicates the number of standard deviations above or below the mean for age, as well as sex and race. A Z-score of ≤-2.0 is below the expected range, indicating an increased likelihood of a secondary form of osteoporosis.¹⁴

Which men to screen?

The US Preventive Services Task Force has concluded that evidence is insufficient to assess the balance of benefits and harms of screening for osteoporosis in men. It therefore makes no recommendation to screen men who don't have evidence of previous fractures or secondary causes of osteoporosis.¹⁵

Other organizations agree that there is insufficient evidence to recommend routine screening for men without known osteoporotic fractures or secondary causes for osteoporosis. There are, however, some guidelines that are useful in clinical practice.

The most common causes of secondary osteoporosis in men include exposure to glucocorticoids, primary or secondary hypogonadism, diabetes, alcohol abuse, and smoking.

The Endocrine Society, American College of Physicians (ACP), and National Osteoporosis Foundation (NOF) recommend screening men ages 70 years or older, and men ages 50 to 69 who have risk factors for fracture and/or a history of fracture sustained after age 50.^5,16,17 (See “Did you know?”)^{1,2,4,5,9-12,16,17} Prior to screening, it is important to do a complete medical history and physical examination.

Screening considerations. The Endocrine Society, ACP, and NOF recommend a DEXA scan of the spine and hip for men who are at increased risk for osteoporosis and have no contraindications to drug therapy.^5,16,17 In patients who have degenerative changes of the spine and hip that would likely obscure DEXA outcomes, a scan of the radius may provide a more accurate assessment of bone status. Men receiving androgen deprivation therapy for prostate cancer will have a greater decline of bone density in the radius than in the hip or spine and are therefore ideal candidates for DEXA of the forearm, as well.^5,11 Keep in mind, however, that no studies have looked at how well, or whether, men with osteoporosis measured only in the radius respond to treatment.⁵

A DEXA scan is not always widely available, nor is it a perfect predictor of fracture risk. In addition, it is not always cost effective. For some patients, the use of a validated clinical predictive tool is preferable as an initial option.

The Male Osteoporosis Risk Estimation Score (MORES) uses age, weight, and history of COPD to identify men 60 years or older who are at risk for osteoporosis (TABLE 2).¹⁸ The score can be easily calculated during a clinical encounter and is beneficial for identifying men who should be referred for DEXA scan. A score of ≥6 has been found to yield an overall sensitivity of 0.93 (95% confidence interval [CI], 0.85-0.97) and a specificity of 0.59 (95% CI, 0.56-0.62), with a number needed to screen to prevent one additional hip fracture of 279.¹⁸

The Osteoporosis Self-assessment Tool (OST) (http://depts.washington.edu/osteoed/tools.php?type=ost) is a calculated value that uses age and weight to determine an individual’s risk for osteoporosis (risk score=weight [in kg] – age [in years]/5).^16,19 Although there is not a defined value to determine a positive OST risk score, scores of -1 to 3 have been used in a variety of studies.¹⁶ In a study of 181 American men, the OST predicted osteoporosis with a sensitivity of 93% and a specificity of 66% when using a cutoff score of 3.²⁰

Treating men at risk

Pharmacologic therapy is recommended for men at an increased risk for fracture. This includes men who have had a hip or vertebral fracture without major trauma, as well as those who have not had such a fracture but have a BMD of the spine, femoral neck, and/or total hip of ≤-2.5.^5,17 This standard also applies to the radius when used as an alternative site.

Several organizations recommend screening men ages ≥70 years and those ages 50 to 69 who have risk factors for fractures or who sustained a fracture after age 50.

The International Society for Clinical Densitometry and International Osteoporosis Foundation endorse the use of the Fracture Risk Assessment Tool (FRAX). Available at http://shef.ac.uk/FRAX/tool.aspx?country=9, FRAX is a computer-based calculator that uses risk factors and BMD of the femoral neck to estimate an individual’s 10-year fracture probability.²¹ Men who are 50 years or older, have a T-score between -1.0 and -2.5 in the spine, femoral neck, or total hip, and a 10-year risk of ≥20% of developing any fracture or ≥3% of developing a hip fracture based on FRAX, should be offered pharmacotherapy.^5,17

Bisphosphonates are first-line therapy

Although oral bisphosphonates are first-line therapy for men who meet these criteria,⁴ pharmacotherapy should be individualized based on factors such as fracture history, severity of osteoporosis, comorbidities (eg, peptic ulcer disease, malignancy, renal disease, or malabsorption), and cost (TABLE 3).^22,23

Alendronate once weekly has been proven to increase BMD and to reduce the risk of fracture in men.^24,25 A randomized, placebo-controlled trial of 241 men with osteoporosis found that alendronate increased BMD by 7.1% (±0.3) at the lumbar spine, 2.5% (±0.4) at the femoral neck, and 2% (±0.2) for the total body. Those in the placebo group had a 1.8% (±0.5) increase in BMD of the lumbar spine, with no significant change in femoral neck or total-body BMD—and a higher incidence of vertebral fractures (7.1% vs. 0.8% for those on alendronate; P=.02).²⁴

Risedronate once daily has also been proven to increase BMD in the lumbar spine and hip, with a reduction in vertebral fractures.²⁶ Another investigation—a 2-year, multicenter double-blind placebo-controlled study of 284 men with osteoporosis—found that risedronate given once a week increased BMD in the spine and hip, but did not reduce the incidence of either vertebral or nonvertebral fractures.²⁷

Because a DEXA scan is not always available or cost effective, a validated clinical predictive tool is preferred as an intial screening option.

Both alendronate and risedronate are effective for secondary causes of bone loss, such as corticosteroid use, androgen deprivation therapy/hypogonadism, and rheumatologic conditions.²⁸ Oral bisphosphonates may cause GI irritation, however. Abdominal pain associated with alendronate use is between 1% and 7%, vs 2% to 12% for risedronate.²³ Neither medication is recommended for use in patients with an estimated glomerular filtration rate <35 mL/min.²³ There is no clearly established duration of therapy for men.

Zoledronic acid infusions, given intravenously (IV) once a year, are available for men who cannot tolerate oral bisphosphonates. In a multicenter double-blind, placebocontrolled trial, zoledronic acid was found to reduce the risk of vertebral fractures in men with primary or hypogonadism-associated osteoporosis by 67% (1.6% vertebral fractures in the treatment group after 24 months vs 4.9% with placebo).²⁹ Given within 90 days of a hip fracture repair, zoledronic acid was associated with both a reduction in the rate of new fractures and an increased survival rate.³⁰

Adverse effects of zoledronic acid include diffuse bone pain (3%-9%), fever (9%-22%) and flu-like symptoms (1%-11%). Osteonecrosis of the jaw has been reported in <1% of patients.²³

Recombinant human parathyroid hormone stimulates bone growth

Pharmacotherapy should be individualized based on factors such as fracture history, severity of osteoporosis, comorbidities (eg, peptic ulcer disease, malignancy), and cost.

Teriparatide, administered subcutaneously (SC) once a day, directly stimulates bone formation. In a randomized placebo controlled trial of 437 men with a T-score of -2, teriparatide was found to increase BMD at the spine and femoral neck. Participants were randomized to receive teriparatide (20 or 40 mcg/d) or placebo. Those who received teriparatide had a doserelated increase in BMD from baseline at the spine (5.9% with 20 mcg and 9% with 40 mcg) and femoral neck (1.5% and 2.9%, respectively) compared with the placebo group.³¹ Teriparatide was shown to reduce vertebral fractures by 51% compared with placebo in a randomized study of 355 men with osteoporosis.³²

Teriparatide is indicated for men with severe osteoporosis and those for whom bisphosphonate treatment has been unsuccessful. Its use is limited to 2 years due to a dose-dependent risk of osteosarcoma. Teriparatide is contraindicated in patients with skeletal metastasis and has been associated with transient hypercalcemia 4 to 6 hours after administration.²³ Its use in combination with bisphosphonates is not recommended due to the lack of proven benefit, risk of adverse effects, and associated cost.⁵

Testosterone boosts bone density

Testosterone therapy is recommended for men with low levels of testosterone (<200 ng/dL), high risk for fracture, and contraindications to pharmacologic agents approved for the treatment of osteoporosis.⁵ Supplementation of testosterone to restore correct physiologic levels will decrease bone turnover and increase bone density.³³ In a meta-analysis of 8 trials with a total of 365 participants, testosterone administered intramuscularly was found to increase lumbar BMD by 8% compared with placebo. The effect on fractures is not known.¹²

Monoclonal antibody reduces fracture risk

Denosumab, a monoclonal antibody that prevents osteoclast formation leading to decreased bone resorption, is administered SC every 6 months.²³ In a placebo-controlled trial of 242 men with low bone mass, denosumab increased BMD at the lumbar spine (5.7%), total hip (2.4%), femoral neck (2.1%), trochanter (3.1%), and one-third radius (0.6%) compared with placebo after one year.³⁴ In men receiving androgen deprivation therapy for nonmetastatic prostate cancer, denosumab has been shown to increase BMD and reduce the incidence of vertebral fractures.³⁵

Adverse effects include hypocalcemia, hypophosphatemia, fatigue, and back pain.²³ No data exist on the ability of denosumab to reduce fracture risk in men without androgen deprivation.

Calcium and vitamin D for men at risk

Men who are at risk for or have osteoporosis should consume 1000 mg to 1200 mg of calcium per day. Ideally, this should come through dietary sources, but calcium supplementation may be added when diet is inadequate.⁵ The Institute of Medicine recommends a calcium intake of 1000 mg/d for men ages 51 to 70 years and 1200 mg/d for men ages 70 and older.³⁶

Supplementation of testosterone to restore correct physiologic levels in men with low testosterone will decrease bone turnover and increase bone density.

Men with vitamin D levels below 30 ng/mL should receive vitamin D supplementation to attain blood 25(OH) D levels of at least 30 ng/mL.⁵ The Institute of Medicine recommends a daily intake of 600 international units (IU) of vitamin D for men ages 51 to 70 and 800 IU for men 70 and older.³⁶ A recent Cochrane review on vitamin D and vitamin D analogues concluded that vitamin D alone was unlikely to prevent fractures in older people; when taken with calcium, however, it may have a preventive effect.³⁷

Counseling and follow-up

Lifestyle modification is an important means of primary prevention for osteoporosis. Advise men at risk for osteoporosis to limit alcohol consumption to 2 drinks daily.^4,5,8,10 Tell those who smoke that doing so increases their risk for osteoporotic fracture and refer them for smoking cessation counseling. Emphasize that weight-bearing exercise can improve BMD and should be done at least 3 days per week.^4,5,8,10 It is important, too, to do a medication review to look for drug-drug interactions and to discuss fall prevention strategies, such as gait training and an environmental assessment and removal of fall hazards.

A Cochrane review concluded that vitamin D alone was unlikely to prevent fractures in older people; when taken with calcium, however, it may have a preventive effect.

The evidence for monitoring treatment using BMD is not very strong.^5,14 However, the Endocrine Society recommends that response to treatment be monitored using DEXA scans every one to 2 years, with reduced frequency once the BMD has stabilized.⁵ Any patient found to have a decrease in BMD after treatment is initiated should undergo further evaluation to determine the cause of the decline.

CORRESPONDENCE
Bryan Farford, DO, Mayo Clinic Division of Regional Medicine, 742 Marsh Landing Parkway, Jacksonville Beach, FL 32250; [email protected]

Colorectal cancers are among the most common cancers worldwide, and there is a high mortality rate for advanced-stage disease. Approximately 132,000 new cases of colorectal cancer will be diagnosed in the United States in 2015, and approximately 40,000 of these cases will be primary rectal cancers. The incidence and mortality rates have been steadily declining over the past two decades, largely through advances in screening and improvements in treatment. However, rectal cancer remains a significant cause of morbidity and mortality in the United States and worldwide.

To read the full article in PDF:

Click here

Colorectal cancers are among the most common cancers worldwide, and there is a high mortality rate for advanced-stage disease. Approximately 132,000 new cases of colorectal cancer will be diagnosed in the United States in 2015, and approximately 40,000 of these cases will be primary rectal cancers. The incidence and mortality rates have been steadily declining over the past two decades, largely through advances in screening and improvements in treatment. However, rectal cancer remains a significant cause of morbidity and mortality in the United States and worldwide.

To read the full article in PDF:

Click here

Colorectal cancers are among the most common cancers worldwide, and there is a high mortality rate for advanced-stage disease. Approximately 132,000 new cases of colorectal cancer will be diagnosed in the United States in 2015, and approximately 40,000 of these cases will be primary rectal cancers. The incidence and mortality rates have been steadily declining over the past two decades, largely through advances in screening and improvements in treatment. However, rectal cancer remains a significant cause of morbidity and mortality in the United States and worldwide.

To read the full article in PDF:

Click here

Total joint arthroplasty (TJA) is a clinically effective, cost-effective treatment for symptomatic arthritis.^1,2 After TJA, patients report reduced pain, restored range of motion, high satisfaction, and ability to return to a more active lifestyle.^3-7 The number of total hip arthroplasties (THAs) performed in the United States is expected to reach 572,000 by 2030, a 174% increase, and the number of total knee arthroplasties (TKAs) 3.5 million, nearly a 7-fold increase.^8,9 Since 2005, the cost of THA has risen more than 4 times, to $13.43 billion, and the cost of TKA has risen more than 5 times, to $40.8 billion.^8,9 Given the demand and price tag, TJA is the single largest cost in the Medicare budget.¹⁰

Given its potential to improve care and reduce costs, reducing readmission rates in the surgical setting is a priority for physicians and policymakers.¹¹ Readmissions for TJA are highly scrutinized as a performance indicator—the Centers for Medicare & Medicaid Services (CMS) started including them in its readmissions penalty program in 2013—and were recently validated as a measure of surgical quality.^12-14 Accurate assessments of readmissions after TJA are unclear, with rates ranging from 1% to 8.5% between 7 and 90 days after surgery.^2,15-17 The early success of TJA as an elective (and more frequently outpatient) procedure has paradoxically translated to less tolerance for readmissions. Post-TJA complications resulting in readmission are subject to financial penalties, and there is an implicit judgment of inadequate surgical management.¹²

Not only is the readmission rate poorly characterized, but there is no consensus on the leading reasons for readmissions after primary elective unilateral TJAs. The range of rates, reasons, and follow-up periods reported in the literature is wide.^18,19 CMS plans to monitor readmissions over 7 to 90 days after surgery (the period depends on the complication), whereas a significant portion of the orthopedic literature documents 90-day rates.¹⁹ In 2012, the Yale New Haven Health Services Corporation/Center for Outcomes Research and Evaluation prepared for CMS a comprehensive report identifying rates of post-TJA complications and readmissions.²⁰ The report, however, is limited to US hospitals and Medicare patients and therefore may overstate the rates, given this population’s documented comorbidities and the reimbursement variations between Medicare and commercial insurance.²¹ Lack of consensus on readmissions after primary elective unilateral TJAs requires that we synthesize available data to answer several questions: What is the overall readmission rate 30 and 90 days after TJA? What are the primary reasons for readmission 30 and 90 days after TJA? What are the cause-specific readmission rates? We performed a systematic review and a meta-analysis to answer these questions and to add clarity to the literature in order to help guide policy.

Materials and Methods

We performed a systematic review in accordance with PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines.²² Two reviewers independently completed structured searches of the Medline and Cochrane Central Register of Controlled Trials databases. Search terms were: (total hip replacement OR hip arthroplasty OR total hip arthroplasty OR total knee replacement OR knee arthroplasty OR total knee arthroplasty) AND (readmission OR complication OR discharge). They updated the search June 1, 2013. Four limits were applied: publication between January 1, 1982 and December 12, 2012; human subjects only; age 19+ years; and English-language articles. Study eligibility was determined by using standardized criteria as defined by the inclusion and exclusion criteria described in 3 stages: title review, abstract review, and full-article review. The reviewers also performed ancestry searches, including searches for major review articles and bibliographies of all retrieved studies, to identify additional studies not identified in the keyword searches. Discrepancies were resolved by author consensus.

Inclusion criteria were original studies that presented level I to III evidence and that were identified in structured online searches; published in English between January 1, 1982 and December 31, 2012; involved patients older than 19 years; and reported both readmission rates and reasons at follow-up 30 or 90 days after elective primary unilateral TJA, regardless of indication. Exclusion criteria were studies that reported data from hip fracture, knee fracture, and pelvis fracture cases; those that reported data from hemiarthroplasty, Birmingham hip resurfacing procedures, other resurfacing procedures, simultaneous bilateral hip or knee arthroplasties, unicompartmental knee arthroplasty, patellofemoral arthroplasty, metastatic or bone cancer, or revision hip or knee arthroplasty; those that did not report extractable reasons for readmission; those that reported complications but did not specify readmission rates; and those that reported readmission data only from after the 90-day follow-up window. In cases in which multiple studies reported data from the same patient population, only the largest or most recent report was used.

Two reviewers extracted the quantitative data from eligible studies. The 2 primary outcomes of interests were all-cause readmission rates, and reasons for readmission 30 and 90 days after TJA. Other extracted data were evidence level; publication journal, year, and country; data source (academic institution, Medicare); study design; number of patients; patient characteristics; surgical approach; follow-up period; overall readmission rate; anticoagulant use; tourniquet use; and compression stocking use. In addition, all post-TJA readmissions were assumed to be unplanned, except for staged sequential bilateral arthroplasty for osteoarthritis (excluded from analysis).

Readmission reasons were divided into 4 major categories as defined by the literature and the authors: thromboembolic disease, joint-specific reasons, surgical site infection, and surgical sequelae. The diagnoses in these categories are listed in Table 1. Other extracted reasons were cardiac dysrhythmia and pneumonia.

In cases in which there were at least 2 comparable studies, a meta-analysis was performed to obtain pooled estimates of the proportion of patients readmitted at 30 or 90 days. We calculated a Higgins I² measure for between-study heterogeneity and random-effects analysis, using the method of DerSimonian and Laird²³ if I² was greater than 0.5. Pooled estimates were obtained for both overall and cause-specific reasons for readmission for all reasons reported in at least 3 studies. Small-study or publication bias was assessed using funnel plot asymmetry when at least 5 studies were analyzed as recommended.²⁴ The meta-analytic findings for both overall and cause-specific readmission are presented as pooled proportions with 95% confidence intervals (CIs). All meta-analyses were performed using Stata 10.0.

Results

Fifteen unique TJA studies (12 THA, 10 TKA) met the criteria for the meta-analysis.^20,25-38Figure 1 depicts the PRISMA flowchart for study identification.²²

Of the 12 studies eligible for the THA analysis (Table 2), 6 were conducted in the United States,^{20,26,27,30,33,34} 5 in Europe,^{25,28,29,32,35} and 1 in Canada.³¹ Seven of the 12 studies reported readmission rates at 30 days, and 7 reported rates at 90 days (2 reported rates at both follow-ups). We analyzed a total of 113,396 patients at the 30-day window and 192,380 patients at the 90-day window. Mean age was 74.2 years. The included studies were variable and sparse in their reporting of specific characteristics (Table 3).

Of the 10 studies (2 prospective, 8 retrospective) eligible for the TKA analysis (Table 4), 6 were conducted in the United States,^{20,26,27,34,36,37} 3 in Europe,^25,29,35 and 1 in Asia.³⁸ Four of the 10 studies reported readmission rates at 30 days, and 7 reported rates at 90 days (1 reported rates at both follow-ups).²⁷ We analyzed a total of 3,278,635 patients at the 30-day window and 272,419 patients at the 90-day window. Mean age was 74.3 years. The included studies were quite variable and sparse in their reporting of specific characteristics (Table 5).

We performed random-effects meta-analyses of all unplanned readmissions at both 30 and 90 days (all I²s > 0.5). Among 5 THA studies that reported overall rates at 30 days,^{20,27,28,32,33} the estimated overall unplanned rate among the 120,272 index surgeries was 5.6% (95% CI, 3.2%-8.0%). Among 5 THA studies that reported overall rates at 90 days,^20,25-27,31 the estimated overall unplanned rate among the 192,380 index surgeries was 7.7% (95% CI, 3.2%-12.2%) (I² = 1.00). Among 3 TKA studies that reported overall rates at 30 days,^27,37,38 the estimated overall unplanned rate among the 3,278,635 index surgeries was 3.3% (95% CI, 0.7%-5.9%). Among 5 TKA studies that reported overall rates at 90 days,^20,25-27,36 the estimated overall unplanned rate among the 272,419 index surgeries was 9.7% (95% CI, 7.1%-12.4%) (I² = 0.97).

30-Day Readmission Rates

The most common reason for readmission 30 days after THA discharge was joint-specific. This reason accounted for 39.3% of all unplanned readmissions among studies that reported joint-specific causes, with an estimated pooled rate of 2.2% (95% CI, 0.0%-4.6%; P < .001; I² = 1.00) among 4 studies. The second and third most common reasons were surgical sequelae (1.6%; 95% CI, 0.8%-2.5%; P < .001; I² = 0.95) and thromboembolic disease (1.5%; 95% CI, 1.0%-1.9%; P < .001; I² = 0.95). See Figure 2 for 30-day THA readmission rates. The fourth most common readmission reason was surgical site infection (0.6%; 95% CI, 0.2%-1.1%; P < .001; I² = 0.94). Only these 4 reasons could be pooled, as cardiac dysrhythmia, pneumonia, and bleeding were reported in only 1 study each.

The most common reason for readmission 30 days after TKA discharge was surgical site infection. This reason accounted for 12.1% of all unplanned readmissions among studies that reported surgical site infections, with an estimated pooled rate of 0.4% (95% CI, 0.3%-0.6%; P < .001; I² = 0.61) among 3 studies. The second and third most common reasons were joint-specific and thromboembolic disease, both occurring 0.3% of the time. Joint-specific reasons were reported in 2 studies (95% CI, 0.0%-0.8%; P = .259; I² = 0.94). Thromboembolic disease was reported in 4 studies (95% CI, 0.0%-0.7%; P = .067; I² = 0.98) (Figure 3). Only these 3 reasons could be pooled, as cardiac dysrhythmia, pneumonia, and “sequelae” were reported in only 1 study each.

90-Day Readmission Rates

Consistent with the 30-day THA results, the most common reason for readmission 90 days after THA discharge was joint-specific. This reason accounted for 31.2% of all unplanned readmissions among studies that reported joint-specific causes, with an estimated pooled rate of 2.4% (95% CI, 0.0%-4.9%; P < .001; I² = 1.00) among 5 studies. The second and third most common reasons were surgical sequelae (1.6%; 95% CI, 1.0%-2.2%; P < .003; I² = 0.83) and thromboembolic disease (1.0%; 95% CI, 0.7%-1.4%; P < .001; I² = 0.97). See Figure 4 for 90-day THA readmission rates. The fourth most common readmission reason was surgical site infection (0.6%; 95% CI, 0.2%-1.0%; P < .001; I² = 0.99). Only these 4 reasons could be pooled, as cardiac dysrhythmia, pneumonia, and bleeding were reported by only 1 study each.

Consistent with the 30-day TKA results, the most common reason for readmission 90 days after TKA discharge was surgical site infection. This reason accounted for 9.3% of all unplanned readmissions among studies that reported surgical site infections, with an estimated pooled rate of 0.9% (95% CI, 0.4%-1.4%; P < .001; I² = 0.93) among 5 studies. The second and third most common reasons were joint-specific and thromboembolic disease, both occurring 0.7% of the time. Joint-specific reasons were reported in 5 studies (95% CI, 0.2%-1.1%; P =.003; I² = 0.94). Thromboembolic disease was reported in 7 studies (95% CI, 0.3%-1.1%; P < .001; I² = 0.97) (Figure 5). Bleeding was reported in 3 studies, with a pooled rate of 0.4% (95% CI, 0.0%-0.9%; P = .128; I² = 0.83). Cardiac dysrhythmia was reported in 2 studies, with an estimated pooled rate of 0.3% (95% CI, 0.2%-0.5%; P < .001). Only these 5 reasons could be pooled, as pneumonia and “sequelae” were reported in only 1 study each.

Discussion

This study is the first systematic review and meta-analysis of the literature to identify overall and cause-specific readmission rates after TJA.

For THA, 30- and 90-day readmission rates were 5.6% and 7.7%, respectively. Joint-specific causes were the most common reason for readmission at both 30 and 90 days after THA. For TKA, 30- and 90-day rates were 3.3% and 9.7%, respectively. Surgical site infection was the most common reason for readmission at both 30 and 90 days after TKA.

Hospital readmissions are an important area of scrutiny for Medicare and the health care systems broadly. Readmissions after surgery are deemed quality indicators potentially suggesting incomplete management of active issues and inadequate preparation for discharge.³⁹ Unplanned readmissions also place a significant economic burden on Medicare: $17.5 billion in 2010.⁴⁰ Given their association with quality of overall surgical care, improved readmission rates have the potential to improve the standard of care and reduce costs.

Higher readmission rates will significantly affect hospitals as CMS shifts to bundling payments for acute-care episodes, such as TJA.^41-43 Further, private and public health care payers are increasingly using unplanned 30- and 90-day readmission rates as a marker of quality of care. However, there is little agreement about readmission rates and reasons, let alone what follow-up window should be used to define orthopedic readmissions. One study involving the MEDPAR (Medicare Provider Analysis and Review) database found that a common reason for readmission after major hip or knee surgery was “aftercare” for surgical sequelae (10.3%)¹⁵; another study found a 15% increase in post-THA hospitalizations, most commonly for a mechanical complication (joint-related).⁴⁴ There are no prior complete systematic reviews or meta-analyses of overall rates of readmissions after primary unilateral TJAs, or of the reasons for these readmissions. The closest such report, the Yale report to CMS, was skewed to a proportion of US hospitals treating a population prone to significant comorbidities.²⁰

Although the strength of this study lies in its rigorous identification and extraction of data, notable clarifications must be made when synthesizing the information. First, the definitions of various thromboembolic events varied greatly. Some studies reported deep vein thrombosis (DVT) and pulmonary embolism (PE) separately, whereas others reported only DVT or only PE. Some studies reported rates of readmission for “thromboembolic disorder,” and one²⁵ reported rates for DVT, PE, and thromboembolic disorder. To pool these related events, we created a composite definition that included DVT, PE, and thromboembolic disorders, which we termed thromboembolic disease. We also created a composite measure for joint-specific reasons for readmission. This category included joint infection that definitely required reentry into the joint, but using this category may have led to underestimation of surgical site infection rates, which were defined separately. Third, there was significant variation in documentation of surgical site infection among the studies included in this review. Some studies specified superficial wounds, whereas others did not categorize complications as superficial, deep, or intracapsular, which would qualify as a “joint-specific” cause. Despite this variation, surgical site infection after TJA was found to be the most common reason for readmission.

Our systematic review and meta-analysis were limited, as any others are, by the quality of studies investigated. Few studies reported cause-specific rates and reasons for readmission. Given the small sample, formal tests for small-study or publication bias could not be performed. Some studies included tremendous amounts of data, and International Classification of Diseases, Ninth Revision (ICD-9) codes were used without physician review of readmission diagnoses. In the absence of oversight, many readmissions could have been misinterpreted and incorrectly logged, or simply miscoded. Saucedo and colleagues^27,45 found that readmission diagnostic codes were often unverified. Numerous other studies corroborated this lack of correlation with physician-derived readmission diagnoses in just 25% of cases.^46-54 Another study limitation is the unknown number of patients who had TJA but presented and were subsequently readmitted to a different hospital. Last, as this review included patients who had surgery performed within a 30-year period, it could not address the shifts in postoperative management that occurred in that time, particularly with respect to anticoagulation. This limitation was partially addressed in THA by dividing final studies into 3 decades. Of these studies, only 1 was from the first decade, 3 were from the second, and the rest were from the third. Of the 3 from the second decade, only the study by Warwick and colleagues²⁹ (1995) explicitly did not use anticoagulation, but compression stockings were used, and consequently there was a 4.0% rate of readmission for thromboembolic disease alone, compared with the study by White and colleagues³⁴ (1998), which explicitly used anticoagulation and boasted a 1.7% rate of readmission for thromboembolic disease. This isolated comparison illustrates the effect of routine anticoagulation and the changes in surgical standards over the 3 decades.

The numbers from this systematic review and meta-analysis represent an international benchmark for TJA as a procedure. Knowing the top reasons for readmission will lead to more focus on joint-related and medical issues (surgical site infection, thromboembolic disease) before discharge to avoid readmission after elective unilateral primary TJA. Although readmission rates have received attention in the United States as a primary means of combating soaring health care costs, knowing the rates for a common procedure applies broadly as an indicator for standard of care worldwide, according to the World Health Organization.⁵⁵ This study is the first systematic review and meta-analysis of documented readmission rates and reasons for readmission to identify overall and cause-specific rates after TJA. The hope is that our findings will add clarity to the literature and help guide the decisions of physicians and policymakers.

Conclusion

Readmission rates are an increasingly important metric in the United States and around the world, yet there is no consensus regarding overall readmission rates and reasons for readmission after primary unilateral TJAs. Our systematic review and meta-analysis of the literature found overall unplanned readmission rates of 5.6% (30 days) and 7.7% (90 days) for THA and 3.3% (30 days) and 9.7% (90 days) for TKA. At both 30 and 90 days, the most common readmission reasons were joint-specific (THA) and surgical site infection (TKA). New investigations should be directed toward developing countermeasures to lower the rates of readmission.

Total joint arthroplasty (TJA) is a clinically effective, cost-effective treatment for symptomatic arthritis.^1,2 After TJA, patients report reduced pain, restored range of motion, high satisfaction, and ability to return to a more active lifestyle.^3-7 The number of total hip arthroplasties (THAs) performed in the United States is expected to reach 572,000 by 2030, a 174% increase, and the number of total knee arthroplasties (TKAs) 3.5 million, nearly a 7-fold increase.^8,9 Since 2005, the cost of THA has risen more than 4 times, to $13.43 billion, and the cost of TKA has risen more than 5 times, to $40.8 billion.^8,9 Given the demand and price tag, TJA is the single largest cost in the Medicare budget.¹⁰

Given its potential to improve care and reduce costs, reducing readmission rates in the surgical setting is a priority for physicians and policymakers.¹¹ Readmissions for TJA are highly scrutinized as a performance indicator—the Centers for Medicare & Medicaid Services (CMS) started including them in its readmissions penalty program in 2013—and were recently validated as a measure of surgical quality.^12-14 Accurate assessments of readmissions after TJA are unclear, with rates ranging from 1% to 8.5% between 7 and 90 days after surgery.^2,15-17 The early success of TJA as an elective (and more frequently outpatient) procedure has paradoxically translated to less tolerance for readmissions. Post-TJA complications resulting in readmission are subject to financial penalties, and there is an implicit judgment of inadequate surgical management.¹²

Not only is the readmission rate poorly characterized, but there is no consensus on the leading reasons for readmissions after primary elective unilateral TJAs. The range of rates, reasons, and follow-up periods reported in the literature is wide.^18,19 CMS plans to monitor readmissions over 7 to 90 days after surgery (the period depends on the complication), whereas a significant portion of the orthopedic literature documents 90-day rates.¹⁹ In 2012, the Yale New Haven Health Services Corporation/Center for Outcomes Research and Evaluation prepared for CMS a comprehensive report identifying rates of post-TJA complications and readmissions.²⁰ The report, however, is limited to US hospitals and Medicare patients and therefore may overstate the rates, given this population’s documented comorbidities and the reimbursement variations between Medicare and commercial insurance.²¹ Lack of consensus on readmissions after primary elective unilateral TJAs requires that we synthesize available data to answer several questions: What is the overall readmission rate 30 and 90 days after TJA? What are the primary reasons for readmission 30 and 90 days after TJA? What are the cause-specific readmission rates? We performed a systematic review and a meta-analysis to answer these questions and to add clarity to the literature in order to help guide policy.

Materials and Methods

We performed a systematic review in accordance with PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines.²² Two reviewers independently completed structured searches of the Medline and Cochrane Central Register of Controlled Trials databases. Search terms were: (total hip replacement OR hip arthroplasty OR total hip arthroplasty OR total knee replacement OR knee arthroplasty OR total knee arthroplasty) AND (readmission OR complication OR discharge). They updated the search June 1, 2013. Four limits were applied: publication between January 1, 1982 and December 12, 2012; human subjects only; age 19+ years; and English-language articles. Study eligibility was determined by using standardized criteria as defined by the inclusion and exclusion criteria described in 3 stages: title review, abstract review, and full-article review. The reviewers also performed ancestry searches, including searches for major review articles and bibliographies of all retrieved studies, to identify additional studies not identified in the keyword searches. Discrepancies were resolved by author consensus.

Inclusion criteria were original studies that presented level I to III evidence and that were identified in structured online searches; published in English between January 1, 1982 and December 31, 2012; involved patients older than 19 years; and reported both readmission rates and reasons at follow-up 30 or 90 days after elective primary unilateral TJA, regardless of indication. Exclusion criteria were studies that reported data from hip fracture, knee fracture, and pelvis fracture cases; those that reported data from hemiarthroplasty, Birmingham hip resurfacing procedures, other resurfacing procedures, simultaneous bilateral hip or knee arthroplasties, unicompartmental knee arthroplasty, patellofemoral arthroplasty, metastatic or bone cancer, or revision hip or knee arthroplasty; those that did not report extractable reasons for readmission; those that reported complications but did not specify readmission rates; and those that reported readmission data only from after the 90-day follow-up window. In cases in which multiple studies reported data from the same patient population, only the largest or most recent report was used.

Two reviewers extracted the quantitative data from eligible studies. The 2 primary outcomes of interests were all-cause readmission rates, and reasons for readmission 30 and 90 days after TJA. Other extracted data were evidence level; publication journal, year, and country; data source (academic institution, Medicare); study design; number of patients; patient characteristics; surgical approach; follow-up period; overall readmission rate; anticoagulant use; tourniquet use; and compression stocking use. In addition, all post-TJA readmissions were assumed to be unplanned, except for staged sequential bilateral arthroplasty for osteoarthritis (excluded from analysis).

Readmission reasons were divided into 4 major categories as defined by the literature and the authors: thromboembolic disease, joint-specific reasons, surgical site infection, and surgical sequelae. The diagnoses in these categories are listed in Table 1. Other extracted reasons were cardiac dysrhythmia and pneumonia.

In cases in which there were at least 2 comparable studies, a meta-analysis was performed to obtain pooled estimates of the proportion of patients readmitted at 30 or 90 days. We calculated a Higgins I² measure for between-study heterogeneity and random-effects analysis, using the method of DerSimonian and Laird²³ if I² was greater than 0.5. Pooled estimates were obtained for both overall and cause-specific reasons for readmission for all reasons reported in at least 3 studies. Small-study or publication bias was assessed using funnel plot asymmetry when at least 5 studies were analyzed as recommended.²⁴ The meta-analytic findings for both overall and cause-specific readmission are presented as pooled proportions with 95% confidence intervals (CIs). All meta-analyses were performed using Stata 10.0.

Results

Fifteen unique TJA studies (12 THA, 10 TKA) met the criteria for the meta-analysis.^20,25-38Figure 1 depicts the PRISMA flowchart for study identification.²²

Of the 12 studies eligible for the THA analysis (Table 2), 6 were conducted in the United States,^{20,26,27,30,33,34} 5 in Europe,^{25,28,29,32,35} and 1 in Canada.³¹ Seven of the 12 studies reported readmission rates at 30 days, and 7 reported rates at 90 days (2 reported rates at both follow-ups). We analyzed a total of 113,396 patients at the 30-day window and 192,380 patients at the 90-day window. Mean age was 74.2 years. The included studies were variable and sparse in their reporting of specific characteristics (Table 3).

Of the 10 studies (2 prospective, 8 retrospective) eligible for the TKA analysis (Table 4), 6 were conducted in the United States,^{20,26,27,34,36,37} 3 in Europe,^25,29,35 and 1 in Asia.³⁸ Four of the 10 studies reported readmission rates at 30 days, and 7 reported rates at 90 days (1 reported rates at both follow-ups).²⁷ We analyzed a total of 3,278,635 patients at the 30-day window and 272,419 patients at the 90-day window. Mean age was 74.3 years. The included studies were quite variable and sparse in their reporting of specific characteristics (Table 5).

We performed random-effects meta-analyses of all unplanned readmissions at both 30 and 90 days (all I²s > 0.5). Among 5 THA studies that reported overall rates at 30 days,^{20,27,28,32,33} the estimated overall unplanned rate among the 120,272 index surgeries was 5.6% (95% CI, 3.2%-8.0%). Among 5 THA studies that reported overall rates at 90 days,^20,25-27,31 the estimated overall unplanned rate among the 192,380 index surgeries was 7.7% (95% CI, 3.2%-12.2%) (I² = 1.00). Among 3 TKA studies that reported overall rates at 30 days,^27,37,38 the estimated overall unplanned rate among the 3,278,635 index surgeries was 3.3% (95% CI, 0.7%-5.9%). Among 5 TKA studies that reported overall rates at 90 days,^20,25-27,36 the estimated overall unplanned rate among the 272,419 index surgeries was 9.7% (95% CI, 7.1%-12.4%) (I² = 0.97).

30-Day Readmission Rates

The most common reason for readmission 30 days after THA discharge was joint-specific. This reason accounted for 39.3% of all unplanned readmissions among studies that reported joint-specific causes, with an estimated pooled rate of 2.2% (95% CI, 0.0%-4.6%; P < .001; I² = 1.00) among 4 studies. The second and third most common reasons were surgical sequelae (1.6%; 95% CI, 0.8%-2.5%; P < .001; I² = 0.95) and thromboembolic disease (1.5%; 95% CI, 1.0%-1.9%; P < .001; I² = 0.95). See Figure 2 for 30-day THA readmission rates. The fourth most common readmission reason was surgical site infection (0.6%; 95% CI, 0.2%-1.1%; P < .001; I² = 0.94). Only these 4 reasons could be pooled, as cardiac dysrhythmia, pneumonia, and bleeding were reported in only 1 study each.

The most common reason for readmission 30 days after TKA discharge was surgical site infection. This reason accounted for 12.1% of all unplanned readmissions among studies that reported surgical site infections, with an estimated pooled rate of 0.4% (95% CI, 0.3%-0.6%; P < .001; I² = 0.61) among 3 studies. The second and third most common reasons were joint-specific and thromboembolic disease, both occurring 0.3% of the time. Joint-specific reasons were reported in 2 studies (95% CI, 0.0%-0.8%; P = .259; I² = 0.94). Thromboembolic disease was reported in 4 studies (95% CI, 0.0%-0.7%; P = .067; I² = 0.98) (Figure 3). Only these 3 reasons could be pooled, as cardiac dysrhythmia, pneumonia, and “sequelae” were reported in only 1 study each.

90-Day Readmission Rates

Consistent with the 30-day THA results, the most common reason for readmission 90 days after THA discharge was joint-specific. This reason accounted for 31.2% of all unplanned readmissions among studies that reported joint-specific causes, with an estimated pooled rate of 2.4% (95% CI, 0.0%-4.9%; P < .001; I² = 1.00) among 5 studies. The second and third most common reasons were surgical sequelae (1.6%; 95% CI, 1.0%-2.2%; P < .003; I² = 0.83) and thromboembolic disease (1.0%; 95% CI, 0.7%-1.4%; P < .001; I² = 0.97). See Figure 4 for 90-day THA readmission rates. The fourth most common readmission reason was surgical site infection (0.6%; 95% CI, 0.2%-1.0%; P < .001; I² = 0.99). Only these 4 reasons could be pooled, as cardiac dysrhythmia, pneumonia, and bleeding were reported by only 1 study each.

Consistent with the 30-day TKA results, the most common reason for readmission 90 days after TKA discharge was surgical site infection. This reason accounted for 9.3% of all unplanned readmissions among studies that reported surgical site infections, with an estimated pooled rate of 0.9% (95% CI, 0.4%-1.4%; P < .001; I² = 0.93) among 5 studies. The second and third most common reasons were joint-specific and thromboembolic disease, both occurring 0.7% of the time. Joint-specific reasons were reported in 5 studies (95% CI, 0.2%-1.1%; P =.003; I² = 0.94). Thromboembolic disease was reported in 7 studies (95% CI, 0.3%-1.1%; P < .001; I² = 0.97) (Figure 5). Bleeding was reported in 3 studies, with a pooled rate of 0.4% (95% CI, 0.0%-0.9%; P = .128; I² = 0.83). Cardiac dysrhythmia was reported in 2 studies, with an estimated pooled rate of 0.3% (95% CI, 0.2%-0.5%; P < .001). Only these 5 reasons could be pooled, as pneumonia and “sequelae” were reported in only 1 study each.

Discussion

This study is the first systematic review and meta-analysis of the literature to identify overall and cause-specific readmission rates after TJA.

For THA, 30- and 90-day readmission rates were 5.6% and 7.7%, respectively. Joint-specific causes were the most common reason for readmission at both 30 and 90 days after THA. For TKA, 30- and 90-day rates were 3.3% and 9.7%, respectively. Surgical site infection was the most common reason for readmission at both 30 and 90 days after TKA.

Hospital readmissions are an important area of scrutiny for Medicare and the health care systems broadly. Readmissions after surgery are deemed quality indicators potentially suggesting incomplete management of active issues and inadequate preparation for discharge.³⁹ Unplanned readmissions also place a significant economic burden on Medicare: $17.5 billion in 2010.⁴⁰ Given their association with quality of overall surgical care, improved readmission rates have the potential to improve the standard of care and reduce costs.

Higher readmission rates will significantly affect hospitals as CMS shifts to bundling payments for acute-care episodes, such as TJA.^41-43 Further, private and public health care payers are increasingly using unplanned 30- and 90-day readmission rates as a marker of quality of care. However, there is little agreement about readmission rates and reasons, let alone what follow-up window should be used to define orthopedic readmissions. One study involving the MEDPAR (Medicare Provider Analysis and Review) database found that a common reason for readmission after major hip or knee surgery was “aftercare” for surgical sequelae (10.3%)¹⁵; another study found a 15% increase in post-THA hospitalizations, most commonly for a mechanical complication (joint-related).⁴⁴ There are no prior complete systematic reviews or meta-analyses of overall rates of readmissions after primary unilateral TJAs, or of the reasons for these readmissions. The closest such report, the Yale report to CMS, was skewed to a proportion of US hospitals treating a population prone to significant comorbidities.²⁰

Although the strength of this study lies in its rigorous identification and extraction of data, notable clarifications must be made when synthesizing the information. First, the definitions of various thromboembolic events varied greatly. Some studies reported deep vein thrombosis (DVT) and pulmonary embolism (PE) separately, whereas others reported only DVT or only PE. Some studies reported rates of readmission for “thromboembolic disorder,” and one²⁵ reported rates for DVT, PE, and thromboembolic disorder. To pool these related events, we created a composite definition that included DVT, PE, and thromboembolic disorders, which we termed thromboembolic disease. We also created a composite measure for joint-specific reasons for readmission. This category included joint infection that definitely required reentry into the joint, but using this category may have led to underestimation of surgical site infection rates, which were defined separately. Third, there was significant variation in documentation of surgical site infection among the studies included in this review. Some studies specified superficial wounds, whereas others did not categorize complications as superficial, deep, or intracapsular, which would qualify as a “joint-specific” cause. Despite this variation, surgical site infection after TJA was found to be the most common reason for readmission.

Our systematic review and meta-analysis were limited, as any others are, by the quality of studies investigated. Few studies reported cause-specific rates and reasons for readmission. Given the small sample, formal tests for small-study or publication bias could not be performed. Some studies included tremendous amounts of data, and International Classification of Diseases, Ninth Revision (ICD-9) codes were used without physician review of readmission diagnoses. In the absence of oversight, many readmissions could have been misinterpreted and incorrectly logged, or simply miscoded. Saucedo and colleagues^27,45 found that readmission diagnostic codes were often unverified. Numerous other studies corroborated this lack of correlation with physician-derived readmission diagnoses in just 25% of cases.^46-54 Another study limitation is the unknown number of patients who had TJA but presented and were subsequently readmitted to a different hospital. Last, as this review included patients who had surgery performed within a 30-year period, it could not address the shifts in postoperative management that occurred in that time, particularly with respect to anticoagulation. This limitation was partially addressed in THA by dividing final studies into 3 decades. Of these studies, only 1 was from the first decade, 3 were from the second, and the rest were from the third. Of the 3 from the second decade, only the study by Warwick and colleagues²⁹ (1995) explicitly did not use anticoagulation, but compression stockings were used, and consequently there was a 4.0% rate of readmission for thromboembolic disease alone, compared with the study by White and colleagues³⁴ (1998), which explicitly used anticoagulation and boasted a 1.7% rate of readmission for thromboembolic disease. This isolated comparison illustrates the effect of routine anticoagulation and the changes in surgical standards over the 3 decades.

The numbers from this systematic review and meta-analysis represent an international benchmark for TJA as a procedure. Knowing the top reasons for readmission will lead to more focus on joint-related and medical issues (surgical site infection, thromboembolic disease) before discharge to avoid readmission after elective unilateral primary TJA. Although readmission rates have received attention in the United States as a primary means of combating soaring health care costs, knowing the rates for a common procedure applies broadly as an indicator for standard of care worldwide, according to the World Health Organization.⁵⁵ This study is the first systematic review and meta-analysis of documented readmission rates and reasons for readmission to identify overall and cause-specific rates after TJA. The hope is that our findings will add clarity to the literature and help guide the decisions of physicians and policymakers.

Conclusion

Readmission rates are an increasingly important metric in the United States and around the world, yet there is no consensus regarding overall readmission rates and reasons for readmission after primary unilateral TJAs. Our systematic review and meta-analysis of the literature found overall unplanned readmission rates of 5.6% (30 days) and 7.7% (90 days) for THA and 3.3% (30 days) and 9.7% (90 days) for TKA. At both 30 and 90 days, the most common readmission reasons were joint-specific (THA) and surgical site infection (TKA). New investigations should be directed toward developing countermeasures to lower the rates of readmission.

Total joint arthroplasty (TJA) is a clinically effective, cost-effective treatment for symptomatic arthritis.^1,2 After TJA, patients report reduced pain, restored range of motion, high satisfaction, and ability to return to a more active lifestyle.^3-7 The number of total hip arthroplasties (THAs) performed in the United States is expected to reach 572,000 by 2030, a 174% increase, and the number of total knee arthroplasties (TKAs) 3.5 million, nearly a 7-fold increase.^8,9 Since 2005, the cost of THA has risen more than 4 times, to $13.43 billion, and the cost of TKA has risen more than 5 times, to $40.8 billion.^8,9 Given the demand and price tag, TJA is the single largest cost in the Medicare budget.¹⁰

Given its potential to improve care and reduce costs, reducing readmission rates in the surgical setting is a priority for physicians and policymakers.¹¹ Readmissions for TJA are highly scrutinized as a performance indicator—the Centers for Medicare & Medicaid Services (CMS) started including them in its readmissions penalty program in 2013—and were recently validated as a measure of surgical quality.^12-14 Accurate assessments of readmissions after TJA are unclear, with rates ranging from 1% to 8.5% between 7 and 90 days after surgery.^2,15-17 The early success of TJA as an elective (and more frequently outpatient) procedure has paradoxically translated to less tolerance for readmissions. Post-TJA complications resulting in readmission are subject to financial penalties, and there is an implicit judgment of inadequate surgical management.¹²

Not only is the readmission rate poorly characterized, but there is no consensus on the leading reasons for readmissions after primary elective unilateral TJAs. The range of rates, reasons, and follow-up periods reported in the literature is wide.^18,19 CMS plans to monitor readmissions over 7 to 90 days after surgery (the period depends on the complication), whereas a significant portion of the orthopedic literature documents 90-day rates.¹⁹ In 2012, the Yale New Haven Health Services Corporation/Center for Outcomes Research and Evaluation prepared for CMS a comprehensive report identifying rates of post-TJA complications and readmissions.²⁰ The report, however, is limited to US hospitals and Medicare patients and therefore may overstate the rates, given this population’s documented comorbidities and the reimbursement variations between Medicare and commercial insurance.²¹ Lack of consensus on readmissions after primary elective unilateral TJAs requires that we synthesize available data to answer several questions: What is the overall readmission rate 30 and 90 days after TJA? What are the primary reasons for readmission 30 and 90 days after TJA? What are the cause-specific readmission rates? We performed a systematic review and a meta-analysis to answer these questions and to add clarity to the literature in order to help guide policy.

Materials and Methods

We performed a systematic review in accordance with PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines.²² Two reviewers independently completed structured searches of the Medline and Cochrane Central Register of Controlled Trials databases. Search terms were: (total hip replacement OR hip arthroplasty OR total hip arthroplasty OR total knee replacement OR knee arthroplasty OR total knee arthroplasty) AND (readmission OR complication OR discharge). They updated the search June 1, 2013. Four limits were applied: publication between January 1, 1982 and December 12, 2012; human subjects only; age 19+ years; and English-language articles. Study eligibility was determined by using standardized criteria as defined by the inclusion and exclusion criteria described in 3 stages: title review, abstract review, and full-article review. The reviewers also performed ancestry searches, including searches for major review articles and bibliographies of all retrieved studies, to identify additional studies not identified in the keyword searches. Discrepancies were resolved by author consensus.

Inclusion criteria were original studies that presented level I to III evidence and that were identified in structured online searches; published in English between January 1, 1982 and December 31, 2012; involved patients older than 19 years; and reported both readmission rates and reasons at follow-up 30 or 90 days after elective primary unilateral TJA, regardless of indication. Exclusion criteria were studies that reported data from hip fracture, knee fracture, and pelvis fracture cases; those that reported data from hemiarthroplasty, Birmingham hip resurfacing procedures, other resurfacing procedures, simultaneous bilateral hip or knee arthroplasties, unicompartmental knee arthroplasty, patellofemoral arthroplasty, metastatic or bone cancer, or revision hip or knee arthroplasty; those that did not report extractable reasons for readmission; those that reported complications but did not specify readmission rates; and those that reported readmission data only from after the 90-day follow-up window. In cases in which multiple studies reported data from the same patient population, only the largest or most recent report was used.

Two reviewers extracted the quantitative data from eligible studies. The 2 primary outcomes of interests were all-cause readmission rates, and reasons for readmission 30 and 90 days after TJA. Other extracted data were evidence level; publication journal, year, and country; data source (academic institution, Medicare); study design; number of patients; patient characteristics; surgical approach; follow-up period; overall readmission rate; anticoagulant use; tourniquet use; and compression stocking use. In addition, all post-TJA readmissions were assumed to be unplanned, except for staged sequential bilateral arthroplasty for osteoarthritis (excluded from analysis).

Readmission reasons were divided into 4 major categories as defined by the literature and the authors: thromboembolic disease, joint-specific reasons, surgical site infection, and surgical sequelae. The diagnoses in these categories are listed in Table 1. Other extracted reasons were cardiac dysrhythmia and pneumonia.

In cases in which there were at least 2 comparable studies, a meta-analysis was performed to obtain pooled estimates of the proportion of patients readmitted at 30 or 90 days. We calculated a Higgins I² measure for between-study heterogeneity and random-effects analysis, using the method of DerSimonian and Laird²³ if I² was greater than 0.5. Pooled estimates were obtained for both overall and cause-specific reasons for readmission for all reasons reported in at least 3 studies. Small-study or publication bias was assessed using funnel plot asymmetry when at least 5 studies were analyzed as recommended.²⁴ The meta-analytic findings for both overall and cause-specific readmission are presented as pooled proportions with 95% confidence intervals (CIs). All meta-analyses were performed using Stata 10.0.

Results

Fifteen unique TJA studies (12 THA, 10 TKA) met the criteria for the meta-analysis.^20,25-38Figure 1 depicts the PRISMA flowchart for study identification.²²

Of the 12 studies eligible for the THA analysis (Table 2), 6 were conducted in the United States,^{20,26,27,30,33,34} 5 in Europe,^{25,28,29,32,35} and 1 in Canada.³¹ Seven of the 12 studies reported readmission rates at 30 days, and 7 reported rates at 90 days (2 reported rates at both follow-ups). We analyzed a total of 113,396 patients at the 30-day window and 192,380 patients at the 90-day window. Mean age was 74.2 years. The included studies were variable and sparse in their reporting of specific characteristics (Table 3).

Of the 10 studies (2 prospective, 8 retrospective) eligible for the TKA analysis (Table 4), 6 were conducted in the United States,^{20,26,27,34,36,37} 3 in Europe,^25,29,35 and 1 in Asia.³⁸ Four of the 10 studies reported readmission rates at 30 days, and 7 reported rates at 90 days (1 reported rates at both follow-ups).²⁷ We analyzed a total of 3,278,635 patients at the 30-day window and 272,419 patients at the 90-day window. Mean age was 74.3 years. The included studies were quite variable and sparse in their reporting of specific characteristics (Table 5).