Imaging

Proximal humerus fractures (PHFs), AO/OTA (Ar­ beitsgemeinschaft für Osteosynthesefragen/Orthopaedic Trauma Association) type 11,¹ are common, representing 4% to 5% of all fractures in adults.² However, there is no consensus as to optimal management of these injuries, with some reports supporting and others rejecting the various fixation methods,³ and there are no evidence-based practice guidelines informing treatment decisions.⁴ Not surprisingly, orthopedic surgeons do not agree on ideal treatment for PHFs^5,6 and differ by region in their rates of surgical management.² In addition, analyses of national databases have found variation in choice of surgical treatment for PHFs between surgeons and between hospitals of different patient volumes.⁴ Few studies have assessed surgeon agreement on treatment decisions. Findings from these limited investigations indicate there is little agreement on treatment choices, but training may have some impact.^5-7 In 3 studies,^5-7 shoulder and trauma fellowship–trained surgeons differed in their management of PHFs both in terms of rates of operative treatment^5,7 and specific operative management choices.^5,6 No study has assessed surgeon agreement on radiographic outcomes.

We conducted a study to compare expert shoulder and trauma surgeons’ treatment decision-making and agreement on final radiographic outcomes of surgically treated PHFs. We hypothesized there would be poor agreement on treatment decisions and better agreement on radiographic outcomes, with a difference between shoulder and trauma fellowship–trained surgeons.

Materials and Methods

After receiving institutional review board approval for this study, we collected data on 100 consecutive PHFs (AO/OTA type 11¹) surgically treated at 2 affiliated level I trauma centers between January 2004 and July 2008. None of the cases in the series was managed by any of the surgeons participating in this study.

We created a PowerPoint (Microsoft, Redmond, Washington) survey that included radiographs (preoperative, immediate postoperative, final postoperative) and, if available, a computed tomography image. This survey was sent to 4 orthopedic surgeons: Drs. Gardner, Gerber, Lorich, and Walch. Two of these authors are fellowship-trained in shoulder surgery, the other 2 in orthopedic traumatology with specialization in treating PHFs. All are internationally renowned in PHF management. Using the survey images and a 4-point Likert scale ranging from disagree strongly to agree strongly, the examiners rated their agreement with treatment decisions (arthroplasty vs fixation). They also rated (very poor to very good) immediate postoperative reduction or arthroplasty placement, immediate postoperative fixation methods for fractures treated with open reduction and internal fixation (ORIF), and final radiographic outcomes.

Interobserver agreement was calculated using the intraclass correlation coefficient (ICC),^8,9 with scores of <0.2 (poor), 0.21 to 0.4 (fair), 0.41 to 0.6 (moderate), 0.61 to 0.8 (good), and >0.8 (excellent) used to indicate agreement among observers. ICC scores were determined by treating the 4 examiners as independent entities. Subgroup analyses were also performed to determine ICC scores comparing the 2 shoulder surgeons, comparing the 2 trauma surgeons, and comparing the shoulder surgeons and trauma surgeons as 2 separate groups. ICC scores were used instead of κ coefficients to assess agreement because ICC scores treat ratings as continuous variables, allow for comparison of 2 or more raters, and allow for assessment of correlation among raters, whereas κ coefficients treat data as categorical variables and assume the ratings have no natural ordering. ICC scores were generated by SAS 9.1.3 software (SAS Institute, Cary, North Carolina).

Results

The 4 surgeons’ overall ICC scores for agreement with the rating of immediate reduction or arthroplasty placement and the rating of final radiographic outcome indicated moderate levels of agreement (Table 1). Regarding treatment decision-making and ratings of fixation, the surgeons demonstrated poor and fair levels of agreement, respectively.

The ICC scores comparing the shoulder and trauma surgeons revealed similar levels of agreement (Table 2): moderate levels of agreement for ratings of both immediate postoperative reduction or arthroplasty placement and final radiographic outcomes, but poor and fair levels of agreement regarding treatment decision-making and the rating of immediate postoperative fixation methods for fractures treated with ORIF, respectively.

Subgroup analysis revealed that the 2 shoulder surgeons had poor and fair levels of agreement for treatment decisions and rating of immediate postoperative fixation, respectively, though they moderately agreed on rating of immediate postoperative reduction or arthroplasty placement and rating of final radiographic outcome (Table 3). When the 2 trauma surgeons were compared with each other, ICC scores revealed higher levels of agreement overall (Table 4). In other words, the 2 trauma surgeons agreed with each other more than the 2 shoulder surgeons agreed with each other.

Discussion

This study had 3 major findings: (1) Surgeons do not agree on treatment decisions, including fixation methods, regarding PHFs; (2) regardless of their opinions on ideal treatment, they moderately agree on reductions and final radiographic outcomes; (3) expert trauma surgeons may agree more on treatment decisions than expert shoulder surgeons do. In other words, surgeons do not agree on the best treatment, but they radiographically recognize when a procedure has been performed technically well or poorly. These results support our hypothesis and the limited current literature.

 

An analysis of Medicare databases showed marked regional variation in rates of operative treatment of PHFs.² Similarly, a Nationwide Inpatient Sample analysis revealed nationwide variation in operative management of PHFs.⁴ Both findings are consistent with our results of poor agreement about treatment decisions and ratings of postoperative fixation of PHFs. In 2010, Petit and colleagues⁶ reported that surgeons do not agree on PHF management. In 2011, Foroohar and colleagues¹⁰ similarly reported low interobserver agreement for treatment recommendations made by 4 upper extremity orthopedic specialists, 4 general orthopedic surgeons, 4 senior residents, and 4 junior residents, for a series of 16 PHFs—also consistent with our findings.

The lack of agreement about PHF treatment may reflect a difference in training, particularly in light of the recent expansion of shoulder and elbow fellowships.² Three separate studies performed at 2 affiliated level I trauma centers demonstrated significant differences in treatment decision-making between shoulder and trauma fellowship–trained surgeons.^5-7 Our results are consistent with the hypothesis that training affects treatment decision-making, as we found poor agreement between shoulder and trauma fellowship–trained surgeons regarding treatment decision for PHFs. Subanalyses revealed that expert trauma surgeons agreed with each other on treatment decisions more than expert shoulder surgeons agreed with each other, further suggesting that training may affect how surgeons manage PHFs. Differences in fellowship training even within the same specialty may account for the observed lesser levels of agreement between the shoulder surgeons, even among experts in the field.

The evidence for optimal treatment historically has been poor,^4,6 with few high-quality prospective, randomized controlled studies on the topic up until the past few years. The most recent Cochrane Review on optimal PHF treatment concluded that there is insufficient evidence to make an evidence-based recommendation and that the long-term benefit of surgery is unclear.¹¹ However, at least 5 controlled trials on the topic have been published within the past 5 years.^12-16 The evidence is striking and generally supports nonoperative treatment for most PHFs, including some displaced fractures—contrary to general orthopedic practice in many parts of the United States,² which hitherto had been based mainly on individual surgeon experience and the limited literature. Without strong evidence to support one treatment option over another, surgeons are left with no objective, scientific way of coming to agreement.

Related to the poor status quo of evidence for PHF treatments is new technology (eg, locking plates, reverse total shoulder arthroplasty) that has expanded surgical indications.^2,17 Although such developments have the potential to improve surgical treatments, they may also exacerbate the disagreement between surgeons regarding optimal operative treatment of PHFs. This potential consequence of new technology may be reflected in our finding of disagreement among surgeons on immediate postoperative fixation methods. Precisely because they are new, such technological innovations have limited evidence supporting their use. This leaves surgeons with little to nothing to inform their decisions to use these devices, other than familiarity with and impressions of the new technology.

Our study had several limitations. First is the small sample size, of surgeons who are leaders in the field. Our sample therefore may not be generalizable to the general population of shoulder and trauma surgeons. Second, we did not calculate intraobserver variability. Third, inherent to studies of interobserver agreement is the uncertainty of their clinical relevance. In the clinical setting, a surgeon has much more information at hand (eg, patient history, physical examination findings, colleague consultations), thus raising the possibility of underestimations of interobserver agreements.¹⁸ Fourth, our comparison of surgeons’ ratings of outcomes was purely radiographic, which may or may not represent or be indicative of clinical outcomes (eg, pain relief, function, range of motion, patient satisfaction). The conclusions we may draw are accordingly limited, as we did not directly evaluate clinical outcome parameters.

Our study had several strengths as well. First, to our knowledge this is the first study to assess interobserver variability in surgeons’ ratings of radiographic outcomes. Its findings may provide further insight into the reasons for poor agreement among orthopedic surgeons on both classification and treatment of PHFs. Second, our surveying of internationally renowned expert surgeons from 4 different institutions may have helped reduce single-institution bias, and it presents the highest level of expertise in the treatment of PHFs.

Although the surgeons in our study moderately agreed on final radiographic outcomes of PHFs, such levels of agreement may still be clinically unacceptable.¹⁹ The overall disagreement on treatment decisions highlights the need for better evidence for optimal treatment of PHFs in order to improve consensus, particularly with anticipated increases in age and comorbidities in the population in coming years.⁴ Subgroup analysis suggested trauma fellowships may contribute to better treatment agreement, though this idea requires further study, perhaps by surveying shoulder and trauma fellowship directors and their curricula for variability in teaching treatment decision-making. The surgeons in our study agreed more on what they consider acceptable final radiographic outcomes, which is encouraging. However, treatment consensus is the primary goal. The recent publication of prospective, randomized studies is helping with this issue, but more studies are needed. It is encouraging that several are planned or under way.^20-22

 

Conclusion

The surgeons surveyed in this study did not agree on ideal treatment for PHFs but moderately agreed on quality of radiographic outcomes. These differences may reflect a difference in training. We conducted this study to compare experienced shoulder and trauma fellowship–trained surgeons’ treatment decision-making and ratings of radiographic outcomes of PHFs when presented with the same group of patients managed at 2 level I trauma centers. We hypothesized there would be little agreement on treatment decisions, better agreement on final radiographic outcome, and a difference between decision-making and ratings of radiographic outcomes between expert shoulder and trauma surgeons. Our results showed that surgeons do not agree on the best treatment for PHFs but radiographically recognize when an operative treatment has been performed well or poorly. Regarding treatment decisions, our results also showed that expert trauma surgeons may agree more with each other than shoulder surgeons agree with each other. These results support our hypothesis and the limited current literature. The overall disagreement among the surgeons in our study and an aging population that grows sicker each year highlight the need for better evidence for the optimal treatment of PHFs in order to improve consensus.

Proximal humerus fractures (PHFs), AO/OTA (Ar­ beitsgemeinschaft für Osteosynthesefragen/Orthopaedic Trauma Association) type 11,¹ are common, representing 4% to 5% of all fractures in adults.² However, there is no consensus as to optimal management of these injuries, with some reports supporting and others rejecting the various fixation methods,³ and there are no evidence-based practice guidelines informing treatment decisions.⁴ Not surprisingly, orthopedic surgeons do not agree on ideal treatment for PHFs^5,6 and differ by region in their rates of surgical management.² In addition, analyses of national databases have found variation in choice of surgical treatment for PHFs between surgeons and between hospitals of different patient volumes.⁴ Few studies have assessed surgeon agreement on treatment decisions. Findings from these limited investigations indicate there is little agreement on treatment choices, but training may have some impact.^5-7 In 3 studies,^5-7 shoulder and trauma fellowship–trained surgeons differed in their management of PHFs both in terms of rates of operative treatment^5,7 and specific operative management choices.^5,6 No study has assessed surgeon agreement on radiographic outcomes.

We conducted a study to compare expert shoulder and trauma surgeons’ treatment decision-making and agreement on final radiographic outcomes of surgically treated PHFs. We hypothesized there would be poor agreement on treatment decisions and better agreement on radiographic outcomes, with a difference between shoulder and trauma fellowship–trained surgeons.

Materials and Methods

After receiving institutional review board approval for this study, we collected data on 100 consecutive PHFs (AO/OTA type 11¹) surgically treated at 2 affiliated level I trauma centers between January 2004 and July 2008. None of the cases in the series was managed by any of the surgeons participating in this study.

We created a PowerPoint (Microsoft, Redmond, Washington) survey that included radiographs (preoperative, immediate postoperative, final postoperative) and, if available, a computed tomography image. This survey was sent to 4 orthopedic surgeons: Drs. Gardner, Gerber, Lorich, and Walch. Two of these authors are fellowship-trained in shoulder surgery, the other 2 in orthopedic traumatology with specialization in treating PHFs. All are internationally renowned in PHF management. Using the survey images and a 4-point Likert scale ranging from disagree strongly to agree strongly, the examiners rated their agreement with treatment decisions (arthroplasty vs fixation). They also rated (very poor to very good) immediate postoperative reduction or arthroplasty placement, immediate postoperative fixation methods for fractures treated with open reduction and internal fixation (ORIF), and final radiographic outcomes.

Interobserver agreement was calculated using the intraclass correlation coefficient (ICC),^8,9 with scores of <0.2 (poor), 0.21 to 0.4 (fair), 0.41 to 0.6 (moderate), 0.61 to 0.8 (good), and >0.8 (excellent) used to indicate agreement among observers. ICC scores were determined by treating the 4 examiners as independent entities. Subgroup analyses were also performed to determine ICC scores comparing the 2 shoulder surgeons, comparing the 2 trauma surgeons, and comparing the shoulder surgeons and trauma surgeons as 2 separate groups. ICC scores were used instead of κ coefficients to assess agreement because ICC scores treat ratings as continuous variables, allow for comparison of 2 or more raters, and allow for assessment of correlation among raters, whereas κ coefficients treat data as categorical variables and assume the ratings have no natural ordering. ICC scores were generated by SAS 9.1.3 software (SAS Institute, Cary, North Carolina).

Results

The 4 surgeons’ overall ICC scores for agreement with the rating of immediate reduction or arthroplasty placement and the rating of final radiographic outcome indicated moderate levels of agreement (Table 1). Regarding treatment decision-making and ratings of fixation, the surgeons demonstrated poor and fair levels of agreement, respectively.

The ICC scores comparing the shoulder and trauma surgeons revealed similar levels of agreement (Table 2): moderate levels of agreement for ratings of both immediate postoperative reduction or arthroplasty placement and final radiographic outcomes, but poor and fair levels of agreement regarding treatment decision-making and the rating of immediate postoperative fixation methods for fractures treated with ORIF, respectively.

Subgroup analysis revealed that the 2 shoulder surgeons had poor and fair levels of agreement for treatment decisions and rating of immediate postoperative fixation, respectively, though they moderately agreed on rating of immediate postoperative reduction or arthroplasty placement and rating of final radiographic outcome (Table 3). When the 2 trauma surgeons were compared with each other, ICC scores revealed higher levels of agreement overall (Table 4). In other words, the 2 trauma surgeons agreed with each other more than the 2 shoulder surgeons agreed with each other.

Discussion

This study had 3 major findings: (1) Surgeons do not agree on treatment decisions, including fixation methods, regarding PHFs; (2) regardless of their opinions on ideal treatment, they moderately agree on reductions and final radiographic outcomes; (3) expert trauma surgeons may agree more on treatment decisions than expert shoulder surgeons do. In other words, surgeons do not agree on the best treatment, but they radiographically recognize when a procedure has been performed technically well or poorly. These results support our hypothesis and the limited current literature.

 

An analysis of Medicare databases showed marked regional variation in rates of operative treatment of PHFs.² Similarly, a Nationwide Inpatient Sample analysis revealed nationwide variation in operative management of PHFs.⁴ Both findings are consistent with our results of poor agreement about treatment decisions and ratings of postoperative fixation of PHFs. In 2010, Petit and colleagues⁶ reported that surgeons do not agree on PHF management. In 2011, Foroohar and colleagues¹⁰ similarly reported low interobserver agreement for treatment recommendations made by 4 upper extremity orthopedic specialists, 4 general orthopedic surgeons, 4 senior residents, and 4 junior residents, for a series of 16 PHFs—also consistent with our findings.

The lack of agreement about PHF treatment may reflect a difference in training, particularly in light of the recent expansion of shoulder and elbow fellowships.² Three separate studies performed at 2 affiliated level I trauma centers demonstrated significant differences in treatment decision-making between shoulder and trauma fellowship–trained surgeons.^5-7 Our results are consistent with the hypothesis that training affects treatment decision-making, as we found poor agreement between shoulder and trauma fellowship–trained surgeons regarding treatment decision for PHFs. Subanalyses revealed that expert trauma surgeons agreed with each other on treatment decisions more than expert shoulder surgeons agreed with each other, further suggesting that training may affect how surgeons manage PHFs. Differences in fellowship training even within the same specialty may account for the observed lesser levels of agreement between the shoulder surgeons, even among experts in the field.

The evidence for optimal treatment historically has been poor,^4,6 with few high-quality prospective, randomized controlled studies on the topic up until the past few years. The most recent Cochrane Review on optimal PHF treatment concluded that there is insufficient evidence to make an evidence-based recommendation and that the long-term benefit of surgery is unclear.¹¹ However, at least 5 controlled trials on the topic have been published within the past 5 years.^12-16 The evidence is striking and generally supports nonoperative treatment for most PHFs, including some displaced fractures—contrary to general orthopedic practice in many parts of the United States,² which hitherto had been based mainly on individual surgeon experience and the limited literature. Without strong evidence to support one treatment option over another, surgeons are left with no objective, scientific way of coming to agreement.

Related to the poor status quo of evidence for PHF treatments is new technology (eg, locking plates, reverse total shoulder arthroplasty) that has expanded surgical indications.^2,17 Although such developments have the potential to improve surgical treatments, they may also exacerbate the disagreement between surgeons regarding optimal operative treatment of PHFs. This potential consequence of new technology may be reflected in our finding of disagreement among surgeons on immediate postoperative fixation methods. Precisely because they are new, such technological innovations have limited evidence supporting their use. This leaves surgeons with little to nothing to inform their decisions to use these devices, other than familiarity with and impressions of the new technology.

Our study had several limitations. First is the small sample size, of surgeons who are leaders in the field. Our sample therefore may not be generalizable to the general population of shoulder and trauma surgeons. Second, we did not calculate intraobserver variability. Third, inherent to studies of interobserver agreement is the uncertainty of their clinical relevance. In the clinical setting, a surgeon has much more information at hand (eg, patient history, physical examination findings, colleague consultations), thus raising the possibility of underestimations of interobserver agreements.¹⁸ Fourth, our comparison of surgeons’ ratings of outcomes was purely radiographic, which may or may not represent or be indicative of clinical outcomes (eg, pain relief, function, range of motion, patient satisfaction). The conclusions we may draw are accordingly limited, as we did not directly evaluate clinical outcome parameters.

Our study had several strengths as well. First, to our knowledge this is the first study to assess interobserver variability in surgeons’ ratings of radiographic outcomes. Its findings may provide further insight into the reasons for poor agreement among orthopedic surgeons on both classification and treatment of PHFs. Second, our surveying of internationally renowned expert surgeons from 4 different institutions may have helped reduce single-institution bias, and it presents the highest level of expertise in the treatment of PHFs.

Although the surgeons in our study moderately agreed on final radiographic outcomes of PHFs, such levels of agreement may still be clinically unacceptable.¹⁹ The overall disagreement on treatment decisions highlights the need for better evidence for optimal treatment of PHFs in order to improve consensus, particularly with anticipated increases in age and comorbidities in the population in coming years.⁴ Subgroup analysis suggested trauma fellowships may contribute to better treatment agreement, though this idea requires further study, perhaps by surveying shoulder and trauma fellowship directors and their curricula for variability in teaching treatment decision-making. The surgeons in our study agreed more on what they consider acceptable final radiographic outcomes, which is encouraging. However, treatment consensus is the primary goal. The recent publication of prospective, randomized studies is helping with this issue, but more studies are needed. It is encouraging that several are planned or under way.^20-22

 

Conclusion

The surgeons surveyed in this study did not agree on ideal treatment for PHFs but moderately agreed on quality of radiographic outcomes. These differences may reflect a difference in training. We conducted this study to compare experienced shoulder and trauma fellowship–trained surgeons’ treatment decision-making and ratings of radiographic outcomes of PHFs when presented with the same group of patients managed at 2 level I trauma centers. We hypothesized there would be little agreement on treatment decisions, better agreement on final radiographic outcome, and a difference between decision-making and ratings of radiographic outcomes between expert shoulder and trauma surgeons. Our results showed that surgeons do not agree on the best treatment for PHFs but radiographically recognize when an operative treatment has been performed well or poorly. Regarding treatment decisions, our results also showed that expert trauma surgeons may agree more with each other than shoulder surgeons agree with each other. These results support our hypothesis and the limited current literature. The overall disagreement among the surgeons in our study and an aging population that grows sicker each year highlight the need for better evidence for the optimal treatment of PHFs in order to improve consensus.

Proximal humerus fractures (PHFs), AO/OTA (Ar­ beitsgemeinschaft für Osteosynthesefragen/Orthopaedic Trauma Association) type 11,¹ are common, representing 4% to 5% of all fractures in adults.² However, there is no consensus as to optimal management of these injuries, with some reports supporting and others rejecting the various fixation methods,³ and there are no evidence-based practice guidelines informing treatment decisions.⁴ Not surprisingly, orthopedic surgeons do not agree on ideal treatment for PHFs^5,6 and differ by region in their rates of surgical management.² In addition, analyses of national databases have found variation in choice of surgical treatment for PHFs between surgeons and between hospitals of different patient volumes.⁴ Few studies have assessed surgeon agreement on treatment decisions. Findings from these limited investigations indicate there is little agreement on treatment choices, but training may have some impact.^5-7 In 3 studies,^5-7 shoulder and trauma fellowship–trained surgeons differed in their management of PHFs both in terms of rates of operative treatment^5,7 and specific operative management choices.^5,6 No study has assessed surgeon agreement on radiographic outcomes.

We conducted a study to compare expert shoulder and trauma surgeons’ treatment decision-making and agreement on final radiographic outcomes of surgically treated PHFs. We hypothesized there would be poor agreement on treatment decisions and better agreement on radiographic outcomes, with a difference between shoulder and trauma fellowship–trained surgeons.

Materials and Methods

After receiving institutional review board approval for this study, we collected data on 100 consecutive PHFs (AO/OTA type 11¹) surgically treated at 2 affiliated level I trauma centers between January 2004 and July 2008. None of the cases in the series was managed by any of the surgeons participating in this study.

We created a PowerPoint (Microsoft, Redmond, Washington) survey that included radiographs (preoperative, immediate postoperative, final postoperative) and, if available, a computed tomography image. This survey was sent to 4 orthopedic surgeons: Drs. Gardner, Gerber, Lorich, and Walch. Two of these authors are fellowship-trained in shoulder surgery, the other 2 in orthopedic traumatology with specialization in treating PHFs. All are internationally renowned in PHF management. Using the survey images and a 4-point Likert scale ranging from disagree strongly to agree strongly, the examiners rated their agreement with treatment decisions (arthroplasty vs fixation). They also rated (very poor to very good) immediate postoperative reduction or arthroplasty placement, immediate postoperative fixation methods for fractures treated with open reduction and internal fixation (ORIF), and final radiographic outcomes.

Interobserver agreement was calculated using the intraclass correlation coefficient (ICC),^8,9 with scores of <0.2 (poor), 0.21 to 0.4 (fair), 0.41 to 0.6 (moderate), 0.61 to 0.8 (good), and >0.8 (excellent) used to indicate agreement among observers. ICC scores were determined by treating the 4 examiners as independent entities. Subgroup analyses were also performed to determine ICC scores comparing the 2 shoulder surgeons, comparing the 2 trauma surgeons, and comparing the shoulder surgeons and trauma surgeons as 2 separate groups. ICC scores were used instead of κ coefficients to assess agreement because ICC scores treat ratings as continuous variables, allow for comparison of 2 or more raters, and allow for assessment of correlation among raters, whereas κ coefficients treat data as categorical variables and assume the ratings have no natural ordering. ICC scores were generated by SAS 9.1.3 software (SAS Institute, Cary, North Carolina).

Results

The 4 surgeons’ overall ICC scores for agreement with the rating of immediate reduction or arthroplasty placement and the rating of final radiographic outcome indicated moderate levels of agreement (Table 1). Regarding treatment decision-making and ratings of fixation, the surgeons demonstrated poor and fair levels of agreement, respectively.

The ICC scores comparing the shoulder and trauma surgeons revealed similar levels of agreement (Table 2): moderate levels of agreement for ratings of both immediate postoperative reduction or arthroplasty placement and final radiographic outcomes, but poor and fair levels of agreement regarding treatment decision-making and the rating of immediate postoperative fixation methods for fractures treated with ORIF, respectively.

Subgroup analysis revealed that the 2 shoulder surgeons had poor and fair levels of agreement for treatment decisions and rating of immediate postoperative fixation, respectively, though they moderately agreed on rating of immediate postoperative reduction or arthroplasty placement and rating of final radiographic outcome (Table 3). When the 2 trauma surgeons were compared with each other, ICC scores revealed higher levels of agreement overall (Table 4). In other words, the 2 trauma surgeons agreed with each other more than the 2 shoulder surgeons agreed with each other.

Discussion

This study had 3 major findings: (1) Surgeons do not agree on treatment decisions, including fixation methods, regarding PHFs; (2) regardless of their opinions on ideal treatment, they moderately agree on reductions and final radiographic outcomes; (3) expert trauma surgeons may agree more on treatment decisions than expert shoulder surgeons do. In other words, surgeons do not agree on the best treatment, but they radiographically recognize when a procedure has been performed technically well or poorly. These results support our hypothesis and the limited current literature.

 

An analysis of Medicare databases showed marked regional variation in rates of operative treatment of PHFs.² Similarly, a Nationwide Inpatient Sample analysis revealed nationwide variation in operative management of PHFs.⁴ Both findings are consistent with our results of poor agreement about treatment decisions and ratings of postoperative fixation of PHFs. In 2010, Petit and colleagues⁶ reported that surgeons do not agree on PHF management. In 2011, Foroohar and colleagues¹⁰ similarly reported low interobserver agreement for treatment recommendations made by 4 upper extremity orthopedic specialists, 4 general orthopedic surgeons, 4 senior residents, and 4 junior residents, for a series of 16 PHFs—also consistent with our findings.

The lack of agreement about PHF treatment may reflect a difference in training, particularly in light of the recent expansion of shoulder and elbow fellowships.² Three separate studies performed at 2 affiliated level I trauma centers demonstrated significant differences in treatment decision-making between shoulder and trauma fellowship–trained surgeons.^5-7 Our results are consistent with the hypothesis that training affects treatment decision-making, as we found poor agreement between shoulder and trauma fellowship–trained surgeons regarding treatment decision for PHFs. Subanalyses revealed that expert trauma surgeons agreed with each other on treatment decisions more than expert shoulder surgeons agreed with each other, further suggesting that training may affect how surgeons manage PHFs. Differences in fellowship training even within the same specialty may account for the observed lesser levels of agreement between the shoulder surgeons, even among experts in the field.

The evidence for optimal treatment historically has been poor,^4,6 with few high-quality prospective, randomized controlled studies on the topic up until the past few years. The most recent Cochrane Review on optimal PHF treatment concluded that there is insufficient evidence to make an evidence-based recommendation and that the long-term benefit of surgery is unclear.¹¹ However, at least 5 controlled trials on the topic have been published within the past 5 years.^12-16 The evidence is striking and generally supports nonoperative treatment for most PHFs, including some displaced fractures—contrary to general orthopedic practice in many parts of the United States,² which hitherto had been based mainly on individual surgeon experience and the limited literature. Without strong evidence to support one treatment option over another, surgeons are left with no objective, scientific way of coming to agreement.

Related to the poor status quo of evidence for PHF treatments is new technology (eg, locking plates, reverse total shoulder arthroplasty) that has expanded surgical indications.^2,17 Although such developments have the potential to improve surgical treatments, they may also exacerbate the disagreement between surgeons regarding optimal operative treatment of PHFs. This potential consequence of new technology may be reflected in our finding of disagreement among surgeons on immediate postoperative fixation methods. Precisely because they are new, such technological innovations have limited evidence supporting their use. This leaves surgeons with little to nothing to inform their decisions to use these devices, other than familiarity with and impressions of the new technology.

Our study had several limitations. First is the small sample size, of surgeons who are leaders in the field. Our sample therefore may not be generalizable to the general population of shoulder and trauma surgeons. Second, we did not calculate intraobserver variability. Third, inherent to studies of interobserver agreement is the uncertainty of their clinical relevance. In the clinical setting, a surgeon has much more information at hand (eg, patient history, physical examination findings, colleague consultations), thus raising the possibility of underestimations of interobserver agreements.¹⁸ Fourth, our comparison of surgeons’ ratings of outcomes was purely radiographic, which may or may not represent or be indicative of clinical outcomes (eg, pain relief, function, range of motion, patient satisfaction). The conclusions we may draw are accordingly limited, as we did not directly evaluate clinical outcome parameters.

Our study had several strengths as well. First, to our knowledge this is the first study to assess interobserver variability in surgeons’ ratings of radiographic outcomes. Its findings may provide further insight into the reasons for poor agreement among orthopedic surgeons on both classification and treatment of PHFs. Second, our surveying of internationally renowned expert surgeons from 4 different institutions may have helped reduce single-institution bias, and it presents the highest level of expertise in the treatment of PHFs.

Although the surgeons in our study moderately agreed on final radiographic outcomes of PHFs, such levels of agreement may still be clinically unacceptable.¹⁹ The overall disagreement on treatment decisions highlights the need for better evidence for optimal treatment of PHFs in order to improve consensus, particularly with anticipated increases in age and comorbidities in the population in coming years.⁴ Subgroup analysis suggested trauma fellowships may contribute to better treatment agreement, though this idea requires further study, perhaps by surveying shoulder and trauma fellowship directors and their curricula for variability in teaching treatment decision-making. The surgeons in our study agreed more on what they consider acceptable final radiographic outcomes, which is encouraging. However, treatment consensus is the primary goal. The recent publication of prospective, randomized studies is helping with this issue, but more studies are needed. It is encouraging that several are planned or under way.^20-22

 

Conclusion

The surgeons surveyed in this study did not agree on ideal treatment for PHFs but moderately agreed on quality of radiographic outcomes. These differences may reflect a difference in training. We conducted this study to compare experienced shoulder and trauma fellowship–trained surgeons’ treatment decision-making and ratings of radiographic outcomes of PHFs when presented with the same group of patients managed at 2 level I trauma centers. We hypothesized there would be little agreement on treatment decisions, better agreement on final radiographic outcome, and a difference between decision-making and ratings of radiographic outcomes between expert shoulder and trauma surgeons. Our results showed that surgeons do not agree on the best treatment for PHFs but radiographically recognize when an operative treatment has been performed well or poorly. Regarding treatment decisions, our results also showed that expert trauma surgeons may agree more with each other than shoulder surgeons agree with each other. These results support our hypothesis and the limited current literature. The overall disagreement among the surgeons in our study and an aging population that grows sicker each year highlight the need for better evidence for the optimal treatment of PHFs in order to improve consensus.

Two years of either triple therapy or treatment with tumor necrosis factor plus methotrexate failed to eliminate joint inflammation on MRI in a subcohort of patients with early rheumatoid arthritis from the randomized, double-blind Treatment of Early Aggressive Rheumatoid Arthritis (TEAR) trial.

In 118 patients with a mean age of 51 years, short disease duration, and severe disease at TEAR trial entry – 92% of whom were seropositive – only 29 had wrist pain, tenderness, or swelling at 2-year follow-up. However, all 118 patients had MRI evidence of residual joint inflammation after 2 years, and 78% had evidence of osteitis, Dr. Veena K. Ranganath of the University of California, Los Angeles, and her colleagues reported (Arthritis Care Res. 2015 Jan. 7 [doi:10.1002/acr.22541]).

Inflammation remained despite significant improvement of disease activity measures at the time of the MRI, compared with baseline (for example, 28-joint disease activity score using erythrocyte sedimentation rate [DAS28-ESR] decreased from 5.8 to 2.9). Total MRI inflammation scores were significantly lower in patients who met 2011 American College of Rheumatology (ACR)/European League Against Rheumatism (EULAR) Boolean remission criteria and remission by Chronic Disease Activity Index (CDAI), but not in those with DAS28-ESR remission, they noted.

The findings demonstrate that total MRI inflammatory scores are “best differentiated by the most stringent clinical remission criteria” – CDAI and 2011 ACR/EULAR Boolean Criteria, as opposed to DAS28-ESR (with a 2.6 cutpoint). Further, no differences were seen in damage or MRI inflammatory scores based on treatment regimen, which supports methotrexate-first recommendations for the TEAR trial, they said, noting that the long-term prognostic implications of the study findings are unclear because of short-follow-up, and that it remains unclear whether attainment of clinical remission warrants a drug holiday or cessation of RA treatment.

Thus, it is “ill-advised to discontinue therapy until future studies suggest otherwise,” they concluded, adding that this is particularly true given that prior published data suggest a link between osteitis – which occurred at a high rate in this study despite clinical remission – and future radiographic progression.

The TEAR trial was supported by Amgen. The current research was supported by a National Institutes of Health/National Center for Advancing Translational Science UCLA CTSI grant, and individual authors were supported by ACR/REF grants, a National Institutes of Health award, the Margaret J. Miller Endowed Professor of Research Chair, and the Agency for Healthcare Research and Quality.

Two years of either triple therapy or treatment with tumor necrosis factor plus methotrexate failed to eliminate joint inflammation on MRI in a subcohort of patients with early rheumatoid arthritis from the randomized, double-blind Treatment of Early Aggressive Rheumatoid Arthritis (TEAR) trial.

In 118 patients with a mean age of 51 years, short disease duration, and severe disease at TEAR trial entry – 92% of whom were seropositive – only 29 had wrist pain, tenderness, or swelling at 2-year follow-up. However, all 118 patients had MRI evidence of residual joint inflammation after 2 years, and 78% had evidence of osteitis, Dr. Veena K. Ranganath of the University of California, Los Angeles, and her colleagues reported (Arthritis Care Res. 2015 Jan. 7 [doi:10.1002/acr.22541]).

Inflammation remained despite significant improvement of disease activity measures at the time of the MRI, compared with baseline (for example, 28-joint disease activity score using erythrocyte sedimentation rate [DAS28-ESR] decreased from 5.8 to 2.9). Total MRI inflammation scores were significantly lower in patients who met 2011 American College of Rheumatology (ACR)/European League Against Rheumatism (EULAR) Boolean remission criteria and remission by Chronic Disease Activity Index (CDAI), but not in those with DAS28-ESR remission, they noted.

The findings demonstrate that total MRI inflammatory scores are “best differentiated by the most stringent clinical remission criteria” – CDAI and 2011 ACR/EULAR Boolean Criteria, as opposed to DAS28-ESR (with a 2.6 cutpoint). Further, no differences were seen in damage or MRI inflammatory scores based on treatment regimen, which supports methotrexate-first recommendations for the TEAR trial, they said, noting that the long-term prognostic implications of the study findings are unclear because of short-follow-up, and that it remains unclear whether attainment of clinical remission warrants a drug holiday or cessation of RA treatment.

Thus, it is “ill-advised to discontinue therapy until future studies suggest otherwise,” they concluded, adding that this is particularly true given that prior published data suggest a link between osteitis – which occurred at a high rate in this study despite clinical remission – and future radiographic progression.

The TEAR trial was supported by Amgen. The current research was supported by a National Institutes of Health/National Center for Advancing Translational Science UCLA CTSI grant, and individual authors were supported by ACR/REF grants, a National Institutes of Health award, the Margaret J. Miller Endowed Professor of Research Chair, and the Agency for Healthcare Research and Quality.

Two years of either triple therapy or treatment with tumor necrosis factor plus methotrexate failed to eliminate joint inflammation on MRI in a subcohort of patients with early rheumatoid arthritis from the randomized, double-blind Treatment of Early Aggressive Rheumatoid Arthritis (TEAR) trial.

In 118 patients with a mean age of 51 years, short disease duration, and severe disease at TEAR trial entry – 92% of whom were seropositive – only 29 had wrist pain, tenderness, or swelling at 2-year follow-up. However, all 118 patients had MRI evidence of residual joint inflammation after 2 years, and 78% had evidence of osteitis, Dr. Veena K. Ranganath of the University of California, Los Angeles, and her colleagues reported (Arthritis Care Res. 2015 Jan. 7 [doi:10.1002/acr.22541]).

Inflammation remained despite significant improvement of disease activity measures at the time of the MRI, compared with baseline (for example, 28-joint disease activity score using erythrocyte sedimentation rate [DAS28-ESR] decreased from 5.8 to 2.9). Total MRI inflammation scores were significantly lower in patients who met 2011 American College of Rheumatology (ACR)/European League Against Rheumatism (EULAR) Boolean remission criteria and remission by Chronic Disease Activity Index (CDAI), but not in those with DAS28-ESR remission, they noted.

The findings demonstrate that total MRI inflammatory scores are “best differentiated by the most stringent clinical remission criteria” – CDAI and 2011 ACR/EULAR Boolean Criteria, as opposed to DAS28-ESR (with a 2.6 cutpoint). Further, no differences were seen in damage or MRI inflammatory scores based on treatment regimen, which supports methotrexate-first recommendations for the TEAR trial, they said, noting that the long-term prognostic implications of the study findings are unclear because of short-follow-up, and that it remains unclear whether attainment of clinical remission warrants a drug holiday or cessation of RA treatment.

Thus, it is “ill-advised to discontinue therapy until future studies suggest otherwise,” they concluded, adding that this is particularly true given that prior published data suggest a link between osteitis – which occurred at a high rate in this study despite clinical remission – and future radiographic progression.

The TEAR trial was supported by Amgen. The current research was supported by a National Institutes of Health/National Center for Advancing Translational Science UCLA CTSI grant, and individual authors were supported by ACR/REF grants, a National Institutes of Health award, the Margaret J. Miller Endowed Professor of Research Chair, and the Agency for Healthcare Research and Quality.

CHICAGO – Absence of coronary artery calcium upon imaging results in an impressively low cardiovascular event rate over the next 10 years regardless of an individual’s level of standard risk factors, according to prospective data from the MESA study.

In contrast, a coronary artery calcium (CAC) score of 1-10, often described as minimal CAC, nearly doubles the 10-year risk, compared with a baseline CAC score of 0.

Prior to these new 10-year data, many cardiologists considered a CAC score of 1-10 as tantamount to no CAC. Not so, Dr. Parag H. Joshi said at the American Heart Association scientific sessions.

Bruce Jancin/Frontline Medical News

“A CAC of 0 is presumably identifying someone without any atherosclerosis. Just the presence of minimal calcium suggests that atherosclerosis is building up. Our data suggest that among individuals with a CAC of 1-10, current smoking, elevated non-HDL cholesterol, and particularly hypertension should be treated aggressively,” said Dr. Joshi, a clinical fellow in cardiovascular diseases and prevention at Johns Hopkins University, Baltimore.

Prior studies totaling more than 50,000 subjects with a CAC score of 0 have shown very low cardiovascular event rates over 4-5 years of follow-up. However, current cardiovascular risk estimates focus on 10-year risk. This new analysis from MESA (Multi-Ethnic Study of Atherosclerosis) is the first study to provide prospective, 10-year events data, and those data are highly reassuring, he added.

MESA is a prospective, population-based cohort study. This analysis included 6,814 subjects aged 45-84 who were free of clinical cardiovascular disease at baseline, when their CAC score was determined. At that time, 3,415 participants had a CAC score of 0 and 508 had a score of 1-10.

During a median 10.3 years of follow-up, 123 cardiovascular events occurred, roughly one-third of which were nonfatal acute MIs and half of which were nonfatal strokes; the remainder were cardiovascular deaths.

The event rate was 2.9/1,000 person-years in subjects with a CAC of 0 and significantly greater at 5.5/1,000 person-years with a score of 1-10. However, since the cardiovascular risk factor profile of the zero CAC group was generally more favorable, Dr. Joshi and coinvestigators carried out a Cox proportional hazards analysis factoring in demographics, standard cardiovascular risk factors, body mass index, C-reactive protein level, and carotid intima media thickness. The adjusted 10-year event risk in the group with a CAC score of 1-10 was 1.9-fold greater than with a CAC of 0.

The highest 10-year event rate was noted in subjects with at least three of the following four risk factors at baseline: hypertension, current smoking, diabetes, and hyperlipidemia. The rate was 6.5/1,000 person-years in such individuals if they had a CAC of 0 and doubled at 13.1/1,000 person-years with a score of 1-10.

In a multivariate Cox analysis, age, smoking, and hypertension proved to be significant predictors of cardiovascular events in the group with a CAC of 0 as well as in those with a CAC of 1-10. But there was one important difference between the two groups: While the hazard ratio for cardiovascular events associated with hypertension versus no hypertension was 2.1 in subjects with a CAC of 0, the presence of hypertension in individuals with a CAC of 1-10 increased their event risk by 10.2-fold, or nearly five times greater than the risk increase associated with hypertension in persons with a CAC of 0, Dr. Joshi observed.

Non–HDL cholesterol level was predictive of cardiovascular risk in subjects with a CAC of 1-10 but not in those with a score of 0.

When actual event rates were compared with those predicted by the atherosclerotic cardiovascular disease (ASCVD) risk estimator introduced in the 2013 AHA/American College of Cardiology cholesterol guidelines, the event rate in subjects with an ASCVD 10-year risk estimate of 7.5%-15% but a CAC of 0 was just 4.4%.

Audience members noted that CAC scores didn’t do a very good job of stratifying stroke risk in MESA. That’s not surprising, since the score reflects coronary but not carotid artery calcium. But it is a limitation of CAC as a predictive tool, especially in light of the fact that strokes accounted for half of all cardiovascular events in the study.

Asked where he and his coinvestigators plan to go from here, Dr. Joshi said a randomized, controlled trial would be ideal, but to date funding isn’t available. However, the observational data from MESA and other studies suggest such a trial may not even be needed.

“Certainly the guidelines do allow for CAC scoring to be used in clinical decision making,” he noted.

 

The MESA study is funded by the National Heart, Lung, and Blood Institute. Dr. Joshi reported having no financial conflicts.

[email protected]

CHICAGO – Absence of coronary artery calcium upon imaging results in an impressively low cardiovascular event rate over the next 10 years regardless of an individual’s level of standard risk factors, according to prospective data from the MESA study.

In contrast, a coronary artery calcium (CAC) score of 1-10, often described as minimal CAC, nearly doubles the 10-year risk, compared with a baseline CAC score of 0.

Prior to these new 10-year data, many cardiologists considered a CAC score of 1-10 as tantamount to no CAC. Not so, Dr. Parag H. Joshi said at the American Heart Association scientific sessions.

Bruce Jancin/Frontline Medical News

“A CAC of 0 is presumably identifying someone without any atherosclerosis. Just the presence of minimal calcium suggests that atherosclerosis is building up. Our data suggest that among individuals with a CAC of 1-10, current smoking, elevated non-HDL cholesterol, and particularly hypertension should be treated aggressively,” said Dr. Joshi, a clinical fellow in cardiovascular diseases and prevention at Johns Hopkins University, Baltimore.

Prior studies totaling more than 50,000 subjects with a CAC score of 0 have shown very low cardiovascular event rates over 4-5 years of follow-up. However, current cardiovascular risk estimates focus on 10-year risk. This new analysis from MESA (Multi-Ethnic Study of Atherosclerosis) is the first study to provide prospective, 10-year events data, and those data are highly reassuring, he added.

MESA is a prospective, population-based cohort study. This analysis included 6,814 subjects aged 45-84 who were free of clinical cardiovascular disease at baseline, when their CAC score was determined. At that time, 3,415 participants had a CAC score of 0 and 508 had a score of 1-10.

During a median 10.3 years of follow-up, 123 cardiovascular events occurred, roughly one-third of which were nonfatal acute MIs and half of which were nonfatal strokes; the remainder were cardiovascular deaths.

The event rate was 2.9/1,000 person-years in subjects with a CAC of 0 and significantly greater at 5.5/1,000 person-years with a score of 1-10. However, since the cardiovascular risk factor profile of the zero CAC group was generally more favorable, Dr. Joshi and coinvestigators carried out a Cox proportional hazards analysis factoring in demographics, standard cardiovascular risk factors, body mass index, C-reactive protein level, and carotid intima media thickness. The adjusted 10-year event risk in the group with a CAC score of 1-10 was 1.9-fold greater than with a CAC of 0.

The highest 10-year event rate was noted in subjects with at least three of the following four risk factors at baseline: hypertension, current smoking, diabetes, and hyperlipidemia. The rate was 6.5/1,000 person-years in such individuals if they had a CAC of 0 and doubled at 13.1/1,000 person-years with a score of 1-10.

In a multivariate Cox analysis, age, smoking, and hypertension proved to be significant predictors of cardiovascular events in the group with a CAC of 0 as well as in those with a CAC of 1-10. But there was one important difference between the two groups: While the hazard ratio for cardiovascular events associated with hypertension versus no hypertension was 2.1 in subjects with a CAC of 0, the presence of hypertension in individuals with a CAC of 1-10 increased their event risk by 10.2-fold, or nearly five times greater than the risk increase associated with hypertension in persons with a CAC of 0, Dr. Joshi observed.

Non–HDL cholesterol level was predictive of cardiovascular risk in subjects with a CAC of 1-10 but not in those with a score of 0.

When actual event rates were compared with those predicted by the atherosclerotic cardiovascular disease (ASCVD) risk estimator introduced in the 2013 AHA/American College of Cardiology cholesterol guidelines, the event rate in subjects with an ASCVD 10-year risk estimate of 7.5%-15% but a CAC of 0 was just 4.4%.

Audience members noted that CAC scores didn’t do a very good job of stratifying stroke risk in MESA. That’s not surprising, since the score reflects coronary but not carotid artery calcium. But it is a limitation of CAC as a predictive tool, especially in light of the fact that strokes accounted for half of all cardiovascular events in the study.

Asked where he and his coinvestigators plan to go from here, Dr. Joshi said a randomized, controlled trial would be ideal, but to date funding isn’t available. However, the observational data from MESA and other studies suggest such a trial may not even be needed.

“Certainly the guidelines do allow for CAC scoring to be used in clinical decision making,” he noted.

 

The MESA study is funded by the National Heart, Lung, and Blood Institute. Dr. Joshi reported having no financial conflicts.

[email protected]

CHICAGO – Absence of coronary artery calcium upon imaging results in an impressively low cardiovascular event rate over the next 10 years regardless of an individual’s level of standard risk factors, according to prospective data from the MESA study.

In contrast, a coronary artery calcium (CAC) score of 1-10, often described as minimal CAC, nearly doubles the 10-year risk, compared with a baseline CAC score of 0.

Prior to these new 10-year data, many cardiologists considered a CAC score of 1-10 as tantamount to no CAC. Not so, Dr. Parag H. Joshi said at the American Heart Association scientific sessions.

Bruce Jancin/Frontline Medical News

“A CAC of 0 is presumably identifying someone without any atherosclerosis. Just the presence of minimal calcium suggests that atherosclerosis is building up. Our data suggest that among individuals with a CAC of 1-10, current smoking, elevated non-HDL cholesterol, and particularly hypertension should be treated aggressively,” said Dr. Joshi, a clinical fellow in cardiovascular diseases and prevention at Johns Hopkins University, Baltimore.

Prior studies totaling more than 50,000 subjects with a CAC score of 0 have shown very low cardiovascular event rates over 4-5 years of follow-up. However, current cardiovascular risk estimates focus on 10-year risk. This new analysis from MESA (Multi-Ethnic Study of Atherosclerosis) is the first study to provide prospective, 10-year events data, and those data are highly reassuring, he added.

MESA is a prospective, population-based cohort study. This analysis included 6,814 subjects aged 45-84 who were free of clinical cardiovascular disease at baseline, when their CAC score was determined. At that time, 3,415 participants had a CAC score of 0 and 508 had a score of 1-10.

During a median 10.3 years of follow-up, 123 cardiovascular events occurred, roughly one-third of which were nonfatal acute MIs and half of which were nonfatal strokes; the remainder were cardiovascular deaths.

The event rate was 2.9/1,000 person-years in subjects with a CAC of 0 and significantly greater at 5.5/1,000 person-years with a score of 1-10. However, since the cardiovascular risk factor profile of the zero CAC group was generally more favorable, Dr. Joshi and coinvestigators carried out a Cox proportional hazards analysis factoring in demographics, standard cardiovascular risk factors, body mass index, C-reactive protein level, and carotid intima media thickness. The adjusted 10-year event risk in the group with a CAC score of 1-10 was 1.9-fold greater than with a CAC of 0.

The highest 10-year event rate was noted in subjects with at least three of the following four risk factors at baseline: hypertension, current smoking, diabetes, and hyperlipidemia. The rate was 6.5/1,000 person-years in such individuals if they had a CAC of 0 and doubled at 13.1/1,000 person-years with a score of 1-10.

In a multivariate Cox analysis, age, smoking, and hypertension proved to be significant predictors of cardiovascular events in the group with a CAC of 0 as well as in those with a CAC of 1-10. But there was one important difference between the two groups: While the hazard ratio for cardiovascular events associated with hypertension versus no hypertension was 2.1 in subjects with a CAC of 0, the presence of hypertension in individuals with a CAC of 1-10 increased their event risk by 10.2-fold, or nearly five times greater than the risk increase associated with hypertension in persons with a CAC of 0, Dr. Joshi observed.

Non–HDL cholesterol level was predictive of cardiovascular risk in subjects with a CAC of 1-10 but not in those with a score of 0.

When actual event rates were compared with those predicted by the atherosclerotic cardiovascular disease (ASCVD) risk estimator introduced in the 2013 AHA/American College of Cardiology cholesterol guidelines, the event rate in subjects with an ASCVD 10-year risk estimate of 7.5%-15% but a CAC of 0 was just 4.4%.

Audience members noted that CAC scores didn’t do a very good job of stratifying stroke risk in MESA. That’s not surprising, since the score reflects coronary but not carotid artery calcium. But it is a limitation of CAC as a predictive tool, especially in light of the fact that strokes accounted for half of all cardiovascular events in the study.

Asked where he and his coinvestigators plan to go from here, Dr. Joshi said a randomized, controlled trial would be ideal, but to date funding isn’t available. However, the observational data from MESA and other studies suggest such a trial may not even be needed.

“Certainly the guidelines do allow for CAC scoring to be used in clinical decision making,” he noted.

 

The MESA study is funded by the National Heart, Lung, and Blood Institute. Dr. Joshi reported having no financial conflicts.

[email protected]

VIENNA – Rapid echocardiographic assessment has become routine for many patients who arrive at an emergency department with suspected acute heart failure, and experts consider these examinations critical for quickly getting patients on the right treatment.

Growing use and the important role for emergency echo exams prompted the European echocardiography community to issue in 2014 both recommendations and a position statement on the practice.

With their actions, European echocardiographers joined their U.S. colleagues who had earlier endorsed rapid, focused echocardiography exams. The European position also highlighted the limitations and pitfalls of emergency echo and the need for proper training.

Mitchel L. Zoler/Frontline Medical News

Use of limited, directed, ultrasound heart examinations on an emergency basis by physicians who are not cardiologists is “an irreversible process, but without appropriate training it may become dangerous,” Dr. Nuno Cardim said at the annual meeting of the European Association of Cardiovascular Imaging (EACVI).

A focused cardiac ultrasound (FoCUS) examination for patients with an emergency cardiac condition such as acute heart failure is not a new concept. In 2010, the American Society of Echocardiography and the American College of Emergency Physicians jointly issued a consensus statement on emergency FoCUS (J. Am. Soc. Echocardiogr. 2010;23:1225-30), and the American Society of Echocardiography followed with additional recommendations in 2013 that also dealt with nonemergency uses for FoCUS (J. Am. Soc. Echocardiogr. 2013;26:567-81).

In its 2014 position statement released last May, the EACVI directly addressed FoCUS for the first time (Eur. Heart J. Cardiovasc. Imaging 2014:15;956-60). The statement acknowledged the important role for a circumscribed, point-of-care ultrasound exam in patients undergoing cardiopulmonary resuscitation and in other critical cardiac conditions, but highlighted that a FoCUS exam does not substitute for a comprehensive echocardiographic exam, and that FoCUS should only be done by properly trained clinicians who appreciate the limits of a FoCUS exam.

The EASVI recommendations, which came out a few months later in collaboration with the Acute Cardiovascular Care Association, said that “echocardiography is now recommended (where appropriately trained practitioners are available) in the management of cardiac arrest. However, FoCUS should always be used and interpreted thoughtfully, since this fundamentally limited approach may lead to missing/misinterpretation of important findings unless the practitioner is aware of its (and their) limitations” (Eur. Heart J. Cardiovasc. Imaging 2014 [doi:10.1093/ehjci/jeu210]).

“Of course all patients with suspected acute heart failure in the emergency department should undergo an echo exam. The question is, who will do it? These are patients who are the most difficult to assess,” said Dr. Susanna Price, a member of the EACVI recommendations panel and a specialist in critical care cardiology at Royal Brompton Hospital in London.

“Without proper training, the person doing FoCUS could make a false positive diagnosis, or might miss something and make a false negative diagnosis,” said Dr. Cardim, professor and director of echocardiography and cardiac imaging at Hospital da Luz in Lisbon, and another member of the EACVI panel.

To avoid this, emergency-medicine physicians and others who often triage patients with acute heart disorders should be trained in echocardiography and especially the FoCUS exam, which aims to quickly evaluate several important abnormalities of cardiac function: pericardial effusion, cardiac tamponade, left and right ventricular size and function, and intravascular volume status. A FoCUS exam also screens for pulmonary embolism. FoCUS assesses each of these in a yes-or-no or present-or-absent way, information critical for guiding emergency management but lacking the quantitative and detailed information available with a comprehensive echocardiography exam.

“FoCUS must never substitute” for the comprehensive exam, which should always also be done, he said. FoCUS “should be used wisely and cautiously because of its limitations.”

The FoCUS exam also has equipment specifications. Ideally, clinicians should use a portable, hand-held ultrasound machine, which is larger than “pocket-sized” ultrasound devices and hence gives much better image quality compared with pocket-sized devices, Dr. Cardim said in an interview.

Dr. Cardim and Dr. Price had no disclosures.

[email protected]

On Twitter @mitchelzoler

VIENNA – Rapid echocardiographic assessment has become routine for many patients who arrive at an emergency department with suspected acute heart failure, and experts consider these examinations critical for quickly getting patients on the right treatment.

Growing use and the important role for emergency echo exams prompted the European echocardiography community to issue in 2014 both recommendations and a position statement on the practice.

With their actions, European echocardiographers joined their U.S. colleagues who had earlier endorsed rapid, focused echocardiography exams. The European position also highlighted the limitations and pitfalls of emergency echo and the need for proper training.

Mitchel L. Zoler/Frontline Medical News

Use of limited, directed, ultrasound heart examinations on an emergency basis by physicians who are not cardiologists is “an irreversible process, but without appropriate training it may become dangerous,” Dr. Nuno Cardim said at the annual meeting of the European Association of Cardiovascular Imaging (EACVI).

A focused cardiac ultrasound (FoCUS) examination for patients with an emergency cardiac condition such as acute heart failure is not a new concept. In 2010, the American Society of Echocardiography and the American College of Emergency Physicians jointly issued a consensus statement on emergency FoCUS (J. Am. Soc. Echocardiogr. 2010;23:1225-30), and the American Society of Echocardiography followed with additional recommendations in 2013 that also dealt with nonemergency uses for FoCUS (J. Am. Soc. Echocardiogr. 2013;26:567-81).

In its 2014 position statement released last May, the EACVI directly addressed FoCUS for the first time (Eur. Heart J. Cardiovasc. Imaging 2014:15;956-60). The statement acknowledged the important role for a circumscribed, point-of-care ultrasound exam in patients undergoing cardiopulmonary resuscitation and in other critical cardiac conditions, but highlighted that a FoCUS exam does not substitute for a comprehensive echocardiographic exam, and that FoCUS should only be done by properly trained clinicians who appreciate the limits of a FoCUS exam.

The EASVI recommendations, which came out a few months later in collaboration with the Acute Cardiovascular Care Association, said that “echocardiography is now recommended (where appropriately trained practitioners are available) in the management of cardiac arrest. However, FoCUS should always be used and interpreted thoughtfully, since this fundamentally limited approach may lead to missing/misinterpretation of important findings unless the practitioner is aware of its (and their) limitations” (Eur. Heart J. Cardiovasc. Imaging 2014 [doi:10.1093/ehjci/jeu210]).

“Of course all patients with suspected acute heart failure in the emergency department should undergo an echo exam. The question is, who will do it? These are patients who are the most difficult to assess,” said Dr. Susanna Price, a member of the EACVI recommendations panel and a specialist in critical care cardiology at Royal Brompton Hospital in London.

“Without proper training, the person doing FoCUS could make a false positive diagnosis, or might miss something and make a false negative diagnosis,” said Dr. Cardim, professor and director of echocardiography and cardiac imaging at Hospital da Luz in Lisbon, and another member of the EACVI panel.

To avoid this, emergency-medicine physicians and others who often triage patients with acute heart disorders should be trained in echocardiography and especially the FoCUS exam, which aims to quickly evaluate several important abnormalities of cardiac function: pericardial effusion, cardiac tamponade, left and right ventricular size and function, and intravascular volume status. A FoCUS exam also screens for pulmonary embolism. FoCUS assesses each of these in a yes-or-no or present-or-absent way, information critical for guiding emergency management but lacking the quantitative and detailed information available with a comprehensive echocardiography exam.

“FoCUS must never substitute” for the comprehensive exam, which should always also be done, he said. FoCUS “should be used wisely and cautiously because of its limitations.”

The FoCUS exam also has equipment specifications. Ideally, clinicians should use a portable, hand-held ultrasound machine, which is larger than “pocket-sized” ultrasound devices and hence gives much better image quality compared with pocket-sized devices, Dr. Cardim said in an interview.

Dr. Cardim and Dr. Price had no disclosures.

[email protected]

On Twitter @mitchelzoler

VIENNA – Rapid echocardiographic assessment has become routine for many patients who arrive at an emergency department with suspected acute heart failure, and experts consider these examinations critical for quickly getting patients on the right treatment.

Growing use and the important role for emergency echo exams prompted the European echocardiography community to issue in 2014 both recommendations and a position statement on the practice.

With their actions, European echocardiographers joined their U.S. colleagues who had earlier endorsed rapid, focused echocardiography exams. The European position also highlighted the limitations and pitfalls of emergency echo and the need for proper training.

Mitchel L. Zoler/Frontline Medical News

Use of limited, directed, ultrasound heart examinations on an emergency basis by physicians who are not cardiologists is “an irreversible process, but without appropriate training it may become dangerous,” Dr. Nuno Cardim said at the annual meeting of the European Association of Cardiovascular Imaging (EACVI).

A focused cardiac ultrasound (FoCUS) examination for patients with an emergency cardiac condition such as acute heart failure is not a new concept. In 2010, the American Society of Echocardiography and the American College of Emergency Physicians jointly issued a consensus statement on emergency FoCUS (J. Am. Soc. Echocardiogr. 2010;23:1225-30), and the American Society of Echocardiography followed with additional recommendations in 2013 that also dealt with nonemergency uses for FoCUS (J. Am. Soc. Echocardiogr. 2013;26:567-81).

In its 2014 position statement released last May, the EACVI directly addressed FoCUS for the first time (Eur. Heart J. Cardiovasc. Imaging 2014:15;956-60). The statement acknowledged the important role for a circumscribed, point-of-care ultrasound exam in patients undergoing cardiopulmonary resuscitation and in other critical cardiac conditions, but highlighted that a FoCUS exam does not substitute for a comprehensive echocardiographic exam, and that FoCUS should only be done by properly trained clinicians who appreciate the limits of a FoCUS exam.

The EASVI recommendations, which came out a few months later in collaboration with the Acute Cardiovascular Care Association, said that “echocardiography is now recommended (where appropriately trained practitioners are available) in the management of cardiac arrest. However, FoCUS should always be used and interpreted thoughtfully, since this fundamentally limited approach may lead to missing/misinterpretation of important findings unless the practitioner is aware of its (and their) limitations” (Eur. Heart J. Cardiovasc. Imaging 2014 [doi:10.1093/ehjci/jeu210]).

“Of course all patients with suspected acute heart failure in the emergency department should undergo an echo exam. The question is, who will do it? These are patients who are the most difficult to assess,” said Dr. Susanna Price, a member of the EACVI recommendations panel and a specialist in critical care cardiology at Royal Brompton Hospital in London.

“Without proper training, the person doing FoCUS could make a false positive diagnosis, or might miss something and make a false negative diagnosis,” said Dr. Cardim, professor and director of echocardiography and cardiac imaging at Hospital da Luz in Lisbon, and another member of the EACVI panel.

To avoid this, emergency-medicine physicians and others who often triage patients with acute heart disorders should be trained in echocardiography and especially the FoCUS exam, which aims to quickly evaluate several important abnormalities of cardiac function: pericardial effusion, cardiac tamponade, left and right ventricular size and function, and intravascular volume status. A FoCUS exam also screens for pulmonary embolism. FoCUS assesses each of these in a yes-or-no or present-or-absent way, information critical for guiding emergency management but lacking the quantitative and detailed information available with a comprehensive echocardiography exam.

“FoCUS must never substitute” for the comprehensive exam, which should always also be done, he said. FoCUS “should be used wisely and cautiously because of its limitations.”

The FoCUS exam also has equipment specifications. Ideally, clinicians should use a portable, hand-held ultrasound machine, which is larger than “pocket-sized” ultrasound devices and hence gives much better image quality compared with pocket-sized devices, Dr. Cardim said in an interview.

Dr. Cardim and Dr. Price had no disclosures.

[email protected]

On Twitter @mitchelzoler

CHICAGO – Coronary artery calcium testing has established itself as a true “game changer” in primary cardiovascular prevention, proponents of the risk-stratification tool said at the American Heart Association scientific sessions.

Knowing a patient’s coronary artery calcium score facilitates a more informed physician-patient discussion and shared decision making regarding whether to go on decades-long statin therapy, according to Dr. Khurram Nasir of the center for prevention and wellness research at Baptist Health Medical Center in Miami Beach.

“In our view, a much underappreciated value of coronary artery calcium testing lies in the power of zero. Roughly half of adults have a coronary artery calcium score of 0, and this results in a very low cardiovascular event rate,” the cardiologist said.

He presented an analysis of 4,758 nondiabetic participants in the prospective, population-based MESA (Multi-Ethnic Study of Atherosclerosis) in which he examined how they fared in terms of cardiovascular events over a median 10.3 years of follow-up. All were free of known cardiovascular disease at baseline. With the risk estimator included in the 2013 AHA/ACC cholesterol management guidelines, 2,377 subjects would be recommended for high-intensity statin therapy at baseline on the basis of a 10-year atherosclerotic cardiovascular disease risk estimate of at least 7.5%. Another 589 participants were recommended for consideration of a moderate-intensity statin based on an estimated 10-year risk of 5%-7.4%.

Forty-one percent of MESA subjects recommended for a high-intensity statin according to the AHA/ACC risk estimator had a coronary artery calcium (CAC) score of 0, and their 10-year composite rate of MI, stroke, or cardiovascular death was just 4.9% – well below the 7.5% threshold recommended for statin therapy. In contrast, if any CAC was present, the event rate was 10.5%.

 

With a relative risk reduction with statin therapy of 30%, the number needed to treat for 5 years to prevent one cardiovascular event in the group with a CAC of 0 would be 128. In the presence of any CAC, the number needed to treat fell to a far more reasonable 56, Dr. Nasir said.

Similarly, among the group recommended for consideration of statin therapy on the basis of a 10-year risk of 5%-7.4%, the actual event rate in the 57% of subjects with a CAC of 0 was just 1.5%. If any CAC was present, the event rate shot up to 7.2%. The number needed to treat in this cohort was 445 among those with a CAC of 0 and 90 with any CAC present.

“I think coronary artery calcium is a game changer in primary prevention,” Dr. Michael J. Blaha commented. “It sufficiently moves the needle to make you think differently about a patient. I’m not sure some of the other tests have sufficient evidence to say, ‘I’m going to think about not treating you if it’s negative and treating you if it’s positive,’ but coronary artery calcium has that evidence.”

In his own cardiology practice at Johns Hopkins University, Baltimore, Dr. Blaha finds himself using CAC testing often, especially in his many statin-reluctant patients.

“I have a lot of patients who would fit under a recommendation for statin therapy under the 2013 AHA/ACC cholesterol management guidelines, but who really don’t want to take medications. I know you see these patients in your practices, too. This is lifelong therapy, and they want a really good reason to take it or not to take it. If a patient is reluctant to take a statin and has a CAC score of 0, I will sometimes emphasize lifestyle therapy. It certainly redoubles my interest in lifestyle therapy. But if the CAC score is elevated, then I can make a specific case that the number needed to treat is very favorable, compared to the number needed to harm,” explained Dr. Blaha, a coinvestigator with Dr. Nasir in the MESA study.

 

Other situations where he finds CAC testing useful in daily practice include uncertainty as to a patient’s true risk level because the individual’s situation isn’t adequately captured by the AHA/ACC risk estimator. A patient with rheumatologic disease would be one example; another would be an individual who is neither white nor African American. He said he also utilizes CAC testing in statin-intolerant patients, where the results are useful in deciding how many different statins to try before saying “enough.”

Audience members asked what it’s going to take to get insurers to cover CAC testing for risk stratification. Dr. Blaha replied that more long-term outcomes and cost-effectiveness data are coming. In the meantime, at an out-of-pocket cost of $75-$100, a lot of his statin-reluctant patients consider CAC testing a good buy.

“They say, ‘I’ll take this test to help me decide whether to take a pill for the rest of my life,’” according to Dr. Blaha.

Dr. Nasir said the evidence in support of CAC testing is now so strong that he believes physicians have an obligation to mention it as an option during the statin treatment decision discussion.

“At this moment, most patients are making their decision based on the guesstimate of their risk we are giving them using the risk calculator. If they have the ability through a $75-$100 test that costs about the same as 18 months of statin therapy to know that their true risk is not, say, 10%, but actually 5%, they’re less likely to choose therapy. Is it even ethical to withhold from our patients that there is a test out there that can reduce their estimated risk to a point that they can avoid statin therapy?” the cardiologist asked.

Dr. Nasir reported serving on an advisory board for Quest Diagnostics. Dr. Blaha reported having no financial conflicts.

[email protected]

CHICAGO – Coronary artery calcium testing has established itself as a true “game changer” in primary cardiovascular prevention, proponents of the risk-stratification tool said at the American Heart Association scientific sessions.

Knowing a patient’s coronary artery calcium score facilitates a more informed physician-patient discussion and shared decision making regarding whether to go on decades-long statin therapy, according to Dr. Khurram Nasir of the center for prevention and wellness research at Baptist Health Medical Center in Miami Beach.

“In our view, a much underappreciated value of coronary artery calcium testing lies in the power of zero. Roughly half of adults have a coronary artery calcium score of 0, and this results in a very low cardiovascular event rate,” the cardiologist said.

He presented an analysis of 4,758 nondiabetic participants in the prospective, population-based MESA (Multi-Ethnic Study of Atherosclerosis) in which he examined how they fared in terms of cardiovascular events over a median 10.3 years of follow-up. All were free of known cardiovascular disease at baseline. With the risk estimator included in the 2013 AHA/ACC cholesterol management guidelines, 2,377 subjects would be recommended for high-intensity statin therapy at baseline on the basis of a 10-year atherosclerotic cardiovascular disease risk estimate of at least 7.5%. Another 589 participants were recommended for consideration of a moderate-intensity statin based on an estimated 10-year risk of 5%-7.4%.

Forty-one percent of MESA subjects recommended for a high-intensity statin according to the AHA/ACC risk estimator had a coronary artery calcium (CAC) score of 0, and their 10-year composite rate of MI, stroke, or cardiovascular death was just 4.9% – well below the 7.5% threshold recommended for statin therapy. In contrast, if any CAC was present, the event rate was 10.5%.

 

With a relative risk reduction with statin therapy of 30%, the number needed to treat for 5 years to prevent one cardiovascular event in the group with a CAC of 0 would be 128. In the presence of any CAC, the number needed to treat fell to a far more reasonable 56, Dr. Nasir said.

Similarly, among the group recommended for consideration of statin therapy on the basis of a 10-year risk of 5%-7.4%, the actual event rate in the 57% of subjects with a CAC of 0 was just 1.5%. If any CAC was present, the event rate shot up to 7.2%. The number needed to treat in this cohort was 445 among those with a CAC of 0 and 90 with any CAC present.

“I think coronary artery calcium is a game changer in primary prevention,” Dr. Michael J. Blaha commented. “It sufficiently moves the needle to make you think differently about a patient. I’m not sure some of the other tests have sufficient evidence to say, ‘I’m going to think about not treating you if it’s negative and treating you if it’s positive,’ but coronary artery calcium has that evidence.”

In his own cardiology practice at Johns Hopkins University, Baltimore, Dr. Blaha finds himself using CAC testing often, especially in his many statin-reluctant patients.

“I have a lot of patients who would fit under a recommendation for statin therapy under the 2013 AHA/ACC cholesterol management guidelines, but who really don’t want to take medications. I know you see these patients in your practices, too. This is lifelong therapy, and they want a really good reason to take it or not to take it. If a patient is reluctant to take a statin and has a CAC score of 0, I will sometimes emphasize lifestyle therapy. It certainly redoubles my interest in lifestyle therapy. But if the CAC score is elevated, then I can make a specific case that the number needed to treat is very favorable, compared to the number needed to harm,” explained Dr. Blaha, a coinvestigator with Dr. Nasir in the MESA study.

 

Other situations where he finds CAC testing useful in daily practice include uncertainty as to a patient’s true risk level because the individual’s situation isn’t adequately captured by the AHA/ACC risk estimator. A patient with rheumatologic disease would be one example; another would be an individual who is neither white nor African American. He said he also utilizes CAC testing in statin-intolerant patients, where the results are useful in deciding how many different statins to try before saying “enough.”

Audience members asked what it’s going to take to get insurers to cover CAC testing for risk stratification. Dr. Blaha replied that more long-term outcomes and cost-effectiveness data are coming. In the meantime, at an out-of-pocket cost of $75-$100, a lot of his statin-reluctant patients consider CAC testing a good buy.

“They say, ‘I’ll take this test to help me decide whether to take a pill for the rest of my life,’” according to Dr. Blaha.

Dr. Nasir said the evidence in support of CAC testing is now so strong that he believes physicians have an obligation to mention it as an option during the statin treatment decision discussion.

“At this moment, most patients are making their decision based on the guesstimate of their risk we are giving them using the risk calculator. If they have the ability through a $75-$100 test that costs about the same as 18 months of statin therapy to know that their true risk is not, say, 10%, but actually 5%, they’re less likely to choose therapy. Is it even ethical to withhold from our patients that there is a test out there that can reduce their estimated risk to a point that they can avoid statin therapy?” the cardiologist asked.

Dr. Nasir reported serving on an advisory board for Quest Diagnostics. Dr. Blaha reported having no financial conflicts.

[email protected]

CHICAGO – Coronary artery calcium testing has established itself as a true “game changer” in primary cardiovascular prevention, proponents of the risk-stratification tool said at the American Heart Association scientific sessions.

Knowing a patient’s coronary artery calcium score facilitates a more informed physician-patient discussion and shared decision making regarding whether to go on decades-long statin therapy, according to Dr. Khurram Nasir of the center for prevention and wellness research at Baptist Health Medical Center in Miami Beach.

“In our view, a much underappreciated value of coronary artery calcium testing lies in the power of zero. Roughly half of adults have a coronary artery calcium score of 0, and this results in a very low cardiovascular event rate,” the cardiologist said.

He presented an analysis of 4,758 nondiabetic participants in the prospective, population-based MESA (Multi-Ethnic Study of Atherosclerosis) in which he examined how they fared in terms of cardiovascular events over a median 10.3 years of follow-up. All were free of known cardiovascular disease at baseline. With the risk estimator included in the 2013 AHA/ACC cholesterol management guidelines, 2,377 subjects would be recommended for high-intensity statin therapy at baseline on the basis of a 10-year atherosclerotic cardiovascular disease risk estimate of at least 7.5%. Another 589 participants were recommended for consideration of a moderate-intensity statin based on an estimated 10-year risk of 5%-7.4%.

Forty-one percent of MESA subjects recommended for a high-intensity statin according to the AHA/ACC risk estimator had a coronary artery calcium (CAC) score of 0, and their 10-year composite rate of MI, stroke, or cardiovascular death was just 4.9% – well below the 7.5% threshold recommended for statin therapy. In contrast, if any CAC was present, the event rate was 10.5%.

 

With a relative risk reduction with statin therapy of 30%, the number needed to treat for 5 years to prevent one cardiovascular event in the group with a CAC of 0 would be 128. In the presence of any CAC, the number needed to treat fell to a far more reasonable 56, Dr. Nasir said.

Similarly, among the group recommended for consideration of statin therapy on the basis of a 10-year risk of 5%-7.4%, the actual event rate in the 57% of subjects with a CAC of 0 was just 1.5%. If any CAC was present, the event rate shot up to 7.2%. The number needed to treat in this cohort was 445 among those with a CAC of 0 and 90 with any CAC present.

“I think coronary artery calcium is a game changer in primary prevention,” Dr. Michael J. Blaha commented. “It sufficiently moves the needle to make you think differently about a patient. I’m not sure some of the other tests have sufficient evidence to say, ‘I’m going to think about not treating you if it’s negative and treating you if it’s positive,’ but coronary artery calcium has that evidence.”

In his own cardiology practice at Johns Hopkins University, Baltimore, Dr. Blaha finds himself using CAC testing often, especially in his many statin-reluctant patients.

“I have a lot of patients who would fit under a recommendation for statin therapy under the 2013 AHA/ACC cholesterol management guidelines, but who really don’t want to take medications. I know you see these patients in your practices, too. This is lifelong therapy, and they want a really good reason to take it or not to take it. If a patient is reluctant to take a statin and has a CAC score of 0, I will sometimes emphasize lifestyle therapy. It certainly redoubles my interest in lifestyle therapy. But if the CAC score is elevated, then I can make a specific case that the number needed to treat is very favorable, compared to the number needed to harm,” explained Dr. Blaha, a coinvestigator with Dr. Nasir in the MESA study.

 

Other situations where he finds CAC testing useful in daily practice include uncertainty as to a patient’s true risk level because the individual’s situation isn’t adequately captured by the AHA/ACC risk estimator. A patient with rheumatologic disease would be one example; another would be an individual who is neither white nor African American. He said he also utilizes CAC testing in statin-intolerant patients, where the results are useful in deciding how many different statins to try before saying “enough.”

Audience members asked what it’s going to take to get insurers to cover CAC testing for risk stratification. Dr. Blaha replied that more long-term outcomes and cost-effectiveness data are coming. In the meantime, at an out-of-pocket cost of $75-$100, a lot of his statin-reluctant patients consider CAC testing a good buy.

“They say, ‘I’ll take this test to help me decide whether to take a pill for the rest of my life,’” according to Dr. Blaha.

Dr. Nasir said the evidence in support of CAC testing is now so strong that he believes physicians have an obligation to mention it as an option during the statin treatment decision discussion.

“At this moment, most patients are making their decision based on the guesstimate of their risk we are giving them using the risk calculator. If they have the ability through a $75-$100 test that costs about the same as 18 months of statin therapy to know that their true risk is not, say, 10%, but actually 5%, they’re less likely to choose therapy. Is it even ethical to withhold from our patients that there is a test out there that can reduce their estimated risk to a point that they can avoid statin therapy?” the cardiologist asked.

Dr. Nasir reported serving on an advisory board for Quest Diagnostics. Dr. Blaha reported having no financial conflicts.

[email protected]

VIENNA – One of the best ways to prevent advanced tricuspid-valve regurgitation and need for tricuspid-valve repair may be a more aggressive approach to mitral valve repair.

“If you operate on the mitral valve early, then tricuspid regurgitation does not tend to progress,” Dr. Sunil V. Mankad said at the annual meeting of the European Association of Cardiovascular Imaging. “If you wait until the mitral valve remodels and the atrium enlarges and remodels or there is pulmonary hypertension, then tricuspid regurgitation will progress,” said Dr. Mankad, a echocardiographer at the Mayo Clinic in Rochester, Minn.

Mitchel L. Zoler/Frontline Medical News

Early intervention on mitral valve prolapse has other benefits as well, he said. Mitral disease causes atrial remodeling, which can then progress to atrial fibrillation, “and once that happens it’s a game changer for the patient, even if they later undergo valve repair,” because of atrial fibrillation’s long-term risks and consequences, Dr. Mankad said in an interview.

“We believe there is also subclinical left ventricular dysfunction” in patients with mitral-valve prolapse “even if their ejection fraction is normal.” Once that happens, even if the mitral valve is repaired “the heart is not normal anymore and there is subtle left ventricular dysfunction that is not captured by just looking at ejection fraction.”

To document the impact a more aggressive approach to mitral-valve repair can have on the tricuspid valve, Dr. Mankad cited a 2011 Mayo Clinic analysis of 699 patients who underwent mitral-valve repair at Mayo for severe mitral-valve prolapse and also had some amount of tricuspid regurgitation at the time of their surgery, including 115 patients (16%) with grade 3 or higher tricuspid regurgitation. One year after surgery, the severity of tricuspid regurgitation in these patients had decreased significantly overall, and throughout follow-up only one patient required surgery for tricuspid-valve repair, 4.5 years after that patient’s mitral-valve repair (J. Thoracic Cardiovasc. Surgery 2011;142:608-13).

 

Dr. Mankad also cited a recent editorial written by several of his Mayo Clinic colleagues that synthesized results from the 2011 report as well as from a second Mayo report published in 2014, and a third report from a different group also published in 2014. The authors of the editorial concluded that results from all three studies showed “the performance of early correction of mitral regurgitation is important not only for its own well known benefits (preservation of survival and minimization of late heart failure risk) but also to diminish the late occurrence of functional tricuspid regurgitation (J. Thoracic Cardiovasc. Surgery 2014;148:2810-2).

Because mitral-valve repair often improves tricuspid-valve function and durability, the editorialists suggested “strongly considering” tricuspid repair for a carefully defined, select subgroup of patients. Their list included patients with tricuspid regurgitation that is worse than moderate, right-heart dysfunction, symptoms of right-heart failure, pulmonary hypertension, reduced left ventricular systolic function, cardiomyopathy, or organic tricuspid pathology.

Existing evidence supports leaving the valve alone when patients have a tricuspid regurgitation that is less than moderate when they have also undergone effective correction of degenerative mitral regurgitation. Patients like these are “unlikely ever to have difficulty with the tricuspid valve or the right ventricle,” wrote the authors of the editorial.

Dr. Mankad offered his own suggestions for identifying patients with a tricuspid valve that requires repair at the time of mitral-valve surgery.

“The evidence supports tricuspid-valve repair at the time of mitral-valve surgery if there is tricuspid annular dilatation of more than 4.0 cm measured by three-dimensional echo or greater than moderate tricuspid regurgitation. This is based on observational data and not on results from randomized control trials, but it is what I recommend,” Dr. Mankad said. “I suggest measuring the tricuspid annulus; it is quite easy to do. Directly measuring the annulus size with three-dimensional echo is pretty basic, and I think it is ready for prime time.”

Dr. Mankad had no disclosures.

[email protected]

On Twitter @mitchelzoler

VIENNA – One of the best ways to prevent advanced tricuspid-valve regurgitation and need for tricuspid-valve repair may be a more aggressive approach to mitral valve repair.

“If you operate on the mitral valve early, then tricuspid regurgitation does not tend to progress,” Dr. Sunil V. Mankad said at the annual meeting of the European Association of Cardiovascular Imaging. “If you wait until the mitral valve remodels and the atrium enlarges and remodels or there is pulmonary hypertension, then tricuspid regurgitation will progress,” said Dr. Mankad, a echocardiographer at the Mayo Clinic in Rochester, Minn.

Mitchel L. Zoler/Frontline Medical News

Early intervention on mitral valve prolapse has other benefits as well, he said. Mitral disease causes atrial remodeling, which can then progress to atrial fibrillation, “and once that happens it’s a game changer for the patient, even if they later undergo valve repair,” because of atrial fibrillation’s long-term risks and consequences, Dr. Mankad said in an interview.

“We believe there is also subclinical left ventricular dysfunction” in patients with mitral-valve prolapse “even if their ejection fraction is normal.” Once that happens, even if the mitral valve is repaired “the heart is not normal anymore and there is subtle left ventricular dysfunction that is not captured by just looking at ejection fraction.”

To document the impact a more aggressive approach to mitral-valve repair can have on the tricuspid valve, Dr. Mankad cited a 2011 Mayo Clinic analysis of 699 patients who underwent mitral-valve repair at Mayo for severe mitral-valve prolapse and also had some amount of tricuspid regurgitation at the time of their surgery, including 115 patients (16%) with grade 3 or higher tricuspid regurgitation. One year after surgery, the severity of tricuspid regurgitation in these patients had decreased significantly overall, and throughout follow-up only one patient required surgery for tricuspid-valve repair, 4.5 years after that patient’s mitral-valve repair (J. Thoracic Cardiovasc. Surgery 2011;142:608-13).

 

Dr. Mankad also cited a recent editorial written by several of his Mayo Clinic colleagues that synthesized results from the 2011 report as well as from a second Mayo report published in 2014, and a third report from a different group also published in 2014. The authors of the editorial concluded that results from all three studies showed “the performance of early correction of mitral regurgitation is important not only for its own well known benefits (preservation of survival and minimization of late heart failure risk) but also to diminish the late occurrence of functional tricuspid regurgitation (J. Thoracic Cardiovasc. Surgery 2014;148:2810-2).

Because mitral-valve repair often improves tricuspid-valve function and durability, the editorialists suggested “strongly considering” tricuspid repair for a carefully defined, select subgroup of patients. Their list included patients with tricuspid regurgitation that is worse than moderate, right-heart dysfunction, symptoms of right-heart failure, pulmonary hypertension, reduced left ventricular systolic function, cardiomyopathy, or organic tricuspid pathology.

Existing evidence supports leaving the valve alone when patients have a tricuspid regurgitation that is less than moderate when they have also undergone effective correction of degenerative mitral regurgitation. Patients like these are “unlikely ever to have difficulty with the tricuspid valve or the right ventricle,” wrote the authors of the editorial.

Dr. Mankad offered his own suggestions for identifying patients with a tricuspid valve that requires repair at the time of mitral-valve surgery.

“The evidence supports tricuspid-valve repair at the time of mitral-valve surgery if there is tricuspid annular dilatation of more than 4.0 cm measured by three-dimensional echo or greater than moderate tricuspid regurgitation. This is based on observational data and not on results from randomized control trials, but it is what I recommend,” Dr. Mankad said. “I suggest measuring the tricuspid annulus; it is quite easy to do. Directly measuring the annulus size with three-dimensional echo is pretty basic, and I think it is ready for prime time.”

Dr. Mankad had no disclosures.

[email protected]

On Twitter @mitchelzoler

VIENNA – One of the best ways to prevent advanced tricuspid-valve regurgitation and need for tricuspid-valve repair may be a more aggressive approach to mitral valve repair.

“If you operate on the mitral valve early, then tricuspid regurgitation does not tend to progress,” Dr. Sunil V. Mankad said at the annual meeting of the European Association of Cardiovascular Imaging. “If you wait until the mitral valve remodels and the atrium enlarges and remodels or there is pulmonary hypertension, then tricuspid regurgitation will progress,” said Dr. Mankad, a echocardiographer at the Mayo Clinic in Rochester, Minn.

Mitchel L. Zoler/Frontline Medical News

Early intervention on mitral valve prolapse has other benefits as well, he said. Mitral disease causes atrial remodeling, which can then progress to atrial fibrillation, “and once that happens it’s a game changer for the patient, even if they later undergo valve repair,” because of atrial fibrillation’s long-term risks and consequences, Dr. Mankad said in an interview.

“We believe there is also subclinical left ventricular dysfunction” in patients with mitral-valve prolapse “even if their ejection fraction is normal.” Once that happens, even if the mitral valve is repaired “the heart is not normal anymore and there is subtle left ventricular dysfunction that is not captured by just looking at ejection fraction.”

To document the impact a more aggressive approach to mitral-valve repair can have on the tricuspid valve, Dr. Mankad cited a 2011 Mayo Clinic analysis of 699 patients who underwent mitral-valve repair at Mayo for severe mitral-valve prolapse and also had some amount of tricuspid regurgitation at the time of their surgery, including 115 patients (16%) with grade 3 or higher tricuspid regurgitation. One year after surgery, the severity of tricuspid regurgitation in these patients had decreased significantly overall, and throughout follow-up only one patient required surgery for tricuspid-valve repair, 4.5 years after that patient’s mitral-valve repair (J. Thoracic Cardiovasc. Surgery 2011;142:608-13).

 

Dr. Mankad also cited a recent editorial written by several of his Mayo Clinic colleagues that synthesized results from the 2011 report as well as from a second Mayo report published in 2014, and a third report from a different group also published in 2014. The authors of the editorial concluded that results from all three studies showed “the performance of early correction of mitral regurgitation is important not only for its own well known benefits (preservation of survival and minimization of late heart failure risk) but also to diminish the late occurrence of functional tricuspid regurgitation (J. Thoracic Cardiovasc. Surgery 2014;148:2810-2).

Because mitral-valve repair often improves tricuspid-valve function and durability, the editorialists suggested “strongly considering” tricuspid repair for a carefully defined, select subgroup of patients. Their list included patients with tricuspid regurgitation that is worse than moderate, right-heart dysfunction, symptoms of right-heart failure, pulmonary hypertension, reduced left ventricular systolic function, cardiomyopathy, or organic tricuspid pathology.

Existing evidence supports leaving the valve alone when patients have a tricuspid regurgitation that is less than moderate when they have also undergone effective correction of degenerative mitral regurgitation. Patients like these are “unlikely ever to have difficulty with the tricuspid valve or the right ventricle,” wrote the authors of the editorial.

Dr. Mankad offered his own suggestions for identifying patients with a tricuspid valve that requires repair at the time of mitral-valve surgery.

“The evidence supports tricuspid-valve repair at the time of mitral-valve surgery if there is tricuspid annular dilatation of more than 4.0 cm measured by three-dimensional echo or greater than moderate tricuspid regurgitation. This is based on observational data and not on results from randomized control trials, but it is what I recommend,” Dr. Mankad said. “I suggest measuring the tricuspid annulus; it is quite easy to do. Directly measuring the annulus size with three-dimensional echo is pretty basic, and I think it is ready for prime time.”

Dr. Mankad had no disclosures.

[email protected]

On Twitter @mitchelzoler

CHICAGO – Insulin glargine showed no effects on left ventricular mass or function during 3 years of follow-up in dysglycemic patients at high cardiovascular risk in the ORIGIN echocardiographic substudy.

This echocardiographic study of the ORIGIN (Outcome Reduction With an Initial Glargine Intervention) trial, the largest reported study of the effects of exogenous insulin on left ventricular mass and LV systolic and diastolic function, provides reassuring new evidence that insulin glargine is safe from a cardiac standpoint, Dr. Michelle Haroun said at the American Heart Association scientific sessions.

“The key here is that we didn’t see any signal whatsoever to suggest that insulin is putting patients at increased risk. We think that this finding is important. While you need to follow patients for a very long time to detect changes in clinical heart failure outcomes, we think we’d be able to detect subtle changes in endpoints like LV mass over a 3-year period if insulin was of harm to patients,” said Dr. Haroun of the Population Health Research Institute at McMaster University in Hamilton, Ont.

ORIGIN-ECHO involved 564 dysglycemic patients at high cardiovascular risk who were randomized to insulin glargine (Lantus) or standard therapy. All had echocardiograms at baseline and after 3 years of therapy. Participants had to have impaired fasting blood glucose, impaired glucose tolerance, or early type 2 diabetes managed with no more than one oral antiglycemic drug at baseline. This was a group at high cardiovascular risk: 32% had a prior MI, 84% had a history of hypertension, obesity was common, and the average age was 64. However, none of the participants had heart failure at baseline.

The study was undertaken because some of the medications used to treat hyperglycemia are associated with increased risk of heart failure. Regulatory agencies, physicians, and patients want to see evidence of cardiovascular safety, and until ORIGIN-ECHO, the effects of exogenous insulin on LV mass and function hadn’t been well studied.

Baseline LV mass and function values were within normal range and did not change significantly over 3 years of follow-up in either treatment arm. For example, left ventricular mass/height averaged 116 g/m at baseline and 115 g/m after 3 years on insulin glargine, and was comparable at 113 and 114 g/m, respectively, with standard therapy. This was an unexpected finding, according to Dr. Haroun.

“We thought patients with diabetes on standard therapy were going to develop left ventricular hypertrophy over a 3-year follow-up period, and they didn’t. That came as a bit of a surprise to us. We expected to see a lower rate of LVH in the patients on insulin glargine. This patient population was relatively early in their course of diabetes, and we believe our findings suggest that adequate management of cardiovascular risk factors – especially hypertension– and the use of cardioprotective drugs in this population may prevent or delay abnormalities in LV structure and function,” she said.

The primary outcomes of the full ORIGIN study involving more than 12,000 patients have previously been published (N. Engl. J. Med. 2012; 367:319-28). ORIGIN was sponsored by Sanofi. Dr. Haroun reported having no financial conflicts.

[email protected]

CHICAGO – Insulin glargine showed no effects on left ventricular mass or function during 3 years of follow-up in dysglycemic patients at high cardiovascular risk in the ORIGIN echocardiographic substudy.

This echocardiographic study of the ORIGIN (Outcome Reduction With an Initial Glargine Intervention) trial, the largest reported study of the effects of exogenous insulin on left ventricular mass and LV systolic and diastolic function, provides reassuring new evidence that insulin glargine is safe from a cardiac standpoint, Dr. Michelle Haroun said at the American Heart Association scientific sessions.

“The key here is that we didn’t see any signal whatsoever to suggest that insulin is putting patients at increased risk. We think that this finding is important. While you need to follow patients for a very long time to detect changes in clinical heart failure outcomes, we think we’d be able to detect subtle changes in endpoints like LV mass over a 3-year period if insulin was of harm to patients,” said Dr. Haroun of the Population Health Research Institute at McMaster University in Hamilton, Ont.

ORIGIN-ECHO involved 564 dysglycemic patients at high cardiovascular risk who were randomized to insulin glargine (Lantus) or standard therapy. All had echocardiograms at baseline and after 3 years of therapy. Participants had to have impaired fasting blood glucose, impaired glucose tolerance, or early type 2 diabetes managed with no more than one oral antiglycemic drug at baseline. This was a group at high cardiovascular risk: 32% had a prior MI, 84% had a history of hypertension, obesity was common, and the average age was 64. However, none of the participants had heart failure at baseline.

The study was undertaken because some of the medications used to treat hyperglycemia are associated with increased risk of heart failure. Regulatory agencies, physicians, and patients want to see evidence of cardiovascular safety, and until ORIGIN-ECHO, the effects of exogenous insulin on LV mass and function hadn’t been well studied.

Baseline LV mass and function values were within normal range and did not change significantly over 3 years of follow-up in either treatment arm. For example, left ventricular mass/height averaged 116 g/m at baseline and 115 g/m after 3 years on insulin glargine, and was comparable at 113 and 114 g/m, respectively, with standard therapy. This was an unexpected finding, according to Dr. Haroun.

“We thought patients with diabetes on standard therapy were going to develop left ventricular hypertrophy over a 3-year follow-up period, and they didn’t. That came as a bit of a surprise to us. We expected to see a lower rate of LVH in the patients on insulin glargine. This patient population was relatively early in their course of diabetes, and we believe our findings suggest that adequate management of cardiovascular risk factors – especially hypertension– and the use of cardioprotective drugs in this population may prevent or delay abnormalities in LV structure and function,” she said.

The primary outcomes of the full ORIGIN study involving more than 12,000 patients have previously been published (N. Engl. J. Med. 2012; 367:319-28). ORIGIN was sponsored by Sanofi. Dr. Haroun reported having no financial conflicts.

[email protected]

CHICAGO – Insulin glargine showed no effects on left ventricular mass or function during 3 years of follow-up in dysglycemic patients at high cardiovascular risk in the ORIGIN echocardiographic substudy.

This echocardiographic study of the ORIGIN (Outcome Reduction With an Initial Glargine Intervention) trial, the largest reported study of the effects of exogenous insulin on left ventricular mass and LV systolic and diastolic function, provides reassuring new evidence that insulin glargine is safe from a cardiac standpoint, Dr. Michelle Haroun said at the American Heart Association scientific sessions.

“The key here is that we didn’t see any signal whatsoever to suggest that insulin is putting patients at increased risk. We think that this finding is important. While you need to follow patients for a very long time to detect changes in clinical heart failure outcomes, we think we’d be able to detect subtle changes in endpoints like LV mass over a 3-year period if insulin was of harm to patients,” said Dr. Haroun of the Population Health Research Institute at McMaster University in Hamilton, Ont.

ORIGIN-ECHO involved 564 dysglycemic patients at high cardiovascular risk who were randomized to insulin glargine (Lantus) or standard therapy. All had echocardiograms at baseline and after 3 years of therapy. Participants had to have impaired fasting blood glucose, impaired glucose tolerance, or early type 2 diabetes managed with no more than one oral antiglycemic drug at baseline. This was a group at high cardiovascular risk: 32% had a prior MI, 84% had a history of hypertension, obesity was common, and the average age was 64. However, none of the participants had heart failure at baseline.

The study was undertaken because some of the medications used to treat hyperglycemia are associated with increased risk of heart failure. Regulatory agencies, physicians, and patients want to see evidence of cardiovascular safety, and until ORIGIN-ECHO, the effects of exogenous insulin on LV mass and function hadn’t been well studied.

Baseline LV mass and function values were within normal range and did not change significantly over 3 years of follow-up in either treatment arm. For example, left ventricular mass/height averaged 116 g/m at baseline and 115 g/m after 3 years on insulin glargine, and was comparable at 113 and 114 g/m, respectively, with standard therapy. This was an unexpected finding, according to Dr. Haroun.

“We thought patients with diabetes on standard therapy were going to develop left ventricular hypertrophy over a 3-year follow-up period, and they didn’t. That came as a bit of a surprise to us. We expected to see a lower rate of LVH in the patients on insulin glargine. This patient population was relatively early in their course of diabetes, and we believe our findings suggest that adequate management of cardiovascular risk factors – especially hypertension– and the use of cardioprotective drugs in this population may prevent or delay abnormalities in LV structure and function,” she said.

The primary outcomes of the full ORIGIN study involving more than 12,000 patients have previously been published (N. Engl. J. Med. 2012; 367:319-28). ORIGIN was sponsored by Sanofi. Dr. Haroun reported having no financial conflicts.

[email protected]

Case

A 46-year-old white woman with sudden onset of numbness in her lower extremities and inability to ambulate was transported to the ED via emergency medical services. At the onset of symptoms, the patient reported a feeling of “heaviness” in her lower extremities, which was greater on the left side than the right. After an unsuccessful attempt at ambulation, she subsequently presented to a community hospital where she could no longer move her left lower extremity. Upon evaluation, the patient was found to have progressive neurological deficits and was transferred by ambulance to the authors’ tertiary medical center for definitive management. 

A review of the patient’s recent symptoms indicated that she had also experienced lower abdominal paresthesias of 5 days’ duration. She described this sensation as sharp, numb, and constant since its onset and unrelieved with the use of a muscle relaxant at home. She further noted that the pain became worse with movement, having no palliative modifying factors. Upon further questioning, the patient acknowledged recent urinary incontinence of unknown duration, nausea, and current menstruation. She denied any recent injury or illness.

Her past medical history was unknown, and she stated that she had not seen a physician in several years. The patient’s surgical history included a tonsillectomy and an appendectomy at a young age. She had no known drug allergies. Although she denied the use of medications, electronic medical records show that the patient had been prescribed baclofen, hydrochlorothiazide, metoprolol, and tramadol. She was unaware of her family’s medical history and denied use of tobacco, alcohol, or illicit drugs.

Upon physical examination, the patient’s vital signs were: blood pressure, 161/99 mm Hg; heart rate, 103 beats/minute; respiratory rate, 16 breaths/minute; oxygen saturation, 97% on room air; and temperature, 97.0°F. She appeared to be a middle-aged obese woman in no apparent distress and was alert with normal mentation, lying comfortably on the gurney.

The head and neck examinations were normal. Lung auscultation demonstrated equal and unlabored breath sounds bilaterally with no adventitious sounds. Incidentally, it was noted at this time that the left breast had a significantly large fungating mass about the areola and within the deep tissue that was visually evidenced by prominent erythema and classic peau d’orange skin. The right breast had minimal skin involvement with a smaller palpable mass below the dermal surface. Both breast masses and enlarged axillary lymph nodes on the left were nontender. The cardiovascular examination demonstrated mild tachycardia with normal heart sounds, no extremity edema, and normal pulses throughout. The gastrointestinal examination had normal borborygmus with mild infraabdominal tenderness to palpation superficially over a nondistended abdomen. Neither organomegaly, hernia, nor masses were appreciated. In addition to urinary incontinence, the patient also had fecal incontinence, which correlated with diminished tone on digital rectal examination.

 Neurological sensation was intact in all extremities and no deficits were noted in the cranial nerves. Patellar and ankle tendon-testing demonstrated left-sided hyperreflexia with ipsilateral Babinski reflex exhibiting up-going toes. Musculoskeletal weakness was grossly noted in the left lower extremity to be +2/5, whereas the right lower limb had +4/5 strength. Palpation of the thoracic and lumbar spines did not elicit tenderness. Aside from the aforementioned observations, no additional integumentary findings were noted. 

The patient was given oxygen by nasal cannula, connected to cardiac monitoring and pulse oximetry. A urinary catheter was inserted, and she was given parenteral dexamethasone,³ morphine sulfate, ondansetron, and normal saline. An electrocardiogram showed a normal sinus rhythm. A chest X-ray and basic blood analysis were ordered in preparation for the likelihood of surgical management. Neurosurgery and radiology were consulted. Emergent magnetic resonance imaging (MRI) of the cervical, thoracic, and lumbar spine with and without contrast was obtained to rule out SCC.

The MRI of the spine revealed pathologic fractures leading to cord compression at T9 and spinal stenosis at the L2 segment (Figure 1); diffuse bone metastasis of the spine was also observed. Subsequent surgical decompressive laminectomy from T7 to L3 was performed without complication. Despite the reportedly poor outcome in CMS,^2,4-6 the patient demonstrated a moderate return of strength, sensation, and function within the first month of postoperative follow-up. At 3 months, she had minimal subjective and objective deficits and was ambulating without difficulty. She denied urinary and fecal incontinence during these periods. The biopsied breast mass was determined to be stage IV infiltrating ductal carcinoma mucinous type, for which she was followed by an oncologist and received radiation and chemotherapy.

 

Discussion

The patient’s chief complaint of lower extremity muscle weakness was a clinical emergency that merited thorough investigation in a timely manner to preserve limb function. Since her medical history did not provide pathologic insight concerning her condition, physical examination by emergency personnel served as the founding evidence for this patient’s diagnosis. Decreased muscle tone of the lower extremities and rectal sphincter raised suspicion for a neurological etiology. These symptoms, along with hyperreflexia, the presence of a Babinski sign, and dual-system incontinence, were suggestive of an underlying central nervous system lesion. Of note, urinary complaints commonly result from retention leading to overflow incontinence, a time-dependent symptom that may not be experienced before presentation to medical personnel. Urinary retention is one of the most consistent findings in patients with CMS and SCC, with a relative prevalence of 90%.^4,7,8

For providers not familiar with CMS presentation, preserved tactile sensation, normoreflexia, and lack of a Babinski sign and/or incontinence are not sufficient indicators to discontinue the consideration of spinal cord lesions in the differential diagnosis and may in fact be misleading.^6,9,10 Although the patient’s deficits were not symmetrical as is commonly reported, this did not rule out the diagnosis. 

Appropriate diagnosis and treatment of such a rare entity in the emergency setting consists of a high clinical suspicion, MRI of the spine, urgent consultations, and early treatment with parenteral corticosteroids.^3,4 The patient did not have a previous diagnosis of breast carcinoma; however, once discovered on examination, the condition became suspect as approximately 80% of patients with SCC have a preexisting cancer. The peak incidence of SCC is in the sixth and seventh decades of life. The most common primary cancers metastasizing to bone are breast, prostate, and lung. When found to affect the spine, roughly 60% will be located in the thoracic spine, 30% at the lumbosacral level, and 10% in the cervical spine.

As demonstrated in this case presentation, a thorough examination cannot be stressed enough in emergent situations. The patient’s dermatological findings and nontender lymphadenopathy were adequately significant to consider the possibility of a metastatic process as the underlying etiology. Although discouraged due to the fast-paced environment of the ED, patients are frequently assessed and examined in street clothing, which in this case, may have masked the underlying cause of the patient’s neurological deficits. As a result, imaging studies, corticosteroid treatment, consultations, and surgical management may have been delayed, leading to a nonreversible outcome for the patient.

Central and Peripheral Nervous System Structures and Deficits

Central and peripheral nervous system structures animate the body through coordinated signaling of upper and lower motor neurons respectively. In most adults, the distal spinal cord terminates at the level of the first or second lumbar vertebrae where the conus medullaris is found, giving rise to S2, S3 and S4 functionality. Lesions at this level exhibit lower motor neuron deficits of the bladder and rectum resulting in incontinence and sexual dysfunction. Deficits of sensorium such as saddle anesthesia or upper motor neuron lesions as evidenced by increased motor tone and abnormal reflexes are not uncommon.¹ Branches of the cauda equina extend caudally from the epiconus, a structure proximal to the conus medullaris, as peripheral nervous system branches that innervate spinal cord segments L4 through S1 (Figure 2). Lesions of the epiconus are clinically distinguished by lower motor neuron deficits wherein muscles of the lower extremities are often weakened with potential sparing of the bulbocavernosus and micturition reflexes.²

Among the many etiologies of CMS, the most common are due to compressive lesions. These include spinal trauma, neoplasm, nucleus pulposus herniation, and spinal infection. When the spinal foramen becomes either stenotic or space-occupying lesions compress, neurological function at the affected level may be compromised. In the case of CMS, neurological deficits may present as lower extremity weakness, perineal pain, or altered deep tendon reflexes (hyperreflexia or areflexia). Tactile sensation is usually spared and incontinence is frequently present. Pure lesions of the conus medullaris are uncommon and are often combined with cauda equina symptoms¹ (Table).

Conclusion

While many EPs are cognizant of cauda equina syndrome and its presentation, CMS is less well known and not commonly documented. Due to symptomatic overlap and epidemiological rarity of these conditions, most of the literature describing these entities combines their discussion. This case contributes to the growing body of literature to assist clinicians in the evaluation and management of CMS.

Dr Batt is an emergency medicine resident, Arrowhead Regional Medical Center, Colton, California. Dr Stone is the emergency medical services director, Travis Air Force Base, Fairfield, California.

Case

A 46-year-old white woman with sudden onset of numbness in her lower extremities and inability to ambulate was transported to the ED via emergency medical services. At the onset of symptoms, the patient reported a feeling of “heaviness” in her lower extremities, which was greater on the left side than the right. After an unsuccessful attempt at ambulation, she subsequently presented to a community hospital where she could no longer move her left lower extremity. Upon evaluation, the patient was found to have progressive neurological deficits and was transferred by ambulance to the authors’ tertiary medical center for definitive management. 

A review of the patient’s recent symptoms indicated that she had also experienced lower abdominal paresthesias of 5 days’ duration. She described this sensation as sharp, numb, and constant since its onset and unrelieved with the use of a muscle relaxant at home. She further noted that the pain became worse with movement, having no palliative modifying factors. Upon further questioning, the patient acknowledged recent urinary incontinence of unknown duration, nausea, and current menstruation. She denied any recent injury or illness.

Her past medical history was unknown, and she stated that she had not seen a physician in several years. The patient’s surgical history included a tonsillectomy and an appendectomy at a young age. She had no known drug allergies. Although she denied the use of medications, electronic medical records show that the patient had been prescribed baclofen, hydrochlorothiazide, metoprolol, and tramadol. She was unaware of her family’s medical history and denied use of tobacco, alcohol, or illicit drugs.

Upon physical examination, the patient’s vital signs were: blood pressure, 161/99 mm Hg; heart rate, 103 beats/minute; respiratory rate, 16 breaths/minute; oxygen saturation, 97% on room air; and temperature, 97.0°F. She appeared to be a middle-aged obese woman in no apparent distress and was alert with normal mentation, lying comfortably on the gurney.

The head and neck examinations were normal. Lung auscultation demonstrated equal and unlabored breath sounds bilaterally with no adventitious sounds. Incidentally, it was noted at this time that the left breast had a significantly large fungating mass about the areola and within the deep tissue that was visually evidenced by prominent erythema and classic peau d’orange skin. The right breast had minimal skin involvement with a smaller palpable mass below the dermal surface. Both breast masses and enlarged axillary lymph nodes on the left were nontender. The cardiovascular examination demonstrated mild tachycardia with normal heart sounds, no extremity edema, and normal pulses throughout. The gastrointestinal examination had normal borborygmus with mild infraabdominal tenderness to palpation superficially over a nondistended abdomen. Neither organomegaly, hernia, nor masses were appreciated. In addition to urinary incontinence, the patient also had fecal incontinence, which correlated with diminished tone on digital rectal examination.

 Neurological sensation was intact in all extremities and no deficits were noted in the cranial nerves. Patellar and ankle tendon-testing demonstrated left-sided hyperreflexia with ipsilateral Babinski reflex exhibiting up-going toes. Musculoskeletal weakness was grossly noted in the left lower extremity to be +2/5, whereas the right lower limb had +4/5 strength. Palpation of the thoracic and lumbar spines did not elicit tenderness. Aside from the aforementioned observations, no additional integumentary findings were noted. 

The patient was given oxygen by nasal cannula, connected to cardiac monitoring and pulse oximetry. A urinary catheter was inserted, and she was given parenteral dexamethasone,³ morphine sulfate, ondansetron, and normal saline. An electrocardiogram showed a normal sinus rhythm. A chest X-ray and basic blood analysis were ordered in preparation for the likelihood of surgical management. Neurosurgery and radiology were consulted. Emergent magnetic resonance imaging (MRI) of the cervical, thoracic, and lumbar spine with and without contrast was obtained to rule out SCC.

The MRI of the spine revealed pathologic fractures leading to cord compression at T9 and spinal stenosis at the L2 segment (Figure 1); diffuse bone metastasis of the spine was also observed. Subsequent surgical decompressive laminectomy from T7 to L3 was performed without complication. Despite the reportedly poor outcome in CMS,^2,4-6 the patient demonstrated a moderate return of strength, sensation, and function within the first month of postoperative follow-up. At 3 months, she had minimal subjective and objective deficits and was ambulating without difficulty. She denied urinary and fecal incontinence during these periods. The biopsied breast mass was determined to be stage IV infiltrating ductal carcinoma mucinous type, for which she was followed by an oncologist and received radiation and chemotherapy.

 

Discussion

The patient’s chief complaint of lower extremity muscle weakness was a clinical emergency that merited thorough investigation in a timely manner to preserve limb function. Since her medical history did not provide pathologic insight concerning her condition, physical examination by emergency personnel served as the founding evidence for this patient’s diagnosis. Decreased muscle tone of the lower extremities and rectal sphincter raised suspicion for a neurological etiology. These symptoms, along with hyperreflexia, the presence of a Babinski sign, and dual-system incontinence, were suggestive of an underlying central nervous system lesion. Of note, urinary complaints commonly result from retention leading to overflow incontinence, a time-dependent symptom that may not be experienced before presentation to medical personnel. Urinary retention is one of the most consistent findings in patients with CMS and SCC, with a relative prevalence of 90%.^4,7,8

For providers not familiar with CMS presentation, preserved tactile sensation, normoreflexia, and lack of a Babinski sign and/or incontinence are not sufficient indicators to discontinue the consideration of spinal cord lesions in the differential diagnosis and may in fact be misleading.^6,9,10 Although the patient’s deficits were not symmetrical as is commonly reported, this did not rule out the diagnosis. 

Appropriate diagnosis and treatment of such a rare entity in the emergency setting consists of a high clinical suspicion, MRI of the spine, urgent consultations, and early treatment with parenteral corticosteroids.^3,4 The patient did not have a previous diagnosis of breast carcinoma; however, once discovered on examination, the condition became suspect as approximately 80% of patients with SCC have a preexisting cancer. The peak incidence of SCC is in the sixth and seventh decades of life. The most common primary cancers metastasizing to bone are breast, prostate, and lung. When found to affect the spine, roughly 60% will be located in the thoracic spine, 30% at the lumbosacral level, and 10% in the cervical spine.

As demonstrated in this case presentation, a thorough examination cannot be stressed enough in emergent situations. The patient’s dermatological findings and nontender lymphadenopathy were adequately significant to consider the possibility of a metastatic process as the underlying etiology. Although discouraged due to the fast-paced environment of the ED, patients are frequently assessed and examined in street clothing, which in this case, may have masked the underlying cause of the patient’s neurological deficits. As a result, imaging studies, corticosteroid treatment, consultations, and surgical management may have been delayed, leading to a nonreversible outcome for the patient.

Central and Peripheral Nervous System Structures and Deficits

Central and peripheral nervous system structures animate the body through coordinated signaling of upper and lower motor neurons respectively. In most adults, the distal spinal cord terminates at the level of the first or second lumbar vertebrae where the conus medullaris is found, giving rise to S2, S3 and S4 functionality. Lesions at this level exhibit lower motor neuron deficits of the bladder and rectum resulting in incontinence and sexual dysfunction. Deficits of sensorium such as saddle anesthesia or upper motor neuron lesions as evidenced by increased motor tone and abnormal reflexes are not uncommon.¹ Branches of the cauda equina extend caudally from the epiconus, a structure proximal to the conus medullaris, as peripheral nervous system branches that innervate spinal cord segments L4 through S1 (Figure 2). Lesions of the epiconus are clinically distinguished by lower motor neuron deficits wherein muscles of the lower extremities are often weakened with potential sparing of the bulbocavernosus and micturition reflexes.²

Among the many etiologies of CMS, the most common are due to compressive lesions. These include spinal trauma, neoplasm, nucleus pulposus herniation, and spinal infection. When the spinal foramen becomes either stenotic or space-occupying lesions compress, neurological function at the affected level may be compromised. In the case of CMS, neurological deficits may present as lower extremity weakness, perineal pain, or altered deep tendon reflexes (hyperreflexia or areflexia). Tactile sensation is usually spared and incontinence is frequently present. Pure lesions of the conus medullaris are uncommon and are often combined with cauda equina symptoms¹ (Table).

Conclusion

While many EPs are cognizant of cauda equina syndrome and its presentation, CMS is less well known and not commonly documented. Due to symptomatic overlap and epidemiological rarity of these conditions, most of the literature describing these entities combines their discussion. This case contributes to the growing body of literature to assist clinicians in the evaluation and management of CMS.

Dr Batt is an emergency medicine resident, Arrowhead Regional Medical Center, Colton, California. Dr Stone is the emergency medical services director, Travis Air Force Base, Fairfield, California.

Case

A 46-year-old white woman with sudden onset of numbness in her lower extremities and inability to ambulate was transported to the ED via emergency medical services. At the onset of symptoms, the patient reported a feeling of “heaviness” in her lower extremities, which was greater on the left side than the right. After an unsuccessful attempt at ambulation, she subsequently presented to a community hospital where she could no longer move her left lower extremity. Upon evaluation, the patient was found to have progressive neurological deficits and was transferred by ambulance to the authors’ tertiary medical center for definitive management. 

A review of the patient’s recent symptoms indicated that she had also experienced lower abdominal paresthesias of 5 days’ duration. She described this sensation as sharp, numb, and constant since its onset and unrelieved with the use of a muscle relaxant at home. She further noted that the pain became worse with movement, having no palliative modifying factors. Upon further questioning, the patient acknowledged recent urinary incontinence of unknown duration, nausea, and current menstruation. She denied any recent injury or illness.

Her past medical history was unknown, and she stated that she had not seen a physician in several years. The patient’s surgical history included a tonsillectomy and an appendectomy at a young age. She had no known drug allergies. Although she denied the use of medications, electronic medical records show that the patient had been prescribed baclofen, hydrochlorothiazide, metoprolol, and tramadol. She was unaware of her family’s medical history and denied use of tobacco, alcohol, or illicit drugs.

Upon physical examination, the patient’s vital signs were: blood pressure, 161/99 mm Hg; heart rate, 103 beats/minute; respiratory rate, 16 breaths/minute; oxygen saturation, 97% on room air; and temperature, 97.0°F. She appeared to be a middle-aged obese woman in no apparent distress and was alert with normal mentation, lying comfortably on the gurney.

The head and neck examinations were normal. Lung auscultation demonstrated equal and unlabored breath sounds bilaterally with no adventitious sounds. Incidentally, it was noted at this time that the left breast had a significantly large fungating mass about the areola and within the deep tissue that was visually evidenced by prominent erythema and classic peau d’orange skin. The right breast had minimal skin involvement with a smaller palpable mass below the dermal surface. Both breast masses and enlarged axillary lymph nodes on the left were nontender. The cardiovascular examination demonstrated mild tachycardia with normal heart sounds, no extremity edema, and normal pulses throughout. The gastrointestinal examination had normal borborygmus with mild infraabdominal tenderness to palpation superficially over a nondistended abdomen. Neither organomegaly, hernia, nor masses were appreciated. In addition to urinary incontinence, the patient also had fecal incontinence, which correlated with diminished tone on digital rectal examination.

 Neurological sensation was intact in all extremities and no deficits were noted in the cranial nerves. Patellar and ankle tendon-testing demonstrated left-sided hyperreflexia with ipsilateral Babinski reflex exhibiting up-going toes. Musculoskeletal weakness was grossly noted in the left lower extremity to be +2/5, whereas the right lower limb had +4/5 strength. Palpation of the thoracic and lumbar spines did not elicit tenderness. Aside from the aforementioned observations, no additional integumentary findings were noted. 

The patient was given oxygen by nasal cannula, connected to cardiac monitoring and pulse oximetry. A urinary catheter was inserted, and she was given parenteral dexamethasone,³ morphine sulfate, ondansetron, and normal saline. An electrocardiogram showed a normal sinus rhythm. A chest X-ray and basic blood analysis were ordered in preparation for the likelihood of surgical management. Neurosurgery and radiology were consulted. Emergent magnetic resonance imaging (MRI) of the cervical, thoracic, and lumbar spine with and without contrast was obtained to rule out SCC.

The MRI of the spine revealed pathologic fractures leading to cord compression at T9 and spinal stenosis at the L2 segment (Figure 1); diffuse bone metastasis of the spine was also observed. Subsequent surgical decompressive laminectomy from T7 to L3 was performed without complication. Despite the reportedly poor outcome in CMS,^2,4-6 the patient demonstrated a moderate return of strength, sensation, and function within the first month of postoperative follow-up. At 3 months, she had minimal subjective and objective deficits and was ambulating without difficulty. She denied urinary and fecal incontinence during these periods. The biopsied breast mass was determined to be stage IV infiltrating ductal carcinoma mucinous type, for which she was followed by an oncologist and received radiation and chemotherapy.

 

Discussion

The patient’s chief complaint of lower extremity muscle weakness was a clinical emergency that merited thorough investigation in a timely manner to preserve limb function. Since her medical history did not provide pathologic insight concerning her condition, physical examination by emergency personnel served as the founding evidence for this patient’s diagnosis. Decreased muscle tone of the lower extremities and rectal sphincter raised suspicion for a neurological etiology. These symptoms, along with hyperreflexia, the presence of a Babinski sign, and dual-system incontinence, were suggestive of an underlying central nervous system lesion. Of note, urinary complaints commonly result from retention leading to overflow incontinence, a time-dependent symptom that may not be experienced before presentation to medical personnel. Urinary retention is one of the most consistent findings in patients with CMS and SCC, with a relative prevalence of 90%.^4,7,8

For providers not familiar with CMS presentation, preserved tactile sensation, normoreflexia, and lack of a Babinski sign and/or incontinence are not sufficient indicators to discontinue the consideration of spinal cord lesions in the differential diagnosis and may in fact be misleading.^6,9,10 Although the patient’s deficits were not symmetrical as is commonly reported, this did not rule out the diagnosis. 

Appropriate diagnosis and treatment of such a rare entity in the emergency setting consists of a high clinical suspicion, MRI of the spine, urgent consultations, and early treatment with parenteral corticosteroids.^3,4 The patient did not have a previous diagnosis of breast carcinoma; however, once discovered on examination, the condition became suspect as approximately 80% of patients with SCC have a preexisting cancer. The peak incidence of SCC is in the sixth and seventh decades of life. The most common primary cancers metastasizing to bone are breast, prostate, and lung. When found to affect the spine, roughly 60% will be located in the thoracic spine, 30% at the lumbosacral level, and 10% in the cervical spine.

As demonstrated in this case presentation, a thorough examination cannot be stressed enough in emergent situations. The patient’s dermatological findings and nontender lymphadenopathy were adequately significant to consider the possibility of a metastatic process as the underlying etiology. Although discouraged due to the fast-paced environment of the ED, patients are frequently assessed and examined in street clothing, which in this case, may have masked the underlying cause of the patient’s neurological deficits. As a result, imaging studies, corticosteroid treatment, consultations, and surgical management may have been delayed, leading to a nonreversible outcome for the patient.

Central and Peripheral Nervous System Structures and Deficits

Central and peripheral nervous system structures animate the body through coordinated signaling of upper and lower motor neurons respectively. In most adults, the distal spinal cord terminates at the level of the first or second lumbar vertebrae where the conus medullaris is found, giving rise to S2, S3 and S4 functionality. Lesions at this level exhibit lower motor neuron deficits of the bladder and rectum resulting in incontinence and sexual dysfunction. Deficits of sensorium such as saddle anesthesia or upper motor neuron lesions as evidenced by increased motor tone and abnormal reflexes are not uncommon.¹ Branches of the cauda equina extend caudally from the epiconus, a structure proximal to the conus medullaris, as peripheral nervous system branches that innervate spinal cord segments L4 through S1 (Figure 2). Lesions of the epiconus are clinically distinguished by lower motor neuron deficits wherein muscles of the lower extremities are often weakened with potential sparing of the bulbocavernosus and micturition reflexes.²

Among the many etiologies of CMS, the most common are due to compressive lesions. These include spinal trauma, neoplasm, nucleus pulposus herniation, and spinal infection. When the spinal foramen becomes either stenotic or space-occupying lesions compress, neurological function at the affected level may be compromised. In the case of CMS, neurological deficits may present as lower extremity weakness, perineal pain, or altered deep tendon reflexes (hyperreflexia or areflexia). Tactile sensation is usually spared and incontinence is frequently present. Pure lesions of the conus medullaris are uncommon and are often combined with cauda equina symptoms¹ (Table).

Conclusion

While many EPs are cognizant of cauda equina syndrome and its presentation, CMS is less well known and not commonly documented. Due to symptomatic overlap and epidemiological rarity of these conditions, most of the literature describing these entities combines their discussion. This case contributes to the growing body of literature to assist clinicians in the evaluation and management of CMS.

Dr Batt is an emergency medicine resident, Arrowhead Regional Medical Center, Colton, California. Dr Stone is the emergency medical services director, Travis Air Force Base, Fairfield, California.

Lung ultrasound can be a valuable addition to the emergency physician’s (EP’s) diagnostic armamentarium. This article reviews how this modality may be used to differentiate between chronic obstructive pulmonary disease (COPD) and coronary heart failure (CHF) exacerbations. As patients often have a history of both of these diseases, it is difficult to distinguish which condition is the cause of a patient’s dyspnea. This examination is easy to learn and in most cases, it can be performed within 3 to 4 minutes. Most importantly, lung ultrasound can assist in making clinical decisions in real time at the bedside. Although the following is not a comprehensive review, it does provide the basic essentials, allowing the clinician to begin using this modality in the ED.

Getting Started

The curvilinear probe is required to perform ultrasound of the lungs. Most studies divide the lung into regions, though consensus on exactly how many regions are required remains unclear. The blue protocol, which is probably the most well-known study, divides the lung into the anterior, lateral, and posterolateral sections.¹ The superior and inferior aspects of each zone are evaluated with a total of six ultrasound views
per lung.

Artifacts

An understanding of artifacts is essential to correct interpretation of the ultrasound images. Two ultrasound findings of normal lungs are “A lines” and “lung sliding.” However, these patterns are seen in normal lungs and in the lungs of patients with asthma and COPD.

Lung sliding is movement of the parietal pleura sliding against the visceral pleura. A lines are a repetitive reverberation artifact of the pleura (Figure 1).  Occasional comet-tail artifacts—short hyperechoic artifacts that arise from the pleural line and descend in a vertical orientation partially down the screen (Figure 2).

B lines are the ultrasound equivalent of the Kerley B lines found on chest X-ray. Bilateral B lines are commonly present in lungs with interstitial edema. For an examination to be considered positive, there must be a minimum three B lines per view (Figure 3). Ultrasonographic B lines are long wide bands of hyperechoic artifact that have been likened to the beam of a flashlight. They originate at the pleural line and traverse the entire ultrasound screen vertically to the bottom of the screen. Causes of unilateral B lines can include pneumonia and pulmonary contusion. As the EP becomes more familiar in performing lung ultrasound, he or she will become more adept at identifying A and B lines.

Differential Diagnosis

When using ultrasound to differentiate between CHF and COPD, this examination has been shown to have a sensitivity of 100% and a specificity of 92%.² By performing lung ultrasound immediately upon a patient’s arrival to the ED, the clinician can obtain quick and accurate insight into whether a patient would benefit from albuterol or nitroglycerin. In the acutely dyspneic patient, combining lung ultrasound with focused echocardiogram and sonographic inferior vena cava assessment will provide additional information to support the diagnosis.

Conclusion

As with other bedside imaging techniques, lung ultrasound in the ED can help to quickly assess the dyspneic patient and facilitate initiation of appropriate treatment.

Dr Taylor is an assistant professor and director of postgraduate medical education, department of emergency medicine, Emory University School of Medicine, Atlanta, Georgia. Dr Meer is an assistant professor and director of emergency ultrasound, department of emergency medicine, Emory University School of Medicine, Atlanta, Georgia. Dr Beck is an assistant professor, department of emergency medicine, Emory University School of Medicine, Atlanta, Georgia.

Lung ultrasound can be a valuable addition to the emergency physician’s (EP’s) diagnostic armamentarium. This article reviews how this modality may be used to differentiate between chronic obstructive pulmonary disease (COPD) and coronary heart failure (CHF) exacerbations. As patients often have a history of both of these diseases, it is difficult to distinguish which condition is the cause of a patient’s dyspnea. This examination is easy to learn and in most cases, it can be performed within 3 to 4 minutes. Most importantly, lung ultrasound can assist in making clinical decisions in real time at the bedside. Although the following is not a comprehensive review, it does provide the basic essentials, allowing the clinician to begin using this modality in the ED.

Getting Started

The curvilinear probe is required to perform ultrasound of the lungs. Most studies divide the lung into regions, though consensus on exactly how many regions are required remains unclear. The blue protocol, which is probably the most well-known study, divides the lung into the anterior, lateral, and posterolateral sections.¹ The superior and inferior aspects of each zone are evaluated with a total of six ultrasound views
per lung.

Artifacts

An understanding of artifacts is essential to correct interpretation of the ultrasound images. Two ultrasound findings of normal lungs are “A lines” and “lung sliding.” However, these patterns are seen in normal lungs and in the lungs of patients with asthma and COPD.

Lung sliding is movement of the parietal pleura sliding against the visceral pleura. A lines are a repetitive reverberation artifact of the pleura (Figure 1).  Occasional comet-tail artifacts—short hyperechoic artifacts that arise from the pleural line and descend in a vertical orientation partially down the screen (Figure 2).

B lines are the ultrasound equivalent of the Kerley B lines found on chest X-ray. Bilateral B lines are commonly present in lungs with interstitial edema. For an examination to be considered positive, there must be a minimum three B lines per view (Figure 3). Ultrasonographic B lines are long wide bands of hyperechoic artifact that have been likened to the beam of a flashlight. They originate at the pleural line and traverse the entire ultrasound screen vertically to the bottom of the screen. Causes of unilateral B lines can include pneumonia and pulmonary contusion. As the EP becomes more familiar in performing lung ultrasound, he or she will become more adept at identifying A and B lines.

Differential Diagnosis

When using ultrasound to differentiate between CHF and COPD, this examination has been shown to have a sensitivity of 100% and a specificity of 92%.² By performing lung ultrasound immediately upon a patient’s arrival to the ED, the clinician can obtain quick and accurate insight into whether a patient would benefit from albuterol or nitroglycerin. In the acutely dyspneic patient, combining lung ultrasound with focused echocardiogram and sonographic inferior vena cava assessment will provide additional information to support the diagnosis.

Conclusion

As with other bedside imaging techniques, lung ultrasound in the ED can help to quickly assess the dyspneic patient and facilitate initiation of appropriate treatment.

Dr Taylor is an assistant professor and director of postgraduate medical education, department of emergency medicine, Emory University School of Medicine, Atlanta, Georgia. Dr Meer is an assistant professor and director of emergency ultrasound, department of emergency medicine, Emory University School of Medicine, Atlanta, Georgia. Dr Beck is an assistant professor, department of emergency medicine, Emory University School of Medicine, Atlanta, Georgia.

Lung ultrasound can be a valuable addition to the emergency physician’s (EP’s) diagnostic armamentarium. This article reviews how this modality may be used to differentiate between chronic obstructive pulmonary disease (COPD) and coronary heart failure (CHF) exacerbations. As patients often have a history of both of these diseases, it is difficult to distinguish which condition is the cause of a patient’s dyspnea. This examination is easy to learn and in most cases, it can be performed within 3 to 4 minutes. Most importantly, lung ultrasound can assist in making clinical decisions in real time at the bedside. Although the following is not a comprehensive review, it does provide the basic essentials, allowing the clinician to begin using this modality in the ED.

Getting Started

The curvilinear probe is required to perform ultrasound of the lungs. Most studies divide the lung into regions, though consensus on exactly how many regions are required remains unclear. The blue protocol, which is probably the most well-known study, divides the lung into the anterior, lateral, and posterolateral sections.¹ The superior and inferior aspects of each zone are evaluated with a total of six ultrasound views
per lung.

Artifacts

An understanding of artifacts is essential to correct interpretation of the ultrasound images. Two ultrasound findings of normal lungs are “A lines” and “lung sliding.” However, these patterns are seen in normal lungs and in the lungs of patients with asthma and COPD.

Lung sliding is movement of the parietal pleura sliding against the visceral pleura. A lines are a repetitive reverberation artifact of the pleura (Figure 1).  Occasional comet-tail artifacts—short hyperechoic artifacts that arise from the pleural line and descend in a vertical orientation partially down the screen (Figure 2).

B lines are the ultrasound equivalent of the Kerley B lines found on chest X-ray. Bilateral B lines are commonly present in lungs with interstitial edema. For an examination to be considered positive, there must be a minimum three B lines per view (Figure 3). Ultrasonographic B lines are long wide bands of hyperechoic artifact that have been likened to the beam of a flashlight. They originate at the pleural line and traverse the entire ultrasound screen vertically to the bottom of the screen. Causes of unilateral B lines can include pneumonia and pulmonary contusion. As the EP becomes more familiar in performing lung ultrasound, he or she will become more adept at identifying A and B lines.

Differential Diagnosis

When using ultrasound to differentiate between CHF and COPD, this examination has been shown to have a sensitivity of 100% and a specificity of 92%.² By performing lung ultrasound immediately upon a patient’s arrival to the ED, the clinician can obtain quick and accurate insight into whether a patient would benefit from albuterol or nitroglycerin. In the acutely dyspneic patient, combining lung ultrasound with focused echocardiogram and sonographic inferior vena cava assessment will provide additional information to support the diagnosis.

Conclusion

As with other bedside imaging techniques, lung ultrasound in the ED can help to quickly assess the dyspneic patient and facilitate initiation of appropriate treatment.

Dr Taylor is an assistant professor and director of postgraduate medical education, department of emergency medicine, Emory University School of Medicine, Atlanta, Georgia. Dr Meer is an assistant professor and director of emergency ultrasound, department of emergency medicine, Emory University School of Medicine, Atlanta, Georgia. Dr Beck is an assistant professor, department of emergency medicine, Emory University School of Medicine, Atlanta, Georgia.

Overview

Candidates for noninvasive ventilation (NIV) most commonly present to the ED with acute respiratory failure (ARF) secondary to chronic obstructive pulmonary disease (COPD) or congestive heart-failure (CHF) exacerbations. The emergency physician (EP) must select patients appropriately, recognizing which would benefit most from NIV, as well as those with contraindications to this therapy. When indicated, early application confers benefit to the patient and can help avoid endotracheal intubation. Once therapy is initiated, clinical deterioration is still possible, and close monitoring and troubleshooting are imperative. Frequently, the clinician must make adjustments in ventilatory parameters to support the patient.

In this article, the author discusses the evidence supporting the use of NIV in appropriately selected patients with ARF, as well as review the types of NIV commonly used in the ED, the physiologic effects of positive-pressure ventilation (PPV), and how to identify and avoid common pitfalls.

Case Presentation Examples

Case 1

A 72-year-old man with a past medical history of COPD was brought to the ED by emergency medical services for evaluation of shortness of breath and wheezing. The patient’s initial oxygen (O₂) saturation was 84%, which responded to bronchodilators and supplemental O₂. At the time of arrival, he was somewhat somnolent, but aroused to verbal stimuli. A nonrebreather mask was placed delivering 15 L/minute of O₂ with a saturation of 96%. His vital signs were: blood pressure (BP), 142/76 mm Hg, heart rate, 108 beats/minute; and respiratory rate (RR), 13 breaths/minute. A cardiac monitor revealed sinus tachycardia, and a portable chest X-ray was obtained (Figure 1). On lung examination, the patient’s breath sounds were diminished in the bases with suboptimal respiratory effort and expiratory wheezes in all lung fields. Venous blood gas measurement revealed a pH of 7.25; end-tidal carbon dioxide (CO₂) was 77.

After the initial assessment, the EP considered NIV as an adjunct to improve ventilation as he suspected the patient was experiencing significant respiratory acidosis secondary to CO₂ retention. The respiratory therapist suggested NIV at 12/5 before titrating down the fraction of inspired O₂ (FiO₂) and sought approval from the EP. 

Discussion Questions: Is the above recommendation from the respiratory therapist the most appropriate therapy for this patient? What are the contraindications to this treatment and how should he be monitored to measure improvement?

Case 2

A 54-year-old woman presented to the ED for shortness of breath. On examination, she was diaphoretic and in severe distress with one- to two-word dyspnea and gasping respirations with pink-tinged sputum. Her BP was 236/158 mm Hg. A portable chest X-ray was obtained (Figure 2); rales were present with significant jugular venous distension. An electrocardiogram revealed a left-ventricular hypertrophy strain pattern but no evidence of ST-segment elevation.

During the assessment, the EP considered hypertensive emergency with resulting flash pulmonary edema as the cause of the patient’s condition; as such, he contemplated NIV to decrease the work of breathing and improve oxygenation. However, the EP had concerns regarding the preload and afterload ramifications. Although there was no respiratory therapist in the ED, the EP was able to set up the machine, but was not certain which mode of NIV or initial settings would be appropriate.

Discussion Questions: What is the protocol for proper set up to ensure a good mask fit? Once therapy is initiated, how should the EP monitor the patient? How should the EP explain this therapy to the patient and instruct her on how to work with the ventilator?

Acute-Care Application

Noninvasive ventilation refers to PPV delivered through a device such as a facemask, nasal mask, nasal plugs, or helmet. This modality was first used in the 1940s to treat respiratory failure, and its use has since grown to parallel that of mechanical ventilation.^1-3 Although the application of NIV does not represent definitive airway management, this therapy has dramatically changed the care and treatment of both chronic and ARF. It serves as a significant intervention to prevent further respiratory compromise; to reverse either existing physiologic, hemodynamic, or ventilatory derangements; and to avoid endotracheal intubation.

Modes of Delivery

In the acute setting, NIV is typically delivered via two modes. Continuous positive-airway pressure (CPAP) is delivered regardless of the phase of respiration, and noninvasive positive-pressure ventilation (NIPPV; typically referred to as bi-level positive-airway pressure [BiPAP] or BPPV) is delivered in the inspiratory and expiratory phases of the respiratory cycle. Inspiratory positive-airway pressure (IPAP) refers to an inspiratory boost that is triggered by the negative airway pressure on inspiration in a synchronous fashion. This inspiratory pressure is fixed, but the volume delivered fluctuates based on the patient’s inspiratory effort. Expiratory positive-airway pressure (EPAP) is the delivery of constant pressure during exhalation. The difference between the IPAP and EPAP is referred to as pressure support, which serves to decrease the work of breathing and improve ventilation. (A list of commonly used abbreviations, terms, and definitions are outlined in Table 1.)

 

Etiology of Respiratory Failure and Treatment Decisions
At the time of initial presentation, the exact etiology of a patient’s respiratory failure may not be known, and treatment decisions will be necessary before all relevant data are present. Patients presenting in acute respiratory distress (ARD) are often suffering from shunt physiology, in which alveoli are perfused but not ventilated due to the presence of fluid or collapse, as in pulmonary edema or COPD.⁴ Regardless of the etiology, patients will benefit from early application of NIV.⁵ Thus, the clinician must be aggressive in the application of this therapy to identify those patients who will benefit the most from treatment. All patients receiving NIV must be monitored closely as failure of therapy is still a possibility.

Patient Selection

The utilization of NIV has increased in the hospital and ED setting and it is now often initiated in the prehospital setting^6-8 with observed improvement in dyspnea scores and oxygenation with early intervention.⁹ Regarding patient selection, in the absence of contraindications (Table 2), all dyspneic patients should be considered eligible for a trial of NIV. ¹³ For some patients, this may be their first use of the therapy; as such, they are in effect learning to “swim while drowning.” The agitated and anxious patient will require coaching to provide reassurance and instruction while he or she learns to synchronize and work with the ventilator. The presence and quality of this instruction, though not previously measured, would intuitively be very helpful and an important determinant of success in the application of NIV in the naïve patient.

Common Conditions and NIV

In the ED, NIV is commonly utilized for the treatment of COPD and acute decompensated heart failure. These two conditions have been extensively studied and a robust amount of literature supports the routine use of NIV in these patients.

Chronic Obstructive Pulmonary Disease
For COPD, BiPAP has been shown and is widely accepted as the modality that confers the most benefit, with one study demonstrating a 462% increase in its use and a 42% decline in mechanical intubation rates from 1998 to 2008.¹⁴ Multiple studies have demonstrated a reduction in the intubation rate, improvement in the work of breathing, and a more rapid improvement in RR and symptoms.^15,16

Acute Decompensated Heart Failure and Pulmonary Edema
Noninvasive ventilation is used commonly for decompensated heart failure and acute cardiogenic pulmonary edema (ACPE). The rapid patient improvement with its use when compared to standard O₂ therapy is well documented. A successful trial and application of NIV demonstrated benefit in a recent retrospective analysis of 2,430 acutely decompensated heart-failure patients in the United States. The study found that the patients who were treated with NIV, but not immediately intubated, had better outcomes.¹⁷ (In these types of patients, pulmonary edema is typically not related to volume overload, but the result of imbalanced hemodynamics with markedly increased cardiac afterload and systemic vascular resistance.)

With respect to type of NIV, the use of CPAP is widely accepted as the primary modality of choice to confer the most benefit in ACPE.¹⁸ Although theoretical advantages do exist for the use of BiPAP over CPAP, this benefit has been noted in smaller studies¹⁹ but not clearly demonstrated in large reviews.^20,21 In addition, patients suffering from long-term CHF develop the syndrome of cardiac cachexia, characterized by the loss of quantity and quality of skeletal muscle.²² This reduction in muscle mass can produce a significant deficit in inspiratory muscle strength and ability, providing an opportunity for benefit with the use of BiPAP.

Previously, BiPAP was considered unsafe in the setting of ACPE due to an increase in myocardial infarction.²³ These results have not been reproduced in larger studies, and it is widely accepted that although BiPAP may not confer any benefit, it also does not increase harm.

Asthma
Because the underlying pathology of asthma differs from COPD, the current evidence for NIV use in patients presenting with an asthmatic episode is not very strong. Chronic obstructive pulmonary disease is characterized by collapse of terminal airways, with destruction of pulmonary architecture, and decreased compliance of the chest wall. In contrast, the airway obstruction in asthma progresses as the severity of the attack increases, and NIV may offer potential benefit in high-risk patients to avoid intubation.²⁴ Several small studies suggest the application of NIV for severe asthma exacerbations is reasonable, with some demonstration of improvement in the work of breathing and ventilatory status.^25-27

The Critically Ill Patient

Critically ill patients represent a high-risk group for desaturation during endotracheal intubation, and NIV should be considered for preoxygenation unless contraindications exist (Table 2). If standard high-flow O₂ without positive pressure does not improve oxygenation, the application of NIV may overcome shunt physiology, improve oxygenation, and lessen peri-intubation time with dangerous desaturation events.^4,28-30

 

Interfaces, Mask Leaks, Patient-Ventilator Interaction, and Respiratory Failure

Interfaces
Patient interfaces (mask types) for NIV include nasal prongs, full facial mask, or most commonly, an oronasal mask.³¹ For successful delivery of positive pressure, there must be an adequate fit or seal with minimal air leak to establish a ventilator circuit. Even though there is no perfect interface, patient comfort and treatment efficacy should be balanced. The interface chosen should minimize skin damage, maximize seal, and optimize patient-ventilator interface. The interfaces have straps that are used to secure the mask in place and balance the tension and stress on the skin to ensure a good seal and to avoid excess focal pressure that may result in complications such as skin breakdown, necrosis, or discomfort. Multiple interfaces and mask types have been evaluated in different acute-care situations, and it is important the clinician be familiar with the various options available for NIV interface and delivery. 

Mask Leaks
Unintentional leaks are an unavoidable reality with NIV use. The ventilators designed for NIV typically use a single-limb circuit with an intentional leak port close to the patient. This port provides resistance and, as the ventilator produces airflow, it can subsequently generate pressure. Because this leak port is incorporated into the interface, it is important to utilize the same manufacturer of the ventilator and interface to avoid interface-ventilator mismatch.³²

In some cases, unintentional leaks have been linked to asynchrony leading to increased work of breathing, ineffective delivery of breaths, and missed triggering events.³³ The goal of any chosen interface is the lowest measurable unintentional leak rate as higher values demonstrate significant variability (and inaccuracy) of measured tidal volumes (V_T).³⁴ Overtightening the mask should be avoided since it can compromise both patient comfort and increase the chance of skin necrosis or breakdown.

Patient-Ventilator Interaction
The importance of the patient-ventilator interaction and the development of synchrony between the two cannot be overstated. After initial application, the patient should be closely monitored as he or she begins to work with the ventilator. This is especially important in BiPAP.

Optimal patient-ventilator synchrony can be difficult to achieve, especially in the NIV-naïve patient with critical respiratory distress. Of note, approximately 20% to 30% of patients with ARD cannot be managed by NIV,¹¹ and asynchrony, though difficult to quantify in the acute-care setting, may contribute to this number. 

Respiratory Failure
Acute respiratory failure is caused by a change in the patient’s baseline gas exchange, resulting in an inability to provide sufficient levels of O₂ or to ventilate adequately. The etiologies of ARF are characterized into four types. 

Type I. Also referred to as hypoxemic respiratory failure, type I is the most common and is characterized by an arterial oxygen tension (PaO₂) of less than 60 mm Hg, with either normal or low levels of arterial CO₂ that is not responsive to supplemental O₂.

Type II. This type of respiratory failure is characterized by alveolar hypoventilation, with a PaCO₂ level greater than 45 mm Hg, although hypoxemia may also be present due to concomitant loss of central nervous system drive.

Type III. Failure primarily occurs in the perioperative setting where the functional residual capacity is reduced in combination with increasing atelectasis.

Type IV. Type IV ARF is secondary to circulatory failure and resolves when shock is corrected.^35,36

Regardless of the respiratory failure etiology, the patient is at risk of further deterioration and the need for endotracheal intubation.

Physiologic effects of NIV

Once the interface is secured, NIV has several important effects on both the cardiac and pulmonary systems. For this discussion, intrathoracic pressure (P_IT) is considered synonymous with mean airway pressure (P_aw).

Noninvasive ventilation improves airflow, lung volumes, and subsequent V_T while overcoming pulmonary atelectasis. The increase in lung volume is directly proportional to an increase in P_aw. This effect is only seen after overcoming airway resistance and chest wall and lung compliance. There is also an improvement in alveolar recruitment and redistribution of pulmonary blood flow³⁷ with decreased work of breathing.

With the increase in P_IT, there is decreased venous return to the right heart and a resulting decrease in cardiac preload.³⁸ In the setting of acute cardiogenic pulmonary edema (ACPE), this effect is highly favorable. However, in the volume-depleted or hemodynamically unstable patient, this may result in a drop in cardiac output and hypotension. The “normal” heart is more sensitive to preload, and the application of positive pressure can cause a significant decrease in cardiac output. Cardiac afterload is reduced through multiple mechanisms, including directly from a decreased left-ventricular (LV) preload and also from a decrease in the LV transmural pressure (referred to as P_TM).

 

The effects of positive pressure on the ventricles are opposite in the normal heart, with a decrease in both right and LV preload, increased right ventricular afterload and decreased LV afterload,^39,40 as well as an overall decrease in cardiac chamber size that is directly proportional to the level of PPV.⁴¹ For the decompensated CHF patient, this can produce an increase in cardiac output simply by shifting the patient to a more favorable (leftward) position on the Frank-Starling curve.^42-44 

Troubleshooting

Once NIV is initiated, it is imperative, at least initially, to remain at bedside to monitor progress and improvement. Even though NIV is beneficial in the acute setting, it should always be viewed as a temporary bridging measure. With improvement, NIV may be discontinued, but in cases of failure, it is necessary to proceed with endotracheal intubation.

As the patient synchronizes with the ventilator, changes should be seen rather quickly, including improvement in the work of breathing, a restoration of mental status (if significant hypercapnia is present), and improved oxygenation. In the patient with severe uncontrolled hypertension and resulting flash pulmonary edema, the reduction in preload and afterload should contribute to a decrease in systolic BP (in addition to medical therapy). There should be a low threshold for obtaining an initial arterial blood gas (or a venous sample coupled with end-tidal CO₂ data) as it may be helpful to guide therapy. 

Noninvasive ventilation is similar to mechanical ventilation in that the clinician should not view it is as a static therapy, but rather as a dynamic process. For application of NIV in the acute setting, it should be recognized that the patient’s physiology is deranged (albeit transiently); as physiology eventually returns to preexisting levels, changes in NIV-pressure levels (or modes) are therefore necessary. Moreover, initial starting pressures may not be adequate to either overcome deficits in oxygenation, ventilation, or provide significant preload/afterload reduction. Knowledge of which parameters or values to adjust contribute to increased patient comfort, patient safety, improved cardiopulmonary dynamics, and a faster restoration of ventilatory status. In essence, the EP at the bedside should always ask himself or herself “what am I trying to fix?”  

When the patient begins to develop synchrony with the ventilator, improvement and stabilization in the measured V_T should be observed. The goal of delivered V_T should be 6 to 10 mg/kg of ideal body weight.  An increase in the IPAP value will improve the V_T and decrease the work of breathing, and it should be the first value increased to reduce PaCO₂. The use of EPAP will help to reduce intrinsic positive-end expiratory pressure and atelectasis and reduce upper airway obstruction. Increasing EPAP will improve oxygenation. Table 3 lists the common starting values for both modes of NIV and provides troubleshooting suggestions.  

To date, no clinical trials have addressed the optimal initiation strategy or application settings for NIV. It should be understood, however, that the initial settings will typically be lower pressures to ensure patient comfort and development of familiarity with the device and interaction. For BiPAP, it is common to start with settings of 10/5 (IPAP/EPAP), and then titrate up (not exceeding 25 cm H₂O) and maintaining minimum pressure support of 4 to 5 cm H₂O. For CPAP, initial settings of 5 to 10 cm H₂O are reasonable. Increased pressures can lead to patient discomfort, unintentional leak, and the development of patient-ventilator associated asynchrony.¹² The goal is to balance therapeutic effect(s) with patient comfort. Higher pressures, even though they may be optimal, must be balanced with patient comfort as long as it is physiologically acceptable.

With increasing support, there may be an increase in mask leak; despite this, increasing levels of pressure or volume ventilation have been shown to increase minute ventilation (referred to as V_E).⁴⁵ In cases such as acute pulmonary edema or significant hypercapnia, initial higher-pressure settings may only be necessary for a brief time to reverse the pathology present and restore normal ventilation and hemodynamics. After the initial application, IPAP, EPAP, and FiO₂ all may require titration.

Patients who fail to show improvement (either clinically or based on ventilatory parameters) or those with persistent mental status abnormalities, agitation, excessive secretions, or ventilator asynchrony after 1 hour of NIV are at high risk for NIV failure.^46,47

Interpreting the Literature

Sizeable and sometimes conflicting literature exists on the subject of NIV.  Despite a lack of clear and consistently reproducible benefit in morbidity, NIV use continues to increase. There are multiple factors that make interpretation of the results difficult and at times seemingly contradictory. Careful examination of the literature therefore must be undertaken before applying NIV to daily practice. Inconsistency of therapy type delivered, NIV pressure settings, pressure adjustments, patient monitoring, differing mask types, ventilator designs, endpoints, patient populations and the influence of cotreatments can all influence outcomes and potential benefit. To further complicate the data, unmeasured factors such as patient tolerance, interface fit, mask leak, and patient-ventilator asynchrony may be grouped as “NIV failure.”

 

For a patient suffering from ARF, the point in time of NIV application may have more to do with study enrollment and study group assignment (NIV or intubation) than the underlying pathology. Specifically, in some cases if NIV had been initiated hours prior, a clear benefit may have been demonstrated. One must also remember that at many institutions, the threshold for intubation (or intensive care unit admission) may be different, as well as the treating provider’s expertise and experience with NIV. In addition, well-established and consistent criteria for NIV failure have not been clearly defined and vary significantly study to study, making generalizations difficult. A comparison of patient groups with equal possible clinical outcomes is necessary to compare the findings “on a level playing field” and determine external validity. 

Conclusion

Noninvasive ventilation represents a critically important intervention—one that should be applied early and aggressively in the ED to patients presenting with ARD in whom there are no contraindications to treatment. The EP should recognize the patient at high risk and, at the time of application, continue to closely monitor him or her for signs of improvement or deterioration.

As NIV use continues to increase, it is important that the clinician have a good working knowledge of its setup, modes of operation, and potential complications. A comfort level should exist for troubleshooting at the bedside. As provider competence increases, standardized quality of care is improved.

Dr Burns is an associate professor, residency director, and vice chair of academic affairs, department of emergency medicine, The University of Oklahoma School of Community Medicine, Tulsa.

Overview

Candidates for noninvasive ventilation (NIV) most commonly present to the ED with acute respiratory failure (ARF) secondary to chronic obstructive pulmonary disease (COPD) or congestive heart-failure (CHF) exacerbations. The emergency physician (EP) must select patients appropriately, recognizing which would benefit most from NIV, as well as those with contraindications to this therapy. When indicated, early application confers benefit to the patient and can help avoid endotracheal intubation. Once therapy is initiated, clinical deterioration is still possible, and close monitoring and troubleshooting are imperative. Frequently, the clinician must make adjustments in ventilatory parameters to support the patient.

In this article, the author discusses the evidence supporting the use of NIV in appropriately selected patients with ARF, as well as review the types of NIV commonly used in the ED, the physiologic effects of positive-pressure ventilation (PPV), and how to identify and avoid common pitfalls.

Case Presentation Examples

Case 1

A 72-year-old man with a past medical history of COPD was brought to the ED by emergency medical services for evaluation of shortness of breath and wheezing. The patient’s initial oxygen (O₂) saturation was 84%, which responded to bronchodilators and supplemental O₂. At the time of arrival, he was somewhat somnolent, but aroused to verbal stimuli. A nonrebreather mask was placed delivering 15 L/minute of O₂ with a saturation of 96%. His vital signs were: blood pressure (BP), 142/76 mm Hg, heart rate, 108 beats/minute; and respiratory rate (RR), 13 breaths/minute. A cardiac monitor revealed sinus tachycardia, and a portable chest X-ray was obtained (Figure 1). On lung examination, the patient’s breath sounds were diminished in the bases with suboptimal respiratory effort and expiratory wheezes in all lung fields. Venous blood gas measurement revealed a pH of 7.25; end-tidal carbon dioxide (CO₂) was 77.

After the initial assessment, the EP considered NIV as an adjunct to improve ventilation as he suspected the patient was experiencing significant respiratory acidosis secondary to CO₂ retention. The respiratory therapist suggested NIV at 12/5 before titrating down the fraction of inspired O₂ (FiO₂) and sought approval from the EP. 

Discussion Questions: Is the above recommendation from the respiratory therapist the most appropriate therapy for this patient? What are the contraindications to this treatment and how should he be monitored to measure improvement?

Case 2

A 54-year-old woman presented to the ED for shortness of breath. On examination, she was diaphoretic and in severe distress with one- to two-word dyspnea and gasping respirations with pink-tinged sputum. Her BP was 236/158 mm Hg. A portable chest X-ray was obtained (Figure 2); rales were present with significant jugular venous distension. An electrocardiogram revealed a left-ventricular hypertrophy strain pattern but no evidence of ST-segment elevation.

During the assessment, the EP considered hypertensive emergency with resulting flash pulmonary edema as the cause of the patient’s condition; as such, he contemplated NIV to decrease the work of breathing and improve oxygenation. However, the EP had concerns regarding the preload and afterload ramifications. Although there was no respiratory therapist in the ED, the EP was able to set up the machine, but was not certain which mode of NIV or initial settings would be appropriate.

Discussion Questions: What is the protocol for proper set up to ensure a good mask fit? Once therapy is initiated, how should the EP monitor the patient? How should the EP explain this therapy to the patient and instruct her on how to work with the ventilator?

Acute-Care Application

Noninvasive ventilation refers to PPV delivered through a device such as a facemask, nasal mask, nasal plugs, or helmet. This modality was first used in the 1940s to treat respiratory failure, and its use has since grown to parallel that of mechanical ventilation.^1-3 Although the application of NIV does not represent definitive airway management, this therapy has dramatically changed the care and treatment of both chronic and ARF. It serves as a significant intervention to prevent further respiratory compromise; to reverse either existing physiologic, hemodynamic, or ventilatory derangements; and to avoid endotracheal intubation.

Modes of Delivery

In the acute setting, NIV is typically delivered via two modes. Continuous positive-airway pressure (CPAP) is delivered regardless of the phase of respiration, and noninvasive positive-pressure ventilation (NIPPV; typically referred to as bi-level positive-airway pressure [BiPAP] or BPPV) is delivered in the inspiratory and expiratory phases of the respiratory cycle. Inspiratory positive-airway pressure (IPAP) refers to an inspiratory boost that is triggered by the negative airway pressure on inspiration in a synchronous fashion. This inspiratory pressure is fixed, but the volume delivered fluctuates based on the patient’s inspiratory effort. Expiratory positive-airway pressure (EPAP) is the delivery of constant pressure during exhalation. The difference between the IPAP and EPAP is referred to as pressure support, which serves to decrease the work of breathing and improve ventilation. (A list of commonly used abbreviations, terms, and definitions are outlined in Table 1.)

 

Etiology of Respiratory Failure and Treatment Decisions
At the time of initial presentation, the exact etiology of a patient’s respiratory failure may not be known, and treatment decisions will be necessary before all relevant data are present. Patients presenting in acute respiratory distress (ARD) are often suffering from shunt physiology, in which alveoli are perfused but not ventilated due to the presence of fluid or collapse, as in pulmonary edema or COPD.⁴ Regardless of the etiology, patients will benefit from early application of NIV.⁵ Thus, the clinician must be aggressive in the application of this therapy to identify those patients who will benefit the most from treatment. All patients receiving NIV must be monitored closely as failure of therapy is still a possibility.

Patient Selection

The utilization of NIV has increased in the hospital and ED setting and it is now often initiated in the prehospital setting^6-8 with observed improvement in dyspnea scores and oxygenation with early intervention.⁹ Regarding patient selection, in the absence of contraindications (Table 2), all dyspneic patients should be considered eligible for a trial of NIV. ¹³ For some patients, this may be their first use of the therapy; as such, they are in effect learning to “swim while drowning.” The agitated and anxious patient will require coaching to provide reassurance and instruction while he or she learns to synchronize and work with the ventilator. The presence and quality of this instruction, though not previously measured, would intuitively be very helpful and an important determinant of success in the application of NIV in the naïve patient.

Common Conditions and NIV

In the ED, NIV is commonly utilized for the treatment of COPD and acute decompensated heart failure. These two conditions have been extensively studied and a robust amount of literature supports the routine use of NIV in these patients.

Chronic Obstructive Pulmonary Disease
For COPD, BiPAP has been shown and is widely accepted as the modality that confers the most benefit, with one study demonstrating a 462% increase in its use and a 42% decline in mechanical intubation rates from 1998 to 2008.¹⁴ Multiple studies have demonstrated a reduction in the intubation rate, improvement in the work of breathing, and a more rapid improvement in RR and symptoms.^15,16

Acute Decompensated Heart Failure and Pulmonary Edema
Noninvasive ventilation is used commonly for decompensated heart failure and acute cardiogenic pulmonary edema (ACPE). The rapid patient improvement with its use when compared to standard O₂ therapy is well documented. A successful trial and application of NIV demonstrated benefit in a recent retrospective analysis of 2,430 acutely decompensated heart-failure patients in the United States. The study found that the patients who were treated with NIV, but not immediately intubated, had better outcomes.¹⁷ (In these types of patients, pulmonary edema is typically not related to volume overload, but the result of imbalanced hemodynamics with markedly increased cardiac afterload and systemic vascular resistance.)

With respect to type of NIV, the use of CPAP is widely accepted as the primary modality of choice to confer the most benefit in ACPE.¹⁸ Although theoretical advantages do exist for the use of BiPAP over CPAP, this benefit has been noted in smaller studies¹⁹ but not clearly demonstrated in large reviews.^20,21 In addition, patients suffering from long-term CHF develop the syndrome of cardiac cachexia, characterized by the loss of quantity and quality of skeletal muscle.²² This reduction in muscle mass can produce a significant deficit in inspiratory muscle strength and ability, providing an opportunity for benefit with the use of BiPAP.

Previously, BiPAP was considered unsafe in the setting of ACPE due to an increase in myocardial infarction.²³ These results have not been reproduced in larger studies, and it is widely accepted that although BiPAP may not confer any benefit, it also does not increase harm.

Asthma
Because the underlying pathology of asthma differs from COPD, the current evidence for NIV use in patients presenting with an asthmatic episode is not very strong. Chronic obstructive pulmonary disease is characterized by collapse of terminal airways, with destruction of pulmonary architecture, and decreased compliance of the chest wall. In contrast, the airway obstruction in asthma progresses as the severity of the attack increases, and NIV may offer potential benefit in high-risk patients to avoid intubation.²⁴ Several small studies suggest the application of NIV for severe asthma exacerbations is reasonable, with some demonstration of improvement in the work of breathing and ventilatory status.^25-27

The Critically Ill Patient

Critically ill patients represent a high-risk group for desaturation during endotracheal intubation, and NIV should be considered for preoxygenation unless contraindications exist (Table 2). If standard high-flow O₂ without positive pressure does not improve oxygenation, the application of NIV may overcome shunt physiology, improve oxygenation, and lessen peri-intubation time with dangerous desaturation events.^4,28-30

 

Interfaces, Mask Leaks, Patient-Ventilator Interaction, and Respiratory Failure

Interfaces
Patient interfaces (mask types) for NIV include nasal prongs, full facial mask, or most commonly, an oronasal mask.³¹ For successful delivery of positive pressure, there must be an adequate fit or seal with minimal air leak to establish a ventilator circuit. Even though there is no perfect interface, patient comfort and treatment efficacy should be balanced. The interface chosen should minimize skin damage, maximize seal, and optimize patient-ventilator interface. The interfaces have straps that are used to secure the mask in place and balance the tension and stress on the skin to ensure a good seal and to avoid excess focal pressure that may result in complications such as skin breakdown, necrosis, or discomfort. Multiple interfaces and mask types have been evaluated in different acute-care situations, and it is important the clinician be familiar with the various options available for NIV interface and delivery. 

Mask Leaks
Unintentional leaks are an unavoidable reality with NIV use. The ventilators designed for NIV typically use a single-limb circuit with an intentional leak port close to the patient. This port provides resistance and, as the ventilator produces airflow, it can subsequently generate pressure. Because this leak port is incorporated into the interface, it is important to utilize the same manufacturer of the ventilator and interface to avoid interface-ventilator mismatch.³²

In some cases, unintentional leaks have been linked to asynchrony leading to increased work of breathing, ineffective delivery of breaths, and missed triggering events.³³ The goal of any chosen interface is the lowest measurable unintentional leak rate as higher values demonstrate significant variability (and inaccuracy) of measured tidal volumes (V_T).³⁴ Overtightening the mask should be avoided since it can compromise both patient comfort and increase the chance of skin necrosis or breakdown.

Patient-Ventilator Interaction
The importance of the patient-ventilator interaction and the development of synchrony between the two cannot be overstated. After initial application, the patient should be closely monitored as he or she begins to work with the ventilator. This is especially important in BiPAP.

Optimal patient-ventilator synchrony can be difficult to achieve, especially in the NIV-naïve patient with critical respiratory distress. Of note, approximately 20% to 30% of patients with ARD cannot be managed by NIV,¹¹ and asynchrony, though difficult to quantify in the acute-care setting, may contribute to this number. 

Respiratory Failure
Acute respiratory failure is caused by a change in the patient’s baseline gas exchange, resulting in an inability to provide sufficient levels of O₂ or to ventilate adequately. The etiologies of ARF are characterized into four types. 

Type I. Also referred to as hypoxemic respiratory failure, type I is the most common and is characterized by an arterial oxygen tension (PaO₂) of less than 60 mm Hg, with either normal or low levels of arterial CO₂ that is not responsive to supplemental O₂.

Type II. This type of respiratory failure is characterized by alveolar hypoventilation, with a PaCO₂ level greater than 45 mm Hg, although hypoxemia may also be present due to concomitant loss of central nervous system drive.

Type III. Failure primarily occurs in the perioperative setting where the functional residual capacity is reduced in combination with increasing atelectasis.

Type IV. Type IV ARF is secondary to circulatory failure and resolves when shock is corrected.^35,36

Regardless of the respiratory failure etiology, the patient is at risk of further deterioration and the need for endotracheal intubation.

Physiologic effects of NIV

Once the interface is secured, NIV has several important effects on both the cardiac and pulmonary systems. For this discussion, intrathoracic pressure (P_IT) is considered synonymous with mean airway pressure (P_aw).

Noninvasive ventilation improves airflow, lung volumes, and subsequent V_T while overcoming pulmonary atelectasis. The increase in lung volume is directly proportional to an increase in P_aw. This effect is only seen after overcoming airway resistance and chest wall and lung compliance. There is also an improvement in alveolar recruitment and redistribution of pulmonary blood flow³⁷ with decreased work of breathing.

With the increase in P_IT, there is decreased venous return to the right heart and a resulting decrease in cardiac preload.³⁸ In the setting of acute cardiogenic pulmonary edema (ACPE), this effect is highly favorable. However, in the volume-depleted or hemodynamically unstable patient, this may result in a drop in cardiac output and hypotension. The “normal” heart is more sensitive to preload, and the application of positive pressure can cause a significant decrease in cardiac output. Cardiac afterload is reduced through multiple mechanisms, including directly from a decreased left-ventricular (LV) preload and also from a decrease in the LV transmural pressure (referred to as P_TM).

 

The effects of positive pressure on the ventricles are opposite in the normal heart, with a decrease in both right and LV preload, increased right ventricular afterload and decreased LV afterload,^39,40 as well as an overall decrease in cardiac chamber size that is directly proportional to the level of PPV.⁴¹ For the decompensated CHF patient, this can produce an increase in cardiac output simply by shifting the patient to a more favorable (leftward) position on the Frank-Starling curve.^42-44 

Troubleshooting

Once NIV is initiated, it is imperative, at least initially, to remain at bedside to monitor progress and improvement. Even though NIV is beneficial in the acute setting, it should always be viewed as a temporary bridging measure. With improvement, NIV may be discontinued, but in cases of failure, it is necessary to proceed with endotracheal intubation.

As the patient synchronizes with the ventilator, changes should be seen rather quickly, including improvement in the work of breathing, a restoration of mental status (if significant hypercapnia is present), and improved oxygenation. In the patient with severe uncontrolled hypertension and resulting flash pulmonary edema, the reduction in preload and afterload should contribute to a decrease in systolic BP (in addition to medical therapy). There should be a low threshold for obtaining an initial arterial blood gas (or a venous sample coupled with end-tidal CO₂ data) as it may be helpful to guide therapy. 

Noninvasive ventilation is similar to mechanical ventilation in that the clinician should not view it is as a static therapy, but rather as a dynamic process. For application of NIV in the acute setting, it should be recognized that the patient’s physiology is deranged (albeit transiently); as physiology eventually returns to preexisting levels, changes in NIV-pressure levels (or modes) are therefore necessary. Moreover, initial starting pressures may not be adequate to either overcome deficits in oxygenation, ventilation, or provide significant preload/afterload reduction. Knowledge of which parameters or values to adjust contribute to increased patient comfort, patient safety, improved cardiopulmonary dynamics, and a faster restoration of ventilatory status. In essence, the EP at the bedside should always ask himself or herself “what am I trying to fix?”  

When the patient begins to develop synchrony with the ventilator, improvement and stabilization in the measured V_T should be observed. The goal of delivered V_T should be 6 to 10 mg/kg of ideal body weight.  An increase in the IPAP value will improve the V_T and decrease the work of breathing, and it should be the first value increased to reduce PaCO₂. The use of EPAP will help to reduce intrinsic positive-end expiratory pressure and atelectasis and reduce upper airway obstruction. Increasing EPAP will improve oxygenation. Table 3 lists the common starting values for both modes of NIV and provides troubleshooting suggestions.  

To date, no clinical trials have addressed the optimal initiation strategy or application settings for NIV. It should be understood, however, that the initial settings will typically be lower pressures to ensure patient comfort and development of familiarity with the device and interaction. For BiPAP, it is common to start with settings of 10/5 (IPAP/EPAP), and then titrate up (not exceeding 25 cm H₂O) and maintaining minimum pressure support of 4 to 5 cm H₂O. For CPAP, initial settings of 5 to 10 cm H₂O are reasonable. Increased pressures can lead to patient discomfort, unintentional leak, and the development of patient-ventilator associated asynchrony.¹² The goal is to balance therapeutic effect(s) with patient comfort. Higher pressures, even though they may be optimal, must be balanced with patient comfort as long as it is physiologically acceptable.

With increasing support, there may be an increase in mask leak; despite this, increasing levels of pressure or volume ventilation have been shown to increase minute ventilation (referred to as V_E).⁴⁵ In cases such as acute pulmonary edema or significant hypercapnia, initial higher-pressure settings may only be necessary for a brief time to reverse the pathology present and restore normal ventilation and hemodynamics. After the initial application, IPAP, EPAP, and FiO₂ all may require titration.

Patients who fail to show improvement (either clinically or based on ventilatory parameters) or those with persistent mental status abnormalities, agitation, excessive secretions, or ventilator asynchrony after 1 hour of NIV are at high risk for NIV failure.^46,47

Interpreting the Literature

Sizeable and sometimes conflicting literature exists on the subject of NIV.  Despite a lack of clear and consistently reproducible benefit in morbidity, NIV use continues to increase. There are multiple factors that make interpretation of the results difficult and at times seemingly contradictory. Careful examination of the literature therefore must be undertaken before applying NIV to daily practice. Inconsistency of therapy type delivered, NIV pressure settings, pressure adjustments, patient monitoring, differing mask types, ventilator designs, endpoints, patient populations and the influence of cotreatments can all influence outcomes and potential benefit. To further complicate the data, unmeasured factors such as patient tolerance, interface fit, mask leak, and patient-ventilator asynchrony may be grouped as “NIV failure.”

 

For a patient suffering from ARF, the point in time of NIV application may have more to do with study enrollment and study group assignment (NIV or intubation) than the underlying pathology. Specifically, in some cases if NIV had been initiated hours prior, a clear benefit may have been demonstrated. One must also remember that at many institutions, the threshold for intubation (or intensive care unit admission) may be different, as well as the treating provider’s expertise and experience with NIV. In addition, well-established and consistent criteria for NIV failure have not been clearly defined and vary significantly study to study, making generalizations difficult. A comparison of patient groups with equal possible clinical outcomes is necessary to compare the findings “on a level playing field” and determine external validity. 

Conclusion

Noninvasive ventilation represents a critically important intervention—one that should be applied early and aggressively in the ED to patients presenting with ARD in whom there are no contraindications to treatment. The EP should recognize the patient at high risk and, at the time of application, continue to closely monitor him or her for signs of improvement or deterioration.

As NIV use continues to increase, it is important that the clinician have a good working knowledge of its setup, modes of operation, and potential complications. A comfort level should exist for troubleshooting at the bedside. As provider competence increases, standardized quality of care is improved.

Dr Burns is an associate professor, residency director, and vice chair of academic affairs, department of emergency medicine, The University of Oklahoma School of Community Medicine, Tulsa.

Overview

Candidates for noninvasive ventilation (NIV) most commonly present to the ED with acute respiratory failure (ARF) secondary to chronic obstructive pulmonary disease (COPD) or congestive heart-failure (CHF) exacerbations. The emergency physician (EP) must select patients appropriately, recognizing which would benefit most from NIV, as well as those with contraindications to this therapy. When indicated, early application confers benefit to the patient and can help avoid endotracheal intubation. Once therapy is initiated, clinical deterioration is still possible, and close monitoring and troubleshooting are imperative. Frequently, the clinician must make adjustments in ventilatory parameters to support the patient.

In this article, the author discusses the evidence supporting the use of NIV in appropriately selected patients with ARF, as well as review the types of NIV commonly used in the ED, the physiologic effects of positive-pressure ventilation (PPV), and how to identify and avoid common pitfalls.

Case Presentation Examples

Case 1

A 72-year-old man with a past medical history of COPD was brought to the ED by emergency medical services for evaluation of shortness of breath and wheezing. The patient’s initial oxygen (O₂) saturation was 84%, which responded to bronchodilators and supplemental O₂. At the time of arrival, he was somewhat somnolent, but aroused to verbal stimuli. A nonrebreather mask was placed delivering 15 L/minute of O₂ with a saturation of 96%. His vital signs were: blood pressure (BP), 142/76 mm Hg, heart rate, 108 beats/minute; and respiratory rate (RR), 13 breaths/minute. A cardiac monitor revealed sinus tachycardia, and a portable chest X-ray was obtained (Figure 1). On lung examination, the patient’s breath sounds were diminished in the bases with suboptimal respiratory effort and expiratory wheezes in all lung fields. Venous blood gas measurement revealed a pH of 7.25; end-tidal carbon dioxide (CO₂) was 77.

After the initial assessment, the EP considered NIV as an adjunct to improve ventilation as he suspected the patient was experiencing significant respiratory acidosis secondary to CO₂ retention. The respiratory therapist suggested NIV at 12/5 before titrating down the fraction of inspired O₂ (FiO₂) and sought approval from the EP. 

Discussion Questions: Is the above recommendation from the respiratory therapist the most appropriate therapy for this patient? What are the contraindications to this treatment and how should he be monitored to measure improvement?

Case 2

A 54-year-old woman presented to the ED for shortness of breath. On examination, she was diaphoretic and in severe distress with one- to two-word dyspnea and gasping respirations with pink-tinged sputum. Her BP was 236/158 mm Hg. A portable chest X-ray was obtained (Figure 2); rales were present with significant jugular venous distension. An electrocardiogram revealed a left-ventricular hypertrophy strain pattern but no evidence of ST-segment elevation.

During the assessment, the EP considered hypertensive emergency with resulting flash pulmonary edema as the cause of the patient’s condition; as such, he contemplated NIV to decrease the work of breathing and improve oxygenation. However, the EP had concerns regarding the preload and afterload ramifications. Although there was no respiratory therapist in the ED, the EP was able to set up the machine, but was not certain which mode of NIV or initial settings would be appropriate.

Discussion Questions: What is the protocol for proper set up to ensure a good mask fit? Once therapy is initiated, how should the EP monitor the patient? How should the EP explain this therapy to the patient and instruct her on how to work with the ventilator?

Acute-Care Application

Noninvasive ventilation refers to PPV delivered through a device such as a facemask, nasal mask, nasal plugs, or helmet. This modality was first used in the 1940s to treat respiratory failure, and its use has since grown to parallel that of mechanical ventilation.^1-3 Although the application of NIV does not represent definitive airway management, this therapy has dramatically changed the care and treatment of both chronic and ARF. It serves as a significant intervention to prevent further respiratory compromise; to reverse either existing physiologic, hemodynamic, or ventilatory derangements; and to avoid endotracheal intubation.

Modes of Delivery

In the acute setting, NIV is typically delivered via two modes. Continuous positive-airway pressure (CPAP) is delivered regardless of the phase of respiration, and noninvasive positive-pressure ventilation (NIPPV; typically referred to as bi-level positive-airway pressure [BiPAP] or BPPV) is delivered in the inspiratory and expiratory phases of the respiratory cycle. Inspiratory positive-airway pressure (IPAP) refers to an inspiratory boost that is triggered by the negative airway pressure on inspiration in a synchronous fashion. This inspiratory pressure is fixed, but the volume delivered fluctuates based on the patient’s inspiratory effort. Expiratory positive-airway pressure (EPAP) is the delivery of constant pressure during exhalation. The difference between the IPAP and EPAP is referred to as pressure support, which serves to decrease the work of breathing and improve ventilation. (A list of commonly used abbreviations, terms, and definitions are outlined in Table 1.)

 

Etiology of Respiratory Failure and Treatment Decisions
At the time of initial presentation, the exact etiology of a patient’s respiratory failure may not be known, and treatment decisions will be necessary before all relevant data are present. Patients presenting in acute respiratory distress (ARD) are often suffering from shunt physiology, in which alveoli are perfused but not ventilated due to the presence of fluid or collapse, as in pulmonary edema or COPD.⁴ Regardless of the etiology, patients will benefit from early application of NIV.⁵ Thus, the clinician must be aggressive in the application of this therapy to identify those patients who will benefit the most from treatment. All patients receiving NIV must be monitored closely as failure of therapy is still a possibility.

Patient Selection

The utilization of NIV has increased in the hospital and ED setting and it is now often initiated in the prehospital setting^6-8 with observed improvement in dyspnea scores and oxygenation with early intervention.⁹ Regarding patient selection, in the absence of contraindications (Table 2), all dyspneic patients should be considered eligible for a trial of NIV. ¹³ For some patients, this may be their first use of the therapy; as such, they are in effect learning to “swim while drowning.” The agitated and anxious patient will require coaching to provide reassurance and instruction while he or she learns to synchronize and work with the ventilator. The presence and quality of this instruction, though not previously measured, would intuitively be very helpful and an important determinant of success in the application of NIV in the naïve patient.

Common Conditions and NIV

In the ED, NIV is commonly utilized for the treatment of COPD and acute decompensated heart failure. These two conditions have been extensively studied and a robust amount of literature supports the routine use of NIV in these patients.

Chronic Obstructive Pulmonary Disease
For COPD, BiPAP has been shown and is widely accepted as the modality that confers the most benefit, with one study demonstrating a 462% increase in its use and a 42% decline in mechanical intubation rates from 1998 to 2008.¹⁴ Multiple studies have demonstrated a reduction in the intubation rate, improvement in the work of breathing, and a more rapid improvement in RR and symptoms.^15,16

Acute Decompensated Heart Failure and Pulmonary Edema
Noninvasive ventilation is used commonly for decompensated heart failure and acute cardiogenic pulmonary edema (ACPE). The rapid patient improvement with its use when compared to standard O₂ therapy is well documented. A successful trial and application of NIV demonstrated benefit in a recent retrospective analysis of 2,430 acutely decompensated heart-failure patients in the United States. The study found that the patients who were treated with NIV, but not immediately intubated, had better outcomes.¹⁷ (In these types of patients, pulmonary edema is typically not related to volume overload, but the result of imbalanced hemodynamics with markedly increased cardiac afterload and systemic vascular resistance.)

With respect to type of NIV, the use of CPAP is widely accepted as the primary modality of choice to confer the most benefit in ACPE.¹⁸ Although theoretical advantages do exist for the use of BiPAP over CPAP, this benefit has been noted in smaller studies¹⁹ but not clearly demonstrated in large reviews.^20,21 In addition, patients suffering from long-term CHF develop the syndrome of cardiac cachexia, characterized by the loss of quantity and quality of skeletal muscle.²² This reduction in muscle mass can produce a significant deficit in inspiratory muscle strength and ability, providing an opportunity for benefit with the use of BiPAP.

Previously, BiPAP was considered unsafe in the setting of ACPE due to an increase in myocardial infarction.²³ These results have not been reproduced in larger studies, and it is widely accepted that although BiPAP may not confer any benefit, it also does not increase harm.

Asthma
Because the underlying pathology of asthma differs from COPD, the current evidence for NIV use in patients presenting with an asthmatic episode is not very strong. Chronic obstructive pulmonary disease is characterized by collapse of terminal airways, with destruction of pulmonary architecture, and decreased compliance of the chest wall. In contrast, the airway obstruction in asthma progresses as the severity of the attack increases, and NIV may offer potential benefit in high-risk patients to avoid intubation.²⁴ Several small studies suggest the application of NIV for severe asthma exacerbations is reasonable, with some demonstration of improvement in the work of breathing and ventilatory status.^25-27

The Critically Ill Patient

Critically ill patients represent a high-risk group for desaturation during endotracheal intubation, and NIV should be considered for preoxygenation unless contraindications exist (Table 2). If standard high-flow O₂ without positive pressure does not improve oxygenation, the application of NIV may overcome shunt physiology, improve oxygenation, and lessen peri-intubation time with dangerous desaturation events.^4,28-30

 

Interfaces, Mask Leaks, Patient-Ventilator Interaction, and Respiratory Failure

Interfaces
Patient interfaces (mask types) for NIV include nasal prongs, full facial mask, or most commonly, an oronasal mask.³¹ For successful delivery of positive pressure, there must be an adequate fit or seal with minimal air leak to establish a ventilator circuit. Even though there is no perfect interface, patient comfort and treatment efficacy should be balanced. The interface chosen should minimize skin damage, maximize seal, and optimize patient-ventilator interface. The interfaces have straps that are used to secure the mask in place and balance the tension and stress on the skin to ensure a good seal and to avoid excess focal pressure that may result in complications such as skin breakdown, necrosis, or discomfort. Multiple interfaces and mask types have been evaluated in different acute-care situations, and it is important the clinician be familiar with the various options available for NIV interface and delivery. 

Mask Leaks
Unintentional leaks are an unavoidable reality with NIV use. The ventilators designed for NIV typically use a single-limb circuit with an intentional leak port close to the patient. This port provides resistance and, as the ventilator produces airflow, it can subsequently generate pressure. Because this leak port is incorporated into the interface, it is important to utilize the same manufacturer of the ventilator and interface to avoid interface-ventilator mismatch.³²

In some cases, unintentional leaks have been linked to asynchrony leading to increased work of breathing, ineffective delivery of breaths, and missed triggering events.³³ The goal of any chosen interface is the lowest measurable unintentional leak rate as higher values demonstrate significant variability (and inaccuracy) of measured tidal volumes (V_T).³⁴ Overtightening the mask should be avoided since it can compromise both patient comfort and increase the chance of skin necrosis or breakdown.

Patient-Ventilator Interaction
The importance of the patient-ventilator interaction and the development of synchrony between the two cannot be overstated. After initial application, the patient should be closely monitored as he or she begins to work with the ventilator. This is especially important in BiPAP.

Optimal patient-ventilator synchrony can be difficult to achieve, especially in the NIV-naïve patient with critical respiratory distress. Of note, approximately 20% to 30% of patients with ARD cannot be managed by NIV,¹¹ and asynchrony, though difficult to quantify in the acute-care setting, may contribute to this number. 

Respiratory Failure
Acute respiratory failure is caused by a change in the patient’s baseline gas exchange, resulting in an inability to provide sufficient levels of O₂ or to ventilate adequately. The etiologies of ARF are characterized into four types. 

Type I. Also referred to as hypoxemic respiratory failure, type I is the most common and is characterized by an arterial oxygen tension (PaO₂) of less than 60 mm Hg, with either normal or low levels of arterial CO₂ that is not responsive to supplemental O₂.

Type II. This type of respiratory failure is characterized by alveolar hypoventilation, with a PaCO₂ level greater than 45 mm Hg, although hypoxemia may also be present due to concomitant loss of central nervous system drive.

Type III. Failure primarily occurs in the perioperative setting where the functional residual capacity is reduced in combination with increasing atelectasis.

Type IV. Type IV ARF is secondary to circulatory failure and resolves when shock is corrected.^35,36

Regardless of the respiratory failure etiology, the patient is at risk of further deterioration and the need for endotracheal intubation.

Physiologic effects of NIV

Once the interface is secured, NIV has several important effects on both the cardiac and pulmonary systems. For this discussion, intrathoracic pressure (P_IT) is considered synonymous with mean airway pressure (P_aw).

Noninvasive ventilation improves airflow, lung volumes, and subsequent V_T while overcoming pulmonary atelectasis. The increase in lung volume is directly proportional to an increase in P_aw. This effect is only seen after overcoming airway resistance and chest wall and lung compliance. There is also an improvement in alveolar recruitment and redistribution of pulmonary blood flow³⁷ with decreased work of breathing.

With the increase in P_IT, there is decreased venous return to the right heart and a resulting decrease in cardiac preload.³⁸ In the setting of acute cardiogenic pulmonary edema (ACPE), this effect is highly favorable. However, in the volume-depleted or hemodynamically unstable patient, this may result in a drop in cardiac output and hypotension. The “normal” heart is more sensitive to preload, and the application of positive pressure can cause a significant decrease in cardiac output. Cardiac afterload is reduced through multiple mechanisms, including directly from a decreased left-ventricular (LV) preload and also from a decrease in the LV transmural pressure (referred to as P_TM).

 

The effects of positive pressure on the ventricles are opposite in the normal heart, with a decrease in both right and LV preload, increased right ventricular afterload and decreased LV afterload,^39,40 as well as an overall decrease in cardiac chamber size that is directly proportional to the level of PPV.⁴¹ For the decompensated CHF patient, this can produce an increase in cardiac output simply by shifting the patient to a more favorable (leftward) position on the Frank-Starling curve.^42-44 

Troubleshooting

Once NIV is initiated, it is imperative, at least initially, to remain at bedside to monitor progress and improvement. Even though NIV is beneficial in the acute setting, it should always be viewed as a temporary bridging measure. With improvement, NIV may be discontinued, but in cases of failure, it is necessary to proceed with endotracheal intubation.

As the patient synchronizes with the ventilator, changes should be seen rather quickly, including improvement in the work of breathing, a restoration of mental status (if significant hypercapnia is present), and improved oxygenation. In the patient with severe uncontrolled hypertension and resulting flash pulmonary edema, the reduction in preload and afterload should contribute to a decrease in systolic BP (in addition to medical therapy). There should be a low threshold for obtaining an initial arterial blood gas (or a venous sample coupled with end-tidal CO₂ data) as it may be helpful to guide therapy. 

Noninvasive ventilation is similar to mechanical ventilation in that the clinician should not view it is as a static therapy, but rather as a dynamic process. For application of NIV in the acute setting, it should be recognized that the patient’s physiology is deranged (albeit transiently); as physiology eventually returns to preexisting levels, changes in NIV-pressure levels (or modes) are therefore necessary. Moreover, initial starting pressures may not be adequate to either overcome deficits in oxygenation, ventilation, or provide significant preload/afterload reduction. Knowledge of which parameters or values to adjust contribute to increased patient comfort, patient safety, improved cardiopulmonary dynamics, and a faster restoration of ventilatory status. In essence, the EP at the bedside should always ask himself or herself “what am I trying to fix?”  

When the patient begins to develop synchrony with the ventilator, improvement and stabilization in the measured V_T should be observed. The goal of delivered V_T should be 6 to 10 mg/kg of ideal body weight.  An increase in the IPAP value will improve the V_T and decrease the work of breathing, and it should be the first value increased to reduce PaCO₂. The use of EPAP will help to reduce intrinsic positive-end expiratory pressure and atelectasis and reduce upper airway obstruction. Increasing EPAP will improve oxygenation. Table 3 lists the common starting values for both modes of NIV and provides troubleshooting suggestions.  

To date, no clinical trials have addressed the optimal initiation strategy or application settings for NIV. It should be understood, however, that the initial settings will typically be lower pressures to ensure patient comfort and development of familiarity with the device and interaction. For BiPAP, it is common to start with settings of 10/5 (IPAP/EPAP), and then titrate up (not exceeding 25 cm H₂O) and maintaining minimum pressure support of 4 to 5 cm H₂O. For CPAP, initial settings of 5 to 10 cm H₂O are reasonable. Increased pressures can lead to patient discomfort, unintentional leak, and the development of patient-ventilator associated asynchrony.¹² The goal is to balance therapeutic effect(s) with patient comfort. Higher pressures, even though they may be optimal, must be balanced with patient comfort as long as it is physiologically acceptable.

With increasing support, there may be an increase in mask leak; despite this, increasing levels of pressure or volume ventilation have been shown to increase minute ventilation (referred to as V_E).⁴⁵ In cases such as acute pulmonary edema or significant hypercapnia, initial higher-pressure settings may only be necessary for a brief time to reverse the pathology present and restore normal ventilation and hemodynamics. After the initial application, IPAP, EPAP, and FiO₂ all may require titration.

Patients who fail to show improvement (either clinically or based on ventilatory parameters) or those with persistent mental status abnormalities, agitation, excessive secretions, or ventilator asynchrony after 1 hour of NIV are at high risk for NIV failure.^46,47

Interpreting the Literature

Sizeable and sometimes conflicting literature exists on the subject of NIV.  Despite a lack of clear and consistently reproducible benefit in morbidity, NIV use continues to increase. There are multiple factors that make interpretation of the results difficult and at times seemingly contradictory. Careful examination of the literature therefore must be undertaken before applying NIV to daily practice. Inconsistency of therapy type delivered, NIV pressure settings, pressure adjustments, patient monitoring, differing mask types, ventilator designs, endpoints, patient populations and the influence of cotreatments can all influence outcomes and potential benefit. To further complicate the data, unmeasured factors such as patient tolerance, interface fit, mask leak, and patient-ventilator asynchrony may be grouped as “NIV failure.”

 

For a patient suffering from ARF, the point in time of NIV application may have more to do with study enrollment and study group assignment (NIV or intubation) than the underlying pathology. Specifically, in some cases if NIV had been initiated hours prior, a clear benefit may have been demonstrated. One must also remember that at many institutions, the threshold for intubation (or intensive care unit admission) may be different, as well as the treating provider’s expertise and experience with NIV. In addition, well-established and consistent criteria for NIV failure have not been clearly defined and vary significantly study to study, making generalizations difficult. A comparison of patient groups with equal possible clinical outcomes is necessary to compare the findings “on a level playing field” and determine external validity. 

Conclusion

Noninvasive ventilation represents a critically important intervention—one that should be applied early and aggressively in the ED to patients presenting with ARD in whom there are no contraindications to treatment. The EP should recognize the patient at high risk and, at the time of application, continue to closely monitor him or her for signs of improvement or deterioration.

As NIV use continues to increase, it is important that the clinician have a good working knowledge of its setup, modes of operation, and potential complications. A comfort level should exist for troubleshooting at the bedside. As provider competence increases, standardized quality of care is improved.

Dr Burns is an associate professor, residency director, and vice chair of academic affairs, department of emergency medicine, The University of Oklahoma School of Community Medicine, Tulsa.