Marcos I. Restrepo, MD, MS

Heart failure costs the United States an excess of $30 billion annually, and costs are projected to increase to nearly $70 billion by 2030.[1] Heart failure accounts for over 1 million hospitalizations and is the leading cause of hospitalization in patients >65 years of age.[2] After hospitalization, approximately 50% of patients are readmitted within 6 months of hospital discharge.[3] Mortality rates from heart failure have improved but remain high.[4] Approximately 50% of patients diagnosed with heart failure die within 5 years, and the overall 1‐year mortality rate is 30%.[1]

Prognostic markers and scoring systems for acute decompensated heart failure (ADHF) continue to emerge, but few bedside tools are available to clinicians. Age, brain natriuretic peptide, and N‐terminal pro‐brain natriuretic peptide (NT‐proBNP) levels have been shown to correlate with postdischarge rates of readmission and mortality.[5] A study evaluating the prognostic value of a bedside inferior vena cava (IVC) ultrasound exam demonstrated that lack of improvement in IVC distention from admission to discharge was associated with higher 30‐day readmission rates.[6] Two studies using data from comprehensive transthoracic echocardiograms in heart failure patients demonstrated that a dilated, noncollapsible IVC is associated with higher risk of mortality; however, it is well recognized that obtaining comprehensive transthoracic echocardiograms in all patients hospitalized with heart failure is neither cost‐effective nor practical.[7]

In recent years, multiple studies have emerged demonstrating that noncardiologists can perform focused cardiac ultrasound exams with high reproducibility and accuracy to guide management of patients with ADHF.[8, 9, 10, 11, 12, 13, 14] However, it is unknown whether IVC characteristics from a focused cardiac ultrasound exam performed by a noncardiologist can predict mortality of patients hospitalized with ADHF. The aim of this study was to assess whether a hospitalist‐performed focused ultrasound exam to measure the IVC diameter at admission and discharge can predict mortality in a general medicine ward population hospitalized with ADHF.

METHODS

RESULTS

Outcomes

For the primary outcome of 90‐day mortality, the ROC curves showed a similar AUC for the admission IVC_max diameter (AUC: 0.69; 95% confidence interval [CI]: 0.53‐0.85), log NT‐proBNP at discharge (AUC: 0.67; 95% CI: 0.49‐0.85), and log NT‐proBNP at admission (AUC: 0.69; 95% CI: 0.52‐0.85). The optimal cutoff value for the admission IVC_max diameter to predict mortality was 1.9 cm (sensitivity 100%, specificity 38%) based on the ROC curves (see Supporting Information, Appendices 1 and 2, in the online version of this article). An admission IVC_max diameter 1.9 cm was associated with a higher mortality rate at 90 days (25.4% vs 3.4%; P = 0.009) and 180 days (29.3% vs 3.4%; P = 0.003). The Cox survival curves showed significantly lower survival rates in patients with an admission IVC_max diameter 1.9 cm (74.1 vs 96.7%; P = 0.012) (Figures 1 and 2). Based on the multivariate Cox proportional hazards regression analysis with age, IVC_max diameter, and log NT‐proBNP at admission, the admission IVC_max diameter and age were independent predictors of 90‐ and 180‐day mortality. The hazard ratios for death by age, admission IVC_max diameter, and log NT‐proBNP are shown in Table 3.

Table 3.Cox Proportional Hazards Regression Analysis

Endpoint	Variable	HR (95% CI)	P Value
NOTE: Abbreviations: CI, confidence interval; HR, hazard ratio; IVC, inferior vena cava; NT‐proBNP, N‐terminal pro‐brain natriuretic protein.
90‐day mortality	Age	1.14 (1.031.26)	0.009
	IVC diameter at admission	5.88 (1.2128.1)	0.025
	Log NT‐proBNP at admission	1.00 (1.001.00)	0.910
90‐day readmission	Age	1.06 (1.001.12)	0.025
	IVC diameter at admission	3.20 (1.248.21)	0.016
	Log NT‐proBNP at discharge	1.00 (1.001.00)	0.910
180‐day mortality	Age	1.12 (1.031.22)	0.007
	IVC diameter at admission	4.77 (1.2118.7)	0.025
	Log NT‐proBNP at admission	1.00 (1.001.00)	0.610
180‐day readmission	Age	1.06 (1.011.11)	0.009
	IVC diameter at admission	2.56 (1.145.74)	0.022
	Log NT‐proBNP at discharge	1.00 (1.001.00)	0.610

Figure 1

Figure 2

For the secondary outcome of 90‐day readmissions, 19 patients (24%) were readmitted, and the mean index admission IVC_max diameter was significantly greater in patients who were readmitted (2.36 vs 1.98 cm; P = 0.04). The ROC curves for readmission at 90 days showed that an index admission IVC_max diameter of 1.9 cm had the greatest AUC (0.61; 95% CI: 0.49‐0.74). The optimal cutoff value of an index admission IVC_max to predict readmission was also 1.9 cm (sensitivity 94%, specificity 42%) (see Supporting Information, Appendices 1 and 2, in the online version of this article). The Cox survival analysis showed that patients with an index admission IVC_max diameter 1.9 cm had a higher readmission rate at 90 days (30.8% vs 10.7%; P = 0.04) and 180 days (38.0 vs 14.3%; P = 0.02) (Figures 1 and 2). Using a multivariate Cox proportional regression analysis, the hazard ratios for the variables of age, admission IVC_max diameter, and log NT‐proBNP are shown in Table 3.

DISCUSSION

Our study found that a dilated IVC at admission is associated with a poor prognosis after hospitalization for ADHF. Patients with a dilated IVC 1.9 cm at admission had higher mortality and readmission rates at 90 and 180 days postdischarge.

The effect of a dilated IVC on mortality may be mediated through unrecognized right ventricular disease with or without significant pulmonary hypertension, supporting the notion that right heart function is an important determinant of prognosis in patients with ADHF.[30, 31] Similar to elevated jugular venous distension, bedside ultrasound examination of the IVC diameter can serve as a rapid and noninvasive measurement of right atrial pressure.[32] Elevated right atrial pressure is most often due to elevated left ventricular filling pressure transmitted via the pulmonary vasculature, but it is important to note that right‐ and left‐sided cardiac pressures are often discordant in heart failure patients.[33, 34]

Few studies have evaluated the prognostic value of IVC diameter and collapsibility in patients with heart failure. Nath et al.[24] evaluated the prognostic value of IVC diameter in stable veterans referred for outpatient echocardiography. Patients with a dilated IVC >2 cm that did not collapse with inspiration had higher 90‐day and 1‐year mortality rates. A subsequent study by Pellicori et al.[22] investigated the relationship between IVC diameter and other prognostic markers in stable cardiac patients. Pellicori et al. demonstrated that IVC diameter and serum NT‐proBNP levels were independent predictors of a composite endpoint of cardiovascular death or heart failure hospitalization at 1 year.[22] Most recently, Lee et al.[23] evaluated whether a dilated IVC in patients with a history of advanced systolic heart failure with a reduced ejection fraction of 30% and repeated hospitalizations (2) predicted worsening renal failure and adverse cardiovascular outcomes (death or hospitalization for ADHF). The study concluded that age, IVC diameter >2.1 cm, and worsening renal failure predicted cardiovascular death or hospitalization for ADHF.[23]

Our study demonstrated that an admission IVC_max 1.9 cm in hospitalized ADHF patients predicted higher postdischarge mortality at 90 and 180 days. Our findings are consistent with the above‐mentioned studies with a few important differences. First, all of our patients were hospitalized with acute decompensated heart failure. Nath et al. and Pellicori et al. evaluated stable ambulatory patients seen in an echocardiography lab and cardiology clinic, respectively. Only 12.1% of patients in the Nath study had a history of heart failure, and none were reported to have ADHF. More importantly, our study improves our understanding of patients with heart failure with a preserved ejection fraction, an important gap in the literature. The mean ejection fraction of patients in our study was 52% consistent with heart failure with preserved ejection fraction, whereas patients in the Pellicori et al. and Lee et al. studies had heart failure with reduced (42%) or severely reduced (30%) ejection fraction, respectively. We did not anticipate finding heart failure with preserved ejection fraction in the majority of patients, but our study's findings will add to our understanding of this increasingly common type of heart failure.

Compared to previous studies that utilized a registered diagnostic cardiac sonographer to obtain a comprehensive TTE to prognosticate patients, our study utilized point‐of‐care ultrasonography. Nath et al. commented that obtaining a comprehensive echocardiogram on every patient with ADHF is unlikely to be cost‐effective or feasible. Our study utilized a more realistic approach with a frontline internal medicinetrained hospitalist acquiring and interpreting images of the IVC at the bedside using a basic portable ultrasound machine.

Our study did not show that plasma natriuretic peptides levels are predictive of death or readmission after hospitalization for ADHF as shown in previous studies.[22, 35, 36] The small sample size, relatively low event rate, or predominance of heart failure with preserved ejection fraction may explain this inconsistency with prior studies.

Previous studies have reported hospital readmission rates for ADHF of 30% to 44% after 1 to 6 months.[6, 37] Goonewardena et al. showed a 41.3% readmission rate at 30 days in patients with severely reduced left ventricular ejection fraction (mean 29%), and readmitted patients had an IVC_max diameter >2 cm and an IVC collapsibility <50% on admission and discharge.[6] Carbone et al. demonstrated absence of improvement in the minimum IVC diameter from admission to discharge using hand‐carried ultrasound in patients with ischemic heart disease (ejection fraction 33%) predicted readmission at 60 days.[38] Hospital readmission rates in our study are consistent with these previously published studies. We found readmission rates for patients with ADHF and an admission IVC_max 1.9 cm to be 30.8% and 38.0% after 90 and 180 days, respectively.

Important limitations of our study are the small sample size and single institution setting. A larger sample size may have demonstrated that change in IVC diameter and NT‐proBNP levels from admission to discharge to be predictive of mortality or readmission. Further, we found an IVC_max diameter 1.9 cm to be the optimal cutoff to predict mortality, which is less than an IVC_max diameter >2.0 cm reported in other studies. The relatively smaller IVC diameter in Spanish heart failure patients may be explained by the lower body mass index of this population. An IVC_max diameter 1.9 cm was found to be the optimal cutoff to predict an elevated right atrial pressure >10 mm Hg in a study of Japanese cardiac patients with a relatively lower body mass index.[39] Another limitation is the timing of the admission IVC measurement within the first 24 hours of arrival to the hospital rather than immediately upon arrival to the emergency department. We were not able to control for interventions given in the emergency department prior to the measurement of the admission IVC, including doses of diuretics. Further, unlike the comprehensive TTEs in the United States, TTEs in Spain do not routinely include an assessment of the IVC. Therefore, we were not able to compare our bedside IVC measurements to those from a comprehensive TTE. An important limitation of our regression analysis is the inclusion of only 3 variables. The selection of variables (age, NT‐proBNP, and IVC diameter) was based on prior studies demonstrating their prognostic value.[6, 22, 25] Due to the low event rate (n = 11), we could not include in the regression model other variables that differed significantly between nonsurvivors and survivors, including NYHA class, presence of atrial fibrillation, and use of ‐blockers.

Perhaps in a larger study population the admission IVC_max diameter may not be as predictive of 90‐day mortality as other variables. The findings of our exploratory analysis should be confirmed in a future study with a larger sample size.

The clinical implications of our study are 3‐fold. First, our study demonstrates that IVC images acquired by a hospitalist at the bedside using a portable ultrasound machine can be used to predict postdischarge mortality and readmission of patients with ADHF. Second, the predominant type of heart failure in our study was heart failure with preserved ejection fraction. Currently, approximately 50% of patients hospitalized with ADHF have heart failure with preserved ejection fraction.[40] Our study adds to the understanding of prognosis of these patients whose heart failure pathophysiology is not well understood. Finally, palliative care services are underutilized in patients with advanced heart failure.[41, 42] IVC measurements and other prognostic markers in heart failure may guide discussions about goals of care with patients and families, and facilitate timely referrals for palliative care services.

CONCLUSIONS

Point‐of‐care ultrasound evaluation of IVC diameter at the time of admission can be used to prognosticate patients hospitalized with acute decompensated heart failure. An admission IVC_max diameter 1.9 cm is associated with a higher rate of 90‐day and 180‐day readmission and mortality after hospitalization. Future studies should evaluate the combination of IVC characteristics with other markers of severity of illness to prognosticate patients with heart failure.

Heart failure costs the United States an excess of $30 billion annually, and costs are projected to increase to nearly $70 billion by 2030.[1] Heart failure accounts for over 1 million hospitalizations and is the leading cause of hospitalization in patients >65 years of age.[2] After hospitalization, approximately 50% of patients are readmitted within 6 months of hospital discharge.[3] Mortality rates from heart failure have improved but remain high.[4] Approximately 50% of patients diagnosed with heart failure die within 5 years, and the overall 1‐year mortality rate is 30%.[1]

Prognostic markers and scoring systems for acute decompensated heart failure (ADHF) continue to emerge, but few bedside tools are available to clinicians. Age, brain natriuretic peptide, and N‐terminal pro‐brain natriuretic peptide (NT‐proBNP) levels have been shown to correlate with postdischarge rates of readmission and mortality.[5] A study evaluating the prognostic value of a bedside inferior vena cava (IVC) ultrasound exam demonstrated that lack of improvement in IVC distention from admission to discharge was associated with higher 30‐day readmission rates.[6] Two studies using data from comprehensive transthoracic echocardiograms in heart failure patients demonstrated that a dilated, noncollapsible IVC is associated with higher risk of mortality; however, it is well recognized that obtaining comprehensive transthoracic echocardiograms in all patients hospitalized with heart failure is neither cost‐effective nor practical.[7]

In recent years, multiple studies have emerged demonstrating that noncardiologists can perform focused cardiac ultrasound exams with high reproducibility and accuracy to guide management of patients with ADHF.[8, 9, 10, 11, 12, 13, 14] However, it is unknown whether IVC characteristics from a focused cardiac ultrasound exam performed by a noncardiologist can predict mortality of patients hospitalized with ADHF. The aim of this study was to assess whether a hospitalist‐performed focused ultrasound exam to measure the IVC diameter at admission and discharge can predict mortality in a general medicine ward population hospitalized with ADHF.

METHODS

RESULTS

Outcomes

For the primary outcome of 90‐day mortality, the ROC curves showed a similar AUC for the admission IVC_max diameter (AUC: 0.69; 95% confidence interval [CI]: 0.53‐0.85), log NT‐proBNP at discharge (AUC: 0.67; 95% CI: 0.49‐0.85), and log NT‐proBNP at admission (AUC: 0.69; 95% CI: 0.52‐0.85). The optimal cutoff value for the admission IVC_max diameter to predict mortality was 1.9 cm (sensitivity 100%, specificity 38%) based on the ROC curves (see Supporting Information, Appendices 1 and 2, in the online version of this article). An admission IVC_max diameter 1.9 cm was associated with a higher mortality rate at 90 days (25.4% vs 3.4%; P = 0.009) and 180 days (29.3% vs 3.4%; P = 0.003). The Cox survival curves showed significantly lower survival rates in patients with an admission IVC_max diameter 1.9 cm (74.1 vs 96.7%; P = 0.012) (Figures 1 and 2). Based on the multivariate Cox proportional hazards regression analysis with age, IVC_max diameter, and log NT‐proBNP at admission, the admission IVC_max diameter and age were independent predictors of 90‐ and 180‐day mortality. The hazard ratios for death by age, admission IVC_max diameter, and log NT‐proBNP are shown in Table 3.

Table 3.Cox Proportional Hazards Regression Analysis

Endpoint	Variable	HR (95% CI)	P Value
NOTE: Abbreviations: CI, confidence interval; HR, hazard ratio; IVC, inferior vena cava; NT‐proBNP, N‐terminal pro‐brain natriuretic protein.
90‐day mortality	Age	1.14 (1.031.26)	0.009
	IVC diameter at admission	5.88 (1.2128.1)	0.025
	Log NT‐proBNP at admission	1.00 (1.001.00)	0.910
90‐day readmission	Age	1.06 (1.001.12)	0.025
	IVC diameter at admission	3.20 (1.248.21)	0.016
	Log NT‐proBNP at discharge	1.00 (1.001.00)	0.910
180‐day mortality	Age	1.12 (1.031.22)	0.007
	IVC diameter at admission	4.77 (1.2118.7)	0.025
	Log NT‐proBNP at admission	1.00 (1.001.00)	0.610
180‐day readmission	Age	1.06 (1.011.11)	0.009
	IVC diameter at admission	2.56 (1.145.74)	0.022
	Log NT‐proBNP at discharge	1.00 (1.001.00)	0.610

Figure 1

Figure 2

For the secondary outcome of 90‐day readmissions, 19 patients (24%) were readmitted, and the mean index admission IVC_max diameter was significantly greater in patients who were readmitted (2.36 vs 1.98 cm; P = 0.04). The ROC curves for readmission at 90 days showed that an index admission IVC_max diameter of 1.9 cm had the greatest AUC (0.61; 95% CI: 0.49‐0.74). The optimal cutoff value of an index admission IVC_max to predict readmission was also 1.9 cm (sensitivity 94%, specificity 42%) (see Supporting Information, Appendices 1 and 2, in the online version of this article). The Cox survival analysis showed that patients with an index admission IVC_max diameter 1.9 cm had a higher readmission rate at 90 days (30.8% vs 10.7%; P = 0.04) and 180 days (38.0 vs 14.3%; P = 0.02) (Figures 1 and 2). Using a multivariate Cox proportional regression analysis, the hazard ratios for the variables of age, admission IVC_max diameter, and log NT‐proBNP are shown in Table 3.

DISCUSSION

Our study found that a dilated IVC at admission is associated with a poor prognosis after hospitalization for ADHF. Patients with a dilated IVC 1.9 cm at admission had higher mortality and readmission rates at 90 and 180 days postdischarge.

The effect of a dilated IVC on mortality may be mediated through unrecognized right ventricular disease with or without significant pulmonary hypertension, supporting the notion that right heart function is an important determinant of prognosis in patients with ADHF.[30, 31] Similar to elevated jugular venous distension, bedside ultrasound examination of the IVC diameter can serve as a rapid and noninvasive measurement of right atrial pressure.[32] Elevated right atrial pressure is most often due to elevated left ventricular filling pressure transmitted via the pulmonary vasculature, but it is important to note that right‐ and left‐sided cardiac pressures are often discordant in heart failure patients.[33, 34]

Few studies have evaluated the prognostic value of IVC diameter and collapsibility in patients with heart failure. Nath et al.[24] evaluated the prognostic value of IVC diameter in stable veterans referred for outpatient echocardiography. Patients with a dilated IVC >2 cm that did not collapse with inspiration had higher 90‐day and 1‐year mortality rates. A subsequent study by Pellicori et al.[22] investigated the relationship between IVC diameter and other prognostic markers in stable cardiac patients. Pellicori et al. demonstrated that IVC diameter and serum NT‐proBNP levels were independent predictors of a composite endpoint of cardiovascular death or heart failure hospitalization at 1 year.[22] Most recently, Lee et al.[23] evaluated whether a dilated IVC in patients with a history of advanced systolic heart failure with a reduced ejection fraction of 30% and repeated hospitalizations (2) predicted worsening renal failure and adverse cardiovascular outcomes (death or hospitalization for ADHF). The study concluded that age, IVC diameter >2.1 cm, and worsening renal failure predicted cardiovascular death or hospitalization for ADHF.[23]

Our study demonstrated that an admission IVC_max 1.9 cm in hospitalized ADHF patients predicted higher postdischarge mortality at 90 and 180 days. Our findings are consistent with the above‐mentioned studies with a few important differences. First, all of our patients were hospitalized with acute decompensated heart failure. Nath et al. and Pellicori et al. evaluated stable ambulatory patients seen in an echocardiography lab and cardiology clinic, respectively. Only 12.1% of patients in the Nath study had a history of heart failure, and none were reported to have ADHF. More importantly, our study improves our understanding of patients with heart failure with a preserved ejection fraction, an important gap in the literature. The mean ejection fraction of patients in our study was 52% consistent with heart failure with preserved ejection fraction, whereas patients in the Pellicori et al. and Lee et al. studies had heart failure with reduced (42%) or severely reduced (30%) ejection fraction, respectively. We did not anticipate finding heart failure with preserved ejection fraction in the majority of patients, but our study's findings will add to our understanding of this increasingly common type of heart failure.

Compared to previous studies that utilized a registered diagnostic cardiac sonographer to obtain a comprehensive TTE to prognosticate patients, our study utilized point‐of‐care ultrasonography. Nath et al. commented that obtaining a comprehensive echocardiogram on every patient with ADHF is unlikely to be cost‐effective or feasible. Our study utilized a more realistic approach with a frontline internal medicinetrained hospitalist acquiring and interpreting images of the IVC at the bedside using a basic portable ultrasound machine.

Our study did not show that plasma natriuretic peptides levels are predictive of death or readmission after hospitalization for ADHF as shown in previous studies.[22, 35, 36] The small sample size, relatively low event rate, or predominance of heart failure with preserved ejection fraction may explain this inconsistency with prior studies.

Previous studies have reported hospital readmission rates for ADHF of 30% to 44% after 1 to 6 months.[6, 37] Goonewardena et al. showed a 41.3% readmission rate at 30 days in patients with severely reduced left ventricular ejection fraction (mean 29%), and readmitted patients had an IVC_max diameter >2 cm and an IVC collapsibility <50% on admission and discharge.[6] Carbone et al. demonstrated absence of improvement in the minimum IVC diameter from admission to discharge using hand‐carried ultrasound in patients with ischemic heart disease (ejection fraction 33%) predicted readmission at 60 days.[38] Hospital readmission rates in our study are consistent with these previously published studies. We found readmission rates for patients with ADHF and an admission IVC_max 1.9 cm to be 30.8% and 38.0% after 90 and 180 days, respectively.

Important limitations of our study are the small sample size and single institution setting. A larger sample size may have demonstrated that change in IVC diameter and NT‐proBNP levels from admission to discharge to be predictive of mortality or readmission. Further, we found an IVC_max diameter 1.9 cm to be the optimal cutoff to predict mortality, which is less than an IVC_max diameter >2.0 cm reported in other studies. The relatively smaller IVC diameter in Spanish heart failure patients may be explained by the lower body mass index of this population. An IVC_max diameter 1.9 cm was found to be the optimal cutoff to predict an elevated right atrial pressure >10 mm Hg in a study of Japanese cardiac patients with a relatively lower body mass index.[39] Another limitation is the timing of the admission IVC measurement within the first 24 hours of arrival to the hospital rather than immediately upon arrival to the emergency department. We were not able to control for interventions given in the emergency department prior to the measurement of the admission IVC, including doses of diuretics. Further, unlike the comprehensive TTEs in the United States, TTEs in Spain do not routinely include an assessment of the IVC. Therefore, we were not able to compare our bedside IVC measurements to those from a comprehensive TTE. An important limitation of our regression analysis is the inclusion of only 3 variables. The selection of variables (age, NT‐proBNP, and IVC diameter) was based on prior studies demonstrating their prognostic value.[6, 22, 25] Due to the low event rate (n = 11), we could not include in the regression model other variables that differed significantly between nonsurvivors and survivors, including NYHA class, presence of atrial fibrillation, and use of ‐blockers.

Perhaps in a larger study population the admission IVC_max diameter may not be as predictive of 90‐day mortality as other variables. The findings of our exploratory analysis should be confirmed in a future study with a larger sample size.

The clinical implications of our study are 3‐fold. First, our study demonstrates that IVC images acquired by a hospitalist at the bedside using a portable ultrasound machine can be used to predict postdischarge mortality and readmission of patients with ADHF. Second, the predominant type of heart failure in our study was heart failure with preserved ejection fraction. Currently, approximately 50% of patients hospitalized with ADHF have heart failure with preserved ejection fraction.[40] Our study adds to the understanding of prognosis of these patients whose heart failure pathophysiology is not well understood. Finally, palliative care services are underutilized in patients with advanced heart failure.[41, 42] IVC measurements and other prognostic markers in heart failure may guide discussions about goals of care with patients and families, and facilitate timely referrals for palliative care services.

CONCLUSIONS

Point‐of‐care ultrasound evaluation of IVC diameter at the time of admission can be used to prognosticate patients hospitalized with acute decompensated heart failure. An admission IVC_max diameter 1.9 cm is associated with a higher rate of 90‐day and 180‐day readmission and mortality after hospitalization. Future studies should evaluate the combination of IVC characteristics with other markers of severity of illness to prognosticate patients with heart failure.

Heart failure costs the United States an excess of $30 billion annually, and costs are projected to increase to nearly $70 billion by 2030.[1] Heart failure accounts for over 1 million hospitalizations and is the leading cause of hospitalization in patients >65 years of age.[2] After hospitalization, approximately 50% of patients are readmitted within 6 months of hospital discharge.[3] Mortality rates from heart failure have improved but remain high.[4] Approximately 50% of patients diagnosed with heart failure die within 5 years, and the overall 1‐year mortality rate is 30%.[1]

Prognostic markers and scoring systems for acute decompensated heart failure (ADHF) continue to emerge, but few bedside tools are available to clinicians. Age, brain natriuretic peptide, and N‐terminal pro‐brain natriuretic peptide (NT‐proBNP) levels have been shown to correlate with postdischarge rates of readmission and mortality.[5] A study evaluating the prognostic value of a bedside inferior vena cava (IVC) ultrasound exam demonstrated that lack of improvement in IVC distention from admission to discharge was associated with higher 30‐day readmission rates.[6] Two studies using data from comprehensive transthoracic echocardiograms in heart failure patients demonstrated that a dilated, noncollapsible IVC is associated with higher risk of mortality; however, it is well recognized that obtaining comprehensive transthoracic echocardiograms in all patients hospitalized with heart failure is neither cost‐effective nor practical.[7]

In recent years, multiple studies have emerged demonstrating that noncardiologists can perform focused cardiac ultrasound exams with high reproducibility and accuracy to guide management of patients with ADHF.[8, 9, 10, 11, 12, 13, 14] However, it is unknown whether IVC characteristics from a focused cardiac ultrasound exam performed by a noncardiologist can predict mortality of patients hospitalized with ADHF. The aim of this study was to assess whether a hospitalist‐performed focused ultrasound exam to measure the IVC diameter at admission and discharge can predict mortality in a general medicine ward population hospitalized with ADHF.

METHODS

RESULTS

Outcomes

For the primary outcome of 90‐day mortality, the ROC curves showed a similar AUC for the admission IVC_max diameter (AUC: 0.69; 95% confidence interval [CI]: 0.53‐0.85), log NT‐proBNP at discharge (AUC: 0.67; 95% CI: 0.49‐0.85), and log NT‐proBNP at admission (AUC: 0.69; 95% CI: 0.52‐0.85). The optimal cutoff value for the admission IVC_max diameter to predict mortality was 1.9 cm (sensitivity 100%, specificity 38%) based on the ROC curves (see Supporting Information, Appendices 1 and 2, in the online version of this article). An admission IVC_max diameter 1.9 cm was associated with a higher mortality rate at 90 days (25.4% vs 3.4%; P = 0.009) and 180 days (29.3% vs 3.4%; P = 0.003). The Cox survival curves showed significantly lower survival rates in patients with an admission IVC_max diameter 1.9 cm (74.1 vs 96.7%; P = 0.012) (Figures 1 and 2). Based on the multivariate Cox proportional hazards regression analysis with age, IVC_max diameter, and log NT‐proBNP at admission, the admission IVC_max diameter and age were independent predictors of 90‐ and 180‐day mortality. The hazard ratios for death by age, admission IVC_max diameter, and log NT‐proBNP are shown in Table 3.

Table 3.Cox Proportional Hazards Regression Analysis

Endpoint	Variable	HR (95% CI)	P Value
NOTE: Abbreviations: CI, confidence interval; HR, hazard ratio; IVC, inferior vena cava; NT‐proBNP, N‐terminal pro‐brain natriuretic protein.
90‐day mortality	Age	1.14 (1.031.26)	0.009
	IVC diameter at admission	5.88 (1.2128.1)	0.025
	Log NT‐proBNP at admission	1.00 (1.001.00)	0.910
90‐day readmission	Age	1.06 (1.001.12)	0.025
	IVC diameter at admission	3.20 (1.248.21)	0.016
	Log NT‐proBNP at discharge	1.00 (1.001.00)	0.910
180‐day mortality	Age	1.12 (1.031.22)	0.007
	IVC diameter at admission	4.77 (1.2118.7)	0.025
	Log NT‐proBNP at admission	1.00 (1.001.00)	0.610
180‐day readmission	Age	1.06 (1.011.11)	0.009
	IVC diameter at admission	2.56 (1.145.74)	0.022
	Log NT‐proBNP at discharge	1.00 (1.001.00)	0.610

Figure 1

Figure 2

For the secondary outcome of 90‐day readmissions, 19 patients (24%) were readmitted, and the mean index admission IVC_max diameter was significantly greater in patients who were readmitted (2.36 vs 1.98 cm; P = 0.04). The ROC curves for readmission at 90 days showed that an index admission IVC_max diameter of 1.9 cm had the greatest AUC (0.61; 95% CI: 0.49‐0.74). The optimal cutoff value of an index admission IVC_max to predict readmission was also 1.9 cm (sensitivity 94%, specificity 42%) (see Supporting Information, Appendices 1 and 2, in the online version of this article). The Cox survival analysis showed that patients with an index admission IVC_max diameter 1.9 cm had a higher readmission rate at 90 days (30.8% vs 10.7%; P = 0.04) and 180 days (38.0 vs 14.3%; P = 0.02) (Figures 1 and 2). Using a multivariate Cox proportional regression analysis, the hazard ratios for the variables of age, admission IVC_max diameter, and log NT‐proBNP are shown in Table 3.

DISCUSSION

Our study found that a dilated IVC at admission is associated with a poor prognosis after hospitalization for ADHF. Patients with a dilated IVC 1.9 cm at admission had higher mortality and readmission rates at 90 and 180 days postdischarge.

The effect of a dilated IVC on mortality may be mediated through unrecognized right ventricular disease with or without significant pulmonary hypertension, supporting the notion that right heart function is an important determinant of prognosis in patients with ADHF.[30, 31] Similar to elevated jugular venous distension, bedside ultrasound examination of the IVC diameter can serve as a rapid and noninvasive measurement of right atrial pressure.[32] Elevated right atrial pressure is most often due to elevated left ventricular filling pressure transmitted via the pulmonary vasculature, but it is important to note that right‐ and left‐sided cardiac pressures are often discordant in heart failure patients.[33, 34]

Few studies have evaluated the prognostic value of IVC diameter and collapsibility in patients with heart failure. Nath et al.[24] evaluated the prognostic value of IVC diameter in stable veterans referred for outpatient echocardiography. Patients with a dilated IVC >2 cm that did not collapse with inspiration had higher 90‐day and 1‐year mortality rates. A subsequent study by Pellicori et al.[22] investigated the relationship between IVC diameter and other prognostic markers in stable cardiac patients. Pellicori et al. demonstrated that IVC diameter and serum NT‐proBNP levels were independent predictors of a composite endpoint of cardiovascular death or heart failure hospitalization at 1 year.[22] Most recently, Lee et al.[23] evaluated whether a dilated IVC in patients with a history of advanced systolic heart failure with a reduced ejection fraction of 30% and repeated hospitalizations (2) predicted worsening renal failure and adverse cardiovascular outcomes (death or hospitalization for ADHF). The study concluded that age, IVC diameter >2.1 cm, and worsening renal failure predicted cardiovascular death or hospitalization for ADHF.[23]

Our study demonstrated that an admission IVC_max 1.9 cm in hospitalized ADHF patients predicted higher postdischarge mortality at 90 and 180 days. Our findings are consistent with the above‐mentioned studies with a few important differences. First, all of our patients were hospitalized with acute decompensated heart failure. Nath et al. and Pellicori et al. evaluated stable ambulatory patients seen in an echocardiography lab and cardiology clinic, respectively. Only 12.1% of patients in the Nath study had a history of heart failure, and none were reported to have ADHF. More importantly, our study improves our understanding of patients with heart failure with a preserved ejection fraction, an important gap in the literature. The mean ejection fraction of patients in our study was 52% consistent with heart failure with preserved ejection fraction, whereas patients in the Pellicori et al. and Lee et al. studies had heart failure with reduced (42%) or severely reduced (30%) ejection fraction, respectively. We did not anticipate finding heart failure with preserved ejection fraction in the majority of patients, but our study's findings will add to our understanding of this increasingly common type of heart failure.

Compared to previous studies that utilized a registered diagnostic cardiac sonographer to obtain a comprehensive TTE to prognosticate patients, our study utilized point‐of‐care ultrasonography. Nath et al. commented that obtaining a comprehensive echocardiogram on every patient with ADHF is unlikely to be cost‐effective or feasible. Our study utilized a more realistic approach with a frontline internal medicinetrained hospitalist acquiring and interpreting images of the IVC at the bedside using a basic portable ultrasound machine.

Our study did not show that plasma natriuretic peptides levels are predictive of death or readmission after hospitalization for ADHF as shown in previous studies.[22, 35, 36] The small sample size, relatively low event rate, or predominance of heart failure with preserved ejection fraction may explain this inconsistency with prior studies.

Previous studies have reported hospital readmission rates for ADHF of 30% to 44% after 1 to 6 months.[6, 37] Goonewardena et al. showed a 41.3% readmission rate at 30 days in patients with severely reduced left ventricular ejection fraction (mean 29%), and readmitted patients had an IVC_max diameter >2 cm and an IVC collapsibility <50% on admission and discharge.[6] Carbone et al. demonstrated absence of improvement in the minimum IVC diameter from admission to discharge using hand‐carried ultrasound in patients with ischemic heart disease (ejection fraction 33%) predicted readmission at 60 days.[38] Hospital readmission rates in our study are consistent with these previously published studies. We found readmission rates for patients with ADHF and an admission IVC_max 1.9 cm to be 30.8% and 38.0% after 90 and 180 days, respectively.

Important limitations of our study are the small sample size and single institution setting. A larger sample size may have demonstrated that change in IVC diameter and NT‐proBNP levels from admission to discharge to be predictive of mortality or readmission. Further, we found an IVC_max diameter 1.9 cm to be the optimal cutoff to predict mortality, which is less than an IVC_max diameter >2.0 cm reported in other studies. The relatively smaller IVC diameter in Spanish heart failure patients may be explained by the lower body mass index of this population. An IVC_max diameter 1.9 cm was found to be the optimal cutoff to predict an elevated right atrial pressure >10 mm Hg in a study of Japanese cardiac patients with a relatively lower body mass index.[39] Another limitation is the timing of the admission IVC measurement within the first 24 hours of arrival to the hospital rather than immediately upon arrival to the emergency department. We were not able to control for interventions given in the emergency department prior to the measurement of the admission IVC, including doses of diuretics. Further, unlike the comprehensive TTEs in the United States, TTEs in Spain do not routinely include an assessment of the IVC. Therefore, we were not able to compare our bedside IVC measurements to those from a comprehensive TTE. An important limitation of our regression analysis is the inclusion of only 3 variables. The selection of variables (age, NT‐proBNP, and IVC diameter) was based on prior studies demonstrating their prognostic value.[6, 22, 25] Due to the low event rate (n = 11), we could not include in the regression model other variables that differed significantly between nonsurvivors and survivors, including NYHA class, presence of atrial fibrillation, and use of ‐blockers.

Perhaps in a larger study population the admission IVC_max diameter may not be as predictive of 90‐day mortality as other variables. The findings of our exploratory analysis should be confirmed in a future study with a larger sample size.

The clinical implications of our study are 3‐fold. First, our study demonstrates that IVC images acquired by a hospitalist at the bedside using a portable ultrasound machine can be used to predict postdischarge mortality and readmission of patients with ADHF. Second, the predominant type of heart failure in our study was heart failure with preserved ejection fraction. Currently, approximately 50% of patients hospitalized with ADHF have heart failure with preserved ejection fraction.[40] Our study adds to the understanding of prognosis of these patients whose heart failure pathophysiology is not well understood. Finally, palliative care services are underutilized in patients with advanced heart failure.[41, 42] IVC measurements and other prognostic markers in heart failure may guide discussions about goals of care with patients and families, and facilitate timely referrals for palliative care services.

CONCLUSIONS

Point‐of‐care ultrasound evaluation of IVC diameter at the time of admission can be used to prognosticate patients hospitalized with acute decompensated heart failure. An admission IVC_max diameter 1.9 cm is associated with a higher rate of 90‐day and 180‐day readmission and mortality after hospitalization. Future studies should evaluate the combination of IVC characteristics with other markers of severity of illness to prognosticate patients with heart failure.

Hospitalists commonly encounter pleural effusions, and their detection and characterization by point‐of‐care ultrasound can guide management. Approximately 44% to 57% of hospitalized patients with bacterial pneumonia,[1, 2] and up to 62% of intensive care unit (ICU) patients[3] have a pleural effusion. For patients with a parapneumonic effusion, hospitalists can use ultrasound to quantify and characterize pleural fluid to determine whether diagnostic or therapeutic drainage is indicated, as well as guide performance of thoracentesis. For patients with lung cancer, detection of a malignant pleural effusion changes staging to stage IV, regardless of tumor size or lymph node involvement, and hospitalists may discuss more appropriate treatment options with patients and consultants.

Routine use of pleural ultrasonography may help hospitalists provide high‐value care by reducing ancillary testing, including computerized tomography (CT) scans that expose patients to ionizing radiation, and reducing complications of thoracentesis. However, many hospitalists may not be familiar with the use of point‐of‐care ultrasound. A national survey in 2012 revealed only 25% of internal medicine residencies have formal curricula to teach point‐of‐care ultrasonography.[4] The purpose of this review is to provide an overview of how point‐of‐care ultrasound can be utilized by hospitalists in the care of patients with pleural effusions. We review the literature on the diagnosis and evaluation of pleural effusions with ultrasound, as well as techniques to examine and drain the pleural space.

DIAGNOSIS OF PLEURAL EFFUSION

PLEURAL ULTRASOUND EXAMINATION

A pleural ultrasound exam may be performed as part of a complete lung ultrasound exam, such as the BLUE (Bedside Lung Ultrasound in Emergency) protocol,[27] or a focused exam to evaluate a suspected or known pleural effusion seen on chest radiograph or CT scan.[27] Free‐flowing pleural effusions accumulate in the most dependent portions of the thorax, most commonly, the posterolateral costophrenic recesses in semirecumbent or seated patients, but anteriorly in mechanically ventilated patients in a prone position.

A low‐frequency (25 MHz) phased‐array transducer is generally preferred for imaging in between the ribs. High‐frequency linear transducers do not provide adequate penetration to visualize deep structures, but do provide superior visualization of the pleural line to assess pleural thickness, measure pleural depth, and evaluate for pneumothorax.

Pleural effusions are best evaluated starting at the level of the diaphragm. Place the transducer in a longitudinal plane on the posterior axillary line at the level of the diaphragm with the transducer orientation marker (notch) pointed cephalad (Figure 1). Five structures must be definitively identified to diagnose a pleural effusion: liver/spleen, diaphragm, pleural fluid, lung, and chest wall (Figure 2A). Large pleural effusions compress the adjacent lung causing atelectasis, which gives the lung a tissue‐like echogenicity similar to the liver (Figure 2B). Static air bronchograms are commonly seen in atelectatic lung bases with pleural effusions.[28]

Figure 1

Figure 2

Color flow Doppler and M‐mode ultrasound may be utilized as adjuncts to routine 2‐dimensional ultrasonography. Free‐flowing pleural effusions will demonstrate flow by color Doppler (Figure 3A). Using M‐mode ultrasound, the lung can been seen moving within a pleural effusion to and from the chest wall (sinusoid sign).[29] Absence of flow or movement is seen with dense pleural loculations, pleural thickening, and peripheral lung or pleural masses (Figure 3B).

Figure 3

CHARACTERIZATION OF PLEURAL EFFUSION

Simple Versus Complex Effusions

Based on its sonographic appearance, pleural effusions are categorized as simple or complex. Simple pleural effusions are anechoic and usually transudative. Complex pleural effusions are subcategorized as homogeneously or heterogeneously echogenic, with or without septations, and are more often exudative.[33]

Effusions with heterogeneous echogenicity with swirling echoes suggest high cellular content that is often associated with malignancy.[34] Fibrinous stranding, septations, and loculations also suggest an exudative effusion (Figure 4A), and are more readily identified and characterized on lung ultrasound than CT scan.[35]

Figure 4

Homogenously echogenic effusions are most often due to hemothorax or empyema.[36] The high cell count of a hemothorax creates a layering effect in costophrenic recesses (hematocrit sign). Empyemas develop from complex effusions that organize into collections of pus and usually have a homogeneously echogenic, speckled appearance (Figure 4B). Sonographic evidence of septations in the presence of empyema predicts the need for intrapleural fibrinolytic therapy, longer duration of drainage, and possible surgical intervention.[37]

Isolated dense loculations may be challenging to differentiate from peripheral lung or pleural lesions, such as abscess or tumor.

PLEURAL FLUID DRAINAGE

Since its first description in 1967, use of ultrasound guidance for thoracentesis has evolved to become the standard of care in many hospitals in the United States.[41] The British Thoracic Society guidelines recommend that all thoracenteses be performed with ultrasound guidance.[42] The American College of Graduate Medical Education now requires proficiency in the use of ultrasound for thoracentesis and pleural catheter insertion by pulmonary and critical care fellows.[43]

The impetus for these recommendations stems from increased procedural success and decreased complications associated with ultrasound‐guided drainage of pleural effusions. A study evaluating thoracentesis site selection based on physical exam and chest radiographs demonstrated inaccurate site selection in 15% of patients, and use of ultrasound for site selection prevented possible accidental organ puncture in 10% of all cases.[44] The success rate of thoracentesis for small pleural effusions has been shown to increase from 66% to 90% with ultrasound guidance.[42] Using ultrasound, the distance from the skin to parietal and visceral pleura can be measured to determine whether thoracentesis can be safely performed, and to guide selection of an adequate length needle (Figure 5). A minimum pleural effusion depth of 1.5 cm between the visceral and parietal pleura has been recommended to perform diagnostic thoracentesis.[28] Diagnostic thoracentesis of complex septated pleural effusions or empyemas may be performed with a straight needle, but therapeutic drainage often requires temporary insertion of a catheter. Traditionally, large‐bore chest tubes (>24 F) had been advocated to drain viscid pus, but recent evidence suggests that small‐bore catheters (1014 F) with instillation of thrombolytics may be as effective and performed with less discomfort.[45] Video‐assisted thoracoscopy to lyse septations and evacuate infected materials is indicated when chest tube drainage has failed.

Figure 5

The most common complication of pleural drainage is pneumothorax. A meta‐analysis demonstrated a reduction in post‐thoracentesis pneumothorax rates from 9% to 4% with use of ultrasound.[46] Transporting patients to radiology for ultrasound marking has not been shown to decrease pneumothorax rates compared to thoracentesis without ultrasound guidance, likely due to changes in patient position and prolonged delays between marking and drainage.[47] Postprocedure pneumothorax can be ruled out if lung sliding is visualized. A meta‐analysis demonstrated superior sensitivity and similar specificity of pleural ultrasonography versus chest radiography to detect pneumothorax (sensitivity 91% vs 50% and specificity 98% vs 99%, respectively).[48] Real‐time ultrasound guidance for thoracentesis, or use of ultrasound to track the needle tip, has not been well studied but may be performed by experienced proceduralists to drain small effusions.

FUTURE RESEARCH

Future research should focus on the clinical effectiveness of point‐of‐care pleural ultrasonography when integrated with other diagnostic tools, and application of new ultrasound technologies to evaluate pleural diseases. Routine use of point‐of‐care ultrasound as the primary imaging modality in a medical ICU demonstrated a highly statistically significant reduction in chest x‐rays (3.75 vs 0.82, P < 0.0001) and chest CT scans (0.10 vs 0.04, P = 0.0007).[49] Similar studies have yet to be performed with the use of ultrasound specifically in the management of pleural diseases. Thus, clinical effectiveness studies are needed to assess the impact of routine use of pleural ultrasound on the initiation of appropriate therapies, length of stay, and costs in the management of pleural disease.

Point‐of‐care pleural ultrasound findings need to be evaluated in the context of other clinical findings and diagnostic tests. Certain ultrasound findings have been associated with exudative pleural effusions, but whether exudative and transudative effusions can be differentiated noninvasively using ultrasound findings alone, or in combination with other clinical data, warrants investigation. Similar to severity of illness scores, models that incorporate clinical, laboratory, and ultrasound findings need to be developed to guide treatment decisions, such as type of drainage procedure, as well as prognostication.

Finally, new technologies may advance the utility of point‐of‐care pleural ultrasonography. Even though 3‐dimensional ultrasonography has been available for over 2 decades, comparative studies of conventional 2‐dimensional versus 3‐dimensional ultrasonography to characterize pleural effusions have yet to be performed. Furthermore, computer‐aided detection has been shown to facilitate interpretation of ultrasound images, but this technology has yet to be applied to pleural ultrasonography.

CONCLUSIONS

Point‐of‐care pleural ultrasound is a powerful bedside tool in the hospitalist's armamentarium that is superior to physical examination and chest radiographs in the detection and characterization of pleural effusions. Furthermore, ultrasound performs similarly when compared to CT scans but offers the advantages of decreased cost, avoidance of ionizing radiation, and availability at the bedside. Ultrasound guidance reduces complications and increases the success rate of pleural drainage procedures, leading to improved patient safety. As clinical effectiveness studies emerge revealing its true value, point‐of‐care pleural ultrasonography is likely to become the standard diagnostic tool to evaluate and manage patients with pleural effusions.

Disclosures: Dr. Restrepo is partially supported by award number K23HL096054 from the National Heart, Lung, and Blood Institute. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Heart, Lung, and Blood Institute or the National Institutes of Health. The authors report no conflicts of interest.

Hospitalists commonly encounter pleural effusions, and their detection and characterization by point‐of‐care ultrasound can guide management. Approximately 44% to 57% of hospitalized patients with bacterial pneumonia,[1, 2] and up to 62% of intensive care unit (ICU) patients[3] have a pleural effusion. For patients with a parapneumonic effusion, hospitalists can use ultrasound to quantify and characterize pleural fluid to determine whether diagnostic or therapeutic drainage is indicated, as well as guide performance of thoracentesis. For patients with lung cancer, detection of a malignant pleural effusion changes staging to stage IV, regardless of tumor size or lymph node involvement, and hospitalists may discuss more appropriate treatment options with patients and consultants.

Routine use of pleural ultrasonography may help hospitalists provide high‐value care by reducing ancillary testing, including computerized tomography (CT) scans that expose patients to ionizing radiation, and reducing complications of thoracentesis. However, many hospitalists may not be familiar with the use of point‐of‐care ultrasound. A national survey in 2012 revealed only 25% of internal medicine residencies have formal curricula to teach point‐of‐care ultrasonography.[4] The purpose of this review is to provide an overview of how point‐of‐care ultrasound can be utilized by hospitalists in the care of patients with pleural effusions. We review the literature on the diagnosis and evaluation of pleural effusions with ultrasound, as well as techniques to examine and drain the pleural space.

DIAGNOSIS OF PLEURAL EFFUSION

PLEURAL ULTRASOUND EXAMINATION

A pleural ultrasound exam may be performed as part of a complete lung ultrasound exam, such as the BLUE (Bedside Lung Ultrasound in Emergency) protocol,[27] or a focused exam to evaluate a suspected or known pleural effusion seen on chest radiograph or CT scan.[27] Free‐flowing pleural effusions accumulate in the most dependent portions of the thorax, most commonly, the posterolateral costophrenic recesses in semirecumbent or seated patients, but anteriorly in mechanically ventilated patients in a prone position.

A low‐frequency (25 MHz) phased‐array transducer is generally preferred for imaging in between the ribs. High‐frequency linear transducers do not provide adequate penetration to visualize deep structures, but do provide superior visualization of the pleural line to assess pleural thickness, measure pleural depth, and evaluate for pneumothorax.

Pleural effusions are best evaluated starting at the level of the diaphragm. Place the transducer in a longitudinal plane on the posterior axillary line at the level of the diaphragm with the transducer orientation marker (notch) pointed cephalad (Figure 1). Five structures must be definitively identified to diagnose a pleural effusion: liver/spleen, diaphragm, pleural fluid, lung, and chest wall (Figure 2A). Large pleural effusions compress the adjacent lung causing atelectasis, which gives the lung a tissue‐like echogenicity similar to the liver (Figure 2B). Static air bronchograms are commonly seen in atelectatic lung bases with pleural effusions.[28]

Figure 1

Figure 2

Color flow Doppler and M‐mode ultrasound may be utilized as adjuncts to routine 2‐dimensional ultrasonography. Free‐flowing pleural effusions will demonstrate flow by color Doppler (Figure 3A). Using M‐mode ultrasound, the lung can been seen moving within a pleural effusion to and from the chest wall (sinusoid sign).[29] Absence of flow or movement is seen with dense pleural loculations, pleural thickening, and peripheral lung or pleural masses (Figure 3B).

Figure 3

CHARACTERIZATION OF PLEURAL EFFUSION

Simple Versus Complex Effusions

Based on its sonographic appearance, pleural effusions are categorized as simple or complex. Simple pleural effusions are anechoic and usually transudative. Complex pleural effusions are subcategorized as homogeneously or heterogeneously echogenic, with or without septations, and are more often exudative.[33]

Effusions with heterogeneous echogenicity with swirling echoes suggest high cellular content that is often associated with malignancy.[34] Fibrinous stranding, septations, and loculations also suggest an exudative effusion (Figure 4A), and are more readily identified and characterized on lung ultrasound than CT scan.[35]

Figure 4

Homogenously echogenic effusions are most often due to hemothorax or empyema.[36] The high cell count of a hemothorax creates a layering effect in costophrenic recesses (hematocrit sign). Empyemas develop from complex effusions that organize into collections of pus and usually have a homogeneously echogenic, speckled appearance (Figure 4B). Sonographic evidence of septations in the presence of empyema predicts the need for intrapleural fibrinolytic therapy, longer duration of drainage, and possible surgical intervention.[37]

Isolated dense loculations may be challenging to differentiate from peripheral lung or pleural lesions, such as abscess or tumor.

PLEURAL FLUID DRAINAGE

Since its first description in 1967, use of ultrasound guidance for thoracentesis has evolved to become the standard of care in many hospitals in the United States.[41] The British Thoracic Society guidelines recommend that all thoracenteses be performed with ultrasound guidance.[42] The American College of Graduate Medical Education now requires proficiency in the use of ultrasound for thoracentesis and pleural catheter insertion by pulmonary and critical care fellows.[43]

The impetus for these recommendations stems from increased procedural success and decreased complications associated with ultrasound‐guided drainage of pleural effusions. A study evaluating thoracentesis site selection based on physical exam and chest radiographs demonstrated inaccurate site selection in 15% of patients, and use of ultrasound for site selection prevented possible accidental organ puncture in 10% of all cases.[44] The success rate of thoracentesis for small pleural effusions has been shown to increase from 66% to 90% with ultrasound guidance.[42] Using ultrasound, the distance from the skin to parietal and visceral pleura can be measured to determine whether thoracentesis can be safely performed, and to guide selection of an adequate length needle (Figure 5). A minimum pleural effusion depth of 1.5 cm between the visceral and parietal pleura has been recommended to perform diagnostic thoracentesis.[28] Diagnostic thoracentesis of complex septated pleural effusions or empyemas may be performed with a straight needle, but therapeutic drainage often requires temporary insertion of a catheter. Traditionally, large‐bore chest tubes (>24 F) had been advocated to drain viscid pus, but recent evidence suggests that small‐bore catheters (1014 F) with instillation of thrombolytics may be as effective and performed with less discomfort.[45] Video‐assisted thoracoscopy to lyse septations and evacuate infected materials is indicated when chest tube drainage has failed.

Figure 5

The most common complication of pleural drainage is pneumothorax. A meta‐analysis demonstrated a reduction in post‐thoracentesis pneumothorax rates from 9% to 4% with use of ultrasound.[46] Transporting patients to radiology for ultrasound marking has not been shown to decrease pneumothorax rates compared to thoracentesis without ultrasound guidance, likely due to changes in patient position and prolonged delays between marking and drainage.[47] Postprocedure pneumothorax can be ruled out if lung sliding is visualized. A meta‐analysis demonstrated superior sensitivity and similar specificity of pleural ultrasonography versus chest radiography to detect pneumothorax (sensitivity 91% vs 50% and specificity 98% vs 99%, respectively).[48] Real‐time ultrasound guidance for thoracentesis, or use of ultrasound to track the needle tip, has not been well studied but may be performed by experienced proceduralists to drain small effusions.

FUTURE RESEARCH

Future research should focus on the clinical effectiveness of point‐of‐care pleural ultrasonography when integrated with other diagnostic tools, and application of new ultrasound technologies to evaluate pleural diseases. Routine use of point‐of‐care ultrasound as the primary imaging modality in a medical ICU demonstrated a highly statistically significant reduction in chest x‐rays (3.75 vs 0.82, P < 0.0001) and chest CT scans (0.10 vs 0.04, P = 0.0007).[49] Similar studies have yet to be performed with the use of ultrasound specifically in the management of pleural diseases. Thus, clinical effectiveness studies are needed to assess the impact of routine use of pleural ultrasound on the initiation of appropriate therapies, length of stay, and costs in the management of pleural disease.

Point‐of‐care pleural ultrasound findings need to be evaluated in the context of other clinical findings and diagnostic tests. Certain ultrasound findings have been associated with exudative pleural effusions, but whether exudative and transudative effusions can be differentiated noninvasively using ultrasound findings alone, or in combination with other clinical data, warrants investigation. Similar to severity of illness scores, models that incorporate clinical, laboratory, and ultrasound findings need to be developed to guide treatment decisions, such as type of drainage procedure, as well as prognostication.

Finally, new technologies may advance the utility of point‐of‐care pleural ultrasonography. Even though 3‐dimensional ultrasonography has been available for over 2 decades, comparative studies of conventional 2‐dimensional versus 3‐dimensional ultrasonography to characterize pleural effusions have yet to be performed. Furthermore, computer‐aided detection has been shown to facilitate interpretation of ultrasound images, but this technology has yet to be applied to pleural ultrasonography.

CONCLUSIONS

Point‐of‐care pleural ultrasound is a powerful bedside tool in the hospitalist's armamentarium that is superior to physical examination and chest radiographs in the detection and characterization of pleural effusions. Furthermore, ultrasound performs similarly when compared to CT scans but offers the advantages of decreased cost, avoidance of ionizing radiation, and availability at the bedside. Ultrasound guidance reduces complications and increases the success rate of pleural drainage procedures, leading to improved patient safety. As clinical effectiveness studies emerge revealing its true value, point‐of‐care pleural ultrasonography is likely to become the standard diagnostic tool to evaluate and manage patients with pleural effusions.

Disclosures: Dr. Restrepo is partially supported by award number K23HL096054 from the National Heart, Lung, and Blood Institute. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Heart, Lung, and Blood Institute or the National Institutes of Health. The authors report no conflicts of interest.

Hospitalists commonly encounter pleural effusions, and their detection and characterization by point‐of‐care ultrasound can guide management. Approximately 44% to 57% of hospitalized patients with bacterial pneumonia,[1, 2] and up to 62% of intensive care unit (ICU) patients[3] have a pleural effusion. For patients with a parapneumonic effusion, hospitalists can use ultrasound to quantify and characterize pleural fluid to determine whether diagnostic or therapeutic drainage is indicated, as well as guide performance of thoracentesis. For patients with lung cancer, detection of a malignant pleural effusion changes staging to stage IV, regardless of tumor size or lymph node involvement, and hospitalists may discuss more appropriate treatment options with patients and consultants.

Routine use of pleural ultrasonography may help hospitalists provide high‐value care by reducing ancillary testing, including computerized tomography (CT) scans that expose patients to ionizing radiation, and reducing complications of thoracentesis. However, many hospitalists may not be familiar with the use of point‐of‐care ultrasound. A national survey in 2012 revealed only 25% of internal medicine residencies have formal curricula to teach point‐of‐care ultrasonography.[4] The purpose of this review is to provide an overview of how point‐of‐care ultrasound can be utilized by hospitalists in the care of patients with pleural effusions. We review the literature on the diagnosis and evaluation of pleural effusions with ultrasound, as well as techniques to examine and drain the pleural space.

DIAGNOSIS OF PLEURAL EFFUSION

PLEURAL ULTRASOUND EXAMINATION

A pleural ultrasound exam may be performed as part of a complete lung ultrasound exam, such as the BLUE (Bedside Lung Ultrasound in Emergency) protocol,[27] or a focused exam to evaluate a suspected or known pleural effusion seen on chest radiograph or CT scan.[27] Free‐flowing pleural effusions accumulate in the most dependent portions of the thorax, most commonly, the posterolateral costophrenic recesses in semirecumbent or seated patients, but anteriorly in mechanically ventilated patients in a prone position.

A low‐frequency (25 MHz) phased‐array transducer is generally preferred for imaging in between the ribs. High‐frequency linear transducers do not provide adequate penetration to visualize deep structures, but do provide superior visualization of the pleural line to assess pleural thickness, measure pleural depth, and evaluate for pneumothorax.

Pleural effusions are best evaluated starting at the level of the diaphragm. Place the transducer in a longitudinal plane on the posterior axillary line at the level of the diaphragm with the transducer orientation marker (notch) pointed cephalad (Figure 1). Five structures must be definitively identified to diagnose a pleural effusion: liver/spleen, diaphragm, pleural fluid, lung, and chest wall (Figure 2A). Large pleural effusions compress the adjacent lung causing atelectasis, which gives the lung a tissue‐like echogenicity similar to the liver (Figure 2B). Static air bronchograms are commonly seen in atelectatic lung bases with pleural effusions.[28]

Figure 1

Figure 2

Color flow Doppler and M‐mode ultrasound may be utilized as adjuncts to routine 2‐dimensional ultrasonography. Free‐flowing pleural effusions will demonstrate flow by color Doppler (Figure 3A). Using M‐mode ultrasound, the lung can been seen moving within a pleural effusion to and from the chest wall (sinusoid sign).[29] Absence of flow or movement is seen with dense pleural loculations, pleural thickening, and peripheral lung or pleural masses (Figure 3B).

Figure 3

CHARACTERIZATION OF PLEURAL EFFUSION

Simple Versus Complex Effusions

Based on its sonographic appearance, pleural effusions are categorized as simple or complex. Simple pleural effusions are anechoic and usually transudative. Complex pleural effusions are subcategorized as homogeneously or heterogeneously echogenic, with or without septations, and are more often exudative.[33]

Effusions with heterogeneous echogenicity with swirling echoes suggest high cellular content that is often associated with malignancy.[34] Fibrinous stranding, septations, and loculations also suggest an exudative effusion (Figure 4A), and are more readily identified and characterized on lung ultrasound than CT scan.[35]

Figure 4

Homogenously echogenic effusions are most often due to hemothorax or empyema.[36] The high cell count of a hemothorax creates a layering effect in costophrenic recesses (hematocrit sign). Empyemas develop from complex effusions that organize into collections of pus and usually have a homogeneously echogenic, speckled appearance (Figure 4B). Sonographic evidence of septations in the presence of empyema predicts the need for intrapleural fibrinolytic therapy, longer duration of drainage, and possible surgical intervention.[37]

Isolated dense loculations may be challenging to differentiate from peripheral lung or pleural lesions, such as abscess or tumor.

PLEURAL FLUID DRAINAGE

Since its first description in 1967, use of ultrasound guidance for thoracentesis has evolved to become the standard of care in many hospitals in the United States.[41] The British Thoracic Society guidelines recommend that all thoracenteses be performed with ultrasound guidance.[42] The American College of Graduate Medical Education now requires proficiency in the use of ultrasound for thoracentesis and pleural catheter insertion by pulmonary and critical care fellows.[43]

The impetus for these recommendations stems from increased procedural success and decreased complications associated with ultrasound‐guided drainage of pleural effusions. A study evaluating thoracentesis site selection based on physical exam and chest radiographs demonstrated inaccurate site selection in 15% of patients, and use of ultrasound for site selection prevented possible accidental organ puncture in 10% of all cases.[44] The success rate of thoracentesis for small pleural effusions has been shown to increase from 66% to 90% with ultrasound guidance.[42] Using ultrasound, the distance from the skin to parietal and visceral pleura can be measured to determine whether thoracentesis can be safely performed, and to guide selection of an adequate length needle (Figure 5). A minimum pleural effusion depth of 1.5 cm between the visceral and parietal pleura has been recommended to perform diagnostic thoracentesis.[28] Diagnostic thoracentesis of complex septated pleural effusions or empyemas may be performed with a straight needle, but therapeutic drainage often requires temporary insertion of a catheter. Traditionally, large‐bore chest tubes (>24 F) had been advocated to drain viscid pus, but recent evidence suggests that small‐bore catheters (1014 F) with instillation of thrombolytics may be as effective and performed with less discomfort.[45] Video‐assisted thoracoscopy to lyse septations and evacuate infected materials is indicated when chest tube drainage has failed.

Figure 5

The most common complication of pleural drainage is pneumothorax. A meta‐analysis demonstrated a reduction in post‐thoracentesis pneumothorax rates from 9% to 4% with use of ultrasound.[46] Transporting patients to radiology for ultrasound marking has not been shown to decrease pneumothorax rates compared to thoracentesis without ultrasound guidance, likely due to changes in patient position and prolonged delays between marking and drainage.[47] Postprocedure pneumothorax can be ruled out if lung sliding is visualized. A meta‐analysis demonstrated superior sensitivity and similar specificity of pleural ultrasonography versus chest radiography to detect pneumothorax (sensitivity 91% vs 50% and specificity 98% vs 99%, respectively).[48] Real‐time ultrasound guidance for thoracentesis, or use of ultrasound to track the needle tip, has not been well studied but may be performed by experienced proceduralists to drain small effusions.

FUTURE RESEARCH

Future research should focus on the clinical effectiveness of point‐of‐care pleural ultrasonography when integrated with other diagnostic tools, and application of new ultrasound technologies to evaluate pleural diseases. Routine use of point‐of‐care ultrasound as the primary imaging modality in a medical ICU demonstrated a highly statistically significant reduction in chest x‐rays (3.75 vs 0.82, P < 0.0001) and chest CT scans (0.10 vs 0.04, P = 0.0007).[49] Similar studies have yet to be performed with the use of ultrasound specifically in the management of pleural diseases. Thus, clinical effectiveness studies are needed to assess the impact of routine use of pleural ultrasound on the initiation of appropriate therapies, length of stay, and costs in the management of pleural disease.

Point‐of‐care pleural ultrasound findings need to be evaluated in the context of other clinical findings and diagnostic tests. Certain ultrasound findings have been associated with exudative pleural effusions, but whether exudative and transudative effusions can be differentiated noninvasively using ultrasound findings alone, or in combination with other clinical data, warrants investigation. Similar to severity of illness scores, models that incorporate clinical, laboratory, and ultrasound findings need to be developed to guide treatment decisions, such as type of drainage procedure, as well as prognostication.

Finally, new technologies may advance the utility of point‐of‐care pleural ultrasonography. Even though 3‐dimensional ultrasonography has been available for over 2 decades, comparative studies of conventional 2‐dimensional versus 3‐dimensional ultrasonography to characterize pleural effusions have yet to be performed. Furthermore, computer‐aided detection has been shown to facilitate interpretation of ultrasound images, but this technology has yet to be applied to pleural ultrasonography.

CONCLUSIONS

Point‐of‐care pleural ultrasound is a powerful bedside tool in the hospitalist's armamentarium that is superior to physical examination and chest radiographs in the detection and characterization of pleural effusions. Furthermore, ultrasound performs similarly when compared to CT scans but offers the advantages of decreased cost, avoidance of ionizing radiation, and availability at the bedside. Ultrasound guidance reduces complications and increases the success rate of pleural drainage procedures, leading to improved patient safety. As clinical effectiveness studies emerge revealing its true value, point‐of‐care pleural ultrasonography is likely to become the standard diagnostic tool to evaluate and manage patients with pleural effusions.

Disclosures: Dr. Restrepo is partially supported by award number K23HL096054 from the National Heart, Lung, and Blood Institute. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Heart, Lung, and Blood Institute or the National Institutes of Health. The authors report no conflicts of interest.