Imaging

Acute dyspnea, with or without hypoxia, is a common patient presentation in the ED, and can be the result of a myriad of mainly cardiac, pulmonary, and metabolic conditions—many of which are life-threatening. Therefore, it is crucial to determine or narrow the diagnosis promptly and initiate appropriate treatment. Focused ultrasound of the lungs can provide important information that can change a patient’s clinical course within minutes of initial evaluation.

Background

Prior to the 1990s, the lung was considered unsuitable for evaluation by ultrasound given the scatter of the ultrasound beam that is produced by the presence of aerated tissue. Lung pathology, however, produces distinct artifacts and signs on ultrasound that correspond with specific disease patterns.

The Bedside Lung Ultrasound in Emergencies (BLUE) protocol¹ was developed by Daniel Lichtenstein, a French intensivist, and published in 2008. The goal of the examination is to improve the speed and precision of identifying common causes of acute dyspnea. The sensitivity of ultrasound for cardiogenic pulmonary edema, asthma/chronic obstructive pulmonary disease (COPD), and pneumothorax were reported as exceeding 88%.² Strictly speaking, the BLUE protocol includes an evaluation of the deep veins as well to exclude thrombus; however, this article will focus on ultrasound imaging of the lung.

Relevant Findings

A-line Artifact

The A-line seen on lung ultrasound (Figure 1) originates from the pleura and can be seen in a normal lung.

B-line Artifact

B-lines, also referred to as “lung rockets,” are a comet-tail artifact arising from the pleura (Figure 2).

Lung Profiles

A patient can have one of three predominant lung profiles: A-profile, B-profile, or AB-profile.

A-profile. A-lines appear bilaterally with lung sliding in the anterior surface of lungs, suggestive of COPD, or pulmonary embolism. Exacerbation of congestive heart failure can be ruled out.

B-profile. The appearance of prominent B-lines bilaterally, suggestive of heart failure, essentially rules out COPD, pulmonary embolism, and pneumothorax.

AB-profile. The appearance of predominant B-lines on one lung and predominant A-lines on the other lung, is consistent with an AB profile. This is usually associated with unilateral pneumonia, especially if seen with other findings such as subpleural consolidation (Figure 3) and air bronchograms (Figure 4).

Lung Point

The lung point sign is the only specific finding in the BLUE protocol, and signifies the limits of a pneumothorax by showing the interface between normal lung sliding and the edge of the pneumothorax. Without a specific search for the lung point, it may not be seen in the anterior assessment of lung sliding, although lung sliding will still be abolished.

Imaging Technique

The mid-to-high frequency phased array transducer is used to examine the anterior and posterolateral chest. The original BLUE protocol assesses three zones, but the most relevant information can be obtained from performing the ultrasound in the anterior and posterolateral locations (Figures 6 and 7).

Anterior Pleural Assessment

The first step is to evaluate the pleural line anteriorly (Figure 1) for lung sliding. This is best accomplished by setting the depth to no more than 5 cm so that the focal zone of the ultrasound beam is directed at the pleural line, and it is centered on the screen. If no sliding is present, it is because the visceral and parietal pleura are not apposed to one another. There are many pathological entities that can cause this finding, but one of the more common is pneumothorax.

After evaluating the pleural line, the depth will then need to be switched to 15 cm to evaluate for B-lines. If B-lines are present without lung sliding, pneumonia should be strongly considered. The appearance of B-lines with lung sliding signifies alveolar interstitial fluid, commonly from pulmonary edema.

Posterolateral Assessment

The posterolateral assessment (Figure 7) evaluates for pleural effusion and consolidation. The dome of the diaphragm is the landmark above which abnormal lung and artifacts will be seen.

Summary

Lung ultrasound can help narrow the differential diagnosis for acute dyspnea within the first few minutes of the patient encounter. The BLUE protocol provides an organized approach to this evaluation. Often, the protocol is combined with focused examinations of the heart, inferior vena cava, and/or deep veins to complete the clinical picture. It is important to keep in mind that patients may have two or more pathological conditions (eg, asthma and pneumonia) that can affect the ultrasound findings. For this reason, ultrasound interpretation should always occur in the context of the clinical condition. If it does not exclude important diagnoses, additional investigations such as plain radiography, cross-sectional imaging, or ventilation/perfusion studies should be pursued.

Acute dyspnea, with or without hypoxia, is a common patient presentation in the ED, and can be the result of a myriad of mainly cardiac, pulmonary, and metabolic conditions—many of which are life-threatening. Therefore, it is crucial to determine or narrow the diagnosis promptly and initiate appropriate treatment. Focused ultrasound of the lungs can provide important information that can change a patient’s clinical course within minutes of initial evaluation.

Background

Prior to the 1990s, the lung was considered unsuitable for evaluation by ultrasound given the scatter of the ultrasound beam that is produced by the presence of aerated tissue. Lung pathology, however, produces distinct artifacts and signs on ultrasound that correspond with specific disease patterns.

The Bedside Lung Ultrasound in Emergencies (BLUE) protocol¹ was developed by Daniel Lichtenstein, a French intensivist, and published in 2008. The goal of the examination is to improve the speed and precision of identifying common causes of acute dyspnea. The sensitivity of ultrasound for cardiogenic pulmonary edema, asthma/chronic obstructive pulmonary disease (COPD), and pneumothorax were reported as exceeding 88%.² Strictly speaking, the BLUE protocol includes an evaluation of the deep veins as well to exclude thrombus; however, this article will focus on ultrasound imaging of the lung.

Relevant Findings

A-line Artifact

The A-line seen on lung ultrasound (Figure 1) originates from the pleura and can be seen in a normal lung.

B-line Artifact

B-lines, also referred to as “lung rockets,” are a comet-tail artifact arising from the pleura (Figure 2).

Lung Profiles

A patient can have one of three predominant lung profiles: A-profile, B-profile, or AB-profile.

A-profile. A-lines appear bilaterally with lung sliding in the anterior surface of lungs, suggestive of COPD, or pulmonary embolism. Exacerbation of congestive heart failure can be ruled out.

B-profile. The appearance of prominent B-lines bilaterally, suggestive of heart failure, essentially rules out COPD, pulmonary embolism, and pneumothorax.

AB-profile. The appearance of predominant B-lines on one lung and predominant A-lines on the other lung, is consistent with an AB profile. This is usually associated with unilateral pneumonia, especially if seen with other findings such as subpleural consolidation (Figure 3) and air bronchograms (Figure 4).

Lung Point

The lung point sign is the only specific finding in the BLUE protocol, and signifies the limits of a pneumothorax by showing the interface between normal lung sliding and the edge of the pneumothorax. Without a specific search for the lung point, it may not be seen in the anterior assessment of lung sliding, although lung sliding will still be abolished.

Imaging Technique

The mid-to-high frequency phased array transducer is used to examine the anterior and posterolateral chest. The original BLUE protocol assesses three zones, but the most relevant information can be obtained from performing the ultrasound in the anterior and posterolateral locations (Figures 6 and 7).

Anterior Pleural Assessment

The first step is to evaluate the pleural line anteriorly (Figure 1) for lung sliding. This is best accomplished by setting the depth to no more than 5 cm so that the focal zone of the ultrasound beam is directed at the pleural line, and it is centered on the screen. If no sliding is present, it is because the visceral and parietal pleura are not apposed to one another. There are many pathological entities that can cause this finding, but one of the more common is pneumothorax.

After evaluating the pleural line, the depth will then need to be switched to 15 cm to evaluate for B-lines. If B-lines are present without lung sliding, pneumonia should be strongly considered. The appearance of B-lines with lung sliding signifies alveolar interstitial fluid, commonly from pulmonary edema.

Posterolateral Assessment

The posterolateral assessment (Figure 7) evaluates for pleural effusion and consolidation. The dome of the diaphragm is the landmark above which abnormal lung and artifacts will be seen.

Summary

Lung ultrasound can help narrow the differential diagnosis for acute dyspnea within the first few minutes of the patient encounter. The BLUE protocol provides an organized approach to this evaluation. Often, the protocol is combined with focused examinations of the heart, inferior vena cava, and/or deep veins to complete the clinical picture. It is important to keep in mind that patients may have two or more pathological conditions (eg, asthma and pneumonia) that can affect the ultrasound findings. For this reason, ultrasound interpretation should always occur in the context of the clinical condition. If it does not exclude important diagnoses, additional investigations such as plain radiography, cross-sectional imaging, or ventilation/perfusion studies should be pursued.

Acute dyspnea, with or without hypoxia, is a common patient presentation in the ED, and can be the result of a myriad of mainly cardiac, pulmonary, and metabolic conditions—many of which are life-threatening. Therefore, it is crucial to determine or narrow the diagnosis promptly and initiate appropriate treatment. Focused ultrasound of the lungs can provide important information that can change a patient’s clinical course within minutes of initial evaluation.

Background

Prior to the 1990s, the lung was considered unsuitable for evaluation by ultrasound given the scatter of the ultrasound beam that is produced by the presence of aerated tissue. Lung pathology, however, produces distinct artifacts and signs on ultrasound that correspond with specific disease patterns.

The Bedside Lung Ultrasound in Emergencies (BLUE) protocol¹ was developed by Daniel Lichtenstein, a French intensivist, and published in 2008. The goal of the examination is to improve the speed and precision of identifying common causes of acute dyspnea. The sensitivity of ultrasound for cardiogenic pulmonary edema, asthma/chronic obstructive pulmonary disease (COPD), and pneumothorax were reported as exceeding 88%.² Strictly speaking, the BLUE protocol includes an evaluation of the deep veins as well to exclude thrombus; however, this article will focus on ultrasound imaging of the lung.

Relevant Findings

A-line Artifact

The A-line seen on lung ultrasound (Figure 1) originates from the pleura and can be seen in a normal lung.

B-line Artifact

B-lines, also referred to as “lung rockets,” are a comet-tail artifact arising from the pleura (Figure 2).

Lung Profiles

A patient can have one of three predominant lung profiles: A-profile, B-profile, or AB-profile.

A-profile. A-lines appear bilaterally with lung sliding in the anterior surface of lungs, suggestive of COPD, or pulmonary embolism. Exacerbation of congestive heart failure can be ruled out.

B-profile. The appearance of prominent B-lines bilaterally, suggestive of heart failure, essentially rules out COPD, pulmonary embolism, and pneumothorax.

AB-profile. The appearance of predominant B-lines on one lung and predominant A-lines on the other lung, is consistent with an AB profile. This is usually associated with unilateral pneumonia, especially if seen with other findings such as subpleural consolidation (Figure 3) and air bronchograms (Figure 4).

Lung Point

The lung point sign is the only specific finding in the BLUE protocol, and signifies the limits of a pneumothorax by showing the interface between normal lung sliding and the edge of the pneumothorax. Without a specific search for the lung point, it may not be seen in the anterior assessment of lung sliding, although lung sliding will still be abolished.

Imaging Technique

The mid-to-high frequency phased array transducer is used to examine the anterior and posterolateral chest. The original BLUE protocol assesses three zones, but the most relevant information can be obtained from performing the ultrasound in the anterior and posterolateral locations (Figures 6 and 7).

Anterior Pleural Assessment

The first step is to evaluate the pleural line anteriorly (Figure 1) for lung sliding. This is best accomplished by setting the depth to no more than 5 cm so that the focal zone of the ultrasound beam is directed at the pleural line, and it is centered on the screen. If no sliding is present, it is because the visceral and parietal pleura are not apposed to one another. There are many pathological entities that can cause this finding, but one of the more common is pneumothorax.

After evaluating the pleural line, the depth will then need to be switched to 15 cm to evaluate for B-lines. If B-lines are present without lung sliding, pneumonia should be strongly considered. The appearance of B-lines with lung sliding signifies alveolar interstitial fluid, commonly from pulmonary edema.

Posterolateral Assessment

The posterolateral assessment (Figure 7) evaluates for pleural effusion and consolidation. The dome of the diaphragm is the landmark above which abnormal lung and artifacts will be seen.

Summary

Lung ultrasound can help narrow the differential diagnosis for acute dyspnea within the first few minutes of the patient encounter. The BLUE protocol provides an organized approach to this evaluation. Often, the protocol is combined with focused examinations of the heart, inferior vena cava, and/or deep veins to complete the clinical picture. It is important to keep in mind that patients may have two or more pathological conditions (eg, asthma and pneumonia) that can affect the ultrasound findings. For this reason, ultrasound interpretation should always occur in the context of the clinical condition. If it does not exclude important diagnoses, additional investigations such as plain radiography, cross-sectional imaging, or ventilation/perfusion studies should be pursued.

Critically ill patients presenting to the ED represent the most time-sensitive patient encounter for the emergency physician (EP), as delays in restoring physiological homeostasis increase the risks of organ dysfunction and death. Management and treatment strategies in critically ill patients have evolved from the routine use of invasive catheters and radiography for cardiopulmonary evaluation to a variety of noninvasive devices and pathways. The widespread adoption of point-of-care ultrasound (POCUS) in EDs provides the opportunity to rapidly obtain invaluable information about the diagnosis and etiology to guide resuscitation in critically ill patients—particularly those in shock and acute dyspnea. 

Over the last two decades, EPs and critical care physicians have employed POCUS to assist in identifying emergent reversible causes of shock and cardiac arrest, including cardiac tamponade, massive pulmonary embolism (PE), and hemoperitoneum. Recent advances in hemodynamic and cardiopulmonary POCUS allow for a nuanced approach to hemodynamic evaluation.¹ In addition, the use of ultrasound “first” in the critical care setting may reduce the dependence on radiographic-based management, catheter-based protocols, and the need for invasive procedures. 

Bedside cardiopulmonary ultrasound to evaluate the hemodynamic status of hypotensive patients can help determine the etiology of shock, provide evidence of fluid-volume responsiveness, visualize hemodynamic abnormalities that would alter fluid resuscitation strategies, and assess patient response to an intervention. The use of ultrasound can also identify the etiology of acute respiratory failure—providing the opportunity to initiate the appropriate interventions prior to patient decompensation. Findings such as pneumothorax or pleural effusion may require immediate procedural intervention, while other findings may only require noninvasive positive pressure ventilation and diuresis. 

The tools to implement these concepts include basic POCUS education common to emergency medicine and critical care (American College of Emergency Physicians Guidelines and American College of Chest Physicians/Society of Critical Care Medicine guidelines); ultrasound machines with phased array, linear, and curvilinear probes; and ultrasonographic instrumentation such as M-Mode, color Doppler, and spectral Doppler. An understanding of common Doppler imaging techniques optimizes the examination, and the use of presets common to cardiac packages may further assist the provider with adoption. 

When evaluating critically ill patients, we recommend the following step-wise approach: 

• Identify a clinical question to be answered prior to doing the examination; 
• Determine the hemodynamic profile of the patient to guide therapeutic maneuvers; and 
• Monitor the response to any therapeutic maneuver and adjust accordingly. (In these complicated patients, repeat examinations are invaluable, as the hemodynamic profile can change rapidly.)

Emergency physicians are increasingly utilizing POCUS to rapidly evaluate the thoracic cavity in critically ill patients. This modality is an appealing alternative to formal chest radiography because of the ease of rapid image acquisition, lack of ionizing radiation, and the ability to repeat the examination in real-time. 

When critically ill patients present in respiratory distress, POCUS allows the EP to rapidly diagnose potential etiologies, such as pleural effusion, pneumothorax, or pulmonary edema, and employ emergent intervention, which can greatly alter the patient’s clinical course. Additionally, the rapid diagnosis of consolidation permits earlier appropriate management of sepsis and respiratory failure when the clinical setting is consistent with pneumonia. 

In many cases, ultrasound has been shown to be superior to traditional chest radiography to assess critically ill patients.^2-8 Although there are several protocols that utilize thoracic ultrasound in evaluating the critical patient, this review focuses solely on the components of thoracic ultrasound, rather than specific protocols.  

Pneumothorax 

Ultrasound imaging with a high-frequency probe is highly sensitive and specific in assessing for pneumothorax in a supine patient.⁹ In the normal lung, the visceral and parietal pleura are visualized as sliding with each breath. In this examination, the transducer is placed on the chest wall to visualize two ribs and the pleura between them (Figures 2a and 2b).

When lung sliding is present, the appearance in M-mode is that of the “seashore” or “sandy beach.” The hyperechoic white pleura is seen as moving with the respiratory cycle. Additionally, lung artifacts such as A-lines, horizontal reverberation artifacts; and B-lines (also referred to as “comet-tails”), vertical lines arising from distended subpleural alveoli, will be seen in a normal lung. If pneumothorax is present, no sliding or comet-tail artifacts will be present at the pleural surface. Although A-lines may also be absent in pneumothorax, studies have shown that the absence of lung sliding and the presence of A-lines are associated with increased specificity (94% vs 78% with absent lung sliding alone) for diagnosing occult pneumothorax.⁹

While the lack of pleural sliding is highly sensitive for pneumothorax, the clinician must place this finding within the clinical context of the patient. For example, an intubated patient may not have left-sided sliding in the case of a right main-stem intubation. Moreover, patients who have an underlying obstructive lung disease (eg, chronic obstructive pulmonary disease [COPD]) and/or emphysema may present a more challenging examination because pleural sliding is often absent, especially in the apical segments, and can mimic pneumothorax in these patients.¹⁰ 

In addition to pleural sliding, presence or absence of a lung pulse also assists in assessing patients for pneumothorax. The detection of a lung pulse on M-mode ultrasound indicates subtle cardiac pulsation at the periphery of the lung; this finding only appears in the nonventilated lung in the absence of a pneumothorax. The presence of lung pulse is therefore useful in distinguishing other causes of nonventilated lung from pneumothorax.¹¹

Pleural Fluid

The low-frequency curvilinear or phased array probes are used to assess for pleural fluid. In this study, the clinician fans the probe cephalad from Morison’s pouch on the patient’s right side, or from the splenorenal recess on the left side, to visualize the bright, hyperechoic diaphragm. If pleural fluid is present, there will be loss of the mirroring artifact, and the fluid will appear as an anechoic collection cephalad to the diaphragm. In addition, when fluid is present, the normal lung may be visualized moving within the effusion, evoking a quad or sinusoid sign with M-mode imaging.^12,13 In the setting of complicated parapneumonic effusion, the echogenicity may be mixed or difficult to detect.  

Visualization of the thoracic spine above the diaphragm may serve as a surrogate marker for the presence of fluid. Typically, the thoracic spine is not visualized on ultrasound due to the scatter caused by the air-filled lungs.

Ultrasound has been shown to be superior to routine chest radiograph for the identification of small pleural effusions.⁷ Given that both critically ill medical and injured patients can present with pleural fluid, the use of POCUS to rapidly determine the presence or absence of fluid is an adjunct in the evaluation of these patients. 

Interstitial Fluid

Evaluation of the thoracic cavity for interstitial fluid in the setting of acute pulmonary edema, acute respiratory distress syndrome (ARDS), or interstitial pneumonia is best accomplished using either the curvilinear low-frequency probe or the phased array probe. The visualization of vertically oriented B-lines in the upper lung fields is very sensitive for interstitial fluid or edema of the interlobular septa (Figures 2a and 2b).^13,15 In this study, B-lines originate at the pleural line, move with the pleura, and extend off the bottom of the monitor without obliteration (in contrast to A-lines). An isolated B-line may be physiological; however, the presence of several B-lines is consistent with an interstitial pathology. On imaging, the presence of three or more B-lines in a single rib space with a convex probe, or more than six B-lines when utilizing the curvilinear, is considered pathological and referred to as “lung rockets.” B-lines may be focal or diffuse, as seen respectively in cases of pneumonia or acute pulmonary edema.¹⁶ 

Pulmonary Assessment for Fluid Resuscitation

Fluid Resuscitation 

Lung ultrasound studies have been proposed as a means of determining adequate fluid resuscitation and preventing complications associated with excessive fluid. The appearance of diffuse B-lines of acute interstitial syndrome on lung ultrasound can uncover the first signs of extravascular lung water and prevent pulmonary alveolar edema and associated morbidity and mortality.¹⁷ The appearance of an A-line predominance throughout the lung does not predict fluid responsiveness, but rather potential fluid tolerance. 

A benefit of lung ultrasound is that it provides information more rapidly than many of the dynamic measures of fluid responsiveness and cardiac output variability. In addition, lung ultrasound studies are much more easily reproduced than repeating a velocity time integral (VTI) measurements.

Lichtenstein’s FALLS Protocol

Lichtenstein’s FALLS (Fluid Administration Limited by Lung Sonography) protocol provides an approach to performing lung ultrasound on patients presenting in shock.¹² In this approach, lung ultrasound studies are performed after echocardiography to evaluate the patient for causes of obstructive shock. The predominance of B-lines on lung ultrasound suggests cardiogenic shock and, by definition, fluid intolerance. The predominance of A-lines on ultrasound may be present in patients in hypovolemic or septic shock. 

In hypovolemic shock, continued fluid boluses will improve hemodynamics with preserved A-line predominance. In septic shock, B-lines will begin to appear, suggesting that other means of improving forward flow should be initiated.

Consolidation

Chest radiography is known to have variable test characteristics for the detection of pneumonia. Consolidation may not be detected in profoundly immunocompromised or dehydrated patients. Additionally, in critically ill patients, it is often challenging to obtain a posteroanterior and lateral chest X-ray, given the patient’s hemodynamic status and stability for transport, and a single portable anteroposterior film will often miss retrocardiac infiltrates. In both of these clinical settings, POCUS can provide a rapid diagnosis, expediting the care of these septic patients. 

In the presence of a dense consolidation, there may be hepatization of the lung parenchyma (Figure 4b). Additionally, hyperechoic air bronchograms are often visualized. Pneumonia is often associated with pleural effusion and localized B-lines. Using lung ultrasound, rapid bedside detection of these pulmonary findings in clinical presentations suggestive of pneumonia can accelerate appropriate antibiotic and respiratory supportive treatment.  

Left Ventricular Systolic Assessment 

Critically ill patients commonly present with a mixed shock picture, and it is rare for a patient to have solely cardiogenic shock, hemorrhagic shock, etc. Rather, a patient who presents in septic shock may have an underlying cardiomyopathy for which she or he is being treated with a beta-blocker. 

Cardiomyopathy associated with sepsis is common¹⁸ and, at least in the case of diastolic dysfunction, it is underdiagnosed and associated with a higher mortality rate.¹⁹ It is therefore essential that the EP evaluate left ventricular (LV) systolic function rapidly and reliably—particularly in critically ill patients whose disease process may be undifferentiated and whose hemodynamic status is unclear.^20-22 Bedside echocardiography by the EP is invaluable in identifying the LV contribution to the hemodynamic profile and tailoring resuscitation to optimize patient outcomes. 

Although gross visual assessment is the most widely used method by which EPs estimate LV systolic function, this strategy is subjective, operator-dependent, and requires at least two quality views to understand the heart’s three-dimensional movement. However, when faced with a rapid diagnostic dilemma, a global visual estimate of the overall contractility (hyperdynamic, normal, depressed, severely depressed) may be more useful than estimating the ejection fraction (EF), especially when the patient’s baseline EF is unknown. 

Regional wall-motion abnormalities can be evaluated by considering  and correlating the coronary artery distributions with the electrocardiographic findings and the clinical scenario (Figure 5).

Simpson’s Rule

Although no one parameter can quantitatively assess LV function, the EF is the one most commonly used. The Simpson’s Rule or the “method of disks” estimates EF by changes in calculated ventricular volumes. The endocardial border is outlined in end-diastole and end-systole (ES) in both the apical four- (AP4) and two-chamber views. The cardiac package on the ultrasound system can divide the selected area into a series of disks, calculate the volume of each disk, and then add these figures to estimate the ventricular volume (Figure 6a). Limitations of this study include potentially difficult visualization of the endocardial border, and the length of time to conduct this study. 

Fractional Shortening

M-mode ultrasound can be used in several ways to estimate LV EF. Fractional shortening (FS) estimates the size reduction of the LV during systole. In the parasternal long axis (PLAX) view, the M-mode cursor is placed over the walls of the LV, just apical to the tips of the mitral valve (MV) leaflets (Figure 6b). Maximal (end-diastolic diameter [EDD]) and minimal (end-systolic diameter [ESD]) dimensions of the LV are measured and FS is calculated as (LVEDD – LVESD)/ LVEDD. A normal value is more than 25%, and a rough estimate of EF is FS x 2.²⁴ Limitations to this study include nonplacement of the M-mode cursor perpendicular to the LV walls, and inaccuracy in patients with regional wall abnormalities. 

E-Point Septal Separation

Another way to assess EF with POCUS is through E-point septal separation (EPSS), which uses the movement of the MV during diastole to estimate the EF during systole. In the PLAX view, the M-mode cursor is placed over the apical tip of the anterior leaflet of the MV to visualize the movement of the leaflet in relation to the interventricular septum (Figure 6c). Two characteristic waves are created during each diastole—the larger first wave representing early filling (the E-wave) and the smaller second wave representing the atrial kick (the A-wave). The E-point is the tallest point of the E-wave, and the EPSS is measured as the distance in millimeters between the E-point and the interventricular septum.²¹ 

The opening of the anterior leaflet of the MV toward the interventricular septum in diastole requires a pressure difference between the left atrium (LA) and LV. In a patient with poor LV systolic function, the LV is still full at the end of systole, the pressure difference is not as great, and the mitral leaflets will not snap open vigorously. The EPSS should be at or less than 6 mm in patients with normal LV systolic function. An EPSS of 6 to 12 mm suggests moderately depressed LV systolic function, and over 12 mm signifies severely decreased LV systolic function.²⁵ Limitations include inaccuracy in patients with valvular abnormalities, such as mitral stenosis or aortic regurgitation, severe LV or septal hypertrophy, regional wall abnormalities or severe LV dilation, limited data, and a wide margin of error when comparing to magnetic resonance imaging measurement of EF.

Cardiac Output 

Left Ventricular Diastolic Assessment

In an aging population of patients who have longstanding, undiagnosed, or untreated hypertension, LV hypertrophy leads to impaired relaxation and diastolic filling, eventually causing elevated LA pressure and, in extreme cases, restrictive cardiomyopathy. It has been reported that approximately half of all symptomatic patients with heart failure have a preserved EF.²⁷ 

Determination of LV pressures allows for the distinction between hydrostatic pulmonary edema and ARDS. Diagnosing elevated LA pressure is not inconsequential, as diastolic dysfunction in septic patients has been associated with increased mortality, likely due to increased pulmonary edema from fluid resuscitation.¹⁹ An invasive method of using a pulmonary artery catheter and measuring the pulmonary artery occlusion pressure to estimate the LA pressure is the gold standard, but is no longer routinely performed. 

Echocardiography is a noninvasive surrogate to estimating LA and LV filling pressures. Two different echocardiographic measurements can be used in conjunction to estimate LV filling pressures: MV inflow velocity and tissue Doppler imaging. 

Mitral Valve Inflow Velocity

Assessment of the MV inflow is performed by placing the pulse-wave Doppler gate between the tips of the MV leaflets in the AP4 view. Early diastolic filling produces the E-wave, and LA contraction produces the late diastolic A-wave (Figure 8a).

Tissue Doppler Imaging

Tissue Doppler imaging enables the clinician to measure myocardial velocities such as the speed of relaxation to evaluate if LV relaxation is due to a drop in LV pressure below LA pressure after systole, pulling the MV open; or if increased LA pressure is required to push open the MV and fill the LV. 

For this study, the tissue Doppler sampling gate is placed at the septal or lateral annulus of the MV in the AP4 view to visualize early diastolic mitral annulus velocity (e’) (Figure 8b). The E/e’ ratio can be helpful for estimating LV filling pressures. An E/e’ of less than 8 is associated with normal LV filling pressure whereas an E/e’ >15 is associated with an elevated LV filling pressure.28,29 When the E/e’ is 8 to 10, other indices such as the E/A ratio and deceleration time, as well as the clinical picture, can provide insight into the presence of hemodynamically significant diastolic dysfunction.

Learning and applying the assessment of diastolic parameters can be challenging; however, these parameters can be used to help predict LV filling pressures in patients with findings of pulmonary edema on chest radiograph. Limitations of these techniques are inter-rater variability, as well as the ability of the operator to acquire the required AP4 view. In addition, these techniques are unreliable in patients with irregular cardiac rhythms, severe mitral disease, and in hypertrophic cardiomyopathy. 

Right Ventricular Assessment

The right ventricle (RV) is a small, thin-walled ventricle with only two layers of muscle, as opposed to the three layers of the LV. In contrast to the rocking motion of LV contraction, the orientation of the two muscle layers of the RV permits mostly longitudinal contraction. The circumferential muscle fibers are shared at the base and apex with the LV, which can provide some of the contractile strength of the RV.³⁰ Because of this orientation, RV strain, which can manifest as decreased longitudinal contraction, speed of contraction, septal movement, and tethering abnormalities through ventricular interdependence, can be measured easily using bedside echocardiography. 

In healthy individuals, the RV is a low-pressure chamber that acts as a conduit for propelling venous return into the pulmonary circulation without much effect on systemic hemodynamics. However, in critical illness, RV abnormalities can have profound effects on hemodynamics, and  the efforts typically used to improve LV performance will worsen a failing RV. 

While RV dysfunction is most commonly due to chronic LV disease, acute RV dysfunction is commonly encountered in critical illness,³¹ including many septic patients with ARDS,^32,33 PE, or decompensated chronic pulmonary hypertension.³⁴ The examinations that follow, allow the EP to assess for the presence of RV dysfunction and to guide resuscitation appropriately to avoid the untoward hemodynamic effects of conventional resuscitation strategies in these patients. 

When evaluating the RV, the clinician must determine (1) if the patient’s RV strain is due to pressure or volume overload; and (2) if the patient’s RV is responsive or nonresponsive to a preload challenge, prompting an alteration in the resuscitation plan in nonresponsive cases. 

Right Ventricular Pressure/Volume Overload

While inferior vena cava (IVC) ultrasound has been shown to be a pre-heart/lung assessment of cardiopulmonary interactions that predicts volume responsiveness, the IVC is also a good predictor of right atrial (RA) pressure.³⁵ If the IVC is dilated and lacks respiratory variation, the patient likely has an elevated RA pressure, which is most likely transmitted from an elevated RV pressure (Figure 9a). However, compliance of the RA, RA pressure and, by extension, IVC prediction of that RA pressure, may underestimate the degree of RV pressure or afterload. 

Right Ventricular Strain and Contractile Reserve 

From the same apical view, tissue Doppler at the lateral tricuspid annulus will give a tricuspid annular peak velocity, a measure of the isovolumetric contraction velocity. This measurement will provide a measure of the contractile reserve of the RV (Figure 10b). A measure of less than 10 cm/sec indicates that further volume and inotropic challenges to the RV will not be effective, and the focus should be to decrease RV afterload with pulmonary vasodilators.^34,39,40 

Fluid Resuscitation Assessment 

Restoring circulating volume to increase cardiac output and improve oxygen delivery is the primary objective when managing patients in shock. Patient outcomes improve dramatically with early aggressive fluid resuscitation.^41-44 However, many critically ill patients do not respond to fluid resuscitation, which is generally defined as the rise of cardiac output of more than 15% in response to volume expansion. Not all patients found to be fluid responsive will require volume expansion.^45,46 

Excessive fluid resuscitation has been shown to increase intensive care unit length of stay, morbidity, and mortality.^47,48 Further, pathophysiological processes such as RV dysfunction and severe diastolic dysfunction can significantly alter the hemodynamic profile such that fluid management can be quite challenging in critically ill patients.

Distinguishing responders from nonresponders prior to fluid administration is the goal of early resuscitation. Unfortunately, this distinction cannot be made based on the patient’s vital signs or the physical examination.⁴⁹ Static filling pressures and volumetric measures are unreliable markers of fluid responsiveness.^50,51 The practice of administering a fluid challenge and observing the clinical effect on cardiac output is undesirable because it requires, by definition, on administering fluids, which ultimately may be harmful to the patient. 

Dynamic measures of fluid responsiveness that reliably predict cardiac response to a preload challenge are proven to be of greater utility.^52,53 These assessments determine volume responsiveness by evaluating the change in LV output with intrathoracic pressure changes due to the respiratory cycle, (ie, cardiopulmonary interaction). Ultrasound studies to assess cardiopulmonary interactions include IVC variability, arterial flow variability, brachial artery peak velocity variability, and common carotid artery (CCA) flow. In addition to echocardiography, lung ultrasound may be used to determine the endpoint of fluid resuscitation by monitoring for the appearance of extravascular lung water. 

Inferior Vena Cava Variability 

The IVC is a large extrathoracic vein which is easily insonated and accessible, even to a clinician with basic bedside ultrasound competency. Static IVC measures, such as diameter alone, correlate with central venous pressure but do not predict fluid responsiveness.^54-56 Dynamic IVC evaluation provides an upstream assessment of cardiopulmonary interactions. 

In the spontaneously breathing patient, the IVC collapses with inspiration as the RA pressure falls below atmospheric pressure, collapsing the intrathoracic veins for a short period until the intravascular pressure at the entry to the thorax exceeds atmospheric pressure, causing a bolus of venous return to the right heart. The overall effect is an increase in venous return⁵⁹. Conversely, in the mechanically ventilated patient, the IVC will distend with insufflation as increased intrathoracic pressure results in increased RV afterload and a transient increase in pulmonary artery pressure with an overall net decrease in venous return.⁶⁰

This IVC variability, termed the caval index, quantifies the degree of change in size of the IVC between end-inspiration and end-expiration. An M-mode imaging evaluation of the IVC allows for measurement of the maximal and minimal diameters for this calculation (Figure 11). Passively mechanically ventilated patients, with tidal volumes (TV) of 8 to 10 cc/kg in sinus rhythm, are predictably volume-responsive when the IVC distends by 12% to 18%.^54,61,62 However, there is considerable debate as to whether evaluating the degree of IVC collapse is of value in spontaneously breathing patients.⁶³ Cardiopulmonary interactions that drive IVC variability are affected by variable TV, intrathoracic pressure changes, etc. Nonetheless, two studies have shown that IVC collapse reliably predicts fluid responsiveness in spontaneously breathing patients.^64,65 

Stroke Volume/Arterial Flow Variability

Intrathoracic pressure changes induce dynamic changes in venous return that ultimately result in alterations in LV stroke volume (LVSV) when the blood volume traverses pulmonary circulation.⁶⁶ This variability in LVSV is the basis for all dynamic assessments of cardiopulmonary interactions, whether by arterial pressure waveform analysis or echocardiographic assessment of arterial flow. 

The LVSV variability reliably predicts fluid responsiveness and may be assessed by esophageal Doppler echocardiography of the ascending aorta.^67,68 Transesophageal echocardiography has also been used to assess SV variability at the LVOT.⁶⁹ Both of these measures require equipment and skill that may not be available in every clinical setting. Fortunately, LVOT SV is easily obtained through transthoracic echocardiography (TTE) (Figures 7a and 7b) using LVOT Doppler velocities as a surrogate for SV variations. A small study of TTE in mechanically ventilated children found that aortic flow variability predicted fluid responsiveness.⁷⁰ Therefore, transthoracic echocardiography provides a well-established alternative to thermodilution in determining cardiac output. Multiplication of the HR by an estimate of the column of blood flowing through the LVOT with each systolic contraction gives the cardiac output.⁷¹ 

Using TTE measurement of SV and cardiac output, the clinician can assess the effect of small fluid challenges on cardiac output.⁷² Cardiac output can be augmented with the passive leg raise (PLR), which is an entirely reversible preload challenge maneuver thought to increase preload by 300 to 500 mL. To assess volume responsiveness using this technique, LVOT cardiac output must first be determined. With the transducer in place, the patient’s legs are lifted to a 45° angle. After a minute of equilibration, the LVOT VTI is repeated and cardiac output recalculated. An increase in VTI of more than 12.5% predicts an increase in cardiac output with volume expansion.^73,74 This procedure requires proficiency with pulsed-wave Doppler and the ability to obtain the apical five-chamber view while a patient’s legs are being manipulated. In addition, the angle of insonation and location of measurement of LVOT and VTI must not vary for this measure to be valid. 

Alternatively, respiratory variation in LVOT peak velocities has been shown to reliably predict volume responsiveness when variability is more than 12% (Figure 7c).⁶⁹ This measurement is easier to obtain in that it does not require multiple views or complex calculations, and can be easily augmented with a passive leg raise maneuver. 

In the search for easily accessible alternatives to cardiac and aortic flow, brachial artery peak velocity variation (BAPVV) was found to be useful for predicting volume responsiveness.⁷⁵ To perform this study, the brachial artery is imaged in the long axis view using a linear transducer. Doppler gating should be adjusted to ensure an angle of less than 60°. The patient’s BAPVV is calculated as the difference between maximum and minimum peak velocity divided by the mean peak velocity. A variability in peak velocity of more than 10% predicts volume responsiveness.⁷⁵ 

Common Carotid Artery Flow

Similarly, CCA flow has attracted attention as a potential surrogate to assess SV response to preload challenge.^76,77 The CCA is large, easily accessible and does not require specialized training to assess (Figure 12).⁷⁸

Even though cardiopulmonary interaction assessment has excellent performance for predicting volume responsiveness, limitations do exist. For example, cardiopulmonary interactions may be exaggerated or diminished—thus decreasing the reliability of this assessment—in patients on mechanical ventilation who have spontaneous breathing, high positive end-expiratory pressures or a high minute ventilation, low TV, dysrhythmias, external compression of extra- or intrathoracic vessels (eg, intra-abdominal hypertension, pericardial tamponade, COPD/asthma exacerbations); and in patients who have decreased arterial elastance, or high RV afterload causing RV dysfunction or failure.

Conclusion

The advanced ultrasound techniques described in this review provide several useful tools to rapidly evaluate and manage cardiopulmonary interactions and assess the hemodynamic profile of critically ill patients. With these bedside techniques added to basic POCUS examinations, a new era in noninvasive critical care management is now available. 

As we enter the days of precision medicine, these examinations will enable EPs to optimize the care of this high-risk patient population. Moreover, future research by the emergency ultrasound and critical care communities on morbidity and mortality associated with resuscitation strategies in the ED will undoubtedly incorporate cardiopulmonary and hemodynamic ultrasound. 

Critically ill patients presenting to the ED represent the most time-sensitive patient encounter for the emergency physician (EP), as delays in restoring physiological homeostasis increase the risks of organ dysfunction and death. Management and treatment strategies in critically ill patients have evolved from the routine use of invasive catheters and radiography for cardiopulmonary evaluation to a variety of noninvasive devices and pathways. The widespread adoption of point-of-care ultrasound (POCUS) in EDs provides the opportunity to rapidly obtain invaluable information about the diagnosis and etiology to guide resuscitation in critically ill patients—particularly those in shock and acute dyspnea. 

Over the last two decades, EPs and critical care physicians have employed POCUS to assist in identifying emergent reversible causes of shock and cardiac arrest, including cardiac tamponade, massive pulmonary embolism (PE), and hemoperitoneum. Recent advances in hemodynamic and cardiopulmonary POCUS allow for a nuanced approach to hemodynamic evaluation.¹ In addition, the use of ultrasound “first” in the critical care setting may reduce the dependence on radiographic-based management, catheter-based protocols, and the need for invasive procedures. 

Bedside cardiopulmonary ultrasound to evaluate the hemodynamic status of hypotensive patients can help determine the etiology of shock, provide evidence of fluid-volume responsiveness, visualize hemodynamic abnormalities that would alter fluid resuscitation strategies, and assess patient response to an intervention. The use of ultrasound can also identify the etiology of acute respiratory failure—providing the opportunity to initiate the appropriate interventions prior to patient decompensation. Findings such as pneumothorax or pleural effusion may require immediate procedural intervention, while other findings may only require noninvasive positive pressure ventilation and diuresis. 

The tools to implement these concepts include basic POCUS education common to emergency medicine and critical care (American College of Emergency Physicians Guidelines and American College of Chest Physicians/Society of Critical Care Medicine guidelines); ultrasound machines with phased array, linear, and curvilinear probes; and ultrasonographic instrumentation such as M-Mode, color Doppler, and spectral Doppler. An understanding of common Doppler imaging techniques optimizes the examination, and the use of presets common to cardiac packages may further assist the provider with adoption. 

When evaluating critically ill patients, we recommend the following step-wise approach: 

• Identify a clinical question to be answered prior to doing the examination; 
• Determine the hemodynamic profile of the patient to guide therapeutic maneuvers; and 
• Monitor the response to any therapeutic maneuver and adjust accordingly. (In these complicated patients, repeat examinations are invaluable, as the hemodynamic profile can change rapidly.)

Emergency physicians are increasingly utilizing POCUS to rapidly evaluate the thoracic cavity in critically ill patients. This modality is an appealing alternative to formal chest radiography because of the ease of rapid image acquisition, lack of ionizing radiation, and the ability to repeat the examination in real-time. 

When critically ill patients present in respiratory distress, POCUS allows the EP to rapidly diagnose potential etiologies, such as pleural effusion, pneumothorax, or pulmonary edema, and employ emergent intervention, which can greatly alter the patient’s clinical course. Additionally, the rapid diagnosis of consolidation permits earlier appropriate management of sepsis and respiratory failure when the clinical setting is consistent with pneumonia. 

In many cases, ultrasound has been shown to be superior to traditional chest radiography to assess critically ill patients.^2-8 Although there are several protocols that utilize thoracic ultrasound in evaluating the critical patient, this review focuses solely on the components of thoracic ultrasound, rather than specific protocols.  

Pneumothorax 

Ultrasound imaging with a high-frequency probe is highly sensitive and specific in assessing for pneumothorax in a supine patient.⁹ In the normal lung, the visceral and parietal pleura are visualized as sliding with each breath. In this examination, the transducer is placed on the chest wall to visualize two ribs and the pleura between them (Figures 2a and 2b).

When lung sliding is present, the appearance in M-mode is that of the “seashore” or “sandy beach.” The hyperechoic white pleura is seen as moving with the respiratory cycle. Additionally, lung artifacts such as A-lines, horizontal reverberation artifacts; and B-lines (also referred to as “comet-tails”), vertical lines arising from distended subpleural alveoli, will be seen in a normal lung. If pneumothorax is present, no sliding or comet-tail artifacts will be present at the pleural surface. Although A-lines may also be absent in pneumothorax, studies have shown that the absence of lung sliding and the presence of A-lines are associated with increased specificity (94% vs 78% with absent lung sliding alone) for diagnosing occult pneumothorax.⁹

While the lack of pleural sliding is highly sensitive for pneumothorax, the clinician must place this finding within the clinical context of the patient. For example, an intubated patient may not have left-sided sliding in the case of a right main-stem intubation. Moreover, patients who have an underlying obstructive lung disease (eg, chronic obstructive pulmonary disease [COPD]) and/or emphysema may present a more challenging examination because pleural sliding is often absent, especially in the apical segments, and can mimic pneumothorax in these patients.¹⁰ 

In addition to pleural sliding, presence or absence of a lung pulse also assists in assessing patients for pneumothorax. The detection of a lung pulse on M-mode ultrasound indicates subtle cardiac pulsation at the periphery of the lung; this finding only appears in the nonventilated lung in the absence of a pneumothorax. The presence of lung pulse is therefore useful in distinguishing other causes of nonventilated lung from pneumothorax.¹¹

Pleural Fluid

The low-frequency curvilinear or phased array probes are used to assess for pleural fluid. In this study, the clinician fans the probe cephalad from Morison’s pouch on the patient’s right side, or from the splenorenal recess on the left side, to visualize the bright, hyperechoic diaphragm. If pleural fluid is present, there will be loss of the mirroring artifact, and the fluid will appear as an anechoic collection cephalad to the diaphragm. In addition, when fluid is present, the normal lung may be visualized moving within the effusion, evoking a quad or sinusoid sign with M-mode imaging.^12,13 In the setting of complicated parapneumonic effusion, the echogenicity may be mixed or difficult to detect.  

Visualization of the thoracic spine above the diaphragm may serve as a surrogate marker for the presence of fluid. Typically, the thoracic spine is not visualized on ultrasound due to the scatter caused by the air-filled lungs.

Ultrasound has been shown to be superior to routine chest radiograph for the identification of small pleural effusions.⁷ Given that both critically ill medical and injured patients can present with pleural fluid, the use of POCUS to rapidly determine the presence or absence of fluid is an adjunct in the evaluation of these patients. 

Interstitial Fluid

Evaluation of the thoracic cavity for interstitial fluid in the setting of acute pulmonary edema, acute respiratory distress syndrome (ARDS), or interstitial pneumonia is best accomplished using either the curvilinear low-frequency probe or the phased array probe. The visualization of vertically oriented B-lines in the upper lung fields is very sensitive for interstitial fluid or edema of the interlobular septa (Figures 2a and 2b).^13,15 In this study, B-lines originate at the pleural line, move with the pleura, and extend off the bottom of the monitor without obliteration (in contrast to A-lines). An isolated B-line may be physiological; however, the presence of several B-lines is consistent with an interstitial pathology. On imaging, the presence of three or more B-lines in a single rib space with a convex probe, or more than six B-lines when utilizing the curvilinear, is considered pathological and referred to as “lung rockets.” B-lines may be focal or diffuse, as seen respectively in cases of pneumonia or acute pulmonary edema.¹⁶ 

Pulmonary Assessment for Fluid Resuscitation

Fluid Resuscitation 

Lung ultrasound studies have been proposed as a means of determining adequate fluid resuscitation and preventing complications associated with excessive fluid. The appearance of diffuse B-lines of acute interstitial syndrome on lung ultrasound can uncover the first signs of extravascular lung water and prevent pulmonary alveolar edema and associated morbidity and mortality.¹⁷ The appearance of an A-line predominance throughout the lung does not predict fluid responsiveness, but rather potential fluid tolerance. 

A benefit of lung ultrasound is that it provides information more rapidly than many of the dynamic measures of fluid responsiveness and cardiac output variability. In addition, lung ultrasound studies are much more easily reproduced than repeating a velocity time integral (VTI) measurements.

Lichtenstein’s FALLS Protocol

Lichtenstein’s FALLS (Fluid Administration Limited by Lung Sonography) protocol provides an approach to performing lung ultrasound on patients presenting in shock.¹² In this approach, lung ultrasound studies are performed after echocardiography to evaluate the patient for causes of obstructive shock. The predominance of B-lines on lung ultrasound suggests cardiogenic shock and, by definition, fluid intolerance. The predominance of A-lines on ultrasound may be present in patients in hypovolemic or septic shock. 

In hypovolemic shock, continued fluid boluses will improve hemodynamics with preserved A-line predominance. In septic shock, B-lines will begin to appear, suggesting that other means of improving forward flow should be initiated.

Consolidation

Chest radiography is known to have variable test characteristics for the detection of pneumonia. Consolidation may not be detected in profoundly immunocompromised or dehydrated patients. Additionally, in critically ill patients, it is often challenging to obtain a posteroanterior and lateral chest X-ray, given the patient’s hemodynamic status and stability for transport, and a single portable anteroposterior film will often miss retrocardiac infiltrates. In both of these clinical settings, POCUS can provide a rapid diagnosis, expediting the care of these septic patients. 

In the presence of a dense consolidation, there may be hepatization of the lung parenchyma (Figure 4b). Additionally, hyperechoic air bronchograms are often visualized. Pneumonia is often associated with pleural effusion and localized B-lines. Using lung ultrasound, rapid bedside detection of these pulmonary findings in clinical presentations suggestive of pneumonia can accelerate appropriate antibiotic and respiratory supportive treatment.  

Left Ventricular Systolic Assessment 

Critically ill patients commonly present with a mixed shock picture, and it is rare for a patient to have solely cardiogenic shock, hemorrhagic shock, etc. Rather, a patient who presents in septic shock may have an underlying cardiomyopathy for which she or he is being treated with a beta-blocker. 

Cardiomyopathy associated with sepsis is common¹⁸ and, at least in the case of diastolic dysfunction, it is underdiagnosed and associated with a higher mortality rate.¹⁹ It is therefore essential that the EP evaluate left ventricular (LV) systolic function rapidly and reliably—particularly in critically ill patients whose disease process may be undifferentiated and whose hemodynamic status is unclear.^20-22 Bedside echocardiography by the EP is invaluable in identifying the LV contribution to the hemodynamic profile and tailoring resuscitation to optimize patient outcomes. 

Although gross visual assessment is the most widely used method by which EPs estimate LV systolic function, this strategy is subjective, operator-dependent, and requires at least two quality views to understand the heart’s three-dimensional movement. However, when faced with a rapid diagnostic dilemma, a global visual estimate of the overall contractility (hyperdynamic, normal, depressed, severely depressed) may be more useful than estimating the ejection fraction (EF), especially when the patient’s baseline EF is unknown. 

Regional wall-motion abnormalities can be evaluated by considering  and correlating the coronary artery distributions with the electrocardiographic findings and the clinical scenario (Figure 5).

Simpson’s Rule

Although no one parameter can quantitatively assess LV function, the EF is the one most commonly used. The Simpson’s Rule or the “method of disks” estimates EF by changes in calculated ventricular volumes. The endocardial border is outlined in end-diastole and end-systole (ES) in both the apical four- (AP4) and two-chamber views. The cardiac package on the ultrasound system can divide the selected area into a series of disks, calculate the volume of each disk, and then add these figures to estimate the ventricular volume (Figure 6a). Limitations of this study include potentially difficult visualization of the endocardial border, and the length of time to conduct this study. 

Fractional Shortening

M-mode ultrasound can be used in several ways to estimate LV EF. Fractional shortening (FS) estimates the size reduction of the LV during systole. In the parasternal long axis (PLAX) view, the M-mode cursor is placed over the walls of the LV, just apical to the tips of the mitral valve (MV) leaflets (Figure 6b). Maximal (end-diastolic diameter [EDD]) and minimal (end-systolic diameter [ESD]) dimensions of the LV are measured and FS is calculated as (LVEDD – LVESD)/ LVEDD. A normal value is more than 25%, and a rough estimate of EF is FS x 2.²⁴ Limitations to this study include nonplacement of the M-mode cursor perpendicular to the LV walls, and inaccuracy in patients with regional wall abnormalities. 

E-Point Septal Separation

Another way to assess EF with POCUS is through E-point septal separation (EPSS), which uses the movement of the MV during diastole to estimate the EF during systole. In the PLAX view, the M-mode cursor is placed over the apical tip of the anterior leaflet of the MV to visualize the movement of the leaflet in relation to the interventricular septum (Figure 6c). Two characteristic waves are created during each diastole—the larger first wave representing early filling (the E-wave) and the smaller second wave representing the atrial kick (the A-wave). The E-point is the tallest point of the E-wave, and the EPSS is measured as the distance in millimeters between the E-point and the interventricular septum.²¹ 

The opening of the anterior leaflet of the MV toward the interventricular septum in diastole requires a pressure difference between the left atrium (LA) and LV. In a patient with poor LV systolic function, the LV is still full at the end of systole, the pressure difference is not as great, and the mitral leaflets will not snap open vigorously. The EPSS should be at or less than 6 mm in patients with normal LV systolic function. An EPSS of 6 to 12 mm suggests moderately depressed LV systolic function, and over 12 mm signifies severely decreased LV systolic function.²⁵ Limitations include inaccuracy in patients with valvular abnormalities, such as mitral stenosis or aortic regurgitation, severe LV or septal hypertrophy, regional wall abnormalities or severe LV dilation, limited data, and a wide margin of error when comparing to magnetic resonance imaging measurement of EF.

Cardiac Output 

Left Ventricular Diastolic Assessment

In an aging population of patients who have longstanding, undiagnosed, or untreated hypertension, LV hypertrophy leads to impaired relaxation and diastolic filling, eventually causing elevated LA pressure and, in extreme cases, restrictive cardiomyopathy. It has been reported that approximately half of all symptomatic patients with heart failure have a preserved EF.²⁷ 

Determination of LV pressures allows for the distinction between hydrostatic pulmonary edema and ARDS. Diagnosing elevated LA pressure is not inconsequential, as diastolic dysfunction in septic patients has been associated with increased mortality, likely due to increased pulmonary edema from fluid resuscitation.¹⁹ An invasive method of using a pulmonary artery catheter and measuring the pulmonary artery occlusion pressure to estimate the LA pressure is the gold standard, but is no longer routinely performed. 

Echocardiography is a noninvasive surrogate to estimating LA and LV filling pressures. Two different echocardiographic measurements can be used in conjunction to estimate LV filling pressures: MV inflow velocity and tissue Doppler imaging. 

Mitral Valve Inflow Velocity

Assessment of the MV inflow is performed by placing the pulse-wave Doppler gate between the tips of the MV leaflets in the AP4 view. Early diastolic filling produces the E-wave, and LA contraction produces the late diastolic A-wave (Figure 8a).

Tissue Doppler Imaging

Tissue Doppler imaging enables the clinician to measure myocardial velocities such as the speed of relaxation to evaluate if LV relaxation is due to a drop in LV pressure below LA pressure after systole, pulling the MV open; or if increased LA pressure is required to push open the MV and fill the LV. 

For this study, the tissue Doppler sampling gate is placed at the septal or lateral annulus of the MV in the AP4 view to visualize early diastolic mitral annulus velocity (e’) (Figure 8b). The E/e’ ratio can be helpful for estimating LV filling pressures. An E/e’ of less than 8 is associated with normal LV filling pressure whereas an E/e’ >15 is associated with an elevated LV filling pressure.28,29 When the E/e’ is 8 to 10, other indices such as the E/A ratio and deceleration time, as well as the clinical picture, can provide insight into the presence of hemodynamically significant diastolic dysfunction.

Learning and applying the assessment of diastolic parameters can be challenging; however, these parameters can be used to help predict LV filling pressures in patients with findings of pulmonary edema on chest radiograph. Limitations of these techniques are inter-rater variability, as well as the ability of the operator to acquire the required AP4 view. In addition, these techniques are unreliable in patients with irregular cardiac rhythms, severe mitral disease, and in hypertrophic cardiomyopathy. 

Right Ventricular Assessment

The right ventricle (RV) is a small, thin-walled ventricle with only two layers of muscle, as opposed to the three layers of the LV. In contrast to the rocking motion of LV contraction, the orientation of the two muscle layers of the RV permits mostly longitudinal contraction. The circumferential muscle fibers are shared at the base and apex with the LV, which can provide some of the contractile strength of the RV.³⁰ Because of this orientation, RV strain, which can manifest as decreased longitudinal contraction, speed of contraction, septal movement, and tethering abnormalities through ventricular interdependence, can be measured easily using bedside echocardiography. 

In healthy individuals, the RV is a low-pressure chamber that acts as a conduit for propelling venous return into the pulmonary circulation without much effect on systemic hemodynamics. However, in critical illness, RV abnormalities can have profound effects on hemodynamics, and  the efforts typically used to improve LV performance will worsen a failing RV. 

While RV dysfunction is most commonly due to chronic LV disease, acute RV dysfunction is commonly encountered in critical illness,³¹ including many septic patients with ARDS,^32,33 PE, or decompensated chronic pulmonary hypertension.³⁴ The examinations that follow, allow the EP to assess for the presence of RV dysfunction and to guide resuscitation appropriately to avoid the untoward hemodynamic effects of conventional resuscitation strategies in these patients. 

When evaluating the RV, the clinician must determine (1) if the patient’s RV strain is due to pressure or volume overload; and (2) if the patient’s RV is responsive or nonresponsive to a preload challenge, prompting an alteration in the resuscitation plan in nonresponsive cases. 

Right Ventricular Pressure/Volume Overload

While inferior vena cava (IVC) ultrasound has been shown to be a pre-heart/lung assessment of cardiopulmonary interactions that predicts volume responsiveness, the IVC is also a good predictor of right atrial (RA) pressure.³⁵ If the IVC is dilated and lacks respiratory variation, the patient likely has an elevated RA pressure, which is most likely transmitted from an elevated RV pressure (Figure 9a). However, compliance of the RA, RA pressure and, by extension, IVC prediction of that RA pressure, may underestimate the degree of RV pressure or afterload. 

Right Ventricular Strain and Contractile Reserve 

From the same apical view, tissue Doppler at the lateral tricuspid annulus will give a tricuspid annular peak velocity, a measure of the isovolumetric contraction velocity. This measurement will provide a measure of the contractile reserve of the RV (Figure 10b). A measure of less than 10 cm/sec indicates that further volume and inotropic challenges to the RV will not be effective, and the focus should be to decrease RV afterload with pulmonary vasodilators.^34,39,40 

Fluid Resuscitation Assessment 

Restoring circulating volume to increase cardiac output and improve oxygen delivery is the primary objective when managing patients in shock. Patient outcomes improve dramatically with early aggressive fluid resuscitation.^41-44 However, many critically ill patients do not respond to fluid resuscitation, which is generally defined as the rise of cardiac output of more than 15% in response to volume expansion. Not all patients found to be fluid responsive will require volume expansion.^45,46 

Excessive fluid resuscitation has been shown to increase intensive care unit length of stay, morbidity, and mortality.^47,48 Further, pathophysiological processes such as RV dysfunction and severe diastolic dysfunction can significantly alter the hemodynamic profile such that fluid management can be quite challenging in critically ill patients.

Distinguishing responders from nonresponders prior to fluid administration is the goal of early resuscitation. Unfortunately, this distinction cannot be made based on the patient’s vital signs or the physical examination.⁴⁹ Static filling pressures and volumetric measures are unreliable markers of fluid responsiveness.^50,51 The practice of administering a fluid challenge and observing the clinical effect on cardiac output is undesirable because it requires, by definition, on administering fluids, which ultimately may be harmful to the patient. 

Dynamic measures of fluid responsiveness that reliably predict cardiac response to a preload challenge are proven to be of greater utility.^52,53 These assessments determine volume responsiveness by evaluating the change in LV output with intrathoracic pressure changes due to the respiratory cycle, (ie, cardiopulmonary interaction). Ultrasound studies to assess cardiopulmonary interactions include IVC variability, arterial flow variability, brachial artery peak velocity variability, and common carotid artery (CCA) flow. In addition to echocardiography, lung ultrasound may be used to determine the endpoint of fluid resuscitation by monitoring for the appearance of extravascular lung water. 

Inferior Vena Cava Variability 

The IVC is a large extrathoracic vein which is easily insonated and accessible, even to a clinician with basic bedside ultrasound competency. Static IVC measures, such as diameter alone, correlate with central venous pressure but do not predict fluid responsiveness.^54-56 Dynamic IVC evaluation provides an upstream assessment of cardiopulmonary interactions. 

In the spontaneously breathing patient, the IVC collapses with inspiration as the RA pressure falls below atmospheric pressure, collapsing the intrathoracic veins for a short period until the intravascular pressure at the entry to the thorax exceeds atmospheric pressure, causing a bolus of venous return to the right heart. The overall effect is an increase in venous return⁵⁹. Conversely, in the mechanically ventilated patient, the IVC will distend with insufflation as increased intrathoracic pressure results in increased RV afterload and a transient increase in pulmonary artery pressure with an overall net decrease in venous return.⁶⁰

This IVC variability, termed the caval index, quantifies the degree of change in size of the IVC between end-inspiration and end-expiration. An M-mode imaging evaluation of the IVC allows for measurement of the maximal and minimal diameters for this calculation (Figure 11). Passively mechanically ventilated patients, with tidal volumes (TV) of 8 to 10 cc/kg in sinus rhythm, are predictably volume-responsive when the IVC distends by 12% to 18%.^54,61,62 However, there is considerable debate as to whether evaluating the degree of IVC collapse is of value in spontaneously breathing patients.⁶³ Cardiopulmonary interactions that drive IVC variability are affected by variable TV, intrathoracic pressure changes, etc. Nonetheless, two studies have shown that IVC collapse reliably predicts fluid responsiveness in spontaneously breathing patients.^64,65 

Stroke Volume/Arterial Flow Variability

Intrathoracic pressure changes induce dynamic changes in venous return that ultimately result in alterations in LV stroke volume (LVSV) when the blood volume traverses pulmonary circulation.⁶⁶ This variability in LVSV is the basis for all dynamic assessments of cardiopulmonary interactions, whether by arterial pressure waveform analysis or echocardiographic assessment of arterial flow. 

The LVSV variability reliably predicts fluid responsiveness and may be assessed by esophageal Doppler echocardiography of the ascending aorta.^67,68 Transesophageal echocardiography has also been used to assess SV variability at the LVOT.⁶⁹ Both of these measures require equipment and skill that may not be available in every clinical setting. Fortunately, LVOT SV is easily obtained through transthoracic echocardiography (TTE) (Figures 7a and 7b) using LVOT Doppler velocities as a surrogate for SV variations. A small study of TTE in mechanically ventilated children found that aortic flow variability predicted fluid responsiveness.⁷⁰ Therefore, transthoracic echocardiography provides a well-established alternative to thermodilution in determining cardiac output. Multiplication of the HR by an estimate of the column of blood flowing through the LVOT with each systolic contraction gives the cardiac output.⁷¹ 

Using TTE measurement of SV and cardiac output, the clinician can assess the effect of small fluid challenges on cardiac output.⁷² Cardiac output can be augmented with the passive leg raise (PLR), which is an entirely reversible preload challenge maneuver thought to increase preload by 300 to 500 mL. To assess volume responsiveness using this technique, LVOT cardiac output must first be determined. With the transducer in place, the patient’s legs are lifted to a 45° angle. After a minute of equilibration, the LVOT VTI is repeated and cardiac output recalculated. An increase in VTI of more than 12.5% predicts an increase in cardiac output with volume expansion.^73,74 This procedure requires proficiency with pulsed-wave Doppler and the ability to obtain the apical five-chamber view while a patient’s legs are being manipulated. In addition, the angle of insonation and location of measurement of LVOT and VTI must not vary for this measure to be valid. 

Alternatively, respiratory variation in LVOT peak velocities has been shown to reliably predict volume responsiveness when variability is more than 12% (Figure 7c).⁶⁹ This measurement is easier to obtain in that it does not require multiple views or complex calculations, and can be easily augmented with a passive leg raise maneuver. 

In the search for easily accessible alternatives to cardiac and aortic flow, brachial artery peak velocity variation (BAPVV) was found to be useful for predicting volume responsiveness.⁷⁵ To perform this study, the brachial artery is imaged in the long axis view using a linear transducer. Doppler gating should be adjusted to ensure an angle of less than 60°. The patient’s BAPVV is calculated as the difference between maximum and minimum peak velocity divided by the mean peak velocity. A variability in peak velocity of more than 10% predicts volume responsiveness.⁷⁵ 

Common Carotid Artery Flow

Similarly, CCA flow has attracted attention as a potential surrogate to assess SV response to preload challenge.^76,77 The CCA is large, easily accessible and does not require specialized training to assess (Figure 12).⁷⁸

Even though cardiopulmonary interaction assessment has excellent performance for predicting volume responsiveness, limitations do exist. For example, cardiopulmonary interactions may be exaggerated or diminished—thus decreasing the reliability of this assessment—in patients on mechanical ventilation who have spontaneous breathing, high positive end-expiratory pressures or a high minute ventilation, low TV, dysrhythmias, external compression of extra- or intrathoracic vessels (eg, intra-abdominal hypertension, pericardial tamponade, COPD/asthma exacerbations); and in patients who have decreased arterial elastance, or high RV afterload causing RV dysfunction or failure.

Conclusion

The advanced ultrasound techniques described in this review provide several useful tools to rapidly evaluate and manage cardiopulmonary interactions and assess the hemodynamic profile of critically ill patients. With these bedside techniques added to basic POCUS examinations, a new era in noninvasive critical care management is now available. 

As we enter the days of precision medicine, these examinations will enable EPs to optimize the care of this high-risk patient population. Moreover, future research by the emergency ultrasound and critical care communities on morbidity and mortality associated with resuscitation strategies in the ED will undoubtedly incorporate cardiopulmonary and hemodynamic ultrasound. 

Critically ill patients presenting to the ED represent the most time-sensitive patient encounter for the emergency physician (EP), as delays in restoring physiological homeostasis increase the risks of organ dysfunction and death. Management and treatment strategies in critically ill patients have evolved from the routine use of invasive catheters and radiography for cardiopulmonary evaluation to a variety of noninvasive devices and pathways. The widespread adoption of point-of-care ultrasound (POCUS) in EDs provides the opportunity to rapidly obtain invaluable information about the diagnosis and etiology to guide resuscitation in critically ill patients—particularly those in shock and acute dyspnea. 

Over the last two decades, EPs and critical care physicians have employed POCUS to assist in identifying emergent reversible causes of shock and cardiac arrest, including cardiac tamponade, massive pulmonary embolism (PE), and hemoperitoneum. Recent advances in hemodynamic and cardiopulmonary POCUS allow for a nuanced approach to hemodynamic evaluation.¹ In addition, the use of ultrasound “first” in the critical care setting may reduce the dependence on radiographic-based management, catheter-based protocols, and the need for invasive procedures. 

Bedside cardiopulmonary ultrasound to evaluate the hemodynamic status of hypotensive patients can help determine the etiology of shock, provide evidence of fluid-volume responsiveness, visualize hemodynamic abnormalities that would alter fluid resuscitation strategies, and assess patient response to an intervention. The use of ultrasound can also identify the etiology of acute respiratory failure—providing the opportunity to initiate the appropriate interventions prior to patient decompensation. Findings such as pneumothorax or pleural effusion may require immediate procedural intervention, while other findings may only require noninvasive positive pressure ventilation and diuresis. 

The tools to implement these concepts include basic POCUS education common to emergency medicine and critical care (American College of Emergency Physicians Guidelines and American College of Chest Physicians/Society of Critical Care Medicine guidelines); ultrasound machines with phased array, linear, and curvilinear probes; and ultrasonographic instrumentation such as M-Mode, color Doppler, and spectral Doppler. An understanding of common Doppler imaging techniques optimizes the examination, and the use of presets common to cardiac packages may further assist the provider with adoption. 

When evaluating critically ill patients, we recommend the following step-wise approach: 

• Identify a clinical question to be answered prior to doing the examination; 
• Determine the hemodynamic profile of the patient to guide therapeutic maneuvers; and 
• Monitor the response to any therapeutic maneuver and adjust accordingly. (In these complicated patients, repeat examinations are invaluable, as the hemodynamic profile can change rapidly.)

Emergency physicians are increasingly utilizing POCUS to rapidly evaluate the thoracic cavity in critically ill patients. This modality is an appealing alternative to formal chest radiography because of the ease of rapid image acquisition, lack of ionizing radiation, and the ability to repeat the examination in real-time. 

When critically ill patients present in respiratory distress, POCUS allows the EP to rapidly diagnose potential etiologies, such as pleural effusion, pneumothorax, or pulmonary edema, and employ emergent intervention, which can greatly alter the patient’s clinical course. Additionally, the rapid diagnosis of consolidation permits earlier appropriate management of sepsis and respiratory failure when the clinical setting is consistent with pneumonia. 

In many cases, ultrasound has been shown to be superior to traditional chest radiography to assess critically ill patients.^2-8 Although there are several protocols that utilize thoracic ultrasound in evaluating the critical patient, this review focuses solely on the components of thoracic ultrasound, rather than specific protocols.  

Pneumothorax 

Ultrasound imaging with a high-frequency probe is highly sensitive and specific in assessing for pneumothorax in a supine patient.⁹ In the normal lung, the visceral and parietal pleura are visualized as sliding with each breath. In this examination, the transducer is placed on the chest wall to visualize two ribs and the pleura between them (Figures 2a and 2b).

When lung sliding is present, the appearance in M-mode is that of the “seashore” or “sandy beach.” The hyperechoic white pleura is seen as moving with the respiratory cycle. Additionally, lung artifacts such as A-lines, horizontal reverberation artifacts; and B-lines (also referred to as “comet-tails”), vertical lines arising from distended subpleural alveoli, will be seen in a normal lung. If pneumothorax is present, no sliding or comet-tail artifacts will be present at the pleural surface. Although A-lines may also be absent in pneumothorax, studies have shown that the absence of lung sliding and the presence of A-lines are associated with increased specificity (94% vs 78% with absent lung sliding alone) for diagnosing occult pneumothorax.⁹

While the lack of pleural sliding is highly sensitive for pneumothorax, the clinician must place this finding within the clinical context of the patient. For example, an intubated patient may not have left-sided sliding in the case of a right main-stem intubation. Moreover, patients who have an underlying obstructive lung disease (eg, chronic obstructive pulmonary disease [COPD]) and/or emphysema may present a more challenging examination because pleural sliding is often absent, especially in the apical segments, and can mimic pneumothorax in these patients.¹⁰ 

In addition to pleural sliding, presence or absence of a lung pulse also assists in assessing patients for pneumothorax. The detection of a lung pulse on M-mode ultrasound indicates subtle cardiac pulsation at the periphery of the lung; this finding only appears in the nonventilated lung in the absence of a pneumothorax. The presence of lung pulse is therefore useful in distinguishing other causes of nonventilated lung from pneumothorax.¹¹

Pleural Fluid

The low-frequency curvilinear or phased array probes are used to assess for pleural fluid. In this study, the clinician fans the probe cephalad from Morison’s pouch on the patient’s right side, or from the splenorenal recess on the left side, to visualize the bright, hyperechoic diaphragm. If pleural fluid is present, there will be loss of the mirroring artifact, and the fluid will appear as an anechoic collection cephalad to the diaphragm. In addition, when fluid is present, the normal lung may be visualized moving within the effusion, evoking a quad or sinusoid sign with M-mode imaging.^12,13 In the setting of complicated parapneumonic effusion, the echogenicity may be mixed or difficult to detect.  

Visualization of the thoracic spine above the diaphragm may serve as a surrogate marker for the presence of fluid. Typically, the thoracic spine is not visualized on ultrasound due to the scatter caused by the air-filled lungs.

Ultrasound has been shown to be superior to routine chest radiograph for the identification of small pleural effusions.⁷ Given that both critically ill medical and injured patients can present with pleural fluid, the use of POCUS to rapidly determine the presence or absence of fluid is an adjunct in the evaluation of these patients. 

Interstitial Fluid

Evaluation of the thoracic cavity for interstitial fluid in the setting of acute pulmonary edema, acute respiratory distress syndrome (ARDS), or interstitial pneumonia is best accomplished using either the curvilinear low-frequency probe or the phased array probe. The visualization of vertically oriented B-lines in the upper lung fields is very sensitive for interstitial fluid or edema of the interlobular septa (Figures 2a and 2b).^13,15 In this study, B-lines originate at the pleural line, move with the pleura, and extend off the bottom of the monitor without obliteration (in contrast to A-lines). An isolated B-line may be physiological; however, the presence of several B-lines is consistent with an interstitial pathology. On imaging, the presence of three or more B-lines in a single rib space with a convex probe, or more than six B-lines when utilizing the curvilinear, is considered pathological and referred to as “lung rockets.” B-lines may be focal or diffuse, as seen respectively in cases of pneumonia or acute pulmonary edema.¹⁶ 

Pulmonary Assessment for Fluid Resuscitation

Fluid Resuscitation 

Lung ultrasound studies have been proposed as a means of determining adequate fluid resuscitation and preventing complications associated with excessive fluid. The appearance of diffuse B-lines of acute interstitial syndrome on lung ultrasound can uncover the first signs of extravascular lung water and prevent pulmonary alveolar edema and associated morbidity and mortality.¹⁷ The appearance of an A-line predominance throughout the lung does not predict fluid responsiveness, but rather potential fluid tolerance. 

A benefit of lung ultrasound is that it provides information more rapidly than many of the dynamic measures of fluid responsiveness and cardiac output variability. In addition, lung ultrasound studies are much more easily reproduced than repeating a velocity time integral (VTI) measurements.

Lichtenstein’s FALLS Protocol

Lichtenstein’s FALLS (Fluid Administration Limited by Lung Sonography) protocol provides an approach to performing lung ultrasound on patients presenting in shock.¹² In this approach, lung ultrasound studies are performed after echocardiography to evaluate the patient for causes of obstructive shock. The predominance of B-lines on lung ultrasound suggests cardiogenic shock and, by definition, fluid intolerance. The predominance of A-lines on ultrasound may be present in patients in hypovolemic or septic shock. 

In hypovolemic shock, continued fluid boluses will improve hemodynamics with preserved A-line predominance. In septic shock, B-lines will begin to appear, suggesting that other means of improving forward flow should be initiated.

Consolidation

Chest radiography is known to have variable test characteristics for the detection of pneumonia. Consolidation may not be detected in profoundly immunocompromised or dehydrated patients. Additionally, in critically ill patients, it is often challenging to obtain a posteroanterior and lateral chest X-ray, given the patient’s hemodynamic status and stability for transport, and a single portable anteroposterior film will often miss retrocardiac infiltrates. In both of these clinical settings, POCUS can provide a rapid diagnosis, expediting the care of these septic patients. 

In the presence of a dense consolidation, there may be hepatization of the lung parenchyma (Figure 4b). Additionally, hyperechoic air bronchograms are often visualized. Pneumonia is often associated with pleural effusion and localized B-lines. Using lung ultrasound, rapid bedside detection of these pulmonary findings in clinical presentations suggestive of pneumonia can accelerate appropriate antibiotic and respiratory supportive treatment.  

Left Ventricular Systolic Assessment 

Critically ill patients commonly present with a mixed shock picture, and it is rare for a patient to have solely cardiogenic shock, hemorrhagic shock, etc. Rather, a patient who presents in septic shock may have an underlying cardiomyopathy for which she or he is being treated with a beta-blocker. 

Cardiomyopathy associated with sepsis is common¹⁸ and, at least in the case of diastolic dysfunction, it is underdiagnosed and associated with a higher mortality rate.¹⁹ It is therefore essential that the EP evaluate left ventricular (LV) systolic function rapidly and reliably—particularly in critically ill patients whose disease process may be undifferentiated and whose hemodynamic status is unclear.^20-22 Bedside echocardiography by the EP is invaluable in identifying the LV contribution to the hemodynamic profile and tailoring resuscitation to optimize patient outcomes. 

Although gross visual assessment is the most widely used method by which EPs estimate LV systolic function, this strategy is subjective, operator-dependent, and requires at least two quality views to understand the heart’s three-dimensional movement. However, when faced with a rapid diagnostic dilemma, a global visual estimate of the overall contractility (hyperdynamic, normal, depressed, severely depressed) may be more useful than estimating the ejection fraction (EF), especially when the patient’s baseline EF is unknown. 

Regional wall-motion abnormalities can be evaluated by considering  and correlating the coronary artery distributions with the electrocardiographic findings and the clinical scenario (Figure 5).

Simpson’s Rule

Although no one parameter can quantitatively assess LV function, the EF is the one most commonly used. The Simpson’s Rule or the “method of disks” estimates EF by changes in calculated ventricular volumes. The endocardial border is outlined in end-diastole and end-systole (ES) in both the apical four- (AP4) and two-chamber views. The cardiac package on the ultrasound system can divide the selected area into a series of disks, calculate the volume of each disk, and then add these figures to estimate the ventricular volume (Figure 6a). Limitations of this study include potentially difficult visualization of the endocardial border, and the length of time to conduct this study. 

Fractional Shortening

M-mode ultrasound can be used in several ways to estimate LV EF. Fractional shortening (FS) estimates the size reduction of the LV during systole. In the parasternal long axis (PLAX) view, the M-mode cursor is placed over the walls of the LV, just apical to the tips of the mitral valve (MV) leaflets (Figure 6b). Maximal (end-diastolic diameter [EDD]) and minimal (end-systolic diameter [ESD]) dimensions of the LV are measured and FS is calculated as (LVEDD – LVESD)/ LVEDD. A normal value is more than 25%, and a rough estimate of EF is FS x 2.²⁴ Limitations to this study include nonplacement of the M-mode cursor perpendicular to the LV walls, and inaccuracy in patients with regional wall abnormalities. 

E-Point Septal Separation

Another way to assess EF with POCUS is through E-point septal separation (EPSS), which uses the movement of the MV during diastole to estimate the EF during systole. In the PLAX view, the M-mode cursor is placed over the apical tip of the anterior leaflet of the MV to visualize the movement of the leaflet in relation to the interventricular septum (Figure 6c). Two characteristic waves are created during each diastole—the larger first wave representing early filling (the E-wave) and the smaller second wave representing the atrial kick (the A-wave). The E-point is the tallest point of the E-wave, and the EPSS is measured as the distance in millimeters between the E-point and the interventricular septum.²¹ 

The opening of the anterior leaflet of the MV toward the interventricular septum in diastole requires a pressure difference between the left atrium (LA) and LV. In a patient with poor LV systolic function, the LV is still full at the end of systole, the pressure difference is not as great, and the mitral leaflets will not snap open vigorously. The EPSS should be at or less than 6 mm in patients with normal LV systolic function. An EPSS of 6 to 12 mm suggests moderately depressed LV systolic function, and over 12 mm signifies severely decreased LV systolic function.²⁵ Limitations include inaccuracy in patients with valvular abnormalities, such as mitral stenosis or aortic regurgitation, severe LV or septal hypertrophy, regional wall abnormalities or severe LV dilation, limited data, and a wide margin of error when comparing to magnetic resonance imaging measurement of EF.

Cardiac Output 

Left Ventricular Diastolic Assessment

In an aging population of patients who have longstanding, undiagnosed, or untreated hypertension, LV hypertrophy leads to impaired relaxation and diastolic filling, eventually causing elevated LA pressure and, in extreme cases, restrictive cardiomyopathy. It has been reported that approximately half of all symptomatic patients with heart failure have a preserved EF.²⁷ 

Determination of LV pressures allows for the distinction between hydrostatic pulmonary edema and ARDS. Diagnosing elevated LA pressure is not inconsequential, as diastolic dysfunction in septic patients has been associated with increased mortality, likely due to increased pulmonary edema from fluid resuscitation.¹⁹ An invasive method of using a pulmonary artery catheter and measuring the pulmonary artery occlusion pressure to estimate the LA pressure is the gold standard, but is no longer routinely performed. 

Echocardiography is a noninvasive surrogate to estimating LA and LV filling pressures. Two different echocardiographic measurements can be used in conjunction to estimate LV filling pressures: MV inflow velocity and tissue Doppler imaging. 

Mitral Valve Inflow Velocity

Assessment of the MV inflow is performed by placing the pulse-wave Doppler gate between the tips of the MV leaflets in the AP4 view. Early diastolic filling produces the E-wave, and LA contraction produces the late diastolic A-wave (Figure 8a).

Tissue Doppler Imaging

Tissue Doppler imaging enables the clinician to measure myocardial velocities such as the speed of relaxation to evaluate if LV relaxation is due to a drop in LV pressure below LA pressure after systole, pulling the MV open; or if increased LA pressure is required to push open the MV and fill the LV. 

For this study, the tissue Doppler sampling gate is placed at the septal or lateral annulus of the MV in the AP4 view to visualize early diastolic mitral annulus velocity (e’) (Figure 8b). The E/e’ ratio can be helpful for estimating LV filling pressures. An E/e’ of less than 8 is associated with normal LV filling pressure whereas an E/e’ >15 is associated with an elevated LV filling pressure.28,29 When the E/e’ is 8 to 10, other indices such as the E/A ratio and deceleration time, as well as the clinical picture, can provide insight into the presence of hemodynamically significant diastolic dysfunction.

Learning and applying the assessment of diastolic parameters can be challenging; however, these parameters can be used to help predict LV filling pressures in patients with findings of pulmonary edema on chest radiograph. Limitations of these techniques are inter-rater variability, as well as the ability of the operator to acquire the required AP4 view. In addition, these techniques are unreliable in patients with irregular cardiac rhythms, severe mitral disease, and in hypertrophic cardiomyopathy. 

Right Ventricular Assessment

The right ventricle (RV) is a small, thin-walled ventricle with only two layers of muscle, as opposed to the three layers of the LV. In contrast to the rocking motion of LV contraction, the orientation of the two muscle layers of the RV permits mostly longitudinal contraction. The circumferential muscle fibers are shared at the base and apex with the LV, which can provide some of the contractile strength of the RV.³⁰ Because of this orientation, RV strain, which can manifest as decreased longitudinal contraction, speed of contraction, septal movement, and tethering abnormalities through ventricular interdependence, can be measured easily using bedside echocardiography. 

In healthy individuals, the RV is a low-pressure chamber that acts as a conduit for propelling venous return into the pulmonary circulation without much effect on systemic hemodynamics. However, in critical illness, RV abnormalities can have profound effects on hemodynamics, and  the efforts typically used to improve LV performance will worsen a failing RV. 

While RV dysfunction is most commonly due to chronic LV disease, acute RV dysfunction is commonly encountered in critical illness,³¹ including many septic patients with ARDS,^32,33 PE, or decompensated chronic pulmonary hypertension.³⁴ The examinations that follow, allow the EP to assess for the presence of RV dysfunction and to guide resuscitation appropriately to avoid the untoward hemodynamic effects of conventional resuscitation strategies in these patients. 

When evaluating the RV, the clinician must determine (1) if the patient’s RV strain is due to pressure or volume overload; and (2) if the patient’s RV is responsive or nonresponsive to a preload challenge, prompting an alteration in the resuscitation plan in nonresponsive cases. 

Right Ventricular Pressure/Volume Overload

While inferior vena cava (IVC) ultrasound has been shown to be a pre-heart/lung assessment of cardiopulmonary interactions that predicts volume responsiveness, the IVC is also a good predictor of right atrial (RA) pressure.³⁵ If the IVC is dilated and lacks respiratory variation, the patient likely has an elevated RA pressure, which is most likely transmitted from an elevated RV pressure (Figure 9a). However, compliance of the RA, RA pressure and, by extension, IVC prediction of that RA pressure, may underestimate the degree of RV pressure or afterload. 

Right Ventricular Strain and Contractile Reserve 

From the same apical view, tissue Doppler at the lateral tricuspid annulus will give a tricuspid annular peak velocity, a measure of the isovolumetric contraction velocity. This measurement will provide a measure of the contractile reserve of the RV (Figure 10b). A measure of less than 10 cm/sec indicates that further volume and inotropic challenges to the RV will not be effective, and the focus should be to decrease RV afterload with pulmonary vasodilators.^34,39,40 

Fluid Resuscitation Assessment 

Restoring circulating volume to increase cardiac output and improve oxygen delivery is the primary objective when managing patients in shock. Patient outcomes improve dramatically with early aggressive fluid resuscitation.^41-44 However, many critically ill patients do not respond to fluid resuscitation, which is generally defined as the rise of cardiac output of more than 15% in response to volume expansion. Not all patients found to be fluid responsive will require volume expansion.^45,46 

Excessive fluid resuscitation has been shown to increase intensive care unit length of stay, morbidity, and mortality.^47,48 Further, pathophysiological processes such as RV dysfunction and severe diastolic dysfunction can significantly alter the hemodynamic profile such that fluid management can be quite challenging in critically ill patients.

Distinguishing responders from nonresponders prior to fluid administration is the goal of early resuscitation. Unfortunately, this distinction cannot be made based on the patient’s vital signs or the physical examination.⁴⁹ Static filling pressures and volumetric measures are unreliable markers of fluid responsiveness.^50,51 The practice of administering a fluid challenge and observing the clinical effect on cardiac output is undesirable because it requires, by definition, on administering fluids, which ultimately may be harmful to the patient. 

Dynamic measures of fluid responsiveness that reliably predict cardiac response to a preload challenge are proven to be of greater utility.^52,53 These assessments determine volume responsiveness by evaluating the change in LV output with intrathoracic pressure changes due to the respiratory cycle, (ie, cardiopulmonary interaction). Ultrasound studies to assess cardiopulmonary interactions include IVC variability, arterial flow variability, brachial artery peak velocity variability, and common carotid artery (CCA) flow. In addition to echocardiography, lung ultrasound may be used to determine the endpoint of fluid resuscitation by monitoring for the appearance of extravascular lung water. 

Inferior Vena Cava Variability 

The IVC is a large extrathoracic vein which is easily insonated and accessible, even to a clinician with basic bedside ultrasound competency. Static IVC measures, such as diameter alone, correlate with central venous pressure but do not predict fluid responsiveness.^54-56 Dynamic IVC evaluation provides an upstream assessment of cardiopulmonary interactions. 

In the spontaneously breathing patient, the IVC collapses with inspiration as the RA pressure falls below atmospheric pressure, collapsing the intrathoracic veins for a short period until the intravascular pressure at the entry to the thorax exceeds atmospheric pressure, causing a bolus of venous return to the right heart. The overall effect is an increase in venous return⁵⁹. Conversely, in the mechanically ventilated patient, the IVC will distend with insufflation as increased intrathoracic pressure results in increased RV afterload and a transient increase in pulmonary artery pressure with an overall net decrease in venous return.⁶⁰

This IVC variability, termed the caval index, quantifies the degree of change in size of the IVC between end-inspiration and end-expiration. An M-mode imaging evaluation of the IVC allows for measurement of the maximal and minimal diameters for this calculation (Figure 11). Passively mechanically ventilated patients, with tidal volumes (TV) of 8 to 10 cc/kg in sinus rhythm, are predictably volume-responsive when the IVC distends by 12% to 18%.^54,61,62 However, there is considerable debate as to whether evaluating the degree of IVC collapse is of value in spontaneously breathing patients.⁶³ Cardiopulmonary interactions that drive IVC variability are affected by variable TV, intrathoracic pressure changes, etc. Nonetheless, two studies have shown that IVC collapse reliably predicts fluid responsiveness in spontaneously breathing patients.^64,65 

Stroke Volume/Arterial Flow Variability

Intrathoracic pressure changes induce dynamic changes in venous return that ultimately result in alterations in LV stroke volume (LVSV) when the blood volume traverses pulmonary circulation.⁶⁶ This variability in LVSV is the basis for all dynamic assessments of cardiopulmonary interactions, whether by arterial pressure waveform analysis or echocardiographic assessment of arterial flow. 

The LVSV variability reliably predicts fluid responsiveness and may be assessed by esophageal Doppler echocardiography of the ascending aorta.^67,68 Transesophageal echocardiography has also been used to assess SV variability at the LVOT.⁶⁹ Both of these measures require equipment and skill that may not be available in every clinical setting. Fortunately, LVOT SV is easily obtained through transthoracic echocardiography (TTE) (Figures 7a and 7b) using LVOT Doppler velocities as a surrogate for SV variations. A small study of TTE in mechanically ventilated children found that aortic flow variability predicted fluid responsiveness.⁷⁰ Therefore, transthoracic echocardiography provides a well-established alternative to thermodilution in determining cardiac output. Multiplication of the HR by an estimate of the column of blood flowing through the LVOT with each systolic contraction gives the cardiac output.⁷¹ 

Using TTE measurement of SV and cardiac output, the clinician can assess the effect of small fluid challenges on cardiac output.⁷² Cardiac output can be augmented with the passive leg raise (PLR), which is an entirely reversible preload challenge maneuver thought to increase preload by 300 to 500 mL. To assess volume responsiveness using this technique, LVOT cardiac output must first be determined. With the transducer in place, the patient’s legs are lifted to a 45° angle. After a minute of equilibration, the LVOT VTI is repeated and cardiac output recalculated. An increase in VTI of more than 12.5% predicts an increase in cardiac output with volume expansion.^73,74 This procedure requires proficiency with pulsed-wave Doppler and the ability to obtain the apical five-chamber view while a patient’s legs are being manipulated. In addition, the angle of insonation and location of measurement of LVOT and VTI must not vary for this measure to be valid. 

Alternatively, respiratory variation in LVOT peak velocities has been shown to reliably predict volume responsiveness when variability is more than 12% (Figure 7c).⁶⁹ This measurement is easier to obtain in that it does not require multiple views or complex calculations, and can be easily augmented with a passive leg raise maneuver. 

In the search for easily accessible alternatives to cardiac and aortic flow, brachial artery peak velocity variation (BAPVV) was found to be useful for predicting volume responsiveness.⁷⁵ To perform this study, the brachial artery is imaged in the long axis view using a linear transducer. Doppler gating should be adjusted to ensure an angle of less than 60°. The patient’s BAPVV is calculated as the difference between maximum and minimum peak velocity divided by the mean peak velocity. A variability in peak velocity of more than 10% predicts volume responsiveness.⁷⁵ 

Common Carotid Artery Flow

Similarly, CCA flow has attracted attention as a potential surrogate to assess SV response to preload challenge.^76,77 The CCA is large, easily accessible and does not require specialized training to assess (Figure 12).⁷⁸

Even though cardiopulmonary interaction assessment has excellent performance for predicting volume responsiveness, limitations do exist. For example, cardiopulmonary interactions may be exaggerated or diminished—thus decreasing the reliability of this assessment—in patients on mechanical ventilation who have spontaneous breathing, high positive end-expiratory pressures or a high minute ventilation, low TV, dysrhythmias, external compression of extra- or intrathoracic vessels (eg, intra-abdominal hypertension, pericardial tamponade, COPD/asthma exacerbations); and in patients who have decreased arterial elastance, or high RV afterload causing RV dysfunction or failure.

Conclusion

The advanced ultrasound techniques described in this review provide several useful tools to rapidly evaluate and manage cardiopulmonary interactions and assess the hemodynamic profile of critically ill patients. With these bedside techniques added to basic POCUS examinations, a new era in noninvasive critical care management is now available. 

As we enter the days of precision medicine, these examinations will enable EPs to optimize the care of this high-risk patient population. Moreover, future research by the emergency ultrasound and critical care communities on morbidity and mortality associated with resuscitation strategies in the ED will undoubtedly incorporate cardiopulmonary and hemodynamic ultrasound. 

ORLANDO – A new predictive method could limit unnecessary computed tomography scans on pediatric, blunt force trauma patients at low risk for intra-abdominal injury, according to a study presented at the annual scientific assembly of the Eastern Association for the Surgery of Trauma.

With values for five clinical variables, the prediction rule would eliminate the need to subject some patients to unwarranted radiation exposure, which has become a growing health and financial concern for medical institutions.

“CT utilization rates in pediatric blunt trauma are very high, at a rate of 40%-60%, despite a relatively low incidence of intra-abdominal injury after abdominal trauma,” according to presenter Chase A. Arbra, MD, of the department of surgery at the Medical University of South Carolina, Charleston. “With increasing concerns regarding the cost and radiation exposure in children, our group is focusing on research to safely avoid these unnecessary scans.”

The rule, developed by the Pediatric Surgery Research Collaborative (PedSRC), evaluates abdominal wall trauma and tenderness, complaint of abdominal pain, aspartate aminotransferase level greater than 200 U/L, abnormal pancreatic enzymes, and abnormal chest x-rays to determine a patient’s risk of having an intra-abdominal injury (IAI). If none of the five variables in a patient is abnormal, the finding is considered negative and the patient is considered to be at very low risk for having an IAI or an IAI requiring acute intervention (IAI-I).

Investigators studied 2,435 pediatric blunt trauma patients with all five clinical variables documented within 6 hours of arrival, using data gathered from the Pediatric Emergency Care Applied Research Network.

Patients were an average of 9.4 years old, with an IAI rate of 9.7% (n = 235) and an IAI-I rate of 2.5% (n = 60); 61.1% of the patients had a CT scan.

Prediction sensitivity of the method was 97.5% for IAI and 100% for IAI-I, said Dr. Arbra. Negative predictive value for the model was 99.3% for IAI and 100% for IAI-I.

Patients who were found to have aspartate aminotransferase level greater than 200 U/L were at the highest risk of IAI (52.6%) and IAI-I (11.9%), according to investigators. One-third of the test population was found to be at very low risk after using the prediction model, according to Dr. Arbra, with 46.8% of them still undergoing a CT scan. Of those tested, six patients had IAI that was not predicted by the model, three of whom were intubated. Because CT scans were not required and there was no follow-up after discharge, investigators are not able to determine if any minor IAI was missed.

Despite these limitations, the highly sensitive rule shows great promise, according to Dr. Arbra.

“Patients with 0-5 variables, even patients who were involved in a high impact mechanism, could potentially forgo CT scans safely.”

A closer look at the 26 patients who only had abdominal pain showed that only 1 had IAI, suggesting that patients with only abdominal pain could be safely observed with only serial exams, according to Dr. Arbra.

Investigators plan to conduct a prospective study that will include older patients.

Dr. Arbra concluded, “The rule could potentially help centers to determine who could avoid imaging prior to transfer and potentially could one day be used to see who could be discharged.”

Dr. Arbra reported no relevant financial disclosures.

[email protected]

SOURCE: Arbra CA. EAST Scientific Assembly 2018, paper #7.

ORLANDO – A new predictive method could limit unnecessary computed tomography scans on pediatric, blunt force trauma patients at low risk for intra-abdominal injury, according to a study presented at the annual scientific assembly of the Eastern Association for the Surgery of Trauma.

With values for five clinical variables, the prediction rule would eliminate the need to subject some patients to unwarranted radiation exposure, which has become a growing health and financial concern for medical institutions.

“CT utilization rates in pediatric blunt trauma are very high, at a rate of 40%-60%, despite a relatively low incidence of intra-abdominal injury after abdominal trauma,” according to presenter Chase A. Arbra, MD, of the department of surgery at the Medical University of South Carolina, Charleston. “With increasing concerns regarding the cost and radiation exposure in children, our group is focusing on research to safely avoid these unnecessary scans.”

The rule, developed by the Pediatric Surgery Research Collaborative (PedSRC), evaluates abdominal wall trauma and tenderness, complaint of abdominal pain, aspartate aminotransferase level greater than 200 U/L, abnormal pancreatic enzymes, and abnormal chest x-rays to determine a patient’s risk of having an intra-abdominal injury (IAI). If none of the five variables in a patient is abnormal, the finding is considered negative and the patient is considered to be at very low risk for having an IAI or an IAI requiring acute intervention (IAI-I).

Investigators studied 2,435 pediatric blunt trauma patients with all five clinical variables documented within 6 hours of arrival, using data gathered from the Pediatric Emergency Care Applied Research Network.

Patients were an average of 9.4 years old, with an IAI rate of 9.7% (n = 235) and an IAI-I rate of 2.5% (n = 60); 61.1% of the patients had a CT scan.

Prediction sensitivity of the method was 97.5% for IAI and 100% for IAI-I, said Dr. Arbra. Negative predictive value for the model was 99.3% for IAI and 100% for IAI-I.

Patients who were found to have aspartate aminotransferase level greater than 200 U/L were at the highest risk of IAI (52.6%) and IAI-I (11.9%), according to investigators. One-third of the test population was found to be at very low risk after using the prediction model, according to Dr. Arbra, with 46.8% of them still undergoing a CT scan. Of those tested, six patients had IAI that was not predicted by the model, three of whom were intubated. Because CT scans were not required and there was no follow-up after discharge, investigators are not able to determine if any minor IAI was missed.

Despite these limitations, the highly sensitive rule shows great promise, according to Dr. Arbra.

“Patients with 0-5 variables, even patients who were involved in a high impact mechanism, could potentially forgo CT scans safely.”

A closer look at the 26 patients who only had abdominal pain showed that only 1 had IAI, suggesting that patients with only abdominal pain could be safely observed with only serial exams, according to Dr. Arbra.

Investigators plan to conduct a prospective study that will include older patients.

Dr. Arbra concluded, “The rule could potentially help centers to determine who could avoid imaging prior to transfer and potentially could one day be used to see who could be discharged.”

Dr. Arbra reported no relevant financial disclosures.

[email protected]

SOURCE: Arbra CA. EAST Scientific Assembly 2018, paper #7.

ORLANDO – A new predictive method could limit unnecessary computed tomography scans on pediatric, blunt force trauma patients at low risk for intra-abdominal injury, according to a study presented at the annual scientific assembly of the Eastern Association for the Surgery of Trauma.

With values for five clinical variables, the prediction rule would eliminate the need to subject some patients to unwarranted radiation exposure, which has become a growing health and financial concern for medical institutions.

“CT utilization rates in pediatric blunt trauma are very high, at a rate of 40%-60%, despite a relatively low incidence of intra-abdominal injury after abdominal trauma,” according to presenter Chase A. Arbra, MD, of the department of surgery at the Medical University of South Carolina, Charleston. “With increasing concerns regarding the cost and radiation exposure in children, our group is focusing on research to safely avoid these unnecessary scans.”

The rule, developed by the Pediatric Surgery Research Collaborative (PedSRC), evaluates abdominal wall trauma and tenderness, complaint of abdominal pain, aspartate aminotransferase level greater than 200 U/L, abnormal pancreatic enzymes, and abnormal chest x-rays to determine a patient’s risk of having an intra-abdominal injury (IAI). If none of the five variables in a patient is abnormal, the finding is considered negative and the patient is considered to be at very low risk for having an IAI or an IAI requiring acute intervention (IAI-I).

Investigators studied 2,435 pediatric blunt trauma patients with all five clinical variables documented within 6 hours of arrival, using data gathered from the Pediatric Emergency Care Applied Research Network.

Patients were an average of 9.4 years old, with an IAI rate of 9.7% (n = 235) and an IAI-I rate of 2.5% (n = 60); 61.1% of the patients had a CT scan.

Prediction sensitivity of the method was 97.5% for IAI and 100% for IAI-I, said Dr. Arbra. Negative predictive value for the model was 99.3% for IAI and 100% for IAI-I.

Patients who were found to have aspartate aminotransferase level greater than 200 U/L were at the highest risk of IAI (52.6%) and IAI-I (11.9%), according to investigators. One-third of the test population was found to be at very low risk after using the prediction model, according to Dr. Arbra, with 46.8% of them still undergoing a CT scan. Of those tested, six patients had IAI that was not predicted by the model, three of whom were intubated. Because CT scans were not required and there was no follow-up after discharge, investigators are not able to determine if any minor IAI was missed.

Despite these limitations, the highly sensitive rule shows great promise, according to Dr. Arbra.

“Patients with 0-5 variables, even patients who were involved in a high impact mechanism, could potentially forgo CT scans safely.”

A closer look at the 26 patients who only had abdominal pain showed that only 1 had IAI, suggesting that patients with only abdominal pain could be safely observed with only serial exams, according to Dr. Arbra.

Investigators plan to conduct a prospective study that will include older patients.

Dr. Arbra concluded, “The rule could potentially help centers to determine who could avoid imaging prior to transfer and potentially could one day be used to see who could be discharged.”

Dr. Arbra reported no relevant financial disclosures.

[email protected]

SOURCE: Arbra CA. EAST Scientific Assembly 2018, paper #7.

Although rare, inadvertent placement of a pacemaker or defibrillator lead in the left ventricle can have serious consequences, including arterial thromboembolism and aortic or mitral valve damage or infection.^1–4

This article discusses situations in which lead malpositioning is likely to occur, how to prevent it, how to detect and correct it immediately, and how to manage cases discovered long after implantation.

RARE, BUT LIKELY UNDERREPORTED

In 2011, Rodriguez et al¹ reviewed 56 reported cases in which an endocardial lead had been mistakenly placed in the left ventricle. A few more cases have been reported since then, but some cases are not reported, so how often this occurs is unknown.

A large single-center retrospective study² reported a 3.4% incidence of inadvertent lead placement in the left side of the heart, including the cardiac veins.

HOW LEADS CAN END UP IN THE WRONG PLACE

Risk factors for lead malpositioning include abnormal thoracic anatomy, underlying congenital heart disease, and operator inexperience.²

Normally, in single- and double-lead systems, leads are inserted into a cephalic, subclavian, or axillary vein and advanced into the right atrium, right ventricle, or both. However, pacing, sensing, and defibrillation leads have inadvertently been placed in the left ventricular endocardium and even on the epicardial surface.

Leads can end up inside the left ventricle by passing through an unrecognized atrial septal defect, patent foramen ovale, or ventricular septal defect, or by perforating the interventricular septum. Another route into the left ventricle is by gaining vascular access through the axillary or subclavian artery and advancing the lead retrograde across the aortic valve.

Epicardial lead placement may result from perforating the right ventricle⁵ or inadvertent positioning within the main coronary sinus or in a cardiac vein.

PREVENTION IS THE BEST MANAGEMENT

The best way to manage lead malpositioning is to prevent it in the first place.

Make sure you are in a vein, not an artery! If you are working from the patient’s left side, you should see the guidewire cross the midline on fluoroscopy. Working from either the left or the right side, you can ensure that the guidewire is in the venous system by advancing it into the inferior vena cava and then all the way below the diaphragm (best seen on anteroposterior views). These observations help avoid lead placement in the left ventricle by an inadvertent retrograde aortic approach.

Suspect that you are taking the wrong route to the heart (ie, through the arterial system) if, in the anteroposterior view, the guidewire bends as it approaches the left spinal border. This sign suggests that you are going backwards through the ascending aorta and bumping up against the aortic cusps. Occasionally, the wire may pass through the aortic valve without resistance and bending. Additional advancement toward the left chest wall will make contact with the left ventricular endocardium and may result in ventricular ectopy. Placement in the left ventricle is best seen in the left anterior oblique projection; the lead will cross the spine or its distal end will point toward the spine in progressive projections from farther to the left.

Make sure you are in the right ventricle. Even if you have gone through the venous system, you are not home free. Advancing the lead into the right ventricular outflow tract (best seen in the right anterior oblique projection) is a key step in avoiding lead misplacement. In the right ventricular outflow tract, the lead tip should move freely; if it does not, it may be in the coronary sinus or middle cardiac vein. 

If a lead passes through a patent foramen ovale or septal defect to the left atrium, a left anterior oblique view should also demonstrate movement toward or beyond the spine. If the lead passes beyond the left heart border, a position in a pulmonary vein is possible. This is often associated with loss of a recordable intracardiac electrogram. A position in a right pulmonary vein is possible but very, very unlikely. If a lead passes through a patent foramen ovale or septal defect to the left ventricle, it will point toward the spine in left anterior oblique projections. (See “Postoperative detection by chest radiography.”)

Ventricular paced QRS complexes should show a left bundle branch pattern on electrocardiography (ECG), not a right bundle branch pattern (more about this below). However, when inserting a pacemaker, the sterile field includes the front of the chest and therefore lead V₁ is usually omitted, depriving the operator of valuable information.

Fortunately, operators may fluoroscopically view leads intended for the right ventricle in left anterior oblique projections. We recommend beginning at 40° left anterior oblique. In this view, septally positioned right ventricular leads may appear to abut the spine. A right ventricular position is confirmed in a steeper left anterior oblique projection, where the lead should be seen to be away from the spine.⁴

Careful evaluation of the 12-lead electrocardiogram during ventricular pacing is important for confirming correct lead placement. If ventricular pacing is absent, eg, if the device fires only if the natural heart rate drops below a set number and the heart happens to be firing on its own when you happen to be looking at it, programming the device to pace the right ventricle 10 beats per minute faster than the intrinsic heart rate usually suffices. Temporarily disabling atrial pacing and cardiac venous pacing in biventricular devices facilitates interpretation of the paced QRS complex.

Bundle branch block patterns

The typical morphology for paced events originating from the right ventricle has a left bundle branch block pattern, ie, a dominant S wave in leads V₁ and V₂.  Nevertheless, many patients with a safely placed lead in the right ventricle can also demonstrate right bundle branch morphology during pacing,⁶ ie, a dominant R wave in leads V₁ and V₂.

Reprinted from reference 6 with permission.

Klein et al⁷ reported on 8 patients who had features of right bundle branch block in leads V₁ and V₂ and noted that placing these leads 1 interspace lower eliminated the right bundle branch block appearance. The utility of this maneuver is demonstrated in Figure 1.

Almehairi et al⁸ demonstrated transition to a left bundle branch block-like pattern in V₁ in 14 of 26 patients after leads V₁ and V₂ were moved to the fifth intercostal space. Moving these leads to the sixth intercostal space produced a left bundle branch block-like pattern in all the remaining patients. Additional study is needed to validate this precordial mapping technique.⁹

Reprinted from reference 6 and reference 14 with permission.

Although the Coman and Trohman algorithm suggests that a frontal plane axis of −90° to –180° is specific for left ventricular pacing,⁶ other reports have identified this axis in the presence of true right ventricular pacing.^6,9–12 Therefore, Barold and Giudici⁹ argue that a frontal plane axis in the right superior quadrant has limited diagnostic value.

POSTOPERATIVE DETECTION BY CHEST RADIOGRAPHY

Adapted with permission from references 14 and 15.

A lead in the left ventricle may be a subtle finding on an anteroposterior or posteroanterior chest radiograph. The definitive view is the lateral projection, which is also true during intraoperative fluoroscopy.^13–15 The tip of a malpositioned left-ventricular lead is characteristically seen farther posterior (toward the spine) in the cardiac silhouette on the lateral view (Figure 3).² If the lead is properly positioned, the general direction of the middle to distal portion should be away from the spine.

ECHOCARDIOGRAPHY TO CONFIRM

Echocardiograms adapted with permission from reference 16; medical illustration by Joseph Pangrace.

Two-dimensional echocardiography can help to confirm left ventricular placement via an atrial septal defect, patent foramen ovale, or perforation of the interventricular septum.^16,17

Three-dimensional echocardiography can facilitate cardiac venous lead placement and assess the impact of right ventricular lead placement on tricuspid valve function.^18,19 In one case report, 3-dimensional echocardiography provided a definitive diagnosis of interventricular septal perforation when findings on computed tomography (CT) were indeterminate.²⁰

CT AND MRI: LIMITED ROLES

When echocardiographic findings are equivocal, CT can help diagnose lead perforation. Electrocardiogram-triggered cardiac CT can help visualize lead positions and potential lead perforation. Unfortunately, the precise location of the lead tip (and the diagnosis) can be missed due to streaking (“star”) artifacts and acoustic shadowing from the metallic lead.^21–26 Because of these limitations, as well as radiation exposure and high costs, CT should be used sparingly, if at all, for diagnosing lead malposition.

Technological advances and the increasing use of magnetic resonance imaging (MRI) in clinical practice have led to the development of “MRI-conditional” cardiac implantable electronic devices (ie, safe for undergoing MRI), as well as more lenient regulation of MRI in patients with nonconditional devices.^27,28 Although the widely held opinion that patients with a pacemaker or implantable cardioverter defibrillator are not eligible to undergo MRI has largely been abandoned, it seems unlikely that cardiac MRI will become a pivotal tool in assessing lead malposition.

Inadvertent left ventricular lead placement provides a nidus for thrombus formation. When inadvertent left ventricular lead malposition is identified acutely, correction of the lead position should be performed immediately by an experienced electrophysiologist.

Treatment of left ventricular lead misplacement discovered late after implantation includes lead removal or chronic anticoagulation with warfarin to prevent thromboemboli.

Long-term anticoagulation

No thromboembolic events have been reported² in patients with lead malposition who take warfarin and maintain an international normalized ratio of 2.5 to 3.5.

Antiplatelet agents are not enough by themselves.¹⁶

The use of direct oral anticoagulants has not been explored in this setting. Use of dabigatran in patients with mechanical heart valves was associated with increased rates of thromboembolic and bleeding complications compared with warfarin.²⁹ Based on these results and an overall lack of evidence, we do not recommend substituting a direct oral anticoagulant for warfarin in the setting of malpositioned left ventricular leads.

Late percutaneous removal

Late lead removal is most appropriate if cardiac surgery is planned for other reasons. Although percutaneous extraction of a malpositioned left ventricular lead was first described over 25 years ago,¹³ the safety of this procedure remains uncertain.

Kosmidou et al¹⁷ reported two cases of percutaneous removal of inadvertent transarterial leads employing standard interventional cardiology methods for cerebral embolic protection. Distal embolic filter wires were deployed in the left and right internal carotid arteries. A covered stent was deployed at the arterial entry site simultaneously with lead removal, providing immediate and effective hemostasis. Similar protection should be considered during transvenous access and extraction via an atrial septal or patent foramen ovale.

Nevertheless, not even transesophageal echocardiography can reliably exclude adhered thrombi, and the risk of embolization of fibrous adhesions or thrombi has been cited as a pivotal contraindication to percutaneous lead extraction regardless of modality.¹⁶

Although rare, inadvertent placement of a pacemaker or defibrillator lead in the left ventricle can have serious consequences, including arterial thromboembolism and aortic or mitral valve damage or infection.^1–4

This article discusses situations in which lead malpositioning is likely to occur, how to prevent it, how to detect and correct it immediately, and how to manage cases discovered long after implantation.

RARE, BUT LIKELY UNDERREPORTED

In 2011, Rodriguez et al¹ reviewed 56 reported cases in which an endocardial lead had been mistakenly placed in the left ventricle. A few more cases have been reported since then, but some cases are not reported, so how often this occurs is unknown.

A large single-center retrospective study² reported a 3.4% incidence of inadvertent lead placement in the left side of the heart, including the cardiac veins.

HOW LEADS CAN END UP IN THE WRONG PLACE

Risk factors for lead malpositioning include abnormal thoracic anatomy, underlying congenital heart disease, and operator inexperience.²

Normally, in single- and double-lead systems, leads are inserted into a cephalic, subclavian, or axillary vein and advanced into the right atrium, right ventricle, or both. However, pacing, sensing, and defibrillation leads have inadvertently been placed in the left ventricular endocardium and even on the epicardial surface.

Leads can end up inside the left ventricle by passing through an unrecognized atrial septal defect, patent foramen ovale, or ventricular septal defect, or by perforating the interventricular septum. Another route into the left ventricle is by gaining vascular access through the axillary or subclavian artery and advancing the lead retrograde across the aortic valve.

Epicardial lead placement may result from perforating the right ventricle⁵ or inadvertent positioning within the main coronary sinus or in a cardiac vein.

PREVENTION IS THE BEST MANAGEMENT

The best way to manage lead malpositioning is to prevent it in the first place.

Make sure you are in a vein, not an artery! If you are working from the patient’s left side, you should see the guidewire cross the midline on fluoroscopy. Working from either the left or the right side, you can ensure that the guidewire is in the venous system by advancing it into the inferior vena cava and then all the way below the diaphragm (best seen on anteroposterior views). These observations help avoid lead placement in the left ventricle by an inadvertent retrograde aortic approach.

Suspect that you are taking the wrong route to the heart (ie, through the arterial system) if, in the anteroposterior view, the guidewire bends as it approaches the left spinal border. This sign suggests that you are going backwards through the ascending aorta and bumping up against the aortic cusps. Occasionally, the wire may pass through the aortic valve without resistance and bending. Additional advancement toward the left chest wall will make contact with the left ventricular endocardium and may result in ventricular ectopy. Placement in the left ventricle is best seen in the left anterior oblique projection; the lead will cross the spine or its distal end will point toward the spine in progressive projections from farther to the left.

Make sure you are in the right ventricle. Even if you have gone through the venous system, you are not home free. Advancing the lead into the right ventricular outflow tract (best seen in the right anterior oblique projection) is a key step in avoiding lead misplacement. In the right ventricular outflow tract, the lead tip should move freely; if it does not, it may be in the coronary sinus or middle cardiac vein. 

If a lead passes through a patent foramen ovale or septal defect to the left atrium, a left anterior oblique view should also demonstrate movement toward or beyond the spine. If the lead passes beyond the left heart border, a position in a pulmonary vein is possible. This is often associated with loss of a recordable intracardiac electrogram. A position in a right pulmonary vein is possible but very, very unlikely. If a lead passes through a patent foramen ovale or septal defect to the left ventricle, it will point toward the spine in left anterior oblique projections. (See “Postoperative detection by chest radiography.”)

Ventricular paced QRS complexes should show a left bundle branch pattern on electrocardiography (ECG), not a right bundle branch pattern (more about this below). However, when inserting a pacemaker, the sterile field includes the front of the chest and therefore lead V₁ is usually omitted, depriving the operator of valuable information.

Fortunately, operators may fluoroscopically view leads intended for the right ventricle in left anterior oblique projections. We recommend beginning at 40° left anterior oblique. In this view, septally positioned right ventricular leads may appear to abut the spine. A right ventricular position is confirmed in a steeper left anterior oblique projection, where the lead should be seen to be away from the spine.⁴

Careful evaluation of the 12-lead electrocardiogram during ventricular pacing is important for confirming correct lead placement. If ventricular pacing is absent, eg, if the device fires only if the natural heart rate drops below a set number and the heart happens to be firing on its own when you happen to be looking at it, programming the device to pace the right ventricle 10 beats per minute faster than the intrinsic heart rate usually suffices. Temporarily disabling atrial pacing and cardiac venous pacing in biventricular devices facilitates interpretation of the paced QRS complex.

Bundle branch block patterns

The typical morphology for paced events originating from the right ventricle has a left bundle branch block pattern, ie, a dominant S wave in leads V₁ and V₂.  Nevertheless, many patients with a safely placed lead in the right ventricle can also demonstrate right bundle branch morphology during pacing,⁶ ie, a dominant R wave in leads V₁ and V₂.

Reprinted from reference 6 with permission.

Klein et al⁷ reported on 8 patients who had features of right bundle branch block in leads V₁ and V₂ and noted that placing these leads 1 interspace lower eliminated the right bundle branch block appearance. The utility of this maneuver is demonstrated in Figure 1.

Almehairi et al⁸ demonstrated transition to a left bundle branch block-like pattern in V₁ in 14 of 26 patients after leads V₁ and V₂ were moved to the fifth intercostal space. Moving these leads to the sixth intercostal space produced a left bundle branch block-like pattern in all the remaining patients. Additional study is needed to validate this precordial mapping technique.⁹

Reprinted from reference 6 and reference 14 with permission.

Although the Coman and Trohman algorithm suggests that a frontal plane axis of −90° to –180° is specific for left ventricular pacing,⁶ other reports have identified this axis in the presence of true right ventricular pacing.^6,9–12 Therefore, Barold and Giudici⁹ argue that a frontal plane axis in the right superior quadrant has limited diagnostic value.

POSTOPERATIVE DETECTION BY CHEST RADIOGRAPHY

Adapted with permission from references 14 and 15.

A lead in the left ventricle may be a subtle finding on an anteroposterior or posteroanterior chest radiograph. The definitive view is the lateral projection, which is also true during intraoperative fluoroscopy.^13–15 The tip of a malpositioned left-ventricular lead is characteristically seen farther posterior (toward the spine) in the cardiac silhouette on the lateral view (Figure 3).² If the lead is properly positioned, the general direction of the middle to distal portion should be away from the spine.

ECHOCARDIOGRAPHY TO CONFIRM

Echocardiograms adapted with permission from reference 16; medical illustration by Joseph Pangrace.

Two-dimensional echocardiography can help to confirm left ventricular placement via an atrial septal defect, patent foramen ovale, or perforation of the interventricular septum.^16,17

Three-dimensional echocardiography can facilitate cardiac venous lead placement and assess the impact of right ventricular lead placement on tricuspid valve function.^18,19 In one case report, 3-dimensional echocardiography provided a definitive diagnosis of interventricular septal perforation when findings on computed tomography (CT) were indeterminate.²⁰

CT AND MRI: LIMITED ROLES

When echocardiographic findings are equivocal, CT can help diagnose lead perforation. Electrocardiogram-triggered cardiac CT can help visualize lead positions and potential lead perforation. Unfortunately, the precise location of the lead tip (and the diagnosis) can be missed due to streaking (“star”) artifacts and acoustic shadowing from the metallic lead.^21–26 Because of these limitations, as well as radiation exposure and high costs, CT should be used sparingly, if at all, for diagnosing lead malposition.

Technological advances and the increasing use of magnetic resonance imaging (MRI) in clinical practice have led to the development of “MRI-conditional” cardiac implantable electronic devices (ie, safe for undergoing MRI), as well as more lenient regulation of MRI in patients with nonconditional devices.^27,28 Although the widely held opinion that patients with a pacemaker or implantable cardioverter defibrillator are not eligible to undergo MRI has largely been abandoned, it seems unlikely that cardiac MRI will become a pivotal tool in assessing lead malposition.

Inadvertent left ventricular lead placement provides a nidus for thrombus formation. When inadvertent left ventricular lead malposition is identified acutely, correction of the lead position should be performed immediately by an experienced electrophysiologist.

Treatment of left ventricular lead misplacement discovered late after implantation includes lead removal or chronic anticoagulation with warfarin to prevent thromboemboli.

Long-term anticoagulation

No thromboembolic events have been reported² in patients with lead malposition who take warfarin and maintain an international normalized ratio of 2.5 to 3.5.

Antiplatelet agents are not enough by themselves.¹⁶

The use of direct oral anticoagulants has not been explored in this setting. Use of dabigatran in patients with mechanical heart valves was associated with increased rates of thromboembolic and bleeding complications compared with warfarin.²⁹ Based on these results and an overall lack of evidence, we do not recommend substituting a direct oral anticoagulant for warfarin in the setting of malpositioned left ventricular leads.

Late percutaneous removal

Late lead removal is most appropriate if cardiac surgery is planned for other reasons. Although percutaneous extraction of a malpositioned left ventricular lead was first described over 25 years ago,¹³ the safety of this procedure remains uncertain.

Kosmidou et al¹⁷ reported two cases of percutaneous removal of inadvertent transarterial leads employing standard interventional cardiology methods for cerebral embolic protection. Distal embolic filter wires were deployed in the left and right internal carotid arteries. A covered stent was deployed at the arterial entry site simultaneously with lead removal, providing immediate and effective hemostasis. Similar protection should be considered during transvenous access and extraction via an atrial septal or patent foramen ovale.

Nevertheless, not even transesophageal echocardiography can reliably exclude adhered thrombi, and the risk of embolization of fibrous adhesions or thrombi has been cited as a pivotal contraindication to percutaneous lead extraction regardless of modality.¹⁶

Although rare, inadvertent placement of a pacemaker or defibrillator lead in the left ventricle can have serious consequences, including arterial thromboembolism and aortic or mitral valve damage or infection.^1–4

This article discusses situations in which lead malpositioning is likely to occur, how to prevent it, how to detect and correct it immediately, and how to manage cases discovered long after implantation.

RARE, BUT LIKELY UNDERREPORTED

In 2011, Rodriguez et al¹ reviewed 56 reported cases in which an endocardial lead had been mistakenly placed in the left ventricle. A few more cases have been reported since then, but some cases are not reported, so how often this occurs is unknown.

A large single-center retrospective study² reported a 3.4% incidence of inadvertent lead placement in the left side of the heart, including the cardiac veins.

HOW LEADS CAN END UP IN THE WRONG PLACE

Risk factors for lead malpositioning include abnormal thoracic anatomy, underlying congenital heart disease, and operator inexperience.²

Normally, in single- and double-lead systems, leads are inserted into a cephalic, subclavian, or axillary vein and advanced into the right atrium, right ventricle, or both. However, pacing, sensing, and defibrillation leads have inadvertently been placed in the left ventricular endocardium and even on the epicardial surface.

Leads can end up inside the left ventricle by passing through an unrecognized atrial septal defect, patent foramen ovale, or ventricular septal defect, or by perforating the interventricular septum. Another route into the left ventricle is by gaining vascular access through the axillary or subclavian artery and advancing the lead retrograde across the aortic valve.

Epicardial lead placement may result from perforating the right ventricle⁵ or inadvertent positioning within the main coronary sinus or in a cardiac vein.

PREVENTION IS THE BEST MANAGEMENT

The best way to manage lead malpositioning is to prevent it in the first place.

Make sure you are in a vein, not an artery! If you are working from the patient’s left side, you should see the guidewire cross the midline on fluoroscopy. Working from either the left or the right side, you can ensure that the guidewire is in the venous system by advancing it into the inferior vena cava and then all the way below the diaphragm (best seen on anteroposterior views). These observations help avoid lead placement in the left ventricle by an inadvertent retrograde aortic approach.

Suspect that you are taking the wrong route to the heart (ie, through the arterial system) if, in the anteroposterior view, the guidewire bends as it approaches the left spinal border. This sign suggests that you are going backwards through the ascending aorta and bumping up against the aortic cusps. Occasionally, the wire may pass through the aortic valve without resistance and bending. Additional advancement toward the left chest wall will make contact with the left ventricular endocardium and may result in ventricular ectopy. Placement in the left ventricle is best seen in the left anterior oblique projection; the lead will cross the spine or its distal end will point toward the spine in progressive projections from farther to the left.

Make sure you are in the right ventricle. Even if you have gone through the venous system, you are not home free. Advancing the lead into the right ventricular outflow tract (best seen in the right anterior oblique projection) is a key step in avoiding lead misplacement. In the right ventricular outflow tract, the lead tip should move freely; if it does not, it may be in the coronary sinus or middle cardiac vein. 

If a lead passes through a patent foramen ovale or septal defect to the left atrium, a left anterior oblique view should also demonstrate movement toward or beyond the spine. If the lead passes beyond the left heart border, a position in a pulmonary vein is possible. This is often associated with loss of a recordable intracardiac electrogram. A position in a right pulmonary vein is possible but very, very unlikely. If a lead passes through a patent foramen ovale or septal defect to the left ventricle, it will point toward the spine in left anterior oblique projections. (See “Postoperative detection by chest radiography.”)

Ventricular paced QRS complexes should show a left bundle branch pattern on electrocardiography (ECG), not a right bundle branch pattern (more about this below). However, when inserting a pacemaker, the sterile field includes the front of the chest and therefore lead V₁ is usually omitted, depriving the operator of valuable information.

Fortunately, operators may fluoroscopically view leads intended for the right ventricle in left anterior oblique projections. We recommend beginning at 40° left anterior oblique. In this view, septally positioned right ventricular leads may appear to abut the spine. A right ventricular position is confirmed in a steeper left anterior oblique projection, where the lead should be seen to be away from the spine.⁴

Careful evaluation of the 12-lead electrocardiogram during ventricular pacing is important for confirming correct lead placement. If ventricular pacing is absent, eg, if the device fires only if the natural heart rate drops below a set number and the heart happens to be firing on its own when you happen to be looking at it, programming the device to pace the right ventricle 10 beats per minute faster than the intrinsic heart rate usually suffices. Temporarily disabling atrial pacing and cardiac venous pacing in biventricular devices facilitates interpretation of the paced QRS complex.

Bundle branch block patterns

The typical morphology for paced events originating from the right ventricle has a left bundle branch block pattern, ie, a dominant S wave in leads V₁ and V₂.  Nevertheless, many patients with a safely placed lead in the right ventricle can also demonstrate right bundle branch morphology during pacing,⁶ ie, a dominant R wave in leads V₁ and V₂.

Reprinted from reference 6 with permission.

Klein et al⁷ reported on 8 patients who had features of right bundle branch block in leads V₁ and V₂ and noted that placing these leads 1 interspace lower eliminated the right bundle branch block appearance. The utility of this maneuver is demonstrated in Figure 1.

Almehairi et al⁸ demonstrated transition to a left bundle branch block-like pattern in V₁ in 14 of 26 patients after leads V₁ and V₂ were moved to the fifth intercostal space. Moving these leads to the sixth intercostal space produced a left bundle branch block-like pattern in all the remaining patients. Additional study is needed to validate this precordial mapping technique.⁹

Reprinted from reference 6 and reference 14 with permission.

Although the Coman and Trohman algorithm suggests that a frontal plane axis of −90° to –180° is specific for left ventricular pacing,⁶ other reports have identified this axis in the presence of true right ventricular pacing.^6,9–12 Therefore, Barold and Giudici⁹ argue that a frontal plane axis in the right superior quadrant has limited diagnostic value.

POSTOPERATIVE DETECTION BY CHEST RADIOGRAPHY

Adapted with permission from references 14 and 15.

A lead in the left ventricle may be a subtle finding on an anteroposterior or posteroanterior chest radiograph. The definitive view is the lateral projection, which is also true during intraoperative fluoroscopy.^13–15 The tip of a malpositioned left-ventricular lead is characteristically seen farther posterior (toward the spine) in the cardiac silhouette on the lateral view (Figure 3).² If the lead is properly positioned, the general direction of the middle to distal portion should be away from the spine.

ECHOCARDIOGRAPHY TO CONFIRM

Echocardiograms adapted with permission from reference 16; medical illustration by Joseph Pangrace.

Two-dimensional echocardiography can help to confirm left ventricular placement via an atrial septal defect, patent foramen ovale, or perforation of the interventricular septum.^16,17

Three-dimensional echocardiography can facilitate cardiac venous lead placement and assess the impact of right ventricular lead placement on tricuspid valve function.^18,19 In one case report, 3-dimensional echocardiography provided a definitive diagnosis of interventricular septal perforation when findings on computed tomography (CT) were indeterminate.²⁰

CT AND MRI: LIMITED ROLES

When echocardiographic findings are equivocal, CT can help diagnose lead perforation. Electrocardiogram-triggered cardiac CT can help visualize lead positions and potential lead perforation. Unfortunately, the precise location of the lead tip (and the diagnosis) can be missed due to streaking (“star”) artifacts and acoustic shadowing from the metallic lead.^21–26 Because of these limitations, as well as radiation exposure and high costs, CT should be used sparingly, if at all, for diagnosing lead malposition.

Technological advances and the increasing use of magnetic resonance imaging (MRI) in clinical practice have led to the development of “MRI-conditional” cardiac implantable electronic devices (ie, safe for undergoing MRI), as well as more lenient regulation of MRI in patients with nonconditional devices.^27,28 Although the widely held opinion that patients with a pacemaker or implantable cardioverter defibrillator are not eligible to undergo MRI has largely been abandoned, it seems unlikely that cardiac MRI will become a pivotal tool in assessing lead malposition.

Inadvertent left ventricular lead placement provides a nidus for thrombus formation. When inadvertent left ventricular lead malposition is identified acutely, correction of the lead position should be performed immediately by an experienced electrophysiologist.

Treatment of left ventricular lead misplacement discovered late after implantation includes lead removal or chronic anticoagulation with warfarin to prevent thromboemboli.

Long-term anticoagulation

No thromboembolic events have been reported² in patients with lead malposition who take warfarin and maintain an international normalized ratio of 2.5 to 3.5.

Antiplatelet agents are not enough by themselves.¹⁶

The use of direct oral anticoagulants has not been explored in this setting. Use of dabigatran in patients with mechanical heart valves was associated with increased rates of thromboembolic and bleeding complications compared with warfarin.²⁹ Based on these results and an overall lack of evidence, we do not recommend substituting a direct oral anticoagulant for warfarin in the setting of malpositioned left ventricular leads.

Late percutaneous removal

Late lead removal is most appropriate if cardiac surgery is planned for other reasons. Although percutaneous extraction of a malpositioned left ventricular lead was first described over 25 years ago,¹³ the safety of this procedure remains uncertain.

Kosmidou et al¹⁷ reported two cases of percutaneous removal of inadvertent transarterial leads employing standard interventional cardiology methods for cerebral embolic protection. Distal embolic filter wires were deployed in the left and right internal carotid arteries. A covered stent was deployed at the arterial entry site simultaneously with lead removal, providing immediate and effective hemostasis. Similar protection should be considered during transvenous access and extraction via an atrial septal or patent foramen ovale.

Nevertheless, not even transesophageal echocardiography can reliably exclude adhered thrombi, and the risk of embolization of fibrous adhesions or thrombi has been cited as a pivotal contraindication to percutaneous lead extraction regardless of modality.¹⁶

Take-Home Points

• Gorham disease is a rare condition that manifests as an acute, spontaneous osteolysis.
• There is no clear hereditary pattern of transmission. Bones of any type or location can be affected.
• Imaging studies are nonspecific, but show permeative osteolysis involving the subcortical and intramedullary regions and typically affect regional, contiguous bones, without adjacent sclerosis, somewhat resembling osteoporosis.
• Tissue biopsy is indicated to rule out other potential etiologies of osteolysis, and the histologic findings help confirm a diagnosis of Gorham disease.
• There is no single or combined treatment modality that is considered as the gold standard. Surgical treatment includes resection of the lesion and reconstruction. Also, antiosteoclastic medication can be used.

Gorham disease, a rare condition of unknown etiology, manifests as acute, spontaneous osteolysis associated with benign hemangiomatosis or lymphangiomatosis, which presents as skeletal lucency on radiographs, prompting the classic eponym of vanishing bone disease.^1-6 There is no evidence supporting the idea that osteoclasts are present in any meaningful amount in the resorption areas or that local reparative osteogenesis occurs.^4,6

Jackson and colleagues first described idiopathic osteolysis in 1838,^1,2 and Gorham and Stout³ introduced the syndrome to the orthopedic community in 1955. Since then, few strides have been made in identifying the disease origin.^1,2,4 Diagnosis is possible only after meticulous work-up has excluded neoplastic and infectious etiologies.^7,8

Clinical Presentation

Gorham disease affects patients ranging widely in age, from 2 months to 78 years, but typically presents in those under 40 years. There is a questionable predilection for males but no correlation with ethnicity or geographic region. There is no clear hereditary pattern of transmission.⁷ Although the bones of the head, neck, and upper extremities are involved in most cases, bone of any type or location can be affected.⁶ Pelvic bones seem to be involved least often.^6,7

Initial clinical presentation varies considerably but typically involves prolonged soreness in the affected region and, rarely, acute pathologic fracture.^1,2,4 The nonspecific nature of complaints, lack of markers of systemic illness, and rarity of the disease contribute to delayed diagnosis.^1,2

Imaging

Computed tomography (CT) better defines the severity and extent of these changes.

Diagnosis

There have been 8 histologic and clinical criteria described to diagnose Gorham disease: (1) biopsy positive for presence of angiomatous tissue, (2) complete absence of any cellular atypia, (3) lack of osteoclastic response and lack of dystrophic calcifications, (4) evidence of progressive resorption of native bone, (5) no evidence of expansive or ulcerative lesion, (6) lack of visceral involvement, (7) osteolytic radiographic pattern, and (8) no concrete diagnosis after hereditary, metabolic, neoplastic, immunologic, and infectious work-up.^4-6 These criteria confirm that the diagnosis can be rendered only after exclusion of neoplastic and infectious etiologies through clinical and laboratory work-up, imaging studies, and tissue sampling.

Tissue biopsy is indicated to rule out other potential etiologies of osteolysis, and the histologic findings help confirm a diagnosis of Gorham disease.

Treatment

Surgical treatment usually includes lesion resection and subsequent reconstruction using combinations of bone grafts (allogenic) and prostheses. Bone graft alone is quickly resorbed and has not been found to be beneficial.^1,2,4,20

Take-Home Points

• Gorham disease is a rare condition that manifests as an acute, spontaneous osteolysis.
• There is no clear hereditary pattern of transmission. Bones of any type or location can be affected.
• Imaging studies are nonspecific, but show permeative osteolysis involving the subcortical and intramedullary regions and typically affect regional, contiguous bones, without adjacent sclerosis, somewhat resembling osteoporosis.
• Tissue biopsy is indicated to rule out other potential etiologies of osteolysis, and the histologic findings help confirm a diagnosis of Gorham disease.
• There is no single or combined treatment modality that is considered as the gold standard. Surgical treatment includes resection of the lesion and reconstruction. Also, antiosteoclastic medication can be used.

Gorham disease, a rare condition of unknown etiology, manifests as acute, spontaneous osteolysis associated with benign hemangiomatosis or lymphangiomatosis, which presents as skeletal lucency on radiographs, prompting the classic eponym of vanishing bone disease.^1-6 There is no evidence supporting the idea that osteoclasts are present in any meaningful amount in the resorption areas or that local reparative osteogenesis occurs.^4,6

Jackson and colleagues first described idiopathic osteolysis in 1838,^1,2 and Gorham and Stout³ introduced the syndrome to the orthopedic community in 1955. Since then, few strides have been made in identifying the disease origin.^1,2,4 Diagnosis is possible only after meticulous work-up has excluded neoplastic and infectious etiologies.^7,8

Clinical Presentation

Gorham disease affects patients ranging widely in age, from 2 months to 78 years, but typically presents in those under 40 years. There is a questionable predilection for males but no correlation with ethnicity or geographic region. There is no clear hereditary pattern of transmission.⁷ Although the bones of the head, neck, and upper extremities are involved in most cases, bone of any type or location can be affected.⁶ Pelvic bones seem to be involved least often.^6,7

Initial clinical presentation varies considerably but typically involves prolonged soreness in the affected region and, rarely, acute pathologic fracture.^1,2,4 The nonspecific nature of complaints, lack of markers of systemic illness, and rarity of the disease contribute to delayed diagnosis.^1,2

Imaging

Computed tomography (CT) better defines the severity and extent of these changes.

Diagnosis

There have been 8 histologic and clinical criteria described to diagnose Gorham disease: (1) biopsy positive for presence of angiomatous tissue, (2) complete absence of any cellular atypia, (3) lack of osteoclastic response and lack of dystrophic calcifications, (4) evidence of progressive resorption of native bone, (5) no evidence of expansive or ulcerative lesion, (6) lack of visceral involvement, (7) osteolytic radiographic pattern, and (8) no concrete diagnosis after hereditary, metabolic, neoplastic, immunologic, and infectious work-up.^4-6 These criteria confirm that the diagnosis can be rendered only after exclusion of neoplastic and infectious etiologies through clinical and laboratory work-up, imaging studies, and tissue sampling.

Tissue biopsy is indicated to rule out other potential etiologies of osteolysis, and the histologic findings help confirm a diagnosis of Gorham disease.

Treatment

Surgical treatment usually includes lesion resection and subsequent reconstruction using combinations of bone grafts (allogenic) and prostheses. Bone graft alone is quickly resorbed and has not been found to be beneficial.^1,2,4,20

Take-Home Points

• Gorham disease is a rare condition that manifests as an acute, spontaneous osteolysis.
• There is no clear hereditary pattern of transmission. Bones of any type or location can be affected.
• Imaging studies are nonspecific, but show permeative osteolysis involving the subcortical and intramedullary regions and typically affect regional, contiguous bones, without adjacent sclerosis, somewhat resembling osteoporosis.
• Tissue biopsy is indicated to rule out other potential etiologies of osteolysis, and the histologic findings help confirm a diagnosis of Gorham disease.
• There is no single or combined treatment modality that is considered as the gold standard. Surgical treatment includes resection of the lesion and reconstruction. Also, antiosteoclastic medication can be used.

Gorham disease, a rare condition of unknown etiology, manifests as acute, spontaneous osteolysis associated with benign hemangiomatosis or lymphangiomatosis, which presents as skeletal lucency on radiographs, prompting the classic eponym of vanishing bone disease.^1-6 There is no evidence supporting the idea that osteoclasts are present in any meaningful amount in the resorption areas or that local reparative osteogenesis occurs.^4,6

Jackson and colleagues first described idiopathic osteolysis in 1838,^1,2 and Gorham and Stout³ introduced the syndrome to the orthopedic community in 1955. Since then, few strides have been made in identifying the disease origin.^1,2,4 Diagnosis is possible only after meticulous work-up has excluded neoplastic and infectious etiologies.^7,8

Clinical Presentation

Gorham disease affects patients ranging widely in age, from 2 months to 78 years, but typically presents in those under 40 years. There is a questionable predilection for males but no correlation with ethnicity or geographic region. There is no clear hereditary pattern of transmission.⁷ Although the bones of the head, neck, and upper extremities are involved in most cases, bone of any type or location can be affected.⁶ Pelvic bones seem to be involved least often.^6,7

Initial clinical presentation varies considerably but typically involves prolonged soreness in the affected region and, rarely, acute pathologic fracture.^1,2,4 The nonspecific nature of complaints, lack of markers of systemic illness, and rarity of the disease contribute to delayed diagnosis.^1,2

Imaging

Computed tomography (CT) better defines the severity and extent of these changes.

Diagnosis

There have been 8 histologic and clinical criteria described to diagnose Gorham disease: (1) biopsy positive for presence of angiomatous tissue, (2) complete absence of any cellular atypia, (3) lack of osteoclastic response and lack of dystrophic calcifications, (4) evidence of progressive resorption of native bone, (5) no evidence of expansive or ulcerative lesion, (6) lack of visceral involvement, (7) osteolytic radiographic pattern, and (8) no concrete diagnosis after hereditary, metabolic, neoplastic, immunologic, and infectious work-up.^4-6 These criteria confirm that the diagnosis can be rendered only after exclusion of neoplastic and infectious etiologies through clinical and laboratory work-up, imaging studies, and tissue sampling.

Tissue biopsy is indicated to rule out other potential etiologies of osteolysis, and the histologic findings help confirm a diagnosis of Gorham disease.

Treatment

Surgical treatment usually includes lesion resection and subsequent reconstruction using combinations of bone grafts (allogenic) and prostheses. Bone graft alone is quickly resorbed and has not been found to be beneficial.^1,2,4,20

Gadolinium-based contrast agents (GBCAs) used for MRI will now carry a warning regarding their potential retention in the bodies and brains of treated patients, according to the Food and Drug Administration.

The FDA is requiring the new class warning, along with other safety measures, based on evidence showing that trace amounts of gadolinium can be retained in the body for months to years after treatment.

Wikimedia Commons/FitzColinGerald/Creative Commons License

Specifically, the agency will require that patients receiving GBCAs first receive a Medication Guide and that GBCA manufacturers conduct human and animal studies to further assess GBCA safety. At this time, the only known adverse health effect of gadolinium retention is nephrogenic systemic fibrosis, which affects a small subgroup of patients with pre-existing kidney failure. No causal association has been established between gadolinium retention and reported adverse events in those with normal kidney function.

The FDA recommended that health care professionals consider the retention characteristics of GBCAs for patients who may be at higher risk for retention, including those requiring multiple lifetime doses, pregnant women, children, and patients with inflammatory conditions, but stressed that, although repeated GBCA imaging studies should be minimized when possible, they should not be avoided or deferred when they are necessary. In the safety alert, the FDA noted that administration of the GBCAs Dotarem (gadoterate meglumine), Gadavist (gadobutrol), and ProHance (gadoteridol) produce the lowest gadolinium levels in the body, and the three agents leave similar gadolinium levels in the body.

The agency encourages reports of adverse events or side effects related to the use of GBCAs to its MedWatch Safety information and Adverse Event Reporting Program. Reports can be submitted online at www.fda.gov/MedWatch/report or by calling 1-800-332-1088 to request a preaddressed form that can be mailed or faxed to 1-800-FDA-0178.

[email protected]

Gadolinium-based contrast agents (GBCAs) used for MRI will now carry a warning regarding their potential retention in the bodies and brains of treated patients, according to the Food and Drug Administration.

The FDA is requiring the new class warning, along with other safety measures, based on evidence showing that trace amounts of gadolinium can be retained in the body for months to years after treatment.

Wikimedia Commons/FitzColinGerald/Creative Commons License

Specifically, the agency will require that patients receiving GBCAs first receive a Medication Guide and that GBCA manufacturers conduct human and animal studies to further assess GBCA safety. At this time, the only known adverse health effect of gadolinium retention is nephrogenic systemic fibrosis, which affects a small subgroup of patients with pre-existing kidney failure. No causal association has been established between gadolinium retention and reported adverse events in those with normal kidney function.

The FDA recommended that health care professionals consider the retention characteristics of GBCAs for patients who may be at higher risk for retention, including those requiring multiple lifetime doses, pregnant women, children, and patients with inflammatory conditions, but stressed that, although repeated GBCA imaging studies should be minimized when possible, they should not be avoided or deferred when they are necessary. In the safety alert, the FDA noted that administration of the GBCAs Dotarem (gadoterate meglumine), Gadavist (gadobutrol), and ProHance (gadoteridol) produce the lowest gadolinium levels in the body, and the three agents leave similar gadolinium levels in the body.

The agency encourages reports of adverse events or side effects related to the use of GBCAs to its MedWatch Safety information and Adverse Event Reporting Program. Reports can be submitted online at www.fda.gov/MedWatch/report or by calling 1-800-332-1088 to request a preaddressed form that can be mailed or faxed to 1-800-FDA-0178.

[email protected]

Gadolinium-based contrast agents (GBCAs) used for MRI will now carry a warning regarding their potential retention in the bodies and brains of treated patients, according to the Food and Drug Administration.

The FDA is requiring the new class warning, along with other safety measures, based on evidence showing that trace amounts of gadolinium can be retained in the body for months to years after treatment.

Wikimedia Commons/FitzColinGerald/Creative Commons License

Specifically, the agency will require that patients receiving GBCAs first receive a Medication Guide and that GBCA manufacturers conduct human and animal studies to further assess GBCA safety. At this time, the only known adverse health effect of gadolinium retention is nephrogenic systemic fibrosis, which affects a small subgroup of patients with pre-existing kidney failure. No causal association has been established between gadolinium retention and reported adverse events in those with normal kidney function.

The FDA recommended that health care professionals consider the retention characteristics of GBCAs for patients who may be at higher risk for retention, including those requiring multiple lifetime doses, pregnant women, children, and patients with inflammatory conditions, but stressed that, although repeated GBCA imaging studies should be minimized when possible, they should not be avoided or deferred when they are necessary. In the safety alert, the FDA noted that administration of the GBCAs Dotarem (gadoterate meglumine), Gadavist (gadobutrol), and ProHance (gadoteridol) produce the lowest gadolinium levels in the body, and the three agents leave similar gadolinium levels in the body.

The agency encourages reports of adverse events or side effects related to the use of GBCAs to its MedWatch Safety information and Adverse Event Reporting Program. Reports can be submitted online at www.fda.gov/MedWatch/report or by calling 1-800-332-1088 to request a preaddressed form that can be mailed or faxed to 1-800-FDA-0178.

[email protected]

Gadolinium-based contrast agents (GBCAs) used for MRI will now carry a warning regarding their potential retention in the bodies and brains of treated patients, according to the Food and Drug Administration.

The FDA is requiring the new class warning, along with other safety measures, based on evidence showing that trace amounts of gadolinium can be retained in the body for months to years after treatment.

Wikimedia Commons/FitzColinGerald/Creative Commons License

[email protected]

Gadolinium-based contrast agents (GBCAs) used for MRI will now carry a warning regarding their potential retention in the bodies and brains of treated patients, according to the Food and Drug Administration.

The FDA is requiring the new class warning, along with other safety measures, based on evidence showing that trace amounts of gadolinium can be retained in the body for months to years after treatment.

Wikimedia Commons/FitzColinGerald/Creative Commons License

[email protected]

Gadolinium-based contrast agents (GBCAs) used for MRI will now carry a warning regarding their potential retention in the bodies and brains of treated patients, according to the Food and Drug Administration.

The FDA is requiring the new class warning, along with other safety measures, based on evidence showing that trace amounts of gadolinium can be retained in the body for months to years after treatment.

Wikimedia Commons/FitzColinGerald/Creative Commons License

[email protected]

Case

A 96-year-old woman with a medical history of sciatica, vertigo, osteoporosis, and dementia presented with atraumatic right leg pain. She stated that the pain, which began 4 weeks prior to presentation, started in her right groin. The patient’s primary care physician diagnosed her with tendonitis, and prescribed acetaminophen/codeine and naproxen sodium for the pain. However, the patient’s pain progressively worsened to the point where she was no longer able to ambulate or bear weight on her right hip, prompting this visit to the ED.

On physical examination, the patient’s right hip was tender to palpation without any signs of physical deformity of the lower extremity. Upon hip flexion, she grimaced and communicated her pain.

Radiographs and computed tomography images taken of the right hip, femur, and pelvis demonstrated low-bone mineral density without fracture.

What is the diagnosis?

Answer

Axial and coronal edema-sensitive images of the pelvis demonstrated edema (increased signal) within the right psoas, iliacus, and iliopsoas muscles (red arrows, Figures 2a-2c), which were in contrast to the normal pelvic muscles on the left side (white arrows, Figures 2a-2c).

Iliopsoas Musculotendinous Unit

The iliopsoas musculotendinous unit consists of the psoas major, the psoas minor, and the iliacus, with the psoas minor absent in 40% to 50% of cases.^1,2 The iliacus muscle arises from the iliac wing and inserts with the psoas tendon onto the lesser trochanter of the femur. These muscles function as primary flexors of the thigh and trunk, as well as lateral flexors of the lower vertebral column.²

Signs and Symptoms

In non-sports-related injuries, iliopsoas tendon tears typically occur in elderly female patients—even in the absence of any trauma or known predisposing factors. Patients with iliopsoas tears typically present with hip or groin pain, and weakness with hip flexion, which clinically may mimic hip or sacral fracture. An anterior thigh mass or ecchymosis may also be present. Complete tear of the iliopsoas tendon usually occurs at or near the distal insertion at the lesser trochanter, and is often associated with proximal retraction of the tendon to the level of the femoral head.¹

Imaging Studies

Iliopsoas tendon injury is best evaluated with MRI, particularly with fluid-sensitive sequences. Patients with iliopsoas tendon tears have abnormal signal in the muscle belly, likely related to edema and hemorrhage, and hematoma or fluid around the torn tendon and at the site of retraction. In pediatric patients, iliopsoas injury is typically an avulsion of the lesser trochanter prior to fusion of the apophysis.^3,4 In adult patients with avulsion of the lesser trochanter, this injury is regarded as a sign of metastatic disease until proven otherwise.⁵

Treatment

Patients with iliopsoas tendon rupture are treated conservatively with rest, ice, and physical therapy (PT). Preservation of the distal muscular insertion of the lateral portion of the iliacus muscle is thought to play a role in positive clinical outcomes.³

The patient in this case was admitted to the hospital and treated for pain with standing acetaminophen, tramadol as needed, and a lidocaine patch. After attending multiple inpatient PT sessions, she was discharged to a subacute rehabilitation facility.

Case

A 96-year-old woman with a medical history of sciatica, vertigo, osteoporosis, and dementia presented with atraumatic right leg pain. She stated that the pain, which began 4 weeks prior to presentation, started in her right groin. The patient’s primary care physician diagnosed her with tendonitis, and prescribed acetaminophen/codeine and naproxen sodium for the pain. However, the patient’s pain progressively worsened to the point where she was no longer able to ambulate or bear weight on her right hip, prompting this visit to the ED.

On physical examination, the patient’s right hip was tender to palpation without any signs of physical deformity of the lower extremity. Upon hip flexion, she grimaced and communicated her pain.

Radiographs and computed tomography images taken of the right hip, femur, and pelvis demonstrated low-bone mineral density without fracture.

What is the diagnosis?

Answer

Axial and coronal edema-sensitive images of the pelvis demonstrated edema (increased signal) within the right psoas, iliacus, and iliopsoas muscles (red arrows, Figures 2a-2c), which were in contrast to the normal pelvic muscles on the left side (white arrows, Figures 2a-2c).

Iliopsoas Musculotendinous Unit

The iliopsoas musculotendinous unit consists of the psoas major, the psoas minor, and the iliacus, with the psoas minor absent in 40% to 50% of cases.^1,2 The iliacus muscle arises from the iliac wing and inserts with the psoas tendon onto the lesser trochanter of the femur. These muscles function as primary flexors of the thigh and trunk, as well as lateral flexors of the lower vertebral column.²

Signs and Symptoms

In non-sports-related injuries, iliopsoas tendon tears typically occur in elderly female patients—even in the absence of any trauma or known predisposing factors. Patients with iliopsoas tears typically present with hip or groin pain, and weakness with hip flexion, which clinically may mimic hip or sacral fracture. An anterior thigh mass or ecchymosis may also be present. Complete tear of the iliopsoas tendon usually occurs at or near the distal insertion at the lesser trochanter, and is often associated with proximal retraction of the tendon to the level of the femoral head.¹

Imaging Studies

Iliopsoas tendon injury is best evaluated with MRI, particularly with fluid-sensitive sequences. Patients with iliopsoas tendon tears have abnormal signal in the muscle belly, likely related to edema and hemorrhage, and hematoma or fluid around the torn tendon and at the site of retraction. In pediatric patients, iliopsoas injury is typically an avulsion of the lesser trochanter prior to fusion of the apophysis.^3,4 In adult patients with avulsion of the lesser trochanter, this injury is regarded as a sign of metastatic disease until proven otherwise.⁵

Treatment

Patients with iliopsoas tendon rupture are treated conservatively with rest, ice, and physical therapy (PT). Preservation of the distal muscular insertion of the lateral portion of the iliacus muscle is thought to play a role in positive clinical outcomes.³

The patient in this case was admitted to the hospital and treated for pain with standing acetaminophen, tramadol as needed, and a lidocaine patch. After attending multiple inpatient PT sessions, she was discharged to a subacute rehabilitation facility.

Case

A 96-year-old woman with a medical history of sciatica, vertigo, osteoporosis, and dementia presented with atraumatic right leg pain. She stated that the pain, which began 4 weeks prior to presentation, started in her right groin. The patient’s primary care physician diagnosed her with tendonitis, and prescribed acetaminophen/codeine and naproxen sodium for the pain. However, the patient’s pain progressively worsened to the point where she was no longer able to ambulate or bear weight on her right hip, prompting this visit to the ED.

On physical examination, the patient’s right hip was tender to palpation without any signs of physical deformity of the lower extremity. Upon hip flexion, she grimaced and communicated her pain.

Radiographs and computed tomography images taken of the right hip, femur, and pelvis demonstrated low-bone mineral density without fracture.

What is the diagnosis?

Answer

Axial and coronal edema-sensitive images of the pelvis demonstrated edema (increased signal) within the right psoas, iliacus, and iliopsoas muscles (red arrows, Figures 2a-2c), which were in contrast to the normal pelvic muscles on the left side (white arrows, Figures 2a-2c).

Iliopsoas Musculotendinous Unit

The iliopsoas musculotendinous unit consists of the psoas major, the psoas minor, and the iliacus, with the psoas minor absent in 40% to 50% of cases.^1,2 The iliacus muscle arises from the iliac wing and inserts with the psoas tendon onto the lesser trochanter of the femur. These muscles function as primary flexors of the thigh and trunk, as well as lateral flexors of the lower vertebral column.²

Signs and Symptoms

In non-sports-related injuries, iliopsoas tendon tears typically occur in elderly female patients—even in the absence of any trauma or known predisposing factors. Patients with iliopsoas tears typically present with hip or groin pain, and weakness with hip flexion, which clinically may mimic hip or sacral fracture. An anterior thigh mass or ecchymosis may also be present. Complete tear of the iliopsoas tendon usually occurs at or near the distal insertion at the lesser trochanter, and is often associated with proximal retraction of the tendon to the level of the femoral head.¹

Imaging Studies

Iliopsoas tendon injury is best evaluated with MRI, particularly with fluid-sensitive sequences. Patients with iliopsoas tendon tears have abnormal signal in the muscle belly, likely related to edema and hemorrhage, and hematoma or fluid around the torn tendon and at the site of retraction. In pediatric patients, iliopsoas injury is typically an avulsion of the lesser trochanter prior to fusion of the apophysis.^3,4 In adult patients with avulsion of the lesser trochanter, this injury is regarded as a sign of metastatic disease until proven otherwise.⁵

Treatment

Patients with iliopsoas tendon rupture are treated conservatively with rest, ice, and physical therapy (PT). Preservation of the distal muscular insertion of the lateral portion of the iliacus muscle is thought to play a role in positive clinical outcomes.³

The patient in this case was admitted to the hospital and treated for pain with standing acetaminophen, tramadol as needed, and a lidocaine patch. After attending multiple inpatient PT sessions, she was discharged to a subacute rehabilitation facility.

A 76-year-old man with ulcerative colitis presented with a 1-week history of low-grade fever and progressive dyspnea. He was taking infliximab for the ulcerative colitis. He was known to be negative for human immunodeficiency virus.

Since the M tuberculosis cultured from his lung proved to be sensitive to the antituberculosis drugs, we suspected that the nodules were a paradoxical reaction to the drug therapy, and thus we continued the treatment because of the continued low-grade fever. After 9 months of therapy, the fever had resolved and the nodules had disappeared, confirming our suspicion of a paradoxical reaction. The number of lymphocytes gradually increased during drug therapy.

Paradoxical reaction during tuberculosis treatment is defined as a worsening of pre-existing lesions or as the emergence of new lesions during appropriate therapy.^1,2 The diagnosis is sometimes difficult, since new lesions can resemble other lung diseases. However, a paradoxical reaction involving randomly distributed nodules is rare and radiographically resembles metastatic lung cancer. Clinicians should be aware of this type of reaction in patients on tuberculosis therapy.

A 76-year-old man with ulcerative colitis presented with a 1-week history of low-grade fever and progressive dyspnea. He was taking infliximab for the ulcerative colitis. He was known to be negative for human immunodeficiency virus.

Since the M tuberculosis cultured from his lung proved to be sensitive to the antituberculosis drugs, we suspected that the nodules were a paradoxical reaction to the drug therapy, and thus we continued the treatment because of the continued low-grade fever. After 9 months of therapy, the fever had resolved and the nodules had disappeared, confirming our suspicion of a paradoxical reaction. The number of lymphocytes gradually increased during drug therapy.

Paradoxical reaction during tuberculosis treatment is defined as a worsening of pre-existing lesions or as the emergence of new lesions during appropriate therapy.^1,2 The diagnosis is sometimes difficult, since new lesions can resemble other lung diseases. However, a paradoxical reaction involving randomly distributed nodules is rare and radiographically resembles metastatic lung cancer. Clinicians should be aware of this type of reaction in patients on tuberculosis therapy.

A 76-year-old man with ulcerative colitis presented with a 1-week history of low-grade fever and progressive dyspnea. He was taking infliximab for the ulcerative colitis. He was known to be negative for human immunodeficiency virus.

Since the M tuberculosis cultured from his lung proved to be sensitive to the antituberculosis drugs, we suspected that the nodules were a paradoxical reaction to the drug therapy, and thus we continued the treatment because of the continued low-grade fever. After 9 months of therapy, the fever had resolved and the nodules had disappeared, confirming our suspicion of a paradoxical reaction. The number of lymphocytes gradually increased during drug therapy.

Paradoxical reaction during tuberculosis treatment is defined as a worsening of pre-existing lesions or as the emergence of new lesions during appropriate therapy.^1,2 The diagnosis is sometimes difficult, since new lesions can resemble other lung diseases. However, a paradoxical reaction involving randomly distributed nodules is rare and radiographically resembles metastatic lung cancer. Clinicians should be aware of this type of reaction in patients on tuberculosis therapy.

An 85-year-old woman presented with night sweats, dry cough, and an unintended 30-pound weight loss over the preceding 6 months. She also reported the sudden onset of “itchy moles” on her back.

KERATOSES AND MALIGNANCY

The Leser-Trélat sign is the sudden development of multiple pruritic seborrheic keratoses, often associated with malignancy.^1–4 Roughly half of these associated malignancies are adenocarcinomas, most commonly of the stomach, breast, colon, or rectum. However, it can be seen in other malignancies, including lymphoma, leukemia, and squamous cell carcinoma, as in this case.

Eruption of seborrheic keratoses has also been observed with benign neoplasms, pregnancy, human immunodeficiency virus infections, and the use of adalimumab, which indicates that the Leser-Trélat sign is not very specific. Despite these concerns, the eruption of multiple seborrheic keratoses should continue to trigger the thought of an internal malignancy in the differential diagnosis.

An 85-year-old woman presented with night sweats, dry cough, and an unintended 30-pound weight loss over the preceding 6 months. She also reported the sudden onset of “itchy moles” on her back.

KERATOSES AND MALIGNANCY

The Leser-Trélat sign is the sudden development of multiple pruritic seborrheic keratoses, often associated with malignancy.^1–4 Roughly half of these associated malignancies are adenocarcinomas, most commonly of the stomach, breast, colon, or rectum. However, it can be seen in other malignancies, including lymphoma, leukemia, and squamous cell carcinoma, as in this case.

Eruption of seborrheic keratoses has also been observed with benign neoplasms, pregnancy, human immunodeficiency virus infections, and the use of adalimumab, which indicates that the Leser-Trélat sign is not very specific. Despite these concerns, the eruption of multiple seborrheic keratoses should continue to trigger the thought of an internal malignancy in the differential diagnosis.

An 85-year-old woman presented with night sweats, dry cough, and an unintended 30-pound weight loss over the preceding 6 months. She also reported the sudden onset of “itchy moles” on her back.

KERATOSES AND MALIGNANCY

The Leser-Trélat sign is the sudden development of multiple pruritic seborrheic keratoses, often associated with malignancy.^1–4 Roughly half of these associated malignancies are adenocarcinomas, most commonly of the stomach, breast, colon, or rectum. However, it can be seen in other malignancies, including lymphoma, leukemia, and squamous cell carcinoma, as in this case.

Eruption of seborrheic keratoses has also been observed with benign neoplasms, pregnancy, human immunodeficiency virus infections, and the use of adalimumab, which indicates that the Leser-Trélat sign is not very specific. Despite these concerns, the eruption of multiple seborrheic keratoses should continue to trigger the thought of an internal malignancy in the differential diagnosis.