Imaging

Computed tomography (CT) plays an important role in the diagnosis and treatment of many clinical conditions¹ involving the chest wall, mediastinum, pleura, pulmonary arteries, and lung parenchyma. The need for enhancement with intravenous (IV) contrast depends on the specific clinical indication (Table 1).

EVALUATION OF SUSPECTED CANCER

CT is commonly used to diagnose, stage, and plan treatment for lung cancer, other primary neoplastic processes involving the chest, and metastatic disease.² The need for contrast varies on a case-by-case basis, and the benefits of contrast should be weighed against the potential risks in each patient.

When the neoplasm has CT attenuation similar to that of adjacent structures (lymph nodes in the hilum, masses in the mediastinum or chest wall), IV contrast can improve identification of the lesion and delineation of its margins and the relationship with adjacent structures (eg, vascular structures) (Figure 1).

CT without contrast for screening

The diagnostic algorithm for lung cancer screening is evolving. The US Preventive Services Task Force currently recommends low-dose CT without contrast, along with appropriate patient counseling, for patients with a history of smoking and an age range as detailed in the Task Force statement.³

Follow-up of a solitary pulmonary nodule also typically does not require contrast enhancement, though some investigators have reported high sensitivity with dynamic contrast enhancement of pulmonary nodules.⁴ This represents a rare clinical application of chest CT with and without contrast.

EVALUATION OF THORACIC VASCULAR DISEASE

For the assessment of vascular disease, CT in most cases requires IV contrast to delineate the vessel lumen. Pulmonary embolic disease is the third most common cause of acute cardiovascular disease.⁵ CT pulmonary angiography is the most common way to assess for pulmonary embolic disease, as it is accurate, fast, and widely available, and can assess alternate pathologies in cases of undifferentiated chest pain. Contrast enhancement of the pulmonary arteries is key, as embolic disease is identified as abnormal filling defects within the pulmonary arteries (Figure 2).

Contrast enhancement is also used to evaluate superior vena cava syndrome. At our institution, the CT protocol includes concomitant injections in the upper-extremity veins, with imaging timed for venous phase enhancement (pulmonary venogram). In cases of suspected arteriovenous malformation, a protocol similar to that used for suspected pulmonary embolus is used (Figure 3), although in some instances, the imaging features of arteriovenous malformation may be detectable without IV contrast.

EVALUATION OF PULMONARY PARENCHYMAL DISEASE

Infection, inflammation, and edema of the lung parenchyma are usually well depicted on CT without contrast enhancement. However, contrast may be helpful if there are concerns about complications such as chest wall involvement, where contrast enhancement may help further delineate the extent of complications.

Assessment of interstitial lung disease does not require use of IV contrast; rather, a tailored protocol with thinner slices and noncontiguous expiratory images can be used to evaluate for air-trapping and dynamic airway compromise (Figure 4). Evaluation of chronic obstructive pulmonary disease also does not require IV contrast.

EVALUATION OF THE PLEURA

In pleural effusion, CT assessment for the presence, location, and extent of the effusion does not require contrast. However, contrast enhancement is used to evaluate suspected or known exudative effusions and empyema.⁶ It also aids the evaluation of metastatic or primary malignancy of the pleura, particularly in cases of occult disease, as enhancement and thickening of the pleura are of diagnostic interest.

EVALUATION OF AIRWAY DISEASE

Diseases of the large airway, such as stenosis and thickening, and diseases of the small airways, such as bronchiolitis, typically do not require contrast enhancement. At our institution, to assess dynamic airway narrowing, we use a dedicated airway protocol, including inspiratory and expiratory phases and multiplanar reformatted images.

EVALUATION OF STERNAL AND MEDIASTINAL INFECTIONS

Postoperative sternal wound infections are not uncommon and range from cellulitis to frank osteomyelitis. Mediastinitis may likewise be iatrogenic or may spread from the oropharynx. CT with contrast can help to depict infection of the chest wall or mediastinum and in some instances can also delineate the route of spread.⁷

TYPES OF IV CONTRAST MEDIA

Contrast media used in CT contain iodine, which causes increased absorption and scattering of radiation in body tissues and blood. Other contrast media, such as those used for magnetic resonance imaging or barium enemas, do not contain iodine. This absorption and scattering in turn results in higher CT attenuation values, or “enhancement” on CT images. The extent of enhancement depends on the amount and rate of contrast material administered, as well as on patient factors (eg, tissue vascularity, permeability, interstitial space) and the energy (tube voltage) of the incident x-rays.⁸

Adverse reactions

Contrast materials are generally safe; however, as with any pharmaceutical, there is the potential for adverse reactions. These reactions are relatively rare and are usually mild but occasionally can be severe.⁹ Anaphylactoid reactions have an unclear etiology but mimic allergic reactions, and they are more likely to occur in patients with a previous reaction to contrast and in patients with asthma or cardiovascular or renal disease.

Nonanaphylactoid reactions are dependent on contrast osmolality and on the volume and route of injection (unlike anaphylactoid reactions).¹⁰ Typical symptoms include warmth, metallic taste, and nausea or vomiting.

Contrast-related nephrotoxicity has been reported,¹¹ although this has been challenged more recently.¹² Suspected risk factors for this complication include advanced age, cardiovascular disease, treatment with chemotherapy, elevated serum creatinine level, dehydration, diabetes, use of nonsteroidal anti-inflammatory medications, myeloma,¹³ renal disease, and kidney transplant.

Detailed protocols for premedication and management of contrast adverse reactions are beyond the scope of this review and the reader is advised to refer to dedicated manuals.¹⁰

Acknowledgment: We are grateful for the editorial assistance of Megan M. Griffiths, scientific writer for the Imaging Institute, Cleveland Clinic.

Computed tomography (CT) plays an important role in the diagnosis and treatment of many clinical conditions¹ involving the chest wall, mediastinum, pleura, pulmonary arteries, and lung parenchyma. The need for enhancement with intravenous (IV) contrast depends on the specific clinical indication (Table 1).

EVALUATION OF SUSPECTED CANCER

CT is commonly used to diagnose, stage, and plan treatment for lung cancer, other primary neoplastic processes involving the chest, and metastatic disease.² The need for contrast varies on a case-by-case basis, and the benefits of contrast should be weighed against the potential risks in each patient.

When the neoplasm has CT attenuation similar to that of adjacent structures (lymph nodes in the hilum, masses in the mediastinum or chest wall), IV contrast can improve identification of the lesion and delineation of its margins and the relationship with adjacent structures (eg, vascular structures) (Figure 1).

CT without contrast for screening

The diagnostic algorithm for lung cancer screening is evolving. The US Preventive Services Task Force currently recommends low-dose CT without contrast, along with appropriate patient counseling, for patients with a history of smoking and an age range as detailed in the Task Force statement.³

Follow-up of a solitary pulmonary nodule also typically does not require contrast enhancement, though some investigators have reported high sensitivity with dynamic contrast enhancement of pulmonary nodules.⁴ This represents a rare clinical application of chest CT with and without contrast.

EVALUATION OF THORACIC VASCULAR DISEASE

For the assessment of vascular disease, CT in most cases requires IV contrast to delineate the vessel lumen. Pulmonary embolic disease is the third most common cause of acute cardiovascular disease.⁵ CT pulmonary angiography is the most common way to assess for pulmonary embolic disease, as it is accurate, fast, and widely available, and can assess alternate pathologies in cases of undifferentiated chest pain. Contrast enhancement of the pulmonary arteries is key, as embolic disease is identified as abnormal filling defects within the pulmonary arteries (Figure 2).

Contrast enhancement is also used to evaluate superior vena cava syndrome. At our institution, the CT protocol includes concomitant injections in the upper-extremity veins, with imaging timed for venous phase enhancement (pulmonary venogram). In cases of suspected arteriovenous malformation, a protocol similar to that used for suspected pulmonary embolus is used (Figure 3), although in some instances, the imaging features of arteriovenous malformation may be detectable without IV contrast.

EVALUATION OF PULMONARY PARENCHYMAL DISEASE

Infection, inflammation, and edema of the lung parenchyma are usually well depicted on CT without contrast enhancement. However, contrast may be helpful if there are concerns about complications such as chest wall involvement, where contrast enhancement may help further delineate the extent of complications.

Assessment of interstitial lung disease does not require use of IV contrast; rather, a tailored protocol with thinner slices and noncontiguous expiratory images can be used to evaluate for air-trapping and dynamic airway compromise (Figure 4). Evaluation of chronic obstructive pulmonary disease also does not require IV contrast.

EVALUATION OF THE PLEURA

In pleural effusion, CT assessment for the presence, location, and extent of the effusion does not require contrast. However, contrast enhancement is used to evaluate suspected or known exudative effusions and empyema.⁶ It also aids the evaluation of metastatic or primary malignancy of the pleura, particularly in cases of occult disease, as enhancement and thickening of the pleura are of diagnostic interest.

EVALUATION OF AIRWAY DISEASE

Diseases of the large airway, such as stenosis and thickening, and diseases of the small airways, such as bronchiolitis, typically do not require contrast enhancement. At our institution, to assess dynamic airway narrowing, we use a dedicated airway protocol, including inspiratory and expiratory phases and multiplanar reformatted images.

EVALUATION OF STERNAL AND MEDIASTINAL INFECTIONS

Postoperative sternal wound infections are not uncommon and range from cellulitis to frank osteomyelitis. Mediastinitis may likewise be iatrogenic or may spread from the oropharynx. CT with contrast can help to depict infection of the chest wall or mediastinum and in some instances can also delineate the route of spread.⁷

TYPES OF IV CONTRAST MEDIA

Contrast media used in CT contain iodine, which causes increased absorption and scattering of radiation in body tissues and blood. Other contrast media, such as those used for magnetic resonance imaging or barium enemas, do not contain iodine. This absorption and scattering in turn results in higher CT attenuation values, or “enhancement” on CT images. The extent of enhancement depends on the amount and rate of contrast material administered, as well as on patient factors (eg, tissue vascularity, permeability, interstitial space) and the energy (tube voltage) of the incident x-rays.⁸

Adverse reactions

Contrast materials are generally safe; however, as with any pharmaceutical, there is the potential for adverse reactions. These reactions are relatively rare and are usually mild but occasionally can be severe.⁹ Anaphylactoid reactions have an unclear etiology but mimic allergic reactions, and they are more likely to occur in patients with a previous reaction to contrast and in patients with asthma or cardiovascular or renal disease.

Nonanaphylactoid reactions are dependent on contrast osmolality and on the volume and route of injection (unlike anaphylactoid reactions).¹⁰ Typical symptoms include warmth, metallic taste, and nausea or vomiting.

Contrast-related nephrotoxicity has been reported,¹¹ although this has been challenged more recently.¹² Suspected risk factors for this complication include advanced age, cardiovascular disease, treatment with chemotherapy, elevated serum creatinine level, dehydration, diabetes, use of nonsteroidal anti-inflammatory medications, myeloma,¹³ renal disease, and kidney transplant.

Detailed protocols for premedication and management of contrast adverse reactions are beyond the scope of this review and the reader is advised to refer to dedicated manuals.¹⁰

Acknowledgment: We are grateful for the editorial assistance of Megan M. Griffiths, scientific writer for the Imaging Institute, Cleveland Clinic.

Computed tomography (CT) plays an important role in the diagnosis and treatment of many clinical conditions¹ involving the chest wall, mediastinum, pleura, pulmonary arteries, and lung parenchyma. The need for enhancement with intravenous (IV) contrast depends on the specific clinical indication (Table 1).

EVALUATION OF SUSPECTED CANCER

CT is commonly used to diagnose, stage, and plan treatment for lung cancer, other primary neoplastic processes involving the chest, and metastatic disease.² The need for contrast varies on a case-by-case basis, and the benefits of contrast should be weighed against the potential risks in each patient.

When the neoplasm has CT attenuation similar to that of adjacent structures (lymph nodes in the hilum, masses in the mediastinum or chest wall), IV contrast can improve identification of the lesion and delineation of its margins and the relationship with adjacent structures (eg, vascular structures) (Figure 1).

CT without contrast for screening

The diagnostic algorithm for lung cancer screening is evolving. The US Preventive Services Task Force currently recommends low-dose CT without contrast, along with appropriate patient counseling, for patients with a history of smoking and an age range as detailed in the Task Force statement.³

Follow-up of a solitary pulmonary nodule also typically does not require contrast enhancement, though some investigators have reported high sensitivity with dynamic contrast enhancement of pulmonary nodules.⁴ This represents a rare clinical application of chest CT with and without contrast.

EVALUATION OF THORACIC VASCULAR DISEASE

For the assessment of vascular disease, CT in most cases requires IV contrast to delineate the vessel lumen. Pulmonary embolic disease is the third most common cause of acute cardiovascular disease.⁵ CT pulmonary angiography is the most common way to assess for pulmonary embolic disease, as it is accurate, fast, and widely available, and can assess alternate pathologies in cases of undifferentiated chest pain. Contrast enhancement of the pulmonary arteries is key, as embolic disease is identified as abnormal filling defects within the pulmonary arteries (Figure 2).

Contrast enhancement is also used to evaluate superior vena cava syndrome. At our institution, the CT protocol includes concomitant injections in the upper-extremity veins, with imaging timed for venous phase enhancement (pulmonary venogram). In cases of suspected arteriovenous malformation, a protocol similar to that used for suspected pulmonary embolus is used (Figure 3), although in some instances, the imaging features of arteriovenous malformation may be detectable without IV contrast.

EVALUATION OF PULMONARY PARENCHYMAL DISEASE

Infection, inflammation, and edema of the lung parenchyma are usually well depicted on CT without contrast enhancement. However, contrast may be helpful if there are concerns about complications such as chest wall involvement, where contrast enhancement may help further delineate the extent of complications.

Assessment of interstitial lung disease does not require use of IV contrast; rather, a tailored protocol with thinner slices and noncontiguous expiratory images can be used to evaluate for air-trapping and dynamic airway compromise (Figure 4). Evaluation of chronic obstructive pulmonary disease also does not require IV contrast.

EVALUATION OF THE PLEURA

In pleural effusion, CT assessment for the presence, location, and extent of the effusion does not require contrast. However, contrast enhancement is used to evaluate suspected or known exudative effusions and empyema.⁶ It also aids the evaluation of metastatic or primary malignancy of the pleura, particularly in cases of occult disease, as enhancement and thickening of the pleura are of diagnostic interest.

EVALUATION OF AIRWAY DISEASE

Diseases of the large airway, such as stenosis and thickening, and diseases of the small airways, such as bronchiolitis, typically do not require contrast enhancement. At our institution, to assess dynamic airway narrowing, we use a dedicated airway protocol, including inspiratory and expiratory phases and multiplanar reformatted images.

EVALUATION OF STERNAL AND MEDIASTINAL INFECTIONS

Postoperative sternal wound infections are not uncommon and range from cellulitis to frank osteomyelitis. Mediastinitis may likewise be iatrogenic or may spread from the oropharynx. CT with contrast can help to depict infection of the chest wall or mediastinum and in some instances can also delineate the route of spread.⁷

TYPES OF IV CONTRAST MEDIA

Contrast media used in CT contain iodine, which causes increased absorption and scattering of radiation in body tissues and blood. Other contrast media, such as those used for magnetic resonance imaging or barium enemas, do not contain iodine. This absorption and scattering in turn results in higher CT attenuation values, or “enhancement” on CT images. The extent of enhancement depends on the amount and rate of contrast material administered, as well as on patient factors (eg, tissue vascularity, permeability, interstitial space) and the energy (tube voltage) of the incident x-rays.⁸

Adverse reactions

Contrast materials are generally safe; however, as with any pharmaceutical, there is the potential for adverse reactions. These reactions are relatively rare and are usually mild but occasionally can be severe.⁹ Anaphylactoid reactions have an unclear etiology but mimic allergic reactions, and they are more likely to occur in patients with a previous reaction to contrast and in patients with asthma or cardiovascular or renal disease.

Nonanaphylactoid reactions are dependent on contrast osmolality and on the volume and route of injection (unlike anaphylactoid reactions).¹⁰ Typical symptoms include warmth, metallic taste, and nausea or vomiting.

Contrast-related nephrotoxicity has been reported,¹¹ although this has been challenged more recently.¹² Suspected risk factors for this complication include advanced age, cardiovascular disease, treatment with chemotherapy, elevated serum creatinine level, dehydration, diabetes, use of nonsteroidal anti-inflammatory medications, myeloma,¹³ renal disease, and kidney transplant.

Detailed protocols for premedication and management of contrast adverse reactions are beyond the scope of this review and the reader is advised to refer to dedicated manuals.¹⁰

Acknowledgment: We are grateful for the editorial assistance of Megan M. Griffiths, scientific writer for the Imaging Institute, Cleveland Clinic.

A 34-year-old woman sought consultation at our clinic for an asymptomatic swelling on her right foot that had been growing very slowly over the last 15 years. She said she had presented to other healthcare facilities, but no diagnosis had been made and no treatment had been offered.

Examination revealed a linear swelling extending from the lower third to the mid-dorsal surface of the right foot (Figure 1). Palpation revealed multiple, closely set nodules arranged in a linear fashion. This finding along with the history raised the suspicion of neurofibroma and other conditions in the differential diagnosis, eg, pure neuritic Hansen disease, phaeohyphomycosis, and palisaded neutrophilic granulomatous dermatitis. The rest of the mucocutaneous examination results were normal. No café-au-lait spots, axillary freckling, or other swelling suggestive of neurofibroma was seen. She had no family history of mucocutaneous disease or other systemic disorder.

Because of the suspicion of neurofibromatosis, slit-lamp examination of the eyes was done to rule out Lisch nodules, a common feature of neurofibromatosis; the results were normal. Plain radiography of the right foot showed only soft-tissue swelling. Magnetic resonance imaging with contrast, done to determine the extent of the lesions, revealed multiple dumbbell-shaped lesions with homogeneous enhancement (Figure 2). Histopathologic study of a biopsy specimen of the lesions showed tumor cells in the dermis. The cells were long, with elongated nuclei with pointed ends, arranged in long and short fascicles—an appearance characteristic of neurofibroma. Areas of hypocellularity and hypercellularity were seen, and on S100 protein immunostaining, the tumor cells showed strong nuclear and cytoplasmic positivity (Figure 3).

The histologic evaluation confirmed neurofibroma. The specific diagnosis of sporadic solitary neurofibroma was made based on the onset of the lesions, the number of lesions (one in this patient), and the absence of features suggestive of neurofibromatosis.

SPORADIC SOLITARY NEUROFIBROMA

Neurofibroma is a common tumor of the peripheral nerve sheath and, when present with features such as café-au-lait spots, axillary freckling, and characteristic bone changes, it is pathognomic of neurofibromatosis type 1.¹ But solitary neurofibromas can occur sporadically in the absence of other features of neurofibromatosis.

Sporadic solitary neurofibroma arises from small nerves, is benign in nature, and carries a lower rate of malignant transformation than its counterpart that occurs in the setting of neurofibromatosis.² Though sporadic solitary neurofibroma can occur in any part of the body, it is commonly seen on the head and neck, and occasionally on the presacral and parasacral space, thigh, intrascrotal area,³ the ankle and foot,^4,5 and the subungual region.⁶ A series of 397 peripheral neural sheath tumors examined over 30 years showed 55 sporadic solitary neurofibromas occurring in the brachial plexus region, 45 in the upper extremities, 10 in the pelvic plexus, and 31 in the lower extremities.⁷

Management of sporadic solitary neurofibroma depends on the patient’s discomfort. For asymptomatic lesions, serial observation is all that is required. Complete surgical excision including the parent nerve is the treatment for large lesions. More research is needed to define the potential role of drugs such as pirfenidone and tipifarnib.

THE DIFFERENTIAL DIAGNOSIS

Sporadic solitary neurofibroma can masquerade as pure neuritic Hansen disease (leprosy), phaeohyphomycosis, and palisaded neutrophilic granulomatous dermatitis. The absence of neural symptoms and no evidence of trophic changes exclude pure neuritic Hansen disease. Phaeohyphomycosis clinically presents as a single cyst that may evolve into pigmented plaques,⁸ and the diagnosis relies on the presence of fungus in tissue. The absence of cystic changes clinically and fungi histopathologically in this patient did not favor phaeohyphomycosis. Palisaded neutrophilic granulomatous dermatitis is characterized clinically by cordlike skin lesions (the “rope sign”) and is accompanied by extracutaneous, mostly articular features. Histopathologically, it shows intense neutrophilic infiltrate and interstitial histiocytic infiltrate along with collagen degeneration. The absence of extracutaneous and classical histologic features negated this possibility in this patient.

Though sporotrichosis and cutaneous atypical mycobacterial infections may present in linear fashion following the course of the lymphatic vessels, the absence of epidermal changes after a disease course of 15 years and the absence of granulomatous infiltrate in histopathology excluded these possibilities in this patient.

The patient was referred to a plastic surgeon, and the lesions were successfully resected. She did not return for additional review after that.

A 34-year-old woman sought consultation at our clinic for an asymptomatic swelling on her right foot that had been growing very slowly over the last 15 years. She said she had presented to other healthcare facilities, but no diagnosis had been made and no treatment had been offered.

Examination revealed a linear swelling extending from the lower third to the mid-dorsal surface of the right foot (Figure 1). Palpation revealed multiple, closely set nodules arranged in a linear fashion. This finding along with the history raised the suspicion of neurofibroma and other conditions in the differential diagnosis, eg, pure neuritic Hansen disease, phaeohyphomycosis, and palisaded neutrophilic granulomatous dermatitis. The rest of the mucocutaneous examination results were normal. No café-au-lait spots, axillary freckling, or other swelling suggestive of neurofibroma was seen. She had no family history of mucocutaneous disease or other systemic disorder.

Because of the suspicion of neurofibromatosis, slit-lamp examination of the eyes was done to rule out Lisch nodules, a common feature of neurofibromatosis; the results were normal. Plain radiography of the right foot showed only soft-tissue swelling. Magnetic resonance imaging with contrast, done to determine the extent of the lesions, revealed multiple dumbbell-shaped lesions with homogeneous enhancement (Figure 2). Histopathologic study of a biopsy specimen of the lesions showed tumor cells in the dermis. The cells were long, with elongated nuclei with pointed ends, arranged in long and short fascicles—an appearance characteristic of neurofibroma. Areas of hypocellularity and hypercellularity were seen, and on S100 protein immunostaining, the tumor cells showed strong nuclear and cytoplasmic positivity (Figure 3).

The histologic evaluation confirmed neurofibroma. The specific diagnosis of sporadic solitary neurofibroma was made based on the onset of the lesions, the number of lesions (one in this patient), and the absence of features suggestive of neurofibromatosis.

SPORADIC SOLITARY NEUROFIBROMA

Neurofibroma is a common tumor of the peripheral nerve sheath and, when present with features such as café-au-lait spots, axillary freckling, and characteristic bone changes, it is pathognomic of neurofibromatosis type 1.¹ But solitary neurofibromas can occur sporadically in the absence of other features of neurofibromatosis.

Sporadic solitary neurofibroma arises from small nerves, is benign in nature, and carries a lower rate of malignant transformation than its counterpart that occurs in the setting of neurofibromatosis.² Though sporadic solitary neurofibroma can occur in any part of the body, it is commonly seen on the head and neck, and occasionally on the presacral and parasacral space, thigh, intrascrotal area,³ the ankle and foot,^4,5 and the subungual region.⁶ A series of 397 peripheral neural sheath tumors examined over 30 years showed 55 sporadic solitary neurofibromas occurring in the brachial plexus region, 45 in the upper extremities, 10 in the pelvic plexus, and 31 in the lower extremities.⁷

Management of sporadic solitary neurofibroma depends on the patient’s discomfort. For asymptomatic lesions, serial observation is all that is required. Complete surgical excision including the parent nerve is the treatment for large lesions. More research is needed to define the potential role of drugs such as pirfenidone and tipifarnib.

THE DIFFERENTIAL DIAGNOSIS

Sporadic solitary neurofibroma can masquerade as pure neuritic Hansen disease (leprosy), phaeohyphomycosis, and palisaded neutrophilic granulomatous dermatitis. The absence of neural symptoms and no evidence of trophic changes exclude pure neuritic Hansen disease. Phaeohyphomycosis clinically presents as a single cyst that may evolve into pigmented plaques,⁸ and the diagnosis relies on the presence of fungus in tissue. The absence of cystic changes clinically and fungi histopathologically in this patient did not favor phaeohyphomycosis. Palisaded neutrophilic granulomatous dermatitis is characterized clinically by cordlike skin lesions (the “rope sign”) and is accompanied by extracutaneous, mostly articular features. Histopathologically, it shows intense neutrophilic infiltrate and interstitial histiocytic infiltrate along with collagen degeneration. The absence of extracutaneous and classical histologic features negated this possibility in this patient.

Though sporotrichosis and cutaneous atypical mycobacterial infections may present in linear fashion following the course of the lymphatic vessels, the absence of epidermal changes after a disease course of 15 years and the absence of granulomatous infiltrate in histopathology excluded these possibilities in this patient.

The patient was referred to a plastic surgeon, and the lesions were successfully resected. She did not return for additional review after that.

A 34-year-old woman sought consultation at our clinic for an asymptomatic swelling on her right foot that had been growing very slowly over the last 15 years. She said she had presented to other healthcare facilities, but no diagnosis had been made and no treatment had been offered.

Examination revealed a linear swelling extending from the lower third to the mid-dorsal surface of the right foot (Figure 1). Palpation revealed multiple, closely set nodules arranged in a linear fashion. This finding along with the history raised the suspicion of neurofibroma and other conditions in the differential diagnosis, eg, pure neuritic Hansen disease, phaeohyphomycosis, and palisaded neutrophilic granulomatous dermatitis. The rest of the mucocutaneous examination results were normal. No café-au-lait spots, axillary freckling, or other swelling suggestive of neurofibroma was seen. She had no family history of mucocutaneous disease or other systemic disorder.

Because of the suspicion of neurofibromatosis, slit-lamp examination of the eyes was done to rule out Lisch nodules, a common feature of neurofibromatosis; the results were normal. Plain radiography of the right foot showed only soft-tissue swelling. Magnetic resonance imaging with contrast, done to determine the extent of the lesions, revealed multiple dumbbell-shaped lesions with homogeneous enhancement (Figure 2). Histopathologic study of a biopsy specimen of the lesions showed tumor cells in the dermis. The cells were long, with elongated nuclei with pointed ends, arranged in long and short fascicles—an appearance characteristic of neurofibroma. Areas of hypocellularity and hypercellularity were seen, and on S100 protein immunostaining, the tumor cells showed strong nuclear and cytoplasmic positivity (Figure 3).

The histologic evaluation confirmed neurofibroma. The specific diagnosis of sporadic solitary neurofibroma was made based on the onset of the lesions, the number of lesions (one in this patient), and the absence of features suggestive of neurofibromatosis.

SPORADIC SOLITARY NEUROFIBROMA

Neurofibroma is a common tumor of the peripheral nerve sheath and, when present with features such as café-au-lait spots, axillary freckling, and characteristic bone changes, it is pathognomic of neurofibromatosis type 1.¹ But solitary neurofibromas can occur sporadically in the absence of other features of neurofibromatosis.

Sporadic solitary neurofibroma arises from small nerves, is benign in nature, and carries a lower rate of malignant transformation than its counterpart that occurs in the setting of neurofibromatosis.² Though sporadic solitary neurofibroma can occur in any part of the body, it is commonly seen on the head and neck, and occasionally on the presacral and parasacral space, thigh, intrascrotal area,³ the ankle and foot,^4,5 and the subungual region.⁶ A series of 397 peripheral neural sheath tumors examined over 30 years showed 55 sporadic solitary neurofibromas occurring in the brachial plexus region, 45 in the upper extremities, 10 in the pelvic plexus, and 31 in the lower extremities.⁷

Management of sporadic solitary neurofibroma depends on the patient’s discomfort. For asymptomatic lesions, serial observation is all that is required. Complete surgical excision including the parent nerve is the treatment for large lesions. More research is needed to define the potential role of drugs such as pirfenidone and tipifarnib.

THE DIFFERENTIAL DIAGNOSIS

Sporadic solitary neurofibroma can masquerade as pure neuritic Hansen disease (leprosy), phaeohyphomycosis, and palisaded neutrophilic granulomatous dermatitis. The absence of neural symptoms and no evidence of trophic changes exclude pure neuritic Hansen disease. Phaeohyphomycosis clinically presents as a single cyst that may evolve into pigmented plaques,⁸ and the diagnosis relies on the presence of fungus in tissue. The absence of cystic changes clinically and fungi histopathologically in this patient did not favor phaeohyphomycosis. Palisaded neutrophilic granulomatous dermatitis is characterized clinically by cordlike skin lesions (the “rope sign”) and is accompanied by extracutaneous, mostly articular features. Histopathologically, it shows intense neutrophilic infiltrate and interstitial histiocytic infiltrate along with collagen degeneration. The absence of extracutaneous and classical histologic features negated this possibility in this patient.

Though sporotrichosis and cutaneous atypical mycobacterial infections may present in linear fashion following the course of the lymphatic vessels, the absence of epidermal changes after a disease course of 15 years and the absence of granulomatous infiltrate in histopathology excluded these possibilities in this patient.

The patient was referred to a plastic surgeon, and the lesions were successfully resected. She did not return for additional review after that.

PARIS – Advances in CT scanner technology make cardiac CT a viable alternative to transesophageal echocardiography for preprocedural detection of left atrial appendage thrombus in candidates for transcatheter aortic valve replacement, Dr. Paul D. Williams said at the annual congress of the European Association of Percutaneous Cardiovascular Interventions.

This strategy helps simplify transcatheter aortic valve replacement (TAVR). That has become a major goal for the field now that TAVR’s safety and effectiveness have been established, said Dr. Williams of James Cook University Hospital in Middlesbrough, England.

“With the use of CT as the preferred method for annular sizing prior to the procedure and the increasing use of conscious sedation, transesophageal echo can be avoided altogether in many patients. And identification of left atrial appendage thrombus [LAAT] on CT may lead to changes in management, including optimization of oral anticoagulation, the use of an embolic protection device, and possibly obtaining consent from patients for a higher risk of procedural stroke,” he added.

Transesophageal echocardiography (TEE) has long been considered the gold standard method for detecting LAAT. But it has several disadvantages: It’s invasive, requires heavy sedation, and poses a small risk of serious complications.

Dr. Williams presented a single-center prospective study involving 198 consecutive patients who underwent dual source CT scanning with retrospective gated acquisition and flash angiographic acquisition during their pre-TAVR workup. The study showed that atrial fibrillation (AF) is very common in TAVR candidates, that LAAT is far more common in the TAVR population with AF than in the general AF population, and that while TAVR can still be performed in patients with LAAT, the periprocedural stroke risk appears to be higher.

Of the 198 TAVR candidates, 32% had AF. Two independent cardiologists with CT expertise rated 11.1% of TAVR candidates as having definite LAAT on the basis of a filling defect in both phases of imaging. Another 83.8% were deemed to definitely not have LAAT, while in 5.1% of cases the CT image quality wasn’t sufficient to render a judgment.

“The literature would suggest only about 5% of patients in the general AF population have LAAT. The rate is much higher in a TAVR population,” the cardiologist observed.

As expected, AF was a strong predictor of LAAT being found on CT, with a 32% prevalence in the AF subgroup, compared with just 1.6% in patients without AF.

Ninety-eight patients with a diagnostic CT also had a TEE. Six of the eight with LAAT on CT also showed LAAT on TEE. Two patients had LAAT on CT but not TEE. Thus, CT had 100% sensitivity, 97.8% specificity, a 75% positive predictive value, and a 100% negative predictive value, Dr. Williams continued.

Of the 198 patients evaluated by CT, 124 actually underwent TAVR. AF was present in 34% of these patients, whose mean CHA₂DS₂-VASc score was 3.7. CT showed that 8.1% of the patients who had TAVR had definite LAAT, and 84.7% definitely did not.

Six of the 124 patients (4.8%) had a stroke during their hospital stay for TAVR. Two of the six had LAAT on their preprocedural CT; both were being anticoagulated with warfarin at the time. The other four patients with periprocedural stroke didn’t have AF, were negative for LAAT on preprocedural CT, and weren’t being anticoagulated.

“Importantly, in the overall TAVR cohort, 8 of the 10 patients with LAAT on CT did not have a clinically evident periprocedural stroke,” Dr. Williams noted.

Session chair Dr. Rajendra Makkar, director of interventional cardiology at the Cedars-Sinai Heart Institute in Los Angeles, commented, “Your study has very, very important implications for how we actually change the management of some of our patients. You’ve shown LAAT is much more important in TAVR patients than I’d thought. A stroke risk of 20% with LAAT versus 3.8% in patients without LAAT is an impressive difference.”

His take away lesson from the study, Dr. Makkar added, is that if a patient has a preprocedural CT scan that’s negative for LAAT, there’s no need to do a TEE. If CT is positive or nondefinitive, it makes sense to review the patient’s anticoagulation regimen, then bring the patient back a few weeks later for a TEE to see if the LAAT has resolved.

Dr. Williams replied that’s exactly the practice now being followed at his hospital. If CT shows LAAT in a patient with AF who’s already on warfarin, physicians will consider aiming for a higher target INR [international normalized ratio], or they’ll switch to one of the novel oral anticoagulants if there’s a warfarin compliance issue. Then they’ll bring the patient back for a TEE.

“If the TEE is positive for LAAT we will still offer them TAVR, with the use of an embolic protection device if the anatomy is suitable, but we will tell them that potentially they may be at higher risk of stroke,” Dr. Williams said.

He reported having no financial conflicts of interest regarding this study.

[email protected]

PARIS – Advances in CT scanner technology make cardiac CT a viable alternative to transesophageal echocardiography for preprocedural detection of left atrial appendage thrombus in candidates for transcatheter aortic valve replacement, Dr. Paul D. Williams said at the annual congress of the European Association of Percutaneous Cardiovascular Interventions.

This strategy helps simplify transcatheter aortic valve replacement (TAVR). That has become a major goal for the field now that TAVR’s safety and effectiveness have been established, said Dr. Williams of James Cook University Hospital in Middlesbrough, England.

“With the use of CT as the preferred method for annular sizing prior to the procedure and the increasing use of conscious sedation, transesophageal echo can be avoided altogether in many patients. And identification of left atrial appendage thrombus [LAAT] on CT may lead to changes in management, including optimization of oral anticoagulation, the use of an embolic protection device, and possibly obtaining consent from patients for a higher risk of procedural stroke,” he added.

Transesophageal echocardiography (TEE) has long been considered the gold standard method for detecting LAAT. But it has several disadvantages: It’s invasive, requires heavy sedation, and poses a small risk of serious complications.

Dr. Williams presented a single-center prospective study involving 198 consecutive patients who underwent dual source CT scanning with retrospective gated acquisition and flash angiographic acquisition during their pre-TAVR workup. The study showed that atrial fibrillation (AF) is very common in TAVR candidates, that LAAT is far more common in the TAVR population with AF than in the general AF population, and that while TAVR can still be performed in patients with LAAT, the periprocedural stroke risk appears to be higher.

Of the 198 TAVR candidates, 32% had AF. Two independent cardiologists with CT expertise rated 11.1% of TAVR candidates as having definite LAAT on the basis of a filling defect in both phases of imaging. Another 83.8% were deemed to definitely not have LAAT, while in 5.1% of cases the CT image quality wasn’t sufficient to render a judgment.

“The literature would suggest only about 5% of patients in the general AF population have LAAT. The rate is much higher in a TAVR population,” the cardiologist observed.

As expected, AF was a strong predictor of LAAT being found on CT, with a 32% prevalence in the AF subgroup, compared with just 1.6% in patients without AF.

Ninety-eight patients with a diagnostic CT also had a TEE. Six of the eight with LAAT on CT also showed LAAT on TEE. Two patients had LAAT on CT but not TEE. Thus, CT had 100% sensitivity, 97.8% specificity, a 75% positive predictive value, and a 100% negative predictive value, Dr. Williams continued.

Of the 198 patients evaluated by CT, 124 actually underwent TAVR. AF was present in 34% of these patients, whose mean CHA₂DS₂-VASc score was 3.7. CT showed that 8.1% of the patients who had TAVR had definite LAAT, and 84.7% definitely did not.

Six of the 124 patients (4.8%) had a stroke during their hospital stay for TAVR. Two of the six had LAAT on their preprocedural CT; both were being anticoagulated with warfarin at the time. The other four patients with periprocedural stroke didn’t have AF, were negative for LAAT on preprocedural CT, and weren’t being anticoagulated.

“Importantly, in the overall TAVR cohort, 8 of the 10 patients with LAAT on CT did not have a clinically evident periprocedural stroke,” Dr. Williams noted.

Session chair Dr. Rajendra Makkar, director of interventional cardiology at the Cedars-Sinai Heart Institute in Los Angeles, commented, “Your study has very, very important implications for how we actually change the management of some of our patients. You’ve shown LAAT is much more important in TAVR patients than I’d thought. A stroke risk of 20% with LAAT versus 3.8% in patients without LAAT is an impressive difference.”

His take away lesson from the study, Dr. Makkar added, is that if a patient has a preprocedural CT scan that’s negative for LAAT, there’s no need to do a TEE. If CT is positive or nondefinitive, it makes sense to review the patient’s anticoagulation regimen, then bring the patient back a few weeks later for a TEE to see if the LAAT has resolved.

Dr. Williams replied that’s exactly the practice now being followed at his hospital. If CT shows LAAT in a patient with AF who’s already on warfarin, physicians will consider aiming for a higher target INR [international normalized ratio], or they’ll switch to one of the novel oral anticoagulants if there’s a warfarin compliance issue. Then they’ll bring the patient back for a TEE.

“If the TEE is positive for LAAT we will still offer them TAVR, with the use of an embolic protection device if the anatomy is suitable, but we will tell them that potentially they may be at higher risk of stroke,” Dr. Williams said.

He reported having no financial conflicts of interest regarding this study.

[email protected]

PARIS – Advances in CT scanner technology make cardiac CT a viable alternative to transesophageal echocardiography for preprocedural detection of left atrial appendage thrombus in candidates for transcatheter aortic valve replacement, Dr. Paul D. Williams said at the annual congress of the European Association of Percutaneous Cardiovascular Interventions.

This strategy helps simplify transcatheter aortic valve replacement (TAVR). That has become a major goal for the field now that TAVR’s safety and effectiveness have been established, said Dr. Williams of James Cook University Hospital in Middlesbrough, England.

“With the use of CT as the preferred method for annular sizing prior to the procedure and the increasing use of conscious sedation, transesophageal echo can be avoided altogether in many patients. And identification of left atrial appendage thrombus [LAAT] on CT may lead to changes in management, including optimization of oral anticoagulation, the use of an embolic protection device, and possibly obtaining consent from patients for a higher risk of procedural stroke,” he added.

Transesophageal echocardiography (TEE) has long been considered the gold standard method for detecting LAAT. But it has several disadvantages: It’s invasive, requires heavy sedation, and poses a small risk of serious complications.

Dr. Williams presented a single-center prospective study involving 198 consecutive patients who underwent dual source CT scanning with retrospective gated acquisition and flash angiographic acquisition during their pre-TAVR workup. The study showed that atrial fibrillation (AF) is very common in TAVR candidates, that LAAT is far more common in the TAVR population with AF than in the general AF population, and that while TAVR can still be performed in patients with LAAT, the periprocedural stroke risk appears to be higher.

Of the 198 TAVR candidates, 32% had AF. Two independent cardiologists with CT expertise rated 11.1% of TAVR candidates as having definite LAAT on the basis of a filling defect in both phases of imaging. Another 83.8% were deemed to definitely not have LAAT, while in 5.1% of cases the CT image quality wasn’t sufficient to render a judgment.

“The literature would suggest only about 5% of patients in the general AF population have LAAT. The rate is much higher in a TAVR population,” the cardiologist observed.

As expected, AF was a strong predictor of LAAT being found on CT, with a 32% prevalence in the AF subgroup, compared with just 1.6% in patients without AF.

Ninety-eight patients with a diagnostic CT also had a TEE. Six of the eight with LAAT on CT also showed LAAT on TEE. Two patients had LAAT on CT but not TEE. Thus, CT had 100% sensitivity, 97.8% specificity, a 75% positive predictive value, and a 100% negative predictive value, Dr. Williams continued.

Of the 198 patients evaluated by CT, 124 actually underwent TAVR. AF was present in 34% of these patients, whose mean CHA₂DS₂-VASc score was 3.7. CT showed that 8.1% of the patients who had TAVR had definite LAAT, and 84.7% definitely did not.

Six of the 124 patients (4.8%) had a stroke during their hospital stay for TAVR. Two of the six had LAAT on their preprocedural CT; both were being anticoagulated with warfarin at the time. The other four patients with periprocedural stroke didn’t have AF, were negative for LAAT on preprocedural CT, and weren’t being anticoagulated.

“Importantly, in the overall TAVR cohort, 8 of the 10 patients with LAAT on CT did not have a clinically evident periprocedural stroke,” Dr. Williams noted.

Session chair Dr. Rajendra Makkar, director of interventional cardiology at the Cedars-Sinai Heart Institute in Los Angeles, commented, “Your study has very, very important implications for how we actually change the management of some of our patients. You’ve shown LAAT is much more important in TAVR patients than I’d thought. A stroke risk of 20% with LAAT versus 3.8% in patients without LAAT is an impressive difference.”

His take away lesson from the study, Dr. Makkar added, is that if a patient has a preprocedural CT scan that’s negative for LAAT, there’s no need to do a TEE. If CT is positive or nondefinitive, it makes sense to review the patient’s anticoagulation regimen, then bring the patient back a few weeks later for a TEE to see if the LAAT has resolved.

Dr. Williams replied that’s exactly the practice now being followed at his hospital. If CT shows LAAT in a patient with AF who’s already on warfarin, physicians will consider aiming for a higher target INR [international normalized ratio], or they’ll switch to one of the novel oral anticoagulants if there’s a warfarin compliance issue. Then they’ll bring the patient back for a TEE.

“If the TEE is positive for LAAT we will still offer them TAVR, with the use of an embolic protection device if the anatomy is suitable, but we will tell them that potentially they may be at higher risk of stroke,” Dr. Williams said.

He reported having no financial conflicts of interest regarding this study.

[email protected]

The extended focused assessment with sonography for trauma (EFAST) examination provides rapid point-of-care (POC) evaluation of patients with thoracoabdominal trauma. This article offers essential clinical pearls to ensure an accurate and thorough examination, including tips on proper gain adjustment, correct probe fanning, shadow removal, visualization of the paracolic gutters, seeking the “spine sign” to determine effusion, and assessing effusion or consolidation of the lung.

Turning Down the Gain

Too much gain (signal amplification) will wash out the ultrasound image, making it challenging to detect small quantities of free fluid. This is especially true in the pelvic windows. Sound waves travel easily through the fluid-filled bladder and a posterior acoustic enhancement artifact will make the far field of the image appear too bright, obscuring small quantities of fluid (Figure 1). To correct this issue without changing the gain of the entire image, the far-field gain can be adjusted on most ultrasound devices by using the time-gain compensation bar or a far field gain knob. 

Fanning Is Key

With the probe placed at a single location on the skin, one can dramatically change the structures visualized by fanning (tilting the probe). The image visualized on the ultrasound screen represents only a single slice of the anatomy—one that is about the thickness of a credit card. A single image therefore can only show structures that are within that thin beam of the probe. Just as one would not make a clinical decision based on a single-slice computed tomography (CT) scan image, the same is true of ultrasound. By fanning the probe toward the anterior and posterior abdomen, the clinician will catch smaller quantities of free fluid within each quadrant. A good rule of thumb is to scan through the entire organ of interest from edge-to-edge (eg, the entire bladder when imaging the pelvic window; the entire kidney in the right upper quadrant (RUQ) window; the entire spleen in the left upper quadrant [LUQ]).

Get Rid of the Rib Shadows

The RUQ and LUQ windows can be difficult to visualize when the view is obscured by rib shadows. To minimize/remove rib shadows, some clinicians prefer to use the phased array probe, which has a small footprint that fits easily in the intercostal space. Clinicians who prefer using the curvilinear probe should place the probe at an oblique angle (Figure 2); this probe will fit between the ribs and remove shadowing artifacts.

Remember the Paracolic

In some patients, the paracolic gutters are the most dependent portion of the abdomen and the first place where free fluid collects. When evaluating the RUQ, the clinician should first identify Morrison’s pouch, which is the interface between the liver and the kidney. After this pouch has been identified, the clinician should slide the probe toward the patient’s feet, paying close attention to the area around the inferior tip of the liver, and continue sliding the probe down to the inferior tip of the kidney, looking for fluid layering above the kidney or the psoas muscle (Figure 3). The same holds true for the LUQ technique. Once one has looked between the spleen and the diaphragm for free fluid, the probe should be moved down to the flank to evaluate the inferior tip of the spleen and the region anterior to the kidney. 

The Left Upper Quadrant—Do Not Let the Stomach Fake You Out

A fluid-filled stomach can be a fake-out for free fluid appearing black on ultrasound (Figure 4). Remember, free fluid in the LUQ window will typically appear between the spleen and the diaphragm or at either pole of the spleen, so the clinician should pay particular attention to these areas. When evaluating the LUQ, a good rule of thumb is to place one’s hand on the patient’s bed while holding the probe; this will ensure that the scan is sufficiently posterior. The probe may also need to be fanned toward the bed to identify the kidneys in the retroperitoneum. 

Look in the Chest and Remember the Spine Sign

Rapidly identifying a hemothorax can be a critical finding on the EFAST examination. Therefore, it is important to remember that air in the lungs scatters sound waves, so one does not normally visualize distinct structures that are deep to the pleural line. This is why the spine is not typically visible in the chest above the level of the diaphragm. When pathology is present, however, the sound waves are not blocked by air-filled lungs and one can see the “spine sign,” which suggests the presence of either effusion or consolidation of the lung (Figure 5).

Tough Cardiac Window? Try These Tips

A subxiphoid window is typically used to assess for pericardial effusion. To obtain this view, the clinician usually needs to increase the depth setting by a few centimeters (typically to around 18 cm). When the patient is able to do so, he or she may assist in the examination by bending his or her knees or taking a deep breath to help bring the heart into view. Despite these efforts, however, in some patients, it is technically impossible to obtain a subxiphoid view. In such cases, switching to an alternate view, such as the parasternal window, may be successful in visualizing the subxiphoid region.

Summary

Proper gain adjustment, thorough scanning of the thoracoabdominal region, and knowledge of common artifacts and signs are essential to ensuring an accurate and thorough POC EFAST examination.

The extended focused assessment with sonography for trauma (EFAST) examination provides rapid point-of-care (POC) evaluation of patients with thoracoabdominal trauma. This article offers essential clinical pearls to ensure an accurate and thorough examination, including tips on proper gain adjustment, correct probe fanning, shadow removal, visualization of the paracolic gutters, seeking the “spine sign” to determine effusion, and assessing effusion or consolidation of the lung.

Turning Down the Gain

Too much gain (signal amplification) will wash out the ultrasound image, making it challenging to detect small quantities of free fluid. This is especially true in the pelvic windows. Sound waves travel easily through the fluid-filled bladder and a posterior acoustic enhancement artifact will make the far field of the image appear too bright, obscuring small quantities of fluid (Figure 1). To correct this issue without changing the gain of the entire image, the far-field gain can be adjusted on most ultrasound devices by using the time-gain compensation bar or a far field gain knob. 

Fanning Is Key

With the probe placed at a single location on the skin, one can dramatically change the structures visualized by fanning (tilting the probe). The image visualized on the ultrasound screen represents only a single slice of the anatomy—one that is about the thickness of a credit card. A single image therefore can only show structures that are within that thin beam of the probe. Just as one would not make a clinical decision based on a single-slice computed tomography (CT) scan image, the same is true of ultrasound. By fanning the probe toward the anterior and posterior abdomen, the clinician will catch smaller quantities of free fluid within each quadrant. A good rule of thumb is to scan through the entire organ of interest from edge-to-edge (eg, the entire bladder when imaging the pelvic window; the entire kidney in the right upper quadrant (RUQ) window; the entire spleen in the left upper quadrant [LUQ]).

Get Rid of the Rib Shadows

The RUQ and LUQ windows can be difficult to visualize when the view is obscured by rib shadows. To minimize/remove rib shadows, some clinicians prefer to use the phased array probe, which has a small footprint that fits easily in the intercostal space. Clinicians who prefer using the curvilinear probe should place the probe at an oblique angle (Figure 2); this probe will fit between the ribs and remove shadowing artifacts.

Remember the Paracolic

In some patients, the paracolic gutters are the most dependent portion of the abdomen and the first place where free fluid collects. When evaluating the RUQ, the clinician should first identify Morrison’s pouch, which is the interface between the liver and the kidney. After this pouch has been identified, the clinician should slide the probe toward the patient’s feet, paying close attention to the area around the inferior tip of the liver, and continue sliding the probe down to the inferior tip of the kidney, looking for fluid layering above the kidney or the psoas muscle (Figure 3). The same holds true for the LUQ technique. Once one has looked between the spleen and the diaphragm for free fluid, the probe should be moved down to the flank to evaluate the inferior tip of the spleen and the region anterior to the kidney. 

The Left Upper Quadrant—Do Not Let the Stomach Fake You Out

A fluid-filled stomach can be a fake-out for free fluid appearing black on ultrasound (Figure 4). Remember, free fluid in the LUQ window will typically appear between the spleen and the diaphragm or at either pole of the spleen, so the clinician should pay particular attention to these areas. When evaluating the LUQ, a good rule of thumb is to place one’s hand on the patient’s bed while holding the probe; this will ensure that the scan is sufficiently posterior. The probe may also need to be fanned toward the bed to identify the kidneys in the retroperitoneum. 

Look in the Chest and Remember the Spine Sign

Rapidly identifying a hemothorax can be a critical finding on the EFAST examination. Therefore, it is important to remember that air in the lungs scatters sound waves, so one does not normally visualize distinct structures that are deep to the pleural line. This is why the spine is not typically visible in the chest above the level of the diaphragm. When pathology is present, however, the sound waves are not blocked by air-filled lungs and one can see the “spine sign,” which suggests the presence of either effusion or consolidation of the lung (Figure 5).

Tough Cardiac Window? Try These Tips

A subxiphoid window is typically used to assess for pericardial effusion. To obtain this view, the clinician usually needs to increase the depth setting by a few centimeters (typically to around 18 cm). When the patient is able to do so, he or she may assist in the examination by bending his or her knees or taking a deep breath to help bring the heart into view. Despite these efforts, however, in some patients, it is technically impossible to obtain a subxiphoid view. In such cases, switching to an alternate view, such as the parasternal window, may be successful in visualizing the subxiphoid region.

Summary

Proper gain adjustment, thorough scanning of the thoracoabdominal region, and knowledge of common artifacts and signs are essential to ensuring an accurate and thorough POC EFAST examination.

The extended focused assessment with sonography for trauma (EFAST) examination provides rapid point-of-care (POC) evaluation of patients with thoracoabdominal trauma. This article offers essential clinical pearls to ensure an accurate and thorough examination, including tips on proper gain adjustment, correct probe fanning, shadow removal, visualization of the paracolic gutters, seeking the “spine sign” to determine effusion, and assessing effusion or consolidation of the lung.

Turning Down the Gain

Too much gain (signal amplification) will wash out the ultrasound image, making it challenging to detect small quantities of free fluid. This is especially true in the pelvic windows. Sound waves travel easily through the fluid-filled bladder and a posterior acoustic enhancement artifact will make the far field of the image appear too bright, obscuring small quantities of fluid (Figure 1). To correct this issue without changing the gain of the entire image, the far-field gain can be adjusted on most ultrasound devices by using the time-gain compensation bar or a far field gain knob. 

Fanning Is Key

With the probe placed at a single location on the skin, one can dramatically change the structures visualized by fanning (tilting the probe). The image visualized on the ultrasound screen represents only a single slice of the anatomy—one that is about the thickness of a credit card. A single image therefore can only show structures that are within that thin beam of the probe. Just as one would not make a clinical decision based on a single-slice computed tomography (CT) scan image, the same is true of ultrasound. By fanning the probe toward the anterior and posterior abdomen, the clinician will catch smaller quantities of free fluid within each quadrant. A good rule of thumb is to scan through the entire organ of interest from edge-to-edge (eg, the entire bladder when imaging the pelvic window; the entire kidney in the right upper quadrant (RUQ) window; the entire spleen in the left upper quadrant [LUQ]).

Get Rid of the Rib Shadows

The RUQ and LUQ windows can be difficult to visualize when the view is obscured by rib shadows. To minimize/remove rib shadows, some clinicians prefer to use the phased array probe, which has a small footprint that fits easily in the intercostal space. Clinicians who prefer using the curvilinear probe should place the probe at an oblique angle (Figure 2); this probe will fit between the ribs and remove shadowing artifacts.

Remember the Paracolic

In some patients, the paracolic gutters are the most dependent portion of the abdomen and the first place where free fluid collects. When evaluating the RUQ, the clinician should first identify Morrison’s pouch, which is the interface between the liver and the kidney. After this pouch has been identified, the clinician should slide the probe toward the patient’s feet, paying close attention to the area around the inferior tip of the liver, and continue sliding the probe down to the inferior tip of the kidney, looking for fluid layering above the kidney or the psoas muscle (Figure 3). The same holds true for the LUQ technique. Once one has looked between the spleen and the diaphragm for free fluid, the probe should be moved down to the flank to evaluate the inferior tip of the spleen and the region anterior to the kidney. 

The Left Upper Quadrant—Do Not Let the Stomach Fake You Out

A fluid-filled stomach can be a fake-out for free fluid appearing black on ultrasound (Figure 4). Remember, free fluid in the LUQ window will typically appear between the spleen and the diaphragm or at either pole of the spleen, so the clinician should pay particular attention to these areas. When evaluating the LUQ, a good rule of thumb is to place one’s hand on the patient’s bed while holding the probe; this will ensure that the scan is sufficiently posterior. The probe may also need to be fanned toward the bed to identify the kidneys in the retroperitoneum. 

Look in the Chest and Remember the Spine Sign

Rapidly identifying a hemothorax can be a critical finding on the EFAST examination. Therefore, it is important to remember that air in the lungs scatters sound waves, so one does not normally visualize distinct structures that are deep to the pleural line. This is why the spine is not typically visible in the chest above the level of the diaphragm. When pathology is present, however, the sound waves are not blocked by air-filled lungs and one can see the “spine sign,” which suggests the presence of either effusion or consolidation of the lung (Figure 5).

Tough Cardiac Window? Try These Tips

A subxiphoid window is typically used to assess for pericardial effusion. To obtain this view, the clinician usually needs to increase the depth setting by a few centimeters (typically to around 18 cm). When the patient is able to do so, he or she may assist in the examination by bending his or her knees or taking a deep breath to help bring the heart into view. Despite these efforts, however, in some patients, it is technically impossible to obtain a subxiphoid view. In such cases, switching to an alternate view, such as the parasternal window, may be successful in visualizing the subxiphoid region.

Summary

Proper gain adjustment, thorough scanning of the thoracoabdominal region, and knowledge of common artifacts and signs are essential to ensuring an accurate and thorough POC EFAST examination.

The musculoskeletal (MSK) ultrasound evaluation of the shoulder provides a cost- and time-efficient imaging modality with similar diagnostic power as magnetic resonance imaging (MRI).^1,2 Its portable point-of-care applications can be used in the office, in the operating room, and in sideline athletic event coverage, as we discussed in Part 1 of this series.³

MSK ultrasound may seem difficult and daunting, and many articles have quoted steep learning curves.^4,5 However, in our experience in teaching many ultrasound courses, this modality can be learned quite quickly with the proper instruction. Physicians are already familiar with anatomy and usually have had some exposure to MRI.⁴ Taking courses in MSK ultrasound or simply learning the basic concepts of ultrasound and then learning the machine controls is usually a good start.^5-8 Practice scanning normal individuals, comparing the images from an MRI to learn how to reproduce the same planes and images. This will allow the user to become familiar with normal anatomy and how to see the images on the ultrasound screen.^5-8 Vollman and colleagues⁹ showed that in trainees, combining MRI images with sonograms enhances the ability to correctly identify MSK ultrasound anatomy from 40.9% to 72.5%, when compared with learning from ultrasound images alone.

There are currently no certifications necessary to perform ultrasound scans or bill for them; however, some insurance carriers may require demonstrating relevant, documented training for reimbursement.³ Various organizations are trying to develop certifications and regulations for ultrasound to standardize the use of this modality. In the United States, the American Institute of Ultrasound in Medicine (AIUM) and the American Registry for Diagnostic Medical Sonography (ARDMS) provide guidelines and particular MSK ultrasound certifications.^10,11

Basic Ultrasound Principles

The ultrasound machine creates electrical impulses that are turned into sound waves by piezoelectric crystals at the probe’s footprint. These sound waves bounce off tissues and return to the probe, where they are converted electronically to an image on the monitor. Depending on the echogenicity of the scanned tissue, the ultrasound beam will either reflect or be absorbed at different rates. This variance is transmitted on the monitor as a grayscale image. When ultrasound waves are highly reflective, like in bone or fat, they are characterized as hyperechoic. The opposite occurs when ultrasound waves are absorbed like in the fluid of a cystic cavity or joint effusion, and the image appears black. This is described as anechoic.¹² Intermediate tissues such as tendons that are less reflective are seen as hypoechoic and appear gray. When a tissue has a similar echogenicity to its surrounding tissues, it is called isoechoic.¹²

The transducer is the scanning component of the ultrasound machine. Transducers come in 2 shapes: linear and curvilinear. The linear probe creates a straight image that is equal to the size of the transducer footprint. The curvilinear probe creates a wider, wedge-shaped panoramic image.

Linear probes are of higher frequency and generate higher resolution images of shallower structures, while curvilinear probes have greater depth penetration but generate lower resolution images. A high frequency of 10 to 15 MHz is preferred for anatomy between 2 cm to 4 cm depth.¹³ Midrange frequency of 5 to 10 MHz is preferred at 5 cm to 6 cm depth, and low-frequency 2 to 5 MHz probes are preferred for anatomical structures >6 cm depth.¹³

Anisotropy is the property of being directionally dependent, as opposed to isotropy, which implies identical properties in all directions. This anisotropic effect is dependent on the angle of the insonating beam. The maximum return echo occurs when the ultrasound beam is perpendicular to the tendon. Decreasing the insonating angle on a normal tendon will cause it to change from brightly hyperechoic (the actual echo from tightly bound tendon fibers) to darkly hypoechoic. If the angle is then increased, the tendon will again appear hyperechoic. If the artifact causes a normal tendon to appear hypoechoic, it may falsely lead to a diagnosis of tendinosis or tear.

Posterior acoustic shadowing is present when a hyperechoic structure reflects the ultrasound beam so much that it creates a dark shadow underneath it.^12,14 This phenomenon is possible since the ultrasound beam cannot penetrate the hyperechoic structure and reflects off its inferior tissues. Reverberation is when the beam is repeated back and forth between 2 parallel highly reflective surfaces. The initial reflection will be displayed correctly, while the subsequent ultrasound waves will be delayed and appear at a farther distance from the transducer.^12,14

The point where the beam is at its narrowest point generates the section of the image that is best visualized.¹⁵ This is called the focal zone, and it can be adjusted to highlight the desired area of evaluation. Gain controls adjust the amount of black, gray, and white on the monitor and can be adjusted to focus the desired image.¹³ Depth settings are fundamental in finding the desired targets. It is recommended to start with a higher depth setting to get an overview and progressively decrease the depth to key in on the desired anatomy.¹³ Color Doppler can be used to view movement within structures and to identify vessels, synovitis, and neovascularization in tendinopathy.¹³

Ultrasound of the Shoulder

Patients should be seated, if possible, on a rotating seat. The examiner’s shoulder should be higher than the patient’s shoulder.¹⁶ The user holds the ultrasound probe between the thumb and index fingers while resting the hypothenar eminence on the patient to serve as a fulcrum and steadying force. The examination should take 5 to 15 minutes, depending on the examiner’s expertise and the amount of anatomy being scanned.

Examining the body requires knowledge of anatomy. The examination and accuracy are determined by the technician using the probe. The probe can be angled any direction and be placed obliquely on the subject. The advantage here is that anatomy in the human body is not always planar. Muscles and tissues can run obliquely or even perpendicular to each other. When evaluating anatomy, the examiner should keep in mind what structure he or she is looking for; where it should be found; what landmarks can be used to easily locate it; what orientation it has; and what the normal anatomy should look like.

Muscle appears as a lattice with larger areas of hypoechoic muscle tissue and hyperechoic fascial perimysium layers traversing through it.¹⁷ The actual muscle tissue appears hypoechoic from the fluid or blood found within. Scarring, fibrosis, calcification, or chronic injury will change the tissue to appear denser or hyperechoic.¹⁷ Acute injury will appear hypoechoic from the inflammatory response and influx of blood. Tendon appears dense and hyperechoic with striations within the tissue, sometimes referred to as a horse’s tail.¹⁷ When torn, there will be a disassociation of the tissue with a hypoechoic region between the 2 ends. The attachment to the bone and muscle tissue should appear uniform. Hyperechoic areas within the tendon may be from calcification. Ligament appears similar to tendon but is more isoechoic and connects bone to bone. Evaluation of the entire length and the attachments to the bone are critical to evaluate for disease.

Bone appears bright hyperechoic, smooth, and flat, while hyaline cartilage is hypoechoic, smooth, and runs superiorly in a parallel pattern to its respective inferior cortical bone.¹⁷

Fibrocartilage is hyperechoic and typically triangularly shaped, such as in the glenohumeral labrum. Nerves appear fascicular and hypoechoic surrounded by hyperechoic epineurium.¹⁴

The epidermis and dermis are the most superficial structure on top of the screen, and are also hyperechoic.¹⁷

The Diagnostic Shoulder Examination

The proximal long head of the biceps tendon (LHBT) is the easiest structure in the shoulder to identify because of the anatomic structure, the bicipital groove. By keeping the arm relaxed, perpendicular to the ground, and in neutral rotation, the probe can be placed perpendicular to the arm over the proximal shoulder (Figure 1A).^16-20 By finding the groove, the biceps tendon will usually be found resting within the groove (Figure 1B). This is the short axis view and is equivalent to an MRI in the axial plane.

The long axis view of the proximal biceps tendon is found by keeping the tendon in the center of the screen/probe. The probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The user should be sure to visualize the entire tendon on the screen. If only part of the tendon is seen along only part of the screen, then the probe is oblique to the tendon. In this case, the probe area showing the tendon must be stabilized as the center or set point. The other part of the probe will then pivot until all of the tendon is seen on the screen. The MRI equivalent to the long axis of the proximal biceps tendon is the sagittal view.

Ultrasound is a dynamic evaluation. Moving the probe or moving the patient will change what and how something is imaged. The proximal biceps tendon is a good example of this concept. The bicipital groove is very deep proximally and flattens out as it travels distally to the mid-humerus. The examiner should continually adjust his or her hand/probe/patient position as well as depth/gain and other console functions to adapt to the dynamics of the scan. While keeping the bicep tendon in a short axis view, the tendon can be dynamically evaluated for subluxation by internally and externally rotating the arm.

To find the subscapularis, the arm remains in a neutral position with the hand supinated and the probe is held parallel with the ground. After finding the bicipital groove, the subscapularis tendon insertion is just medial to the groove (Figure 1B). By externally rotating the arm, the subscapularis tendon/muscle will come into a long axis view.^16-20 The MRI equivalent to the long axis view of the subscapularis is the axial view. Dynamic testing can be done by internally and externally rotating the arm to evaluate for impingement of the subscapularis tendon as it slides underneath the coracoid process. To view the subscapularis tendon in short axis, the tendon is kept in the center of the screen/probe, and the probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The MRI equivalent is the sagittal view.

Some have recommended using the modified Crass or Middleton position to evaluate the supraspinatus, where the hand is in the “back pocket”.¹⁹ However, many patients with shoulder pain have trouble with this position. By resting the ipsilateral hand on the ipsilateral hip and then dropping the elbow, the supraspinatus insertion can still be brought out from under the acromion. This does bring the insertion anterior out of the scapular plane, so an adjustment is required in probe positioning to properly see the supraspinatus short and long axis. To find the long axis, the probe is placed parallel to a plane that spans the contralateral shoulder and ipsilateral hip (Figure 2A). The fibers of the supraspinatus should be inserting directly lateral to the humeral head without any intervening space (Figure 2B). If any space exists, a partial articular supraspinatus tendon avulsion (PASTA) lesion is present, and its thickness can be directly measured. Moving more posterior will show the flattening of the tuberosity and the fibers of the infraspinatus moving away from the humeral head—the bare spot. The MRI equivalent is the coronal view.

To view the supraspinatus tendon in short axis, maintain the arm in the same position, keeping the tendon in the center of the screen/probe. The probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The probe should now be in a parallel plane between the ipsilateral shoulder and the contralateral hip. The biceps tendon in cross-section will be found anteriorly, and the articular cartilage will appear as a black layer over the bone. Dynamic testing includes placing the probe in a coronal plane between the acromion and greater tuberosity. When the patient abducts the arm while in internal rotation, the supraspinatus tendon will slide underneath the coracoacromial arch showing potential external impingement.¹⁵ The MRI equivalent is the sagittal plane.

The glenohumeral joint is best viewed posteriorly, limiting how much of the intra-articular portion of the joint can be imaged. The arm remains in a neutral position; palpate for the posterior acromion and place the probe just inferior to it, wedging up against it (Figure 3A). The glenohumeral joint will be seen by keeping the probe parallel to the ground (Figure 3B). The MRI equivalent is the axial plane. If a joint effusion exists, it can be seen in the posterior recess.¹⁵ A hyperechoic triangular region in between the humeral head and the glenoid will represent the glenoid labrum (Figure 3B). By internally and externally rotating the arm, the joint and labrum complex can be dynamically examined. From the labrum, scanning superior and medial can sometimes show the spinoglenoid notch where a paralabral cyst might be seen.¹⁵

Using the glenohumeral joint as a reference, the infraspinatus muscle is easily visualized. Maintaining the arm in neutral position with the probe over the glenohumeral joint, the infraspinatus will become apparent as it lays in long axis view superficially between the posterior deltoid and glenohumeral joint (Figure 3B).^16-20 The teres minor lies just inferiorly. The MRI equivalent is the axial plane. To view the infraspinatus and teres minor in short axis, the probe is then rotated 90° on its center axis. The infraspinatus (superiorly) and teres minor (inferiorly) muscles will be visible in short axis within the infraspinatus fossa.¹⁵ The MRI equivalent is the sagittal view.

The acromioclavicular joint is superficial and easy to image. The arm remains in a neutral position, and we can palpate the joint for easy localization. The probe is placed anteriorly in a coronal plane over the acromion and clavicle. By scanning anteriorly and posteriorly, a joint effusion referred to as a Geyser sign might be seen. The MRI equivalent is the coronal view.

Available Certifications

The AIUM certification is a voluntary peer reviewed process that acknowledges that a practice is meeting national standards and aids in improving their respective MSK ultrasound protocols. They also provide guidelines on demonstrating training and competence on performing and/or interpreting diagnostic MSK examinations (Table).¹⁰ The ARDMS certification provides an actual individual certification referred to as “Registered” in MSK ultrasound.¹¹ The physician must perform 150 diagnostic MSK ultrasound evaluations within 36 months of applying and pass a 200-question examination that is offered twice per year.¹¹ None of these certifications are mandated by the American Medical Association (AMA) or American Osteopathic Association (AOA).

Maintenance and Continuing Medical Education (CME)

The AIUM recommends that a minimum of 50 diagnostic MSK ultrasound evaluations be performed per year for skill maintenance.¹⁰ Furthermore, 10 hours of AMA PRA Category 1 Credits™ or American Osteopathic Association Category 1-A Credits specific to MSK ultrasound must be completed by physicians performing and/or interpreting these examinations every 3 years.¹⁰ ARDMS recommends a minimum of 30 MSK ultrasound-specific CMEs in preparation for their “Registered” MSK evaluation.¹

Conclusion

MSK ultrasound is a dynamic, real-time imaging modality that can improve cost efficiency and patient care. Its portability allows for its use anywhere. Learning the skill may seem daunting, but with the proper courses and education, the technology can be easily learned. By correlating a known modality like MRI, the user will easily begin to read ultrasound images. No current certification is needed to use or bill for ultrasound, but various institutions are developing criteria and testing. Two organizations, AIUM and ARDMS, provide guidelines and certifications to demonstrate competency, which may become necessary in the very near future.

The musculoskeletal (MSK) ultrasound evaluation of the shoulder provides a cost- and time-efficient imaging modality with similar diagnostic power as magnetic resonance imaging (MRI).^1,2 Its portable point-of-care applications can be used in the office, in the operating room, and in sideline athletic event coverage, as we discussed in Part 1 of this series.³

MSK ultrasound may seem difficult and daunting, and many articles have quoted steep learning curves.^4,5 However, in our experience in teaching many ultrasound courses, this modality can be learned quite quickly with the proper instruction. Physicians are already familiar with anatomy and usually have had some exposure to MRI.⁴ Taking courses in MSK ultrasound or simply learning the basic concepts of ultrasound and then learning the machine controls is usually a good start.^5-8 Practice scanning normal individuals, comparing the images from an MRI to learn how to reproduce the same planes and images. This will allow the user to become familiar with normal anatomy and how to see the images on the ultrasound screen.^5-8 Vollman and colleagues⁹ showed that in trainees, combining MRI images with sonograms enhances the ability to correctly identify MSK ultrasound anatomy from 40.9% to 72.5%, when compared with learning from ultrasound images alone.

There are currently no certifications necessary to perform ultrasound scans or bill for them; however, some insurance carriers may require demonstrating relevant, documented training for reimbursement.³ Various organizations are trying to develop certifications and regulations for ultrasound to standardize the use of this modality. In the United States, the American Institute of Ultrasound in Medicine (AIUM) and the American Registry for Diagnostic Medical Sonography (ARDMS) provide guidelines and particular MSK ultrasound certifications.^10,11

Basic Ultrasound Principles

The ultrasound machine creates electrical impulses that are turned into sound waves by piezoelectric crystals at the probe’s footprint. These sound waves bounce off tissues and return to the probe, where they are converted electronically to an image on the monitor. Depending on the echogenicity of the scanned tissue, the ultrasound beam will either reflect or be absorbed at different rates. This variance is transmitted on the monitor as a grayscale image. When ultrasound waves are highly reflective, like in bone or fat, they are characterized as hyperechoic. The opposite occurs when ultrasound waves are absorbed like in the fluid of a cystic cavity or joint effusion, and the image appears black. This is described as anechoic.¹² Intermediate tissues such as tendons that are less reflective are seen as hypoechoic and appear gray. When a tissue has a similar echogenicity to its surrounding tissues, it is called isoechoic.¹²

The transducer is the scanning component of the ultrasound machine. Transducers come in 2 shapes: linear and curvilinear. The linear probe creates a straight image that is equal to the size of the transducer footprint. The curvilinear probe creates a wider, wedge-shaped panoramic image.

Linear probes are of higher frequency and generate higher resolution images of shallower structures, while curvilinear probes have greater depth penetration but generate lower resolution images. A high frequency of 10 to 15 MHz is preferred for anatomy between 2 cm to 4 cm depth.¹³ Midrange frequency of 5 to 10 MHz is preferred at 5 cm to 6 cm depth, and low-frequency 2 to 5 MHz probes are preferred for anatomical structures >6 cm depth.¹³

Anisotropy is the property of being directionally dependent, as opposed to isotropy, which implies identical properties in all directions. This anisotropic effect is dependent on the angle of the insonating beam. The maximum return echo occurs when the ultrasound beam is perpendicular to the tendon. Decreasing the insonating angle on a normal tendon will cause it to change from brightly hyperechoic (the actual echo from tightly bound tendon fibers) to darkly hypoechoic. If the angle is then increased, the tendon will again appear hyperechoic. If the artifact causes a normal tendon to appear hypoechoic, it may falsely lead to a diagnosis of tendinosis or tear.

Posterior acoustic shadowing is present when a hyperechoic structure reflects the ultrasound beam so much that it creates a dark shadow underneath it.^12,14 This phenomenon is possible since the ultrasound beam cannot penetrate the hyperechoic structure and reflects off its inferior tissues. Reverberation is when the beam is repeated back and forth between 2 parallel highly reflective surfaces. The initial reflection will be displayed correctly, while the subsequent ultrasound waves will be delayed and appear at a farther distance from the transducer.^12,14

The point where the beam is at its narrowest point generates the section of the image that is best visualized.¹⁵ This is called the focal zone, and it can be adjusted to highlight the desired area of evaluation. Gain controls adjust the amount of black, gray, and white on the monitor and can be adjusted to focus the desired image.¹³ Depth settings are fundamental in finding the desired targets. It is recommended to start with a higher depth setting to get an overview and progressively decrease the depth to key in on the desired anatomy.¹³ Color Doppler can be used to view movement within structures and to identify vessels, synovitis, and neovascularization in tendinopathy.¹³

Ultrasound of the Shoulder

Patients should be seated, if possible, on a rotating seat. The examiner’s shoulder should be higher than the patient’s shoulder.¹⁶ The user holds the ultrasound probe between the thumb and index fingers while resting the hypothenar eminence on the patient to serve as a fulcrum and steadying force. The examination should take 5 to 15 minutes, depending on the examiner’s expertise and the amount of anatomy being scanned.

Examining the body requires knowledge of anatomy. The examination and accuracy are determined by the technician using the probe. The probe can be angled any direction and be placed obliquely on the subject. The advantage here is that anatomy in the human body is not always planar. Muscles and tissues can run obliquely or even perpendicular to each other. When evaluating anatomy, the examiner should keep in mind what structure he or she is looking for; where it should be found; what landmarks can be used to easily locate it; what orientation it has; and what the normal anatomy should look like.

Muscle appears as a lattice with larger areas of hypoechoic muscle tissue and hyperechoic fascial perimysium layers traversing through it.¹⁷ The actual muscle tissue appears hypoechoic from the fluid or blood found within. Scarring, fibrosis, calcification, or chronic injury will change the tissue to appear denser or hyperechoic.¹⁷ Acute injury will appear hypoechoic from the inflammatory response and influx of blood. Tendon appears dense and hyperechoic with striations within the tissue, sometimes referred to as a horse’s tail.¹⁷ When torn, there will be a disassociation of the tissue with a hypoechoic region between the 2 ends. The attachment to the bone and muscle tissue should appear uniform. Hyperechoic areas within the tendon may be from calcification. Ligament appears similar to tendon but is more isoechoic and connects bone to bone. Evaluation of the entire length and the attachments to the bone are critical to evaluate for disease.

Bone appears bright hyperechoic, smooth, and flat, while hyaline cartilage is hypoechoic, smooth, and runs superiorly in a parallel pattern to its respective inferior cortical bone.¹⁷

Fibrocartilage is hyperechoic and typically triangularly shaped, such as in the glenohumeral labrum. Nerves appear fascicular and hypoechoic surrounded by hyperechoic epineurium.¹⁴

The epidermis and dermis are the most superficial structure on top of the screen, and are also hyperechoic.¹⁷

The Diagnostic Shoulder Examination

The proximal long head of the biceps tendon (LHBT) is the easiest structure in the shoulder to identify because of the anatomic structure, the bicipital groove. By keeping the arm relaxed, perpendicular to the ground, and in neutral rotation, the probe can be placed perpendicular to the arm over the proximal shoulder (Figure 1A).^16-20 By finding the groove, the biceps tendon will usually be found resting within the groove (Figure 1B). This is the short axis view and is equivalent to an MRI in the axial plane.

The long axis view of the proximal biceps tendon is found by keeping the tendon in the center of the screen/probe. The probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The user should be sure to visualize the entire tendon on the screen. If only part of the tendon is seen along only part of the screen, then the probe is oblique to the tendon. In this case, the probe area showing the tendon must be stabilized as the center or set point. The other part of the probe will then pivot until all of the tendon is seen on the screen. The MRI equivalent to the long axis of the proximal biceps tendon is the sagittal view.

Ultrasound is a dynamic evaluation. Moving the probe or moving the patient will change what and how something is imaged. The proximal biceps tendon is a good example of this concept. The bicipital groove is very deep proximally and flattens out as it travels distally to the mid-humerus. The examiner should continually adjust his or her hand/probe/patient position as well as depth/gain and other console functions to adapt to the dynamics of the scan. While keeping the bicep tendon in a short axis view, the tendon can be dynamically evaluated for subluxation by internally and externally rotating the arm.

To find the subscapularis, the arm remains in a neutral position with the hand supinated and the probe is held parallel with the ground. After finding the bicipital groove, the subscapularis tendon insertion is just medial to the groove (Figure 1B). By externally rotating the arm, the subscapularis tendon/muscle will come into a long axis view.^16-20 The MRI equivalent to the long axis view of the subscapularis is the axial view. Dynamic testing can be done by internally and externally rotating the arm to evaluate for impingement of the subscapularis tendon as it slides underneath the coracoid process. To view the subscapularis tendon in short axis, the tendon is kept in the center of the screen/probe, and the probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The MRI equivalent is the sagittal view.

Some have recommended using the modified Crass or Middleton position to evaluate the supraspinatus, where the hand is in the “back pocket”.¹⁹ However, many patients with shoulder pain have trouble with this position. By resting the ipsilateral hand on the ipsilateral hip and then dropping the elbow, the supraspinatus insertion can still be brought out from under the acromion. This does bring the insertion anterior out of the scapular plane, so an adjustment is required in probe positioning to properly see the supraspinatus short and long axis. To find the long axis, the probe is placed parallel to a plane that spans the contralateral shoulder and ipsilateral hip (Figure 2A). The fibers of the supraspinatus should be inserting directly lateral to the humeral head without any intervening space (Figure 2B). If any space exists, a partial articular supraspinatus tendon avulsion (PASTA) lesion is present, and its thickness can be directly measured. Moving more posterior will show the flattening of the tuberosity and the fibers of the infraspinatus moving away from the humeral head—the bare spot. The MRI equivalent is the coronal view.

To view the supraspinatus tendon in short axis, maintain the arm in the same position, keeping the tendon in the center of the screen/probe. The probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The probe should now be in a parallel plane between the ipsilateral shoulder and the contralateral hip. The biceps tendon in cross-section will be found anteriorly, and the articular cartilage will appear as a black layer over the bone. Dynamic testing includes placing the probe in a coronal plane between the acromion and greater tuberosity. When the patient abducts the arm while in internal rotation, the supraspinatus tendon will slide underneath the coracoacromial arch showing potential external impingement.¹⁵ The MRI equivalent is the sagittal plane.

The glenohumeral joint is best viewed posteriorly, limiting how much of the intra-articular portion of the joint can be imaged. The arm remains in a neutral position; palpate for the posterior acromion and place the probe just inferior to it, wedging up against it (Figure 3A). The glenohumeral joint will be seen by keeping the probe parallel to the ground (Figure 3B). The MRI equivalent is the axial plane. If a joint effusion exists, it can be seen in the posterior recess.¹⁵ A hyperechoic triangular region in between the humeral head and the glenoid will represent the glenoid labrum (Figure 3B). By internally and externally rotating the arm, the joint and labrum complex can be dynamically examined. From the labrum, scanning superior and medial can sometimes show the spinoglenoid notch where a paralabral cyst might be seen.¹⁵

Using the glenohumeral joint as a reference, the infraspinatus muscle is easily visualized. Maintaining the arm in neutral position with the probe over the glenohumeral joint, the infraspinatus will become apparent as it lays in long axis view superficially between the posterior deltoid and glenohumeral joint (Figure 3B).^16-20 The teres minor lies just inferiorly. The MRI equivalent is the axial plane. To view the infraspinatus and teres minor in short axis, the probe is then rotated 90° on its center axis. The infraspinatus (superiorly) and teres minor (inferiorly) muscles will be visible in short axis within the infraspinatus fossa.¹⁵ The MRI equivalent is the sagittal view.

The acromioclavicular joint is superficial and easy to image. The arm remains in a neutral position, and we can palpate the joint for easy localization. The probe is placed anteriorly in a coronal plane over the acromion and clavicle. By scanning anteriorly and posteriorly, a joint effusion referred to as a Geyser sign might be seen. The MRI equivalent is the coronal view.

Available Certifications

The AIUM certification is a voluntary peer reviewed process that acknowledges that a practice is meeting national standards and aids in improving their respective MSK ultrasound protocols. They also provide guidelines on demonstrating training and competence on performing and/or interpreting diagnostic MSK examinations (Table).¹⁰ The ARDMS certification provides an actual individual certification referred to as “Registered” in MSK ultrasound.¹¹ The physician must perform 150 diagnostic MSK ultrasound evaluations within 36 months of applying and pass a 200-question examination that is offered twice per year.¹¹ None of these certifications are mandated by the American Medical Association (AMA) or American Osteopathic Association (AOA).

Maintenance and Continuing Medical Education (CME)

The AIUM recommends that a minimum of 50 diagnostic MSK ultrasound evaluations be performed per year for skill maintenance.¹⁰ Furthermore, 10 hours of AMA PRA Category 1 Credits™ or American Osteopathic Association Category 1-A Credits specific to MSK ultrasound must be completed by physicians performing and/or interpreting these examinations every 3 years.¹⁰ ARDMS recommends a minimum of 30 MSK ultrasound-specific CMEs in preparation for their “Registered” MSK evaluation.¹

Conclusion

MSK ultrasound is a dynamic, real-time imaging modality that can improve cost efficiency and patient care. Its portability allows for its use anywhere. Learning the skill may seem daunting, but with the proper courses and education, the technology can be easily learned. By correlating a known modality like MRI, the user will easily begin to read ultrasound images. No current certification is needed to use or bill for ultrasound, but various institutions are developing criteria and testing. Two organizations, AIUM and ARDMS, provide guidelines and certifications to demonstrate competency, which may become necessary in the very near future.

The musculoskeletal (MSK) ultrasound evaluation of the shoulder provides a cost- and time-efficient imaging modality with similar diagnostic power as magnetic resonance imaging (MRI).^1,2 Its portable point-of-care applications can be used in the office, in the operating room, and in sideline athletic event coverage, as we discussed in Part 1 of this series.³

MSK ultrasound may seem difficult and daunting, and many articles have quoted steep learning curves.^4,5 However, in our experience in teaching many ultrasound courses, this modality can be learned quite quickly with the proper instruction. Physicians are already familiar with anatomy and usually have had some exposure to MRI.⁴ Taking courses in MSK ultrasound or simply learning the basic concepts of ultrasound and then learning the machine controls is usually a good start.^5-8 Practice scanning normal individuals, comparing the images from an MRI to learn how to reproduce the same planes and images. This will allow the user to become familiar with normal anatomy and how to see the images on the ultrasound screen.^5-8 Vollman and colleagues⁹ showed that in trainees, combining MRI images with sonograms enhances the ability to correctly identify MSK ultrasound anatomy from 40.9% to 72.5%, when compared with learning from ultrasound images alone.

There are currently no certifications necessary to perform ultrasound scans or bill for them; however, some insurance carriers may require demonstrating relevant, documented training for reimbursement.³ Various organizations are trying to develop certifications and regulations for ultrasound to standardize the use of this modality. In the United States, the American Institute of Ultrasound in Medicine (AIUM) and the American Registry for Diagnostic Medical Sonography (ARDMS) provide guidelines and particular MSK ultrasound certifications.^10,11

Basic Ultrasound Principles

The ultrasound machine creates electrical impulses that are turned into sound waves by piezoelectric crystals at the probe’s footprint. These sound waves bounce off tissues and return to the probe, where they are converted electronically to an image on the monitor. Depending on the echogenicity of the scanned tissue, the ultrasound beam will either reflect or be absorbed at different rates. This variance is transmitted on the monitor as a grayscale image. When ultrasound waves are highly reflective, like in bone or fat, they are characterized as hyperechoic. The opposite occurs when ultrasound waves are absorbed like in the fluid of a cystic cavity or joint effusion, and the image appears black. This is described as anechoic.¹² Intermediate tissues such as tendons that are less reflective are seen as hypoechoic and appear gray. When a tissue has a similar echogenicity to its surrounding tissues, it is called isoechoic.¹²

The transducer is the scanning component of the ultrasound machine. Transducers come in 2 shapes: linear and curvilinear. The linear probe creates a straight image that is equal to the size of the transducer footprint. The curvilinear probe creates a wider, wedge-shaped panoramic image.

Linear probes are of higher frequency and generate higher resolution images of shallower structures, while curvilinear probes have greater depth penetration but generate lower resolution images. A high frequency of 10 to 15 MHz is preferred for anatomy between 2 cm to 4 cm depth.¹³ Midrange frequency of 5 to 10 MHz is preferred at 5 cm to 6 cm depth, and low-frequency 2 to 5 MHz probes are preferred for anatomical structures >6 cm depth.¹³

Anisotropy is the property of being directionally dependent, as opposed to isotropy, which implies identical properties in all directions. This anisotropic effect is dependent on the angle of the insonating beam. The maximum return echo occurs when the ultrasound beam is perpendicular to the tendon. Decreasing the insonating angle on a normal tendon will cause it to change from brightly hyperechoic (the actual echo from tightly bound tendon fibers) to darkly hypoechoic. If the angle is then increased, the tendon will again appear hyperechoic. If the artifact causes a normal tendon to appear hypoechoic, it may falsely lead to a diagnosis of tendinosis or tear.

Posterior acoustic shadowing is present when a hyperechoic structure reflects the ultrasound beam so much that it creates a dark shadow underneath it.^12,14 This phenomenon is possible since the ultrasound beam cannot penetrate the hyperechoic structure and reflects off its inferior tissues. Reverberation is when the beam is repeated back and forth between 2 parallel highly reflective surfaces. The initial reflection will be displayed correctly, while the subsequent ultrasound waves will be delayed and appear at a farther distance from the transducer.^12,14

The point where the beam is at its narrowest point generates the section of the image that is best visualized.¹⁵ This is called the focal zone, and it can be adjusted to highlight the desired area of evaluation. Gain controls adjust the amount of black, gray, and white on the monitor and can be adjusted to focus the desired image.¹³ Depth settings are fundamental in finding the desired targets. It is recommended to start with a higher depth setting to get an overview and progressively decrease the depth to key in on the desired anatomy.¹³ Color Doppler can be used to view movement within structures and to identify vessels, synovitis, and neovascularization in tendinopathy.¹³

Ultrasound of the Shoulder

Patients should be seated, if possible, on a rotating seat. The examiner’s shoulder should be higher than the patient’s shoulder.¹⁶ The user holds the ultrasound probe between the thumb and index fingers while resting the hypothenar eminence on the patient to serve as a fulcrum and steadying force. The examination should take 5 to 15 minutes, depending on the examiner’s expertise and the amount of anatomy being scanned.

Examining the body requires knowledge of anatomy. The examination and accuracy are determined by the technician using the probe. The probe can be angled any direction and be placed obliquely on the subject. The advantage here is that anatomy in the human body is not always planar. Muscles and tissues can run obliquely or even perpendicular to each other. When evaluating anatomy, the examiner should keep in mind what structure he or she is looking for; where it should be found; what landmarks can be used to easily locate it; what orientation it has; and what the normal anatomy should look like.

Muscle appears as a lattice with larger areas of hypoechoic muscle tissue and hyperechoic fascial perimysium layers traversing through it.¹⁷ The actual muscle tissue appears hypoechoic from the fluid or blood found within. Scarring, fibrosis, calcification, or chronic injury will change the tissue to appear denser or hyperechoic.¹⁷ Acute injury will appear hypoechoic from the inflammatory response and influx of blood. Tendon appears dense and hyperechoic with striations within the tissue, sometimes referred to as a horse’s tail.¹⁷ When torn, there will be a disassociation of the tissue with a hypoechoic region between the 2 ends. The attachment to the bone and muscle tissue should appear uniform. Hyperechoic areas within the tendon may be from calcification. Ligament appears similar to tendon but is more isoechoic and connects bone to bone. Evaluation of the entire length and the attachments to the bone are critical to evaluate for disease.

Bone appears bright hyperechoic, smooth, and flat, while hyaline cartilage is hypoechoic, smooth, and runs superiorly in a parallel pattern to its respective inferior cortical bone.¹⁷

Fibrocartilage is hyperechoic and typically triangularly shaped, such as in the glenohumeral labrum. Nerves appear fascicular and hypoechoic surrounded by hyperechoic epineurium.¹⁴

The epidermis and dermis are the most superficial structure on top of the screen, and are also hyperechoic.¹⁷

The Diagnostic Shoulder Examination

The proximal long head of the biceps tendon (LHBT) is the easiest structure in the shoulder to identify because of the anatomic structure, the bicipital groove. By keeping the arm relaxed, perpendicular to the ground, and in neutral rotation, the probe can be placed perpendicular to the arm over the proximal shoulder (Figure 1A).^16-20 By finding the groove, the biceps tendon will usually be found resting within the groove (Figure 1B). This is the short axis view and is equivalent to an MRI in the axial plane.

The long axis view of the proximal biceps tendon is found by keeping the tendon in the center of the screen/probe. The probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The user should be sure to visualize the entire tendon on the screen. If only part of the tendon is seen along only part of the screen, then the probe is oblique to the tendon. In this case, the probe area showing the tendon must be stabilized as the center or set point. The other part of the probe will then pivot until all of the tendon is seen on the screen. The MRI equivalent to the long axis of the proximal biceps tendon is the sagittal view.

Ultrasound is a dynamic evaluation. Moving the probe or moving the patient will change what and how something is imaged. The proximal biceps tendon is a good example of this concept. The bicipital groove is very deep proximally and flattens out as it travels distally to the mid-humerus. The examiner should continually adjust his or her hand/probe/patient position as well as depth/gain and other console functions to adapt to the dynamics of the scan. While keeping the bicep tendon in a short axis view, the tendon can be dynamically evaluated for subluxation by internally and externally rotating the arm.

To find the subscapularis, the arm remains in a neutral position with the hand supinated and the probe is held parallel with the ground. After finding the bicipital groove, the subscapularis tendon insertion is just medial to the groove (Figure 1B). By externally rotating the arm, the subscapularis tendon/muscle will come into a long axis view.^16-20 The MRI equivalent to the long axis view of the subscapularis is the axial view. Dynamic testing can be done by internally and externally rotating the arm to evaluate for impingement of the subscapularis tendon as it slides underneath the coracoid process. To view the subscapularis tendon in short axis, the tendon is kept in the center of the screen/probe, and the probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The MRI equivalent is the sagittal view.

Some have recommended using the modified Crass or Middleton position to evaluate the supraspinatus, where the hand is in the “back pocket”.¹⁹ However, many patients with shoulder pain have trouble with this position. By resting the ipsilateral hand on the ipsilateral hip and then dropping the elbow, the supraspinatus insertion can still be brought out from under the acromion. This does bring the insertion anterior out of the scapular plane, so an adjustment is required in probe positioning to properly see the supraspinatus short and long axis. To find the long axis, the probe is placed parallel to a plane that spans the contralateral shoulder and ipsilateral hip (Figure 2A). The fibers of the supraspinatus should be inserting directly lateral to the humeral head without any intervening space (Figure 2B). If any space exists, a partial articular supraspinatus tendon avulsion (PASTA) lesion is present, and its thickness can be directly measured. Moving more posterior will show the flattening of the tuberosity and the fibers of the infraspinatus moving away from the humeral head—the bare spot. The MRI equivalent is the coronal view.

To view the supraspinatus tendon in short axis, maintain the arm in the same position, keeping the tendon in the center of the screen/probe. The probe is then rotated 90° on its center axis, keeping the tendon centered on the probe. The probe should now be in a parallel plane between the ipsilateral shoulder and the contralateral hip. The biceps tendon in cross-section will be found anteriorly, and the articular cartilage will appear as a black layer over the bone. Dynamic testing includes placing the probe in a coronal plane between the acromion and greater tuberosity. When the patient abducts the arm while in internal rotation, the supraspinatus tendon will slide underneath the coracoacromial arch showing potential external impingement.¹⁵ The MRI equivalent is the sagittal plane.

The glenohumeral joint is best viewed posteriorly, limiting how much of the intra-articular portion of the joint can be imaged. The arm remains in a neutral position; palpate for the posterior acromion and place the probe just inferior to it, wedging up against it (Figure 3A). The glenohumeral joint will be seen by keeping the probe parallel to the ground (Figure 3B). The MRI equivalent is the axial plane. If a joint effusion exists, it can be seen in the posterior recess.¹⁵ A hyperechoic triangular region in between the humeral head and the glenoid will represent the glenoid labrum (Figure 3B). By internally and externally rotating the arm, the joint and labrum complex can be dynamically examined. From the labrum, scanning superior and medial can sometimes show the spinoglenoid notch where a paralabral cyst might be seen.¹⁵

Using the glenohumeral joint as a reference, the infraspinatus muscle is easily visualized. Maintaining the arm in neutral position with the probe over the glenohumeral joint, the infraspinatus will become apparent as it lays in long axis view superficially between the posterior deltoid and glenohumeral joint (Figure 3B).^16-20 The teres minor lies just inferiorly. The MRI equivalent is the axial plane. To view the infraspinatus and teres minor in short axis, the probe is then rotated 90° on its center axis. The infraspinatus (superiorly) and teres minor (inferiorly) muscles will be visible in short axis within the infraspinatus fossa.¹⁵ The MRI equivalent is the sagittal view.

The acromioclavicular joint is superficial and easy to image. The arm remains in a neutral position, and we can palpate the joint for easy localization. The probe is placed anteriorly in a coronal plane over the acromion and clavicle. By scanning anteriorly and posteriorly, a joint effusion referred to as a Geyser sign might be seen. The MRI equivalent is the coronal view.

Available Certifications

The AIUM certification is a voluntary peer reviewed process that acknowledges that a practice is meeting national standards and aids in improving their respective MSK ultrasound protocols. They also provide guidelines on demonstrating training and competence on performing and/or interpreting diagnostic MSK examinations (Table).¹⁰ The ARDMS certification provides an actual individual certification referred to as “Registered” in MSK ultrasound.¹¹ The physician must perform 150 diagnostic MSK ultrasound evaluations within 36 months of applying and pass a 200-question examination that is offered twice per year.¹¹ None of these certifications are mandated by the American Medical Association (AMA) or American Osteopathic Association (AOA).

Maintenance and Continuing Medical Education (CME)

The AIUM recommends that a minimum of 50 diagnostic MSK ultrasound evaluations be performed per year for skill maintenance.¹⁰ Furthermore, 10 hours of AMA PRA Category 1 Credits™ or American Osteopathic Association Category 1-A Credits specific to MSK ultrasound must be completed by physicians performing and/or interpreting these examinations every 3 years.¹⁰ ARDMS recommends a minimum of 30 MSK ultrasound-specific CMEs in preparation for their “Registered” MSK evaluation.¹

Conclusion

MSK ultrasound is a dynamic, real-time imaging modality that can improve cost efficiency and patient care. Its portability allows for its use anywhere. Learning the skill may seem daunting, but with the proper courses and education, the technology can be easily learned. By correlating a known modality like MRI, the user will easily begin to read ultrasound images. No current certification is needed to use or bill for ultrasound, but various institutions are developing criteria and testing. Two organizations, AIUM and ARDMS, provide guidelines and certifications to demonstrate competency, which may become necessary in the very near future.

CHICAGO – CMX-2043, a novel agent intended for prevention of contrast-induced nephropathy, failed in the phase II, double-blind, placebo-controlled CARIN clinical trial presented at the annual meeting of the American College of Cardiology.

The drug had also shown promise in small preliminary studies for the prevention of periprocedural myocardial infarction in patients undergoing coronary stenting. There again, however, CMX-2043 – a derivative of alpha lipoic acid with antioxidant and cell membrane–stabilizing properties – proved ineffective in the 361-patient, 31-center phase II trial, reported Dr. Deepak L. Bhatt, professor of medicine at Harvard Medical School and executive director of interventional cardiovascular programs at Brigham and Women’s Hospital, both in Boston.

All participants in CARIN had baseline severe impairment of kidney function or mild to moderate renal impairment plus another risk factor, such as diabetes or age greater than 75 years. One hour prior to coronary angiography, they received various doses of CMX-2043 or placebo.

Unfortunately, no difference between the four treatment arms was present in terms of the primary study endpoint: the incidence of acute kidney injury as defined by at least a 0.3 mg/dL rise in serum creatinine from baseline on day 4. No dose response to CMX-2043 was evident, nor did the investigational agent have any impact on the risk of major adverse cardiovascular events.

Immediately prior to Dr. Bhatt’s presentation, Dr. Michelle L. O’Donoghue of Brigham and Women’s Hospital presented the equally negative results of the LATITUDE-TIMI 60 trial, a phase III trial of the investigational mitogen-activated protein kinase inhibitor losmapimod, a drug developed to improve outcomes in patients with an acute coronary syndrome.

“It’s a bit distressing” to witness back to back presentations of clinical trials that proved resoundingly negative despite very strong-looking preliminary data, commented discussant Dr. Anthony N. DeMaria, professor of medicine at the University of California, San Diego. What’s going on here? he asked.

“I think it’s a fundamental truth that a lot of things that look good in preclinical work, even when backed up by a lot of solid science, don’t pan out in human studies,” Dr. Bhatt replied. “That’s a challenge, and probably in no other arena more so than in tackling inflammation and antioxidant therapy.

“There’s a graveyard of compounds that have not worked, and now we’ve perhaps added another one,” Dr. Bhatt continued. “But it doesn’t mean that scientific inquiry isn’t important, because I think eventually we’ll have drugs for these problems, whether it’s reperfusion injury or contrast-induced nephropathy. It’ll probably just take a lot more time and effort.”

The one solace regarding the CARIN trial, in Dr. Bhatt’s view, is that it highlighted the advantages of what is known as an adaptive trial design. Instead of jumping from positive early-phase results straight to a definitive 10,000-patient phase III clinical trial, investigators were able to obtain answers regarding the drug’s ability to prevent two major problems in patients undergoing coronary angiography – contrast-induced nephropathy and major adverse cardiac events – by means of a single 361-patient trial that was comparatively inexpensive.

Acute kidney injury secondary to exposure to contrast agents remains a significant problem, with an incidence of 20%-25% in high-risk patients. Numerous proposed prophylactic agents have ultimately proved not useful, including sodium bicarbonate, N-acetylcysteine, and intravenous fenoldopam.

Indeed, the only preventive measures of proven effectiveness are hydration with saline for 12 hours preangioplasty, and limiting the volume of contrast agent used. In real-world clinical practice, however, it’s often impractical to administer the optimal 12 hours of saline because of hospital pressure to get patients out quickly, Dr. Bhatt observed.

“There remains an important unmet clinical need to find agents that reduce the occurrence of contrast nephropathy,” he stressed.

Ischemix funded the CARIN trial. Dr. Bhatt reported receiving a research grant from the company that was directed to Brigham and Women’s Hospital.

[email protected]

CHICAGO – CMX-2043, a novel agent intended for prevention of contrast-induced nephropathy, failed in the phase II, double-blind, placebo-controlled CARIN clinical trial presented at the annual meeting of the American College of Cardiology.

The drug had also shown promise in small preliminary studies for the prevention of periprocedural myocardial infarction in patients undergoing coronary stenting. There again, however, CMX-2043 – a derivative of alpha lipoic acid with antioxidant and cell membrane–stabilizing properties – proved ineffective in the 361-patient, 31-center phase II trial, reported Dr. Deepak L. Bhatt, professor of medicine at Harvard Medical School and executive director of interventional cardiovascular programs at Brigham and Women’s Hospital, both in Boston.

All participants in CARIN had baseline severe impairment of kidney function or mild to moderate renal impairment plus another risk factor, such as diabetes or age greater than 75 years. One hour prior to coronary angiography, they received various doses of CMX-2043 or placebo.

Unfortunately, no difference between the four treatment arms was present in terms of the primary study endpoint: the incidence of acute kidney injury as defined by at least a 0.3 mg/dL rise in serum creatinine from baseline on day 4. No dose response to CMX-2043 was evident, nor did the investigational agent have any impact on the risk of major adverse cardiovascular events.

Immediately prior to Dr. Bhatt’s presentation, Dr. Michelle L. O’Donoghue of Brigham and Women’s Hospital presented the equally negative results of the LATITUDE-TIMI 60 trial, a phase III trial of the investigational mitogen-activated protein kinase inhibitor losmapimod, a drug developed to improve outcomes in patients with an acute coronary syndrome.

“It’s a bit distressing” to witness back to back presentations of clinical trials that proved resoundingly negative despite very strong-looking preliminary data, commented discussant Dr. Anthony N. DeMaria, professor of medicine at the University of California, San Diego. What’s going on here? he asked.

“I think it’s a fundamental truth that a lot of things that look good in preclinical work, even when backed up by a lot of solid science, don’t pan out in human studies,” Dr. Bhatt replied. “That’s a challenge, and probably in no other arena more so than in tackling inflammation and antioxidant therapy.

“There’s a graveyard of compounds that have not worked, and now we’ve perhaps added another one,” Dr. Bhatt continued. “But it doesn’t mean that scientific inquiry isn’t important, because I think eventually we’ll have drugs for these problems, whether it’s reperfusion injury or contrast-induced nephropathy. It’ll probably just take a lot more time and effort.”

The one solace regarding the CARIN trial, in Dr. Bhatt’s view, is that it highlighted the advantages of what is known as an adaptive trial design. Instead of jumping from positive early-phase results straight to a definitive 10,000-patient phase III clinical trial, investigators were able to obtain answers regarding the drug’s ability to prevent two major problems in patients undergoing coronary angiography – contrast-induced nephropathy and major adverse cardiac events – by means of a single 361-patient trial that was comparatively inexpensive.

Acute kidney injury secondary to exposure to contrast agents remains a significant problem, with an incidence of 20%-25% in high-risk patients. Numerous proposed prophylactic agents have ultimately proved not useful, including sodium bicarbonate, N-acetylcysteine, and intravenous fenoldopam.

Indeed, the only preventive measures of proven effectiveness are hydration with saline for 12 hours preangioplasty, and limiting the volume of contrast agent used. In real-world clinical practice, however, it’s often impractical to administer the optimal 12 hours of saline because of hospital pressure to get patients out quickly, Dr. Bhatt observed.

“There remains an important unmet clinical need to find agents that reduce the occurrence of contrast nephropathy,” he stressed.

Ischemix funded the CARIN trial. Dr. Bhatt reported receiving a research grant from the company that was directed to Brigham and Women’s Hospital.

[email protected]

CHICAGO – CMX-2043, a novel agent intended for prevention of contrast-induced nephropathy, failed in the phase II, double-blind, placebo-controlled CARIN clinical trial presented at the annual meeting of the American College of Cardiology.

The drug had also shown promise in small preliminary studies for the prevention of periprocedural myocardial infarction in patients undergoing coronary stenting. There again, however, CMX-2043 – a derivative of alpha lipoic acid with antioxidant and cell membrane–stabilizing properties – proved ineffective in the 361-patient, 31-center phase II trial, reported Dr. Deepak L. Bhatt, professor of medicine at Harvard Medical School and executive director of interventional cardiovascular programs at Brigham and Women’s Hospital, both in Boston.

All participants in CARIN had baseline severe impairment of kidney function or mild to moderate renal impairment plus another risk factor, such as diabetes or age greater than 75 years. One hour prior to coronary angiography, they received various doses of CMX-2043 or placebo.

Unfortunately, no difference between the four treatment arms was present in terms of the primary study endpoint: the incidence of acute kidney injury as defined by at least a 0.3 mg/dL rise in serum creatinine from baseline on day 4. No dose response to CMX-2043 was evident, nor did the investigational agent have any impact on the risk of major adverse cardiovascular events.

Immediately prior to Dr. Bhatt’s presentation, Dr. Michelle L. O’Donoghue of Brigham and Women’s Hospital presented the equally negative results of the LATITUDE-TIMI 60 trial, a phase III trial of the investigational mitogen-activated protein kinase inhibitor losmapimod, a drug developed to improve outcomes in patients with an acute coronary syndrome.

“It’s a bit distressing” to witness back to back presentations of clinical trials that proved resoundingly negative despite very strong-looking preliminary data, commented discussant Dr. Anthony N. DeMaria, professor of medicine at the University of California, San Diego. What’s going on here? he asked.

“I think it’s a fundamental truth that a lot of things that look good in preclinical work, even when backed up by a lot of solid science, don’t pan out in human studies,” Dr. Bhatt replied. “That’s a challenge, and probably in no other arena more so than in tackling inflammation and antioxidant therapy.

“There’s a graveyard of compounds that have not worked, and now we’ve perhaps added another one,” Dr. Bhatt continued. “But it doesn’t mean that scientific inquiry isn’t important, because I think eventually we’ll have drugs for these problems, whether it’s reperfusion injury or contrast-induced nephropathy. It’ll probably just take a lot more time and effort.”

The one solace regarding the CARIN trial, in Dr. Bhatt’s view, is that it highlighted the advantages of what is known as an adaptive trial design. Instead of jumping from positive early-phase results straight to a definitive 10,000-patient phase III clinical trial, investigators were able to obtain answers regarding the drug’s ability to prevent two major problems in patients undergoing coronary angiography – contrast-induced nephropathy and major adverse cardiac events – by means of a single 361-patient trial that was comparatively inexpensive.

Acute kidney injury secondary to exposure to contrast agents remains a significant problem, with an incidence of 20%-25% in high-risk patients. Numerous proposed prophylactic agents have ultimately proved not useful, including sodium bicarbonate, N-acetylcysteine, and intravenous fenoldopam.

Indeed, the only preventive measures of proven effectiveness are hydration with saline for 12 hours preangioplasty, and limiting the volume of contrast agent used. In real-world clinical practice, however, it’s often impractical to administer the optimal 12 hours of saline because of hospital pressure to get patients out quickly, Dr. Bhatt observed.

“There remains an important unmet clinical need to find agents that reduce the occurrence of contrast nephropathy,” he stressed.

Ischemix funded the CARIN trial. Dr. Bhatt reported receiving a research grant from the company that was directed to Brigham and Women’s Hospital.

[email protected]

SAN DIEGO – Head CTs for patients with in-hospital delirium. Ammonia tests to check for hepatic encephalopathy in chronic liver disease. Renal ultrasounds for acute kidney injury.

Those are three low value tests highlighted in hospitalist Dr. Leonard Feldman’s latest iteration of his lecture series “Things We Do for No Reason.”

Dr. Feldman, associate professor of internal medicine and pediatrics at Johns Hopkins University, Baltimore, has presented his list of usually unnecessary hospitalist practices for five years at the Society of Hospital Medicine’s annual meetings. With three new ones explained during the 2016 meeting, there are now 19 on the list and more to come, he said.

“So far, I’ve picked things that are relatively low-hanging fruit, things for which there’s good evidence we shouldn’t be doing and if you saw the evidence, you’d say ‘that’s right, we shouldn’t,’” he said.

Dr. Feldman’s intent is to help clinicians stop certain “learned behaviors,” tests and procedures which research and experience now show “are not helping people, sometimes harm people, and often result in a cascade” of further unnecessary tests and care.

The conference presentations have been so popular, the Journal of Hospital Medicine in October 2015 started a “Things We Do for No Reason” series.

Here are the three most recent tests hospitalists should avoid:

Ammonia levels for chronic liver disease

Dr. Feldman said doctors were taught in medical school that ammonia levels rise in patients with cirrhosis and when they rise too high, the patient may develop hepatic encephalopathy. They also learned that if levels are normal, the patient should not have hepatic encephalopathy.

But a number of studies have found “neither of those is true,” he said. What’s possibly worse is that “you close your mind to other possible diagnoses way too early.” Nevertheless, the practice at many hospitals is to perform multiple tests to trend those levels.”

“I had a patient who had an ammonia test sent the other day while in the emergency room, and it was elevated,” Dr. Feldman recalled in a recent phone interview. “The patient got admitted, but when we re-tested, it wasn’t.”

Part of the problem is that blood samples are often incorrectly processed. “When you draw the blood, you have to put it on ice and it needs to get to the lab very quickly. And I think we do neither of those things on a regular basis,” he said. Also, if the patient has a tourniquet or is clenching a fist, use of muscle creates ammonia.

Dr. Feldman said that at a hospital like Johns Hopkins in Baltimore, where there are high rates of hepatitis C, there might be 50 patients with chronic liver disease, or 20% of patients on medicine service. It’s not the cost of the blood test that he’s worried about because that’s probably minimal. Rather, it’s the test’s downstream provocation of more unnecessary care “and missed opportunities to intervene with a treatable diagnosis.”

In general, he said, “for patients with chronic liver disease, we shouldn’t be checking ammonia.”

Head CTs for inpatients with new onset delirium

Performing a costly head CT scan on a patient who presents in the emergency department with delirium is appropriate. But for low-risk patients who develop delirium inside the hospital without a clear reason, such as a fall or focal neurologic symptoms suggesting a stroke, a head CT is probably not necessary, Dr. Feldman said.

“But we have this knee-jerk reaction, this reflex, that when a patient becomes delirious, we probably should run a head CT on them,” he added.

Dr. Feldman acknowledged that the frequency of head CTs on inpatients with delirium has been hard to tease out.

“But all the studies indicate that patients who develop delirium while in the hospital, without any sort of risk factor, are very unlikely to have pathology found on a head CT,” he said, noting that the cause of their delirium is likely something else, like dehydration, an infection, disruption of sleep, urinary retention, or medication effect.

Of course, if patients aren’t getting better without the CT, order the CT, he said. “Even if the patient has no risk factor, there’s still a 3% chance of having an abnormality like a tumor or stroke.”

Renal ultrasound for patients with new acute kidney injury

To determine if an acute kidney injury is caused by a treatable obstruction, such as a large prostate causing urinary retention, doctors often first order a renal ultrasound, a test that can cost $300, and must be read by a radiologist.

But a much less expensive simple bladder scan, which can be performed by a nurse, is a much better substitute for the first pass, Dr. Feldman said. He said it’s logical that “a bladder scan is a much higher value test” in the early diagnostic process.

“The studies have been pretty clear. If you don’t have risk factors for having an obstruction, a history of kidney stones, it hasn’t happened before, or other reasons kidneys aren’t working, it’s extraordinarily unlikely you’re going to find anything on that renal ultrasound that could be intervened to fix that acute kidney injury,” Dr. Feldman said. He pointed to a study that found 223 renal ultrasounds were necessary to find one patient who needed an intervention.

“You can probably get a good sense from the history and physical” and start to treat them, he said, and if they’re not getting better, then order the ultrasound.

Each of the items on Feldman’s list don’t necessarily save a lot of money, but they add up. “The more we ask ‘Why are we doing this? Can we stop it if it’s not helping people, and particularly if it’s harming people?’ the more we can prevent the cascade that happens because you did one unnecessary diagnostic test,” he concluded.

SAN DIEGO – Head CTs for patients with in-hospital delirium. Ammonia tests to check for hepatic encephalopathy in chronic liver disease. Renal ultrasounds for acute kidney injury.

Those are three low value tests highlighted in hospitalist Dr. Leonard Feldman’s latest iteration of his lecture series “Things We Do for No Reason.”

Dr. Feldman, associate professor of internal medicine and pediatrics at Johns Hopkins University, Baltimore, has presented his list of usually unnecessary hospitalist practices for five years at the Society of Hospital Medicine’s annual meetings. With three new ones explained during the 2016 meeting, there are now 19 on the list and more to come, he said.

“So far, I’ve picked things that are relatively low-hanging fruit, things for which there’s good evidence we shouldn’t be doing and if you saw the evidence, you’d say ‘that’s right, we shouldn’t,’” he said.

Dr. Feldman’s intent is to help clinicians stop certain “learned behaviors,” tests and procedures which research and experience now show “are not helping people, sometimes harm people, and often result in a cascade” of further unnecessary tests and care.

The conference presentations have been so popular, the Journal of Hospital Medicine in October 2015 started a “Things We Do for No Reason” series.

Here are the three most recent tests hospitalists should avoid:

Ammonia levels for chronic liver disease

Dr. Feldman said doctors were taught in medical school that ammonia levels rise in patients with cirrhosis and when they rise too high, the patient may develop hepatic encephalopathy. They also learned that if levels are normal, the patient should not have hepatic encephalopathy.

But a number of studies have found “neither of those is true,” he said. What’s possibly worse is that “you close your mind to other possible diagnoses way too early.” Nevertheless, the practice at many hospitals is to perform multiple tests to trend those levels.”

“I had a patient who had an ammonia test sent the other day while in the emergency room, and it was elevated,” Dr. Feldman recalled in a recent phone interview. “The patient got admitted, but when we re-tested, it wasn’t.”

Part of the problem is that blood samples are often incorrectly processed. “When you draw the blood, you have to put it on ice and it needs to get to the lab very quickly. And I think we do neither of those things on a regular basis,” he said. Also, if the patient has a tourniquet or is clenching a fist, use of muscle creates ammonia.

Dr. Feldman said that at a hospital like Johns Hopkins in Baltimore, where there are high rates of hepatitis C, there might be 50 patients with chronic liver disease, or 20% of patients on medicine service. It’s not the cost of the blood test that he’s worried about because that’s probably minimal. Rather, it’s the test’s downstream provocation of more unnecessary care “and missed opportunities to intervene with a treatable diagnosis.”

In general, he said, “for patients with chronic liver disease, we shouldn’t be checking ammonia.”

Head CTs for inpatients with new onset delirium

Performing a costly head CT scan on a patient who presents in the emergency department with delirium is appropriate. But for low-risk patients who develop delirium inside the hospital without a clear reason, such as a fall or focal neurologic symptoms suggesting a stroke, a head CT is probably not necessary, Dr. Feldman said.

“But we have this knee-jerk reaction, this reflex, that when a patient becomes delirious, we probably should run a head CT on them,” he added.

Dr. Feldman acknowledged that the frequency of head CTs on inpatients with delirium has been hard to tease out.

“But all the studies indicate that patients who develop delirium while in the hospital, without any sort of risk factor, are very unlikely to have pathology found on a head CT,” he said, noting that the cause of their delirium is likely something else, like dehydration, an infection, disruption of sleep, urinary retention, or medication effect.

Of course, if patients aren’t getting better without the CT, order the CT, he said. “Even if the patient has no risk factor, there’s still a 3% chance of having an abnormality like a tumor or stroke.”

Renal ultrasound for patients with new acute kidney injury

To determine if an acute kidney injury is caused by a treatable obstruction, such as a large prostate causing urinary retention, doctors often first order a renal ultrasound, a test that can cost $300, and must be read by a radiologist.

But a much less expensive simple bladder scan, which can be performed by a nurse, is a much better substitute for the first pass, Dr. Feldman said. He said it’s logical that “a bladder scan is a much higher value test” in the early diagnostic process.

“The studies have been pretty clear. If you don’t have risk factors for having an obstruction, a history of kidney stones, it hasn’t happened before, or other reasons kidneys aren’t working, it’s extraordinarily unlikely you’re going to find anything on that renal ultrasound that could be intervened to fix that acute kidney injury,” Dr. Feldman said. He pointed to a study that found 223 renal ultrasounds were necessary to find one patient who needed an intervention.

“You can probably get a good sense from the history and physical” and start to treat them, he said, and if they’re not getting better, then order the ultrasound.

Each of the items on Feldman’s list don’t necessarily save a lot of money, but they add up. “The more we ask ‘Why are we doing this? Can we stop it if it’s not helping people, and particularly if it’s harming people?’ the more we can prevent the cascade that happens because you did one unnecessary diagnostic test,” he concluded.

SAN DIEGO – Head CTs for patients with in-hospital delirium. Ammonia tests to check for hepatic encephalopathy in chronic liver disease. Renal ultrasounds for acute kidney injury.

Those are three low value tests highlighted in hospitalist Dr. Leonard Feldman’s latest iteration of his lecture series “Things We Do for No Reason.”

Dr. Feldman, associate professor of internal medicine and pediatrics at Johns Hopkins University, Baltimore, has presented his list of usually unnecessary hospitalist practices for five years at the Society of Hospital Medicine’s annual meetings. With three new ones explained during the 2016 meeting, there are now 19 on the list and more to come, he said.

“So far, I’ve picked things that are relatively low-hanging fruit, things for which there’s good evidence we shouldn’t be doing and if you saw the evidence, you’d say ‘that’s right, we shouldn’t,’” he said.

Dr. Feldman’s intent is to help clinicians stop certain “learned behaviors,” tests and procedures which research and experience now show “are not helping people, sometimes harm people, and often result in a cascade” of further unnecessary tests and care.

The conference presentations have been so popular, the Journal of Hospital Medicine in October 2015 started a “Things We Do for No Reason” series.

Here are the three most recent tests hospitalists should avoid:

Ammonia levels for chronic liver disease

Dr. Feldman said doctors were taught in medical school that ammonia levels rise in patients with cirrhosis and when they rise too high, the patient may develop hepatic encephalopathy. They also learned that if levels are normal, the patient should not have hepatic encephalopathy.

But a number of studies have found “neither of those is true,” he said. What’s possibly worse is that “you close your mind to other possible diagnoses way too early.” Nevertheless, the practice at many hospitals is to perform multiple tests to trend those levels.”

“I had a patient who had an ammonia test sent the other day while in the emergency room, and it was elevated,” Dr. Feldman recalled in a recent phone interview. “The patient got admitted, but when we re-tested, it wasn’t.”

Part of the problem is that blood samples are often incorrectly processed. “When you draw the blood, you have to put it on ice and it needs to get to the lab very quickly. And I think we do neither of those things on a regular basis,” he said. Also, if the patient has a tourniquet or is clenching a fist, use of muscle creates ammonia.

Dr. Feldman said that at a hospital like Johns Hopkins in Baltimore, where there are high rates of hepatitis C, there might be 50 patients with chronic liver disease, or 20% of patients on medicine service. It’s not the cost of the blood test that he’s worried about because that’s probably minimal. Rather, it’s the test’s downstream provocation of more unnecessary care “and missed opportunities to intervene with a treatable diagnosis.”

In general, he said, “for patients with chronic liver disease, we shouldn’t be checking ammonia.”

Head CTs for inpatients with new onset delirium

Performing a costly head CT scan on a patient who presents in the emergency department with delirium is appropriate. But for low-risk patients who develop delirium inside the hospital without a clear reason, such as a fall or focal neurologic symptoms suggesting a stroke, a head CT is probably not necessary, Dr. Feldman said.

“But we have this knee-jerk reaction, this reflex, that when a patient becomes delirious, we probably should run a head CT on them,” he added.

Dr. Feldman acknowledged that the frequency of head CTs on inpatients with delirium has been hard to tease out.

“But all the studies indicate that patients who develop delirium while in the hospital, without any sort of risk factor, are very unlikely to have pathology found on a head CT,” he said, noting that the cause of their delirium is likely something else, like dehydration, an infection, disruption of sleep, urinary retention, or medication effect.

Of course, if patients aren’t getting better without the CT, order the CT, he said. “Even if the patient has no risk factor, there’s still a 3% chance of having an abnormality like a tumor or stroke.”

Renal ultrasound for patients with new acute kidney injury

To determine if an acute kidney injury is caused by a treatable obstruction, such as a large prostate causing urinary retention, doctors often first order a renal ultrasound, a test that can cost $300, and must be read by a radiologist.

But a much less expensive simple bladder scan, which can be performed by a nurse, is a much better substitute for the first pass, Dr. Feldman said. He said it’s logical that “a bladder scan is a much higher value test” in the early diagnostic process.

“The studies have been pretty clear. If you don’t have risk factors for having an obstruction, a history of kidney stones, it hasn’t happened before, or other reasons kidneys aren’t working, it’s extraordinarily unlikely you’re going to find anything on that renal ultrasound that could be intervened to fix that acute kidney injury,” Dr. Feldman said. He pointed to a study that found 223 renal ultrasounds were necessary to find one patient who needed an intervention.

“You can probably get a good sense from the history and physical” and start to treat them, he said, and if they’re not getting better, then order the ultrasound.

Each of the items on Feldman’s list don’t necessarily save a lot of money, but they add up. “The more we ask ‘Why are we doing this? Can we stop it if it’s not helping people, and particularly if it’s harming people?’ the more we can prevent the cascade that happens because you did one unnecessary diagnostic test,” he concluded.

There’s no need to let fear of electronic interference between computed tomography and electronic medical devices preclude the ordering of such scans for patients with insulin pumps, cardiac implantable electronic devices, or neurostimulators, the Food and Drug Administration said in a written notification.

“The probability of an adverse event being caused by exposing these devices to CT irradiation is extremely low, and it is greatly outweighed by the clinical benefit of a medically indicated CT examination,” according to the new notification, which updates and replaces a preliminary health notification released on July 14, 2008.

The preliminary notification said there was a “possibility that the x-rays used during CT examinations may cause some implanted and external electronic medical devices to malfunction.” It also included recommendations to reduce the potential risk of such events from occurring and cited adverse events experienced by a few patients with medical devices who had undergone CT scanning, including unintended shocks from neurostimulators, malfunctions of insulin infusion pumps, and transient changes in pacemaker output pulse rate.

The new notification says there is an extremely low probability that a CT scanner directly irradiating the circuitry of certain implantable or wearable electronic medical devices can cause sufficient electronic interference to affect the function and operation of the medical device, and this probability is even lower when the radiation dose and the radiation dose rate are reduced. The FDA also notes that the interference is completely avoided when the medical device is outside of the primary x-ray beam of the CT scanner.

The update, which provides additional reports of adverse events by patients with electronic medical devices who had CT scans, states that the number of such events was small, compared with the number of patients with insulin pumps, cardiac implantable electronic devices, and neurostimulators who were scanned without adverse effects.

The FDA encourages health care providers and patients who suspect a problem with a medical imaging device to file a voluntary report through MedWatch, the FDA Safety Information and Adverse Event Reporting Program.

[email protected]

There’s no need to let fear of electronic interference between computed tomography and electronic medical devices preclude the ordering of such scans for patients with insulin pumps, cardiac implantable electronic devices, or neurostimulators, the Food and Drug Administration said in a written notification.

“The probability of an adverse event being caused by exposing these devices to CT irradiation is extremely low, and it is greatly outweighed by the clinical benefit of a medically indicated CT examination,” according to the new notification, which updates and replaces a preliminary health notification released on July 14, 2008.

The preliminary notification said there was a “possibility that the x-rays used during CT examinations may cause some implanted and external electronic medical devices to malfunction.” It also included recommendations to reduce the potential risk of such events from occurring and cited adverse events experienced by a few patients with medical devices who had undergone CT scanning, including unintended shocks from neurostimulators, malfunctions of insulin infusion pumps, and transient changes in pacemaker output pulse rate.

The new notification says there is an extremely low probability that a CT scanner directly irradiating the circuitry of certain implantable or wearable electronic medical devices can cause sufficient electronic interference to affect the function and operation of the medical device, and this probability is even lower when the radiation dose and the radiation dose rate are reduced. The FDA also notes that the interference is completely avoided when the medical device is outside of the primary x-ray beam of the CT scanner.

The update, which provides additional reports of adverse events by patients with electronic medical devices who had CT scans, states that the number of such events was small, compared with the number of patients with insulin pumps, cardiac implantable electronic devices, and neurostimulators who were scanned without adverse effects.

The FDA encourages health care providers and patients who suspect a problem with a medical imaging device to file a voluntary report through MedWatch, the FDA Safety Information and Adverse Event Reporting Program.

[email protected]

There’s no need to let fear of electronic interference between computed tomography and electronic medical devices preclude the ordering of such scans for patients with insulin pumps, cardiac implantable electronic devices, or neurostimulators, the Food and Drug Administration said in a written notification.

“The probability of an adverse event being caused by exposing these devices to CT irradiation is extremely low, and it is greatly outweighed by the clinical benefit of a medically indicated CT examination,” according to the new notification, which updates and replaces a preliminary health notification released on July 14, 2008.

The preliminary notification said there was a “possibility that the x-rays used during CT examinations may cause some implanted and external electronic medical devices to malfunction.” It also included recommendations to reduce the potential risk of such events from occurring and cited adverse events experienced by a few patients with medical devices who had undergone CT scanning, including unintended shocks from neurostimulators, malfunctions of insulin infusion pumps, and transient changes in pacemaker output pulse rate.

The new notification says there is an extremely low probability that a CT scanner directly irradiating the circuitry of certain implantable or wearable electronic medical devices can cause sufficient electronic interference to affect the function and operation of the medical device, and this probability is even lower when the radiation dose and the radiation dose rate are reduced. The FDA also notes that the interference is completely avoided when the medical device is outside of the primary x-ray beam of the CT scanner.

The update, which provides additional reports of adverse events by patients with electronic medical devices who had CT scans, states that the number of such events was small, compared with the number of patients with insulin pumps, cardiac implantable electronic devices, and neurostimulators who were scanned without adverse effects.

The FDA encourages health care providers and patients who suspect a problem with a medical imaging device to file a voluntary report through MedWatch, the FDA Safety Information and Adverse Event Reporting Program.

[email protected]

The incidental finding of high systolic pulmonary artery pressure on echocardiography is common. What we should do about it varies according to clinical presentation, comorbidities, and results of other tests, including assessment of the right ventricle. Thus, the optimal approach ranges from no further investigation to right heart catheterization and, in some cases, referral to a pulmonary hypertension center.

THE TWO MEASUREMENTS COMPARED

Although it raises concern, the finding of high systolic pulmonary artery pressure is not enough to diagnose pulmonary hypertension. In fact, several other conditions are associated with high systolic pulmonary artery pressure on echocardiography (Table 1). The diagnosis must be confirmed with right heart catheterization.¹

Echocardiography provides an estimate of the systolic pulmonary artery pressure that is calculated from other values, whereas right heart catheterization gives a direct measurement of the mean pulmonary artery pressure, which is necessary for diagnosing pulmonary hypertension. The two values are correlated, but the differences are noteworthy.

WHAT IS PULMONARY HYPERTENSION?

Pulmonary hypertension is defined by a resting mean pulmonary artery pressure 25 mm Hg or greater during right heart catheterization.¹ The large number of conditions associated with pulmonary hypertension can be divided into five groups²:

• Group 1, pulmonary artery hypertension
• Group 2, pulmonary hypertension associated with left heart disease
• Group 3, pulmonary hypertension due to chronic lung disease or hypoxia
• Group 4, chronic thromboembolic pulmonary hypertension
• Group 5, pulmonary hypertension due to unclear multifactorial mechanisms.²

Pulmonary artery hypertension (group 1) is a syndrome characterized by a restricted flow of small pulmonary arteries that can be idiopathic, heritable, or induced by anorexigens, connective tissue disease, congenital heart disease, portal hypertension, human immunodeficiency virus (HIV), or schistosomiasis.^2,3 In spite of significant advances in therapy in the last 3 decades, pulmonary artery hypertension continues to lead to right heart failure and death,⁴ and the diagnosis has adverse prognostic implications. Therefore, it is essential to be attentive when reviewing the echocardiogram, since an elevated systolic pulmonary artery pressure may be an important clue to pulmonary hypertension.

ESTIMATED PRESSURE: HOW HIGH IS TOO HIGH?

There is no consensus on the optimal cutoff of echocardiographic systolic pulmonary artery pressure to trigger a further evaluation for pulmonary hypertension.

A retrospective evaluation of nearly 16,000 normal echocardiograms found that the 95% upper limit for systolic pulmonary artery pressure was 37 mm Hg.⁵

European guidelines⁶ propose that pulmonary hypertension is unlikely if the estimated systolic pulmonary artery pressure is 36 mm Hg or lower, possible if it is 37 to 50 mm Hg, and likely if it is higher than 50 mm Hg.⁶

The 2009 consensus document of the American College of Cardiology Foundation and American Heart Association³ recommends a systolic pulmonary artery pressure greater than 40 mm Hg as the threshold to suggest further evaluation in a patient with unexplained dyspnea.

Converting the systolic pulmonary artery pressure to the mean pressure

Although not validated to use with echocardiography, the most accurate estimate of mean pulmonary artery pressure was shown in one study⁷ to be obtained with the equation:

0.61 × systolic pulmonary artery pressure
+ 2 mm Hg

Using this formula, a systolic pulmonary artery pressure of 37 mm Hg would correspond to a mean pulmonary artery pressure of 24.6 mm Hg. A systolic pulmonary artery pressure of 40 mm Hg would correspond to a mean pulmonary artery pressure of 26.4 mm Hg.

Estimated systolic pulmonary artery pressure depends on several variables

Systolic pulmonary artery pressure is estimated using the simplified Bernoulli equation⁸:

4 × tricuspid regurgitation jet velocity² (m/s)
+ right atrial pressure (mm Hg)

Tricuspid regurgitation is present in over 75% of the normal population. The regurgitation velocity across the tricuspid valve must be measured to estimate the pressure gradient between the right ventricle and the right atrium. The right atrial pressure is estimated from the diameter of the inferior vena cava and the degree of inspiratory collapse with the sniff test. As the right atrial pressure increases, the inferior vena cava dilates and inspiratory collapse decreases.⁸ If there is no gradient across the right ventricular outflow tract or pulmonary valve, the right ventricular systolic pressure is equal to the systolic pulmonary artery pressure.

Since tricuspid regurgitation velocity is squared and then multiplied by 4, small deviations of this measurement lead to markedly different systolic pulmonary artery pressure values. To avoid this problem, the tricuspid regurgitation velocity needs to be looked at in multiple echocardiographic views to find the best alignment with the flow and an adequate envelope.

Many causes of high estimated systolic pulmonary artery pressure

Table 1 shows conditions associated with a high estimated systolic pulmonary artery pressure. Echocardiographic limitations, constitutional factors, and high cardiac output states can lead to an apparent elevation in systolic pulmonary artery pressure, which is not confirmed later during right heart catheterization.

Systolic pulmonary artery pressure increases with age and body mass index as a result of worsening left ventricular diastolic dysfunction.⁸ In fact, an estimated pressure greater than 40 mm Hg is found⁵ in 6% of people over age 50 and in 5% of people with a body mass index greater than 30 kg/m². It can also be high in conditions in which there is an increase in cardiac output, such as pregnancy, anemia (sickle cell disease, thalassemia), cirrhosis, and arteriovenous fistula.

The estimated systolic value often differs from the measured value

Studies have compared the systolic pulmonary artery pressure measured during right heart catheterization with the estimated value on echocardiography.^9,10 These studies noted a reasonable degree of agreement between the tests but a substantial variability.

Both underestimation and overestimation of the systolic pulmonary artery pressure by echocardiography were common, with 95% limits of agreement ranging from minus 40 mm Hg to plus 40 mm Hg.^9,10 A difference of plus or minus 10 mm Hg in systolic pulmonary artery pressure between echocardiography and catheterization was observed in 48% to 51% of patients with pulmonary hypertension, particularly in those with higher systolic pulmonary artery pressure.^9,10

An important reason for overestimation of systolic pulmonary artery pressure is the inaccurate estimation of the right atrial pressure by echocardiography.^9,10 Indeed, this factor may account for half of the cases in which the systolic pulmonary artery pressure is overestimated.¹⁰ Although the traditional methods to estimate the right atrial pressure have been revisited,^8,11 this estimation is less reliable for intermediate pressure values, for patients on mechanical ventilation, and for young athletes.⁸

Other explanations for the variability between measured and estimated systolic pulmonary artery pressure include suboptimal alignment between the Doppler beam and the regurgitant jet, severe tricuspid regurgitation, arrhythmias, and limitations inherent to the simplified Bernoulli equation.¹² The estimated value is particularly inaccurate in patients with advanced lung disease, possibly owing to lung hyperinflation and alteration in the thoracic cavity and position of the heart—all factors that limit visualization and measurement of the tricuspid regurgitant jet.¹³

OTHER SIGNS OF PULMONARY HYPERTENSION ON ECHOCARDIOGRAPHY

Echocardiography provides information that is useful in assessing the accuracy of the estimated systolic pulmonary artery pressure, particularly right ventricular size and function.

As pulmonary hypertension progresses, the right ventricle dilates, and its function is compromised. Therefore, it is important to determine the right ventricular size and function by using objective echocardiographic findings such as right ventricular diameters (basal, mid, apical) and area, right ventricular fractional area change, tricuspid annular plane systolic excursion, myocardial performance index, and the pulsed tissue Doppler tricuspid annular peak systolic excursion velocity.⁸

Other echocardiographic features that suggest pulmonary hypertension include a dilated right atrial area, flattening of the interventricular septum, notching of the right ventricular outflow tract flow, and dilation of the main pulmonary artery. Interestingly, left ventricular diastolic dysfunction of the impaired relaxation type (grade I) is commonly observed in pulmonary hypertension¹⁴; however, more advanced degrees of diastolic dysfunction, ie, pseudonormalization (grade II) or restrictive left ventricular filling (grade III),¹⁵ particularly when associated with a left atrial enlargement, suggest pulmonary hypertension associated with left heart disease and not pulmonary artery hypertension.

WHAT TO DO IF ECHOCARDIOGRAPHY INDICATES PULMONARY HYPERTENSION

Adapted in part from the diagnostic approach to pulmonary hypertension recommended by the Fifth World Symposium on Pulmonary Hypertension (reference 6).

An algorithm showing the approach to an elevated systolic pulmonary artery pressure on echocardiography is presented in Figure 1.

In the appropriate clinical setting, if the systolic pulmonary artery pressure is 40 mm Hg or greater or if other echocardiographic variables suggest pulmonary hypertension, our practice is to proceed with right heart catheterization.

Clinical variables that suggest pulmonary hypertension include progressive dyspnea, chest pain, presyncope-syncope, lower extremity edema, hepatomegaly, jugular vein distention, hepatojugular reflux, sternal heave, loud second heart sound (P2), murmur of tricuspid or pulmonary regurgitation, and right ventricular third heart sound.¹⁶ These are of particular interest when associated with conditions known to cause pulmonary hypertension,²such as connective tissue disease, portal hypertension, congenital heart disease, HIV infection, and certain drugs and toxins.

Other tests that raise suspicion of pulmonary hypertension are an electrocardiogram suggesting a dilated right atrium or ventricle, an elevated brain natriuretic peptide level, a low carbon monoxide diffusing capacity on pulmonary function testing, and an enlarged pulmonary artery diameter on imaging.

Given the high prevalence of pulmonary hypertension, the Fifth World Symposium on Pulmonary Hypertension recommended first considering heart or parenchymal lung disease when an echocardiogram suggests pulmonary hypertension.⁶ If there are signs of severe pulmonary hypertension or right ventricular dysfunction, referral to a center specializing in pulmonary hypertension is recommended. Referral is also appropriate when there is no major heart or lung disease and the echocardiogram shows an elevated systolic pulmonary artery pressure, particularly when the clinical presentation or results of other testing suggest pulmonary hypertension.

TAKE-HOME POINTS

In the appropriate context, a high systolic pulmonary artery pressure on echocardiography suggests pulmonary hypertension, but right heart catheterization is needed to confirm the diagnosis. Estimating the systolic pulmonary artery pressure with echocardiography has limitations, including false-positive results, predominantly when the pretest probability of pulmonary hypertension is low.

The incidental finding of high systolic pulmonary artery pressure on echocardiography is common. What we should do about it varies according to clinical presentation, comorbidities, and results of other tests, including assessment of the right ventricle. Thus, the optimal approach ranges from no further investigation to right heart catheterization and, in some cases, referral to a pulmonary hypertension center.

THE TWO MEASUREMENTS COMPARED

Although it raises concern, the finding of high systolic pulmonary artery pressure is not enough to diagnose pulmonary hypertension. In fact, several other conditions are associated with high systolic pulmonary artery pressure on echocardiography (Table 1). The diagnosis must be confirmed with right heart catheterization.¹

Echocardiography provides an estimate of the systolic pulmonary artery pressure that is calculated from other values, whereas right heart catheterization gives a direct measurement of the mean pulmonary artery pressure, which is necessary for diagnosing pulmonary hypertension. The two values are correlated, but the differences are noteworthy.

WHAT IS PULMONARY HYPERTENSION?

Pulmonary hypertension is defined by a resting mean pulmonary artery pressure 25 mm Hg or greater during right heart catheterization.¹ The large number of conditions associated with pulmonary hypertension can be divided into five groups²:

• Group 1, pulmonary artery hypertension
• Group 2, pulmonary hypertension associated with left heart disease
• Group 3, pulmonary hypertension due to chronic lung disease or hypoxia
• Group 4, chronic thromboembolic pulmonary hypertension
• Group 5, pulmonary hypertension due to unclear multifactorial mechanisms.²

Pulmonary artery hypertension (group 1) is a syndrome characterized by a restricted flow of small pulmonary arteries that can be idiopathic, heritable, or induced by anorexigens, connective tissue disease, congenital heart disease, portal hypertension, human immunodeficiency virus (HIV), or schistosomiasis.^2,3 In spite of significant advances in therapy in the last 3 decades, pulmonary artery hypertension continues to lead to right heart failure and death,⁴ and the diagnosis has adverse prognostic implications. Therefore, it is essential to be attentive when reviewing the echocardiogram, since an elevated systolic pulmonary artery pressure may be an important clue to pulmonary hypertension.

ESTIMATED PRESSURE: HOW HIGH IS TOO HIGH?

There is no consensus on the optimal cutoff of echocardiographic systolic pulmonary artery pressure to trigger a further evaluation for pulmonary hypertension.

A retrospective evaluation of nearly 16,000 normal echocardiograms found that the 95% upper limit for systolic pulmonary artery pressure was 37 mm Hg.⁵

European guidelines⁶ propose that pulmonary hypertension is unlikely if the estimated systolic pulmonary artery pressure is 36 mm Hg or lower, possible if it is 37 to 50 mm Hg, and likely if it is higher than 50 mm Hg.⁶

The 2009 consensus document of the American College of Cardiology Foundation and American Heart Association³ recommends a systolic pulmonary artery pressure greater than 40 mm Hg as the threshold to suggest further evaluation in a patient with unexplained dyspnea.

Converting the systolic pulmonary artery pressure to the mean pressure

Although not validated to use with echocardiography, the most accurate estimate of mean pulmonary artery pressure was shown in one study⁷ to be obtained with the equation:

0.61 × systolic pulmonary artery pressure
+ 2 mm Hg

Using this formula, a systolic pulmonary artery pressure of 37 mm Hg would correspond to a mean pulmonary artery pressure of 24.6 mm Hg. A systolic pulmonary artery pressure of 40 mm Hg would correspond to a mean pulmonary artery pressure of 26.4 mm Hg.

Estimated systolic pulmonary artery pressure depends on several variables

Systolic pulmonary artery pressure is estimated using the simplified Bernoulli equation⁸:

4 × tricuspid regurgitation jet velocity² (m/s)
+ right atrial pressure (mm Hg)

Tricuspid regurgitation is present in over 75% of the normal population. The regurgitation velocity across the tricuspid valve must be measured to estimate the pressure gradient between the right ventricle and the right atrium. The right atrial pressure is estimated from the diameter of the inferior vena cava and the degree of inspiratory collapse with the sniff test. As the right atrial pressure increases, the inferior vena cava dilates and inspiratory collapse decreases.⁸ If there is no gradient across the right ventricular outflow tract or pulmonary valve, the right ventricular systolic pressure is equal to the systolic pulmonary artery pressure.

Since tricuspid regurgitation velocity is squared and then multiplied by 4, small deviations of this measurement lead to markedly different systolic pulmonary artery pressure values. To avoid this problem, the tricuspid regurgitation velocity needs to be looked at in multiple echocardiographic views to find the best alignment with the flow and an adequate envelope.

Many causes of high estimated systolic pulmonary artery pressure

Table 1 shows conditions associated with a high estimated systolic pulmonary artery pressure. Echocardiographic limitations, constitutional factors, and high cardiac output states can lead to an apparent elevation in systolic pulmonary artery pressure, which is not confirmed later during right heart catheterization.

Systolic pulmonary artery pressure increases with age and body mass index as a result of worsening left ventricular diastolic dysfunction.⁸ In fact, an estimated pressure greater than 40 mm Hg is found⁵ in 6% of people over age 50 and in 5% of people with a body mass index greater than 30 kg/m². It can also be high in conditions in which there is an increase in cardiac output, such as pregnancy, anemia (sickle cell disease, thalassemia), cirrhosis, and arteriovenous fistula.

The estimated systolic value often differs from the measured value

Studies have compared the systolic pulmonary artery pressure measured during right heart catheterization with the estimated value on echocardiography.^9,10 These studies noted a reasonable degree of agreement between the tests but a substantial variability.

Both underestimation and overestimation of the systolic pulmonary artery pressure by echocardiography were common, with 95% limits of agreement ranging from minus 40 mm Hg to plus 40 mm Hg.^9,10 A difference of plus or minus 10 mm Hg in systolic pulmonary artery pressure between echocardiography and catheterization was observed in 48% to 51% of patients with pulmonary hypertension, particularly in those with higher systolic pulmonary artery pressure.^9,10

An important reason for overestimation of systolic pulmonary artery pressure is the inaccurate estimation of the right atrial pressure by echocardiography.^9,10 Indeed, this factor may account for half of the cases in which the systolic pulmonary artery pressure is overestimated.¹⁰ Although the traditional methods to estimate the right atrial pressure have been revisited,^8,11 this estimation is less reliable for intermediate pressure values, for patients on mechanical ventilation, and for young athletes.⁸

Other explanations for the variability between measured and estimated systolic pulmonary artery pressure include suboptimal alignment between the Doppler beam and the regurgitant jet, severe tricuspid regurgitation, arrhythmias, and limitations inherent to the simplified Bernoulli equation.¹² The estimated value is particularly inaccurate in patients with advanced lung disease, possibly owing to lung hyperinflation and alteration in the thoracic cavity and position of the heart—all factors that limit visualization and measurement of the tricuspid regurgitant jet.¹³

OTHER SIGNS OF PULMONARY HYPERTENSION ON ECHOCARDIOGRAPHY

Echocardiography provides information that is useful in assessing the accuracy of the estimated systolic pulmonary artery pressure, particularly right ventricular size and function.

As pulmonary hypertension progresses, the right ventricle dilates, and its function is compromised. Therefore, it is important to determine the right ventricular size and function by using objective echocardiographic findings such as right ventricular diameters (basal, mid, apical) and area, right ventricular fractional area change, tricuspid annular plane systolic excursion, myocardial performance index, and the pulsed tissue Doppler tricuspid annular peak systolic excursion velocity.⁸

Other echocardiographic features that suggest pulmonary hypertension include a dilated right atrial area, flattening of the interventricular septum, notching of the right ventricular outflow tract flow, and dilation of the main pulmonary artery. Interestingly, left ventricular diastolic dysfunction of the impaired relaxation type (grade I) is commonly observed in pulmonary hypertension¹⁴; however, more advanced degrees of diastolic dysfunction, ie, pseudonormalization (grade II) or restrictive left ventricular filling (grade III),¹⁵ particularly when associated with a left atrial enlargement, suggest pulmonary hypertension associated with left heart disease and not pulmonary artery hypertension.

WHAT TO DO IF ECHOCARDIOGRAPHY INDICATES PULMONARY HYPERTENSION

Adapted in part from the diagnostic approach to pulmonary hypertension recommended by the Fifth World Symposium on Pulmonary Hypertension (reference 6).

An algorithm showing the approach to an elevated systolic pulmonary artery pressure on echocardiography is presented in Figure 1.

In the appropriate clinical setting, if the systolic pulmonary artery pressure is 40 mm Hg or greater or if other echocardiographic variables suggest pulmonary hypertension, our practice is to proceed with right heart catheterization.

Clinical variables that suggest pulmonary hypertension include progressive dyspnea, chest pain, presyncope-syncope, lower extremity edema, hepatomegaly, jugular vein distention, hepatojugular reflux, sternal heave, loud second heart sound (P2), murmur of tricuspid or pulmonary regurgitation, and right ventricular third heart sound.¹⁶ These are of particular interest when associated with conditions known to cause pulmonary hypertension,²such as connective tissue disease, portal hypertension, congenital heart disease, HIV infection, and certain drugs and toxins.

Other tests that raise suspicion of pulmonary hypertension are an electrocardiogram suggesting a dilated right atrium or ventricle, an elevated brain natriuretic peptide level, a low carbon monoxide diffusing capacity on pulmonary function testing, and an enlarged pulmonary artery diameter on imaging.

Given the high prevalence of pulmonary hypertension, the Fifth World Symposium on Pulmonary Hypertension recommended first considering heart or parenchymal lung disease when an echocardiogram suggests pulmonary hypertension.⁶ If there are signs of severe pulmonary hypertension or right ventricular dysfunction, referral to a center specializing in pulmonary hypertension is recommended. Referral is also appropriate when there is no major heart or lung disease and the echocardiogram shows an elevated systolic pulmonary artery pressure, particularly when the clinical presentation or results of other testing suggest pulmonary hypertension.

TAKE-HOME POINTS

In the appropriate context, a high systolic pulmonary artery pressure on echocardiography suggests pulmonary hypertension, but right heart catheterization is needed to confirm the diagnosis. Estimating the systolic pulmonary artery pressure with echocardiography has limitations, including false-positive results, predominantly when the pretest probability of pulmonary hypertension is low.

The incidental finding of high systolic pulmonary artery pressure on echocardiography is common. What we should do about it varies according to clinical presentation, comorbidities, and results of other tests, including assessment of the right ventricle. Thus, the optimal approach ranges from no further investigation to right heart catheterization and, in some cases, referral to a pulmonary hypertension center.

THE TWO MEASUREMENTS COMPARED

Although it raises concern, the finding of high systolic pulmonary artery pressure is not enough to diagnose pulmonary hypertension. In fact, several other conditions are associated with high systolic pulmonary artery pressure on echocardiography (Table 1). The diagnosis must be confirmed with right heart catheterization.¹

Echocardiography provides an estimate of the systolic pulmonary artery pressure that is calculated from other values, whereas right heart catheterization gives a direct measurement of the mean pulmonary artery pressure, which is necessary for diagnosing pulmonary hypertension. The two values are correlated, but the differences are noteworthy.

WHAT IS PULMONARY HYPERTENSION?

Pulmonary hypertension is defined by a resting mean pulmonary artery pressure 25 mm Hg or greater during right heart catheterization.¹ The large number of conditions associated with pulmonary hypertension can be divided into five groups²:

• Group 1, pulmonary artery hypertension
• Group 2, pulmonary hypertension associated with left heart disease
• Group 3, pulmonary hypertension due to chronic lung disease or hypoxia
• Group 4, chronic thromboembolic pulmonary hypertension
• Group 5, pulmonary hypertension due to unclear multifactorial mechanisms.²

Pulmonary artery hypertension (group 1) is a syndrome characterized by a restricted flow of small pulmonary arteries that can be idiopathic, heritable, or induced by anorexigens, connective tissue disease, congenital heart disease, portal hypertension, human immunodeficiency virus (HIV), or schistosomiasis.^2,3 In spite of significant advances in therapy in the last 3 decades, pulmonary artery hypertension continues to lead to right heart failure and death,⁴ and the diagnosis has adverse prognostic implications. Therefore, it is essential to be attentive when reviewing the echocardiogram, since an elevated systolic pulmonary artery pressure may be an important clue to pulmonary hypertension.

ESTIMATED PRESSURE: HOW HIGH IS TOO HIGH?

There is no consensus on the optimal cutoff of echocardiographic systolic pulmonary artery pressure to trigger a further evaluation for pulmonary hypertension.

A retrospective evaluation of nearly 16,000 normal echocardiograms found that the 95% upper limit for systolic pulmonary artery pressure was 37 mm Hg.⁵

European guidelines⁶ propose that pulmonary hypertension is unlikely if the estimated systolic pulmonary artery pressure is 36 mm Hg or lower, possible if it is 37 to 50 mm Hg, and likely if it is higher than 50 mm Hg.⁶

The 2009 consensus document of the American College of Cardiology Foundation and American Heart Association³ recommends a systolic pulmonary artery pressure greater than 40 mm Hg as the threshold to suggest further evaluation in a patient with unexplained dyspnea.

Converting the systolic pulmonary artery pressure to the mean pressure

Although not validated to use with echocardiography, the most accurate estimate of mean pulmonary artery pressure was shown in one study⁷ to be obtained with the equation:

0.61 × systolic pulmonary artery pressure
+ 2 mm Hg

Using this formula, a systolic pulmonary artery pressure of 37 mm Hg would correspond to a mean pulmonary artery pressure of 24.6 mm Hg. A systolic pulmonary artery pressure of 40 mm Hg would correspond to a mean pulmonary artery pressure of 26.4 mm Hg.

Estimated systolic pulmonary artery pressure depends on several variables

Systolic pulmonary artery pressure is estimated using the simplified Bernoulli equation⁸:

4 × tricuspid regurgitation jet velocity² (m/s)
+ right atrial pressure (mm Hg)

Tricuspid regurgitation is present in over 75% of the normal population. The regurgitation velocity across the tricuspid valve must be measured to estimate the pressure gradient between the right ventricle and the right atrium. The right atrial pressure is estimated from the diameter of the inferior vena cava and the degree of inspiratory collapse with the sniff test. As the right atrial pressure increases, the inferior vena cava dilates and inspiratory collapse decreases.⁸ If there is no gradient across the right ventricular outflow tract or pulmonary valve, the right ventricular systolic pressure is equal to the systolic pulmonary artery pressure.

Since tricuspid regurgitation velocity is squared and then multiplied by 4, small deviations of this measurement lead to markedly different systolic pulmonary artery pressure values. To avoid this problem, the tricuspid regurgitation velocity needs to be looked at in multiple echocardiographic views to find the best alignment with the flow and an adequate envelope.

Many causes of high estimated systolic pulmonary artery pressure

Table 1 shows conditions associated with a high estimated systolic pulmonary artery pressure. Echocardiographic limitations, constitutional factors, and high cardiac output states can lead to an apparent elevation in systolic pulmonary artery pressure, which is not confirmed later during right heart catheterization.

Systolic pulmonary artery pressure increases with age and body mass index as a result of worsening left ventricular diastolic dysfunction.⁸ In fact, an estimated pressure greater than 40 mm Hg is found⁵ in 6% of people over age 50 and in 5% of people with a body mass index greater than 30 kg/m². It can also be high in conditions in which there is an increase in cardiac output, such as pregnancy, anemia (sickle cell disease, thalassemia), cirrhosis, and arteriovenous fistula.

The estimated systolic value often differs from the measured value

Studies have compared the systolic pulmonary artery pressure measured during right heart catheterization with the estimated value on echocardiography.^9,10 These studies noted a reasonable degree of agreement between the tests but a substantial variability.

Both underestimation and overestimation of the systolic pulmonary artery pressure by echocardiography were common, with 95% limits of agreement ranging from minus 40 mm Hg to plus 40 mm Hg.^9,10 A difference of plus or minus 10 mm Hg in systolic pulmonary artery pressure between echocardiography and catheterization was observed in 48% to 51% of patients with pulmonary hypertension, particularly in those with higher systolic pulmonary artery pressure.^9,10

An important reason for overestimation of systolic pulmonary artery pressure is the inaccurate estimation of the right atrial pressure by echocardiography.^9,10 Indeed, this factor may account for half of the cases in which the systolic pulmonary artery pressure is overestimated.¹⁰ Although the traditional methods to estimate the right atrial pressure have been revisited,^8,11 this estimation is less reliable for intermediate pressure values, for patients on mechanical ventilation, and for young athletes.⁸

Other explanations for the variability between measured and estimated systolic pulmonary artery pressure include suboptimal alignment between the Doppler beam and the regurgitant jet, severe tricuspid regurgitation, arrhythmias, and limitations inherent to the simplified Bernoulli equation.¹² The estimated value is particularly inaccurate in patients with advanced lung disease, possibly owing to lung hyperinflation and alteration in the thoracic cavity and position of the heart—all factors that limit visualization and measurement of the tricuspid regurgitant jet.¹³

OTHER SIGNS OF PULMONARY HYPERTENSION ON ECHOCARDIOGRAPHY

Echocardiography provides information that is useful in assessing the accuracy of the estimated systolic pulmonary artery pressure, particularly right ventricular size and function.

As pulmonary hypertension progresses, the right ventricle dilates, and its function is compromised. Therefore, it is important to determine the right ventricular size and function by using objective echocardiographic findings such as right ventricular diameters (basal, mid, apical) and area, right ventricular fractional area change, tricuspid annular plane systolic excursion, myocardial performance index, and the pulsed tissue Doppler tricuspid annular peak systolic excursion velocity.⁸

Other echocardiographic features that suggest pulmonary hypertension include a dilated right atrial area, flattening of the interventricular septum, notching of the right ventricular outflow tract flow, and dilation of the main pulmonary artery. Interestingly, left ventricular diastolic dysfunction of the impaired relaxation type (grade I) is commonly observed in pulmonary hypertension¹⁴; however, more advanced degrees of diastolic dysfunction, ie, pseudonormalization (grade II) or restrictive left ventricular filling (grade III),¹⁵ particularly when associated with a left atrial enlargement, suggest pulmonary hypertension associated with left heart disease and not pulmonary artery hypertension.

WHAT TO DO IF ECHOCARDIOGRAPHY INDICATES PULMONARY HYPERTENSION

Adapted in part from the diagnostic approach to pulmonary hypertension recommended by the Fifth World Symposium on Pulmonary Hypertension (reference 6).

An algorithm showing the approach to an elevated systolic pulmonary artery pressure on echocardiography is presented in Figure 1.

In the appropriate clinical setting, if the systolic pulmonary artery pressure is 40 mm Hg or greater or if other echocardiographic variables suggest pulmonary hypertension, our practice is to proceed with right heart catheterization.

Clinical variables that suggest pulmonary hypertension include progressive dyspnea, chest pain, presyncope-syncope, lower extremity edema, hepatomegaly, jugular vein distention, hepatojugular reflux, sternal heave, loud second heart sound (P2), murmur of tricuspid or pulmonary regurgitation, and right ventricular third heart sound.¹⁶ These are of particular interest when associated with conditions known to cause pulmonary hypertension,²such as connective tissue disease, portal hypertension, congenital heart disease, HIV infection, and certain drugs and toxins.

Other tests that raise suspicion of pulmonary hypertension are an electrocardiogram suggesting a dilated right atrium or ventricle, an elevated brain natriuretic peptide level, a low carbon monoxide diffusing capacity on pulmonary function testing, and an enlarged pulmonary artery diameter on imaging.

Given the high prevalence of pulmonary hypertension, the Fifth World Symposium on Pulmonary Hypertension recommended first considering heart or parenchymal lung disease when an echocardiogram suggests pulmonary hypertension.⁶ If there are signs of severe pulmonary hypertension or right ventricular dysfunction, referral to a center specializing in pulmonary hypertension is recommended. Referral is also appropriate when there is no major heart or lung disease and the echocardiogram shows an elevated systolic pulmonary artery pressure, particularly when the clinical presentation or results of other testing suggest pulmonary hypertension.

TAKE-HOME POINTS

In the appropriate context, a high systolic pulmonary artery pressure on echocardiography suggests pulmonary hypertension, but right heart catheterization is needed to confirm the diagnosis. Estimating the systolic pulmonary artery pressure with echocardiography has limitations, including false-positive results, predominantly when the pretest probability of pulmonary hypertension is low.