Imaging

A 39-year-old woman with a history of human immunodeficiency virus (HIV) and hepatitis B virus infection was brought to the emergency department for evaluation of seizures, which had started a few days earlier. She was born and raised in a state bordering the Ohio River, an area where Histoplasma capsulatum is endemic. She denied any recent travel.

Her vital signs and neurologic examination were normal. Computed tomography of the head showed two areas of increased attenuation anterior to the frontal horns. To better characterize those lesions, magnetic resonance imaging (MRI) with contrast was done, which showed about a dozen 1-cm ring-enhancing lesions in the right cerebellum and both cerebral hemispheres (Figure 1).

Results of a complete blood cell count, metabolic profile, and chest radiography were normal. Her CD4 count was 428/μL (reference range 533–1,674) and 20% (60%–89%); her HIV viral load was 326,000 copies/mL.

She was initially treated empirically with sulfadiazine, pyrimethamine, and leukovorin for possible toxoplasmosis, which is the most common cause of ring-enhancing brain lesions in HIV patients. In the meantime, cerebrospinal fluid, blood, and urine were sent for a detailed workup for fungi, including Histoplasma. Results of the Histoplasma antibody and antigen studies of the serum, urine, and cerebrospinal fluid were positive, while cerebrospinal fluid testing for Toxoplasma by polymerase chain reaction testing was negative. Empirical treatment for toxoplasmosis was stopped and amphotericin B was started to treat disseminated histoplasmosis.

During her hospital course, she underwent brain biopsy via right frontotemporal craniotomy with resection of right frontal lesions. Pathologic study showed partially organizing abscesses with central necrosis (Figure 2), microscopy with Grocott-Gomori methenamine silver stain was positive for budding yeast forms consistent with H capsulatum (Figure 3), and special stain for acid-fast bacilli was negative for mycobacteria. Cultures of the brain biopsy specimen, blood, and cerebrospinal fluid for fungi, acid-fast bacilli, and bacteria did not reveal any growth after 28 days.

The patient was discharged home with instructions to take amphotericin B for a total of 6 weeks and then itraconazole. About 1 year later, she remained free of symptoms, although repeat MRI did not show any significant change in the size or number of histoplasmomas.

She did not comply well with her HIV treatment, and her immune status did not improve, so we decided to continue her itraconazole treatment for more than 1 year.

CEREBRAL HISTOPLASMOMA

The term “histoplasmoma” was introduced by Shapiro et al¹ in 1955, when they first described numerous focal areas of softening, up to 1 cm in diameter, scattered throughout the brain at autopsy in a 41-year-old man who had died of disseminated histoplasmosis. They coined the word to describe these discrete areas of necrosis that might resemble tumors on the basis of their size, location, and capability of causing increased intracranial pressure.

Central nervous system involvement can either be a manifestation of disseminated disease or present as an isolated illness.² It occurs in 5% to 10% of cases of disseminated histoplasmosis.³ Histoplasmosis of the central nervous system can have different manifestations; the most common presentation is chronic meningitis.⁴

Laboratory diagnosis is based on detecting H capsulatum antigen and antibody in the urine, blood, and cerebrospinal fluid. Tissue biopsy (histopathology) as well as cultures of tissue samples or body fluids may also establish the diagnosis.⁴

Toxoplasmosis and primary central nervous system lymphoma are the most common causes of brain ring-enhancing lesions in HIV patients in developed countries, while in the developing world neurocysticercosis and tuberculomas are more common.^5,6 Much less common causes include brain abscesses secondary to bacterial infections (pyogenic abscess),⁷ cryptococcomas,⁸ syphilitic cerebral gummata,⁹ primary brain tumors (gliomas), and metastases.¹⁰

Compared with other forms of the disease, histoplasmosis of the central nervous system has higher rates of treatment failure and relapse, so treatment should be prolonged and aggressive.^2,3 The cure rate with amphotericin B ranges from 33% to 61%, and higher doses produce better response rates.³

Current treatment recommendations are based on 2007 guidelines of the Infectious Diseases Society of America.¹¹ Liposomal amphotericin B is the drug of choice because it achieves higher concentrations in the central nervous system than other drugs and is less toxic. It is given for 4 to 6 weeks, followed by itraconazole for at least 1 year and until the cerebrospinal fluid Histoplasma antigen test is negative and other cerebrospinal fluid abnormalities are resolved.

In patients who have primary disseminated histoplasmosis that includes the central nervous system, itraconazole can be given for more than 1 year or until immune recovery is achieved—or lifelong if necessary.^2,12 Long-term suppressive antifungal therapy also should be considered in patients for whom appropriate initial therapy fails.²

Nephrotoxicity (acute kidney injury, hypokalemia, and hypomagnesemia), infusion-related drug reactions, and rash are among the well-described side effects of amphotericin B. Maintenance of intravascular volume and replacement of electrolytes should be an integral part of the amphotericin B treatment regimen.¹³

TAKE-AWAY POINTS

• Histoplasmomas should be considered in the differential diagnosis of ring-enhancing lesions of the central nervous system, along with toxoplasmosis and primary central nervous system lymphoma. This will allow timely initiation of the diagnostic workup, avoiding unnecessary and potentially risky interventions and delays in starting targeted antifungal therapy.
• There is no single gold standard test for central nervous system histoplasmosis. Rather, the final diagnosis is based on the combination of clinical, laboratory, and radiologic findings.

Acknowledgment: Library research assistance provided by HSHS St. John’s Hospital Health Sciences Library staff.

A 39-year-old woman with a history of human immunodeficiency virus (HIV) and hepatitis B virus infection was brought to the emergency department for evaluation of seizures, which had started a few days earlier. She was born and raised in a state bordering the Ohio River, an area where Histoplasma capsulatum is endemic. She denied any recent travel.

Her vital signs and neurologic examination were normal. Computed tomography of the head showed two areas of increased attenuation anterior to the frontal horns. To better characterize those lesions, magnetic resonance imaging (MRI) with contrast was done, which showed about a dozen 1-cm ring-enhancing lesions in the right cerebellum and both cerebral hemispheres (Figure 1).

Results of a complete blood cell count, metabolic profile, and chest radiography were normal. Her CD4 count was 428/μL (reference range 533–1,674) and 20% (60%–89%); her HIV viral load was 326,000 copies/mL.

She was initially treated empirically with sulfadiazine, pyrimethamine, and leukovorin for possible toxoplasmosis, which is the most common cause of ring-enhancing brain lesions in HIV patients. In the meantime, cerebrospinal fluid, blood, and urine were sent for a detailed workup for fungi, including Histoplasma. Results of the Histoplasma antibody and antigen studies of the serum, urine, and cerebrospinal fluid were positive, while cerebrospinal fluid testing for Toxoplasma by polymerase chain reaction testing was negative. Empirical treatment for toxoplasmosis was stopped and amphotericin B was started to treat disseminated histoplasmosis.

During her hospital course, she underwent brain biopsy via right frontotemporal craniotomy with resection of right frontal lesions. Pathologic study showed partially organizing abscesses with central necrosis (Figure 2), microscopy with Grocott-Gomori methenamine silver stain was positive for budding yeast forms consistent with H capsulatum (Figure 3), and special stain for acid-fast bacilli was negative for mycobacteria. Cultures of the brain biopsy specimen, blood, and cerebrospinal fluid for fungi, acid-fast bacilli, and bacteria did not reveal any growth after 28 days.

The patient was discharged home with instructions to take amphotericin B for a total of 6 weeks and then itraconazole. About 1 year later, she remained free of symptoms, although repeat MRI did not show any significant change in the size or number of histoplasmomas.

She did not comply well with her HIV treatment, and her immune status did not improve, so we decided to continue her itraconazole treatment for more than 1 year.

CEREBRAL HISTOPLASMOMA

The term “histoplasmoma” was introduced by Shapiro et al¹ in 1955, when they first described numerous focal areas of softening, up to 1 cm in diameter, scattered throughout the brain at autopsy in a 41-year-old man who had died of disseminated histoplasmosis. They coined the word to describe these discrete areas of necrosis that might resemble tumors on the basis of their size, location, and capability of causing increased intracranial pressure.

Central nervous system involvement can either be a manifestation of disseminated disease or present as an isolated illness.² It occurs in 5% to 10% of cases of disseminated histoplasmosis.³ Histoplasmosis of the central nervous system can have different manifestations; the most common presentation is chronic meningitis.⁴

Laboratory diagnosis is based on detecting H capsulatum antigen and antibody in the urine, blood, and cerebrospinal fluid. Tissue biopsy (histopathology) as well as cultures of tissue samples or body fluids may also establish the diagnosis.⁴

Toxoplasmosis and primary central nervous system lymphoma are the most common causes of brain ring-enhancing lesions in HIV patients in developed countries, while in the developing world neurocysticercosis and tuberculomas are more common.^5,6 Much less common causes include brain abscesses secondary to bacterial infections (pyogenic abscess),⁷ cryptococcomas,⁸ syphilitic cerebral gummata,⁹ primary brain tumors (gliomas), and metastases.¹⁰

Compared with other forms of the disease, histoplasmosis of the central nervous system has higher rates of treatment failure and relapse, so treatment should be prolonged and aggressive.^2,3 The cure rate with amphotericin B ranges from 33% to 61%, and higher doses produce better response rates.³

Current treatment recommendations are based on 2007 guidelines of the Infectious Diseases Society of America.¹¹ Liposomal amphotericin B is the drug of choice because it achieves higher concentrations in the central nervous system than other drugs and is less toxic. It is given for 4 to 6 weeks, followed by itraconazole for at least 1 year and until the cerebrospinal fluid Histoplasma antigen test is negative and other cerebrospinal fluid abnormalities are resolved.

In patients who have primary disseminated histoplasmosis that includes the central nervous system, itraconazole can be given for more than 1 year or until immune recovery is achieved—or lifelong if necessary.^2,12 Long-term suppressive antifungal therapy also should be considered in patients for whom appropriate initial therapy fails.²

Nephrotoxicity (acute kidney injury, hypokalemia, and hypomagnesemia), infusion-related drug reactions, and rash are among the well-described side effects of amphotericin B. Maintenance of intravascular volume and replacement of electrolytes should be an integral part of the amphotericin B treatment regimen.¹³

TAKE-AWAY POINTS

• Histoplasmomas should be considered in the differential diagnosis of ring-enhancing lesions of the central nervous system, along with toxoplasmosis and primary central nervous system lymphoma. This will allow timely initiation of the diagnostic workup, avoiding unnecessary and potentially risky interventions and delays in starting targeted antifungal therapy.
• There is no single gold standard test for central nervous system histoplasmosis. Rather, the final diagnosis is based on the combination of clinical, laboratory, and radiologic findings.

Acknowledgment: Library research assistance provided by HSHS St. John’s Hospital Health Sciences Library staff.

A 39-year-old woman with a history of human immunodeficiency virus (HIV) and hepatitis B virus infection was brought to the emergency department for evaluation of seizures, which had started a few days earlier. She was born and raised in a state bordering the Ohio River, an area where Histoplasma capsulatum is endemic. She denied any recent travel.

Her vital signs and neurologic examination were normal. Computed tomography of the head showed two areas of increased attenuation anterior to the frontal horns. To better characterize those lesions, magnetic resonance imaging (MRI) with contrast was done, which showed about a dozen 1-cm ring-enhancing lesions in the right cerebellum and both cerebral hemispheres (Figure 1).

Results of a complete blood cell count, metabolic profile, and chest radiography were normal. Her CD4 count was 428/μL (reference range 533–1,674) and 20% (60%–89%); her HIV viral load was 326,000 copies/mL.

She was initially treated empirically with sulfadiazine, pyrimethamine, and leukovorin for possible toxoplasmosis, which is the most common cause of ring-enhancing brain lesions in HIV patients. In the meantime, cerebrospinal fluid, blood, and urine were sent for a detailed workup for fungi, including Histoplasma. Results of the Histoplasma antibody and antigen studies of the serum, urine, and cerebrospinal fluid were positive, while cerebrospinal fluid testing for Toxoplasma by polymerase chain reaction testing was negative. Empirical treatment for toxoplasmosis was stopped and amphotericin B was started to treat disseminated histoplasmosis.

During her hospital course, she underwent brain biopsy via right frontotemporal craniotomy with resection of right frontal lesions. Pathologic study showed partially organizing abscesses with central necrosis (Figure 2), microscopy with Grocott-Gomori methenamine silver stain was positive for budding yeast forms consistent with H capsulatum (Figure 3), and special stain for acid-fast bacilli was negative for mycobacteria. Cultures of the brain biopsy specimen, blood, and cerebrospinal fluid for fungi, acid-fast bacilli, and bacteria did not reveal any growth after 28 days.

The patient was discharged home with instructions to take amphotericin B for a total of 6 weeks and then itraconazole. About 1 year later, she remained free of symptoms, although repeat MRI did not show any significant change in the size or number of histoplasmomas.

She did not comply well with her HIV treatment, and her immune status did not improve, so we decided to continue her itraconazole treatment for more than 1 year.

CEREBRAL HISTOPLASMOMA

The term “histoplasmoma” was introduced by Shapiro et al¹ in 1955, when they first described numerous focal areas of softening, up to 1 cm in diameter, scattered throughout the brain at autopsy in a 41-year-old man who had died of disseminated histoplasmosis. They coined the word to describe these discrete areas of necrosis that might resemble tumors on the basis of their size, location, and capability of causing increased intracranial pressure.

Central nervous system involvement can either be a manifestation of disseminated disease or present as an isolated illness.² It occurs in 5% to 10% of cases of disseminated histoplasmosis.³ Histoplasmosis of the central nervous system can have different manifestations; the most common presentation is chronic meningitis.⁴

Laboratory diagnosis is based on detecting H capsulatum antigen and antibody in the urine, blood, and cerebrospinal fluid. Tissue biopsy (histopathology) as well as cultures of tissue samples or body fluids may also establish the diagnosis.⁴

Toxoplasmosis and primary central nervous system lymphoma are the most common causes of brain ring-enhancing lesions in HIV patients in developed countries, while in the developing world neurocysticercosis and tuberculomas are more common.^5,6 Much less common causes include brain abscesses secondary to bacterial infections (pyogenic abscess),⁷ cryptococcomas,⁸ syphilitic cerebral gummata,⁹ primary brain tumors (gliomas), and metastases.¹⁰

Compared with other forms of the disease, histoplasmosis of the central nervous system has higher rates of treatment failure and relapse, so treatment should be prolonged and aggressive.^2,3 The cure rate with amphotericin B ranges from 33% to 61%, and higher doses produce better response rates.³

Current treatment recommendations are based on 2007 guidelines of the Infectious Diseases Society of America.¹¹ Liposomal amphotericin B is the drug of choice because it achieves higher concentrations in the central nervous system than other drugs and is less toxic. It is given for 4 to 6 weeks, followed by itraconazole for at least 1 year and until the cerebrospinal fluid Histoplasma antigen test is negative and other cerebrospinal fluid abnormalities are resolved.

In patients who have primary disseminated histoplasmosis that includes the central nervous system, itraconazole can be given for more than 1 year or until immune recovery is achieved—or lifelong if necessary.^2,12 Long-term suppressive antifungal therapy also should be considered in patients for whom appropriate initial therapy fails.²

Nephrotoxicity (acute kidney injury, hypokalemia, and hypomagnesemia), infusion-related drug reactions, and rash are among the well-described side effects of amphotericin B. Maintenance of intravascular volume and replacement of electrolytes should be an integral part of the amphotericin B treatment regimen.¹³

TAKE-AWAY POINTS

• Histoplasmomas should be considered in the differential diagnosis of ring-enhancing lesions of the central nervous system, along with toxoplasmosis and primary central nervous system lymphoma. This will allow timely initiation of the diagnostic workup, avoiding unnecessary and potentially risky interventions and delays in starting targeted antifungal therapy.
• There is no single gold standard test for central nervous system histoplasmosis. Rather, the final diagnosis is based on the combination of clinical, laboratory, and radiologic findings.

Acknowledgment: Library research assistance provided by HSHS St. John’s Hospital Health Sciences Library staff.

Despite advances in therapy, more than 10% of patients with acute bacterial meningitis still die of it, and more suffer significant morbidity, including cognitive dysfunction and deafness. Well-defined protocols that include empiric antibiotics and systemic corticosteroids have improved the outcomes of patients with meningitis. But, as with other closed-space infections such as septic arthritis, any delay in providing appropriate antibiotic treatment is associated with a worse prognosis. In the case of bacterial meningitis, a retrospective analysis concluded that each hour of delay in delivering antibiotics and a corticosteroid can be associated with a relative (not absolute) increase in mortality of 13%.¹

The precise diagnosis of bacterial meningitis depends entirely on obtaining cerebrospinal fluid for analysis, including culture and antibiotic sensitivity testing. But that simple statement belies several current and historical complexities. From my experience, getting a prompt diagnostic lumbar puncture is not as simple as it once was.

Many hospitals have imposed patient safety initiatives, which overall have been beneficial but have had the effect that medical residents and probably even hospitalists in some medical centers are less frequently the ones doing interventional procedures. Some procedures, such as placement of pulmonary arterial catheters in the medical intensive care unit, have been shown to be less useful and to pose more risk than once believed. The tasks of placing other central lines and performing thoracenteses have been relegated to special procedure teams trained in using ultrasound guidance. Interventional radiologists now often do the visceral biopsies and lumbar punctures, and as a result, it is hoped that procedural complication rates will decline. On the other hand, these changes mean that medical residents and future staff are less experienced in performing these procedures, even though there are times that they are the only ones available to perform them. The result is a potential delay in performing a necessary lumbar puncture.

Another reason that a lumbar puncture may be delayed is concern over iatrogenic herniation if the procedure is done in a patient who has elevated intracranial pressure. We do not know precisely how often this occurs if there is an undiagnosed brain mass lesion such as an abscess, which can mimic bacterial meningitis, or a malignancy, and meningitis itself may be associated with herniation. Yet, for years physicians have hesitated to perform lumbar punctures in some patients without first ruling out a brain mass by computed tomography (CT), a diagnostic flow algorithm that often introduces at least an hour of delay in performing the procedure and in obtaining cultures before starting antibiotics.

When I was in training, we were perhaps more cavalier, appropriately or not. If the history and examination did not suggest a brain mass and the patient had retinal vein pulsations without papilledema, we did the lumbar puncture. It was a different time, and there was a different perspective on risks and benefits. More recently, the trend has been to obtain a CT scan before a lumbar puncture in several subsets of patients.

A 2015 analysis from Sweden¹ showed that we can probably do a lumbar puncture for suspected bacterial meningitis without first doing a CT scan in most patients, even in patients with moderately impaired mentation. Perhaps some other concerns can also be assuaged if evaluated, but we don’t have data. Mirrakhimov et al, in this issue of the Journal, review the current evidence on when to do CT before a lumbar puncture, even if it may significantly delay the procedure and the timely delivery of antibiotics. A perfect algorithm that balances the risks of delaying treatment, initiating less-than-ideal empiric antibiotics potentially without definitive culture, and inducing complications from a procedure done promptly may well be impossible to develop. Evidence helps us refine the diagnostic approach, but with limited data, some important decisions unfortunately remain within the “art” rather than the science of medicine.

Despite advances in therapy, more than 10% of patients with acute bacterial meningitis still die of it, and more suffer significant morbidity, including cognitive dysfunction and deafness. Well-defined protocols that include empiric antibiotics and systemic corticosteroids have improved the outcomes of patients with meningitis. But, as with other closed-space infections such as septic arthritis, any delay in providing appropriate antibiotic treatment is associated with a worse prognosis. In the case of bacterial meningitis, a retrospective analysis concluded that each hour of delay in delivering antibiotics and a corticosteroid can be associated with a relative (not absolute) increase in mortality of 13%.¹

The precise diagnosis of bacterial meningitis depends entirely on obtaining cerebrospinal fluid for analysis, including culture and antibiotic sensitivity testing. But that simple statement belies several current and historical complexities. From my experience, getting a prompt diagnostic lumbar puncture is not as simple as it once was.

Many hospitals have imposed patient safety initiatives, which overall have been beneficial but have had the effect that medical residents and probably even hospitalists in some medical centers are less frequently the ones doing interventional procedures. Some procedures, such as placement of pulmonary arterial catheters in the medical intensive care unit, have been shown to be less useful and to pose more risk than once believed. The tasks of placing other central lines and performing thoracenteses have been relegated to special procedure teams trained in using ultrasound guidance. Interventional radiologists now often do the visceral biopsies and lumbar punctures, and as a result, it is hoped that procedural complication rates will decline. On the other hand, these changes mean that medical residents and future staff are less experienced in performing these procedures, even though there are times that they are the only ones available to perform them. The result is a potential delay in performing a necessary lumbar puncture.

Another reason that a lumbar puncture may be delayed is concern over iatrogenic herniation if the procedure is done in a patient who has elevated intracranial pressure. We do not know precisely how often this occurs if there is an undiagnosed brain mass lesion such as an abscess, which can mimic bacterial meningitis, or a malignancy, and meningitis itself may be associated with herniation. Yet, for years physicians have hesitated to perform lumbar punctures in some patients without first ruling out a brain mass by computed tomography (CT), a diagnostic flow algorithm that often introduces at least an hour of delay in performing the procedure and in obtaining cultures before starting antibiotics.

When I was in training, we were perhaps more cavalier, appropriately or not. If the history and examination did not suggest a brain mass and the patient had retinal vein pulsations without papilledema, we did the lumbar puncture. It was a different time, and there was a different perspective on risks and benefits. More recently, the trend has been to obtain a CT scan before a lumbar puncture in several subsets of patients.

A 2015 analysis from Sweden¹ showed that we can probably do a lumbar puncture for suspected bacterial meningitis without first doing a CT scan in most patients, even in patients with moderately impaired mentation. Perhaps some other concerns can also be assuaged if evaluated, but we don’t have data. Mirrakhimov et al, in this issue of the Journal, review the current evidence on when to do CT before a lumbar puncture, even if it may significantly delay the procedure and the timely delivery of antibiotics. A perfect algorithm that balances the risks of delaying treatment, initiating less-than-ideal empiric antibiotics potentially without definitive culture, and inducing complications from a procedure done promptly may well be impossible to develop. Evidence helps us refine the diagnostic approach, but with limited data, some important decisions unfortunately remain within the “art” rather than the science of medicine.

Despite advances in therapy, more than 10% of patients with acute bacterial meningitis still die of it, and more suffer significant morbidity, including cognitive dysfunction and deafness. Well-defined protocols that include empiric antibiotics and systemic corticosteroids have improved the outcomes of patients with meningitis. But, as with other closed-space infections such as septic arthritis, any delay in providing appropriate antibiotic treatment is associated with a worse prognosis. In the case of bacterial meningitis, a retrospective analysis concluded that each hour of delay in delivering antibiotics and a corticosteroid can be associated with a relative (not absolute) increase in mortality of 13%.¹

The precise diagnosis of bacterial meningitis depends entirely on obtaining cerebrospinal fluid for analysis, including culture and antibiotic sensitivity testing. But that simple statement belies several current and historical complexities. From my experience, getting a prompt diagnostic lumbar puncture is not as simple as it once was.

Many hospitals have imposed patient safety initiatives, which overall have been beneficial but have had the effect that medical residents and probably even hospitalists in some medical centers are less frequently the ones doing interventional procedures. Some procedures, such as placement of pulmonary arterial catheters in the medical intensive care unit, have been shown to be less useful and to pose more risk than once believed. The tasks of placing other central lines and performing thoracenteses have been relegated to special procedure teams trained in using ultrasound guidance. Interventional radiologists now often do the visceral biopsies and lumbar punctures, and as a result, it is hoped that procedural complication rates will decline. On the other hand, these changes mean that medical residents and future staff are less experienced in performing these procedures, even though there are times that they are the only ones available to perform them. The result is a potential delay in performing a necessary lumbar puncture.

Another reason that a lumbar puncture may be delayed is concern over iatrogenic herniation if the procedure is done in a patient who has elevated intracranial pressure. We do not know precisely how often this occurs if there is an undiagnosed brain mass lesion such as an abscess, which can mimic bacterial meningitis, or a malignancy, and meningitis itself may be associated with herniation. Yet, for years physicians have hesitated to perform lumbar punctures in some patients without first ruling out a brain mass by computed tomography (CT), a diagnostic flow algorithm that often introduces at least an hour of delay in performing the procedure and in obtaining cultures before starting antibiotics.

When I was in training, we were perhaps more cavalier, appropriately or not. If the history and examination did not suggest a brain mass and the patient had retinal vein pulsations without papilledema, we did the lumbar puncture. It was a different time, and there was a different perspective on risks and benefits. More recently, the trend has been to obtain a CT scan before a lumbar puncture in several subsets of patients.

A 2015 analysis from Sweden¹ showed that we can probably do a lumbar puncture for suspected bacterial meningitis without first doing a CT scan in most patients, even in patients with moderately impaired mentation. Perhaps some other concerns can also be assuaged if evaluated, but we don’t have data. Mirrakhimov et al, in this issue of the Journal, review the current evidence on when to do CT before a lumbar puncture, even if it may significantly delay the procedure and the timely delivery of antibiotics. A perfect algorithm that balances the risks of delaying treatment, initiating less-than-ideal empiric antibiotics potentially without definitive culture, and inducing complications from a procedure done promptly may well be impossible to develop. Evidence helps us refine the diagnostic approach, but with limited data, some important decisions unfortunately remain within the “art” rather than the science of medicine.

Cardiac ultrasound is among the many beneficial applications of point-of-care (POC) ultrasound in the ED. This modality can prove extremely beneficial in evaluating the critically ill patient. For example, POC cardiac ultrasound not only permits the emergency physician (EP) to diagnose a pericardial effusion and cardiac tamponade, but also perform a pericardiocentesis.¹ The EP can also employ beside ultrasound to estimate an ejection fraction (EF) almost as well as cardiology services,² look for signs of right-heart strain in patients with pulmonary embolism (PE),³ and guide fluid management in patients who have septic shock.⁴ In addition to only taking a few minutes to perform, POC cardiac ultrasound can also drastically change the course of management in some patients. Our case illustrates the use of POC ultrasound to diagnose Takotsubo cardiomyopathy in a 64-year-old patient and guide management when she became unstable prior to cardiac catheterization.

Case

A 64-year-old white woman with a medical history of diabetes, obesity, and nephrolithiasis presented to the ED with chest pain and shortness of breath, which she stated had begun earlier in the day. The patient’s chest pain did not intensify upon exertion, but the shortness of breath worsened when she was in the supine position.

Three months prior, the patient had also presented to our ED with chest pain. Evaluation during that visit included a negative stress echocardiogram with an EF of 55%. At this second visit, an electrocardiogram (ECG) showed new T-wave inversions in the anterior, lateral, and inferior leads. Vital signs at presentation were: blood pressure, 107/63 mm Hg; heart rate, 100 beats/min; respiratory rate, 18 breaths/min; and temperature, 97.9°F. Oxygen saturation was 97% on room air when patient was sitting upright, but decreased to 90% when she was supine. A chest X-ray showed left basilar atelectasis with a trace effusion. Laboratory evaluation was remarkable for the following: troponin I, 2.99 ng/mL; D-dimer, 294 ng/mL; and brain natriuretic peptide, 559 pg/mL.

Given the patient’s vital signs and positive troponin I level, a computed tomography (CT) scan was ordered to assess for a PE. This was done despite the patient’s negative D-dimer results, as it was felt that she was not low-risk for PE. At the same time the CT scan was ordered, a POC cardiac ultrasound was performed to assess for signs of right heart strain.

Discussion

Takotsubo cardiomyopathy is an acute, stress-induced cardiomyopathy that was first described in Japan in the early 1990s.⁵ It is thought to be due to catecholamine-induced dysfunction from a stressful event,^6-8 such as the death of a loved one, which is why it is often referred to as “broken heart syndrome.” However there are case reports highlighting other causes of Takotsubo cardiomyopathy, such as cocaine use,⁹ scuba diving,¹⁰ and diabetic ketoacidosis combined with hypothermia.¹¹

Patients with Takotsubo cardiomyopathy will frequently have ECG abnormalities, including ST-segment elevation or depression, or T-wave changes; troponin levels also may be elevated. The majority of patients (>80%) are postmenopausal women, typically aged 50 to 75 years.^6,12 Echocardiogram findings in Takotsubo cardiomyopathy show significant left ventricular (LV) dysfunction or regional dysfunction that is not in one coronary artery distribution.^12,13 There will often be apical dilation or ballooning with dyskinesia but more preserved function at the base and normal dimensions.^14,15 A negative cardiac catheterization or catheterization in the absence of significant disease is required to confirm the diagnosis.¹⁶ The LV function usually returns to baseline in 1 to 4 weeks, but there can be recurrence in some patients.^6,17 The condition is also associated with a large burden of morbidity and mortality.^6,18 In a case series by Gopalakrishnan et al⁶ of 56 patients, there was an 8.9% in-hospital mortality rate and an additional 17.9% out-of-hospital mortality rate even in patients in whom LV function had returned to normal.

In a review by Gianni et al,¹⁹ 4.2% of patients with Takotsubo cardiomyopathy present with or go into cardiogenic shock at some point during admission, and up to 2% of patients who present with acute myocardial infarction have Takotsubo cardiomyopathy. Patients can go into cardiogenic shock due to depressed EF or LV outflow tract obstruction from hyperkinesis of the basilar segments. Some of these patients may be sent directly to the catheter laboratory based on ST elevations on ECG, in which case the diagnosis is made there. Our patient, however, did not have ST elevation and later became unstable on the floor. Citro et al²⁰ suggest that a patient with a predisposition for Takotsubo cardiomyopathy (eg, postmenopausal patients, those who experienced a trigger event), in the right clinical setting and without ST-segment elevation on ECG, could be managed more conservatively with delayed cardiac angiography or CT angiography (CTA) evaluation of the coronary arteries (sparing the patient an invasive procedure)—as long as ultrasound was consistent with typical Takotsubo cardiomyopathy findings. However, CTA is still needed to make the diagnosis.

At this time, Takotsubo cardiomyopathy should remain an important part of the differential diagnosis for emergency patients who have chest pain—especially for postmenopausal women with a history of significant stressor—as early recognition can lead to better patient care.

Conclusion

This case highlights the importance of POC ultrasound in the management of patients in the ED and after admission. The care of our patient was enhanced by the ability to take a real-time look at her EF and cardiac function at the time of admission through bedside ultrasound. This information guided her management and optimized stabilization.

Cardiac ultrasound is among the many beneficial applications of point-of-care (POC) ultrasound in the ED. This modality can prove extremely beneficial in evaluating the critically ill patient. For example, POC cardiac ultrasound not only permits the emergency physician (EP) to diagnose a pericardial effusion and cardiac tamponade, but also perform a pericardiocentesis.¹ The EP can also employ beside ultrasound to estimate an ejection fraction (EF) almost as well as cardiology services,² look for signs of right-heart strain in patients with pulmonary embolism (PE),³ and guide fluid management in patients who have septic shock.⁴ In addition to only taking a few minutes to perform, POC cardiac ultrasound can also drastically change the course of management in some patients. Our case illustrates the use of POC ultrasound to diagnose Takotsubo cardiomyopathy in a 64-year-old patient and guide management when she became unstable prior to cardiac catheterization.

Case

A 64-year-old white woman with a medical history of diabetes, obesity, and nephrolithiasis presented to the ED with chest pain and shortness of breath, which she stated had begun earlier in the day. The patient’s chest pain did not intensify upon exertion, but the shortness of breath worsened when she was in the supine position.

Three months prior, the patient had also presented to our ED with chest pain. Evaluation during that visit included a negative stress echocardiogram with an EF of 55%. At this second visit, an electrocardiogram (ECG) showed new T-wave inversions in the anterior, lateral, and inferior leads. Vital signs at presentation were: blood pressure, 107/63 mm Hg; heart rate, 100 beats/min; respiratory rate, 18 breaths/min; and temperature, 97.9°F. Oxygen saturation was 97% on room air when patient was sitting upright, but decreased to 90% when she was supine. A chest X-ray showed left basilar atelectasis with a trace effusion. Laboratory evaluation was remarkable for the following: troponin I, 2.99 ng/mL; D-dimer, 294 ng/mL; and brain natriuretic peptide, 559 pg/mL.

Given the patient’s vital signs and positive troponin I level, a computed tomography (CT) scan was ordered to assess for a PE. This was done despite the patient’s negative D-dimer results, as it was felt that she was not low-risk for PE. At the same time the CT scan was ordered, a POC cardiac ultrasound was performed to assess for signs of right heart strain.

Discussion

Takotsubo cardiomyopathy is an acute, stress-induced cardiomyopathy that was first described in Japan in the early 1990s.⁵ It is thought to be due to catecholamine-induced dysfunction from a stressful event,^6-8 such as the death of a loved one, which is why it is often referred to as “broken heart syndrome.” However there are case reports highlighting other causes of Takotsubo cardiomyopathy, such as cocaine use,⁹ scuba diving,¹⁰ and diabetic ketoacidosis combined with hypothermia.¹¹

Patients with Takotsubo cardiomyopathy will frequently have ECG abnormalities, including ST-segment elevation or depression, or T-wave changes; troponin levels also may be elevated. The majority of patients (>80%) are postmenopausal women, typically aged 50 to 75 years.^6,12 Echocardiogram findings in Takotsubo cardiomyopathy show significant left ventricular (LV) dysfunction or regional dysfunction that is not in one coronary artery distribution.^12,13 There will often be apical dilation or ballooning with dyskinesia but more preserved function at the base and normal dimensions.^14,15 A negative cardiac catheterization or catheterization in the absence of significant disease is required to confirm the diagnosis.¹⁶ The LV function usually returns to baseline in 1 to 4 weeks, but there can be recurrence in some patients.^6,17 The condition is also associated with a large burden of morbidity and mortality.^6,18 In a case series by Gopalakrishnan et al⁶ of 56 patients, there was an 8.9% in-hospital mortality rate and an additional 17.9% out-of-hospital mortality rate even in patients in whom LV function had returned to normal.

In a review by Gianni et al,¹⁹ 4.2% of patients with Takotsubo cardiomyopathy present with or go into cardiogenic shock at some point during admission, and up to 2% of patients who present with acute myocardial infarction have Takotsubo cardiomyopathy. Patients can go into cardiogenic shock due to depressed EF or LV outflow tract obstruction from hyperkinesis of the basilar segments. Some of these patients may be sent directly to the catheter laboratory based on ST elevations on ECG, in which case the diagnosis is made there. Our patient, however, did not have ST elevation and later became unstable on the floor. Citro et al²⁰ suggest that a patient with a predisposition for Takotsubo cardiomyopathy (eg, postmenopausal patients, those who experienced a trigger event), in the right clinical setting and without ST-segment elevation on ECG, could be managed more conservatively with delayed cardiac angiography or CT angiography (CTA) evaluation of the coronary arteries (sparing the patient an invasive procedure)—as long as ultrasound was consistent with typical Takotsubo cardiomyopathy findings. However, CTA is still needed to make the diagnosis.

At this time, Takotsubo cardiomyopathy should remain an important part of the differential diagnosis for emergency patients who have chest pain—especially for postmenopausal women with a history of significant stressor—as early recognition can lead to better patient care.

Conclusion

This case highlights the importance of POC ultrasound in the management of patients in the ED and after admission. The care of our patient was enhanced by the ability to take a real-time look at her EF and cardiac function at the time of admission through bedside ultrasound. This information guided her management and optimized stabilization.

Cardiac ultrasound is among the many beneficial applications of point-of-care (POC) ultrasound in the ED. This modality can prove extremely beneficial in evaluating the critically ill patient. For example, POC cardiac ultrasound not only permits the emergency physician (EP) to diagnose a pericardial effusion and cardiac tamponade, but also perform a pericardiocentesis.¹ The EP can also employ beside ultrasound to estimate an ejection fraction (EF) almost as well as cardiology services,² look for signs of right-heart strain in patients with pulmonary embolism (PE),³ and guide fluid management in patients who have septic shock.⁴ In addition to only taking a few minutes to perform, POC cardiac ultrasound can also drastically change the course of management in some patients. Our case illustrates the use of POC ultrasound to diagnose Takotsubo cardiomyopathy in a 64-year-old patient and guide management when she became unstable prior to cardiac catheterization.

Case

A 64-year-old white woman with a medical history of diabetes, obesity, and nephrolithiasis presented to the ED with chest pain and shortness of breath, which she stated had begun earlier in the day. The patient’s chest pain did not intensify upon exertion, but the shortness of breath worsened when she was in the supine position.

Three months prior, the patient had also presented to our ED with chest pain. Evaluation during that visit included a negative stress echocardiogram with an EF of 55%. At this second visit, an electrocardiogram (ECG) showed new T-wave inversions in the anterior, lateral, and inferior leads. Vital signs at presentation were: blood pressure, 107/63 mm Hg; heart rate, 100 beats/min; respiratory rate, 18 breaths/min; and temperature, 97.9°F. Oxygen saturation was 97% on room air when patient was sitting upright, but decreased to 90% when she was supine. A chest X-ray showed left basilar atelectasis with a trace effusion. Laboratory evaluation was remarkable for the following: troponin I, 2.99 ng/mL; D-dimer, 294 ng/mL; and brain natriuretic peptide, 559 pg/mL.

Given the patient’s vital signs and positive troponin I level, a computed tomography (CT) scan was ordered to assess for a PE. This was done despite the patient’s negative D-dimer results, as it was felt that she was not low-risk for PE. At the same time the CT scan was ordered, a POC cardiac ultrasound was performed to assess for signs of right heart strain.

Discussion

Takotsubo cardiomyopathy is an acute, stress-induced cardiomyopathy that was first described in Japan in the early 1990s.⁵ It is thought to be due to catecholamine-induced dysfunction from a stressful event,^6-8 such as the death of a loved one, which is why it is often referred to as “broken heart syndrome.” However there are case reports highlighting other causes of Takotsubo cardiomyopathy, such as cocaine use,⁹ scuba diving,¹⁰ and diabetic ketoacidosis combined with hypothermia.¹¹

Patients with Takotsubo cardiomyopathy will frequently have ECG abnormalities, including ST-segment elevation or depression, or T-wave changes; troponin levels also may be elevated. The majority of patients (>80%) are postmenopausal women, typically aged 50 to 75 years.^6,12 Echocardiogram findings in Takotsubo cardiomyopathy show significant left ventricular (LV) dysfunction or regional dysfunction that is not in one coronary artery distribution.^12,13 There will often be apical dilation or ballooning with dyskinesia but more preserved function at the base and normal dimensions.^14,15 A negative cardiac catheterization or catheterization in the absence of significant disease is required to confirm the diagnosis.¹⁶ The LV function usually returns to baseline in 1 to 4 weeks, but there can be recurrence in some patients.^6,17 The condition is also associated with a large burden of morbidity and mortality.^6,18 In a case series by Gopalakrishnan et al⁶ of 56 patients, there was an 8.9% in-hospital mortality rate and an additional 17.9% out-of-hospital mortality rate even in patients in whom LV function had returned to normal.

In a review by Gianni et al,¹⁹ 4.2% of patients with Takotsubo cardiomyopathy present with or go into cardiogenic shock at some point during admission, and up to 2% of patients who present with acute myocardial infarction have Takotsubo cardiomyopathy. Patients can go into cardiogenic shock due to depressed EF or LV outflow tract obstruction from hyperkinesis of the basilar segments. Some of these patients may be sent directly to the catheter laboratory based on ST elevations on ECG, in which case the diagnosis is made there. Our patient, however, did not have ST elevation and later became unstable on the floor. Citro et al²⁰ suggest that a patient with a predisposition for Takotsubo cardiomyopathy (eg, postmenopausal patients, those who experienced a trigger event), in the right clinical setting and without ST-segment elevation on ECG, could be managed more conservatively with delayed cardiac angiography or CT angiography (CTA) evaluation of the coronary arteries (sparing the patient an invasive procedure)—as long as ultrasound was consistent with typical Takotsubo cardiomyopathy findings. However, CTA is still needed to make the diagnosis.

At this time, Takotsubo cardiomyopathy should remain an important part of the differential diagnosis for emergency patients who have chest pain—especially for postmenopausal women with a history of significant stressor—as early recognition can lead to better patient care.

Conclusion

This case highlights the importance of POC ultrasound in the management of patients in the ED and after admission. The care of our patient was enhanced by the ability to take a real-time look at her EF and cardiac function at the time of admission through bedside ultrasound. This information guided her management and optimized stabilization.

Hip ultrasound has long been considered an effective diagnostic and interventional tool to identify hip effusions and perform guided arthrocentesis in patients with suspected septic arthritis. Although imaging and interventional techniques are typically performed by interventional radiologists, several case reports support the use of these techniques by the emergency physician (EP) in both pediatric and adult patients presenting with hip pain.^1,2

Hip ultrasound permits rapid visualization of the joint space to assess the presence of a hip effusion, and provides the opportunity for the clinician to quickly perform hip arthrocentesis and to obtain synovial fluid for analysis—the current gold standard of diagnosis. The current literature shows treatment of effusion in the adult hip via ultrasound-guided interventional methods to be more convenient and less painful than traditional fluoroscopic-guided techniques, and to have the same procedural success rate.³ With the increasing utilization of point-of-care (POC) ultrasound in the ED, ultrasound-guided hip arthrocentesis has become a powerful tool in the EP’s armamentarium to aid in evaluating and treating patients in the ED presenting with hip pain.

Imaging Technique

To perform an ultrasound-guided arthrocentesis, the patient should be placed in the supine position, with both knees bent and the hips externally rotated in the frog leg position (Figure 1).

Arthrocentesis

When an effusion is present, arthrocentesis is warranted. To perform this procedure, the femoral vessels should be identified inferior to the inguinal ligament and avoided laterally. The hip should be prepared in a sterile fashion and a lubricated probe should be placed in a sterile dressing with a cord cover. The effusion should be visualized again, and the area should be anesthetized superficially and deeply with local anesthetic, aspirating prior to infusing at the deeper levels. An 18-gauge spinal needle affixed to a 20-mL syringe should be introduced and advanced while aspirating under direct visualization through the capsule of the hip into the effusion. The fluid is then aspirated and sent for laboratory analysis.

Summary

A delayed diagnosis of hip effusion and failure to initiate prompt treatment are the most common causes of late complications of septic arthritis.⁴ Point-of-care diagnostic and interventional ultrasound of the hip permit instant visualization and implementation of immediate diagnostic and therapeutic measures, which decrease morbidity in adult patients with septic arthritis. Hip arthrocentesis with subsequent synovial fluid analysis, the gold standard of diagnosis, has traditionally been performed by radiology services. Recent literature, however, has shown performance of these ultrasound-guided techniques by EPs to be safe and efficient, facilitating time to treatment.

Hip ultrasound has long been considered an effective diagnostic and interventional tool to identify hip effusions and perform guided arthrocentesis in patients with suspected septic arthritis. Although imaging and interventional techniques are typically performed by interventional radiologists, several case reports support the use of these techniques by the emergency physician (EP) in both pediatric and adult patients presenting with hip pain.^1,2

Hip ultrasound permits rapid visualization of the joint space to assess the presence of a hip effusion, and provides the opportunity for the clinician to quickly perform hip arthrocentesis and to obtain synovial fluid for analysis—the current gold standard of diagnosis. The current literature shows treatment of effusion in the adult hip via ultrasound-guided interventional methods to be more convenient and less painful than traditional fluoroscopic-guided techniques, and to have the same procedural success rate.³ With the increasing utilization of point-of-care (POC) ultrasound in the ED, ultrasound-guided hip arthrocentesis has become a powerful tool in the EP’s armamentarium to aid in evaluating and treating patients in the ED presenting with hip pain.

Imaging Technique

To perform an ultrasound-guided arthrocentesis, the patient should be placed in the supine position, with both knees bent and the hips externally rotated in the frog leg position (Figure 1).

Arthrocentesis

When an effusion is present, arthrocentesis is warranted. To perform this procedure, the femoral vessels should be identified inferior to the inguinal ligament and avoided laterally. The hip should be prepared in a sterile fashion and a lubricated probe should be placed in a sterile dressing with a cord cover. The effusion should be visualized again, and the area should be anesthetized superficially and deeply with local anesthetic, aspirating prior to infusing at the deeper levels. An 18-gauge spinal needle affixed to a 20-mL syringe should be introduced and advanced while aspirating under direct visualization through the capsule of the hip into the effusion. The fluid is then aspirated and sent for laboratory analysis.

Summary

A delayed diagnosis of hip effusion and failure to initiate prompt treatment are the most common causes of late complications of septic arthritis.⁴ Point-of-care diagnostic and interventional ultrasound of the hip permit instant visualization and implementation of immediate diagnostic and therapeutic measures, which decrease morbidity in adult patients with septic arthritis. Hip arthrocentesis with subsequent synovial fluid analysis, the gold standard of diagnosis, has traditionally been performed by radiology services. Recent literature, however, has shown performance of these ultrasound-guided techniques by EPs to be safe and efficient, facilitating time to treatment.

Hip ultrasound has long been considered an effective diagnostic and interventional tool to identify hip effusions and perform guided arthrocentesis in patients with suspected septic arthritis. Although imaging and interventional techniques are typically performed by interventional radiologists, several case reports support the use of these techniques by the emergency physician (EP) in both pediatric and adult patients presenting with hip pain.^1,2

Hip ultrasound permits rapid visualization of the joint space to assess the presence of a hip effusion, and provides the opportunity for the clinician to quickly perform hip arthrocentesis and to obtain synovial fluid for analysis—the current gold standard of diagnosis. The current literature shows treatment of effusion in the adult hip via ultrasound-guided interventional methods to be more convenient and less painful than traditional fluoroscopic-guided techniques, and to have the same procedural success rate.³ With the increasing utilization of point-of-care (POC) ultrasound in the ED, ultrasound-guided hip arthrocentesis has become a powerful tool in the EP’s armamentarium to aid in evaluating and treating patients in the ED presenting with hip pain.

Imaging Technique

To perform an ultrasound-guided arthrocentesis, the patient should be placed in the supine position, with both knees bent and the hips externally rotated in the frog leg position (Figure 1).

Arthrocentesis

When an effusion is present, arthrocentesis is warranted. To perform this procedure, the femoral vessels should be identified inferior to the inguinal ligament and avoided laterally. The hip should be prepared in a sterile fashion and a lubricated probe should be placed in a sterile dressing with a cord cover. The effusion should be visualized again, and the area should be anesthetized superficially and deeply with local anesthetic, aspirating prior to infusing at the deeper levels. An 18-gauge spinal needle affixed to a 20-mL syringe should be introduced and advanced while aspirating under direct visualization through the capsule of the hip into the effusion. The fluid is then aspirated and sent for laboratory analysis.

Summary

A delayed diagnosis of hip effusion and failure to initiate prompt treatment are the most common causes of late complications of septic arthritis.⁴ Point-of-care diagnostic and interventional ultrasound of the hip permit instant visualization and implementation of immediate diagnostic and therapeutic measures, which decrease morbidity in adult patients with septic arthritis. Hip arthrocentesis with subsequent synovial fluid analysis, the gold standard of diagnosis, has traditionally been performed by radiology services. Recent literature, however, has shown performance of these ultrasound-guided techniques by EPs to be safe and efficient, facilitating time to treatment.

Take-Home Points

• Be sure to have a well centered AP pelvis without rotation.
• Get at least 3 plain radiographs—AP pelvis, false profile, and lateral hip view.
• Ensure that there is sufficient acetabular coverage, LCEA >20° on AP pelvis and ACEA >20° on false profile view.
• CT scans are helpful for precise hip pathomor­phology but must be weighed against risk of radiation exposure.
• MRI or MRA can be helpful to diagnose intra-articular as well as extra-articular hip and pelvis abnormalities.

In the work-up for nonarthritic hip pain, the value of diagnostic imaging is in objective findings, which can support or weaken the leading diagnoses based on subjective complaints, recalled history, and, in some cases, elusive physical examination findings. Morphologic changes alone, however, do not always indicate pathology.^1,2 At presentation and at each step in the work-up, it is imperative to evaluate the entire clinical picture. The prudent clinician uses both clinical and radiographic findings to make the diagnosis and direct treatment.

Radiography

The first step in diagnostic imaging is radiography. Although use of plain radiographs is routine, their value cannot be understated. Standard hip radiographs—an anteroposterior (AP) radiograph of the pelvis and AP and frog-leg (cross-table lateral) radiographs of the hip—provide a wealth of information.^3-6

Evaluated first is the radiograph itself. For example, the ideal AP radiograph of the pelvis (Figure 1) is centered on the lower sacrum, and the patient is not rotated.

13

Computed Tomography

The benefits of computed tomography (CT) outweigh the risk of radiation exposure. CT is most useful in characterizing osseous morphology.²¹ In FAI cases, CT can distinguish acetabular version abnormalities from femoral torsion (Figures 7A-7C), entities with very different treatment approaches.²¹

Magnetic Resonance Imaging

MRI is becoming essential in the work-up for nonarthritic hip pain.^11,22 It is used for assessment of osseous, chondral, and musculotendinous soft tissues. Further, it affords appreciation of outside-the-hip-joint pathology that may mimic joint-centered pathology.

MRI techniques range from noncontrast to indirect and direct magnetic resonance arthrography (MRA).²² Indirect MRA is performed with contrast medium administered through an intravenous line. Direct MRA has contrast administered intra-articularly and is more sensitive and specific for labral tears and ligamentous injury.²³ Excellent detection of intra-articular pathology on noncontrast studies questions the need for MRA.²⁴ Nevertheless, direct MRA can also be used as a therapeutic procedure when lidocaine is included in the injected gadolinium.

Labral tears, focal chondral defects, and stress or insufficiency fractures are important differentials in the work-up for nonarthritic hip pain. Over the dysplasia-to-FAI spectrum, MRI distinguishes symptomatic pathoanatomy from asymptomatic anatomical variants by revealing underlying bone edema. Capsule findings should also be considered.²¹The most practical classification of labral tears, proposed by Blankenbaker and colleagues,²⁵ is based on tear type (frayed, unstable, flap), location, and extent. More than half of labral tears occur in the anterosuperior quadrant of the labrum.²⁵

26

MRI detects osseous pathology from surrounding soft-tissue edema and bone remodeling to stress and fragility fractures. In athletes, the most common fractures are pubic rami, sacral, and apophyseal avulsion fractures.²⁸ In all patients, attention should be given to the lower spine and the proximal femurs. Aside from MRI, nuclear medicine bone scan might also identify active osseous reaction representative of a fracture.

Conclusion

The work-up for nonarthritic hip pain substantiates differential diagnoses. A case’s complexity determines the course of diagnostic imaging. At presentation and at each step in the work-up, it is imperative to evaluate the entire clinical picture. The prudent clinician uses both clinical and radiographic findings to make the diagnosis and direct treatment.

Am J Orthop . 2017;46(1):17-22. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Be sure to have a well centered AP pelvis without rotation.
• Get at least 3 plain radiographs—AP pelvis, false profile, and lateral hip view.
• Ensure that there is sufficient acetabular coverage, LCEA >20° on AP pelvis and ACEA >20° on false profile view.
• CT scans are helpful for precise hip pathomor­phology but must be weighed against risk of radiation exposure.
• MRI or MRA can be helpful to diagnose intra-articular as well as extra-articular hip and pelvis abnormalities.

In the work-up for nonarthritic hip pain, the value of diagnostic imaging is in objective findings, which can support or weaken the leading diagnoses based on subjective complaints, recalled history, and, in some cases, elusive physical examination findings. Morphologic changes alone, however, do not always indicate pathology.^1,2 At presentation and at each step in the work-up, it is imperative to evaluate the entire clinical picture. The prudent clinician uses both clinical and radiographic findings to make the diagnosis and direct treatment.

Radiography

The first step in diagnostic imaging is radiography. Although use of plain radiographs is routine, their value cannot be understated. Standard hip radiographs—an anteroposterior (AP) radiograph of the pelvis and AP and frog-leg (cross-table lateral) radiographs of the hip—provide a wealth of information.^3-6

Evaluated first is the radiograph itself. For example, the ideal AP radiograph of the pelvis (Figure 1) is centered on the lower sacrum, and the patient is not rotated.

13

Computed Tomography

The benefits of computed tomography (CT) outweigh the risk of radiation exposure. CT is most useful in characterizing osseous morphology.²¹ In FAI cases, CT can distinguish acetabular version abnormalities from femoral torsion (Figures 7A-7C), entities with very different treatment approaches.²¹

Magnetic Resonance Imaging

MRI is becoming essential in the work-up for nonarthritic hip pain.^11,22 It is used for assessment of osseous, chondral, and musculotendinous soft tissues. Further, it affords appreciation of outside-the-hip-joint pathology that may mimic joint-centered pathology.

MRI techniques range from noncontrast to indirect and direct magnetic resonance arthrography (MRA).²² Indirect MRA is performed with contrast medium administered through an intravenous line. Direct MRA has contrast administered intra-articularly and is more sensitive and specific for labral tears and ligamentous injury.²³ Excellent detection of intra-articular pathology on noncontrast studies questions the need for MRA.²⁴ Nevertheless, direct MRA can also be used as a therapeutic procedure when lidocaine is included in the injected gadolinium.

Labral tears, focal chondral defects, and stress or insufficiency fractures are important differentials in the work-up for nonarthritic hip pain. Over the dysplasia-to-FAI spectrum, MRI distinguishes symptomatic pathoanatomy from asymptomatic anatomical variants by revealing underlying bone edema. Capsule findings should also be considered.²¹The most practical classification of labral tears, proposed by Blankenbaker and colleagues,²⁵ is based on tear type (frayed, unstable, flap), location, and extent. More than half of labral tears occur in the anterosuperior quadrant of the labrum.²⁵

26

MRI detects osseous pathology from surrounding soft-tissue edema and bone remodeling to stress and fragility fractures. In athletes, the most common fractures are pubic rami, sacral, and apophyseal avulsion fractures.²⁸ In all patients, attention should be given to the lower spine and the proximal femurs. Aside from MRI, nuclear medicine bone scan might also identify active osseous reaction representative of a fracture.

Conclusion

The work-up for nonarthritic hip pain substantiates differential diagnoses. A case’s complexity determines the course of diagnostic imaging. At presentation and at each step in the work-up, it is imperative to evaluate the entire clinical picture. The prudent clinician uses both clinical and radiographic findings to make the diagnosis and direct treatment.

Am J Orthop . 2017;46(1):17-22. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Be sure to have a well centered AP pelvis without rotation.
• Get at least 3 plain radiographs—AP pelvis, false profile, and lateral hip view.
• Ensure that there is sufficient acetabular coverage, LCEA >20° on AP pelvis and ACEA >20° on false profile view.
• CT scans are helpful for precise hip pathomor­phology but must be weighed against risk of radiation exposure.
• MRI or MRA can be helpful to diagnose intra-articular as well as extra-articular hip and pelvis abnormalities.

In the work-up for nonarthritic hip pain, the value of diagnostic imaging is in objective findings, which can support or weaken the leading diagnoses based on subjective complaints, recalled history, and, in some cases, elusive physical examination findings. Morphologic changes alone, however, do not always indicate pathology.^1,2 At presentation and at each step in the work-up, it is imperative to evaluate the entire clinical picture. The prudent clinician uses both clinical and radiographic findings to make the diagnosis and direct treatment.

Radiography

The first step in diagnostic imaging is radiography. Although use of plain radiographs is routine, their value cannot be understated. Standard hip radiographs—an anteroposterior (AP) radiograph of the pelvis and AP and frog-leg (cross-table lateral) radiographs of the hip—provide a wealth of information.^3-6

Evaluated first is the radiograph itself. For example, the ideal AP radiograph of the pelvis (Figure 1) is centered on the lower sacrum, and the patient is not rotated.

13

Computed Tomography

The benefits of computed tomography (CT) outweigh the risk of radiation exposure. CT is most useful in characterizing osseous morphology.²¹ In FAI cases, CT can distinguish acetabular version abnormalities from femoral torsion (Figures 7A-7C), entities with very different treatment approaches.²¹

Magnetic Resonance Imaging

MRI is becoming essential in the work-up for nonarthritic hip pain.^11,22 It is used for assessment of osseous, chondral, and musculotendinous soft tissues. Further, it affords appreciation of outside-the-hip-joint pathology that may mimic joint-centered pathology.

MRI techniques range from noncontrast to indirect and direct magnetic resonance arthrography (MRA).²² Indirect MRA is performed with contrast medium administered through an intravenous line. Direct MRA has contrast administered intra-articularly and is more sensitive and specific for labral tears and ligamentous injury.²³ Excellent detection of intra-articular pathology on noncontrast studies questions the need for MRA.²⁴ Nevertheless, direct MRA can also be used as a therapeutic procedure when lidocaine is included in the injected gadolinium.

Labral tears, focal chondral defects, and stress or insufficiency fractures are important differentials in the work-up for nonarthritic hip pain. Over the dysplasia-to-FAI spectrum, MRI distinguishes symptomatic pathoanatomy from asymptomatic anatomical variants by revealing underlying bone edema. Capsule findings should also be considered.²¹The most practical classification of labral tears, proposed by Blankenbaker and colleagues,²⁵ is based on tear type (frayed, unstable, flap), location, and extent. More than half of labral tears occur in the anterosuperior quadrant of the labrum.²⁵

26

MRI detects osseous pathology from surrounding soft-tissue edema and bone remodeling to stress and fragility fractures. In athletes, the most common fractures are pubic rami, sacral, and apophyseal avulsion fractures.²⁸ In all patients, attention should be given to the lower spine and the proximal femurs. Aside from MRI, nuclear medicine bone scan might also identify active osseous reaction representative of a fracture.

Conclusion

The work-up for nonarthritic hip pain substantiates differential diagnoses. A case’s complexity determines the course of diagnostic imaging. At presentation and at each step in the work-up, it is imperative to evaluate the entire clinical picture. The prudent clinician uses both clinical and radiographic findings to make the diagnosis and direct treatment.

Am J Orthop . 2017;46(1):17-22. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

A 66-year-old man with chronic obstructive pulmonary disease (COPD) was brought to the emergency department with a 2-week history of progressive dyspnea followed by altered mental status. He had no history of diabetes mellitus, hypertension, or drug abuse.

On physical examination, he was stuporous. He had no fever or hypotension, but his pulse and breathing were rapid, and he had central cyanosis, bilateral conjunctival congestion, a puffy face, generalized wheezing, basilar crackles in both lungs, and leg edema.

Laboratory testing showed hypoxia and severe hypercarbia. His hematocrit was 65% (reference range 39–51) and his hemoglobin level was 21.5 g/dL (13–17).

The patient was diagnosed with an exacerbation of COPD. He was intubated, placed on mechanical ventilation, and admitted to the intensive care unit.

Computed tomography (CT) performed because of his decreased level of consciousness (Figure 1) showed increased attenuation in the ambient cistern and the lateral aspect of the lateral cerebral fissure, suggesting subarachnoid hemorrhage. The attenuation value in these areas was 89 Hounsfield units (typical values for brain tissue are in the 20s to 30s, and for blood in the 30s to 40s). To further evaluate for subarachnoid hemorrhage, lumbar puncture was performed, but analysis of the fluid sample showed normal protein and glucose levels and no cells.

Based on the results of cerebrospinal fluid evaluation and on the CT attenuation value, a diagnosis of pseudosubarachnoid hemorrhage due to polycythemia was made.

SUBARACHNOID VS PSEUDOSUBARACHNOID HEMORRHAGE

Subarachnoid hemorrhage typically begins with a “thunder-clap” headache (beginning suddenly and described by patients as “the worst headache ever.”) While not all patients have this presentation, if imaging suggests subarachnoid hemorrhage but the patient has atypical signs and symptoms (eg, other than headache), then pseudosubarachnoid hemorrhage should be considered.

Brain CT is one of the most reliable tools for diagnosing subarachnoid hemorrhage in the emergency department. Done within 6 hours of symptom onset, it has a sensitivity of 98.7% and a specificity of 99.9%.¹ Magnetic resonance imaging can also visualize subarachnoid hemorrhage within the first 12 hours, typically as a hyperintensity in the subarachnoid space on fluid-attenuated inversion-recovery sequences² and on susceptibility-weighted sequences.

Lumbar puncture is also an important diagnostic tool but carries a risk of brain herniation in patients with brain edema.

Pseudosubarachnoid hemorrhage is an artifact of CT imaging. It is rare, and its prevalence is unknown.³ However, it may be seen in up to 20% of patients after resuscitation, as a result of diffuse cerebral edema that lowers the attenuation of brain tissue on CT, making the vessels relatively conspicuous. It can also be seen in purulent meningitis (due to proteinaceous influx after blood-brain barrier disruption),⁴ in meningeal leukemia (due to increased cellularity in the leptomeninges), and in severe polycythemia (from a higher concentration of blood and hemoglobin in the vessels).^3,5–7

Although the level of attenuation on CT may help distinguish subarachnoid from pseudosubarachnoid hemorrhage, its accuracy has not been defined. Inspecting the CT images may clarify whether areas with high attenuation look like blood vessels vs subarachnoid hemorrhage.

Our patient recovered and had an uneventful follow-up. The cause of his elevated hematocrit was likely chronic hypoxia from COPD.

Acknowledgment: We thank Dr. Saeide Khanbagi and Dr. Azade Nasr-lari for their cooperation.

A 66-year-old man with chronic obstructive pulmonary disease (COPD) was brought to the emergency department with a 2-week history of progressive dyspnea followed by altered mental status. He had no history of diabetes mellitus, hypertension, or drug abuse.

On physical examination, he was stuporous. He had no fever or hypotension, but his pulse and breathing were rapid, and he had central cyanosis, bilateral conjunctival congestion, a puffy face, generalized wheezing, basilar crackles in both lungs, and leg edema.

Laboratory testing showed hypoxia and severe hypercarbia. His hematocrit was 65% (reference range 39–51) and his hemoglobin level was 21.5 g/dL (13–17).

The patient was diagnosed with an exacerbation of COPD. He was intubated, placed on mechanical ventilation, and admitted to the intensive care unit.

Computed tomography (CT) performed because of his decreased level of consciousness (Figure 1) showed increased attenuation in the ambient cistern and the lateral aspect of the lateral cerebral fissure, suggesting subarachnoid hemorrhage. The attenuation value in these areas was 89 Hounsfield units (typical values for brain tissue are in the 20s to 30s, and for blood in the 30s to 40s). To further evaluate for subarachnoid hemorrhage, lumbar puncture was performed, but analysis of the fluid sample showed normal protein and glucose levels and no cells.

Based on the results of cerebrospinal fluid evaluation and on the CT attenuation value, a diagnosis of pseudosubarachnoid hemorrhage due to polycythemia was made.

SUBARACHNOID VS PSEUDOSUBARACHNOID HEMORRHAGE

Subarachnoid hemorrhage typically begins with a “thunder-clap” headache (beginning suddenly and described by patients as “the worst headache ever.”) While not all patients have this presentation, if imaging suggests subarachnoid hemorrhage but the patient has atypical signs and symptoms (eg, other than headache), then pseudosubarachnoid hemorrhage should be considered.

Brain CT is one of the most reliable tools for diagnosing subarachnoid hemorrhage in the emergency department. Done within 6 hours of symptom onset, it has a sensitivity of 98.7% and a specificity of 99.9%.¹ Magnetic resonance imaging can also visualize subarachnoid hemorrhage within the first 12 hours, typically as a hyperintensity in the subarachnoid space on fluid-attenuated inversion-recovery sequences² and on susceptibility-weighted sequences.

Lumbar puncture is also an important diagnostic tool but carries a risk of brain herniation in patients with brain edema.

Pseudosubarachnoid hemorrhage is an artifact of CT imaging. It is rare, and its prevalence is unknown.³ However, it may be seen in up to 20% of patients after resuscitation, as a result of diffuse cerebral edema that lowers the attenuation of brain tissue on CT, making the vessels relatively conspicuous. It can also be seen in purulent meningitis (due to proteinaceous influx after blood-brain barrier disruption),⁴ in meningeal leukemia (due to increased cellularity in the leptomeninges), and in severe polycythemia (from a higher concentration of blood and hemoglobin in the vessels).^3,5–7

Although the level of attenuation on CT may help distinguish subarachnoid from pseudosubarachnoid hemorrhage, its accuracy has not been defined. Inspecting the CT images may clarify whether areas with high attenuation look like blood vessels vs subarachnoid hemorrhage.

Our patient recovered and had an uneventful follow-up. The cause of his elevated hematocrit was likely chronic hypoxia from COPD.

Acknowledgment: We thank Dr. Saeide Khanbagi and Dr. Azade Nasr-lari for their cooperation.

A 66-year-old man with chronic obstructive pulmonary disease (COPD) was brought to the emergency department with a 2-week history of progressive dyspnea followed by altered mental status. He had no history of diabetes mellitus, hypertension, or drug abuse.

On physical examination, he was stuporous. He had no fever or hypotension, but his pulse and breathing were rapid, and he had central cyanosis, bilateral conjunctival congestion, a puffy face, generalized wheezing, basilar crackles in both lungs, and leg edema.

Laboratory testing showed hypoxia and severe hypercarbia. His hematocrit was 65% (reference range 39–51) and his hemoglobin level was 21.5 g/dL (13–17).

The patient was diagnosed with an exacerbation of COPD. He was intubated, placed on mechanical ventilation, and admitted to the intensive care unit.

Computed tomography (CT) performed because of his decreased level of consciousness (Figure 1) showed increased attenuation in the ambient cistern and the lateral aspect of the lateral cerebral fissure, suggesting subarachnoid hemorrhage. The attenuation value in these areas was 89 Hounsfield units (typical values for brain tissue are in the 20s to 30s, and for blood in the 30s to 40s). To further evaluate for subarachnoid hemorrhage, lumbar puncture was performed, but analysis of the fluid sample showed normal protein and glucose levels and no cells.

Based on the results of cerebrospinal fluid evaluation and on the CT attenuation value, a diagnosis of pseudosubarachnoid hemorrhage due to polycythemia was made.

SUBARACHNOID VS PSEUDOSUBARACHNOID HEMORRHAGE

Subarachnoid hemorrhage typically begins with a “thunder-clap” headache (beginning suddenly and described by patients as “the worst headache ever.”) While not all patients have this presentation, if imaging suggests subarachnoid hemorrhage but the patient has atypical signs and symptoms (eg, other than headache), then pseudosubarachnoid hemorrhage should be considered.

Brain CT is one of the most reliable tools for diagnosing subarachnoid hemorrhage in the emergency department. Done within 6 hours of symptom onset, it has a sensitivity of 98.7% and a specificity of 99.9%.¹ Magnetic resonance imaging can also visualize subarachnoid hemorrhage within the first 12 hours, typically as a hyperintensity in the subarachnoid space on fluid-attenuated inversion-recovery sequences² and on susceptibility-weighted sequences.

Lumbar puncture is also an important diagnostic tool but carries a risk of brain herniation in patients with brain edema.

Pseudosubarachnoid hemorrhage is an artifact of CT imaging. It is rare, and its prevalence is unknown.³ However, it may be seen in up to 20% of patients after resuscitation, as a result of diffuse cerebral edema that lowers the attenuation of brain tissue on CT, making the vessels relatively conspicuous. It can also be seen in purulent meningitis (due to proteinaceous influx after blood-brain barrier disruption),⁴ in meningeal leukemia (due to increased cellularity in the leptomeninges), and in severe polycythemia (from a higher concentration of blood and hemoglobin in the vessels).^3,5–7

Although the level of attenuation on CT may help distinguish subarachnoid from pseudosubarachnoid hemorrhage, its accuracy has not been defined. Inspecting the CT images may clarify whether areas with high attenuation look like blood vessels vs subarachnoid hemorrhage.

Our patient recovered and had an uneventful follow-up. The cause of his elevated hematocrit was likely chronic hypoxia from COPD.

Acknowledgment: We thank Dr. Saeide Khanbagi and Dr. Azade Nasr-lari for their cooperation.

An 89-year-old man presented to the ED with facial trauma due to a mechanical fall after losing his balance on uneven pavement and hitting the right side of his face. Physical examination revealed an ecchymosis inferior to the right eye and tenderness to palpation at the right maxilla and bilateral nasolabial folds. Maxillofacial computed tomography (CT) was ordered for further evaluation; representative images are presented above (Figure 1a and 1b).

What is the diagnosis?

Answer

A noncontrast CT of the maxillofacial bones demonstrated acute fractures through the bilateral pterygoid plates (white arrows, Figure 2a). The fractures extended through the medial and lateral walls of the bilateral maxillary sinuses (red arrows, Figure 2a), and propagated to the frontal processes of the maxilla (red arrows, Figure 2b), extending toward the alveolar process, indicating involvement of the anterolateral margin of the nasal fossa. The full extent of the fracture is best seen on a 3D-reconstructed image (red arrows, Figure 3). Additional images (not presented here) confirmed no fracture involvement of the orbital floors, nasal bones, or zygomatic arches. Expected posttraumatic hemorrhage was appreciated within the maxillary sinuses (white asterisks, Figure 2a).

Le Fort Fractures

The findings described above are characteristic of a Le Fort I fracture pattern. Initially described in 1901 by René Le Fort, a French surgeon, the Le Fort classification system details somewhat predictable midface fracture patterns resulting in various degrees of craniofacial disassociation.¹ Using weights that were dropped on cadaveric heads, Le Fort discovered that the pterygoid plates must be disrupted in order for the midface facial bones to separate from the skull base. As such, when diagnosing a Le Fort fracture, fracture of the pterygoid plate must be present, regardless of the fracture type (Le Fort I, II, and III).²

Le Fort I Fracture. This fracture pattern (red line, Figure 4) is referred to as a “floating palate” and involves separation of the hard palate from the skull base via fracture extension from the pterygoid plates into the maxillary sinus walls, as demonstrated in this case. The key distinguisher of the Le Fort I pattern is involvement of the anterolateral margin of the nasal fossa.²

Le Fort II Fracture. This fracture pattern (blue line, Figure 4) describes a “floating maxilla” wherein the pterygoid plate fractures are met with a pyramidal-type fracture pattern of the midface. The maxillary teeth form the base of the pyramid, and the fracture extends superiorly through the infraorbital rims bilaterally and toward the nasofrontal suture.^2,3 Le Fort II fractures result in the maxilla floating freely from the rest of the midface and skull base.

Le Fort III Fracture. This fracture pattern (green lines, Figure 4) describes a “floating face” with complete craniofacial disjunction resulting from fracture of the pterygoid plates, nasofrontal suture, maxillofrontal suture, orbital wall, and zygomatic arch/zygomaticofrontal suture.^2,3

It is important to note that midface trauma represents a complex spectrum of injuries, and Le Fort fractures only account for a small percentage of facial bone fractures that present through Level 1 trauma centers.² Le Fort fracture patterns can coexist with other fracture patterns and also can be seen in combination with each other. For example, one side of the face may demonstrate a Le Fort II pattern while the other side concurrently demonstrates a Le Fort III pattern. Though not robust enough for complete description of and surgical planning for facial fractures, this classification system is a succinct and well-accepted means of describing major fracture planes.

An 89-year-old man presented to the ED with facial trauma due to a mechanical fall after losing his balance on uneven pavement and hitting the right side of his face. Physical examination revealed an ecchymosis inferior to the right eye and tenderness to palpation at the right maxilla and bilateral nasolabial folds. Maxillofacial computed tomography (CT) was ordered for further evaluation; representative images are presented above (Figure 1a and 1b).

What is the diagnosis?

Answer

A noncontrast CT of the maxillofacial bones demonstrated acute fractures through the bilateral pterygoid plates (white arrows, Figure 2a). The fractures extended through the medial and lateral walls of the bilateral maxillary sinuses (red arrows, Figure 2a), and propagated to the frontal processes of the maxilla (red arrows, Figure 2b), extending toward the alveolar process, indicating involvement of the anterolateral margin of the nasal fossa. The full extent of the fracture is best seen on a 3D-reconstructed image (red arrows, Figure 3). Additional images (not presented here) confirmed no fracture involvement of the orbital floors, nasal bones, or zygomatic arches. Expected posttraumatic hemorrhage was appreciated within the maxillary sinuses (white asterisks, Figure 2a).

Le Fort Fractures

The findings described above are characteristic of a Le Fort I fracture pattern. Initially described in 1901 by René Le Fort, a French surgeon, the Le Fort classification system details somewhat predictable midface fracture patterns resulting in various degrees of craniofacial disassociation.¹ Using weights that were dropped on cadaveric heads, Le Fort discovered that the pterygoid plates must be disrupted in order for the midface facial bones to separate from the skull base. As such, when diagnosing a Le Fort fracture, fracture of the pterygoid plate must be present, regardless of the fracture type (Le Fort I, II, and III).²

Le Fort I Fracture. This fracture pattern (red line, Figure 4) is referred to as a “floating palate” and involves separation of the hard palate from the skull base via fracture extension from the pterygoid plates into the maxillary sinus walls, as demonstrated in this case. The key distinguisher of the Le Fort I pattern is involvement of the anterolateral margin of the nasal fossa.²

Le Fort II Fracture. This fracture pattern (blue line, Figure 4) describes a “floating maxilla” wherein the pterygoid plate fractures are met with a pyramidal-type fracture pattern of the midface. The maxillary teeth form the base of the pyramid, and the fracture extends superiorly through the infraorbital rims bilaterally and toward the nasofrontal suture.^2,3 Le Fort II fractures result in the maxilla floating freely from the rest of the midface and skull base.

Le Fort III Fracture. This fracture pattern (green lines, Figure 4) describes a “floating face” with complete craniofacial disjunction resulting from fracture of the pterygoid plates, nasofrontal suture, maxillofrontal suture, orbital wall, and zygomatic arch/zygomaticofrontal suture.^2,3

It is important to note that midface trauma represents a complex spectrum of injuries, and Le Fort fractures only account for a small percentage of facial bone fractures that present through Level 1 trauma centers.² Le Fort fracture patterns can coexist with other fracture patterns and also can be seen in combination with each other. For example, one side of the face may demonstrate a Le Fort II pattern while the other side concurrently demonstrates a Le Fort III pattern. Though not robust enough for complete description of and surgical planning for facial fractures, this classification system is a succinct and well-accepted means of describing major fracture planes.

An 89-year-old man presented to the ED with facial trauma due to a mechanical fall after losing his balance on uneven pavement and hitting the right side of his face. Physical examination revealed an ecchymosis inferior to the right eye and tenderness to palpation at the right maxilla and bilateral nasolabial folds. Maxillofacial computed tomography (CT) was ordered for further evaluation; representative images are presented above (Figure 1a and 1b).

What is the diagnosis?

Answer

A noncontrast CT of the maxillofacial bones demonstrated acute fractures through the bilateral pterygoid plates (white arrows, Figure 2a). The fractures extended through the medial and lateral walls of the bilateral maxillary sinuses (red arrows, Figure 2a), and propagated to the frontal processes of the maxilla (red arrows, Figure 2b), extending toward the alveolar process, indicating involvement of the anterolateral margin of the nasal fossa. The full extent of the fracture is best seen on a 3D-reconstructed image (red arrows, Figure 3). Additional images (not presented here) confirmed no fracture involvement of the orbital floors, nasal bones, or zygomatic arches. Expected posttraumatic hemorrhage was appreciated within the maxillary sinuses (white asterisks, Figure 2a).

Le Fort Fractures

The findings described above are characteristic of a Le Fort I fracture pattern. Initially described in 1901 by René Le Fort, a French surgeon, the Le Fort classification system details somewhat predictable midface fracture patterns resulting in various degrees of craniofacial disassociation.¹ Using weights that were dropped on cadaveric heads, Le Fort discovered that the pterygoid plates must be disrupted in order for the midface facial bones to separate from the skull base. As such, when diagnosing a Le Fort fracture, fracture of the pterygoid plate must be present, regardless of the fracture type (Le Fort I, II, and III).²

Le Fort I Fracture. This fracture pattern (red line, Figure 4) is referred to as a “floating palate” and involves separation of the hard palate from the skull base via fracture extension from the pterygoid plates into the maxillary sinus walls, as demonstrated in this case. The key distinguisher of the Le Fort I pattern is involvement of the anterolateral margin of the nasal fossa.²

Le Fort II Fracture. This fracture pattern (blue line, Figure 4) describes a “floating maxilla” wherein the pterygoid plate fractures are met with a pyramidal-type fracture pattern of the midface. The maxillary teeth form the base of the pyramid, and the fracture extends superiorly through the infraorbital rims bilaterally and toward the nasofrontal suture.^2,3 Le Fort II fractures result in the maxilla floating freely from the rest of the midface and skull base.

Le Fort III Fracture. This fracture pattern (green lines, Figure 4) describes a “floating face” with complete craniofacial disjunction resulting from fracture of the pterygoid plates, nasofrontal suture, maxillofrontal suture, orbital wall, and zygomatic arch/zygomaticofrontal suture.^2,3

It is important to note that midface trauma represents a complex spectrum of injuries, and Le Fort fractures only account for a small percentage of facial bone fractures that present through Level 1 trauma centers.² Le Fort fracture patterns can coexist with other fracture patterns and also can be seen in combination with each other. For example, one side of the face may demonstrate a Le Fort II pattern while the other side concurrently demonstrates a Le Fort III pattern. Though not robust enough for complete description of and surgical planning for facial fractures, this classification system is a succinct and well-accepted means of describing major fracture planes.

A 77-year-old man presented with a 5-day history of painful swelling of his right leg. He reported no trauma, no recent surgery, no history of thrombophilic disorder, and no prolonged immobilization. However, he had a history of prostate cancer, treated 10 years earlier with pelvic radiation.

Examination revealed massive right leg swelling extending from the thigh to the ankle, along with bluish-red skin discoloration (Figure 1). Doppler ultrasonography demonstrated acute thrombosis involving the right iliofemoral veins. These findings were consistent with phlegmasia cerulea dolens.

Urgent percutaneous catheter-directed thrombolysis was performed. Venography revealed extensive thrombosis of the femoral vein (Figure 2A) extending into the right external iliac vein. This was treated with catheter-directed pharmacomechanical thrombectomy.

Venography after this procedure showed significant improvement in venous blood flow (Figure 2B). However, stenosis of the right external iliac vein was also noted (Figure 2C) and was treated with balloon angioplasty (Figure 2D) followed by placement of a stent (14 × 40 mm).

In the immediate postprocedural period, there was marked reduction in swelling and normalization of skin color (Figure 3). The patient did not experience significant bleeding during or after the procedure. Treatment with intravenous unfractionated heparin was continued during the hospital stay, and he was discharged on warfarin with a therapeutic international normalized ratio. At a follow-up visit 3 months later, he was asymptomatic.

A RARE BUT SEVERE TYPE OF ACUTE DEEP VEIN THROMBOSIS

Phlegmasia cerulea dolens (painful cyanotic swollen leg) is a rare and severe form of acute deep vein thrombosis (DVT) characterized by marked limb pain, swelling, and blue discoloration.¹ DVT is the most common cause of acute-onset unilateral leg pain, swelling, and skin discoloration.²

The differential diagnosis

The differential diagnosis includes infection (cellulitis, necrotizing fasciitis), compartment syndrome from limb injury, musculoskeletal conditions such as ruptured Baker cyst, venous stasis due to external compression (May-Thurner syndrome, iliac vein compression syndrome, pelvic tumor), acute limb ischemia from arterial obstruction, and complex regional pain syndrome (reflex sympathetic dystrophy).

Management recommendations

As in most cases of DVT, initial treatment of phlegmasia cerulea dolens involves systemic anticoagulation with heparin, elevation of the affected extremity, and fluid resuscitation if the patient is hypotensive. However, phlegmasia cerulea dolens is a major indication for catheter-directed thrombolysis,^3,4 so an urgent vascular surgery or interventional cardiology consultation is also required. The American College of Chest Physicians recommends catheter-directed thrombolysis for acute DVT of the iliofemoral veins in patients with symptoms for less than 14 days, good functional capacity, and a life expectancy beyond 1 year.⁵ This intervention results in reduced incidence of postthrombotic syndrome and improved quality of life^5,6 compared with anticoagulation therapy alone.

Who is at risk?

Risk factors for phlegmasia cerulea dolens include a history of malignancy, inherited or acquired thrombophilia, surgery, radiation therapy, trauma, placement of an inferior vena cava filter, and pregnancy. In our patient, the iliac vein stenosis most likely was the result of the radiation therapy he had undergone for prostate cancer.

Arterial stenosis is a well-known complication of radiation therapy and is associated with an increased risk of cardiovascular events.^7,8 Radiation induces endothelial damage followed by proliferation of smooth muscle cells, resulting in luminal stenosis and thrombosis. At the cellular level, radiation leads to an acute increase in pro-inflammatory cytokines and endothelial adhesion molecules, causing the recruitment of inflammatory cells to radiation-exposed vessels and chronic activation of transcription factor NF-kappa B, leading to long-term inflammation and angiogenesis.⁹

Carotid, coronary, and iliac artery stenosis are known to occur around 10 years after radiation therapy to the head, neck, breast, and pelvis. Radiation-induced iliac vein stenosis is rare and can manifest as acute proximal DVT.

A 77-year-old man presented with a 5-day history of painful swelling of his right leg. He reported no trauma, no recent surgery, no history of thrombophilic disorder, and no prolonged immobilization. However, he had a history of prostate cancer, treated 10 years earlier with pelvic radiation.

Examination revealed massive right leg swelling extending from the thigh to the ankle, along with bluish-red skin discoloration (Figure 1). Doppler ultrasonography demonstrated acute thrombosis involving the right iliofemoral veins. These findings were consistent with phlegmasia cerulea dolens.

Urgent percutaneous catheter-directed thrombolysis was performed. Venography revealed extensive thrombosis of the femoral vein (Figure 2A) extending into the right external iliac vein. This was treated with catheter-directed pharmacomechanical thrombectomy.

Venography after this procedure showed significant improvement in venous blood flow (Figure 2B). However, stenosis of the right external iliac vein was also noted (Figure 2C) and was treated with balloon angioplasty (Figure 2D) followed by placement of a stent (14 × 40 mm).

In the immediate postprocedural period, there was marked reduction in swelling and normalization of skin color (Figure 3). The patient did not experience significant bleeding during or after the procedure. Treatment with intravenous unfractionated heparin was continued during the hospital stay, and he was discharged on warfarin with a therapeutic international normalized ratio. At a follow-up visit 3 months later, he was asymptomatic.

A RARE BUT SEVERE TYPE OF ACUTE DEEP VEIN THROMBOSIS

Phlegmasia cerulea dolens (painful cyanotic swollen leg) is a rare and severe form of acute deep vein thrombosis (DVT) characterized by marked limb pain, swelling, and blue discoloration.¹ DVT is the most common cause of acute-onset unilateral leg pain, swelling, and skin discoloration.²

The differential diagnosis

The differential diagnosis includes infection (cellulitis, necrotizing fasciitis), compartment syndrome from limb injury, musculoskeletal conditions such as ruptured Baker cyst, venous stasis due to external compression (May-Thurner syndrome, iliac vein compression syndrome, pelvic tumor), acute limb ischemia from arterial obstruction, and complex regional pain syndrome (reflex sympathetic dystrophy).

Management recommendations

As in most cases of DVT, initial treatment of phlegmasia cerulea dolens involves systemic anticoagulation with heparin, elevation of the affected extremity, and fluid resuscitation if the patient is hypotensive. However, phlegmasia cerulea dolens is a major indication for catheter-directed thrombolysis,^3,4 so an urgent vascular surgery or interventional cardiology consultation is also required. The American College of Chest Physicians recommends catheter-directed thrombolysis for acute DVT of the iliofemoral veins in patients with symptoms for less than 14 days, good functional capacity, and a life expectancy beyond 1 year.⁵ This intervention results in reduced incidence of postthrombotic syndrome and improved quality of life^5,6 compared with anticoagulation therapy alone.

Who is at risk?

Risk factors for phlegmasia cerulea dolens include a history of malignancy, inherited or acquired thrombophilia, surgery, radiation therapy, trauma, placement of an inferior vena cava filter, and pregnancy. In our patient, the iliac vein stenosis most likely was the result of the radiation therapy he had undergone for prostate cancer.

Arterial stenosis is a well-known complication of radiation therapy and is associated with an increased risk of cardiovascular events.^7,8 Radiation induces endothelial damage followed by proliferation of smooth muscle cells, resulting in luminal stenosis and thrombosis. At the cellular level, radiation leads to an acute increase in pro-inflammatory cytokines and endothelial adhesion molecules, causing the recruitment of inflammatory cells to radiation-exposed vessels and chronic activation of transcription factor NF-kappa B, leading to long-term inflammation and angiogenesis.⁹

Carotid, coronary, and iliac artery stenosis are known to occur around 10 years after radiation therapy to the head, neck, breast, and pelvis. Radiation-induced iliac vein stenosis is rare and can manifest as acute proximal DVT.

A 77-year-old man presented with a 5-day history of painful swelling of his right leg. He reported no trauma, no recent surgery, no history of thrombophilic disorder, and no prolonged immobilization. However, he had a history of prostate cancer, treated 10 years earlier with pelvic radiation.

Examination revealed massive right leg swelling extending from the thigh to the ankle, along with bluish-red skin discoloration (Figure 1). Doppler ultrasonography demonstrated acute thrombosis involving the right iliofemoral veins. These findings were consistent with phlegmasia cerulea dolens.

Urgent percutaneous catheter-directed thrombolysis was performed. Venography revealed extensive thrombosis of the femoral vein (Figure 2A) extending into the right external iliac vein. This was treated with catheter-directed pharmacomechanical thrombectomy.

Venography after this procedure showed significant improvement in venous blood flow (Figure 2B). However, stenosis of the right external iliac vein was also noted (Figure 2C) and was treated with balloon angioplasty (Figure 2D) followed by placement of a stent (14 × 40 mm).

In the immediate postprocedural period, there was marked reduction in swelling and normalization of skin color (Figure 3). The patient did not experience significant bleeding during or after the procedure. Treatment with intravenous unfractionated heparin was continued during the hospital stay, and he was discharged on warfarin with a therapeutic international normalized ratio. At a follow-up visit 3 months later, he was asymptomatic.

A RARE BUT SEVERE TYPE OF ACUTE DEEP VEIN THROMBOSIS

Phlegmasia cerulea dolens (painful cyanotic swollen leg) is a rare and severe form of acute deep vein thrombosis (DVT) characterized by marked limb pain, swelling, and blue discoloration.¹ DVT is the most common cause of acute-onset unilateral leg pain, swelling, and skin discoloration.²

The differential diagnosis

The differential diagnosis includes infection (cellulitis, necrotizing fasciitis), compartment syndrome from limb injury, musculoskeletal conditions such as ruptured Baker cyst, venous stasis due to external compression (May-Thurner syndrome, iliac vein compression syndrome, pelvic tumor), acute limb ischemia from arterial obstruction, and complex regional pain syndrome (reflex sympathetic dystrophy).

Management recommendations

As in most cases of DVT, initial treatment of phlegmasia cerulea dolens involves systemic anticoagulation with heparin, elevation of the affected extremity, and fluid resuscitation if the patient is hypotensive. However, phlegmasia cerulea dolens is a major indication for catheter-directed thrombolysis,^3,4 so an urgent vascular surgery or interventional cardiology consultation is also required. The American College of Chest Physicians recommends catheter-directed thrombolysis for acute DVT of the iliofemoral veins in patients with symptoms for less than 14 days, good functional capacity, and a life expectancy beyond 1 year.⁵ This intervention results in reduced incidence of postthrombotic syndrome and improved quality of life^5,6 compared with anticoagulation therapy alone.

Who is at risk?

Risk factors for phlegmasia cerulea dolens include a history of malignancy, inherited or acquired thrombophilia, surgery, radiation therapy, trauma, placement of an inferior vena cava filter, and pregnancy. In our patient, the iliac vein stenosis most likely was the result of the radiation therapy he had undergone for prostate cancer.

Arterial stenosis is a well-known complication of radiation therapy and is associated with an increased risk of cardiovascular events.^7,8 Radiation induces endothelial damage followed by proliferation of smooth muscle cells, resulting in luminal stenosis and thrombosis. At the cellular level, radiation leads to an acute increase in pro-inflammatory cytokines and endothelial adhesion molecules, causing the recruitment of inflammatory cells to radiation-exposed vessels and chronic activation of transcription factor NF-kappa B, leading to long-term inflammation and angiogenesis.⁹

Carotid, coronary, and iliac artery stenosis are known to occur around 10 years after radiation therapy to the head, neck, breast, and pelvis. Radiation-induced iliac vein stenosis is rare and can manifest as acute proximal DVT.

A 69-year-old diabetic woman with stage 4 non–small-cell lung cancer presented with a 3-day history of abdominal pain and loss of appetite. She was being treated with corticosteroids for a brain metastasis.

Computed tomography (CT) (Figure 1) revealed air within the bladder wall and lumen; diffuse air in the intraperitoneum and retroperitoneum; air distributed from the left iliopsoas muscle to the left femur that spread around the obturator muscle; air in the left ureter; and an abscess in the psoas major muscle extending to the ala of the ilium. A diagnosis of emphysematous cystitis complicated by extensive abdominal emphysema and abscess was made.

Blood cultures were negative, but urine cultures grew extended-spectrum beta-lactamase-producing Escherichia coli, which was sensitive to meropenem. Meropenem was given intravenously for 24 days and was stopped when levels of inflammatory markers improved and urine cultures were negative. However, on day 29, the patient developed a fever. Follow-up CT showed that the abscess in the psoas muscle had enlarged (Figure 2). We chose not to surgically drain the abscess because the patient had terminal lung cancer. The patient expired 6 days later, 35 days after her hospital admission.

EMPHYSEMATOUS CYSTITIS ASSOCIATED WITH A PSOAS MUSCLE ABSCESS

Emphysematous cystitis is an uncommon urinary tract infection characterized by air within the bladder wall and lumen that is caused by gas-producing pathogens.^1,2 The disease is often found in elderly diabetic women. Treatment of emphysematous cystitis typically includes intravenous antibiotics, adequate bladder drainage, and, for diabetic patients, appropriate glycemic control.

Psoas muscle abscess is a collection of pus in the retroperitoneal space.³ It can be primary, caused by hematogenous spread from the site of an occult infection, or secondary, caused by contiguous spread from adjacent infected organs, including those of the urinary tract. Psoas muscle abscess associated with emphysematous cystitis, as in our patient, is rare. We have seen only one other report in the medical literature.⁴

TREATMENT

The treatment of psoas muscle abscess involves the use of broad-spectrum antibiotics and drainage.⁵ Small abscesses (less than 3.5 cm) can be controlled with antibiotics alone. Image-guided percutaneous drainage is a safe, minimally invasive option. Surgery is indicated for unsuccessful percutaneous drainage, loculated abscesses, and abscesses difficult to approach percutaneously, or when the underlying disease requires definitive surgical management.

As in our patient, the presence of additional comorbid immunosuppressive conditions² such as lung cancer and treatment with corticosteroids can allow the infection to become widespread and life-threatening.

A 69-year-old diabetic woman with stage 4 non–small-cell lung cancer presented with a 3-day history of abdominal pain and loss of appetite. She was being treated with corticosteroids for a brain metastasis.

Computed tomography (CT) (Figure 1) revealed air within the bladder wall and lumen; diffuse air in the intraperitoneum and retroperitoneum; air distributed from the left iliopsoas muscle to the left femur that spread around the obturator muscle; air in the left ureter; and an abscess in the psoas major muscle extending to the ala of the ilium. A diagnosis of emphysematous cystitis complicated by extensive abdominal emphysema and abscess was made.

Blood cultures were negative, but urine cultures grew extended-spectrum beta-lactamase-producing Escherichia coli, which was sensitive to meropenem. Meropenem was given intravenously for 24 days and was stopped when levels of inflammatory markers improved and urine cultures were negative. However, on day 29, the patient developed a fever. Follow-up CT showed that the abscess in the psoas muscle had enlarged (Figure 2). We chose not to surgically drain the abscess because the patient had terminal lung cancer. The patient expired 6 days later, 35 days after her hospital admission.

EMPHYSEMATOUS CYSTITIS ASSOCIATED WITH A PSOAS MUSCLE ABSCESS

Emphysematous cystitis is an uncommon urinary tract infection characterized by air within the bladder wall and lumen that is caused by gas-producing pathogens.^1,2 The disease is often found in elderly diabetic women. Treatment of emphysematous cystitis typically includes intravenous antibiotics, adequate bladder drainage, and, for diabetic patients, appropriate glycemic control.

Psoas muscle abscess is a collection of pus in the retroperitoneal space.³ It can be primary, caused by hematogenous spread from the site of an occult infection, or secondary, caused by contiguous spread from adjacent infected organs, including those of the urinary tract. Psoas muscle abscess associated with emphysematous cystitis, as in our patient, is rare. We have seen only one other report in the medical literature.⁴

TREATMENT

The treatment of psoas muscle abscess involves the use of broad-spectrum antibiotics and drainage.⁵ Small abscesses (less than 3.5 cm) can be controlled with antibiotics alone. Image-guided percutaneous drainage is a safe, minimally invasive option. Surgery is indicated for unsuccessful percutaneous drainage, loculated abscesses, and abscesses difficult to approach percutaneously, or when the underlying disease requires definitive surgical management.

As in our patient, the presence of additional comorbid immunosuppressive conditions² such as lung cancer and treatment with corticosteroids can allow the infection to become widespread and life-threatening.

A 69-year-old diabetic woman with stage 4 non–small-cell lung cancer presented with a 3-day history of abdominal pain and loss of appetite. She was being treated with corticosteroids for a brain metastasis.

Computed tomography (CT) (Figure 1) revealed air within the bladder wall and lumen; diffuse air in the intraperitoneum and retroperitoneum; air distributed from the left iliopsoas muscle to the left femur that spread around the obturator muscle; air in the left ureter; and an abscess in the psoas major muscle extending to the ala of the ilium. A diagnosis of emphysematous cystitis complicated by extensive abdominal emphysema and abscess was made.

Blood cultures were negative, but urine cultures grew extended-spectrum beta-lactamase-producing Escherichia coli, which was sensitive to meropenem. Meropenem was given intravenously for 24 days and was stopped when levels of inflammatory markers improved and urine cultures were negative. However, on day 29, the patient developed a fever. Follow-up CT showed that the abscess in the psoas muscle had enlarged (Figure 2). We chose not to surgically drain the abscess because the patient had terminal lung cancer. The patient expired 6 days later, 35 days after her hospital admission.

EMPHYSEMATOUS CYSTITIS ASSOCIATED WITH A PSOAS MUSCLE ABSCESS

Emphysematous cystitis is an uncommon urinary tract infection characterized by air within the bladder wall and lumen that is caused by gas-producing pathogens.^1,2 The disease is often found in elderly diabetic women. Treatment of emphysematous cystitis typically includes intravenous antibiotics, adequate bladder drainage, and, for diabetic patients, appropriate glycemic control.

Psoas muscle abscess is a collection of pus in the retroperitoneal space.³ It can be primary, caused by hematogenous spread from the site of an occult infection, or secondary, caused by contiguous spread from adjacent infected organs, including those of the urinary tract. Psoas muscle abscess associated with emphysematous cystitis, as in our patient, is rare. We have seen only one other report in the medical literature.⁴

TREATMENT

The treatment of psoas muscle abscess involves the use of broad-spectrum antibiotics and drainage.⁵ Small abscesses (less than 3.5 cm) can be controlled with antibiotics alone. Image-guided percutaneous drainage is a safe, minimally invasive option. Surgery is indicated for unsuccessful percutaneous drainage, loculated abscesses, and abscesses difficult to approach percutaneously, or when the underlying disease requires definitive surgical management.

As in our patient, the presence of additional comorbid immunosuppressive conditions² such as lung cancer and treatment with corticosteroids can allow the infection to become widespread and life-threatening.

Ultrasound has classically been marketed and used as a diagnostic tool. Radiologists, emergency physicians, and sports physicians used ultrasound units to rapidly and appropriately diagnose numerous injuries and disorders, in a timely and cost effective manner. Part 1¹ and Part 2² of this series showed how to use ultrasound in the shoulder for diagnosis and how to code and get reimbursed for its use.Ultrasound can also be used to help guide procedures and interventions performed to treat patients. Currently, more physicians are beginning to recognize the utility of this modality as an aid to interventional procedures.

First-generation procedures use ultrasound to improve accuracy of joint, bursal, tendon, and muscular injections.³ Recent studies have shown a significant improvement in accuracy, outcomes, and patient satisfaction using ultrasound guidance for injections.^3-12 Within the limitation of using a needle, second-generation procedures—hydrodissection of peripherally entrapped nerves, capsular distention, mechanical disruption of neovascularization, and needle fenestration or barbotage in chronic tendinopathy—try to simulate surgical objectives while minimizing tissue burden and other complications of surgery.³ More advanced procedures include needle fenestration/release of the carpal ligament in carpal tunnel syndrome and A1 pulley needle release in the setting of trigger finger.³ Innovative third-generation procedures involve the use of surgical tools such as hook blades under ultrasound guidance to perform surgical procedures. Surgeons are now improving already established percutaneous, arthroscopic, and open surgical procedures with ultrasound assistance.³ Aside from better guidance, reducing cost and improving surgeon comfort may be additional benefits of ultrasound assisted surgery.

Image-Guided Treatment Options

Prior to image guidance, palpation of surface anatomy helped physicians determine the anatomic placement of injections, incisions, or portals. Joints and bursas that do not have any inflammation or fluid can sometimes be difficult to identify or locate by palpation alone. Palpation-guided joint injections often miss their target and cause significant pain when the therapeutic agent is injected into a muscle, tendon, ligament, fat, or other tissue. Ultrasound-guided injections have proven to be more accurate and have better patient satisfaction when compared to blind injections.^3-12

X-ray fluoroscopy has been the primary option for surgeons to assist in surgery. This is a natural modality for orthopedic surgeons; their primary use is for bone to help with fracture reduction and fixation as the bone, instrumentation, and fixation methods are usually radio-opaque. With the advancement in technology, many orthopedic surgeons are regularly using radiolucent fixation devices and working with soft tissue as opposed to bone. Fixation of tendons, ligaments, and muscles would be done using a large incision, palpation of the anatomy, then fixation or repair. Many surgeons began looking for ways to minimize the incisions. Turning to fluoroscopy, a traditional and well-used modality, was a natural progression. Guides and methods were developed to isolate insertions and drill placements. However, fluoroscopy is limited by its difficulty in changing planes and the large equipment required. Also, it is limited in its ability to image soft tissue.

Computed tomography (CT) scans and magnetic resonance imaging (MRI) are far better at imaging soft tissue but cannot be taken for use into the office or surgical suite. These modalities are also far more expensive and take up significant space.

Ultrasound Procedural Basics

Appropriate use of ultrasound still remains highly technician-dependent. Unlike other imaging modalities, ultrasound requires a higher skill level by the physician to implement the use of ultrasound and identification of pathology to treat these disease processes. However, this is no different from the use of arthroscopy or fluoroscopy to treat patients. Training is required, as well as an understanding of the ultrasound machine, anatomy, and sono-anatomy—identification of anatomy and pathology as shown by the ultrasound machine.²

In ultrasound, the long axis refers to looking at a structure along its length, as in longitudinal. The short axis refers to evaluating a structure in cross-section, transverse, or along its shortest length. “In plane” refers to performing a procedure where the needle or object being used enters the ultrasound field along the plane of the transducer, allowing visualization of the majority of the needle as it crosses tissue planes. “Out of plane” has the needle entering perpendicular to the plane of the transducer, showing the needle on the monitor as a bright, hyperechoic dot. Some studies have suggested that novice ultrasonographers should start in a long axis view and use the in plane technique when injecting, as doing so may decrease time to identify the target and improve mean imaging quality during needle advancement.¹³

Anisotropy is the property of being directionally dependent. The ultrasound beam needs to be perpendicular to the structure being imaged to give the optimal image. When the beam hits a longitudinal structure like a needle at an angle <90°, the linear structure might reflect most of the beam away from the transducer. So when using a needle to localize or inject a specific area, maintaining the probe as close to perpendicular as possible with the needle will give a better image. New technology exists to better visualize needles even at high acuity angles by using a multi-beam processing algorithm, which can significantly aid the physician without the need for specialized needles.

Despite better technology, advance planning is key to a successful procedure. Positioning the patient and ultrasound machine in a manner that is comfortable and makes the desired target accessible while being able to visualize the ultrasound monitor comes first. Identifying the target, mapping the needle trajectory using depth markings, and scanning for nerves, vessels, and other structures that may be damaged along the needle path comes next. Using the in plane ultrasound technique with color Doppler and the nerve contrast setting can ensure that the physician has placed the therapeutic agent to the proper location while avoiding any nerves, arteries, or veins. Marking the borders of the ultrasound probe and needle entry site can be helpful to return to the same area after sterile preparation is done. As in any procedure, sterile technique is paramount. Sterile technique considerations may include using sterile gloves and a probe cover with sterile gel, cleaning the area thoroughly, planning the needle entry point 3 cm to 5 cm away from the probe, and maintaining a dry and gel-free needle entry.^14-15 The probe should be sterilized between patients to avoid cross-contamination; note that certain solutions like alcohol or ethyl chloride can damage the transducer.^14-15 However, simple injections do not require such stringent standards when simple sterile technique is observed by cleaning and then never touching the cleaned area again except with the needle to avoid contamination. Also, ethyl chloride has been found to not contaminate a sterile site and can be used safely to anesthetize the skin.

Ultrasound-Guided Procedures

Many injectable therapeutic options exist as interventions. Cortisone, hyaluronic acid, platelet-rich plasma (PRP), stem cells/bone marrow concentrate (BMC), amniotic fluid, prolotherapy, and saline are now commonly used.^16-17 A meta-analysis of the literature assessing the accuracy of ultrasound-guided shoulder girdle injections vs a landmark-guided injection was done in 2015.¹⁸ It showed that for the acromioclavicular joint, accuracy was 93.6% vs 68.2% (P < .0001), based on single studies. The accuracy of ultrasound vs a landmark-guided injection was 65% vs 70% for the subacromial space (P > .05); 86.7% vs 26.7% for the biceps tendon sheath (P < .05); and 92.5% vs 72.5% for the glenohumeral joint (P = .025).¹⁸ 

With cortisone, injecting into muscle, ligament, or tendons could potentially harm the tissue or cause worsening of the disease process.^19-20 With the advent of orthobiologics, injecting into these structures is now desirable, instead of a potential complication.^19-20 Ultrasound has become even more important to the accurate delivery of these therapies to the disease locations. Multiple studies using leukocyte-poor PRP for osteoarthritis show significant differences in pain scores.^21-23 Peerbooms and colleagues^24,25 also showed that PRP reduced pain and increased function compared to cortisone injections for lateral epicondylitis in 1- and 2-year double-blind randomized controlled trials. Centeno and colleagues²⁶ performed a prospective, multi-site registry study on 102 patients with symptomatic osteoarthritis and/or rotator cuff tears that were injected with bone marrow concentrate. There was a statistically significant improvement in Disabilities of the Arm, Shoulder and Hand (DASH) scores from 36.1 to 17.1 (P < .001) and numeric pain scores improved from 4.3 to 2.4 (P < .001).

By being able to see the pathology, like a hypoechoic region in a tendon, ligament, or muscle, the physician can reliably place the therapeutic agent into the precise location. Also, adjacent para-tendon or para-ligament injections allow for in-season athletes to get some relief from symptoms while allowing to return to play quickly; injections into muscle, ligament, or tendon can damage the structure and require days or weeks of rest, while para-tendon and para-ligament injections are far less painful.

Second-generation techniques have provided patients with great options that can help avoid surgery. Calcific tendonitis appears brightly hyperechoic on ultrasound and is easily identified. The physician can attempt to break up the calcium by fenestration or barbotage of the calcium. The same can be accomplished by injecting the density with PRP or stem cells. If the calcium is soft or “toothpaste-like,” the negative pressure will make it easy to aspirate it into the syringe. A 2-year, longitudinal prospective study of 121 patients demonstrated that visual analog score (VAS) pain scores and size of calcium significantly decreased with ultrasound-guided percutaneous needle lavage; 89% of patients were pain-free at 1-year follow-up.²⁷ Moreover, a randomized controlled trial of 48 patients comparing needle lavage vs subacromial steroid injection showed statistically significant radiographic and clinically better outcomes with the needle lavage group at the 1-year mark.²⁸

The Tenex procedure is a novel technique that uses ultrasonic energy to fenestrate diseased tendon tissue. It also can be used to break up calcific deposits. After the Tenex probe is guided to the diseased tendon/calcium, the TX-1 tip oscillates at the speed of sound, fenestrating/cutting through the tendon or calcium while lavaging the tendon with saline. Multiple prospective, noncontrolled studies done in common extensor, patellar, and rotator cuff tendinopathy have demonstrated good to excellent improvements in pain scores with the Tenex procedure.^29-31

Ultrasound is extremely useful in the treatment of adhesive capsulitis.³² The posterior glenohumeral capsule can be distended using a large volume (60 cc) of saline to loosen adhesions in preparation for manipulation. Because the manipulation can be an extremely painful procedure, ultrasound can be used to perform an inter-scalene block for regional anesthesia prior to the procedure. In 2014, Park and colleagues³³ performed a randomized prospective trial that showed that capsular distension followed by manipulation was more effective than cortisone injection alone for the treatment of adhesive capsulitis.Ultrasound guidance was found to be just as efficacious as fluoroscopy in a randomized controlled trial in 2014; the authors noted that ultrasound does not expose the patient or clinician to radiation and can be done in office.³⁴

Currently, techniques to perform ultrasound-guided percutaneous tenotomies of the long head of the biceps tendon using hook blades are being studied.³⁵

Ultrasound-Assisted Surgery

Ultrasound has been a boon to surgeons who perform minimally invasive procedures. It is far less cumbersome than classic fluoroscopy. Fluoroscopy requires the use of heavy lead aprons by the surgeons. Combining this with the impervious gowns and hot lights, the surgeons’ comfort level is severely sacrificed. When having to do many long surgeries in a row, this situation can take a toll on the surgeons’ endurance and strength. Improving the comfort of the surgeon is not the primary goal of surgery, but can significantly help our ability to do a better job.

Ultrasound allows the surgeon to localize any superficial foreign objects, especially with radiolucent objects like fragments of glass. Small glass fragments or pieces of wood have always been extremely difficult to remove. X-rays cannot localize these objects, so getting a proper orientation is difficult. MRI and CT scans easily identify these types of foreign objects, but cannot be used intraoperatively (Figure 1A). Often, these objects cannot be felt and therefore require a large dissection. The objects may encapsulate and be easily confused with other soft tissues.

Conclusion

Ultrasound is quickly becoming a popular imaging modality due to its simplicity, portability, and cost efficiency. Its use as a diagnostic tool is widely known. As an adjunct for procedures and interventions, its advantages over larger, more expensive modalities such as fluoroscopy, CT, or MRI make it stand out. Ultrasound is not the perfect solution to all problems, but it is clearly a technology that is gaining traction. Ultrasound is another imaging modality and tool that physicians and surgeons can use to improve their patients’ treatment.

Ultrasound has classically been marketed and used as a diagnostic tool. Radiologists, emergency physicians, and sports physicians used ultrasound units to rapidly and appropriately diagnose numerous injuries and disorders, in a timely and cost effective manner. Part 1¹ and Part 2² of this series showed how to use ultrasound in the shoulder for diagnosis and how to code and get reimbursed for its use.Ultrasound can also be used to help guide procedures and interventions performed to treat patients. Currently, more physicians are beginning to recognize the utility of this modality as an aid to interventional procedures.

First-generation procedures use ultrasound to improve accuracy of joint, bursal, tendon, and muscular injections.³ Recent studies have shown a significant improvement in accuracy, outcomes, and patient satisfaction using ultrasound guidance for injections.^3-12 Within the limitation of using a needle, second-generation procedures—hydrodissection of peripherally entrapped nerves, capsular distention, mechanical disruption of neovascularization, and needle fenestration or barbotage in chronic tendinopathy—try to simulate surgical objectives while minimizing tissue burden and other complications of surgery.³ More advanced procedures include needle fenestration/release of the carpal ligament in carpal tunnel syndrome and A1 pulley needle release in the setting of trigger finger.³ Innovative third-generation procedures involve the use of surgical tools such as hook blades under ultrasound guidance to perform surgical procedures. Surgeons are now improving already established percutaneous, arthroscopic, and open surgical procedures with ultrasound assistance.³ Aside from better guidance, reducing cost and improving surgeon comfort may be additional benefits of ultrasound assisted surgery.

Image-Guided Treatment Options

Prior to image guidance, palpation of surface anatomy helped physicians determine the anatomic placement of injections, incisions, or portals. Joints and bursas that do not have any inflammation or fluid can sometimes be difficult to identify or locate by palpation alone. Palpation-guided joint injections often miss their target and cause significant pain when the therapeutic agent is injected into a muscle, tendon, ligament, fat, or other tissue. Ultrasound-guided injections have proven to be more accurate and have better patient satisfaction when compared to blind injections.^3-12

X-ray fluoroscopy has been the primary option for surgeons to assist in surgery. This is a natural modality for orthopedic surgeons; their primary use is for bone to help with fracture reduction and fixation as the bone, instrumentation, and fixation methods are usually radio-opaque. With the advancement in technology, many orthopedic surgeons are regularly using radiolucent fixation devices and working with soft tissue as opposed to bone. Fixation of tendons, ligaments, and muscles would be done using a large incision, palpation of the anatomy, then fixation or repair. Many surgeons began looking for ways to minimize the incisions. Turning to fluoroscopy, a traditional and well-used modality, was a natural progression. Guides and methods were developed to isolate insertions and drill placements. However, fluoroscopy is limited by its difficulty in changing planes and the large equipment required. Also, it is limited in its ability to image soft tissue.

Computed tomography (CT) scans and magnetic resonance imaging (MRI) are far better at imaging soft tissue but cannot be taken for use into the office or surgical suite. These modalities are also far more expensive and take up significant space.

Ultrasound Procedural Basics

Appropriate use of ultrasound still remains highly technician-dependent. Unlike other imaging modalities, ultrasound requires a higher skill level by the physician to implement the use of ultrasound and identification of pathology to treat these disease processes. However, this is no different from the use of arthroscopy or fluoroscopy to treat patients. Training is required, as well as an understanding of the ultrasound machine, anatomy, and sono-anatomy—identification of anatomy and pathology as shown by the ultrasound machine.²

In ultrasound, the long axis refers to looking at a structure along its length, as in longitudinal. The short axis refers to evaluating a structure in cross-section, transverse, or along its shortest length. “In plane” refers to performing a procedure where the needle or object being used enters the ultrasound field along the plane of the transducer, allowing visualization of the majority of the needle as it crosses tissue planes. “Out of plane” has the needle entering perpendicular to the plane of the transducer, showing the needle on the monitor as a bright, hyperechoic dot. Some studies have suggested that novice ultrasonographers should start in a long axis view and use the in plane technique when injecting, as doing so may decrease time to identify the target and improve mean imaging quality during needle advancement.¹³

Anisotropy is the property of being directionally dependent. The ultrasound beam needs to be perpendicular to the structure being imaged to give the optimal image. When the beam hits a longitudinal structure like a needle at an angle <90°, the linear structure might reflect most of the beam away from the transducer. So when using a needle to localize or inject a specific area, maintaining the probe as close to perpendicular as possible with the needle will give a better image. New technology exists to better visualize needles even at high acuity angles by using a multi-beam processing algorithm, which can significantly aid the physician without the need for specialized needles.

Despite better technology, advance planning is key to a successful procedure. Positioning the patient and ultrasound machine in a manner that is comfortable and makes the desired target accessible while being able to visualize the ultrasound monitor comes first. Identifying the target, mapping the needle trajectory using depth markings, and scanning for nerves, vessels, and other structures that may be damaged along the needle path comes next. Using the in plane ultrasound technique with color Doppler and the nerve contrast setting can ensure that the physician has placed the therapeutic agent to the proper location while avoiding any nerves, arteries, or veins. Marking the borders of the ultrasound probe and needle entry site can be helpful to return to the same area after sterile preparation is done. As in any procedure, sterile technique is paramount. Sterile technique considerations may include using sterile gloves and a probe cover with sterile gel, cleaning the area thoroughly, planning the needle entry point 3 cm to 5 cm away from the probe, and maintaining a dry and gel-free needle entry.^14-15 The probe should be sterilized between patients to avoid cross-contamination; note that certain solutions like alcohol or ethyl chloride can damage the transducer.^14-15 However, simple injections do not require such stringent standards when simple sterile technique is observed by cleaning and then never touching the cleaned area again except with the needle to avoid contamination. Also, ethyl chloride has been found to not contaminate a sterile site and can be used safely to anesthetize the skin.

Ultrasound-Guided Procedures

Many injectable therapeutic options exist as interventions. Cortisone, hyaluronic acid, platelet-rich plasma (PRP), stem cells/bone marrow concentrate (BMC), amniotic fluid, prolotherapy, and saline are now commonly used.^16-17 A meta-analysis of the literature assessing the accuracy of ultrasound-guided shoulder girdle injections vs a landmark-guided injection was done in 2015.¹⁸ It showed that for the acromioclavicular joint, accuracy was 93.6% vs 68.2% (P < .0001), based on single studies. The accuracy of ultrasound vs a landmark-guided injection was 65% vs 70% for the subacromial space (P > .05); 86.7% vs 26.7% for the biceps tendon sheath (P < .05); and 92.5% vs 72.5% for the glenohumeral joint (P = .025).¹⁸ 

With cortisone, injecting into muscle, ligament, or tendons could potentially harm the tissue or cause worsening of the disease process.^19-20 With the advent of orthobiologics, injecting into these structures is now desirable, instead of a potential complication.^19-20 Ultrasound has become even more important to the accurate delivery of these therapies to the disease locations. Multiple studies using leukocyte-poor PRP for osteoarthritis show significant differences in pain scores.^21-23 Peerbooms and colleagues^24,25 also showed that PRP reduced pain and increased function compared to cortisone injections for lateral epicondylitis in 1- and 2-year double-blind randomized controlled trials. Centeno and colleagues²⁶ performed a prospective, multi-site registry study on 102 patients with symptomatic osteoarthritis and/or rotator cuff tears that were injected with bone marrow concentrate. There was a statistically significant improvement in Disabilities of the Arm, Shoulder and Hand (DASH) scores from 36.1 to 17.1 (P < .001) and numeric pain scores improved from 4.3 to 2.4 (P < .001).

By being able to see the pathology, like a hypoechoic region in a tendon, ligament, or muscle, the physician can reliably place the therapeutic agent into the precise location. Also, adjacent para-tendon or para-ligament injections allow for in-season athletes to get some relief from symptoms while allowing to return to play quickly; injections into muscle, ligament, or tendon can damage the structure and require days or weeks of rest, while para-tendon and para-ligament injections are far less painful.

Second-generation techniques have provided patients with great options that can help avoid surgery. Calcific tendonitis appears brightly hyperechoic on ultrasound and is easily identified. The physician can attempt to break up the calcium by fenestration or barbotage of the calcium. The same can be accomplished by injecting the density with PRP or stem cells. If the calcium is soft or “toothpaste-like,” the negative pressure will make it easy to aspirate it into the syringe. A 2-year, longitudinal prospective study of 121 patients demonstrated that visual analog score (VAS) pain scores and size of calcium significantly decreased with ultrasound-guided percutaneous needle lavage; 89% of patients were pain-free at 1-year follow-up.²⁷ Moreover, a randomized controlled trial of 48 patients comparing needle lavage vs subacromial steroid injection showed statistically significant radiographic and clinically better outcomes with the needle lavage group at the 1-year mark.²⁸

The Tenex procedure is a novel technique that uses ultrasonic energy to fenestrate diseased tendon tissue. It also can be used to break up calcific deposits. After the Tenex probe is guided to the diseased tendon/calcium, the TX-1 tip oscillates at the speed of sound, fenestrating/cutting through the tendon or calcium while lavaging the tendon with saline. Multiple prospective, noncontrolled studies done in common extensor, patellar, and rotator cuff tendinopathy have demonstrated good to excellent improvements in pain scores with the Tenex procedure.^29-31

Ultrasound is extremely useful in the treatment of adhesive capsulitis.³² The posterior glenohumeral capsule can be distended using a large volume (60 cc) of saline to loosen adhesions in preparation for manipulation. Because the manipulation can be an extremely painful procedure, ultrasound can be used to perform an inter-scalene block for regional anesthesia prior to the procedure. In 2014, Park and colleagues³³ performed a randomized prospective trial that showed that capsular distension followed by manipulation was more effective than cortisone injection alone for the treatment of adhesive capsulitis.Ultrasound guidance was found to be just as efficacious as fluoroscopy in a randomized controlled trial in 2014; the authors noted that ultrasound does not expose the patient or clinician to radiation and can be done in office.³⁴

Currently, techniques to perform ultrasound-guided percutaneous tenotomies of the long head of the biceps tendon using hook blades are being studied.³⁵

Ultrasound-Assisted Surgery

Ultrasound has been a boon to surgeons who perform minimally invasive procedures. It is far less cumbersome than classic fluoroscopy. Fluoroscopy requires the use of heavy lead aprons by the surgeons. Combining this with the impervious gowns and hot lights, the surgeons’ comfort level is severely sacrificed. When having to do many long surgeries in a row, this situation can take a toll on the surgeons’ endurance and strength. Improving the comfort of the surgeon is not the primary goal of surgery, but can significantly help our ability to do a better job.

Ultrasound allows the surgeon to localize any superficial foreign objects, especially with radiolucent objects like fragments of glass. Small glass fragments or pieces of wood have always been extremely difficult to remove. X-rays cannot localize these objects, so getting a proper orientation is difficult. MRI and CT scans easily identify these types of foreign objects, but cannot be used intraoperatively (Figure 1A). Often, these objects cannot be felt and therefore require a large dissection. The objects may encapsulate and be easily confused with other soft tissues.

Conclusion

Ultrasound is quickly becoming a popular imaging modality due to its simplicity, portability, and cost efficiency. Its use as a diagnostic tool is widely known. As an adjunct for procedures and interventions, its advantages over larger, more expensive modalities such as fluoroscopy, CT, or MRI make it stand out. Ultrasound is not the perfect solution to all problems, but it is clearly a technology that is gaining traction. Ultrasound is another imaging modality and tool that physicians and surgeons can use to improve their patients’ treatment.

Ultrasound has classically been marketed and used as a diagnostic tool. Radiologists, emergency physicians, and sports physicians used ultrasound units to rapidly and appropriately diagnose numerous injuries and disorders, in a timely and cost effective manner. Part 1¹ and Part 2² of this series showed how to use ultrasound in the shoulder for diagnosis and how to code and get reimbursed for its use.Ultrasound can also be used to help guide procedures and interventions performed to treat patients. Currently, more physicians are beginning to recognize the utility of this modality as an aid to interventional procedures.

First-generation procedures use ultrasound to improve accuracy of joint, bursal, tendon, and muscular injections.³ Recent studies have shown a significant improvement in accuracy, outcomes, and patient satisfaction using ultrasound guidance for injections.^3-12 Within the limitation of using a needle, second-generation procedures—hydrodissection of peripherally entrapped nerves, capsular distention, mechanical disruption of neovascularization, and needle fenestration or barbotage in chronic tendinopathy—try to simulate surgical objectives while minimizing tissue burden and other complications of surgery.³ More advanced procedures include needle fenestration/release of the carpal ligament in carpal tunnel syndrome and A1 pulley needle release in the setting of trigger finger.³ Innovative third-generation procedures involve the use of surgical tools such as hook blades under ultrasound guidance to perform surgical procedures. Surgeons are now improving already established percutaneous, arthroscopic, and open surgical procedures with ultrasound assistance.³ Aside from better guidance, reducing cost and improving surgeon comfort may be additional benefits of ultrasound assisted surgery.

Image-Guided Treatment Options

Prior to image guidance, palpation of surface anatomy helped physicians determine the anatomic placement of injections, incisions, or portals. Joints and bursas that do not have any inflammation or fluid can sometimes be difficult to identify or locate by palpation alone. Palpation-guided joint injections often miss their target and cause significant pain when the therapeutic agent is injected into a muscle, tendon, ligament, fat, or other tissue. Ultrasound-guided injections have proven to be more accurate and have better patient satisfaction when compared to blind injections.^3-12

X-ray fluoroscopy has been the primary option for surgeons to assist in surgery. This is a natural modality for orthopedic surgeons; their primary use is for bone to help with fracture reduction and fixation as the bone, instrumentation, and fixation methods are usually radio-opaque. With the advancement in technology, many orthopedic surgeons are regularly using radiolucent fixation devices and working with soft tissue as opposed to bone. Fixation of tendons, ligaments, and muscles would be done using a large incision, palpation of the anatomy, then fixation or repair. Many surgeons began looking for ways to minimize the incisions. Turning to fluoroscopy, a traditional and well-used modality, was a natural progression. Guides and methods were developed to isolate insertions and drill placements. However, fluoroscopy is limited by its difficulty in changing planes and the large equipment required. Also, it is limited in its ability to image soft tissue.

Computed tomography (CT) scans and magnetic resonance imaging (MRI) are far better at imaging soft tissue but cannot be taken for use into the office or surgical suite. These modalities are also far more expensive and take up significant space.

Ultrasound Procedural Basics

Appropriate use of ultrasound still remains highly technician-dependent. Unlike other imaging modalities, ultrasound requires a higher skill level by the physician to implement the use of ultrasound and identification of pathology to treat these disease processes. However, this is no different from the use of arthroscopy or fluoroscopy to treat patients. Training is required, as well as an understanding of the ultrasound machine, anatomy, and sono-anatomy—identification of anatomy and pathology as shown by the ultrasound machine.²

In ultrasound, the long axis refers to looking at a structure along its length, as in longitudinal. The short axis refers to evaluating a structure in cross-section, transverse, or along its shortest length. “In plane” refers to performing a procedure where the needle or object being used enters the ultrasound field along the plane of the transducer, allowing visualization of the majority of the needle as it crosses tissue planes. “Out of plane” has the needle entering perpendicular to the plane of the transducer, showing the needle on the monitor as a bright, hyperechoic dot. Some studies have suggested that novice ultrasonographers should start in a long axis view and use the in plane technique when injecting, as doing so may decrease time to identify the target and improve mean imaging quality during needle advancement.¹³

Anisotropy is the property of being directionally dependent. The ultrasound beam needs to be perpendicular to the structure being imaged to give the optimal image. When the beam hits a longitudinal structure like a needle at an angle <90°, the linear structure might reflect most of the beam away from the transducer. So when using a needle to localize or inject a specific area, maintaining the probe as close to perpendicular as possible with the needle will give a better image. New technology exists to better visualize needles even at high acuity angles by using a multi-beam processing algorithm, which can significantly aid the physician without the need for specialized needles.

Despite better technology, advance planning is key to a successful procedure. Positioning the patient and ultrasound machine in a manner that is comfortable and makes the desired target accessible while being able to visualize the ultrasound monitor comes first. Identifying the target, mapping the needle trajectory using depth markings, and scanning for nerves, vessels, and other structures that may be damaged along the needle path comes next. Using the in plane ultrasound technique with color Doppler and the nerve contrast setting can ensure that the physician has placed the therapeutic agent to the proper location while avoiding any nerves, arteries, or veins. Marking the borders of the ultrasound probe and needle entry site can be helpful to return to the same area after sterile preparation is done. As in any procedure, sterile technique is paramount. Sterile technique considerations may include using sterile gloves and a probe cover with sterile gel, cleaning the area thoroughly, planning the needle entry point 3 cm to 5 cm away from the probe, and maintaining a dry and gel-free needle entry.^14-15 The probe should be sterilized between patients to avoid cross-contamination; note that certain solutions like alcohol or ethyl chloride can damage the transducer.^14-15 However, simple injections do not require such stringent standards when simple sterile technique is observed by cleaning and then never touching the cleaned area again except with the needle to avoid contamination. Also, ethyl chloride has been found to not contaminate a sterile site and can be used safely to anesthetize the skin.

Ultrasound-Guided Procedures

Many injectable therapeutic options exist as interventions. Cortisone, hyaluronic acid, platelet-rich plasma (PRP), stem cells/bone marrow concentrate (BMC), amniotic fluid, prolotherapy, and saline are now commonly used.^16-17 A meta-analysis of the literature assessing the accuracy of ultrasound-guided shoulder girdle injections vs a landmark-guided injection was done in 2015.¹⁸ It showed that for the acromioclavicular joint, accuracy was 93.6% vs 68.2% (P < .0001), based on single studies. The accuracy of ultrasound vs a landmark-guided injection was 65% vs 70% for the subacromial space (P > .05); 86.7% vs 26.7% for the biceps tendon sheath (P < .05); and 92.5% vs 72.5% for the glenohumeral joint (P = .025).¹⁸ 

With cortisone, injecting into muscle, ligament, or tendons could potentially harm the tissue or cause worsening of the disease process.^19-20 With the advent of orthobiologics, injecting into these structures is now desirable, instead of a potential complication.^19-20 Ultrasound has become even more important to the accurate delivery of these therapies to the disease locations. Multiple studies using leukocyte-poor PRP for osteoarthritis show significant differences in pain scores.^21-23 Peerbooms and colleagues^24,25 also showed that PRP reduced pain and increased function compared to cortisone injections for lateral epicondylitis in 1- and 2-year double-blind randomized controlled trials. Centeno and colleagues²⁶ performed a prospective, multi-site registry study on 102 patients with symptomatic osteoarthritis and/or rotator cuff tears that were injected with bone marrow concentrate. There was a statistically significant improvement in Disabilities of the Arm, Shoulder and Hand (DASH) scores from 36.1 to 17.1 (P < .001) and numeric pain scores improved from 4.3 to 2.4 (P < .001).

By being able to see the pathology, like a hypoechoic region in a tendon, ligament, or muscle, the physician can reliably place the therapeutic agent into the precise location. Also, adjacent para-tendon or para-ligament injections allow for in-season athletes to get some relief from symptoms while allowing to return to play quickly; injections into muscle, ligament, or tendon can damage the structure and require days or weeks of rest, while para-tendon and para-ligament injections are far less painful.

Second-generation techniques have provided patients with great options that can help avoid surgery. Calcific tendonitis appears brightly hyperechoic on ultrasound and is easily identified. The physician can attempt to break up the calcium by fenestration or barbotage of the calcium. The same can be accomplished by injecting the density with PRP or stem cells. If the calcium is soft or “toothpaste-like,” the negative pressure will make it easy to aspirate it into the syringe. A 2-year, longitudinal prospective study of 121 patients demonstrated that visual analog score (VAS) pain scores and size of calcium significantly decreased with ultrasound-guided percutaneous needle lavage; 89% of patients were pain-free at 1-year follow-up.²⁷ Moreover, a randomized controlled trial of 48 patients comparing needle lavage vs subacromial steroid injection showed statistically significant radiographic and clinically better outcomes with the needle lavage group at the 1-year mark.²⁸

The Tenex procedure is a novel technique that uses ultrasonic energy to fenestrate diseased tendon tissue. It also can be used to break up calcific deposits. After the Tenex probe is guided to the diseased tendon/calcium, the TX-1 tip oscillates at the speed of sound, fenestrating/cutting through the tendon or calcium while lavaging the tendon with saline. Multiple prospective, noncontrolled studies done in common extensor, patellar, and rotator cuff tendinopathy have demonstrated good to excellent improvements in pain scores with the Tenex procedure.^29-31

Ultrasound is extremely useful in the treatment of adhesive capsulitis.³² The posterior glenohumeral capsule can be distended using a large volume (60 cc) of saline to loosen adhesions in preparation for manipulation. Because the manipulation can be an extremely painful procedure, ultrasound can be used to perform an inter-scalene block for regional anesthesia prior to the procedure. In 2014, Park and colleagues³³ performed a randomized prospective trial that showed that capsular distension followed by manipulation was more effective than cortisone injection alone for the treatment of adhesive capsulitis.Ultrasound guidance was found to be just as efficacious as fluoroscopy in a randomized controlled trial in 2014; the authors noted that ultrasound does not expose the patient or clinician to radiation and can be done in office.³⁴

Currently, techniques to perform ultrasound-guided percutaneous tenotomies of the long head of the biceps tendon using hook blades are being studied.³⁵

Ultrasound-Assisted Surgery

Ultrasound has been a boon to surgeons who perform minimally invasive procedures. It is far less cumbersome than classic fluoroscopy. Fluoroscopy requires the use of heavy lead aprons by the surgeons. Combining this with the impervious gowns and hot lights, the surgeons’ comfort level is severely sacrificed. When having to do many long surgeries in a row, this situation can take a toll on the surgeons’ endurance and strength. Improving the comfort of the surgeon is not the primary goal of surgery, but can significantly help our ability to do a better job.

Ultrasound allows the surgeon to localize any superficial foreign objects, especially with radiolucent objects like fragments of glass. Small glass fragments or pieces of wood have always been extremely difficult to remove. X-rays cannot localize these objects, so getting a proper orientation is difficult. MRI and CT scans easily identify these types of foreign objects, but cannot be used intraoperatively (Figure 1A). Often, these objects cannot be felt and therefore require a large dissection. The objects may encapsulate and be easily confused with other soft tissues.

Conclusion

Ultrasound is quickly becoming a popular imaging modality due to its simplicity, portability, and cost efficiency. Its use as a diagnostic tool is widely known. As an adjunct for procedures and interventions, its advantages over larger, more expensive modalities such as fluoroscopy, CT, or MRI make it stand out. Ultrasound is not the perfect solution to all problems, but it is clearly a technology that is gaining traction. Ultrasound is another imaging modality and tool that physicians and surgeons can use to improve their patients’ treatment.