Imaging

A   43-year-old woman presented to the  clinic complaining of bilateral ankle joint pain for 2 months. She denied a history of fever, weight loss, addictions, cough, or trauma. On physical examinatio, she had swelling of the ankle and wrist joints and digital clubbing (Figure 1). Active movement of the ankles and wrists was restricted due to pain. The examination was otherwise unremarkable.

Radiography of both ankles showed a lamellar type periosteal reaction suggestive of periostitis (Figure 2). Computed tomography of the chest revealed a spiculated mass over the right lower lobe. Biopsy study of the mass was positive for squamous cell carcinoma. She was referred to the oncology center for further management.

FEATURES OF HYPERTROPHIC OSTEOARTHROPATHY

Digital clubbing is one of the oldest signs in clinical medicine. It is characterized by bulbous enlargement of the terminal segments of the fingers and toes due to proliferation of subungual connective tissue. It usually appears as a painless finger deformity and is clinically appreciated as a loss of the normal angle between the nail bed and proximal nail fold.

Hypertrophic osteoarthropathy is a symptomatic form of clubbing associated with proliferative periostosis of the distal end of long tubular bones, commonly those adjacent to the wrist and ankle joints.¹ The laminated appearance of these bones on radiography is due to the excess connective tissue secondary to new osteoid material deposited under the periosteum.

There is evidence to suggest that clubbing and hypertrophic osteoarthropathy represent different stages of the same disease process.² In most cases, finger deformity is the first manifestation; as the disease progresses, periostosis becomes evident.

Hypertrophic osteoarthropathy can be classified as primary or secondary. The primary form, also known as primary pachydermoperiostosis, is rare and constitutes only 3% of all cases.³ The exact cause is not yet known; it occurs as a hereditary disease with autosomal dominant inheritance with variable penetrance. Congenital clubbing without periostosis is of no clinical significance.⁴

CONDITIONS ASSOCIATED WITH CLUBBING

Primary bronchogenic carcinoma is the most common cause of clubbing and hypertrophic osteoarthropathy. In one retrospective series, 4.5% of patients with lung cancer had radiologic evidence of hypertrophic osteoarthropathy.⁵ Other malignancies associated with this condition are mesothelioma, hepatocellular carcinoma, and certain types of gastrointestinal adenocarcinoma.

Other conditions associated with clubbing include:

• Cardiovascular disease such as congenital cyanotic heart disease and infective endocarditis
• Gastrointestinal conditions such as cirrhosis, primary sclerosing cholangitis, Crohn disease, and ulcerative colitis
• Infections such as lung abscess and empyema.

Clubbing is generally bilaterally symmetrical. Asymmetric clubbing is rare and usually indicates impaired regional blood flow due to vascular disease. Unilateral clubbing or hypertrophic osteoarthropathy restricted to 1 upper limb can result from an anomaly of the aortic arch or from a subclavian or brachial artery aneurysm. Clubbing affecting predominantly the lower limbs has been reported in coarctation of aorta and patent ductus arteriosus.⁶ Rare cases of unidigital clubbing are reported in sarcoidosis.⁷

The importance of recognizing hypertrophic osteoarthropathy cannot be overemphasized. If any of the manifestations of the syndrome become evident in a previously healthy person, a thorough evaluation for an underlying disease should be done.

Clubbing should be differentiated from pseudoclubbing, which is seen in conditions such as hyperparathyroidism and scleroderma. The central mechanism for nail deformity in pseudoclubbing is acro-osteolysis with the resulting collapse of the subungual soft tissues. The important features differentiating it from true clubbing are preservation of the angle between the nail bed and proximal nail fold and asymmetric finger involvement.⁸

MANAGEMENT

The management of primary hypertrophic osteoarthropathy focuses on relieving the symptoms of periosteitis. Secondary forms require a detailed evaluation to rule out the underlying disease. In refractory cases, a bone-modifying agent (eg, zoledronic acid),⁹ octreotide,¹⁰ nonsteroidal anti-inflammatory drugs, or vagotomy¹¹ may help.

A   43-year-old woman presented to the  clinic complaining of bilateral ankle joint pain for 2 months. She denied a history of fever, weight loss, addictions, cough, or trauma. On physical examinatio, she had swelling of the ankle and wrist joints and digital clubbing (Figure 1). Active movement of the ankles and wrists was restricted due to pain. The examination was otherwise unremarkable.

Radiography of both ankles showed a lamellar type periosteal reaction suggestive of periostitis (Figure 2). Computed tomography of the chest revealed a spiculated mass over the right lower lobe. Biopsy study of the mass was positive for squamous cell carcinoma. She was referred to the oncology center for further management.

FEATURES OF HYPERTROPHIC OSTEOARTHROPATHY

Digital clubbing is one of the oldest signs in clinical medicine. It is characterized by bulbous enlargement of the terminal segments of the fingers and toes due to proliferation of subungual connective tissue. It usually appears as a painless finger deformity and is clinically appreciated as a loss of the normal angle between the nail bed and proximal nail fold.

Hypertrophic osteoarthropathy is a symptomatic form of clubbing associated with proliferative periostosis of the distal end of long tubular bones, commonly those adjacent to the wrist and ankle joints.¹ The laminated appearance of these bones on radiography is due to the excess connective tissue secondary to new osteoid material deposited under the periosteum.

There is evidence to suggest that clubbing and hypertrophic osteoarthropathy represent different stages of the same disease process.² In most cases, finger deformity is the first manifestation; as the disease progresses, periostosis becomes evident.

Hypertrophic osteoarthropathy can be classified as primary or secondary. The primary form, also known as primary pachydermoperiostosis, is rare and constitutes only 3% of all cases.³ The exact cause is not yet known; it occurs as a hereditary disease with autosomal dominant inheritance with variable penetrance. Congenital clubbing without periostosis is of no clinical significance.⁴

CONDITIONS ASSOCIATED WITH CLUBBING

Primary bronchogenic carcinoma is the most common cause of clubbing and hypertrophic osteoarthropathy. In one retrospective series, 4.5% of patients with lung cancer had radiologic evidence of hypertrophic osteoarthropathy.⁵ Other malignancies associated with this condition are mesothelioma, hepatocellular carcinoma, and certain types of gastrointestinal adenocarcinoma.

Other conditions associated with clubbing include:

• Cardiovascular disease such as congenital cyanotic heart disease and infective endocarditis
• Gastrointestinal conditions such as cirrhosis, primary sclerosing cholangitis, Crohn disease, and ulcerative colitis
• Infections such as lung abscess and empyema.

Clubbing is generally bilaterally symmetrical. Asymmetric clubbing is rare and usually indicates impaired regional blood flow due to vascular disease. Unilateral clubbing or hypertrophic osteoarthropathy restricted to 1 upper limb can result from an anomaly of the aortic arch or from a subclavian or brachial artery aneurysm. Clubbing affecting predominantly the lower limbs has been reported in coarctation of aorta and patent ductus arteriosus.⁶ Rare cases of unidigital clubbing are reported in sarcoidosis.⁷

The importance of recognizing hypertrophic osteoarthropathy cannot be overemphasized. If any of the manifestations of the syndrome become evident in a previously healthy person, a thorough evaluation for an underlying disease should be done.

Clubbing should be differentiated from pseudoclubbing, which is seen in conditions such as hyperparathyroidism and scleroderma. The central mechanism for nail deformity in pseudoclubbing is acro-osteolysis with the resulting collapse of the subungual soft tissues. The important features differentiating it from true clubbing are preservation of the angle between the nail bed and proximal nail fold and asymmetric finger involvement.⁸

MANAGEMENT

The management of primary hypertrophic osteoarthropathy focuses on relieving the symptoms of periosteitis. Secondary forms require a detailed evaluation to rule out the underlying disease. In refractory cases, a bone-modifying agent (eg, zoledronic acid),⁹ octreotide,¹⁰ nonsteroidal anti-inflammatory drugs, or vagotomy¹¹ may help.

A   43-year-old woman presented to the  clinic complaining of bilateral ankle joint pain for 2 months. She denied a history of fever, weight loss, addictions, cough, or trauma. On physical examinatio, she had swelling of the ankle and wrist joints and digital clubbing (Figure 1). Active movement of the ankles and wrists was restricted due to pain. The examination was otherwise unremarkable.

Radiography of both ankles showed a lamellar type periosteal reaction suggestive of periostitis (Figure 2). Computed tomography of the chest revealed a spiculated mass over the right lower lobe. Biopsy study of the mass was positive for squamous cell carcinoma. She was referred to the oncology center for further management.

FEATURES OF HYPERTROPHIC OSTEOARTHROPATHY

Digital clubbing is one of the oldest signs in clinical medicine. It is characterized by bulbous enlargement of the terminal segments of the fingers and toes due to proliferation of subungual connective tissue. It usually appears as a painless finger deformity and is clinically appreciated as a loss of the normal angle between the nail bed and proximal nail fold.

Hypertrophic osteoarthropathy is a symptomatic form of clubbing associated with proliferative periostosis of the distal end of long tubular bones, commonly those adjacent to the wrist and ankle joints.¹ The laminated appearance of these bones on radiography is due to the excess connective tissue secondary to new osteoid material deposited under the periosteum.

There is evidence to suggest that clubbing and hypertrophic osteoarthropathy represent different stages of the same disease process.² In most cases, finger deformity is the first manifestation; as the disease progresses, periostosis becomes evident.

Hypertrophic osteoarthropathy can be classified as primary or secondary. The primary form, also known as primary pachydermoperiostosis, is rare and constitutes only 3% of all cases.³ The exact cause is not yet known; it occurs as a hereditary disease with autosomal dominant inheritance with variable penetrance. Congenital clubbing without periostosis is of no clinical significance.⁴

CONDITIONS ASSOCIATED WITH CLUBBING

Primary bronchogenic carcinoma is the most common cause of clubbing and hypertrophic osteoarthropathy. In one retrospective series, 4.5% of patients with lung cancer had radiologic evidence of hypertrophic osteoarthropathy.⁵ Other malignancies associated with this condition are mesothelioma, hepatocellular carcinoma, and certain types of gastrointestinal adenocarcinoma.

Other conditions associated with clubbing include:

• Cardiovascular disease such as congenital cyanotic heart disease and infective endocarditis
• Gastrointestinal conditions such as cirrhosis, primary sclerosing cholangitis, Crohn disease, and ulcerative colitis
• Infections such as lung abscess and empyema.

Clubbing is generally bilaterally symmetrical. Asymmetric clubbing is rare and usually indicates impaired regional blood flow due to vascular disease. Unilateral clubbing or hypertrophic osteoarthropathy restricted to 1 upper limb can result from an anomaly of the aortic arch or from a subclavian or brachial artery aneurysm. Clubbing affecting predominantly the lower limbs has been reported in coarctation of aorta and patent ductus arteriosus.⁶ Rare cases of unidigital clubbing are reported in sarcoidosis.⁷

The importance of recognizing hypertrophic osteoarthropathy cannot be overemphasized. If any of the manifestations of the syndrome become evident in a previously healthy person, a thorough evaluation for an underlying disease should be done.

Clubbing should be differentiated from pseudoclubbing, which is seen in conditions such as hyperparathyroidism and scleroderma. The central mechanism for nail deformity in pseudoclubbing is acro-osteolysis with the resulting collapse of the subungual soft tissues. The important features differentiating it from true clubbing are preservation of the angle between the nail bed and proximal nail fold and asymmetric finger involvement.⁸

MANAGEMENT

The management of primary hypertrophic osteoarthropathy focuses on relieving the symptoms of periosteitis. Secondary forms require a detailed evaluation to rule out the underlying disease. In refractory cases, a bone-modifying agent (eg, zoledronic acid),⁹ octreotide,¹⁰ nonsteroidal anti-inflammatory drugs, or vagotomy¹¹ may help.

Laboratory studies revealed leukocytosis with a left shift. Chest radiographs were negative for pneumonia. A magnetic resonance image (MRI) of the lumbar spine was obtained to evaluate for diskitis osteomyelitis. A radiograph of the pelvis was also obtained to evaluate the patient’s THAs, and a computed tomography scan (CT) of the abdomen and pelvis with contrast was obtained for further evaluation. Representative CT, radiographic, and MRI images are shown at left (Figures 1-3).

What is the suspected diagnosis?

Answer

The MRI of the lumbar spine demonstrated no evidence of diskitis osteomyelitis. However, T₂-weighted axial images showed enlarged heterogeneous bilateral psoas muscles with bright signal, indicating the presence of fluid (white arrows, Figure 4).

On the pelvic radiographs, both femoral heads appeared off-center within the acetabular cups (red arrows, Figure 5). This eccentric positioning indicated wear of the polyethylene in the THAs that normally occupies the space between the acetabular cup and the femoral head. In addition, focal lucency in the right acetabulum indicated breakdown of the bone, a condition referred to as osteolysis (white asterisk, Figure 5).

An abdominopelvic CT scan with contrast was performed and confirmed the findings of polyethylene wear and osteolysis. The CT scan also demonstrated large bilateral hip joint effusions (white arrows, Figure 6), decompressed along distended bilateral iliopsoas bursae (red asterisks, Figure 6), and communicating with the bilateral psoas muscle collections (red arrows, Figure 6).

Osteolysis With Iliopsoas Bursitis

Bursae are fluid-filled sacs lined by synovial tissue located throughout the body to reduce friction at sites of movement between muscles, bones, and tendons. Bursitis develops when these sacs become inflamed and/or infected and fill with fluid. The iliopsoas bursa lies between the anterior capsule of the hip and the psoas tendon, iliacus tendon, and muscle fibers.^1,2 This bursa frequently communicates with the hip joint.^3,4 Iliopsoas bursal distension has been reported following THA in the setting of polyethylene wear,⁵ and aseptic bursitis is a commonly seen incidental finding at the time of revision surgery.⁶

In this patient, long-standing polyethylene-induced synovitis had markedly expanded the hip joints and iliopsoas bursae, eventually resulting in superinfection, which accounted for the patient’s symptoms.

Treatment

Based on the imaging findings, interventional radiology services were contacted. The interventional radiologist drained the bilateral psoas abscesses. Cultures of the fluid were positive for both methicillin-resistant Staphylococcus aureus (MRSA) and methicillin-susceptible S aureus (MSSA). The patient was admitted to the hospital for treatment of MRSA and MSSA with intravenous antibiotic therapy. He recovered from the infection and was discharged on hospital day 2, with instructions to follow up with an orthopedic surgeon to discuss eventual revision of the bilateral THAs.

Laboratory studies revealed leukocytosis with a left shift. Chest radiographs were negative for pneumonia. A magnetic resonance image (MRI) of the lumbar spine was obtained to evaluate for diskitis osteomyelitis. A radiograph of the pelvis was also obtained to evaluate the patient’s THAs, and a computed tomography scan (CT) of the abdomen and pelvis with contrast was obtained for further evaluation. Representative CT, radiographic, and MRI images are shown at left (Figures 1-3).

What is the suspected diagnosis?

Answer

The MRI of the lumbar spine demonstrated no evidence of diskitis osteomyelitis. However, T₂-weighted axial images showed enlarged heterogeneous bilateral psoas muscles with bright signal, indicating the presence of fluid (white arrows, Figure 4).

On the pelvic radiographs, both femoral heads appeared off-center within the acetabular cups (red arrows, Figure 5). This eccentric positioning indicated wear of the polyethylene in the THAs that normally occupies the space between the acetabular cup and the femoral head. In addition, focal lucency in the right acetabulum indicated breakdown of the bone, a condition referred to as osteolysis (white asterisk, Figure 5).

An abdominopelvic CT scan with contrast was performed and confirmed the findings of polyethylene wear and osteolysis. The CT scan also demonstrated large bilateral hip joint effusions (white arrows, Figure 6), decompressed along distended bilateral iliopsoas bursae (red asterisks, Figure 6), and communicating with the bilateral psoas muscle collections (red arrows, Figure 6).

Osteolysis With Iliopsoas Bursitis

Bursae are fluid-filled sacs lined by synovial tissue located throughout the body to reduce friction at sites of movement between muscles, bones, and tendons. Bursitis develops when these sacs become inflamed and/or infected and fill with fluid. The iliopsoas bursa lies between the anterior capsule of the hip and the psoas tendon, iliacus tendon, and muscle fibers.^1,2 This bursa frequently communicates with the hip joint.^3,4 Iliopsoas bursal distension has been reported following THA in the setting of polyethylene wear,⁵ and aseptic bursitis is a commonly seen incidental finding at the time of revision surgery.⁶

In this patient, long-standing polyethylene-induced synovitis had markedly expanded the hip joints and iliopsoas bursae, eventually resulting in superinfection, which accounted for the patient’s symptoms.

Treatment

Based on the imaging findings, interventional radiology services were contacted. The interventional radiologist drained the bilateral psoas abscesses. Cultures of the fluid were positive for both methicillin-resistant Staphylococcus aureus (MRSA) and methicillin-susceptible S aureus (MSSA). The patient was admitted to the hospital for treatment of MRSA and MSSA with intravenous antibiotic therapy. He recovered from the infection and was discharged on hospital day 2, with instructions to follow up with an orthopedic surgeon to discuss eventual revision of the bilateral THAs.

Laboratory studies revealed leukocytosis with a left shift. Chest radiographs were negative for pneumonia. A magnetic resonance image (MRI) of the lumbar spine was obtained to evaluate for diskitis osteomyelitis. A radiograph of the pelvis was also obtained to evaluate the patient’s THAs, and a computed tomography scan (CT) of the abdomen and pelvis with contrast was obtained for further evaluation. Representative CT, radiographic, and MRI images are shown at left (Figures 1-3).

What is the suspected diagnosis?

Answer

The MRI of the lumbar spine demonstrated no evidence of diskitis osteomyelitis. However, T₂-weighted axial images showed enlarged heterogeneous bilateral psoas muscles with bright signal, indicating the presence of fluid (white arrows, Figure 4).

On the pelvic radiographs, both femoral heads appeared off-center within the acetabular cups (red arrows, Figure 5). This eccentric positioning indicated wear of the polyethylene in the THAs that normally occupies the space between the acetabular cup and the femoral head. In addition, focal lucency in the right acetabulum indicated breakdown of the bone, a condition referred to as osteolysis (white asterisk, Figure 5).

An abdominopelvic CT scan with contrast was performed and confirmed the findings of polyethylene wear and osteolysis. The CT scan also demonstrated large bilateral hip joint effusions (white arrows, Figure 6), decompressed along distended bilateral iliopsoas bursae (red asterisks, Figure 6), and communicating with the bilateral psoas muscle collections (red arrows, Figure 6).

Osteolysis With Iliopsoas Bursitis

Bursae are fluid-filled sacs lined by synovial tissue located throughout the body to reduce friction at sites of movement between muscles, bones, and tendons. Bursitis develops when these sacs become inflamed and/or infected and fill with fluid. The iliopsoas bursa lies between the anterior capsule of the hip and the psoas tendon, iliacus tendon, and muscle fibers.^1,2 This bursa frequently communicates with the hip joint.^3,4 Iliopsoas bursal distension has been reported following THA in the setting of polyethylene wear,⁵ and aseptic bursitis is a commonly seen incidental finding at the time of revision surgery.⁶

In this patient, long-standing polyethylene-induced synovitis had markedly expanded the hip joints and iliopsoas bursae, eventually resulting in superinfection, which accounted for the patient’s symptoms.

Treatment

Based on the imaging findings, interventional radiology services were contacted. The interventional radiologist drained the bilateral psoas abscesses. Cultures of the fluid were positive for both methicillin-resistant Staphylococcus aureus (MRSA) and methicillin-susceptible S aureus (MSSA). The patient was admitted to the hospital for treatment of MRSA and MSSA with intravenous antibiotic therapy. He recovered from the infection and was discharged on hospital day 2, with instructions to follow up with an orthopedic surgeon to discuss eventual revision of the bilateral THAs.

The diagnosis of aortic dissection is often challenging due to its various presentations and the frequent absence of classic findings. This high-morbidity and high-mortality condition may present with nonspecific chest, back, or abdominal pain, and is often associated with hypotension.¹ Point-of-care (POC) ultrasound in the ED allows for rapid diagnosis of this time-sensitive disease.

Case

A 70-year-old woman presented to the ED for evaluation of acute sharp chest pain, which she stated began while she was exercising earlier that day. The pain was substernal and radiated to her upper back. The patient also described associated lightheadedness and dyspnea, but denied any focal weakness or paresthesias. Her vital signs were remarkable for a blood pressure of 90/31 mm Hg and a heart rate of 42 beats/min. A bedside ultrasound of the patient’s aortic root and abdominal aorta was performed to assess for evidence of aortic dissection.

Imaging Technique

To evaluate for aortic dissection using POC ultrasound, views of the aortic root and the abdominal aorta should be obtained with the patient in the supine position. The phased array (cardiac) probe is used to obtain the parasternal long axis (PSLA) view of the heart to visualize the aortic root. The PSLA view is obtained by placing the probe in the third or fourth intercostal space, adjacent to the left sternal border, with the probe parallel to the long axis of the left ventricle (Figure 1). The American Society of Echocardiography recommends measuring the aortic diameter at the sinus of Valsalva, but measurement of the largest visible portion of the aortic root may be more practical.^2,3 Measurement of the aortic root diameter should occur at end diastole.^2,3 Tricks for better visualization of the aortic root include tilting the probe tail 10° toward the patient’s right elbow (ie, aiming the probe footprint toward the patient’s left shoulder), or placing the patient in the left lateral decubitus position. Values greater than 4 cm indicate aortic root dilatation.⁴ Figure 2 demonstrates the PSLA view in our patient, showing the dilated aortic root, which measured roughly 5 cm. 

The abdominal aorta is best visualized using a low-frequency curvilinear (abdominal) probe. The aorta should be visualized in the transverse plane from the diaphragm to its bifurcation by placing the probe in the epigastrium and slowly moving it inferiorly to the level of the umbilicus (Figure 3). The aorta can then be visualized in the longitudinal plane by rotating the probe clockwise until it is parallel with the long axis of the aorta (Figure 4). Visualization of an intimal flap is the most common sonographic finding associated with an abdominal aortic dissection. In our patient, an intimal flap was visualized in both the transverse and longitudinal views (Figures 5 and 6).

Discussion

Aortic dissection is a medical emergency—one that has a reported in-hospital mortality of 27.4%.¹ Therefore, prompt diagnosis of an aortic dissection in the ED is crucial to improving patient outcomes. Traditionally, emergency physicians (EPs) have relied on aortography and contrast-enhanced computed tomography (CT) to diagnose aortic dissection. However, both of these modalities require a considerable length of time, injection of contrast material, and often transportation of the patient from the ED.

Point-of-care ultrasound provides a fast and noninvasive tool for the diagnosis of aortic dissection. Several recent case reports and case series have highlighted the utility of POC ultrasound to diagnose aortic dissection in the ED.^5-7

Case Conclusion

After the results of the POC transthoracic and transabdominal ultrasound were reviewed, we promptly consulted the vascular surgery team. They performed a CT scan verifying a DeBakey type I aortic dissection involving both the ascending aorta and the descending aorta. The patient was subsequently taken to the operating room for definitive repair with a graft. She was discharged home on hospital day 9 in good condition.

Summary

Point-of-care ultrasound is a useful bedside tool for the rapid diagnosis of aortic dissection in the ED. The aortic root dilatation seen on the PSLA view and the presence of an intimal flap seen on either transthoracic or transabdominal views of the aorta are both highly sensitive for aortic dissection.

The diagnosis of aortic dissection is often challenging due to its various presentations and the frequent absence of classic findings. This high-morbidity and high-mortality condition may present with nonspecific chest, back, or abdominal pain, and is often associated with hypotension.¹ Point-of-care (POC) ultrasound in the ED allows for rapid diagnosis of this time-sensitive disease.

Case

A 70-year-old woman presented to the ED for evaluation of acute sharp chest pain, which she stated began while she was exercising earlier that day. The pain was substernal and radiated to her upper back. The patient also described associated lightheadedness and dyspnea, but denied any focal weakness or paresthesias. Her vital signs were remarkable for a blood pressure of 90/31 mm Hg and a heart rate of 42 beats/min. A bedside ultrasound of the patient’s aortic root and abdominal aorta was performed to assess for evidence of aortic dissection.

Imaging Technique

To evaluate for aortic dissection using POC ultrasound, views of the aortic root and the abdominal aorta should be obtained with the patient in the supine position. The phased array (cardiac) probe is used to obtain the parasternal long axis (PSLA) view of the heart to visualize the aortic root. The PSLA view is obtained by placing the probe in the third or fourth intercostal space, adjacent to the left sternal border, with the probe parallel to the long axis of the left ventricle (Figure 1). The American Society of Echocardiography recommends measuring the aortic diameter at the sinus of Valsalva, but measurement of the largest visible portion of the aortic root may be more practical.^2,3 Measurement of the aortic root diameter should occur at end diastole.^2,3 Tricks for better visualization of the aortic root include tilting the probe tail 10° toward the patient’s right elbow (ie, aiming the probe footprint toward the patient’s left shoulder), or placing the patient in the left lateral decubitus position. Values greater than 4 cm indicate aortic root dilatation.⁴ Figure 2 demonstrates the PSLA view in our patient, showing the dilated aortic root, which measured roughly 5 cm. 

The abdominal aorta is best visualized using a low-frequency curvilinear (abdominal) probe. The aorta should be visualized in the transverse plane from the diaphragm to its bifurcation by placing the probe in the epigastrium and slowly moving it inferiorly to the level of the umbilicus (Figure 3). The aorta can then be visualized in the longitudinal plane by rotating the probe clockwise until it is parallel with the long axis of the aorta (Figure 4). Visualization of an intimal flap is the most common sonographic finding associated with an abdominal aortic dissection. In our patient, an intimal flap was visualized in both the transverse and longitudinal views (Figures 5 and 6).

Discussion

Aortic dissection is a medical emergency—one that has a reported in-hospital mortality of 27.4%.¹ Therefore, prompt diagnosis of an aortic dissection in the ED is crucial to improving patient outcomes. Traditionally, emergency physicians (EPs) have relied on aortography and contrast-enhanced computed tomography (CT) to diagnose aortic dissection. However, both of these modalities require a considerable length of time, injection of contrast material, and often transportation of the patient from the ED.

Point-of-care ultrasound provides a fast and noninvasive tool for the diagnosis of aortic dissection. Several recent case reports and case series have highlighted the utility of POC ultrasound to diagnose aortic dissection in the ED.^5-7

Case Conclusion

After the results of the POC transthoracic and transabdominal ultrasound were reviewed, we promptly consulted the vascular surgery team. They performed a CT scan verifying a DeBakey type I aortic dissection involving both the ascending aorta and the descending aorta. The patient was subsequently taken to the operating room for definitive repair with a graft. She was discharged home on hospital day 9 in good condition.

Summary

Point-of-care ultrasound is a useful bedside tool for the rapid diagnosis of aortic dissection in the ED. The aortic root dilatation seen on the PSLA view and the presence of an intimal flap seen on either transthoracic or transabdominal views of the aorta are both highly sensitive for aortic dissection.

The diagnosis of aortic dissection is often challenging due to its various presentations and the frequent absence of classic findings. This high-morbidity and high-mortality condition may present with nonspecific chest, back, or abdominal pain, and is often associated with hypotension.¹ Point-of-care (POC) ultrasound in the ED allows for rapid diagnosis of this time-sensitive disease.

Case

A 70-year-old woman presented to the ED for evaluation of acute sharp chest pain, which she stated began while she was exercising earlier that day. The pain was substernal and radiated to her upper back. The patient also described associated lightheadedness and dyspnea, but denied any focal weakness or paresthesias. Her vital signs were remarkable for a blood pressure of 90/31 mm Hg and a heart rate of 42 beats/min. A bedside ultrasound of the patient’s aortic root and abdominal aorta was performed to assess for evidence of aortic dissection.

Imaging Technique

To evaluate for aortic dissection using POC ultrasound, views of the aortic root and the abdominal aorta should be obtained with the patient in the supine position. The phased array (cardiac) probe is used to obtain the parasternal long axis (PSLA) view of the heart to visualize the aortic root. The PSLA view is obtained by placing the probe in the third or fourth intercostal space, adjacent to the left sternal border, with the probe parallel to the long axis of the left ventricle (Figure 1). The American Society of Echocardiography recommends measuring the aortic diameter at the sinus of Valsalva, but measurement of the largest visible portion of the aortic root may be more practical.^2,3 Measurement of the aortic root diameter should occur at end diastole.^2,3 Tricks for better visualization of the aortic root include tilting the probe tail 10° toward the patient’s right elbow (ie, aiming the probe footprint toward the patient’s left shoulder), or placing the patient in the left lateral decubitus position. Values greater than 4 cm indicate aortic root dilatation.⁴ Figure 2 demonstrates the PSLA view in our patient, showing the dilated aortic root, which measured roughly 5 cm. 

The abdominal aorta is best visualized using a low-frequency curvilinear (abdominal) probe. The aorta should be visualized in the transverse plane from the diaphragm to its bifurcation by placing the probe in the epigastrium and slowly moving it inferiorly to the level of the umbilicus (Figure 3). The aorta can then be visualized in the longitudinal plane by rotating the probe clockwise until it is parallel with the long axis of the aorta (Figure 4). Visualization of an intimal flap is the most common sonographic finding associated with an abdominal aortic dissection. In our patient, an intimal flap was visualized in both the transverse and longitudinal views (Figures 5 and 6).

Discussion

Aortic dissection is a medical emergency—one that has a reported in-hospital mortality of 27.4%.¹ Therefore, prompt diagnosis of an aortic dissection in the ED is crucial to improving patient outcomes. Traditionally, emergency physicians (EPs) have relied on aortography and contrast-enhanced computed tomography (CT) to diagnose aortic dissection. However, both of these modalities require a considerable length of time, injection of contrast material, and often transportation of the patient from the ED.

Point-of-care ultrasound provides a fast and noninvasive tool for the diagnosis of aortic dissection. Several recent case reports and case series have highlighted the utility of POC ultrasound to diagnose aortic dissection in the ED.^5-7

Case Conclusion

After the results of the POC transthoracic and transabdominal ultrasound were reviewed, we promptly consulted the vascular surgery team. They performed a CT scan verifying a DeBakey type I aortic dissection involving both the ascending aorta and the descending aorta. The patient was subsequently taken to the operating room for definitive repair with a graft. She was discharged home on hospital day 9 in good condition.

Summary

Point-of-care ultrasound is a useful bedside tool for the rapid diagnosis of aortic dissection in the ED. The aortic root dilatation seen on the PSLA view and the presence of an intimal flap seen on either transthoracic or transabdominal views of the aorta are both highly sensitive for aortic dissection.

Arthrex Synergy MSK Ultrasound by Clarius(http://www.synergy-ultrasound.com/)

Arthrex Synergy MSK Ultrasound by Clarius is a new wireless ultrasound scanner that can connect to any iOS or Android device through a secure WiFi Direct connection. The scanner sets up the connection to an app on the device. Ultrasound and wireless technology have been around for decades, but combinations thereof have produced poor results. The main challenge has been to create and wirelessly transmit high-quality images without latency to a display while maintaining a reasonably sized transducer. Handheld ultrasound transducers scan effectively and process the scanned information in compact form. Recent advances in image processing and proprietary imaging algorithms now allow creation of high-resolution images comparable to those produced by most midrange or high-range machines costing $30,000 to $50,000. This new unit costs about $12,000. Ultrasound use has increased over the past decade. Numerous studies have found improved accuracy, efficacy, and outcomes of injections, and reduced pain, with ultrasound-guided injections over blind injections, and cost savings over magnetic resonance imaging.^1-12

Three scanners are capable of targeting different tissue types and depths. We prefer the Synergy MSK Linear Ultrasound by Clarius, a linear transducer that can evaluate tissue to depths of 7 cm and use frequencies from 4 MHz to 13 MHz. Its battery holds a standby charge for 7 days and can be actively used for 45 minutes. The unit has a magnesium shell; with the battery removed, the unit can be completely immersed in liquid without being damaged, which allows for easy cleaning and, potentially, sterilization with a soak solution. Color Doppler (for blood-flow assessment) and proprietary advanced needle visualization technology will be available in June.

The app is simply controlled with typical smart-device gestures. Depth control requires a finger swipe, and zoom takes a pinch. Other controls, such as optimal gain and frequency settings, are automated. Images and videos can be stored on the device and uploaded either to the Clarius Cloud or to a PACS (picture archiving and communication system) device. New features will allow the device to use a Synergy arthroscopy tower (Arthrex) as its display for surgeons and anesthesiologists in the surgical suite.

This technology finally allows ultrasound to be used in the operating room without the hassles of cumbersome machines and the potential contamination by the sleeves covering the cord that connects the transducer and the base unit (Figure 1).

Arthrex Synergy MSK Ultrasound by Clarius(http://www.synergy-ultrasound.com/)

Arthrex Synergy MSK Ultrasound by Clarius is a new wireless ultrasound scanner that can connect to any iOS or Android device through a secure WiFi Direct connection. The scanner sets up the connection to an app on the device. Ultrasound and wireless technology have been around for decades, but combinations thereof have produced poor results. The main challenge has been to create and wirelessly transmit high-quality images without latency to a display while maintaining a reasonably sized transducer. Handheld ultrasound transducers scan effectively and process the scanned information in compact form. Recent advances in image processing and proprietary imaging algorithms now allow creation of high-resolution images comparable to those produced by most midrange or high-range machines costing $30,000 to $50,000. This new unit costs about $12,000. Ultrasound use has increased over the past decade. Numerous studies have found improved accuracy, efficacy, and outcomes of injections, and reduced pain, with ultrasound-guided injections over blind injections, and cost savings over magnetic resonance imaging.^1-12

Three scanners are capable of targeting different tissue types and depths. We prefer the Synergy MSK Linear Ultrasound by Clarius, a linear transducer that can evaluate tissue to depths of 7 cm and use frequencies from 4 MHz to 13 MHz. Its battery holds a standby charge for 7 days and can be actively used for 45 minutes. The unit has a magnesium shell; with the battery removed, the unit can be completely immersed in liquid without being damaged, which allows for easy cleaning and, potentially, sterilization with a soak solution. Color Doppler (for blood-flow assessment) and proprietary advanced needle visualization technology will be available in June.

The app is simply controlled with typical smart-device gestures. Depth control requires a finger swipe, and zoom takes a pinch. Other controls, such as optimal gain and frequency settings, are automated. Images and videos can be stored on the device and uploaded either to the Clarius Cloud or to a PACS (picture archiving and communication system) device. New features will allow the device to use a Synergy arthroscopy tower (Arthrex) as its display for surgeons and anesthesiologists in the surgical suite.

This technology finally allows ultrasound to be used in the operating room without the hassles of cumbersome machines and the potential contamination by the sleeves covering the cord that connects the transducer and the base unit (Figure 1).

Arthrex Synergy MSK Ultrasound by Clarius(http://www.synergy-ultrasound.com/)

Arthrex Synergy MSK Ultrasound by Clarius is a new wireless ultrasound scanner that can connect to any iOS or Android device through a secure WiFi Direct connection. The scanner sets up the connection to an app on the device. Ultrasound and wireless technology have been around for decades, but combinations thereof have produced poor results. The main challenge has been to create and wirelessly transmit high-quality images without latency to a display while maintaining a reasonably sized transducer. Handheld ultrasound transducers scan effectively and process the scanned information in compact form. Recent advances in image processing and proprietary imaging algorithms now allow creation of high-resolution images comparable to those produced by most midrange or high-range machines costing $30,000 to $50,000. This new unit costs about $12,000. Ultrasound use has increased over the past decade. Numerous studies have found improved accuracy, efficacy, and outcomes of injections, and reduced pain, with ultrasound-guided injections over blind injections, and cost savings over magnetic resonance imaging.^1-12

Three scanners are capable of targeting different tissue types and depths. We prefer the Synergy MSK Linear Ultrasound by Clarius, a linear transducer that can evaluate tissue to depths of 7 cm and use frequencies from 4 MHz to 13 MHz. Its battery holds a standby charge for 7 days and can be actively used for 45 minutes. The unit has a magnesium shell; with the battery removed, the unit can be completely immersed in liquid without being damaged, which allows for easy cleaning and, potentially, sterilization with a soak solution. Color Doppler (for blood-flow assessment) and proprietary advanced needle visualization technology will be available in June.

The app is simply controlled with typical smart-device gestures. Depth control requires a finger swipe, and zoom takes a pinch. Other controls, such as optimal gain and frequency settings, are automated. Images and videos can be stored on the device and uploaded either to the Clarius Cloud or to a PACS (picture archiving and communication system) device. New features will allow the device to use a Synergy arthroscopy tower (Arthrex) as its display for surgeons and anesthesiologists in the surgical suite.

This technology finally allows ultrasound to be used in the operating room without the hassles of cumbersome machines and the potential contamination by the sleeves covering the cord that connects the transducer and the base unit (Figure 1).

A 58-year-old man with end-stage renal disease due to diabetic nephropathy was admitted with aggravated exertional dyspnea and intermittent chest pain for 1 week. He had been on hemodialysis for 15 years.

His blood pressure was 124/69 mm Hg, pulse 96 beats per minute, and temperature 35.8°C. On physical examination, he had bilateral diffuse crackles, elevated jugular venous pressure (9.5 cm H₂O) with positive hepatojugular reflux, and apparent dependent pedal edema. The Kussmaul sign was not observed.

Cardiac enzymes were in the normal range (creatine kinase 73 U/L, troponin I 0.032 ng/mL), but the brain-natriuretic peptide level was elevated at 340 pg/mL. Other laboratory findings included calcium 9 mg/dL (reference range 8.4–10.2 mg/dL), inorganic phosphate 5 mg/dL (2.5–4.5 mg/dL), and intact parathyroid hormone 1,457 pg/mL (10–69 pg/mL).

Electrocardiography showed sinus tachycardia with low voltage in diffuse leads and generalized flattening of the T wave. Chest radiography showed a bilateral reticulo­nodular pattern, mild costo­phrenic angle obliteration, and notable calcifications along the cardiac contour. Thoracic computed tomography showed a porcelain-like encasement of the heart (Figure 1). Transthoracic echocardiography showed thickened pericardium, pericardial calcification, and mild interventricular septal bounce in diastole, with no dyskinesia of ventricular wall motion. We decided not to perform an invasive hemodynamic assessment.

CAUSES OF PERICARDIAL CALCIFICATION

Pericardial calcification, abnormal calcium deposits in response to inflammation,¹ has become more widely reported as the use of chest computed tomography has become more widespread. The common identifiable causes of pericardial calcification include recurrent or chronic pericarditis, radiation therapy for Hodgkin lymphoma or breast cancer, tuberculosis, and end-stage kidney disease.^2,3 Other possible causes are retention of uremic metabolites, metastatic calcification induced by secondary hyperparathyroidism, and calcium-phosphate deposition induced by hyperphosphatemia.⁴

In chronic kidney disease, the amount of pericardial fluid and fibrinous pericardial deposition is thought to contribute to increased pericardial thickness and constriction. In some patients, pericardial calcification and thickening would lead to constrictive pericarditis, which could be confirmed by echocardiography and cardiac catheterization. About 25% to 50% of cases of pericardial calcification are complicated by constrictive pericarditis.^5,6 Constrictive pericarditis occurs in up to 4% of patients with end-stage renal disease, even with successful dialysis.⁷

Partial clinical improvement may be obtained with intensive hemodialysis, strict volume control, and decreased catabolism in patients with multiple comorbidities.⁸ However, the definite treatment is total pericardiectomy, which reduces symptoms substantially and offers a favorable long-term outcome.⁷

SECONDARY HYPERPARATHYROIDISM

Secondary hyperparathyroidism is a common complication in patients with end-stage renal disease and is characterized by derangements in the homeostasis of calcium, phosphorus, and vitamin D.⁹

Because renal function is decreased, phosphate is retained and calcitriol synthesis is reduced, resulting in hypocalcemia, which induces parathyroid gland hyperplasia and parathyroid hormone secretion.¹⁰ Moreover, some patents with long-standing secondary hyperparathyroidism may develop tertiary hyperparathyroidism associated with autonomous parathyroid hormone secretion, hypercalcemia, and hyperphosphatemia.¹¹

The Kidney Disease: Improving Global Outcomes (KDIGO) Work Group recommends screening for and managing secondary hyperparathyroidism in all patients with stage 3 chronic kidney disease (estimated glomerular filtration rate < 60 mL/min). In patients with stage 5 chronic kidney disease or on dialysis, the serum calcium and phosphorus levels should be monitored every 1 to 3 months and the parathyroid hormone levels every 3 to 6 months.¹²

According to KDIGO guidelines, the target level of calcium is less than 10.2 mg/dL, and the target phosphorus level is less than 4.6 mg/dL. The level of parathyroid hormone should be maintained at 2 to 9 times the upper limit of normal for the assay.

The management of secondary hyperparathyroidism includes a low-phosphorus diet, calcium-containing or calcium-free phosphate binders, a calcitriol supplement, and calcimimetics. If medical treatment fails and manifestations are significant, parathyroidectomy may be indicated.¹³

A 58-year-old man with end-stage renal disease due to diabetic nephropathy was admitted with aggravated exertional dyspnea and intermittent chest pain for 1 week. He had been on hemodialysis for 15 years.

His blood pressure was 124/69 mm Hg, pulse 96 beats per minute, and temperature 35.8°C. On physical examination, he had bilateral diffuse crackles, elevated jugular venous pressure (9.5 cm H₂O) with positive hepatojugular reflux, and apparent dependent pedal edema. The Kussmaul sign was not observed.

Cardiac enzymes were in the normal range (creatine kinase 73 U/L, troponin I 0.032 ng/mL), but the brain-natriuretic peptide level was elevated at 340 pg/mL. Other laboratory findings included calcium 9 mg/dL (reference range 8.4–10.2 mg/dL), inorganic phosphate 5 mg/dL (2.5–4.5 mg/dL), and intact parathyroid hormone 1,457 pg/mL (10–69 pg/mL).

Electrocardiography showed sinus tachycardia with low voltage in diffuse leads and generalized flattening of the T wave. Chest radiography showed a bilateral reticulo­nodular pattern, mild costo­phrenic angle obliteration, and notable calcifications along the cardiac contour. Thoracic computed tomography showed a porcelain-like encasement of the heart (Figure 1). Transthoracic echocardiography showed thickened pericardium, pericardial calcification, and mild interventricular septal bounce in diastole, with no dyskinesia of ventricular wall motion. We decided not to perform an invasive hemodynamic assessment.

CAUSES OF PERICARDIAL CALCIFICATION

Pericardial calcification, abnormal calcium deposits in response to inflammation,¹ has become more widely reported as the use of chest computed tomography has become more widespread. The common identifiable causes of pericardial calcification include recurrent or chronic pericarditis, radiation therapy for Hodgkin lymphoma or breast cancer, tuberculosis, and end-stage kidney disease.^2,3 Other possible causes are retention of uremic metabolites, metastatic calcification induced by secondary hyperparathyroidism, and calcium-phosphate deposition induced by hyperphosphatemia.⁴

In chronic kidney disease, the amount of pericardial fluid and fibrinous pericardial deposition is thought to contribute to increased pericardial thickness and constriction. In some patients, pericardial calcification and thickening would lead to constrictive pericarditis, which could be confirmed by echocardiography and cardiac catheterization. About 25% to 50% of cases of pericardial calcification are complicated by constrictive pericarditis.^5,6 Constrictive pericarditis occurs in up to 4% of patients with end-stage renal disease, even with successful dialysis.⁷

Partial clinical improvement may be obtained with intensive hemodialysis, strict volume control, and decreased catabolism in patients with multiple comorbidities.⁸ However, the definite treatment is total pericardiectomy, which reduces symptoms substantially and offers a favorable long-term outcome.⁷

SECONDARY HYPERPARATHYROIDISM

Secondary hyperparathyroidism is a common complication in patients with end-stage renal disease and is characterized by derangements in the homeostasis of calcium, phosphorus, and vitamin D.⁹

Because renal function is decreased, phosphate is retained and calcitriol synthesis is reduced, resulting in hypocalcemia, which induces parathyroid gland hyperplasia and parathyroid hormone secretion.¹⁰ Moreover, some patents with long-standing secondary hyperparathyroidism may develop tertiary hyperparathyroidism associated with autonomous parathyroid hormone secretion, hypercalcemia, and hyperphosphatemia.¹¹

The Kidney Disease: Improving Global Outcomes (KDIGO) Work Group recommends screening for and managing secondary hyperparathyroidism in all patients with stage 3 chronic kidney disease (estimated glomerular filtration rate < 60 mL/min). In patients with stage 5 chronic kidney disease or on dialysis, the serum calcium and phosphorus levels should be monitored every 1 to 3 months and the parathyroid hormone levels every 3 to 6 months.¹²

According to KDIGO guidelines, the target level of calcium is less than 10.2 mg/dL, and the target phosphorus level is less than 4.6 mg/dL. The level of parathyroid hormone should be maintained at 2 to 9 times the upper limit of normal for the assay.

The management of secondary hyperparathyroidism includes a low-phosphorus diet, calcium-containing or calcium-free phosphate binders, a calcitriol supplement, and calcimimetics. If medical treatment fails and manifestations are significant, parathyroidectomy may be indicated.¹³

A 58-year-old man with end-stage renal disease due to diabetic nephropathy was admitted with aggravated exertional dyspnea and intermittent chest pain for 1 week. He had been on hemodialysis for 15 years.

His blood pressure was 124/69 mm Hg, pulse 96 beats per minute, and temperature 35.8°C. On physical examination, he had bilateral diffuse crackles, elevated jugular venous pressure (9.5 cm H₂O) with positive hepatojugular reflux, and apparent dependent pedal edema. The Kussmaul sign was not observed.

Cardiac enzymes were in the normal range (creatine kinase 73 U/L, troponin I 0.032 ng/mL), but the brain-natriuretic peptide level was elevated at 340 pg/mL. Other laboratory findings included calcium 9 mg/dL (reference range 8.4–10.2 mg/dL), inorganic phosphate 5 mg/dL (2.5–4.5 mg/dL), and intact parathyroid hormone 1,457 pg/mL (10–69 pg/mL).

Electrocardiography showed sinus tachycardia with low voltage in diffuse leads and generalized flattening of the T wave. Chest radiography showed a bilateral reticulo­nodular pattern, mild costo­phrenic angle obliteration, and notable calcifications along the cardiac contour. Thoracic computed tomography showed a porcelain-like encasement of the heart (Figure 1). Transthoracic echocardiography showed thickened pericardium, pericardial calcification, and mild interventricular septal bounce in diastole, with no dyskinesia of ventricular wall motion. We decided not to perform an invasive hemodynamic assessment.

CAUSES OF PERICARDIAL CALCIFICATION

Pericardial calcification, abnormal calcium deposits in response to inflammation,¹ has become more widely reported as the use of chest computed tomography has become more widespread. The common identifiable causes of pericardial calcification include recurrent or chronic pericarditis, radiation therapy for Hodgkin lymphoma or breast cancer, tuberculosis, and end-stage kidney disease.^2,3 Other possible causes are retention of uremic metabolites, metastatic calcification induced by secondary hyperparathyroidism, and calcium-phosphate deposition induced by hyperphosphatemia.⁴

In chronic kidney disease, the amount of pericardial fluid and fibrinous pericardial deposition is thought to contribute to increased pericardial thickness and constriction. In some patients, pericardial calcification and thickening would lead to constrictive pericarditis, which could be confirmed by echocardiography and cardiac catheterization. About 25% to 50% of cases of pericardial calcification are complicated by constrictive pericarditis.^5,6 Constrictive pericarditis occurs in up to 4% of patients with end-stage renal disease, even with successful dialysis.⁷

Partial clinical improvement may be obtained with intensive hemodialysis, strict volume control, and decreased catabolism in patients with multiple comorbidities.⁸ However, the definite treatment is total pericardiectomy, which reduces symptoms substantially and offers a favorable long-term outcome.⁷

SECONDARY HYPERPARATHYROIDISM

Secondary hyperparathyroidism is a common complication in patients with end-stage renal disease and is characterized by derangements in the homeostasis of calcium, phosphorus, and vitamin D.⁹

Because renal function is decreased, phosphate is retained and calcitriol synthesis is reduced, resulting in hypocalcemia, which induces parathyroid gland hyperplasia and parathyroid hormone secretion.¹⁰ Moreover, some patents with long-standing secondary hyperparathyroidism may develop tertiary hyperparathyroidism associated with autonomous parathyroid hormone secretion, hypercalcemia, and hyperphosphatemia.¹¹

The Kidney Disease: Improving Global Outcomes (KDIGO) Work Group recommends screening for and managing secondary hyperparathyroidism in all patients with stage 3 chronic kidney disease (estimated glomerular filtration rate < 60 mL/min). In patients with stage 5 chronic kidney disease or on dialysis, the serum calcium and phosphorus levels should be monitored every 1 to 3 months and the parathyroid hormone levels every 3 to 6 months.¹²

According to KDIGO guidelines, the target level of calcium is less than 10.2 mg/dL, and the target phosphorus level is less than 4.6 mg/dL. The level of parathyroid hormone should be maintained at 2 to 9 times the upper limit of normal for the assay.

The management of secondary hyperparathyroidism includes a low-phosphorus diet, calcium-containing or calcium-free phosphate binders, a calcitriol supplement, and calcimimetics. If medical treatment fails and manifestations are significant, parathyroidectomy may be indicated.¹³

A 35-year-old woman with a history of migraine presented with a headache that had worsened over the past 2 weeks. The headache was occipital and was associated with blurred vision, photophobia, tingling of the hands, episodes of flashing lights and images, and difficulty concentrating. The headache was similar to her typical migraines, but with the addition of flashing lights and images.

Her medical history included a cystic mass in the right occipital lobe that had been found incidentally on magnetic resonance imaging (MRI) during a workup for pituitary adenoma. The mass was thought to be a congenital lesion or arachnoid cyst, and intermittent screening had been recommended.

The patient had grown up in Honduras and had lived in the jungle until age 12, when she moved to the United States.

EVALUATION AND MANAGEMENT

Physical examination was remarkable for partial visual field loss in the periphery of the left temporal quadrant in both eyes (partial homonymous hemianopia). Repeat MRI showed a cystic lesion with scolex (the anterior end of a tapeworm) in the right occipital lobe, with surrounding edema (Figure 1).

Cystic brain lesions are associated with arachnoid cyst, glioma, and malignancy, but the presence of the scolex placed neurocysticercosis as the leading diagnosis. Testing for cysticercus antibody was negative. This test was done in the hope of confirming our high suspicion; while a negative test result does not exclude this diagnosis, a positive test would have been helpful to corroborate what we suspected. However, her imaging and clinical features were sufficient to warrant treating her for neurocysticercosis

She was treated with albendazole 400 mg twice a day for 10 days, and prednisone 1 mg/kg/day for 10 days followed by a taper. Because of the frequency with which neurocysticercosis causes seizures, an anti­epileptic drug is also recommended, at least until active lesions have subsided.¹ In this patient, levetiracetam 1,000 mg twice a day was prescribed for 6 months for seizure prophylaxis.

Repeat MRI 2 months later showed improvement (Figure 2). Her acute neurologic signs and symptoms had resolved, but she continued to be followed for chronic migraines (Figure 3). She has had no seizures despite weaning from levetiracetam.

TAPEWORM AND MIGRAINE

Neurocysticercosis is caused by the cestode Taenia solium, acquired by eating undercooked pork contaminated with the cysts or eggs.¹ The oncospheres released by the eggs migrate through the host body and encyst in end organs.

Neuroimaging can show 4 stages of the cysts—vesicular with living larva, colloidal with larva degeneration, granulonodular with thickening of the cyst, and calcification.¹

For patients who have lived in or visited high-risk areas of the world such as Central America, South America, sub-Saharan Africa, India, and Asia, it is important to include neurocysticercosis in the differential diagnosis of migraine with focal deficits or migraine with an evolving quality. Encysted larvae can remain asymptomatic for years but can cause brain edema, often leading to seizures.

Serum testing for cysticercus antibody can indicate acute infection, chronic infection, and possibly the immune response to treatment; however, serum testing has limited sensitivity in patients who have single or calcified lesions.² A negative test result does not exclude infection and is more likely to be a false negative in patients with a single or calcified lesion.

Current treatment guidelines recommend albendazole 400 mg twice daily along with dexamethasone or prednisolone to decrease the number of cysts and the development of lesional epilepsy.¹ Albendazole in combination with praziquantel 50 mg/kg/day kills more cysts than albendazole alone and should be considered in patients with more than 2 cysts.³

A 35-year-old woman with a history of migraine presented with a headache that had worsened over the past 2 weeks. The headache was occipital and was associated with blurred vision, photophobia, tingling of the hands, episodes of flashing lights and images, and difficulty concentrating. The headache was similar to her typical migraines, but with the addition of flashing lights and images.

Her medical history included a cystic mass in the right occipital lobe that had been found incidentally on magnetic resonance imaging (MRI) during a workup for pituitary adenoma. The mass was thought to be a congenital lesion or arachnoid cyst, and intermittent screening had been recommended.

The patient had grown up in Honduras and had lived in the jungle until age 12, when she moved to the United States.

EVALUATION AND MANAGEMENT

Physical examination was remarkable for partial visual field loss in the periphery of the left temporal quadrant in both eyes (partial homonymous hemianopia). Repeat MRI showed a cystic lesion with scolex (the anterior end of a tapeworm) in the right occipital lobe, with surrounding edema (Figure 1).

Cystic brain lesions are associated with arachnoid cyst, glioma, and malignancy, but the presence of the scolex placed neurocysticercosis as the leading diagnosis. Testing for cysticercus antibody was negative. This test was done in the hope of confirming our high suspicion; while a negative test result does not exclude this diagnosis, a positive test would have been helpful to corroborate what we suspected. However, her imaging and clinical features were sufficient to warrant treating her for neurocysticercosis

She was treated with albendazole 400 mg twice a day for 10 days, and prednisone 1 mg/kg/day for 10 days followed by a taper. Because of the frequency with which neurocysticercosis causes seizures, an anti­epileptic drug is also recommended, at least until active lesions have subsided.¹ In this patient, levetiracetam 1,000 mg twice a day was prescribed for 6 months for seizure prophylaxis.

Repeat MRI 2 months later showed improvement (Figure 2). Her acute neurologic signs and symptoms had resolved, but she continued to be followed for chronic migraines (Figure 3). She has had no seizures despite weaning from levetiracetam.

TAPEWORM AND MIGRAINE

Neurocysticercosis is caused by the cestode Taenia solium, acquired by eating undercooked pork contaminated with the cysts or eggs.¹ The oncospheres released by the eggs migrate through the host body and encyst in end organs.

Neuroimaging can show 4 stages of the cysts—vesicular with living larva, colloidal with larva degeneration, granulonodular with thickening of the cyst, and calcification.¹

For patients who have lived in or visited high-risk areas of the world such as Central America, South America, sub-Saharan Africa, India, and Asia, it is important to include neurocysticercosis in the differential diagnosis of migraine with focal deficits or migraine with an evolving quality. Encysted larvae can remain asymptomatic for years but can cause brain edema, often leading to seizures.

Serum testing for cysticercus antibody can indicate acute infection, chronic infection, and possibly the immune response to treatment; however, serum testing has limited sensitivity in patients who have single or calcified lesions.² A negative test result does not exclude infection and is more likely to be a false negative in patients with a single or calcified lesion.

Current treatment guidelines recommend albendazole 400 mg twice daily along with dexamethasone or prednisolone to decrease the number of cysts and the development of lesional epilepsy.¹ Albendazole in combination with praziquantel 50 mg/kg/day kills more cysts than albendazole alone and should be considered in patients with more than 2 cysts.³

A 35-year-old woman with a history of migraine presented with a headache that had worsened over the past 2 weeks. The headache was occipital and was associated with blurred vision, photophobia, tingling of the hands, episodes of flashing lights and images, and difficulty concentrating. The headache was similar to her typical migraines, but with the addition of flashing lights and images.

Her medical history included a cystic mass in the right occipital lobe that had been found incidentally on magnetic resonance imaging (MRI) during a workup for pituitary adenoma. The mass was thought to be a congenital lesion or arachnoid cyst, and intermittent screening had been recommended.

The patient had grown up in Honduras and had lived in the jungle until age 12, when she moved to the United States.

EVALUATION AND MANAGEMENT

Physical examination was remarkable for partial visual field loss in the periphery of the left temporal quadrant in both eyes (partial homonymous hemianopia). Repeat MRI showed a cystic lesion with scolex (the anterior end of a tapeworm) in the right occipital lobe, with surrounding edema (Figure 1).

Cystic brain lesions are associated with arachnoid cyst, glioma, and malignancy, but the presence of the scolex placed neurocysticercosis as the leading diagnosis. Testing for cysticercus antibody was negative. This test was done in the hope of confirming our high suspicion; while a negative test result does not exclude this diagnosis, a positive test would have been helpful to corroborate what we suspected. However, her imaging and clinical features were sufficient to warrant treating her for neurocysticercosis

She was treated with albendazole 400 mg twice a day for 10 days, and prednisone 1 mg/kg/day for 10 days followed by a taper. Because of the frequency with which neurocysticercosis causes seizures, an anti­epileptic drug is also recommended, at least until active lesions have subsided.¹ In this patient, levetiracetam 1,000 mg twice a day was prescribed for 6 months for seizure prophylaxis.

Repeat MRI 2 months later showed improvement (Figure 2). Her acute neurologic signs and symptoms had resolved, but she continued to be followed for chronic migraines (Figure 3). She has had no seizures despite weaning from levetiracetam.

TAPEWORM AND MIGRAINE

Neurocysticercosis is caused by the cestode Taenia solium, acquired by eating undercooked pork contaminated with the cysts or eggs.¹ The oncospheres released by the eggs migrate through the host body and encyst in end organs.

Neuroimaging can show 4 stages of the cysts—vesicular with living larva, colloidal with larva degeneration, granulonodular with thickening of the cyst, and calcification.¹

For patients who have lived in or visited high-risk areas of the world such as Central America, South America, sub-Saharan Africa, India, and Asia, it is important to include neurocysticercosis in the differential diagnosis of migraine with focal deficits or migraine with an evolving quality. Encysted larvae can remain asymptomatic for years but can cause brain edema, often leading to seizures.

Serum testing for cysticercus antibody can indicate acute infection, chronic infection, and possibly the immune response to treatment; however, serum testing has limited sensitivity in patients who have single or calcified lesions.² A negative test result does not exclude infection and is more likely to be a false negative in patients with a single or calcified lesion.

Current treatment guidelines recommend albendazole 400 mg twice daily along with dexamethasone or prednisolone to decrease the number of cysts and the development of lesional epilepsy.¹ Albendazole in combination with praziquantel 50 mg/kg/day kills more cysts than albendazole alone and should be considered in patients with more than 2 cysts.³

SNOWMASS, COLO. – The use of coronary artery calcium screening in the subset of asymptomatic diabetes patients at higher clinical risk of CAD appears to offer a practical strategy for identifying a subgroup in whom costlier stress cardiac imaging may be justified, Marcelo F. di Carli, MD, said at the Annual Cardiovascular Conference at Snowmass.

The ultimate goal is to reliably identify those patients who have asymptomatic diabetes with significant CAD warranting revascularization or maximal medical therapy for primary cardiovascular prevention.

“Coronary artery calcium is a simple test that’s accessible and inexpensive and can give us a quick read on the extent of atherosclerosis in the coronary arteries,” said Dr. di Carli, professor of radiology and medicine at Harvard University in Boston. “There’s good data that in diabetic patients there’s a gradation of risk across the spectrum of calcium scores. Risk increases exponentially from a coronary artery calcium score of 0 to more than 400. The calcium score can also provide a snapshot of which patients are more likely to have flow-limiting coronary disease.”

Bruce Jancin/Frontline Medical News

[email protected]

SNOWMASS, COLO. – The use of coronary artery calcium screening in the subset of asymptomatic diabetes patients at higher clinical risk of CAD appears to offer a practical strategy for identifying a subgroup in whom costlier stress cardiac imaging may be justified, Marcelo F. di Carli, MD, said at the Annual Cardiovascular Conference at Snowmass.

The ultimate goal is to reliably identify those patients who have asymptomatic diabetes with significant CAD warranting revascularization or maximal medical therapy for primary cardiovascular prevention.

“Coronary artery calcium is a simple test that’s accessible and inexpensive and can give us a quick read on the extent of atherosclerosis in the coronary arteries,” said Dr. di Carli, professor of radiology and medicine at Harvard University in Boston. “There’s good data that in diabetic patients there’s a gradation of risk across the spectrum of calcium scores. Risk increases exponentially from a coronary artery calcium score of 0 to more than 400. The calcium score can also provide a snapshot of which patients are more likely to have flow-limiting coronary disease.”

Bruce Jancin/Frontline Medical News

[email protected]

SNOWMASS, COLO. – The use of coronary artery calcium screening in the subset of asymptomatic diabetes patients at higher clinical risk of CAD appears to offer a practical strategy for identifying a subgroup in whom costlier stress cardiac imaging may be justified, Marcelo F. di Carli, MD, said at the Annual Cardiovascular Conference at Snowmass.

The ultimate goal is to reliably identify those patients who have asymptomatic diabetes with significant CAD warranting revascularization or maximal medical therapy for primary cardiovascular prevention.

“Coronary artery calcium is a simple test that’s accessible and inexpensive and can give us a quick read on the extent of atherosclerosis in the coronary arteries,” said Dr. di Carli, professor of radiology and medicine at Harvard University in Boston. “There’s good data that in diabetic patients there’s a gradation of risk across the spectrum of calcium scores. Risk increases exponentially from a coronary artery calcium score of 0 to more than 400. The calcium score can also provide a snapshot of which patients are more likely to have flow-limiting coronary disease.”

Bruce Jancin/Frontline Medical News

[email protected]

Case

A 31-year-old white man presented to the ED with abdominal and rectal pain accompanied by multiple episodes of bloody diarrhea. He stated he had mild rectal pain the previous night but was pain-free and in his usual state of health the morning of his presentation. Approximately 2 hours before presenting to the ED, however, he began experiencing mild stomach pain, then bloody diarrhea which he described as bright red and “filling the toilet bowl with blood.” He had no history of inflammatory bowel disease or other gastrointestinal (GI) disorder, no recent travel, no complaints of nausea or vomiting, and no infectious symptoms. He described a remote history of external hemorrhoids, and review of his family history was significant for multiple paternal relatives with aortic aneurysms. He was not taking any medications and was a nonsmoker with a normal body mass index (24.3 kg/m²).

Upon arrival at the ED, the patient’s vital signs were: heart rate, 112 beats/min; and blood pressure, 139/102 mm Hg; respiratory rate and temperature were normal, as was the patient’s oxygen saturation on room air. Physical examination was notable for no subjective or objective findings of orthostatic hypotension; increased bowel sounds and diffuse mild abdominal tenderness; and no external hemorrhoids, fissures, or rectal tenderness. Laboratory evaluation was significant for hemoglobin (Hgb), 15.0 g/dL; blood urea nitrogen (BUN)-to-creatinine (Cr) ratio, 11.6; and anion gap, 17 mEq/L.

Upon initial presentation, there was some concern for an infection. However, as the patient continued to have bowel movements consisting almost entirely of frank blood and did not have any infectious signs, a vascular etiology was more strongly considered. Given the patient’s relatively stable vital signs, BUN-to-Cr ratio of less than 20, and lack of orthostatic hypotension, there was low concern for an upper GI etiology, and endoscopy was not obtained emergently. The patient instead underwent abdominal computed tomography angiography (CTA), which identified active extravasation and contrast pooling within the cecum and appendix (Figure 1).

Discussion

Acute lower GI bleeding has an estimated annual hospitalization rate of 36 patients per 100,000, or about half the rate for upper GI bleeding.^1,2 The majority of patients (>80%) will have spontaneous resolution and can be worked up nonemergently.³ Of the remaining 20%, some patients will have severe hematochezia (defined as continuous bleeding during the first 24 hours of hospitalization that results in a decreased Hgb level of 2 g/dL or more, or a decreased Hgb level that necessitates transfusion of 2 U or more of PRBCs). In patients with significant bleeding, the first priority in the ED is hemodynamic stabilization, including close monitoring, establishing two large-bore intravenous (IV) lines, and volume resuscitation, with transfusion as needed.

Etiology and Work-Up

Assessment of the etiology of hematochezia begins with ruling out an upper GI source of the bleed; 10% to 15% of patients presenting with hematochezia without hematemesis are ultimately diagnosed with an upper GI etiology. ^4,5

BUN-to-Cr Ratio. In a study of patients presenting with hematochezia but no hematemesis or renal failure, Srygley et al⁶ found a BUN-to-Cr ratio greater than 93% to be sensitive for an upper GI source, with a likelihood ratio of 7.5. The proposed etiology is some combination of absorption of digested blood products and prerenal azotemia due to hypovolemia.

Tachycardia and Orthostatic Hypotension. There have been discussions in the literature about other findings to rule in/out upper GI bleeding. While some studies have found statistically significant results between upper and lower GI bleeding for tachycardia and orthostatic hypotension (increased percentage of both in upper GI bleeding), there is disagreement about whether these findings are clinically significant.^7-9

Nasogastric Lavage. Although nasogastric (NG) lavage is no longer the standard of care in the ED due to poor sensitivity and marked discomfort to the patient, most current gastroenterology guidelines still recommend its use; therefore, NG may be requested by the GI consultant.^10-12

Diagnosis

Once an upper GI source has been ruled out, identification of the lesion is the next step. The differential diagnosis includes common sources such as diverticular disease, angiodysplasia, colitis, anorectal sources, and neoplasm.⁵ Less common, but associated with a high risk of mortality, is aortoenteric fistula (100% mortality without surgical intervention).⁵

Colonoscopy. Emergent colonoscopy can be used for both diagnosis and (potential) therapeutic intervention and is therefore the first option of choice.^1,3,4,9 However, as seen in our case, some patients experience such profound hemorrhage that visualization of the colon may be difficult or impossible; patients may also be too unstable to await bowel preparation or undergo a procedure.

Computed Tomography Angiography. For patients in whom colonoscopy is contraindicated, CTA is the imaging modality of choice, and has a 91% to 92% sensitivity in identifying active bleeding (>0.35 mL/min).^13-16

Computed tomography of the abdomen and pelvis with contrast alone, as opposed to CTA, is insufficient for detecting GI bleeding, as it is timed so that imaging is obtained when the contrast is in the portal venous capillary beds, rather than in the arteries or arterioles. By protocol, though, many institutions require abdominal and pelvic CTA to include both arterial phase and venous phase images, allowing for assessment of both active arterial bleeding and alternative lower GI sources of hematochezia (eg, mesenteric ischemia).

When ordering a CT study, an awareness of local practice is important in understanding the information that will be obtained from the study. Protocols for lower GI bleed that include CTA have reported accuracy and efficiency without worsening of renal function, despite the increased contrast load.¹⁷

Triphasic CT Enterography. Another CT modality to consider is triphasic CT enterography, which uses IV and oral contrast. In a preliminary trial, this modality achieved a specificity of 100% (sensitivity 42%) in detecting GI bleeding.¹⁸

Red Blood Cell Scintigraphy. An additional imaging modality that has been the subject of much debate in the GI literature is tagged RBC scintigraphy with Technetium-99m. Various studies have found bleeding-site confirmation in 24% to 97% of patients, and correct localization in 41% to 100% of patients. Given the extensive variability within the literature on selection criteria, localization, site confirmation, and other variables, as well as evidence from one prospective trial by Zink et al¹⁹ that found a significant disagreement between CTA and scintigraphy, RBC scintigraphy is not recommended as an alternative imaging modality for the rapid diagnosis of an acute lower GI bleed.

Conclusion

Severe hematochezia is a potential surgical emergency with a broad differential diagnosis. While emergent colonoscopy is an excellent first option, in patients with severe hematochezia, there may be too much blood in the colon to obtain adequate visual images; additionally, depending on practice setting, emergency colonoscopy may not be immediately available. In either case, CTA—a readily available, noninvasive, rapid, and repeatable diagnostic tool—should be considered as an alternate to colonoscopy, particularly in patients with brisk hematochezia.

If a patient with severe hematochezia presents to the ED, the emergency physician (EP) must recognize that the degree of hemorrhage may not correlate with the patient’s vital signs or initial laboratory values. For this reason, the EP must have a high index of suspicion, and consider CTA to allow for a rapid definitive diagnosis and prompt discussion between surgical, interventional radiology, and/or gastroenterology teams to improve clinical outcomes and decrease morbidity and mortality.²⁰

Case

A 31-year-old white man presented to the ED with abdominal and rectal pain accompanied by multiple episodes of bloody diarrhea. He stated he had mild rectal pain the previous night but was pain-free and in his usual state of health the morning of his presentation. Approximately 2 hours before presenting to the ED, however, he began experiencing mild stomach pain, then bloody diarrhea which he described as bright red and “filling the toilet bowl with blood.” He had no history of inflammatory bowel disease or other gastrointestinal (GI) disorder, no recent travel, no complaints of nausea or vomiting, and no infectious symptoms. He described a remote history of external hemorrhoids, and review of his family history was significant for multiple paternal relatives with aortic aneurysms. He was not taking any medications and was a nonsmoker with a normal body mass index (24.3 kg/m²).

Upon arrival at the ED, the patient’s vital signs were: heart rate, 112 beats/min; and blood pressure, 139/102 mm Hg; respiratory rate and temperature were normal, as was the patient’s oxygen saturation on room air. Physical examination was notable for no subjective or objective findings of orthostatic hypotension; increased bowel sounds and diffuse mild abdominal tenderness; and no external hemorrhoids, fissures, or rectal tenderness. Laboratory evaluation was significant for hemoglobin (Hgb), 15.0 g/dL; blood urea nitrogen (BUN)-to-creatinine (Cr) ratio, 11.6; and anion gap, 17 mEq/L.

Upon initial presentation, there was some concern for an infection. However, as the patient continued to have bowel movements consisting almost entirely of frank blood and did not have any infectious signs, a vascular etiology was more strongly considered. Given the patient’s relatively stable vital signs, BUN-to-Cr ratio of less than 20, and lack of orthostatic hypotension, there was low concern for an upper GI etiology, and endoscopy was not obtained emergently. The patient instead underwent abdominal computed tomography angiography (CTA), which identified active extravasation and contrast pooling within the cecum and appendix (Figure 1).

Discussion

Acute lower GI bleeding has an estimated annual hospitalization rate of 36 patients per 100,000, or about half the rate for upper GI bleeding.^1,2 The majority of patients (>80%) will have spontaneous resolution and can be worked up nonemergently.³ Of the remaining 20%, some patients will have severe hematochezia (defined as continuous bleeding during the first 24 hours of hospitalization that results in a decreased Hgb level of 2 g/dL or more, or a decreased Hgb level that necessitates transfusion of 2 U or more of PRBCs). In patients with significant bleeding, the first priority in the ED is hemodynamic stabilization, including close monitoring, establishing two large-bore intravenous (IV) lines, and volume resuscitation, with transfusion as needed.

Etiology and Work-Up

Assessment of the etiology of hematochezia begins with ruling out an upper GI source of the bleed; 10% to 15% of patients presenting with hematochezia without hematemesis are ultimately diagnosed with an upper GI etiology. ^4,5

BUN-to-Cr Ratio. In a study of patients presenting with hematochezia but no hematemesis or renal failure, Srygley et al⁶ found a BUN-to-Cr ratio greater than 93% to be sensitive for an upper GI source, with a likelihood ratio of 7.5. The proposed etiology is some combination of absorption of digested blood products and prerenal azotemia due to hypovolemia.

Tachycardia and Orthostatic Hypotension. There have been discussions in the literature about other findings to rule in/out upper GI bleeding. While some studies have found statistically significant results between upper and lower GI bleeding for tachycardia and orthostatic hypotension (increased percentage of both in upper GI bleeding), there is disagreement about whether these findings are clinically significant.^7-9

Nasogastric Lavage. Although nasogastric (NG) lavage is no longer the standard of care in the ED due to poor sensitivity and marked discomfort to the patient, most current gastroenterology guidelines still recommend its use; therefore, NG may be requested by the GI consultant.^10-12

Diagnosis

Once an upper GI source has been ruled out, identification of the lesion is the next step. The differential diagnosis includes common sources such as diverticular disease, angiodysplasia, colitis, anorectal sources, and neoplasm.⁵ Less common, but associated with a high risk of mortality, is aortoenteric fistula (100% mortality without surgical intervention).⁵

Colonoscopy. Emergent colonoscopy can be used for both diagnosis and (potential) therapeutic intervention and is therefore the first option of choice.^1,3,4,9 However, as seen in our case, some patients experience such profound hemorrhage that visualization of the colon may be difficult or impossible; patients may also be too unstable to await bowel preparation or undergo a procedure.

Computed Tomography Angiography. For patients in whom colonoscopy is contraindicated, CTA is the imaging modality of choice, and has a 91% to 92% sensitivity in identifying active bleeding (>0.35 mL/min).^13-16

Computed tomography of the abdomen and pelvis with contrast alone, as opposed to CTA, is insufficient for detecting GI bleeding, as it is timed so that imaging is obtained when the contrast is in the portal venous capillary beds, rather than in the arteries or arterioles. By protocol, though, many institutions require abdominal and pelvic CTA to include both arterial phase and venous phase images, allowing for assessment of both active arterial bleeding and alternative lower GI sources of hematochezia (eg, mesenteric ischemia).

When ordering a CT study, an awareness of local practice is important in understanding the information that will be obtained from the study. Protocols for lower GI bleed that include CTA have reported accuracy and efficiency without worsening of renal function, despite the increased contrast load.¹⁷

Triphasic CT Enterography. Another CT modality to consider is triphasic CT enterography, which uses IV and oral contrast. In a preliminary trial, this modality achieved a specificity of 100% (sensitivity 42%) in detecting GI bleeding.¹⁸

Red Blood Cell Scintigraphy. An additional imaging modality that has been the subject of much debate in the GI literature is tagged RBC scintigraphy with Technetium-99m. Various studies have found bleeding-site confirmation in 24% to 97% of patients, and correct localization in 41% to 100% of patients. Given the extensive variability within the literature on selection criteria, localization, site confirmation, and other variables, as well as evidence from one prospective trial by Zink et al¹⁹ that found a significant disagreement between CTA and scintigraphy, RBC scintigraphy is not recommended as an alternative imaging modality for the rapid diagnosis of an acute lower GI bleed.

Conclusion

Severe hematochezia is a potential surgical emergency with a broad differential diagnosis. While emergent colonoscopy is an excellent first option, in patients with severe hematochezia, there may be too much blood in the colon to obtain adequate visual images; additionally, depending on practice setting, emergency colonoscopy may not be immediately available. In either case, CTA—a readily available, noninvasive, rapid, and repeatable diagnostic tool—should be considered as an alternate to colonoscopy, particularly in patients with brisk hematochezia.

If a patient with severe hematochezia presents to the ED, the emergency physician (EP) must recognize that the degree of hemorrhage may not correlate with the patient’s vital signs or initial laboratory values. For this reason, the EP must have a high index of suspicion, and consider CTA to allow for a rapid definitive diagnosis and prompt discussion between surgical, interventional radiology, and/or gastroenterology teams to improve clinical outcomes and decrease morbidity and mortality.²⁰

Case

A 31-year-old white man presented to the ED with abdominal and rectal pain accompanied by multiple episodes of bloody diarrhea. He stated he had mild rectal pain the previous night but was pain-free and in his usual state of health the morning of his presentation. Approximately 2 hours before presenting to the ED, however, he began experiencing mild stomach pain, then bloody diarrhea which he described as bright red and “filling the toilet bowl with blood.” He had no history of inflammatory bowel disease or other gastrointestinal (GI) disorder, no recent travel, no complaints of nausea or vomiting, and no infectious symptoms. He described a remote history of external hemorrhoids, and review of his family history was significant for multiple paternal relatives with aortic aneurysms. He was not taking any medications and was a nonsmoker with a normal body mass index (24.3 kg/m²).

Upon arrival at the ED, the patient’s vital signs were: heart rate, 112 beats/min; and blood pressure, 139/102 mm Hg; respiratory rate and temperature were normal, as was the patient’s oxygen saturation on room air. Physical examination was notable for no subjective or objective findings of orthostatic hypotension; increased bowel sounds and diffuse mild abdominal tenderness; and no external hemorrhoids, fissures, or rectal tenderness. Laboratory evaluation was significant for hemoglobin (Hgb), 15.0 g/dL; blood urea nitrogen (BUN)-to-creatinine (Cr) ratio, 11.6; and anion gap, 17 mEq/L.

Upon initial presentation, there was some concern for an infection. However, as the patient continued to have bowel movements consisting almost entirely of frank blood and did not have any infectious signs, a vascular etiology was more strongly considered. Given the patient’s relatively stable vital signs, BUN-to-Cr ratio of less than 20, and lack of orthostatic hypotension, there was low concern for an upper GI etiology, and endoscopy was not obtained emergently. The patient instead underwent abdominal computed tomography angiography (CTA), which identified active extravasation and contrast pooling within the cecum and appendix (Figure 1).

Discussion

Acute lower GI bleeding has an estimated annual hospitalization rate of 36 patients per 100,000, or about half the rate for upper GI bleeding.^1,2 The majority of patients (>80%) will have spontaneous resolution and can be worked up nonemergently.³ Of the remaining 20%, some patients will have severe hematochezia (defined as continuous bleeding during the first 24 hours of hospitalization that results in a decreased Hgb level of 2 g/dL or more, or a decreased Hgb level that necessitates transfusion of 2 U or more of PRBCs). In patients with significant bleeding, the first priority in the ED is hemodynamic stabilization, including close monitoring, establishing two large-bore intravenous (IV) lines, and volume resuscitation, with transfusion as needed.

Etiology and Work-Up

Assessment of the etiology of hematochezia begins with ruling out an upper GI source of the bleed; 10% to 15% of patients presenting with hematochezia without hematemesis are ultimately diagnosed with an upper GI etiology. ^4,5

BUN-to-Cr Ratio. In a study of patients presenting with hematochezia but no hematemesis or renal failure, Srygley et al⁶ found a BUN-to-Cr ratio greater than 93% to be sensitive for an upper GI source, with a likelihood ratio of 7.5. The proposed etiology is some combination of absorption of digested blood products and prerenal azotemia due to hypovolemia.

Tachycardia and Orthostatic Hypotension. There have been discussions in the literature about other findings to rule in/out upper GI bleeding. While some studies have found statistically significant results between upper and lower GI bleeding for tachycardia and orthostatic hypotension (increased percentage of both in upper GI bleeding), there is disagreement about whether these findings are clinically significant.^7-9

Nasogastric Lavage. Although nasogastric (NG) lavage is no longer the standard of care in the ED due to poor sensitivity and marked discomfort to the patient, most current gastroenterology guidelines still recommend its use; therefore, NG may be requested by the GI consultant.^10-12

Diagnosis

Once an upper GI source has been ruled out, identification of the lesion is the next step. The differential diagnosis includes common sources such as diverticular disease, angiodysplasia, colitis, anorectal sources, and neoplasm.⁵ Less common, but associated with a high risk of mortality, is aortoenteric fistula (100% mortality without surgical intervention).⁵

Colonoscopy. Emergent colonoscopy can be used for both diagnosis and (potential) therapeutic intervention and is therefore the first option of choice.^1,3,4,9 However, as seen in our case, some patients experience such profound hemorrhage that visualization of the colon may be difficult or impossible; patients may also be too unstable to await bowel preparation or undergo a procedure.

Computed Tomography Angiography. For patients in whom colonoscopy is contraindicated, CTA is the imaging modality of choice, and has a 91% to 92% sensitivity in identifying active bleeding (>0.35 mL/min).^13-16

Computed tomography of the abdomen and pelvis with contrast alone, as opposed to CTA, is insufficient for detecting GI bleeding, as it is timed so that imaging is obtained when the contrast is in the portal venous capillary beds, rather than in the arteries or arterioles. By protocol, though, many institutions require abdominal and pelvic CTA to include both arterial phase and venous phase images, allowing for assessment of both active arterial bleeding and alternative lower GI sources of hematochezia (eg, mesenteric ischemia).

When ordering a CT study, an awareness of local practice is important in understanding the information that will be obtained from the study. Protocols for lower GI bleed that include CTA have reported accuracy and efficiency without worsening of renal function, despite the increased contrast load.¹⁷

Triphasic CT Enterography. Another CT modality to consider is triphasic CT enterography, which uses IV and oral contrast. In a preliminary trial, this modality achieved a specificity of 100% (sensitivity 42%) in detecting GI bleeding.¹⁸

Red Blood Cell Scintigraphy. An additional imaging modality that has been the subject of much debate in the GI literature is tagged RBC scintigraphy with Technetium-99m. Various studies have found bleeding-site confirmation in 24% to 97% of patients, and correct localization in 41% to 100% of patients. Given the extensive variability within the literature on selection criteria, localization, site confirmation, and other variables, as well as evidence from one prospective trial by Zink et al¹⁹ that found a significant disagreement between CTA and scintigraphy, RBC scintigraphy is not recommended as an alternative imaging modality for the rapid diagnosis of an acute lower GI bleed.

Conclusion

Severe hematochezia is a potential surgical emergency with a broad differential diagnosis. While emergent colonoscopy is an excellent first option, in patients with severe hematochezia, there may be too much blood in the colon to obtain adequate visual images; additionally, depending on practice setting, emergency colonoscopy may not be immediately available. In either case, CTA—a readily available, noninvasive, rapid, and repeatable diagnostic tool—should be considered as an alternate to colonoscopy, particularly in patients with brisk hematochezia.

If a patient with severe hematochezia presents to the ED, the emergency physician (EP) must recognize that the degree of hemorrhage may not correlate with the patient’s vital signs or initial laboratory values. For this reason, the EP must have a high index of suspicion, and consider CTA to allow for a rapid definitive diagnosis and prompt discussion between surgical, interventional radiology, and/or gastroenterology teams to improve clinical outcomes and decrease morbidity and mortality.²⁰

A 45-year-old woman with a history of polycystic ovary syndrome presented to the ED for evaluation of acute abdominal pain. The patient’s surgical history was significant for a cesarean delivery 6 months prior to presentation. Abdominal examination revealed a well-healed suprapubic cesarean incision scar, which was tender upon palpation. A computed tomography (CT) scan of the abdomen and pelvis with contrast were ordered; representative images are shown above (Figure 1a-1d).

What is the diagnosis? What are the associated complications and preferred management for this entity?

Answer

The scout image from the CT scan shows multiple dilated loops of small bowel (white arrows, Figure 2a) and only a small amount of air within a decompressed colon (red arrow, Figure 2a). The multiplanar CT image confirmed multiple dilated small bowel loops (white arrows, Figure 2b) and the decompressed large bowel (red arrows, Figure 2b), indicating the presence of a small bowel obstruction. A distal small bowel loop (white arrows, Figure 2c and 2d) was identified in a hernia sac within the walls of the rectus abdominis muscle (red arrows, Figure 2c and 2d). Mesenteric stranding within the hernia sac was suggestive of incarceration (black arrow, Figure 2d). No signs of intestinal ischemia, such as pneumatosis or wall thickening, were present.

An exploratory laparotomy was emergently performed, which confirmed the presence of incarcerated small bowel within the posterior rectus sheath defect without evidence of strangulation. Reduction of small bowel and primary closure of the hernia defect was subsequently performed without complication.

Abdominal Wall Hernias

Abdominal wall hernias are common in the United States, with more than 1 million abdominal wall hernia repairs performed annually.¹ A posterior rectus sheath hernia is a rare type of abdominal wall hernia; the majority are postsurgical (as seen in this patient) or posttraumatic, with only a few reported congenital cases.²

Anatomy

The rectus sheath encloses the rectus abdominis muscle and is composed of the aponeuroses of the transversus abdominis, external oblique, and internal oblique muscles. The aponeuroses form an anterior and posterior sheath, which together serve as a strong barrier against the herniation of abdominal contents, accounting for the rarity of a spontaneous rectus sheath hernia. However, inferior to the umbilicus (below the arcuate line), the posterior rectus sheath is composed primarily of transversalis fascia, which may make this region more susceptible to herniation.³ Additional predisposing factors to herniation include increased muscle weakness and elevated intra-abdominal pressure, such as that which occurs during pregnancy or from ascites.⁴

Clinical Presentation

Like other abdominal wall hernias, the clinical presentation of posterior rectus sheath hernias is nonspecific. Patients may be asymptomatic or may develop abdominal pain, distension, and vomiting as a result of acute complications that necessitate emergent surgery. During history-taking, inquiry into a patient’s surgical history is crucial because it may raise clinical suspicion for an abdominal wall hernia, as was the case in our patient, who recently had a cesarean delivery.

Diagnosis

Because prompt and accurate diagnosis of acute complications of abdominal wall hernias is essential, imaging studies are typically required for diagnosis. Computed tomography is the modality of choice based on its ability to provide superior anatomic detail of the abdominal wall, permitting identification of hernias and differentiating them from other abdominal masses, such as hematomas, abscesses, or tumors. Additionally, CT is able to detect early signs of hernia sac complications, including bowel obstruction, incarceration, and strangulation.⁵

Treatment

Treatment for a posterior rectus sheath hernia is surgical with primary closure being the preferred method. Prosthetic repair may also be performed, particularly when the hernia defect is large, but it has been shown to be associated with an increased risk of intestinal strangulation.³

A 45-year-old woman with a history of polycystic ovary syndrome presented to the ED for evaluation of acute abdominal pain. The patient’s surgical history was significant for a cesarean delivery 6 months prior to presentation. Abdominal examination revealed a well-healed suprapubic cesarean incision scar, which was tender upon palpation. A computed tomography (CT) scan of the abdomen and pelvis with contrast were ordered; representative images are shown above (Figure 1a-1d).

What is the diagnosis? What are the associated complications and preferred management for this entity?

Answer

The scout image from the CT scan shows multiple dilated loops of small bowel (white arrows, Figure 2a) and only a small amount of air within a decompressed colon (red arrow, Figure 2a). The multiplanar CT image confirmed multiple dilated small bowel loops (white arrows, Figure 2b) and the decompressed large bowel (red arrows, Figure 2b), indicating the presence of a small bowel obstruction. A distal small bowel loop (white arrows, Figure 2c and 2d) was identified in a hernia sac within the walls of the rectus abdominis muscle (red arrows, Figure 2c and 2d). Mesenteric stranding within the hernia sac was suggestive of incarceration (black arrow, Figure 2d). No signs of intestinal ischemia, such as pneumatosis or wall thickening, were present.

An exploratory laparotomy was emergently performed, which confirmed the presence of incarcerated small bowel within the posterior rectus sheath defect without evidence of strangulation. Reduction of small bowel and primary closure of the hernia defect was subsequently performed without complication.

Abdominal Wall Hernias

Abdominal wall hernias are common in the United States, with more than 1 million abdominal wall hernia repairs performed annually.¹ A posterior rectus sheath hernia is a rare type of abdominal wall hernia; the majority are postsurgical (as seen in this patient) or posttraumatic, with only a few reported congenital cases.²

Anatomy

The rectus sheath encloses the rectus abdominis muscle and is composed of the aponeuroses of the transversus abdominis, external oblique, and internal oblique muscles. The aponeuroses form an anterior and posterior sheath, which together serve as a strong barrier against the herniation of abdominal contents, accounting for the rarity of a spontaneous rectus sheath hernia. However, inferior to the umbilicus (below the arcuate line), the posterior rectus sheath is composed primarily of transversalis fascia, which may make this region more susceptible to herniation.³ Additional predisposing factors to herniation include increased muscle weakness and elevated intra-abdominal pressure, such as that which occurs during pregnancy or from ascites.⁴

Clinical Presentation

Like other abdominal wall hernias, the clinical presentation of posterior rectus sheath hernias is nonspecific. Patients may be asymptomatic or may develop abdominal pain, distension, and vomiting as a result of acute complications that necessitate emergent surgery. During history-taking, inquiry into a patient’s surgical history is crucial because it may raise clinical suspicion for an abdominal wall hernia, as was the case in our patient, who recently had a cesarean delivery.

Diagnosis

Because prompt and accurate diagnosis of acute complications of abdominal wall hernias is essential, imaging studies are typically required for diagnosis. Computed tomography is the modality of choice based on its ability to provide superior anatomic detail of the abdominal wall, permitting identification of hernias and differentiating them from other abdominal masses, such as hematomas, abscesses, or tumors. Additionally, CT is able to detect early signs of hernia sac complications, including bowel obstruction, incarceration, and strangulation.⁵

Treatment

Treatment for a posterior rectus sheath hernia is surgical with primary closure being the preferred method. Prosthetic repair may also be performed, particularly when the hernia defect is large, but it has been shown to be associated with an increased risk of intestinal strangulation.³

A 45-year-old woman with a history of polycystic ovary syndrome presented to the ED for evaluation of acute abdominal pain. The patient’s surgical history was significant for a cesarean delivery 6 months prior to presentation. Abdominal examination revealed a well-healed suprapubic cesarean incision scar, which was tender upon palpation. A computed tomography (CT) scan of the abdomen and pelvis with contrast were ordered; representative images are shown above (Figure 1a-1d).

What is the diagnosis? What are the associated complications and preferred management for this entity?

Answer

The scout image from the CT scan shows multiple dilated loops of small bowel (white arrows, Figure 2a) and only a small amount of air within a decompressed colon (red arrow, Figure 2a). The multiplanar CT image confirmed multiple dilated small bowel loops (white arrows, Figure 2b) and the decompressed large bowel (red arrows, Figure 2b), indicating the presence of a small bowel obstruction. A distal small bowel loop (white arrows, Figure 2c and 2d) was identified in a hernia sac within the walls of the rectus abdominis muscle (red arrows, Figure 2c and 2d). Mesenteric stranding within the hernia sac was suggestive of incarceration (black arrow, Figure 2d). No signs of intestinal ischemia, such as pneumatosis or wall thickening, were present.

An exploratory laparotomy was emergently performed, which confirmed the presence of incarcerated small bowel within the posterior rectus sheath defect without evidence of strangulation. Reduction of small bowel and primary closure of the hernia defect was subsequently performed without complication.

Abdominal Wall Hernias

Abdominal wall hernias are common in the United States, with more than 1 million abdominal wall hernia repairs performed annually.¹ A posterior rectus sheath hernia is a rare type of abdominal wall hernia; the majority are postsurgical (as seen in this patient) or posttraumatic, with only a few reported congenital cases.²

Anatomy

The rectus sheath encloses the rectus abdominis muscle and is composed of the aponeuroses of the transversus abdominis, external oblique, and internal oblique muscles. The aponeuroses form an anterior and posterior sheath, which together serve as a strong barrier against the herniation of abdominal contents, accounting for the rarity of a spontaneous rectus sheath hernia. However, inferior to the umbilicus (below the arcuate line), the posterior rectus sheath is composed primarily of transversalis fascia, which may make this region more susceptible to herniation.³ Additional predisposing factors to herniation include increased muscle weakness and elevated intra-abdominal pressure, such as that which occurs during pregnancy or from ascites.⁴

Clinical Presentation

Like other abdominal wall hernias, the clinical presentation of posterior rectus sheath hernias is nonspecific. Patients may be asymptomatic or may develop abdominal pain, distension, and vomiting as a result of acute complications that necessitate emergent surgery. During history-taking, inquiry into a patient’s surgical history is crucial because it may raise clinical suspicion for an abdominal wall hernia, as was the case in our patient, who recently had a cesarean delivery.

Diagnosis

Because prompt and accurate diagnosis of acute complications of abdominal wall hernias is essential, imaging studies are typically required for diagnosis. Computed tomography is the modality of choice based on its ability to provide superior anatomic detail of the abdominal wall, permitting identification of hernias and differentiating them from other abdominal masses, such as hematomas, abscesses, or tumors. Additionally, CT is able to detect early signs of hernia sac complications, including bowel obstruction, incarceration, and strangulation.⁵

Treatment

Treatment for a posterior rectus sheath hernia is surgical with primary closure being the preferred method. Prosthetic repair may also be performed, particularly when the hernia defect is large, but it has been shown to be associated with an increased risk of intestinal strangulation.³

Brain imaging should precede lumbar puncture in patients with focal neurologic deficits or immunodeficiency, or with altered mental status or seizures during the previous week. However, lumbar puncture can be safely done in most patients without first obtaining brain imaging. Empiric antibiotic and corticosteroid therapy must not be delayed; they should be started immediately after the lumber puncture is done, without waiting for the results. If the lumbar puncture is going to be delayed, these treatments should be started immediately after obtaining blood samples for culture.

A MEDICAL EMERGENCY

Bacterial meningitis is a medical emergency and requires prompt recognition and treatment. It is associated with a nearly 15% death rate as well as neurologic effects such as deafness, seizures, and cognitive decline in about the same percentage of patients.¹ Microbiologic information from lumbar puncture and cerebrospinal fluid analysis is an essential part of the initial workup, whenever possible. Lumbar puncture can be done safely at the bedside in most patients and so should not be delayed unless certain contraindications exist, as discussed below.²

INDICATIONS FOR BRAIN IMAGING BEFORE LUMBAR PUNCTURE

Table 1 lists common indications for brain imaging before lumbar puncture. However, there is a lack of good evidence to support them.

Current guidelines on acute bacterial meningitis from the Infectious Diseases Society of America recommend computed tomography (CT) of the brain before lumbar puncture in patients presenting with:

• Altered mental status
• A new focal neurologic deficit (eg, cranial nerve palsy, extremity weakness or drift, dysarthria, aphasia)
• Papilledema
• Seizure within the past week
• History of central nervous system disease (eg, stroke, tumor)
• Age 60 or older (likely because of the association with previous central nervous system disease)
• Immunocompromised state (due to human immunodeficiency virus infection, chemotherapy, or immunosuppressive drugs for transplant or rheumatologic disease)
• A high clinical suspicion for subarachnoid hemorrhage.^3–5

However, a normal result on head CT does not rule out the possibility of increased intracranial pressure and the risk of brain herniation. Actually, patients with acute bacterial meningitis are inherently at higher risk of spontaneous brain herniation even without lumbar puncture, and some cases of brain herniation after lumbar puncture could have represented the natural course of disease. Importantly, lumbar puncture may not be independently associated with the risk of brain herniation in patients with altered mental status (Glasgow Coma Scale score ≤ 8).⁶ A prospective randomized study is needed to better understand when to order brain imaging before lumbar puncture and when it is safe to proceed directly to lumbar puncture.

CONTRAINDICATIONS TO LUMBAR PUNCTURE

General contraindications to lumbar puncture are listed in Table 2.

Gopal et al³ analyzed clinical and radiographic data for 113 adults requiring urgent lumbar puncture and reported that altered mental status (likelihood ratio [LR] 2.2), focal neurologic deficit (LR 4.3), papilledema (LR 11.1), and clinical impression (LR 18.8) were associated with abnormalities on CT.

Hasbun et al⁴ prospectively analyzed whether clinical variables correlated with abnormal results of head CT that would preclude lumbar puncture in 301 patients requiring urgent lumbar puncture. They found that age 60 and older, immunodeficiency, a history of central nervous system disease, recent seizure (within 1 week), and neurologic deficits were associated with abnormal findings on head CT (eg, lesion with mass effect, midline shift). Importantly, absence of these characteristics had a 97% negative predictive value for abnormal findings on head CT. However, neither a normal head CT nor a normal clinical neurologic examination rules out increased intracranial pressure.^4,7

CHIEF CONCERNS ABOUT LUMBAR PUNCTURE

Lumbar puncture is generally well tolerated. Major complications are rare² and can be prevented by checking for contraindications and by using appropriate procedural hygiene and technique. Complications include pain at the puncture site, postprocedural headache, epidural hematoma, meningitis, osteomyelitis or discitis, bleeding, epidermoid tumor, and, most worrisome, brain herniation.

Brain herniation

Concern about causing brain herniation is the reason imaging may be ordered before lumbar puncture. Cerebral edema and increased intracranial pressure are common in patients with bacterial meningitis, as well as in other conditions such as bleeding, tumor, and abscess.¹ If intracranial pressure is elevated, lumbar puncture can cause cerebral herniation with further neurologic compromise and possibly death. Herniation is believed to be due to a sudden decrease in pressure in the spinal cord caused by removal of cerebrospinal fluid. However, the only information we have about this complication comes from case reports and case series, so we don’t really know how often it happens.

On the other hand, ordering ancillary tests before lumbar puncture and starting empiric antibiotics in patients with suspected bacterial meningitis may delay treatment and lead to worse clinical outcomes and thus should be discouraged.⁸

Also important to note is the lack of good data regarding the safety of lumbar puncture in patients with potential hemostatic problems (thrombocytopenia, coagulopathy). The recommendation not to do lumbar puncture in these situations (Table 1) is taken from neuraxial anesthesia guidelines.⁹ Further, a small retrospective study of thrombocytopenic oncology patients requiring lumbar puncture did not demonstrate an increased risk of complications.¹⁰

ADDITIONAL CONSIDERATIONS

In a retrospective study in 2015, Glimåker et al⁶ demonstrated that lumbar puncture without prior brain CT was safe in patients with suspected acute bacterial meningitis with moderate to severe impairment of mental status, and that it led to a shorter “door-to-antibiotic time.” Lumbar puncture before imaging was also associated with a concomitant decrease in the risk of death, with no increase in the rate of complications.⁶

If brain imaging is to be done before lumbar puncture, then blood cultures (and cultures of other fluids, whenever appropriate) should be collected and the patient should be started on empiric management for central nervous system infection first. CT evidence of diffuse cerebral edema, focal lesions with mass effect, and ventriculomegaly should be viewed as further contraindications to lumbar puncture.¹

Antibiotic therapy

When contraindications to lumbar puncture exist, the choice of antibiotic and the duration of therapy should be based on the patient’s history, demographics, risk factors, and microbiologic data from blood culture, urine culture, sputum culture, and detection of microbiological antigens.¹ The choice of antibiotic is beyond the scope of this article. However, empiric antibiotic therapy with a third-generation cephalosporin (eg, ceftriaxone) and vancomycin and anti-inflammatory therapy (dexamethasone) should in most cases be started immediately after collecting samples for blood culture and must not be delayed by neuroimaging and lumbar puncture with cerebrospinal fluid sampling, given the high rates of mortality and morbidity if treatment is delayed.^5,8

Consultation with the neurosurgery service regarding alternative brain ventricular fluid sampling should be considered.¹¹

Brain imaging should precede lumbar puncture in patients with focal neurologic deficits or immunodeficiency, or with altered mental status or seizures during the previous week. However, lumbar puncture can be safely done in most patients without first obtaining brain imaging. Empiric antibiotic and corticosteroid therapy must not be delayed; they should be started immediately after the lumber puncture is done, without waiting for the results. If the lumbar puncture is going to be delayed, these treatments should be started immediately after obtaining blood samples for culture.

A MEDICAL EMERGENCY

Bacterial meningitis is a medical emergency and requires prompt recognition and treatment. It is associated with a nearly 15% death rate as well as neurologic effects such as deafness, seizures, and cognitive decline in about the same percentage of patients.¹ Microbiologic information from lumbar puncture and cerebrospinal fluid analysis is an essential part of the initial workup, whenever possible. Lumbar puncture can be done safely at the bedside in most patients and so should not be delayed unless certain contraindications exist, as discussed below.²

INDICATIONS FOR BRAIN IMAGING BEFORE LUMBAR PUNCTURE

Table 1 lists common indications for brain imaging before lumbar puncture. However, there is a lack of good evidence to support them.

Current guidelines on acute bacterial meningitis from the Infectious Diseases Society of America recommend computed tomography (CT) of the brain before lumbar puncture in patients presenting with:

• Altered mental status
• A new focal neurologic deficit (eg, cranial nerve palsy, extremity weakness or drift, dysarthria, aphasia)
• Papilledema
• Seizure within the past week
• History of central nervous system disease (eg, stroke, tumor)
• Age 60 or older (likely because of the association with previous central nervous system disease)
• Immunocompromised state (due to human immunodeficiency virus infection, chemotherapy, or immunosuppressive drugs for transplant or rheumatologic disease)
• A high clinical suspicion for subarachnoid hemorrhage.^3–5

However, a normal result on head CT does not rule out the possibility of increased intracranial pressure and the risk of brain herniation. Actually, patients with acute bacterial meningitis are inherently at higher risk of spontaneous brain herniation even without lumbar puncture, and some cases of brain herniation after lumbar puncture could have represented the natural course of disease. Importantly, lumbar puncture may not be independently associated with the risk of brain herniation in patients with altered mental status (Glasgow Coma Scale score ≤ 8).⁶ A prospective randomized study is needed to better understand when to order brain imaging before lumbar puncture and when it is safe to proceed directly to lumbar puncture.

CONTRAINDICATIONS TO LUMBAR PUNCTURE

General contraindications to lumbar puncture are listed in Table 2.

Gopal et al³ analyzed clinical and radiographic data for 113 adults requiring urgent lumbar puncture and reported that altered mental status (likelihood ratio [LR] 2.2), focal neurologic deficit (LR 4.3), papilledema (LR 11.1), and clinical impression (LR 18.8) were associated with abnormalities on CT.

Hasbun et al⁴ prospectively analyzed whether clinical variables correlated with abnormal results of head CT that would preclude lumbar puncture in 301 patients requiring urgent lumbar puncture. They found that age 60 and older, immunodeficiency, a history of central nervous system disease, recent seizure (within 1 week), and neurologic deficits were associated with abnormal findings on head CT (eg, lesion with mass effect, midline shift). Importantly, absence of these characteristics had a 97% negative predictive value for abnormal findings on head CT. However, neither a normal head CT nor a normal clinical neurologic examination rules out increased intracranial pressure.^4,7

CHIEF CONCERNS ABOUT LUMBAR PUNCTURE

Lumbar puncture is generally well tolerated. Major complications are rare² and can be prevented by checking for contraindications and by using appropriate procedural hygiene and technique. Complications include pain at the puncture site, postprocedural headache, epidural hematoma, meningitis, osteomyelitis or discitis, bleeding, epidermoid tumor, and, most worrisome, brain herniation.

Brain herniation

Concern about causing brain herniation is the reason imaging may be ordered before lumbar puncture. Cerebral edema and increased intracranial pressure are common in patients with bacterial meningitis, as well as in other conditions such as bleeding, tumor, and abscess.¹ If intracranial pressure is elevated, lumbar puncture can cause cerebral herniation with further neurologic compromise and possibly death. Herniation is believed to be due to a sudden decrease in pressure in the spinal cord caused by removal of cerebrospinal fluid. However, the only information we have about this complication comes from case reports and case series, so we don’t really know how often it happens.

On the other hand, ordering ancillary tests before lumbar puncture and starting empiric antibiotics in patients with suspected bacterial meningitis may delay treatment and lead to worse clinical outcomes and thus should be discouraged.⁸

Also important to note is the lack of good data regarding the safety of lumbar puncture in patients with potential hemostatic problems (thrombocytopenia, coagulopathy). The recommendation not to do lumbar puncture in these situations (Table 1) is taken from neuraxial anesthesia guidelines.⁹ Further, a small retrospective study of thrombocytopenic oncology patients requiring lumbar puncture did not demonstrate an increased risk of complications.¹⁰

ADDITIONAL CONSIDERATIONS

In a retrospective study in 2015, Glimåker et al⁶ demonstrated that lumbar puncture without prior brain CT was safe in patients with suspected acute bacterial meningitis with moderate to severe impairment of mental status, and that it led to a shorter “door-to-antibiotic time.” Lumbar puncture before imaging was also associated with a concomitant decrease in the risk of death, with no increase in the rate of complications.⁶

If brain imaging is to be done before lumbar puncture, then blood cultures (and cultures of other fluids, whenever appropriate) should be collected and the patient should be started on empiric management for central nervous system infection first. CT evidence of diffuse cerebral edema, focal lesions with mass effect, and ventriculomegaly should be viewed as further contraindications to lumbar puncture.¹

Antibiotic therapy

When contraindications to lumbar puncture exist, the choice of antibiotic and the duration of therapy should be based on the patient’s history, demographics, risk factors, and microbiologic data from blood culture, urine culture, sputum culture, and detection of microbiological antigens.¹ The choice of antibiotic is beyond the scope of this article. However, empiric antibiotic therapy with a third-generation cephalosporin (eg, ceftriaxone) and vancomycin and anti-inflammatory therapy (dexamethasone) should in most cases be started immediately after collecting samples for blood culture and must not be delayed by neuroimaging and lumbar puncture with cerebrospinal fluid sampling, given the high rates of mortality and morbidity if treatment is delayed.^5,8

Consultation with the neurosurgery service regarding alternative brain ventricular fluid sampling should be considered.¹¹

Brain imaging should precede lumbar puncture in patients with focal neurologic deficits or immunodeficiency, or with altered mental status or seizures during the previous week. However, lumbar puncture can be safely done in most patients without first obtaining brain imaging. Empiric antibiotic and corticosteroid therapy must not be delayed; they should be started immediately after the lumber puncture is done, without waiting for the results. If the lumbar puncture is going to be delayed, these treatments should be started immediately after obtaining blood samples for culture.

A MEDICAL EMERGENCY

Bacterial meningitis is a medical emergency and requires prompt recognition and treatment. It is associated with a nearly 15% death rate as well as neurologic effects such as deafness, seizures, and cognitive decline in about the same percentage of patients.¹ Microbiologic information from lumbar puncture and cerebrospinal fluid analysis is an essential part of the initial workup, whenever possible. Lumbar puncture can be done safely at the bedside in most patients and so should not be delayed unless certain contraindications exist, as discussed below.²

INDICATIONS FOR BRAIN IMAGING BEFORE LUMBAR PUNCTURE

Table 1 lists common indications for brain imaging before lumbar puncture. However, there is a lack of good evidence to support them.

Current guidelines on acute bacterial meningitis from the Infectious Diseases Society of America recommend computed tomography (CT) of the brain before lumbar puncture in patients presenting with:

• Altered mental status
• A new focal neurologic deficit (eg, cranial nerve palsy, extremity weakness or drift, dysarthria, aphasia)
• Papilledema
• Seizure within the past week
• History of central nervous system disease (eg, stroke, tumor)
• Age 60 or older (likely because of the association with previous central nervous system disease)
• Immunocompromised state (due to human immunodeficiency virus infection, chemotherapy, or immunosuppressive drugs for transplant or rheumatologic disease)
• A high clinical suspicion for subarachnoid hemorrhage.^3–5

However, a normal result on head CT does not rule out the possibility of increased intracranial pressure and the risk of brain herniation. Actually, patients with acute bacterial meningitis are inherently at higher risk of spontaneous brain herniation even without lumbar puncture, and some cases of brain herniation after lumbar puncture could have represented the natural course of disease. Importantly, lumbar puncture may not be independently associated with the risk of brain herniation in patients with altered mental status (Glasgow Coma Scale score ≤ 8).⁶ A prospective randomized study is needed to better understand when to order brain imaging before lumbar puncture and when it is safe to proceed directly to lumbar puncture.

CONTRAINDICATIONS TO LUMBAR PUNCTURE

General contraindications to lumbar puncture are listed in Table 2.

Gopal et al³ analyzed clinical and radiographic data for 113 adults requiring urgent lumbar puncture and reported that altered mental status (likelihood ratio [LR] 2.2), focal neurologic deficit (LR 4.3), papilledema (LR 11.1), and clinical impression (LR 18.8) were associated with abnormalities on CT.

Hasbun et al⁴ prospectively analyzed whether clinical variables correlated with abnormal results of head CT that would preclude lumbar puncture in 301 patients requiring urgent lumbar puncture. They found that age 60 and older, immunodeficiency, a history of central nervous system disease, recent seizure (within 1 week), and neurologic deficits were associated with abnormal findings on head CT (eg, lesion with mass effect, midline shift). Importantly, absence of these characteristics had a 97% negative predictive value for abnormal findings on head CT. However, neither a normal head CT nor a normal clinical neurologic examination rules out increased intracranial pressure.^4,7

CHIEF CONCERNS ABOUT LUMBAR PUNCTURE

Lumbar puncture is generally well tolerated. Major complications are rare² and can be prevented by checking for contraindications and by using appropriate procedural hygiene and technique. Complications include pain at the puncture site, postprocedural headache, epidural hematoma, meningitis, osteomyelitis or discitis, bleeding, epidermoid tumor, and, most worrisome, brain herniation.

Brain herniation

Concern about causing brain herniation is the reason imaging may be ordered before lumbar puncture. Cerebral edema and increased intracranial pressure are common in patients with bacterial meningitis, as well as in other conditions such as bleeding, tumor, and abscess.¹ If intracranial pressure is elevated, lumbar puncture can cause cerebral herniation with further neurologic compromise and possibly death. Herniation is believed to be due to a sudden decrease in pressure in the spinal cord caused by removal of cerebrospinal fluid. However, the only information we have about this complication comes from case reports and case series, so we don’t really know how often it happens.

On the other hand, ordering ancillary tests before lumbar puncture and starting empiric antibiotics in patients with suspected bacterial meningitis may delay treatment and lead to worse clinical outcomes and thus should be discouraged.⁸

Also important to note is the lack of good data regarding the safety of lumbar puncture in patients with potential hemostatic problems (thrombocytopenia, coagulopathy). The recommendation not to do lumbar puncture in these situations (Table 1) is taken from neuraxial anesthesia guidelines.⁹ Further, a small retrospective study of thrombocytopenic oncology patients requiring lumbar puncture did not demonstrate an increased risk of complications.¹⁰

ADDITIONAL CONSIDERATIONS

In a retrospective study in 2015, Glimåker et al⁶ demonstrated that lumbar puncture without prior brain CT was safe in patients with suspected acute bacterial meningitis with moderate to severe impairment of mental status, and that it led to a shorter “door-to-antibiotic time.” Lumbar puncture before imaging was also associated with a concomitant decrease in the risk of death, with no increase in the rate of complications.⁶

If brain imaging is to be done before lumbar puncture, then blood cultures (and cultures of other fluids, whenever appropriate) should be collected and the patient should be started on empiric management for central nervous system infection first. CT evidence of diffuse cerebral edema, focal lesions with mass effect, and ventriculomegaly should be viewed as further contraindications to lumbar puncture.¹

Antibiotic therapy

When contraindications to lumbar puncture exist, the choice of antibiotic and the duration of therapy should be based on the patient’s history, demographics, risk factors, and microbiologic data from blood culture, urine culture, sputum culture, and detection of microbiological antigens.¹ The choice of antibiotic is beyond the scope of this article. However, empiric antibiotic therapy with a third-generation cephalosporin (eg, ceftriaxone) and vancomycin and anti-inflammatory therapy (dexamethasone) should in most cases be started immediately after collecting samples for blood culture and must not be delayed by neuroimaging and lumbar puncture with cerebrospinal fluid sampling, given the high rates of mortality and morbidity if treatment is delayed.^5,8

Consultation with the neurosurgery service regarding alternative brain ventricular fluid sampling should be considered.¹¹