DOPPLER ĐỘNG MẠCH NÃO GIỮA ĐỂ CHẨN ĐOÁN THIẾU MÁU SƠ SINH

© 2012 by the American Institute of Ultrasound in Medicine

More than a decade ago, Mari et al1,2 achieved a major breakthrough in the treatment of Rh-sensitized fetuses with their pioneering work that showed a correlation between the Doppler middle cerebral artery peak systolic velocity (PSV) and fetal hemoglobin levels. This technique has virtually eliminated the need for invasive procedures such as amniocentesis and cordocentesis that have been used for diagnosis of fetal anemia with their inherent complications. Since then, the middle cerebral artery PSV has been the standard of care for treatment of anemic fetuses. Doppler studies have also been used in neonates with different cerebral conditions (eg, intraventricular hemorrhage, brain lesions, and hydrocephalus).3–6 However, this approach has not been attempted in neonates suspected to have blood volume disorders such as anemia and polycythemia. If a correlation between neonatal hemoglobin levels and the middle cerebral artery PSV is found, it may be similarly applied for rapid, noninvasive bedside diagnosis of acute life-threatening conditions in neonates until the standard blood tests can be performed.

The aims of this study were therefore to determine whether a correlation exists between the neonatal middle cerebral artery PSV and hemoglobin levels and to assess the possibility of implementing this indicator for rapid, noninvasive diagnosis of blood volume disorders in neonates.

Materials and Methods

Study Population

This prospective study included 151 healthy neonates, weight appropriate for gestational age, born at our medical center during a 6-month period. All neonates were delivered at 37 weeks’ gestation or later with Apgar scores of 7 or higher at 5 minutes. We excluded all neonates with malformations, intrauterine growth restriction, perinatal asphyxia, and infections. The local Research Ethics Institutional Review Committee approved the study, and informed consent was obtained from the mother of each neonate enrolled in the study. Medical examinations by a senior pediatrician confirmed that all neonates enrolled in the study were healthy without dysmorphic features. The neonates were born by spontaneous vaginal delivery or cesarean delivery. All neonates were prospectively studied on the second day of life (between 24 and 36 hours after delivery). Anemia was defined as a hemoglobin level of 13.5 g/dL or less or a hematocrit value 45% or less, and polycythemia was defined as a hemoglobin level greater than 22 g/dL or a hematocrit value greater than 65%.7

Doppler Studies

Doppler examinations of the middle cerebral artery were performed with a Voluson 730 ultrasound system (GE Healthcare, Solingen, Germany) and a convex transducer (4–8 MHz) in a quiet room. The neonates were sleeping in a crib without gross body or limb movements and were breathing quietly. The examinations were performed by using an axial plane on the temporal bone anterior to the external auditory canal and superior to the zygomatic process, identifying the middle cerebral artery. Measurements were obtained just distal to the middle cerebral artery origin from the internal carotid artery. The angle of insonation was close to 0°, thus obviating the need for angle correction (Figure 1). The sample gate was 3 to 4 mm. The total examination time was 1 to 3 minutes. Five Doppler waves were recorded, and the highest PSV waveform was used for analysis.

Statistics

An analysis of variance was performed to evaluate the different variables in the 3 groups studied (normal, anemic, and polycythemic neonates). Multiple comparison analyses were performed as well to determine whether the variable means were statistically different from each other. A regression analysis was conducted to test correlations between hemoglobin levels and middle cerebral artery PSVs in the whole groups. P < .05 was considered significant.

Results

The study population included 122 normocythemic, 24 anemic, and 5 polycythemic neonates. The mean gestational age ± SD of the neonates at delivery was 39 ± 1.5 weeks, with a median Apgar score of 10 at 5 minutes and a mean birth weight of 3290 ± 446 g.

Table 1 presents the hemoglobin, hematocrit, and PSV values of the 3 groups. There were significant differences in the hemoglobin, hematocrit, and PSV values between the normocythemic neonates and the anemic and polycythemic neonates (P < .001). Of the 24 anemic neonates, 20 (83%) had a middle cerebral artery PSV that was higher than the 95% confidence interval (CI) for normocythemic neonates, and all 5 polycythemic neonates had a PSV that was lower than the 95% CI for normocythemic neonates.

 

 

 

In Figure 2, the means and 95% CIs of the middle cerebral artery PSV values in the 3 groups (anemic, normocythemic, and polycythemic) are shown. Although there are overlapping values, the means of the 3 groups are significantly different and can be easily distinguished from each other (P < .01). Figure 3 depicts the middle cerebral artery PSV according to different hemoglobin levels (with the means and 95 percent CIs). A clear decrease in the PSV is evident with increasing hemoglobin levels (P < .01).



 

 

In Figure 4, the middle cerebral artery PSV of the 3 groups combined is depicted with a third-order polynomial fit regression line. Although there are overlapping values, the trend is clear (especially at the extremes of the hemoglobin levels) that the lower the hemoglobin concentration, the higher the PSV and vice versa. A significant correlation between the PSV and hemoglobin levels was found (P < .01). It is interesting to note that a plateau exists at hemoglobin levels considered to be within the normal range (±2 SDs) for neonates (at ≈13–22 g/dL), but below or above these limits, there are acute changes in the PSV.



 

In Figure 5, we show a vector plot of several anemic neonates who underwent partial exchange transfusion. The hemoglobin level and middle cerebral artery PSV were obtained at the bedside before the blood transfusion and 1 hour after the transfusion. The plot shows the trend of changes in the PSV, and the lines span from the starting to ending hemoglobin levels. Once more, it is clear that an increasing hemoglobin level caused an immediate decrease in the PSV. These fetuses with initial hemoglobin levels of 7.8 to 11.9 g/dL had PSVs of 51 to 144 cm/s, which rapidly decreased to approximately 32 to 80 cm/s when the hemoglobin levels increased to the normal range (>13 g/dL).



Discussion

This study shows that there is a significant correlation between hemoglobin levels and the middle cerebral artery PSV in neonates. Although overlapping measurements in the normal range of hemoglobin levels exist, the more severe degrees of anemia and polycythemia can be readily diagnosed by examining the middle cerebral artery PSV. Similarly to the well-established technique used in fetuses, this procedure can also be suitable in neonates for prompt diagnosis of life-threatening blood volume disorders. Obviously, we do not imply that this method can replace the traditional direct blood examination. However, it may be used as an ancillary, rapid means of noninvasively estimating the degree of anemia or polycythemia in neonates suspected to have blood volume disorders, thus allowing prompt action. There are several neonatal conditions in which middle cerebral artery PSV can be rapidly used for diagnosis of anemia and polycythemia. These include anticipated deliveries of twins affected by twin-twin transfusion syndrome, neonates affected by Rh and Kell isoimmunization, thalassemia, parvovirus B19 infection, and hydrops. In addition, acute intrapartum events such as intracranial hemorrhage, a large cephalhematoma, and other hemorrhages associated with traumatic instrumental delivery with loss of a substantial amount of blood or a sudden decrease in blood volume can be immediately recognized at the bedside when clinical suspicion dictates. Even critically ill neonates for whom venous access is difficult (eg, hydropic neonates) can have a prompt diagnosis until blood tests can be safely performed. The appealing aspect of this technique is that it can be easily studied and mastered even by novice users in a very short period.

The underlying pathophysiologic mechanism of increased cardiac output and decreased blood viscosity in anemic fetuses is valid also for neonates, as shown in this study. Anemia causes an increase in the cardiac stroke volume, heart rate, and peripheral resistance and decreased blood viscosity, leading to an increase in cerebral blood flow to maintain adequate oxygen transport to the brain.8,9 Neonates, similarly to fetuses, obey the same physical laws of flow velocities in blood vessels.

Polycythemia, on the other hand, occurs in 2% to 5% of term neonates,10 usually as a compensatory mechanism in intrauterine hypoxia or uncontrolled diabetic pregnancies with macrosomic neonates or as a result of delayed cord clamping.11 This condition may lead to hyperviscosity of the blood with altered rheologic properties and flow disturbances, which can result in impaired perfusion to multiple organs. This situation can cause neurologic, cardiorespiratory, gastrointestinal, and renal abnormalities.12–15 Although these symptoms are usually transient, prompt diagnosis and treatment may be life saving with reversal of the potential damage.16,17

We found that for the established normal range of hemoglobin levels, the middle cerebral artery PSV has a plateau, whereas in anemia and polycythemia, the PSV changes rapidly (increasing and decreasing, respectively). The correlation between hemoglobin levels and the PSV becomes more pronounced as the severity of anemia or polycythemia increases (Figure 2). This factor may be due to the rheologic properties of the blood in neonates. Flow remains almost constant for a wide range of hemoglobin levels but rapidly changes as the hemoglobin levels decrease or increase beyond certain limits. It is interesting to note that the middle cerebral artery PSVs of the term neonates in this study (Table 1) were very similar to those reported by Mari et al2 in term fetuses, and anemic fetuses had PSVs similar to those of anemic neonates.

As to the question of whether this technique can be implemented in clinical practice, we have shown several neonates who underwent partial exchange transfusion because of anemia and were studied with the Doppler middle cerebral artery PSV before and after the transfusion (Figure 4). It is evident that normalizing the hemoglobin level rapidly corrects the PSV. We think that in polycythemic neonates, the contrary occurs as well.

This study had some limitations. We studied only term neonates 24 to 36 hours after delivery, examining our hypothesis that the Doppler middle cerebral artery PSV can be helpful in managing neonatal emergencies occurring in the first days after delivery (eg, intracerebral bleeding due to traumatic delivery). Because it has been reported that the PSV progressively changes during the first month of life,18 the flow velocities may be different later, and caution should be used in interpreting hemoglobin levels as a function of the middle cerebral artery PSV in older neonates.

Although it is appealing to also use this technique in premature neonates to diagnose acute anemia caused by massive hemorrhage, a caveat should be addressed in this group as well. The situation may be different in premature neonates in whom the proportion of hemoglobin F is different, and there may be different rheologic properties of the blood due to a different elasticity or size of the red blood cells. This issue should be further studied in the future. An additional factor that was not controlled for but may potentially alter the middle cerebral artery PSV is the presence or absence of a patent ductus arteriosus. However, the impact of the ductus on blood flow to the brain has been reported to be minimal19; therefore, we think that this factor may have only a marginal effect on middle cerebral artery PSV measurements in anemic and polycythemic neonates.

In conclusion, Doppler measurement of the middle cerebral artery PSV appears to be helpful for estimating the hemoglobin concentration in neonates and can be used as a screening tool for diagnosing neonatal anemia and polycythemia. This technique may allow a rapid, noninvasive determination of the neonatal hemoglobin level, dictating the urgency of treatment.



VÌ SAO NÊN SIÊU ÂM KHỚP VAI

Shoulder Sonography: Why We Do It

  Sharlene A. Teefey, MD
 Mallinckrodt Institute of Radiology, St Louis, Missouri USA.
J Ultrasound Med 2012; 31:1325–1331

 

One of the most common causes of shoulder pain is rotator cuff disease. It is the third most prevalent musculoskeletal disorder after low back and neck pain. Shoulder pain is usually due to one of several causes: subacromial impingement and bursopathy, tendinopathy, a tendon tear, a frozen shoulder, ligamentous instability, and osteoarthritis. Rotator cuff disease (tendinopathy or tear) highly correlates with increasing age. In one study, the average age for patients with a painful unilateral partial- or full-thickness tear was 58.7 years, and it was 68.7 years for those with bilateral partial- or full-thickness tears. This study also showed that patients with a painful unilateral full-thickness tear had a 35.5% prevalence of an asymptomatic tear on the contralateral side. This is important because a substantial number of patients with asymptomatic tears become symptomatic after short-term follow-up (which has been associated with tear size progression) and have deterioration of shoulder function.

There are several imaging techniques that can be used to diagnose rotator cuff disease, including sonography, magnetic resonance imaging (MRI), magnetic resonance arthrography, and computed tomographic arthrography. This article will focus on the role of sonography in evaluating the patient with shoulder pain, in particular, rotator cuff disease.

Accuracy of Sonography

Sonography has become an accepted imaging technique for evaluating the patient with suspected cuff disease. It can be used to accurately diagnose and quantify full- and partial-thickness tears and recurrent tears in the postoperative shoulder, determine the tear location, and evaluate the cuff muscles for fatty degeneration. It can also be used to diagnose other cuff disorders such as tendinopathy and calcific tendinitis and noncuff pathology of the biceps tendon, acromioclavicular joint, posterior labrum (paralabral cyst), and sub-deltoid bursa.

Several studies have reported high sensitivity, specificity, and accuracy for diagnosing full- and partial-thickness tears. A meta-analysis by de Jesus et al showed that sonography and MRI were comparable in both sensitivity and specificity for diagnosing full-and partial-thickness cuff tears. It is important to accurately diagnose and characterize cuff tears for treatment planning. Sonographic findings help the orthopedic surgeon decide whether treatment should be surgical or nonsurgical; if arthroscopy is indicated, sono-graphic findings help the orthopedic surgeon counsel patients regarding surgical and functional outcomes. If a nonsurgical approach is chosen, sonography can be used to follow patients for tear size progression. It can also be used to evaluate the cuff muscles for fatty degeneration, which is an important prognostic factor regarding the patient outcome; fatty degeneration portends a poor functional outcome and places the patient at risk of a retear. Two studies have shown that there is a good correlation between sonography and MRI for assessing cuff muscle atrophy and fatty degeneration, and that the diagnostic performance between the two studies was comparable for diagnosing fatty degeneration.

Sonography has also been shown to be very sensitive for diagnosing calcific tendinitis and may be used to guide aspiration of calcific deposits. Aspiration has been shown to provide prompt and long-term pain relief at 1 year. Little has been published regarding cuff tendinopathy, although it has been described in a few textbooks. A cadaveric study comparing sonographic findings to histopathologic changes showed a significant relationship between cuff tendinopathy and thickening in 21 cadaver shoulders (N. Dahiga, MD, S. Teefey, MD, W. Middleton, MD, M. Kim, MD, and C. Hildebolt, PhD, unpublished data, 2007). The diagnosis should be considered when the cuff measures greater than 5.5 mm, based on data from a study that measured cuff thickness in 100 asymptomatic men and showed a mean thickness ± SD of 4.6 ± 0.9 mm. These authors also showed that there were no significant relationships between sex, age, and cuff thickness in the absence or presence of shoulder pain. Thus, this value can be generalized to men and women regardless of age and the presence of shoulder pain.

Sonography is very accurate for diagnosing biceps tendon subluxation, dislocation, and rupture, although it was not able to distinguish a high-grade (≥70%) partial-thickness tear from a rupture. It has low sensitivity for diagnosing tenosynovitis, tendinopathy, and low-grade partial-thickness tears.

Changes to the acromioclavicular joint such as synovitis, effusion, osteoarthritis, and osteolysis are easily diagnosed with sonography. A paralabral cyst, which is usually located in the spinoglenoid notch, can be identified with sonography and aspirated under sonographic guidance for pain relief before definitive surgery. Subdeltoid bursal disorders such as an effusion and bursitis can readily be diagnosed with sonography.

Sonographic Technique

Shoulder sonography is performed using a high-frequency linear array transducer. At our institution, the patient is seated on a rotatable stool. The radiologist stands behind the patient to scan; however, at other institutions, the radiologist sits and faces the patient. The biceps tendon is the first structure to be examined; the arm is slightly externally rotated with the forearm in a supinated position resting on the thigh. This positioning ensures optimal visualization of the bicipital groove. The tendon is initially examined in a transverse plane from the level where it emerges beneath the acromion to the musculotendinous junction. The transducer is gently rocked to maintain the normal echogenicity of the biceps tendon. The transducer is then rotated 90° to examine the tendon in a longitudinal plane. It is important to orient the ultrasound beam perpendicular to the long axis of the tendon to visualize the normal echogenic, fibrillar pattern. This process may require gently pushing the inferior aspect of the transducer against the patient’s arm to ensure that the tendon fibers are oriented perpendicular to the ultrasound beam.

The subscapularis tendon is imaged next. The patient’s arm may need to be further externally rotated to optimally visualize the tendon. The transducer is initially placed in a transverse orientation at the level of the lesser tuberosity and moved medially along the long axis of the tendon. Internal and external rotation of the arm confirms that the tendon is intact. The transducer is then turned 90° to view the tendon fibers perpendicular to their long axis. This view is useful to diagnose superior partial- or full-thickness tears.

To visualize the supraspinatus and infraspinatus tendons, the patient is asked to extend his or her arm posteriorly and place the palmar side of the hand on the superior aspect of the iliac wing with the elbow flexed and directed toward the midline of the back. When scanning the cuff tendons in their long axis, it is important to remember that the long axis of the tendons is approximately 45° between the sagittal and coronal planes. It is also important to recognize that the cuff begins within a few millimeters posterior to the intra-articular portion of the biceps tendon. This portion of the biceps tendon should be identified when scanning in the long axis to ensure that the anterior aspect of the cuff is visualized. The cuff should be evaluated from the most lateral aspect of the greater tuberosity where it inserts to as far medially as possible to ensure that more medial mid substance tears are not missed. Because the cuff assumes a convex curvilinear course as it passes over the humeral head, the transducer should be gently rocked to visualize the various portions of the cuff in a plane perpendicular to the ultrasound beam as it is moved anterior to posterior. It is also important to compress the transducer against the deltoid muscle to detect any nonretracted tears. The transducer is then turned 90° to visualize the cuff in a transverse (short-axis) orientation. This view is useful to measure the width and determine the location of a cuff tear. Next, the posterior glenohumeral joint and the posterior aspect of the infraspinatus and teres minor tendons are evaluated from a posterior approach with the patient resting his or her forearm on the thigh. To identify the glenohumeral joint and the more posterior aspect of the infraspinatus tendon, the transducer is placed immediately below the scapular spine and angled slightly inferiorly. Internal and external rotation of the arm helps better visualize the infraspinatus attachment and the posterior cartilaginous labrum.

Finally, each of the posterior cuff muscles should be evaluated in long and short axes for fatty degeneration. The transducer is first placed superior to the scapular spine to image the supraspinatus muscle and then moved inferior to the scapular spine to visualize the infraspinatus muscle. The transducer is then moved slightly more inferiorly to visualize the teres minor muscle and its short tendon, most of which attaches to the surgical neck of the humerus. To visualize the entire tendon and its muscle, the transducer should be placed at the level of the surgical neck in a sagittal orientation and moved lateral to medial along the muscle.

Figure 1: Full-thickness cuff tear in a 74-year-old woman. A, The longitudinal image shows that the cuff is retracted medially, and the torn tendon end (T) is surrounded by fluid. B, The transverse image shows the width of the tear (between cursors).

The acromioclavicular joint can be imaged in both coronal and sagittal planes but is best evaluated when the transducer is oriented along the long axis of the clavicle. This view optimizes visualization of the joint space, synovium, capsule, and bony margins of the joint.

Figure 2: Full-thickness cuff tear in a 69-year-old woman. A, The longitudinal image shows the cuff tear (between cursors). The torn tendon end is not surrounded by fluid. B, The transverse image shows the width of the tear (between cursors).

 

Sonographic Findings of Shoulder Disorders

Most cuff tears begin approximately 15 mm posterior to the intra-articular portion of the biceps tendon. There may be associated bony changes on the greater tuberosity. On sonography, a full-thickness cuff tear is characterized by a focal defect created by a variable degree of retraction between the torn tendon ends. When there is fluid between the torn tendon ends, it is easy to visualize a tear (Figure 1). In the absence of an effusion, the deltoid muscle and peribursal fat occupy the space created by the defect and oppose the overlying humeral head cartilage (Figure 2). If the subdeltoid synovial tissue is thickened and inflamed, the tissue will abut the cartilage, and on sonography, a subtle loss of the normal convexity of the cuff or flattening of the cuff will be visualized. Nonretracted tears are difficult to identify. It is important to compress the deltoid with the transducer in an attempt to show the defect. Less often, a tear will occur more medially within the mid substance of the cuff; thus, it is important to evaluate the cuff where it exits beneath the acromion to the lateral aspect of the greater tuberosity. In a patient with a massive tear, the cuff is often not visualized and is retracted beneath the acromion on longitudinal views (Figure 3). Because of the size of the tear, it is usually not possible to measure an accurate width. These cuff tears are often chronic and most commonly seen in elderly patients. Subscapularis tears are uncommon and usually occur in patients with massive cuff tears or recurrent anterior shoulder dislocation. It is important to diagnose a subscapularis tear because it may alter the surgical approach.

Figure 3: Massive full-thickness cuff tear in a 53-year-old man. A, The longitudinal image shows nonvisualization of the cuff. Only the deltoid muscle overlying the humeral head is visualized. B, The transverse image also shows absence of the cuff.

Partial-thickness tears can be more difficult to identify than full-thickness tears. These tears usually occur along the deep side of the cuff at the level of anatomic humeral neck and can be recognized as distinct hypoechoic or mixed hyperechoic and hypoechoic defects on both longitudinal and transverse views (Figure 4). It is important not to mistake anisotropy for a partial-thickness tear; anisotropy produces a much less well-defined, uniformly hypoechoic region in the deep portion of the cuff. By angling the transducer such that those fibers become perpendicular to the ultrasound beam, normal tendon fibers will be noted inserting onto the greater tuberosity. A partial-thickness tear that involves more than 50% of the substance of the cuff may be compressible with the transducer and simulate a full-thickness tear. Misdiagnosing an extensive partial-thickness tear for a full-thickness tear is usually not clinically relevant because it is often treated as if it were a full-thickness tear. Partial-thickness tears may occur on the bursal side of the cuff but are much less common; small bursal-side tears are often difficult to distinguish from small full-thickness tears because both produce a focal defect or concavity on the bursal side of the cuff. Linear tears may also occur within the substance of the cuff but are more difficult to visualize than on MRI.

Figure 4: Partial-thickness articular-side cuff tear in a 55-year-old woman. A, The longitudinal image shows a distinct hypoechoic defect in the cuff (between cursors). B, The transverse image shows the width of the tear (between cursors).

Fatty degeneration of the cuff muscles can be diagnosed as described by Strobel et al.These authors evaluated the visibility of the muscle contours, pennate pattern, and central tendon and assessed the echogenicity of the cuff muscles in comparison to the deltoid muscle to grade the degree of fatty degeneration. When fatty degeneration is severe, one or more muscles will become homogeneously hyperechoic (Figure 5). A recent study showed that fatty degeneration of the cuff muscles is closely associated with the tear size and location. The greater the size of the tear, the greater the risk of fatty degeneration, and the closer the tear begins to the intra-articular portion of the biceps tendon, the greater the risk of fatty degeneration. The mechanism for the latter may be due to disruption of the rotator cable insertion (the anterior part of the supraspinatus tendon is the site of the anterior cable insertion), resulting in greater retraction of the tendon and subsequent fatty degeneration over time.

Although little has been published on the sonographic appearance of tendinopathy, on the basis of our observations, it may be a focal or diffuse process; the cuff is typically thickened, heterogeneous, and hypoechoic (Figure 6). Calcific tendinitis may be diagnosed when echogenic foci of varying size that may or may not shadow are visualized within the substance of the tendon. The calcifications are often located at the most lateral aspect of the greater tuberosity.

 

Figure 5: Marked fatty degeneration of the supraspinatus tendon in a 70-year-old man with a full-thickness cuff tear. The longitudinal image shows a homogeneously echogenic supraspinatus muscle.

Disorders of the biceps tendon are commonly associated with rotator cuff disease and are important sources of shoulder pain. When the biceps tendon is thickened and hypoechoic, tendinopathy should be considered. Tendinopathy usually occurs in patients with large chronic cuff tears. Intrasubstance tears may also occur and appear as linear hypoechoic defects. Tenosynovitis is often associated with an effusion. A thickened tendon sheath with or without flow on color or power Doppler imaging is diagnostic of tenosynovitis (Figure 7). Tendon subluxation is considered present when the tendon partially extends above a line drawn from the lesser to the greater tuberosity and dislocated when perched or medial to the lesser tuberosity. Tendon rupture can be diagnosed when the bicipital groove is empty; however, a 70% or greater high-grade partial-thickness tear cannot be distinguished from rupture because the few remaining fibers are usually not visible on sonography.

 

Figure 6: Marked tendinopathy in a 75-year-old man. The longitudinal image shows a hypoechoic and very thickened cuff.

The subdeltoid bursa is a potential space and normally does not contain fluid. The presence of fluid is abnormal, and if there is concern for infection, sonography can be used to provide guidance for aspiration. Bursitis can be an overlooked cause of shoulder pain. It can be diagnosed if the subdeltoid bursa is thicker than the humeral head cartilage (Figure 8). Shoulder abduction with real-time observation helps distinguish the cuff from thickened bursa.

 

Figure 7: Tenosynovitis of the biceps tendon sheath in an 81-year-old woman. The transverse image shows thickening of the biceps tendon sheath. There is increased flow of the thickened synovium on color Doppler imaging.

A paralabral cyst is caused by a posterior capsulolabral avulsion or tear with subsequent leakage of fluid. It is best seen from a posterior approach; the transducer should be placed at the level of the infraspinatus muscle. These anechoic cysts typically occur in the spinoglenoid notch and may extend into the supraspinous or infraspinous fossa. It is important to evaluate the supraspinatus and infraspinatus muscles for fatty degeneration, which may occur if the suprascapular nerve (a mixed motor/sensory nerve) is compressed by the cyst.

The acromioclavicular joint may become infected or inflamed, causing the joint to distend with fluid and the capsule to bulge. The fluid is easily aspirated under sonographic guidance. A synovial cyst, which may be anechoic or contain debris on sonography, if found to communicate with the acromioclavicular joint, should prompt investigation of the rotator cuff because it is associated with a longstanding full-thickness cuff tear. Osteolysis appears as joint space widening and irregularity and erosions of the bony margins.

Figure 8: Bursitis in a 34-year-old woman. The transverse image shows marked thickening of the subdeltoid bursa (between cursors).

Conclusions

In summary, sonography is an excellent modality for diagnosing rotator cuff disease. It is preferred by patients, accurate, noninvasive, rapidly performed, and less expensive than MRI. Furthermore, it is a dynamic, global examination and can provide bilateral information. There is also the opportunity to interact with the patient and explain the results of the examination. However, it is important to recognize that the learning curve is long and steep, and results are operator dependent. It is also more difficult to visualize the entire cuff in obese patients and in patients with decreased range of motion, and evaluation of the labrum, joint capsule, ligaments, bone, and cartilage is limited. Thus, whereas sonography and MRI have comparable accuracy for diagnosing rotator cuff disease, these tests should be viewed as complementary rather than competitive. Which test to perform should be based on the clinical information sought and the inherent strengths and weaknesses of each test.