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Scoliosis is a common deformity in many types of neuromuscular diseases most severe in nonambulatory patients
the prevalence of spinal deformity in the patient with a neuromuscular disorder is much higher than in the general population
It ranges from 20% in children with cerebral palsy to 60% in patients with myelodysplasia.
The prevalence rises to 90% in males with Duchenne muscular dystrophy. In general, the greater the neuromuscular involvement, the greater the likelihood and severity of scoliosis.
Neuropathic: 1. upper motor neuron lesions includes diseases such as cerebral palsy, syringomyelia, and spinal cord trauma
2. lower motor neuron lesions includes poliomyelitis and spinal muscular atrophy
Myopathic - include muscular dystrophy, and other forms of myopathy.
The pathophysiology is not well understood.
The evaluation of a patient with neuromuscular scoliosis entails a thorough assessment of all body systems. Accurate diagnosis of the underlying disease entity is essential and may require muscle biopsy.
Assessing nutritional status and pulmonary function is extremely important The orthopedic examination includes assessment of all extremities and joints for contractures. Spinal deformity, decompensation, and shoulder balance are documented. Ambulatory status is also evaluated, and patients are classified as walkers, sitters, or nonsitters.
Laboratory Studies Total lymphocyte count
The total lymphocyte count should be greater
than 1500 cells/mm3.
Hemoglobin Total protein Albumin: Patients with serum albumin levels greater than 3.5 mg/dL have a much lower incidence of postoperative wound infection
Electrolytes Serum blood urea nitrogen Creatinine Transferrin
Supine anteroposterior and lateral spinal radiographs: These are ordered for very young patients and older patients who cannot sit. Upright anteroposterior and lateral spinal radiographs
Standing upright radiographs should be used for
patients who can stand, and sitting radiographs should be used for patients who cannot stand.
Traction spinal radiographs: These radiographs are obtained to evaluate the flexibility of the curves.
Medical Therapy - The goal of nonoperative and operative treatment of patients with neuromuscular scoliosis is the same: to maintain the spine in a balanced position in the coronal and sagittal planes over a level pelvis. -This goal is achieved with a custom molded thoracolumbosacral orthosis (TLSO) and molded seating supports. - The aim is to control the curve during spinal growth rather than to correct the spinal deformity.
The surgical principles in the management of neuromuscular scoliosis differ from those in idiopathic scoliosis. Fusion is necessary at a younger age, and the fused portion of the spine is longer. Fusion to the sacrum is fairly common because many of these children do not have sitting balance or have pelvic obliquity.
Combined anterior and posterior fusion is common in the treatment of patients with neuromuscular scoliosis: - posterior elements are absent, as in myelodysplasia - necessary to gain correction in a rigid lumbar or thoracolumbar curve and achieve a spine fused in balance over a level pelvis
The instrumentation used is segmental, with either a multiple hook-rod system, with or without the addition of sublaminar wires, or a Luque rod and sublaminar wires or a unit rod device. When fusion to the sacrum is necessary, it can be performed with the Luque-Galveston technique or with iliac screws
Hospital stays are usually 7-10 days. Modifications in the child's wheelchair should be made as soon as possible to accommodate the new sitting position. The number of hours spent upright each day should be gradually increased. The wound should be assessed 3 weeks postoperatively. Radiographs should be obtained 6 weeks postoperatively and again 3 and 6 months after surgery.
respiratory problems ileus nutritional problems hip problems crankshaft phenomenon.
With care in surgical technique and adequate postoperative care, complications can be minimized. The patient can return to the preoperative functional level with a successful surgical result, which consists of a solidly fused spine in balance in the coronal and sagittal planes over a level pelvis.
is the most common type of spinal deformity confronting orthopedic surgeons. Its onset can be rather insidious, its progression relentless, and its end results deadly. Proper recognition and treatment of idiopathic scoliosis help to optimize patient outcomes.
The precise etiology of idiopathic scoliosis remains unknown, but several intriguing research avenues exist. A primary muscle disorder has been postulated as a possible etiology of idiopathic scoliosis. -The contractile proteins of platelets resemble those of skeletal muscle, and calmodulin is an important mediator of calcium-induced contractility
An elastic fiber system defect (abnormal fibrillin metabolism) has been offered as one potential etiologic explanation for idiopathic scoliosis. Disorganized skeletal growth, probably with its root cause at a gene locus or group of loci, has been discussed as a possible etiologic explanation for idiopathic scoliosis.
Much has been written regarding the potential influence of melatonin on the development of idiopathic scoliosis. Some authors have suggested that a posterior column lesion within the central nervous system might be present in patients who have idiopathic scoliosis
The vast majority of patients initially present due to perceived deformity. -Adams forward-bending test (in conjunction with the use of a scoliometer) has been found to be an effective screening tool. Patient's history include information relative to other family members with spinal deformity, assessment of physiologic maturity (eg, menarche), and presence or absence of pain.
Physical examination should include a baseline assessment of posture and body contour. Shoulder unleveling and protruding scapulae are common. In the most common curve pattern (right thoracic), the right shoulder is consistently rotated forward and the medial border of the right scapula protrudes posteriorly. Assessment of lower (and often upper) extremity reflexes should be performed.
Abdominal reflex patterns should also be assessed. The presence or absence of hamstring tightness should be investigated screening should be performed for ataxia and/or poor balance or proprioception (ie, Romberg test). One or two different methods of measuring leg length will prove valuable, as a significant percentage of patients presenting with scoliosis have several centimeters of limb-length discrepancy.
The main treatment options for idiopathic scoliosis may be summarized as "the 3 O's": (1) observation (2) orthosis (3) operative intervention
Infantile Idiopathic Scoliosis: -defined by a seemingly arbitrary age limit (<3 y at the time of diagnosis) -only type of idiopathic scoliosis whose most common curve pattern is left thoracic. - only type of scoliosis that is more common in boys. - more common in European patients or those of immediate European descent.
- spontaneous resolution (20-92%) - Nonoperative treatment of progressive infantile idiopathic scoliosis predominates and may involve the use of conventional thoracolumbosacral orthosis (TLSO)–type braces, Milwaukee-type braces, and even intermittent Risser casting If surgical treatment becomes necessary, anterior release and fusion followed by posterior spinal fusion with instrumentation is considered to be the functional treatment.
rib vertebral angle difference (RVAD) originally described by Mehta in 1972. - measurement carried out at the apical vertebra of the curve
Curves less than 25° with an RVAD less than 20° are preferentially observed and monitored with spinal radiographs at regular intervals. Curves exceeding these parameters are typically braced, with some consideration given to the value of intermittent Risser casting. Surgery is considered for curves not adequately controlled with nonoperative measures.
most closely mimics the epidemiology and demographics of the adolescent version of the disease. It is more common in females, and its most common curve pattern is a right thoracic curve. might be considered to be a malignant subtype of adolescent idiopathic scoliosis
Observation for curves less than 25° with follow-up radiographs at regular intervals Bracing for curves that range from 25-40° and at least consideration of bracing (based on curve flexibility) for curves from 40-50°
Bracing for smaller curves that demonstrate rapid progression to the 20-25° range Surgical intervention for inflexible curves that exceed 40° or virtually any curve that exceeds 50°.
most common type of idiopathic scoliosis and the most common type of scoliosis overall. Treatment recommendations for adolescent idiopathic scoliosis are driven almost totally by curve magnitude (the only caveat being that brace treatment is thought to be effective only in patients who are still growing).
observation for curves less than 30°, bracing of curves that reach the 30-40° range, and consideration of surgery for curves that exceed 40°.
most commonly referred to as frozen shoulder (FS), is an idiopathic disease with 2 principal characteristics: pain and contracture.
In 1934, Codman stated, "This entity [FS] is difficult to define, difficult to treat, and difficult to explain from the point of view of pathology." Codman's statement continues to hold true today.
In 1992, the American Shoulder and Elbow Surgeons Society agreed on the following definition of FS by consensus: a condition of uncertain etiology that is characterized by clinically significant restriction of active and passive shoulder motion that occurs in the absence of a known intrinsic shoulder disorder.
Pain Shoulder pain associated with FS is progressive and initially felt mostly at night or when the shoulder is moved close to the end of its range of motion (ROM). It can be caused by certain combined movements of the shoulder, such as abduction and external rotation (eg, grooming one's hair, reaching for a seatbelt overhead) or extension and internal rotation (eg, reaching for a back pocket or bra strap).
In approximately 90% of patients with FS, this pain usually lasts 1-2 years before subsiding.
Contracture The second principal characteristic of FS is progressive loss of passive ROM (PROM) and active ROM (AROM) of the glenohumeral joint in a capsular pattern
Evaluation of anatomic, histologic, and surgical specimens from subjects affected by idiopathic FS demonstrates that the glenohumeral joint synovial capsule is often involved in this disease process.
active process of hyperplastic fibroplasia and excessive type III collagen secretion that lead to soft-tissue contractures of the aforementioned structures (ie, the coracohumeral ligament, soft tissues of rotator interval, the subscapularis muscle, the subacromial bursae)
Shoulder pain is the third most common cause of musculoskeletal disability after low back pain (LBP) and neck pain. The prevalence of FS in the general population is reported to be 2%, with an 11% prevalence in unselected individuals with diabetes. For patients with type I diabetes, the risk of developing FS in their lifetime is approximately 40%.
FS may affect both shoulders, either simultaneously or sequentially, in as many as 16% of patients. The frequency of bilateral FS is higher in subjects with diabetes than in those without diabetes.
In 14% of patients, while FS still is active in the initial shoulder, the contralateral shoulder also becomes affected.
Contralateral FS usually occurs within 5 years of disease onset. A relapse of FS in the same shoulder is unusual.
FS most frequently occurs in subjects with hyperthyroidism and hypertriglyceridemia.
Although various authors report that heart disease, tuberculosis, and many other medical conditions are associated with FS
FS will undoubtedly become increasingly common as the baby-boom generation ages, because this condition most frequently occurs in the fifth and sixth decades of life.
Patients who present with an idiopathic FS when they are younger than 40 years should definitely be examined to rule out occult diabetes, hyperthyroidism, hypertriglyceridemia, or concomitant neurologic or systemic rheumatologic disorder affecting the upper extremity.
FS affects women more frequently than men, with a female-to-male ratio of about 1.4:1. Menopause is often reported as a cause of FS in women.
mean ages of onset are 52 years for women and 55 years for men
1. Phase 1 - The painful phase; the patient describes an insidious onset of predominantly nocturnal pain, usually without a precipitating factor. - The pain is not related to activity, although the farthest ROM can increase the pain. As the disease progresses, patients have pain at rest. - In this phase, which lasts 2-9 months, ROM is not restricted, and the diagnosis may remain unclear.
2. Phase 2 - The frozen, or adhesive, phase; the pain from phase 1 can persist, although it may decrease. - Progressive limitation in ROM occurs in a capsular pattern (that is, in all directions). Normal daily activities can be severely affected. -Hallmarks of this phase are an inability to move at great amplitude and an inability to move on the affected side. -Diagnosis is easier in this phase than in phase 1. Although phase 2 is reported to last 3-9 months, it can persist longer than this.
3. Phase 3 - The thawing, or regressive, phase; pain progressively decreases, and limitations in ROM progressively increase over 12-24 months. - approximately 40% of patients have slight, persistent limitations in ROM, only 10% have clinically significant long-term functional limitations.
Careful neurologic examination should be conducted in all patients presenting with signs and symptoms associated with FS.
Patients who have a history of smoking should undergo chest radiography with apical views to rule out a Pancoast tumor irritating the brachial plexus, which can cause FS.
All patients should receive a thorough neurologic examination of the upper extremities and neck to rule out cervical radiculopathy and brachial plexopathy.
Care also should be taken to look for signs of Parkinson disease, because the prevalence of shoulder pain in patients with this treatable condition is 4-5 times that of the healthy population. Furthermore, shoulder pain often is an early manifestation of Parkinson disease, and it sometimes precedes the tremor by many years.10
Proper and complete musculoskeletal and integumentary examination should be performed to rule out concomitant systemic rheumatologic, inflammatory, metastatic, or infectious disorders.
Clinicians should also take the time to properly examine the thyroid gland to rule out concomitant hyperthyroidism.
Physicians should remain alert to signs of unsuspected diabetes, which may be present in approximately 25% of subjects presenting with FS.
Laboratory Studies - The scientific literature shows an elevated incidence of diabetes, hyperthyroidism, and hypertriglyceridemia in patients with FS.
a. Lequesne and colleagues found that 28% of 60 new patients who presented with idiopathic FS had unsuspected diabetes.11
b. This association should prompt possible testing of thyroid-stimulating hormone (TSH), serum triglyceride, and fasting blood sugar levels in most patients, particularly those presenting with bilateral disease and patients presenting with FS who are younger than 45 years.
In general, idiopathic FS is considered a clinical
diagnosis that does not require confirmation with radiologic imaging. Current radiologic studies do not seem to confer any useful information, prognostic or otherwise, that changes the way the patient is treated.
For the moment, the principal utility of these tests is in ruling out concomitant conditions that may influence the treatment of an individual patient
All patients presenting with FS should undergo
plain radiography of the shoulder, with the acquisition of soft-tissue views of the rotator cuff to rule out a septic or metastatic process. A plain radiograph may also show evidence of a large calcification of the rotator cuff in the painful resorptive phase, an avascular necrosis of the humeral head (that is, Milwaukee shoulder), or a Charcot joint.
Gallium nuclear scanning - Patients who are immunocompromised, as well as those who abuse intravenous (IV) drugs, should undergo gallium nuclear scanning to rule out a septic joint.
Arthrography of the glenohumeral joint
arthrography is used mostly to treat FS, rather
than to diagnose the condition. The injection of contrast medium into the glenohumeral joint helps to determine its volume and configuration. The normal volume of the joint is 13 mL. In FS, the volume can be reduced to 5-8 mL.
99m Tc methylene diphosphonate (MDP) bone
-In general, the problem with bone scans in the
practice of musculoskeletal medicine is that they are highly sensitive but not specific
Other studies - Computed tomography (CT) scanning, CT arthrography, ultrasonography, and magnetic resonance imaging (MRI) are sensitive imaging modalities that depict specific signs for FS. However, use of these modalities is rarely indicated.
Rehabilitation Program -Physical Therapy ---Although studies have shown the efficacy of physical therapy, no current evidence has suggested that physical therapy alone improves function in the treatment of FS. ---physical therapy associated with an intra-articular injection of corticosteroid improves function and ROM more rapidly than does intra-articular corticosteroid injection alone
Therapeutic exercises - Therapeutic exercises that have been studied include articular stretching and pulley therapy. - Passive articular stretching exercises improve ROM.
Manual therapy ---Data from 2 studies support the use of manual therapy to improve ROM in the short term.
Physical modalities Many electroanalgesic and thermoanalgesic modalities are often used in physical therapy.
Occupational Therapy Patients with severe FS may benefit from a referral to an occupational therapist for assistance and instruction in performing activities of daily living (ADLs). The occupational therapist helps the patient learn how to use adaptive equipment and suggest home and workplace modifications that may be necessary and beneficial for completing professional activities and routine daily tasks (eg, dressing, bathing, grooming)
Duplay, the first person to describe the syndrome of FS, in 1872, proposed treating this condition with manipulation of the glenohumeral joint, with the patient under general anesthesia.
▪ --some orthopedic surgeons continue to practice this technique, the benefits of this approach have not been demonstrated in controlled clinical trials.
A 2009 study by Jacobs et al also found no evidence that manipulation provides a better treatment outcome in FS.
Various improvements in surgical techniques, such as the advent of controlled capsular release by using arthroscopic access to the anterior glenohumeral joint capsule and the coracohumeral ligament, appear to offer promising treatments. However, the effectiveness of these surgical techniques has yet to be demonstrated in controlled clinical trials
Considering the favorable prognosis for patients with idiopathic FS, surgical intervention should probably be reserved for rare patients whose condition does not respond to maximal conservative modalities implemented over a sufficient period of time.
The pathophysiology of rotator cuff degeneration is a controversial topic that still is not fully understood. 2 hypotheses: extrinsic and intrinsic
The extrinsic hypothesis -In this theory, the lesion results mainly from repeated impingement of the rotator cuff tendon against different structures of the glenohumeral joint.
1. The anterosuperior impingement syndrome 2. The posterosuperior impingement syndrome 3. The anterointernal impingement syndrome
Impingement of the rotator cuff beneath the coracoacromial arch is an established cause of chronic shoulder pain. impingement occurs against the under surface of the anterior third of the acromion, the coracoacromial ligament, and at times, the acromioclavicular joint.
Located anterior to the coracoacromial arch in the neutral position, the supraspinatus tendon insertion to the greater tuberosity and the bicipital groove must past beneath the arch with forward flexion of the shoulder, especially if internally rotated, causing an impingement.
Neer believed that 95% of tears of the rotator cuff were initiated by impingement wear, rather than circulatory impairment or trauma. He observed proliferative traction spurs at the undersurface of the anterior acromion that he explained by the repeated impingement of the cuff.
He stated that the variation in shape and slope of the acromion could make people more susceptible to impingement and tear, making it appear logical to perform an anterior acromioplasty at the time of every cuff repair.
Biglianni described 3 different shapes of acromia in cadavers, according to the anterior slope: Type 1 - Flat Type 2 - Curved Type 3 - Hooked
Only 3% of tears are associated with a type 1 acromion. Curved and hooked acromia appear to be due to a degenerative process with formation of the osteophyte-enthesophyte complex at the acromion-coracoacromial ligament junction that is increasingly prevalent with age.
Neer described impingement lesions in the following 3 progressive stages: - In stage 1, edema and hemorrhage result from excessive overhead use and are observed in patients younger than 25 years.
-In stage 2, fibrosis and tendinitis affect the bursa and the cuff following repeated episodes of mechanical inflammation in patients aged 25-40 years. -In stage 3, bone spurs and incomplete and complete tears of the rotator cuff and long head of the biceps tendon are found almost exclusively in patients older than 40 years.
In 1991, Walch et al described, an impingement occurring between the articular side of the supraspinatus tendon and the posterosuperior edge of the glenoid cavity.
With the shoulder held at 120° of abduction, retropulsion, and in extreme external rotation, the labrum moves away from the glenoid and the glenoid rim comes in contact with the deep surface of the tendon, producing repeated microtrauma and leading to partial tears.
This process has been confirmed by MRI studies and may explain some of the articular side tears, especially in overhead sport athletes; however, it does not account for all the tears observed in older patients.
In 1985, Gerber described, from CT scan studies and from surgery observations, impingement of the cuff in the coracohumeral interval
the shoulder is held in flexion and internal rotation the coracohumeral distance is reduced from 8.6 mm when the arm is at the side to 6.7 mm
In this position, the lesser tuberosity, and also the biceps tendon and the supraspinatus tendon, become closer to the coracoid process, creating subcoracoid impingement and cuff lesions.
Subcoracoid impingement can be:
idiopathic (eg, large coracoid tip) iatrogenic (eg, following a Trillat procedure)
following a fracture (eg, humeral head or neck
In this theory, the lesions result from progressive age-related degeneration of the tendon. Von Meyer was probably the first to introduce the concept that degeneration of the tendon plays a major role in the production of cuff lesions.
Observations from various sources (eg, cadaver, surgical, MRI, ultrasonographic, arthrographic studies) show that cuff tears rarely are seen in patients before age 40 years and that the number observed after the patient has reached 50 years increases progressively.
In 1934, Codman introduced the concept that most tears originate on the articular side of the tendon. Most of the tears have been observed on the articular surface of the tendon, near its insertion on the greater tuberosity, in an area Codman called the critical zone.
In all probability, the intrinsic and the extrinsic theories coexist and explain the pathophysiology of rotator cuff degeneration.
Shoulder pain is the third most common cause of musculoskeletal disorder after low back pain (LBP) and cervical pain.
The annual incidence is estimated at 10 cases per 1000 population, peaking at 25 cases per 1000 population in the age category of 42-46 years. In the population aged 70 years or more, 21% of persons were found to have shoulder symptoms, most of which were attributed to the rotator cuff.
No known race variation associated with rotator cuff disease. predominance of male patients (66%) seeking consultation for rotator disease, but, in other studies, the male-to-female ratio is 1:1. Rotator cuff disease is more common after age 40 years. average age of onset is estimated at 55 years.
The shoulder joint is a complex structure comprising not 1, but 5 joints : 3 synovial joints -sternoclavicular - acromioclavicular - glenohumeral joints 2 physiologic joints -scapulothoracic joint -subdeltoid joint]
5 joints fall into the following 2 groups: First group
Glenohumeral joint, a true joint
Subdeltoid joint, a physiologic joint
Sternoclavicular joint, a true joint
Acromioclavicular joint, a true joint Scapulothoracic joint, a physiologic joint
The rotator cuff is made up of 4 interrelated muscles arising from the scapula and attaching to the tuberosities.
Their tendons form a continuous cuff around the head that allows the cuff muscles to provide an infinite variety of moments to rotate and adjust the humeral head in the glenoid fossa.
providing the optimal muscle balance for precise
The supraspinatus muscle arises from the medial two thirds of the supraspinous fossa of the scapula.
This muscle passes under the acromion and
acromioclavicular joint and inserts onto the superior aspect of the greater tuberosity and joint capsule. innervated by the suprascapular nerve (C4-C5-C6) Its primary role is to stabilize the head of the humerus in the glenoid fossa and to abduct the shoulder.
The infraspinatus muscle arises from the medial two thirds of the infraspinous fossa of the scapula and inserts on the middle facet of the greater tuberosity and joint capsule
This muscle is innervated by the suprascapular
nerve (C4-C5-C6). Its primary role is to stabilize and externally rotate the head of the humerus
The teres minor muscle arises from the upper two thirds of the dorsal aspect of the lateral border of the scapula and inserts onto the lower facet of the greater tuberosity and joint capsule. Its primary role is to stabilize and externally rotate the head of the humerus.
The subscapularis muscle arises from the subscapular fossa of the scapula and inserts to the lesser tuberosity and joint capsule.
This muscle is innervated by the upper and lower
subscapular nerve (C5-C6-C7). Its primary role is to stabilize and externally rotate the head of the humerus.
The long head of the biceps tendon arises from the supraglenoid tubercle of the scapula, runs between the supraspinatus and subscapularis muscles, exits the shoulder through the bicipital groove under the transverse humeral ligament, and inserts onto the tuberosity of the radius.
The long head of the biceps is innervated by the
musculocutaneous nerve (C5-C6). Its primary role is to stabilize and flex the humeral head and flex the elbow.
Most glenohumeral motion, especially in overhead activities, occurs around the plane of the scapula, which is approximately 30-45° anterior to the frontal plane. Any time the arm is raised in flexion or abduction, movements from the scapula and the clavicle accompany the glenohumeral joint In the first 30° of abduction or 45-60° of flexion, the scapula moves either toward or away from the spine to seek a position of stability on the thorax.
Consequently, the scapulothoracic joint does not participate in the early elevation of the arm, and the movement of the first 30° comes from the glenohumeral joint. After stabilization has been achieved, the scapula moves laterally, anteriorly, and superiorly, causing an upward rotation of the scapula and glenoid fossa.
1. Maintains the glenoid fossa in an optimal position to receive the head of the humerus, thus increasing the range of motion (ROM) 2. Permits the muscles acting on the humeral head to maintain a satisfactory lengthtension relationship
Beyond the first 30° of abduction (or 45-60° of flexion), scapulothoracic motion occurs and contributes to the scapulohumeral rhythm. As the abduction progress, according to widely accepted belief, there is a 2:1 ratio of motion between the glenohumeral and scapulothoracic motion. Toward the end of the elevation, the scapula contributes more motion and the humerus less.
In total, the glenohumeral joint contributes 90-120° to shoulder abduction and the scapulothoracic joint supplies 60°. The contributing joint actions to the scapular motions are 20° produced by the acromioclavicular joint, 40° produced at the sternoclavicular joint, and 50° of clavicle elevation and 30° of posterior rotation.
For the glenohumeral joint to realize 120° of abduction, external rotation of the humerus must occur. When internally rotated, the humerus can abduct to approximately 90° before the greater tuberosity hits the coracoacromial arch; however, when externally rotated, the greater tuberosity and cuff tendons avoid the coracoacromial arch, and 120° of abduction can be obtained. Full abduction cannot be achieved without trunk extension and contralateral flexion.
A complete medical history should be obtained in order to direct the physical examination and make the right diagnosis.
The following questions should help the physician in assessing the patient: What is the patient's age?
Shoulder pain in young overhead athletes suggests
underlying shoulder instability. In older patients, degenerative rotator cuff disease or frozen shoulder is suggested by shoulder pain.
What is the patient's occupation or sport? Repetitive overhead activities and sports predispose to rotator cuff tendinitis.
What was the mechanism of injury?
A fall on an outstretched arm could indicate a dislocation
What was the onset?
of the glenohumeral joint or a fracture of the humeral neck. Repetitive overhead motions can cause tendinitis and, in the long run, chronic degenerative changes. A fall or a trauma on the tip of the shoulder can result in an acromioclavicular sprain.
Insidious slow onset may suggest tendinitis or
osteoarthritis. Sudden onset usually is due to a trauma causing a fracture, dislocation, or a rotator cuff tear.
Where is the pain located?
Pain located on the superior or lateral aspect of the
What is the severity of the pain?
degenerative rotator cuff disease.
shoulder suggests rotator cuff tendinitis. Pain on the anterior aspect of the shoulder may result from bicipital tendinitis, an acromioclavicular sprain, or anterior instability. Neck pain and radicular pain or paresthesias suggest a cervical spine disorder.
An acute burning pain could indicate an acute bursitis. An intermittent dull pain may be due to a
What is the type of pain?
Sharp burning pain suggests a neurologic origin. Bone and tendon pain is deep, boring, and localized. Muscle pain is dull and aching, not localized, and may be
referred to other areas. Vascular pain is aching, cramplike, poorly localized, and may be referred to other areas.
What is the duration of the symptoms?
Frozen shoulder goes through 3 stages that can last up to
3-4 years. Acute bursitis has a short-term evolution and responds well to nonsteroidal anti-inflammatory drugs (NSAIDs).
What is the timing of the pain?
Predominantly night pain suggests frozen shoulder. Morning pain and stiffness improved by activity may be
Which activities/positions increase the pain?
caused by a synovitis. Pain that increases with activity is usually the result of a rotator cuff tendinitis.
Pain increased by overhead activities or arm-length
activities suggests rotator cuff tendinitis. Pain increased when throwing is likely to be due to anterior instability. Pain increased by lying on the affected shoulder may be caused by an acromioclavicular sprain.
Which activities/positions relieve the pain? Is there any weakness or paresthesias in the upper extremities? Neurologic symptoms are caused by a cervical radiculopathy or peripheral nerve entrapment/lesion. Are the symptoms constant or intermittent?
Intermittent symptoms usually result from soft
tissues or joint disorders. Constant symptoms suggest a neurologic lesion.
Are there any joint motion restrictions?
Passive and active joint restriction in all directions of
Is some crepitus noted?
ROM is caused by a frozen shoulder or glenohumeral synovitis. Restriction in internal rotation suggests an impingement syndrome due to rotator cuff tendinitis. Inability to perform active abduction suggests a rotator cuff tear or a frozen shoulder.
Crepitus is the result of degenerative rotator cuff
changes. Crepitus is not a normal finding in the shoulder.
Are there any changes in the color of the arm?
Color changes may be due to ischemia secondary
to vascular insufficiency. Reflex sympathetic dystrophy (also called complex regional pain syndrome, type 1) can cause skin color changes.
Has the patient had any treatments like oral medication, injections, or physical therapy to date?
Has the patient had any diagnostic tests performed to date? What is the evolution of the symptoms?
Has the pain changed?
Has the pain spread or moved? Has the pain subsided or increased?
Physical A systematic examination of the shoulder region includes a careful observation, the palpation of the bones and soft tissues, passive and active ROM, impingement and topographic tests complemented, as needed, by instability tests, labrum tests, and special tests. The examination is completed by a cervical spine examination, along with neurologic and vascular examination.
Range of motion Both active and passive ROM must be evaluated. Although some authors suggest that there is no need to assess passive ROM if the patient is able to perform a complete active ROM without pain, passive ROM must be assessed systematically.
The following movements (with the normal ranges provided) should be assessed: Abduction (70-180°) Adduction (30-45°) Flexion (160-180°) Extension (45-50°) External rotation (80-90°) Internal rotation (90-110°)
Active movements are evaluated first.
With the observer behind the patient who is standing,
active abduction is performed.
The scapulohumeral rhythm is observed.
If a painful arc (ie, pain or inability to abduct because
of pain) is observed between 45-120°, a subacromial impingement syndrome is suggested. If the pain is greater after 120°, when full elevation is reached, an acromioclavicular joint disorder is suggested.
If a reverse scapulohumeral rhythm (ie, an abduction initiated by the scapulothoracic joint rather than by the glenohumeral joint) is observed, a frozen shoulder is suggested. Look for a winging of the scapula caused by a trapezius or rhomboid muscle weakness. Active flexion also is evaluated.
In the presence of a subacromial impingement
syndrome, this movement also can be painful. Active flexion also can elicit a winging of the scapula caused by a serratus anterior weakness.
Passive range of motion
The evaluation can be performed with the patient standing, sitting, or lying down. For practical purposes, the examination is performed with the patient standing. Passive abduction is assessed with the observer behind the patient. Full abduction is performed first to evaluate the combination of scapulothoracic and glenohumeral motion.
Then, the scapulothoracic joint is locked by
putting one hand over the scapula and the clavicle to resist any motion of this joint. This maneuver allows for a more selective evaluation of the glenohumeral joint (90-120°).
Impingement tests Positive impingement tests result from the reproduction of the impingement of the rotator cuff tendon by different provocative maneuvers.
In the case of an anterosuperior impingement syndrome, the impingement takes place underneath the coracoacromial arch; Iin the case of the posterosuperior impingement syndrome, the impingement is on the posterosuperior border of the glenoid cavity, In the case of the anterointernal impingement syndrome, the impingement takes place in the subcoracoid space or in the coracohumeral interval.
The Neer impingement test
With the examiner standing behind the patient, the
shoulder is flexed passively.
When positive, this test produces pain
that is caused by the contact of the bursal side of the rotator cuff on the anterior third of the undersurface of the acromion and the coracoacromial ligament, as well as by contact of the articular side of the tendon with the anterosuperior glenoid rim.
A positive test suggests an anterosuperior
impingement syndrome. The sensitivity of this test, assessed by operatively observed anatomic lesions, is 89%
The Hawkins-Kennedy test
With the examiner standing behind the patient, the
shoulder is flexed passively to 90°, followed by repeated internal rotation. When positive, this test produces pain that is caused by the contact of the bursal side of the rotator cuff on the coracoacromial ligament and by the contact between the articular surface of the tendon and the anterosuperior glenoid rim. Contact between the subscapularis tendon and the coracoid process also is observed.
A positive test suggests an anterosuperior or an
anterointernal impingement test. A modified version of this test with the shoulder positioned initially at 90° of abduction and 30° of flexion, in the plane of the scapula. With repeated internal rotation motion, the shoulder is brought progressively to 90° of flexion.
If pain is present when the shoulder is flexed at
30°, it is caused by an anterosuperior impingement syndrome. If the pain is present only when the shoulder is brought to 90° of flexion, reducing the coracohumeral interval, an anterointernal impingement syndrome is suggested. The sensitivity of this test is 87%.
The Yocum test
With the examiner standing behind the patient,
the hand on the ipsilateral side of the examined shoulder is placed on the contralateral shoulder. The elevation of the elbow is resisted by the examiner. When positive, this test produces pain caused by the contact of the bursal side of the cuff tendon with the coracoacromial ligament and possibly the undersurface of the acromioclavicular joint.
A positive test suggests an anterosuperior or an
anterointernal impingement syndrome. The sensitivity of this test is only 78%
the sensitivity of the 3 tests together is 100%, which justifies that the 3 tests should be systematically performed together
The posterior impingement test
With the patient lying down, the shoulder is
positioned at 90-100° of abduction and maximally externally rotated.
When positive, this test produces pain in the
posterior aspect of the shoulder that is caused by the impingement of the articular side of the cuff tendon between the greater tuberosity and the posterosuperior glenoid rim and labrum. The relocation of the humeral head, performed by applying a posteriorly directed force to the humeral head, causes a reduction in pain.
The sensitivity of this test is 90%. Impingement tests confirm an impingement
syndrome; however, they do not determine the location of the rotator cuff lesion.
Topographic tests - Using resisted isometric contraction of specific muscles of the rotator cuff, it is possible to identify the location of the tendon lesion causing the impingement.
The Jobe test
The shoulder is placed at 90° of abduction and 30° of
flexion in the plane of the scapula. Shoulder elevation is resisted. The test is positive if pain is noted. When compared with surgical observations, the sensitivity of this test is 86%, and its specificity is 50%. The positive predictive value (the ratio of true positive tests on all the positive tests) of the Jobe test is 96%, and its negative predictive value (the ratio of all the negative tests on all the negative tests) is 22%.
The full can test
The shoulder is placed at 90° of flexion and 45° of
external humeral rotation (thumb pointing upward, like someone holding a full can, right-side-up). Shoulder elevation is resisted. The test is positive if it produces pain. An electromyographic (EMG) study showed that this test results in the greatest supraspinatus activation with the least activation from the infraspinatus.
The infraspinatus isolation test
The shoulder is positioned at 0° of elevation
(elbows against the waist flexed at 90°) and 45° of internal rotation. Shoulder external rotation is resisted. The test is positive if it produces pain. EMG shows that this is the optimal infraspinatus isolation test.
The Patte test
The shoulder is placed at 90° of abduction, neutral
rotation, and in the plane of the scapula. The examiner holds the elbow of the patient and the external rotation is resisted. The test is positive if it produces pain. The sensitivity of the test is 92%, but its specificity is only 30%. The positive predictive value is 29%, and its negative predictive value is 93%.
With the elbow held against the waist, the shoulder is positioned passively in external rotation. The test is positive when the patient is unable to maintain the shoulder in external rotation, suggesting a full tear of the external rotators.
No specific teres minor isolation tests exist. The same tests used to test the infraspinatus tendon serves for the teres minor.
The Gerber lift-off test
The shoulder is placed passively in internal
rotation and slight extension by placing the hand 5-10 cm from the back with the palm facing outward and the elbow flexed at 90°. The test is positive when the patient cannot hold this position, with the back of the hand hitting the patient's back. The sensitivity and specificity of this test are 100% when there is a full tear of the subscapularis.
The Gerber push with force test
The shoulder is placed in the same position as the
lift-off test; however, the patient has to keep his hand away from the back and resists a push in the palm of the hand. EMG shows that this is the optimal subscapularis isolation test with minimal activation of the pectoralis and latissimus dorsi muscles.
The Speed palm up test
The shoulder is placed at 90° of flexion with the
elbow in extension and the forearm in supination, bringing the palm of the hand up. The flexion of the shoulder is resisted. The test is positive if it produces pain. The sensitivity of this test is 63%, but its specificity is only 35%. The positive predictive value is 43%, and its negative predictive value is 55%.
Rotator cuff disease may result from a variety of causes. Damage to the rotator cuff commonly is caused by degeneration associated with aging. Other causes of injury to the rotator cuff may include tendinitis, bursitis, or arthritis.
These injuries are particularly common in individuals who perform repetitive overhead activities at work or through involvement in sports. Throwing athletes are prone to this problem secondary to the repetitive stress and trauma to the rotator cuff. Rotator cuff disease also may be the result of a traumatic injury (eg, a fall onto the shoulder, motor vehicle accident).
Laboratory Studies Laboratory studies are not necessary for diagnosing rotator cuff disease.
Imaging Studies A wide variety of radiological examinations are offered to image the rotator cuff. To prescribe the most useful examination, one must start with a good clinical history and physical examination. Imaging should be used to confirm the anomaly, describe its extension and the associated findings.
Plain film radiography
Indication ▪ Plain films are not very specific or sensitive to rotator cuff disease, but they remain the first examination to perform. ▪ Radiographs give a gross evaluation of the mineralization of the bone, the alignment, posttraumatic changes, the normal variant of the acromion shape, the presence of degenerative changes, and the presence of fine soft tissue calcifications that could be missed otherwise by other modalities.
▪ This is most useful test in trauma or chronic complete tear. ▪ In the last stage of complete chronic rotator cuff tear, it could be the only imaging modality needed to confirm the diagnosis.
Technique: Plain films are acquired routinely in 3 planes (ie, neutral, internal, external rotation)
Partial rotator cuff tear: All of the above can be present, but no specific signs can help in the diagnosis of a partial tear, as tendons are not visible on plain film. Complete rotator cuff tear:
In acute tears, the presence of synovial effusion or
hemorrhage can subluxate the humeral head caudally. Chronic tears, the humeral head migrates superiorly as the rotator cuff loses its ability to stabilize the humeral head in the glenoid cavity.
▪ Radiographically, an acromiohumeral space less than 6 mm, with or without erosion, on the inferior aspect of the acromion is a good semiologic landmark for chronic complete tear.
Rotator cuff tendinitis
Signs of chronic tendinitis without tear: ▪ subchondral sclerosis of humeral head ▪ flattening and geode of the greater tuberosity ▪ sclerosis of the acromion ▪ calcifications located in the presumed area of rotator cuff ▪ acromion, or a type 2 or 3 acromion. ▪
Normal X X
Soft tissue calcification(s) Greater tuberosity flattening or hypertrophy
Humeral head cysts X Acromial sclerosis X
Acromion type 2 and 3 Acromioclavicular osteoarthritis Upward migration of humeral head (
Indication ▪ The main indication of arthrography is to identify complete rotator cuff tears and intra-articular infiltration of corticoid. ▪ As a diagnostic tool, it is combined generally with arthro-CT.
Magnetic resonance imaging
Magnetic resonance imaging (MRI) is the stateof- the-art diagnostic tool for a full evaluation of the shoulder. MRI allows a fine evaluation of the bone marrow, tendons, muscles, ligaments, capsules, bursae, and labrum. MRI combines the advantage of visualization of the bony structures, as well as all the soft tissues about the shoulder and in any plane desirable.
Indication: The main purpose of ultrasonography is to
study the soft tissues. In experienced hands, ultrasonography has a sensitivity of 93-100% and a respective specificity of 85-97% for complete tear and a sensitivity of 69-93% for partial tear.
▪ The advantages of this technique reside in its low cost, high availability, and high resolution. Ultrasonography is a dynamic study for demonstrating impingement syndrome. ▪ The disadvantages are that it is time consuming for the radiologist and is operator-dependent. Ultrasonography cannot study bone structures, as sound does not penetrate bone very well.
Nuclear medicine imaging: Bone scintigraphy is not used routinely in the rotator cuff disease imaging.
Physical Therapy Physical therapy can be a useful adjunct in the conservative treatment of patients with degenerative rotator cuffs.
The conservative treatment of the degenerative rotator cuff Pain relief
Avoidance of painful motions and activities Simple analgesics Nonsteroidal anti-inflammatory drugs Physical modalities Manual physical therapy Subacromial corticosteroid injection A new promising procedure called the bupivacaine suprascapular nerve block
Restoration of motion
Stretching of the glenohumeral capsule and
muscles Manual physical therapy of the glenohumeral, scapulothoracic, acromioclavicular, and sternoclavicular joints and the parascapular and scapula-stabilizer muscles Normal scapulohumeral rhythm must be restored.
Manual therapy of the cervicodorsal
spine, because of its close relationship with the shoulder, often is necessary.
Restoration of strength and function: - Restoration of strength is achieved
by strengthening of the rotator cuff muscles, the scapula-stabilizer muscles and the long humeral depressor muscles (latissimus dorsi and pectoralis major).
Proprioception: In a young individual who has premature degenerative rotator cuff changes because of shoulder instability, proprioceptive exercises must complement strengthening exercises. Sport-specific rehabilitation
In a young individual or athlete, sport-specific
exercises must be included before resuming normal sport activities. With the aging of the active population, this aspect of the rehabilitation, combined with progressive return to sport activities should not be omitted.
Physical modalities for rotator cuff disease Physical modalities are used widely in the treatment of rotator cuff disease. Based on review studies, it appears that ultrasonographic therapy, transcutaneous electrical nerve stimulation (TENS), magnetotherapy, and different methods of thermotherapy are not effective in the treatment of shoulder disorder
Pulsed electromagnetic field therapy and low power laser could have short-term efficacy as compared with placebo.
- This theory may explain why the use of
ultrasonography is only significantly effective in the short term. The short-term efficacy of ultrasonographic therapy has been demonstrated only in calcifying tendinitis.
Another modality that looks promising is extracorporeal shock wave therapy.
Passing a strong electric current through a flat
coil inducing a magnetic field generates shock waves.
Manual therapy Exercises Surgical Intervention
Subacromial corticosteroid injection Bupivacaine suprascapular nerve block
Edetate disodium (disodium EDTA) Analgesic
A follow-up visit should be scheduled 6-8 weeks following the initial evaluation. Following visits depend on the responsiveness to the treatment. Recommend 2 months of follow-up visits until the condition has improved or stabilized.
No medication or homeopathic agent is known to
prevent tendon degeneration. Avoidance of highly repetitive activities or sustained shoulder posture with greater than 60° of flexion or abduction is probably the best prevention.
Acute LBP if it has a duration of about one month or less. Chronic LBP is usually defined by symptoms of two months or more.
Both acute and chronic LBP can be further
defined by the presence or absence of neurologic symptoms and signs. Nonspecific or nonradicular LBP is not associated with neurologic symptoms or signs.
In general, the pain is localized to the spine and/or paraspinal regions and does not radiate into the leg. In general, nonspecific LBP is not associated with spinal nerve root compression.
LBP may or may not be associated with significant pathology on magnetic resonance imaging (MRI) and is often a result of simple soft tissue disorders such as strain, but may also be caused by serious medical disorders arising in the bony spine, parameningeal, or retroperitoneal regions
: Differential Diagnosis of Low Back Pain
Causes of Referred Pain
Malignancy Infection Inflammatory spondyloarthropathy (ankylosing spondylitis, psoriatic spondylitis, Reiter's syndrome, inflammatory bowel disease)
Idiopathic (sprain, strain) Spondylosis (disk, annulus, facet)
Pelvic disease (prostatitis, endometriosis, pelvic inflammatory disease)
Renal disease (kidney stones, pyelonephritis, perinephric abscess)
Compression fracture Traumatic fracture Alignment disorders (kyphosis, scoliosis, spondylolisthesis)
Gastrointestinal disease (pancreatitis, cholecystitis, penetrating ulcer)
Osteochondrosis Paget's disease of bone
LBP accompanied by spinal nerve root damage is usually associated with neurologic signs or symptoms, and is described as radiculopathy.
Low back pain is second only to upper respiratory illness as a cause for visiting a physician Up to two thirds of the population will have low back symptoms at some time in their lives
Among individuals with chronic LBP without neurologic deficits, a number of factors play a role in the length of disability.
Recurrent LBP and prolonged disability tend to correlate with:
prior history of LBP advancing age job dissatisfaction emotional distress heavy or repetitive lifting and physical work prolonged sitting or standing the presence of a worker's compensation claim or pending litigation.
Lumbosacral radiculopathy and radicular LBP are less common than nonspecific LBP.
L5 radiculopathy is the most common
lumbosacral radiculopathy, usually produced by disk herniation between the fourth and fifth lumbar vertebral bodies. S1 radiculopathy is the next most common, followed by L3 to L4 radiculopathy.
The pathophysiology of nonradicular LBP is usually indeterminate.
Pain may arise from a number of sites, including
the vertebral column, surrounding muscles, tendons, ligaments, and fascia Stretching, tearing, or contusion of these tissues may occur after sudden unexpected force applied to the spine from events such as heavy lifting, torsion of the spine, and whiplash injury.
The pathophysiology of radicular spine pain and lumbosacral radiculopathy is usually more obvious.
Disk herniation through the annulus fibrosis does
not in itself produce pain, but compression by disk of the dural lining around the spinal nerve root sleeve is one likely explanation for the back pain associated with acute disk herniation.
History and physical examination are critical to the diagnosis and thus to the formulation of a rational approach to management.
Warning Signals of Systemic Disease Underlying Back Pain Cancer
1. Prior history of malignancy 2. Advanced age 3. Unexplained weight loss 4. No pain relief with bed rest 5. Pain duration greater than 4 to 6 weeks 6. Failure to respond to standard therapies
1. History of intravenous drug use 2. Urinary tract infection 3. Skin infection Compression fracture 1. Advanced age 2. Trauma 3. Prolonged corticosteroid use Rheumatologic disorders
Rheumatologic disorders Waddell and colleagues have described a number of historical features that point to nonorganic causes for low back pain, predicting delayed recovery and suggesting the need for a multidisciplinary approach to treatment.
Historical Symptoms Suggesting Nonorganic Causes of Back Pain Pain at the tip of the tailbone
Whole-leg pain in global distribution
Whole-leg numbness in a global distribution Sudden give-way weakness of the leg
Absence of even brief periods of relative pain relief
Failure or intolerance of numerous treatments Numerous urgent care visits or hospitalizations for back pain
A general examination should be performed to identify potential systemic disorders, such as rheumatologic disease, skin disease, or bony deformities. The spine should be inspected for alignment, curvature, range of motion, focal tenderness, and overlying skin abnormalities such as a tuft of hair or pore. Mechanical maneuvers to elicit radicular and hip-joint symptoms should be considered, including straight-leg raising, reverse straightleg raising, Patrick's test, and Lasègue's sign.
A careful neurologic examination should be undertaken to exclude motor and sensory deficits. Muscle strength in the L2 through S1 myotomes should be examined.
The sensory examination should include soft-touch and
pain sensation in the same segmental distributions.
Muscle stretch reflexes should be elicited at the knee for the L3 to L4 segment and at the ankle for the S1 segment, and can also be performed in the posterior thigh at the tendinous insertion of internal hamstrings for the L5 segment.
Signs on the Physical Examination Indicating Nonorganic Causes of Low Back Pain Superficial tenderness over the lumbar region to light touch
Nonanatomic tenderness Exacerbation of pain by applying a few pounds of pressure with the hands to the top of the head
Exacerbation of pain by simulated rotation of the spine Ability to sit up straight from a supine position, but intolerance of the straight-leg-raising test Nonanatomic distribution of sensory changes
Routine Radiographs of the Spine Computerized Tomography (CT) and Magnetic Resonance Imaging (MRI) CT-Myelography Electrodiagnosis
The initial management of acute spine pain must be directed toward determining if a serious neurologic condition exists If there is a history of recent trauma or serious underlying medical illness, more aggressive evaluation is warranted.
Acute spine pain is very common, and the likelihood of spontaneous recovery is in the range of 80% to 90%. Prolonged inactivity will prolong recovery. treatment regimens tend to be nonspecific.
There is general agreement that patients with acute nonspecific spine pain or nonlocalizable lumbosacral radiculopathy (without neurologic signs or significant neurologic symptoms) require only conservative medical management.
The initial treatment of the patient with lumbosacral radiculopathy presenting with sensory symptoms and pain without significant neurologic deficits is not different from the approach for the patient with uncomplicated low back pain. Patients require observation for possible worsening of their neurologic status.
The treatment plan should fit the severity of the symptoms and signs. The management approach for radiculopathy covers the gamut from avoidance of heavy lifting to laminectomy and fusion. In acute radiculopathy, the goals of treatment should be the reduction of pain and the stabilization or amelioration of neurologic deficits.
When symptoms of spine pain extend beyond 4 to 8 weeks, the condition has moved from the acute to the chronic phase. In the face of true radiculopathy with new or worsening neurologic deficits, a surgical opinion should be considered.
The standard approach to the patient with nonspecific chronic spine pain is physical therapy. By 3 to 4 weeks after onset of symptoms, unless there is serious underlying structural disease, there is no reason the patient should not be enrolled in an aggressive program of mobilization, postural improvement, and increased endurance.
The long-term outlook is good for significant spontaneous recovery in patients with lumbosacral radiculopathy. The pain of acute radiculopathy can persist beyond 3 or 4 weeks, becoming chronic, at which point acute remedies such as rest, analgesics, and cervical traction may be less effective and other therapeutic options must be sought.
Another local injection procedure, selective nerve root block, has been used for diagnostic and therapeutic purposes at the lumbosacral and cervical levels. This diagnostic technique has been used when there is lack of agreement between clinical and neuroimaging findings, when there is atypical limb pain, and when there is a history of failed surgery at the level in question. Nerve root blocks are contraindicated in the presence of systemic infection, local infection, or bleeding diathesis.
For the therapeutic procedure at the cervical level, it is standard practice to use a combination of 0.5 mL of 1% Xylocaine (lidocaine HCl) and a long-acting corticosteroid. The therapeutic injection is preceded by a localization procedure under fluoroscopic guidance using a nonionic contrast medium to outline the selected nerve root.
Some patients have chronic spine pain without evidence of structural intraspinal pathology, others have had previously treated structural lesions, and some have had multiple previous surgical interventions—a condition described as the failed-back syndrome. The goal in these patients is to improve the ability to perform activities of daily living and to diminish pain perception.
Recurrences of low back pain are common. - Studies have shown recurrence rates between 30% and 75% within 3 years of the first episode For patients with radiculopathy, there is less likelihood of early recovery; however, about 50% of patients can return to work after 4 to 6 weeks without surgery
Low back pain is usually caused by mechanical disorders of the spine, with or without involvement of the spinal nerve roots, but it may be a result of nonmechanical causes or may be referred from retroperitoneal sources. Diagnosis starts with a careful examination, followed by consideration for neuroimaging studies and electrodiagnostic studies.
Specific management decisions are based on the duration of symptoms and the presence or absence of neurologic deficits. Chronic pain syndromes are often perpetuated by nonmedical factors. Treatment requires a multidisciplinary approach.
Rheumatoid Arthritis (RA) is a chronic, progressive, systemic inflamatory disorder which affecting the synovial joints and can lead to joint destruction. no known cure
The goal of treatment now aims toward achieving the lowest possible level of arthritis disease activity and remission if possible, the minimization of joint damage, and enhancing physical function and quality of life. The optimal treatment of RA requires a comprehensive program that combines medical, social, and emotional support for the patient
There are three general classes of drugs commonly used in the treatment of rheumatoid arthritis: non-steroidal antiinflammatory agents (NSAIDs), corticosteroids, and disease modifying antirheumatic drugs (DMARDs).
NSAIDs and corticosteroids have a short onset of action while DMARDs can take several weeks or months to demonstrate a clinical effect.
DMARDs include methotrexate, sulfasalazine, leflunomide, etanercept, infliximab, adalimumab, abatacept, rituximab, anakinra, antimalarials, gold salts, d-penicillamine, cyclosporin A, cyclophosphamide and azathioprine .
Because cartilage damage and bony erosions frequently occur within the first two years of disease, rheumatologists now move more aggressively to a DMARD agent early in the course of disease, usually as soon as a diagnosis is confirmed.
Rheumatoid arthritis is the most common form of inflammatory arthritis It is an apparent autoimmune response that involves synovium, articular cartilage, and soft tissue. The joints of the hand are most commonly involved, but wrists, feet, knees, and hips are frequently affected.
This disease is often symmetric, i.e., both knees and both hands. Patients frequently suffer from morning stiffness. Subcutaneous nodules may be palpated, especially at the proximal ulna. The rheumatoid arthritis (RA) factor is positive in approximately 80% of patients.
Radiographic changes in rheumatoid arthritis:
▪ -severe destruction of radiocarpal articulation with subluxation and ulna deviation at the wrist ▪ loss of ulnar styloid bilaterally ▪ dislocation of the proximal interphalangeal joint of the left thumb and dislocation of the right fourth and fifth finger metacarpophalangeal joints and left metacarpophalangeal joint ▪ diffuse joint space narrowing of many interphalangeal joints.
Typical radiographs show loss of articular cartilage, osteopenia, and periarticular erosions A typical hip deformity of the femoral protruding medially into the pelvis (protrusio acetabulum) is not uncommon. These patients can have vasculitis, pericarditis, and pulmonary involvement.
Treatment is initially medical and often by a rheumatologist. A variety of medications are available that can either relieve symptoms or possibly alter the course of the disease (disease-modifying agents). Intra-articular cortisone injections can be a benefit in an acute flare.
For those with persistent joint damage, total joint replacement is the most beneficial method to relieve pain and disability and to restore function. When endotracheal intubation is a possibility it is wise to obtain cervical spine radiographs.
Instability of the cervical spine is not rare and this should be
Patients with systemic lupus erythematoid (SLE) may have a rheumatoid arthritis-like syndrome. many also develop osteonecrosis as a result of the common treatment of their disease with corticosteroids. MRI is useful in making the diagnosis of osteonecrosis.
checked prior to the manipulations required for anesthetic intubation.
Osteoarthritis (OA) is the most common form of arthritis, with up to 40 million people in the United States having been diagnosed with it. Also known as degenerative joint disease generally considered to be noninflammatory. the same cytokines and interleukins seen in inflammatory arthritis are also seen in osteoarthritis, although in lesser quantity.
Theories of etiology include both primary biomechanical, or primary biochemical effects and secondary biomechanical-derived effects leading to a gradual loss of articular cartilage. Many patients do not have a clearly identifiable source for their OA
Other patients may demonstrate problems such as chronic instability, malalignment, prior injury, crystalline disease, past history of meniscectomy, or excessive and repetitive loading
A genetic predisposition is present in some patients.
The knee is the most commonly affected joint.
Radiographic evidence of OA is common by age
40 years, but clinically significant osteoarthritis is less common until about age 60 years
Typical findings on a radiographic examination reveal loss of articular cartilage shown by "joint narrowing" especially on weight-bearing films. Osteophytes and subchondral cysts are common radiographic findings.
Physical examination reveals pain upon walking (an antalgic gait pattern) or motion of the involved joint. Patients have some degree of limitation of motion, pain and/or crepitus with that motion. Usually there is an effusion in the joint.
The initial treatment includes
activity modification weight reduction if indicated
the use of a cane for lower-extremity problems nonsteroidal anti-inflammatory and nonnarcotic
analgesic medications if required.
Patients should be encouraged to maintain their joint motion and muscular strength. Rarely, an intra-articular corticosteroid injection can be used for an acutely painful joint, but it is only a temporary solution
Surgical options are based on the dramatic success of joint replacement to relieve pain and restore function to the arthritic joint.
Clinical Example Normal
Noninflammatory Inflammatory (Osteoarthrosis) (Rheumatoid)
Opalescent yellow Turbid yellow to green Low Low
WBC/mm3 % PMM leukocytes
Culture Mucin clot Glucose (% of serum glucose) Total protein
Negative Firm 100%
Negative Firm 100%
Negative Friable 50–75%
Positive Friable <50%
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