Degenerative Lumbar spinal stenosis

                                    Degenerative Lumbar spinal stenosis

                                                     Dr KS DHILLON

 

What is degenerative lumbar spinal stenosis?

A narrowing of the spinal canal, as a result of degenerative disease of the spine, which reduces the space available for the neural and vascular elements within the canal, is known as spinal stenosis. The narrowing of the canal can be symptomatic or asymptomatic. Clinical or symptomatic spinal stenosis is a syndrome which is characterised by the presence of ‘gluteal and/or lower extremity pain and/or fatigue which may occur with or without back pain’ (1). Classically the presentation is that of neurogenic claudication where the patient has pain, numbness and or weakness of the lower limb on standing and walking and the symptoms are relieved on sitting and lying down. They usually have relief of symptom on bending forward which increases the size of the lumbar canal and aggravation of symptoms on spinal extension.

Natural history of degenerative lumbar spinal stenosis

The North American Spine Society (NASS) evidence-based clinical guidelines committee (1) reviewed the literature to study the natural history of degenerative lumbar spinal stenosis. The question the committee posed was “What happens
to patients with symptomatic lumbar stenosis who do not receive treatment?” They identified 54 articles in the literature which broached the topic of the natural history of spinal stenosis and found that none of the publications answered the question because none of the studies had a cohort of patients who had no treatment. The workgroup concluded that there is insufficient evidence in the literature to define the natural history of degenerative spinal stenosis. Although there is no reliable evidence in the literature, the workgroup came to the following conclusions based on the available evidence:
1. The natural history of mild to moderate degenerative lumbar stenosis
may be favourable in one third to half the of patients.
2. In patients with mild to moderate lumbar spinal stenosis a ‘rapid or catastrophic
neurologic decline’ is unlikely.
3. The natural history of clinically or radiographically severe degenerative lumbar stenosis is unknown.

Diagnosis of lumbar spinal stenosis

 

Clinical diagnosis

Konno et al (2 and 3) developed a simple clinical diagnostic support tool to diagnose lumbar spinal stenosis (LSS) which has a sensitivity of 92.8% and a specificity of 72.0%. Patients who presented with back and leg symptoms were asked to fill up a simple questionnaire.  The questions included age, history of diabetes, presences and absences of intermittent claudication, aggravation of symptoms by standing and relief of symptoms on bending forward. This was followed by a short clinical examination consisting of checking for postural changes in their leg symptoms, Achilles' tendon reflex, SLR test and the measurement of ABI. With these measures, the diagnosis of LSS can be established with high sensitivity and specificity without imaging studies.
Classically patients with LSS will have numbness and or pain in the thighs down to the leg after walking or standing for a while and these symptoms will improve on bending forward and after sitting down. The physical examination usually includes ‘a gait-loading test to confirm neurogenic intermittent claudication’. The patient is asked to walk for a while till neurogenic symptoms develop and then the patient is examined for sensory and motor deficit and the knee and ankle reflexes are tested (2). The presences of peripheral vascular disease which can produce vascular claudication has to excluded.
Katz et al. (4) studied the diagnostic value of history and physical examination in the diagnosis of LSS.They used the opinions of several expert physicians including two orthopaedic surgeons to define the presence or absences of LSS. They found that the factors strongly associated with a diagnosis of LSS ‘were greater age,
severe lower-extremity pain, and absence of pain when seated’. The physical findings strongly associated with the diagnosis ‘were a wide-based gait, an abnormal Romberg test, thigh pain following 30 seconds of lumbar extension, and neuromuscular deficits’.
The clinical diagnosis can be confirmed with and correlated with radiological imaging.

Radiological imaging for spinal stenosis
The presences of spinal canal narrowing on radiological imaging does not indicate a diagnosis of spinal stenosis because degenerative changes in the spine are common in asymptomatic individuals. Brinjiki et al (5) did a systematic review of literature of imaging features of spinal degeneration in asymptomatic populations. They found that the prevalence of disk degeneration in asymptomatic individuals increased from 37% among 20-year-old individuals to 96% among 80-year-old individuals. The prevalence of disk bulge increased from 30% among 20 years old individuals to 84% among 80 years old individuals. The prevalence of disc protrusion increased from 29% of those 20 years of age to 43% of those 80 years of age.
Boden et al (6) did MRI scans in 67 individuals who never had back pain, sciatica and neurogenic claudication in the past. They found 21% of the individuals had radiological evidence of spinal stenosis.
Wiesel et al (7) did CT scans of the spine in asymptomatic individuals and found the presence of disc herniation, facet degeneration or spinal stenosis in about 50% of the subjects. They also found that there was no significant correlation between the area of the dural sac in axially loaded CT and the clinical symptoms of spinal stenosis.
False positive and false negative CT scan and MRI findings of nerve compression have been well documented, which makes radiological imaging as a sole means of diagnosing spinal stenosis untenable (6,7,8). There is also an element of significant variation of image interpretation of  MRI and CT scan in the diagnosis of spinal stenosis (9).
Therefore the diagnosis of spinal stenosis has to be clinical and it can be confirmed and correlated with imaging studies.
What are the most useful imaging studies? In patients where a clinical diagnosis of lumbar spinal stenosis has been made, an MRI of the lumbar spine would be the most appropriate non-invasive investigation to confirm spinal canal narrowing and nerve root compression (1).
Kent et al (10) did a systematic review of the literature to compare the usefulness of CT, MRI and myelography in the diagnosis of spinal stenosis. They found that the sensitivity of MRI in the diagnosis of adult spinal stenosis was 81-97%, the sensitivity of CT was between 70-100% and sensitivity of myelography was about 67-78%. The sensitivity of all three modes of imaging for diagnosis is about the same and no one mode is superior to the other.
There are several other studies in literature (11,12,13) which have compared the value of MRI, myelography and CT myelography in the diagnosis of LSS and they all showed that the accuracy of all three modalities is about equal in the diagnosis of spinal stenosis. MRI is widely used and accepted as a mode of investigation since it is non-invasive and it does not expose the patient to contrast media and ionizing radiations.
Barz et al (14) did a study to evaluate the usefulness of the nerve root sediment sign on MRI’s of the lumbar spine. The studied 100 patients with clinical lumbar stenosis and 100 patients who had low back pain and no clinical evidence of spinal stenosis. Ninety-four of the 100 patients with clinical spinal stenosis had a positive sediment sign whereas none of the patients with low back pain had a positive sign. The authors concluded that ‘a positive sedimentation sign exclusively and reliably occurs in patients with LSS, suggesting its usefulness in clinical practice’. However, critics have pointed out that the sign does not ‘discriminate between symptomatic and asymptomatic patients with Dural Sac Area (DSA)<80mm2,(patients with LSS) and hence is of limited clinical value. A positive sediment sign is expected with a DSA of less than 80mm2 (1).
In patients with a clinical diagnosis of LSS in whom an MRI is contraindicated, inconclusive or cannot be done, a CT myelogram would be the imaging study of choice (1). Several studies (11,13,15) have shown that MRI and CT myelograms are equally effective in confirming narrowing of spinal canal and root compression in LSS.
When an MRI or CT myelogram cannot be done, a CT scan would be an appropriate imaging modality, although the sensitivity is slightly lower with a CT scan in diagnosing spinal canal narrowing and nerve root compression (10).
The radiological criteria for defining the severity of spinal stenosis is unclear. The are several classifications for defining radiological spinal stenosis that has been published in the literature (16).
Lee et al. (17) have recently offered a more simple MRI based classification system for central stenosis. They described a 4-grade (0, 1, 2, and 3) system based on the degree of separation of the cauda equina on T2-weighted axial images. They did not measure the parameters. They defined grade 0 as no lumbar stenosis when there was no obliteration of the CSF space in front of the cauda equina; mild or grade 1 stenosis was present when there was no csf in front of the cauda equina and the cauda equina remained separated; grade 2 or moderate stenosis was present when there was  some cauda equina aggregation or bunching and grade 3 or severe stenosis was present when there was no space between the cauda equina elements and the roots cannot be visually separated. They found that with this classification the interobserver reliability was substantial to excellent for all levels and the intraobserver reliability was excellent. This classification system has been independently validated by Park et al (18) who showed that there was substantial interobserver reliability in the diagnosis of spinal stenosis with this classification. The authors also showed that none of the patients with grade 0 stenosis had neurological symptoms and almost all patients with grade 3 stenosis had neurological symptoms. The relevance of grade 1 and 2 stenosis remained unclear.
Lee et al (19) have also developed a grading system for foraminal stenosis. They divided the stenosis into 4 grades, from 0 to 3 based on sagittal MRI images of the lumbar spine. In this classification grade 0 refers to the absence of foraminal stenosis. In grade 1 stenosis there is mild foraminal stenosis with perineural fat obliteration in the two opposing directions, vertical or transverse. In grade 2  stenosis there is moderate foraminal stenosis with perineural fat obliteration in all four directions without morphologic change and grade 3 refers to a severe foraminal stenosis with nerve root collapse or morphologic change. The authors concluded that this ‘new grading system for foraminal stenosis of the lumbar spine showed nearly perfect interobserver and intraobserver agreement and would be helpful for clinical study and routine practice’.
Wildermuth et al (20) have similarly divided foraminal stenosis into four Grades (1-4) based on the presence of perineural fat as seen on MRI imaging. Grade 1 is the absences of stenosis with normal perineural fat. In grade 2 or slight stenosis, there is compression of perineural fat but the fat is still present all around the nerve root. In grade 3 or marked stenosis there is a loss of perineural fat on at least one side of the nerve and in grade 4 or advanced stenosis, there is a complete loss of perineural fat.
There are no universally accepted criteria for the radiological diagnosis of lateral canal stenosis. Steuer et al (21) did a systematic review of the literature and found that the height and the depth of the lateral recess and the lateral recess angle are the criteria used for describing lateral canal stenosis. The measurements are done on a CT scan or an MRI (axial T2 weighted) images of the lumbar spine. The depth refers to the measurement between the top of the pedicle and the superior articular facet. The height refers to the distance between the most anterior point of the superior articular facet and the posterior border of the vertebral body and the lateral recess angle as the angle between the lines parallel to the floor and the roof of the lateral recess. A lateral recess height ≤ 2 mm and/or lateral recess depth ≤ 3 mm or a lateral recess angle < 30° has been described as diagnostic for lateral recess stenosis.

Treatment of lumbar spinal stenosis

There is no evidence in the literature to show that the outcome of treatment of spinal stenosis is better as compared to the natural history of the disease (no treatment) (1).

Conservative treatment

Anti-inflammatory medications, physical therapy and conditioning is the usual mode of conservative treatment to relieve pain and improve function in patients with spinal stenosis (22). In the elderly population, the non-steroidal anti-inflammatory drugs (NSAIDs) have to be used with caution because of their potential gastrointestinal and cardiovascular adverse effects.
There is no credible evidence that other pharmaceutical agents such as methylcobalamin, gabapentin, prostaglandin E, intranasal calcitonin, and intramuscular calcitonin are of value in the treatment of spinal stenosis (1).
Unfortunately, there is insufficient evidence in literature ‘to make a recommendation for or against the use of pharmacological treatment in the management of spinal stenosis’ (1).
There is level II therapeutic evidence that an exercise program which includes stretching, strengthening and low-intensity cycling exercises, in the short term, improves pain and disability in patients with lumbar spinal stenosis (23).
Physical therapy has shown some improvement in physical function in patients with spinal stenosis although the evidence is not so robust (24,25).

Epidural steroid injections

Epidural steroid injections are widely used for the treatment of patients with spinal stenosis despite the absences of credible evidence regarding its efficacy and safety. Friedly et al (26) carried out a multisite, double-blind, randomised trial in 400 patients with spinal stenosis who had moderate to severe leg pain and disability. One group was given epidural injections of glucocorticoids plus lidocaine and the other group lidocaine alone. The epidural injections were fluoroscopically guided. At six weeks they found no difference between the two groups in the primary outcomes as measured by the Roland-Morris Disability Questionnaire (RMDQ) scores and the rating of the intensity of leg pain. Likewise, there was no difference between the subgroups who received interlaminar or foraminal injections. The authors concluded that ‘in the treatment of lumbar spinal stenosis, epidural injection of glucocorticoids plus lidocaine offered minimal or no short-term benefit as compared with epidural injection of lidocaine alone’.
Complications with epidural injections were not uncommon. The complication rate in the glucocorticoid–lidocaine group was 21.5% and in the lidocaine-alone Group was 15.5%. Complication rates were higher in the transforaminal injection group. Cortisol suppression was significantly higher in the glucocorticoid–lidocaine group.
In this study patients in both treatment groups had improvement in function and decreased pain probably due to a placebo effect, the natural history of spinal stenosis, and other factors present in both study groups. Unfortunately, this excellent study did not have a sham group.
Chou et al (27) in 2015 did a systematic review and meta-analysis of the published data on the use of epidural corticosteroids in the treatment of lumbar radiculopathy and spinal stenosis. They evaluated 30 placebo-controlled trials of epidural corticosteroid injections for radiculopathy, and 8 trials were for spinal stenosis. They found that with epidural corticosteroid injections for radiculopathy there was an immediate reduction in pain and function but the benefits were small and not sustained. There was also no effect on long-term surgical risk. There was some evidence to suggest that there are no benefits of epidural steroids in the treatment of spinal stenosis. They found that ‘serious harms were rare, but harms reporting was suboptimal’.
Nancy E. Epstein (28) in 2013 did a comprehensive review of the literature to assess the risks of epidural and transforaminal steroid injections in the spine. Epidural injections for the management of spinal conditions, though not approved by the FDA, is increasingly being used in the management of patients with spinal disorders. They are typically short-acting with no long-term benefit and their use can be associated with major risks/complications.
There have been reports of contaminated epidural steroid injections which had resulted in meningitis, stroke, paralysis, and even death. Though many of the complications go unreported, other reported complications include ‘life-threatening infections, spinal fluid leaks (0.4-6%), positional headaches (28%), adhesive arachnoiditis (6-16%), hydrocephalus, air embolism, urinary retention, allergic reactions, intravascular injections (7.9-11.6%), stroke, blindness, neurological deficits/paralysis, hematomas, seizures, and death’ (28).
In 2009 FDA started investigations into adverse events related to epidural injections and they found that between 1997 and 2014 there were 90 serious and sometimes fatal neurological complications associated with the use epidural glucocorticoid injections. The complications included paraplegia, quadriplegia, spinal cord infarction, and stroke. Following this investigations, in 2014, the FDA issued a mandatory requirement that ‘all injectable glucocorticoid product labels carry a warning stating that “serious neurologic events, some resulting in death, have been reported with epidural injection of corticosteroids” and that the “safety and effectiveness of epidural administration of corticosteroids have not been established and corticosteroids are not approved for this use” (29).

Ammendolia et al (30) in 2013 did a Cochrane database systematic review to evaluate the effectiveness of non-operative treatment of patients with spinal stenosis and neurogenic claudication. The review included pharmaceutical and physical therapy interventions, as well as epidural injections and they, found that ‘moderate and high-quality evidence for nonoperative treatment is lacking’. What about surgical treatment for spinal stenosis?

Surgical treatment of spinal stenosis

Spinal decompression

Since the symptoms of spinal stenosis are due to narrowing of the spinal canal, surgical decompression was considered to be the logical treatment for symptomatic spinal stenosis from time immemorial. However, over the years clinical experience showed that many patients did well without surgery.
There have been many reports in literature with variable outcome after surgical treatment for spinal stenosis. The outcome varied from 26% to 100% good results at 4 years (31 ), 77% good results at 8 years (32), and  68% good results at 12 years (33).
Johnsson et al (34) compared the outcome of surgical and conservative treatment of patients with spinal stenosis. They found that 60% of the patients treated surgically improved and 25% deteriorated at 53 months follow up and of those treated conservatively 30% improved and 60% remained unchanged at 31 months follow up.
Amundsen et al (35) did a long-term prospective study in 100 patients to compare the outcome of conservative and surgical treatment of spinal stenosis. In this study, there were 19 patients with severe symptoms who had surgical treatment and 50 patients with moderate symptoms had conservative treatment, and another 31 patients were randomized between the conservative treatment group (18 pts) and surgical treatment group (13 pts). All patients were followed up for 10 years.
In the conservative treatment group, good results were reported in 70% of the patients at 6 months, 64% at 1 year and 57% at 4 years. In the surgical group, good results were reported in 79% at 6 months, 89% at 1 year and 84% at 4 years. In patients who were randomly assigned to the conservative and surgical group, the results were much better in the surgical group as compared to the conservative group.
This study provides Level IV evidence that patients with severe symptoms at presentation, who undergo surgical decompression, the outcome will be good 80-90% of the time and in patients with moderate symptoms who undergo conservative treatment, the results will be good in about 70% of the time (1).
Mariconda et al (36) reported a prospective study, of 44 patients, which compared laminectomy with conservative treatment in patients with mild to moderate leg pain. At 4 years follow up they found that 68% of the surgical group had good results while 33% in the conservative group had good results. There was a 9 percent reoperation rate in the surgical group and 9% crossover rate. This study provides level IV evidence that surgical decompression gives good results in 68% of the patients (1).

Spinal fusion

Spinal fusion is often done after spinal decompression due to a belief that posterior spinal decompression can destabilize the spine. Spinal fusion prolongs the operating time and increases the blood loss and can be associated with more complications. Is spinal fusion necessary after posterior decompression?
 Grob et al (37) did a study to address this issue. They did a randomized, controlled trial of 45 patients with symptomatic lumbar stenosis with no spinal instability. The patients were randomly assigned to one of the three groups. Group 1 patients had laminotomy with medial facetectomy. In group 2 the patients had decompression with fusion of the most stenotic segment and in group 3 the patients had decompression with fusion of all decompressed segments. At an average follow up  28 months all groups showed an increase in walking ability and a decrease in pain and there was no difference in the outcome between the groups. This study provides Level II therapeutic evidence that there is no difference in the clinical outcome in patients, with spinal stenosis and no spinal instability, who had posterior decompression alone and in those who had decompression with fusion (1).
Patients with spinal instability as defined by Posner’s method generally do not do well if a laminectomy is done without fusion. Yone and Sakou (38) studied 60 patients who had surgery for spinal stenosis. Thirty-three of the 60 patients had spinal instability as defined by the Posner’s criteria. Of the 33 patients with instability 19 had laminectomy with fusion and the other 14 refused fusion and had laminectomy alone. Twenty-seven other patients without instability had laminectomy alone. Eighty percent of the patients without instability and 80% of those with instability and fusion had good outcome whereas only 43% of patients with instability and no fusion had a good outcome.This study provides Level II  evidence that in patients with spinal stenosis and spinal instability, decompression with fusion is more effective than decompression alone (1). There are other authors who believe that all patients with spinal stenosis can be treated by decompression alone without fusion.
Iguchi et al (39) studied the long-term outcome of posterior spinal decompression without fusion in patients with spinal stenosis. They did laminectomy with partial facetectomy without fusion in 122 patients with spinal stenosis. At a minimum of 10 years (average 13 years) follow up, 37 patients were available for evaluation. In 62.2% of the patients, there was no impairment in activities of daily living. The outcome was excellent in 13 (35.1%), good in 8 (21.6%), fair in 8 (21.6%) , and poor in 8 patients (21.6%). Three of the 8 patients (8.1%) required additional surgery. The outcome was the same in patients with preoperative spondylolisthesis and those without spondylolisthesis. Similarly, the outcome was the same in patients with preoperative scoliosis and those without scoliosis. At least 2 levels of laminectomy was performed in each patient. Preoperative sagittal rotation of more than 10° with multilevel laminectomy was thought to be a risk factor for poor outcome. The authors concluded that acceptable results can be obtained with a laminectomy without spinal fusion in patients with spinal stenosis on long-term follow-up.
Satisfactory long-term outcome (8 years to 13 years) of surgical treatment for spinal stenosis ranges from 55% (40), 56.7% (39) and  71% (35).

The risk factors for unsatisfactory outcome following surgery for spinal stenosis are numerous. Katz et al (41) found that poor long-term outcome, defined as severe pain or the need for a repeat operation, or both, included comorbidities such as osteoarthrosis, cardiac disease, rheumatoid arthritis, or chronic pulmonary disease, longer duration of follow-up, and laminectomy at a single level. However Iguchi et al (39) found that patients who had multilevel laminectomies and a 10° or more of sagittal rotation had a poorer outcome. Patients undergoing repeat spinal surgery has a poorer prognosis (42). Lower income, presences of anxiety and depression, the existence of compensation claims, absences of preoperative neurological deficit, less severe canal stenosis and absences of preoperative subjective difficulty in walking, are all associated with poorer outcome after surgery (43).
Despite the existence of a large number of publications in the scientific literature regarding the treatment of spinal stenosis, there appears to no consensus as to what is the best form of treatment for spinal stenosis. Zaina et al (44), in 2016, did a systematic review of the literature for the Cochrane group to compare conservative and surgical treatment for spinal stenosis. They were unable to conclude whether surgical treatment or a conservative approach is better for lumbar spinal stenosis. They, however, noted that there was a complication rate of between 10% to 24% in patients treated with surgery and there were no side effects of conservative treatment. There were no clear benefits of surgery when a comparison was made with conservative treatment. Their conclusion was that ‘clinicians should be very careful in informing patients about possible treatment options, especially given that conservative treatment options have resulted in no reported side effects’.
There is also no good evidence in the literature on the efficacy of surgery for spinal stenosis. Machado et al (45) in 2016 did a systematic review of literature for the Cochrane group to evaluate the outcome of surgical treatment for spinal stenosis. They found that there was very little literature on the efficacy of surgical treatment of spinal stenosis. There were no trials comparing ‘surgery with no treatment, placebo or sham surgery’ though ‘placebo-controlled trials in surgery are feasible and needed in the field of lumbar spinal stenosis’. They also found that decompression with fusion and interspinous process spacers were not superior to decompression alone.

Conclusions

Clinical or symptomatic spinal stenosis has been well defined with little ambiguity. Radiological narrowing of the spinal canal due to degenerative disease of the spine has been well studied and classified. However, the natural history of symptomatic spinal stenosis is not known because there no studies comparing treatment and no treatment. However, from the little evidence available it appears that the outcome is favourable in one third to half of the patients with mild to moderate spinal stenosis even without treatment.The natural history of patients with severe stenosis is unknown. Rapid neurological decline does not happen in patients with spinal stenosis.
The use of anti-inflammatory medications, physical therapy and conditioning remains the mainstay of conservative treatment of symptomatic spinal stenosis. There is no robust evidence to support the use of other pharmaceutical agents in the treatment of spinal stenosis.
 Epidural steroid injections are widely used for the treatment of patients with spinal stenosis despite the absences of credible evidence regarding its efficacy and safety. Complications are not uncommon with an epidural injection. Complication rates as high as 21.5% have been reported in the literature. Life-threatening infections, paralysis and even death have been reported.
Despite the presences of a large number of publications in the scientific literature regarding treatment of spinal stenosis, there appears to be no consensus as to what is the best form of treatment for spinal stenosis. There is no evidence in literature as to whether surgical or conservative treatment is better for treatment of spinal stenosis. Surgical treatment can be associated with up to 24% complication rate. Conservative treatment is not known to be associated with side effects. There is no good evidence on the efficacy of surgical treatment for spinal stenosis. Studies show that the outcome of spinal decompression alone is the same as that with decompression with fusion. Interspinous process spacers do not provide any additional benefits to patients in the treatment of spinal stenosis.
Till good evidence is available the treatment of patients has to be individualized and the least invasive treatment which will provide maximum relief with minimal or no side effects should be offered to the patient.

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Rotator cuff tears: prevalence and management

                              Rotator cuff tears: prevalence and management

                                                                Dr KS Dhillon

Anatomy of rotator cuff
 

The rotator cuff consists of four muscles that arise from the scapula and and insert on the proximal humerus. The four muscles are, the supraspinatus, infraspinatus, teres minor and the subscapularis. The supraspinatus arises from the supraspinatus fossa, the infraspinatus from the infraspinatus fossa and teres minor from the lateral border of the scapula. All three insert on the greater tubercle of the humerus, with the supraspinatus most proximally and the teres minor most distally and the infraspinatus in between the two. The subscapularis arise from the subscapular fossa and inserts on the lesser tubercle.Though superficially the four muscles are separate,the deeper portions merge with each other and with the glenohumeral capsule and the long head of the bicep tendon.
The subscapularis is an internal/medial rotator and acts together with the latissimus dorsi, pectoralis major, and the teres major to produce medial rotation of the humerus. The infraspinatus is a strong external/lateral rotator and is assisted by the teres minor which is a weak rotator. The supraspinatus is the initiator of abduction of the shoulder and after 30 degrees of abduction the deltoid takes over. Besides producing rotation and abduction forces, the rotator cuff muscles lock the humeral head in the glenoid and provide a stable scapulohumeral link for upper limb function. They also provide muscle balance and capsular stability for the glenohumeral joint (1).

Prevalence of rotator cuff tears

Chronic shoulder pain is the most common orthopedic complaint after knee pain. Atraumatic rotator cuff tear is a frequent cause of pain and dysfunction of the shoulder in individuals over the age of 60 years and is present in about half of the patients with a history of shoulder complaints.
Rotator cuff tears may or may not be symptomatic. Tempelhof et al (2) studied the prevalence of rotator cuff tears in asymptomatic shoulders.They did a prospective clinical and ultrasonographic study in 411 volunteers. They found that the  overall incidence of rotator cuff tear was 23%. The incidence in the age group between 50 to 59 years was 13%, 60 to 69 years was 20%, 70 to 79 age group it was 31% and above 80 years it was 51%. The authors concluded that ‘rotator cuff tears must to a certain extent be regarded as "normal" degenerative attrition, not necessarily causing pain and functional impairment’.
Milgrom et al (3) studied the integrity of the rotator cuff using ultrasound in 90 asymptomatic adults between the age of 30 to 99 years. They found no significant difference between the dominant and nondominant arm as well as between genders. The found that the prevalence of partial and full thickness tears of the cuff increased markedly after the age of 50 years. Rotator cuff tears were present in 50% of dominant shoulders in the seventh decade and in 80% of subjects after the age of 80 years. They concluded that ‘that rotator-cuff lesions are a natural correlate of ageing, and are often present with no clinical symptoms’ hence logically ‘treatment should be based on clinical
findings and not on the results of imaging’.
Reilly et al (4) reviewed the literature to study the cadaveric and radiological prevalence of rotator cuff tears. The prevalence of cadaveric partial tears was 18.49% and cadaveric complete tears was 11.75% (total 30.24%). The ultrasonic incidence of tears in asymptomatic subjects was 38.9% and symptomatic subjects 41.4%. The incidence of MRI tears in asymptomatic subjects was 26.2% and in symptomatic subjects it was 49.4%. The authors concluded that rotator cuff tears are frequently asymptomatic and  radiological findings of rotator cuff tears should be correlated with clinical findings.
Yamamoto et al (5) did a population based study to elucidate the true prevalence of rotator cuff tears regardless of the presence or absences of symptoms. They examined clinically and with ultrasound, 683 people (1366 shoulders) in a village in Japan. There were 229 males and 454 females with an average age of 57.9 years (22 to 87 years). They found a 20.7% prevalence of rotator cuff tears. In symptomatic subject the incidence of tears was 36% and in asymptomatic subjects the incidence was 16.9%. They found that age, dominant arm and trauma were risk factors for tears of the rotator cuff.
In an another population based study, Minagawa et al (6) used ultrasound to elucidate the prevalence of rotator cuff tears in symptomatic and asymptomatic individuals. Out of 664 subjects studied 147 (22.1%) had full thickness tears of the rotator cuff.In the 20 to 40 age group the incidence was 0%, in the 50s 10.7%, in the 60s 15.2%, in the 70s 26.5% and in the 80s the incidence was 36.6%. The prevalence of symptomatic tears was 34.7% and  65.3% of all tears were in asymptomatic individuals. In the 50s one-half of all tears were asymptomatic whereas over the age of 60 two-third of the tears were asymptomatic.In this study the incidence of rotator cuff tears was 22.1% and the incidence increased with age. They also found that asymptomatic tears were  twice as common as symptomatic tear.
Asymptomatic tears can become symptomatic and can show anatomical deterioration with time (7 and 8).

Etiology of rotator cuff tears

Seventy five percent of the rotator cuff tears are due to impingement syndrome, 15% due to shoulder instability (anterior or multidirectional) and 10% due to trauma (9). Rotator cuff tears are broadly classified into two i.e degenerative tears and traumatic tears. Traumatic tears are due to significant trauma and are rare. The most common cause of rotator cuff tears is degeneration of the tendons caused by both intrinsic and extrinsic factors (10).The proponents of the extrinsic theory (Neer, Bigliani and others) have attributed the tendon degeneration to anatomical factors such as downsloping acromion (Bigliani type 2 and type 3 acromion), acromial spur, os acromiale, acromioclavicular spur and lateral extension of acromion (10). The intrinsic factors responsible for degenerative tears include ‘degenerative-microtrauma’, collagen thinning and disorganization, hyaline and myxoid degeneration, vascular proliferation and fatty infiltration (10). Other intrinsic factors responsible include ‘oxidative stress’ in the local environment and poor cuff vascularity(10).
Park et al (11) in a study involving a general population with atraumatic posterosuperior rotator cuff tears diagnosed with an MRI of the shoulder found that age, BMI, waist circumference, dominant-side involvement, manual labor, diabetes, hypertension, metabolic syndrome, ipsilateral carpal tunnel syndrome, HDL, and hypo-HDLemia were significant independent factors associated with development of posterosuperior rotator cuff tears.

Treatment of rotator cuff tears

Literature on the outcome of treatment of partial rotator cuff tears is sparse. However the treatment of partial tears is similar to the treatment for complete rotator cuff tears (12).

Conservative treatment

About one third of rotator cuff tears are symptomatic and the other two third are asymptomatic. Ninety nine percent of the patients with symptomatic tears present with pain (13).The severity of pain has no correlation with the severity of the rotator cuff tear (14). Inflammation of the shoulder seems to be the main cause of pain in patients with rotator cuff tears. The inflammation and pain often settles with NSAIDs and intra-articular steroid injections.
The reported successful outcome of conservative treatment of complete tears of the rotator cuff varies widely from 33% (15) to 82% (16). Itoi and Tabata (16) reported the outcome of conservative treatment of complete rotator cuff tears in 62 shoulders (54 patients) at an average follow up of 3.4 years. They found good to excellent outcome, as measured by the modified Wolfgang criteria, in 82% of the patients. The outcome was good in patients who had ‘well preserved motion and strength’ at the beginning of treatment. Unsatisfactory outcome was seen in patients who had limited motion and muscle weakness at the beginning of treatment.
Minagawa et al (17) reported good or excellent results in 75% of 100 patients (102 shoulders) with complete tears of the rotator cuff who were treated conservative. The average follow up was 32 (12 to 48 months). Fifty percent had no pain and 40% had mild pain which did not require medication.
The Moon shoulder group did a multicentre prospective cohort study (18)  to assess the effectiveness of physical therapy for treatment of atraumatic complete tears of the rotator cuff. The patients were initially instructed by physical therapist and then they continued their therapy at home. Supervised therapy was need only once a week. The patient were given an option for surgery if they were not better at any time during the treatment. If the patient opted for surgery than the conservative treatment was considered a failure. At 6 weeks follow up the success rate of conservative treatment was 91%, at 12 weeks it was 85%, at 1 year 79% and at 2 years the success rate of conservative treatment was 74%. They found that if the patient does not opt for surgery in the first 6 weeks he is unlikely to opt for surgery after that.
Kijima et al (19) published the 13 years follow up results of a prospective cohort of 103 shoulders with rotator cuff tear who were treated conservatively. The found that 90% of the patients had no or very little pain and 70% had no limitation of activities of daily living.
Lee et al (20 ) compared the effectiveness of conservative treatment with arthroscopic  repair for rotator cuff tears. They found that at one year follow up, conservative treatment is as effective as surgical repair in patients, with medium sized rotator cuff tears, who were  50 years of age or older.
From these studies it is clear that conservative treatment for complete tears of the rotator cuff is successful in 74% to 82% of the patients. Kuhn in 2009 (21) did a systematic review of the literature to evaluate the effectiveness of exercise in the treatment rotator cuff impingement. They found that ‘exercise has statistically and clinically significant effects on pain reduction and improving function, but not on range of motion or strength’. According to the review ‘manual therapy augments the effects of exercise, yet supervised exercise was not different than home exercise programs’.
Despite these successes of conservative treatment, a cochrane review (22) of manual therapy and exercise for treatment of rotator cuff disease paints a very different picture. The authors of the review included 60 trials in the study. There was only one trial comparing manual therapy and exercise with placebo. There was no clinically important difference between the two groups. They also found that there was low quality evidence to show that the’ effects of manual therapy and exercise may be similar to those of glucocorticoid injection and arthroscopic subacromial decompression’. The incidence of adverse events were more frequent with manual therapy and exercise as compared with placebo but the adverse events but mild in nature.
There is also no good quality evidence to support the use of electrotherapy modalities  for the treatment of rotator cuff disease (23).

Surgical treatment

Anecdotal evidence suggests that there is misplaced belief that all ligament and tendon tears must be repaired. Despite the popularity of such beliefs, literature on indications for repair of rotator cuff tears is sparse.
 The indications for surgery for atraumatic rotator cuff tears have not yet been defined. Even the MOON shoulder group were unable, by consensus, to develop standard indications for surgery (14).
 In 2007 Oh et al (24) reviewed the literature to investigate factors that influence decision making when patients present with full thickness rotator cuff tears. They looked at how ‘demographic variables, duration of symptoms, timing of surgery, physical examination findings, and size of tear’ affect outcome and indications for surgery. They found that muscle weakness and substantial functional disability maybe an indication for early surgical intervention. There was no clear link between demographic variables and treatment outcome. Although there have been reports of poor outcome of surgery in older patients, the authors did not find evidence to support such a belief. There is evidence in literature to suggest that the outcome of treatment is poorer in patients who have pending worker’s compensation claims. The authors concluded by saying that further research is needed to clearly define the indications for surgery in patients with complete tears of the rotator cuff.
Baysal et al (25) reported good outcome of repair of rotator cuff tears using a mini open technique. They reported improved shoulder function and health-related quality of life upto 5 years postoperatively. Ninety six percent of the patients were satisfied or very satisfied with the outcome of the surgery and 78% returned to their previous job within a year. The size of the tear and age of the patient did not affect the range of motion or the health-related quality of life.
There is apparently no difference in the outcome when comparing arthroscopic versus open repairs (26) and arthroscopic versus mini open repairs (27). Although good outcome of surgery is reported by many authors, the high complication rate and high rerupture rates are often not highlighted. Mansat et al (28) reported a 38% complication rate in patients undergoing rotator cuff repair. Sixteen percent of the patients had major complications affected the functional outcome. Some of the complications reported included frozen shoulder, deep infection and dislocations.
Brislin et al (29) reported a 10.6% incidence of complications after arthroscopic rotator cuff repair. Some of the complications reported included, ‘shoulder stiffness, failure of healing, infection, reflex sympathetic dystrophy, deep venous thrombosis, and death’. The complications are apparently similar to that with open repair of the rotator cuff.
Re-rupture rates of between 13% to 68% have been reported after repair of the rotator cuff  but interestingly patients suffering re-ruptures have significant improvement in pain and function (30). The re-rupture rates as detected by MRI vary between 20% to 39% and in patients with large tears the re-rupture rates at 2 years vary between 41% to 94% (29). The outcome of revision surgery after re-rupture is not as good as for primary repair. Djurasovic et al (31) reported excellent to satisfactory results in 69% of patients who had revision surgery. Despite structural failure of rotator cuff tears and complications, repairs of the rotator cuff do reduce pain, significantly improve function and strength (32).
Coghlan et al (33) did a systematic review of the literature for the Cochrane group, to review the effectiveness and safety of surgery for rotator cuff disease. They included 14 RCTs (829 participants) which compared surgical intervention to placebo, to no treatment or to any other treatment. They concluded that all the trials were ‘susceptible to bias’ and that they ‘cannot draw firm conclusions about the effectiveness or safety of surgery for rotator cuff disease’. There found that there was "Silver" level evidence from three trials ‘that there are no significant differences in outcome between open or arthroscopic subacromial decompression and active non-operative treatment for impingement’.
More recently there have been two prospective randomized studies which compared surgical and conservative treatments for rotator cuff tears and they found that there was no clinically significant difference in outcome between the two groups (34 and 35).
Chalmers et al [36] in 2018 carried out a systematic review of the intermediate to long-term (minimum 5-year) outcome of operative rotator cuff repair and no repair of rotator cuff injuries. The review included 29 studies with 1,583 patients. They compared patient-based outcomes, future surgical intervention, future tear progression or recurrence, and tear size in the two groups.
They found that there was no differences between rotator cuff repair and no repair with respect to strength and range of motion. Rotator cuff repair did not improve outcomes as measured with the Constant score even after adjustment for age, sex, duration of follow-up, and tear size. The rotator cuff repair appears to protect the shoulder from the need for future operative intervention but it does not, however, decrease the likelihood of sustaining a future tear. Rotator cuff repair may not alter natural history rotator cuff pathology.
Recurrent tears after rotator cuff repair are common and the treatment for these recurrent tears vary between conservative and open or arthroscopic revisions. Lädermann et al (37) in 2015 carried out systematic review of the management of failed rotator cuff repairs. They found that the mid to long-term outcome of patients treated conservatively was acceptable and a
persistent defect is usually well-tolerated and only occasionally will this defect require subsequent surgery. Hence conservative treatment can be recommended in most patients especially in patients with posterosuperior involvement and poor preoperative range of motion. In young patients with a repairable lesion, a 3 tendon tear, and in those with involvement of the subscapularis revision surgery may be necessary.

Conclusions

The rotator cuff comprising of the supraspinatus, infraspinatus, teres minor and the subscapularis muscles produce abduction and rotatory forces, stabilize the humeral head in the glenoid, stabilize the capsule and also provide muscular balance around the glenohumeral joint. The rotator cuff frequently tears due impingement syndrome (75%), shoulder instability(15) or trauma (10%). Non traumatic tears are asymptomatic in two third of the individuals and only symptomatic in about a third of the individuals. The prevalence of rotator cuff tears increase with age. The severity of symptoms does not correlate with severity of the cuff tear.
Rotator cuff tears which present with pain are commonly treated conservatively with NSAIDs, intra-articular steroids and physical therapy. Conservative treatment is successful in about 70% to 90% of the individuals. The evidence in support of physical therapy as a mode of treatment remains weak.
 Though there are many reports of successful treatment of symptomatic rotator cuff tears with surgery, the evidence to support the use of surgery for rotator cuff tears remains weak. Surgery can be associated high complication rate with some of them serious. Following surgery rerupture rate can be high.
 Recent studies show that the outcome of conservative treatment of cuff tears is clinically not significantly different from that of surgical treatment. Since the outcome of conservative and surgical treatment is similar, then logically conservative treatment should be the treatment of choice for symptomatic rotator cuff tears.

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