Neurological complications of lumbar epidural anesthesia and analgesia.

      Neurological complications of lumbar epidural anesthesia and analgesia.

                                     Dr KS Dhillon

Introduction

Epidural anesthesia and analgesia (EAA) are widely used in clinical practice for surgery and postoperative analgesia. Epidural anesthesia and analgesia reduces or eliminates perioperative physiological stress responses to surgery and this inturn decreases surgical complications and improve clinical outcomes[1-3].

Studies have shown a significant reduction in perioperative cardiac morbidity, pulmonary infections, deep vein thrombosis, pulmonary embolism, ileus, acute renal failure, blood loss and need for transfusion. The length of hospital stay and the 30 day mortality is also reduced with EAA [4]. EAA is also believed to preserve postoperative immune function by attenuating the stress response of surgery. Studies have shown significant reductions in the incidence of postoperative infections in patients treated with EAA [5,6].

EAA is generally regarded as safe and effective but EAA can be associated with serious complications. Though the complications are rare they can sometimes be devastating.

Neurological complications of lumbar epidural anesthesia and analgesia.

Studies show that the frequency of severe, permanent neurological complications related to epidural catheterisation is low at about  0.1–1/10,000 procedures [7-12]. Epidural anesthesia can be associated with radiculopathy, cauda equina syndrome and myelopathy leading to permanent neurological disability [13]. Compression of the spinal cord or nerve roots can occur from extradural abscesses or haematomas. Arterial and venous infarction of the spinal cord and nerve root trauma can occur during catheter placement. Chemically induced arachnoiditis by the drugs used for the epidural has also been implicated in causing permanent neurological disability [14-18].

Lumbar epidural injections in patients with pre-existing spinal stenosis can  precipitate severe and widespread lumbosacral polyradiculopathy [13,19].

Neurotoxicity from local anesthetics is a well known phenomenon and is related to the type and concentration of anesthetic and its systemic absorption. Intrathecal lignocaine at high doses has been associated with neurologic side effects [20,21].

Epidural catheters can inadvertently penetrate the dural space, cause damage to neurovascular structures and also can lead to infection. The incidence of accidental dural puncture during needle insertion is about 0.16–1.3% and the incidence of postdural headache in these patients is about 16–86% [22-25].

Nerve root irritation by the catheter and intrathecal injection of local anesthesia can produce transient neurologic symptoms (TNS) such as  sharp radicular back pain and paresthesias [26].

Risk factors for TNS include the use of lidocaine as the local anesthetic, lithotomy position, obesity, and performance of the procedure in the outpatient department [27].The TNS usually usually resolve once the catheter is removed. Epidural abscesses and meningitis following epidural and spinal anesthesia is rare [28].

Risk factors for meningitis include dural puncture, non sterile technique, prolonged indwelling catheter and septicemia [29,30]. Paraplegia, the most serious complication of epidural anesthesia can be caused by an epidural hematoma which forms during catheter placement or removal. The secondary cause of this complication is the concomitant pre-, intra-, or postoperative administration of drugs that affect blood coagulation (anticoagulants) [31].  Spinal abscesses and anterior spinal artery syndrome are also known to cause paraplegia. Epidural haematoma formation is a rare complication with an incidence of less than 1 in 150,000 [32].

Injury to the spinal vasculature during catheter placement has been described and the incidence is about 3–12%. Despite injury to spinal vasculature symptomatic epidural hematomas are rare [33,34]. Early recognition of symptomatic epidural haematomas and decompressive laminectomy within 8 hours have been shown to improve clinical outcomes [35].

Epidural abscess and meningitis

The reported incidence of epidural abscess after epidural catheterisation is about 1 : 1000 and for meningitis is about 1 : 50 000 [36].

There are several ways in which bacteria may enter the epidural space. One of the sources of infection is needle or catheter contamination and lack of barrier precautions, such as the use of chlorhexidine 0.5% in 70% alcohol for skin disinfection [37-39]. Contamination of the needle or catheter by oropharyngeal and nasal flora of the anesthetist has been proven by cultures obtained from the epidural abscess and from the anaesthetist [40,41].

Epidural solution can be a source of epidural infection despite the use of bacterial filter. There is some evidence to suggest that frequent syringe changes could be associated with a higher rate of epidural infection  [42-44]. The 500-ml bags of epidural infusion fluid has not been found to be  associated with epidural abscesses or meningitis [45].

Infection of the insertion site of the catheter with migration of the bacteria along the catheter tract is a common mechanism of epidural infections. A haematogenous source of epidural infection after epidural catheterisation is uncommon [46-48].

There are several predisposing factors for epidural infection. Patients who are immunocompromised are more likely to develop infection [49-51]. Difficulty in insertion of epidural catheter is also a known risk factor for infection. Difficulty in insertion is associated with the formation of asymptomatic epidural haematoma [49,52,53] or subcutaneous haematoma which can act as a nidus for infection [54]. Epidural analgesia of more then 3 days is associated with higher infection rates [51].

Staphylococcus is the most common organism cultured from epidural abscesses [49,50,51,55]. Methicillin resistant staphylococcus has also been cultured in some of these abscesses.

Patients with an epidural abscess usually presents with midline back pain and fever about 5 days after epidural insertion [49-51]. If untreated neurological deficit with paraplegia usually develops within a week [49]. The prognosis for recovery is poor once paraplegia develops [49,56].
Meningitis usually results from dural puncture and patients present with headache and fever, with some patients developing neck rigidity [50]. In some patients who developed meningitis there were no reports of dural puncture [45].

In patients suspected to have an epidural abscess, an MRI scan is the investigation of choice [58]. Sometimes back pain is ascribed to musculoskeletal pain and a delay in diagnosis can result. Therefore a high index of suspicion is necessary to prevent delays in diagnosis.

A lumbar puncture with csf microscopy is necessary for the diagnosis of meningitis [45].
Epidural abscesses are treated with a combination of early surgical decompression and prolonged antibiotic therapy [53]. Patients with minimal or no neurological deficit can be managed with antibiotics alone [55].

Epidural haematoma

Coagulopathies predispose patients to epidural haematomas following epidural catheter insertion [56]. Hence the timing of anticoagulant administration is important in reducing the risk of epidural haematomas [59,60]. The newer recommendations, recommend that low molecular weight heparin administration for prevention of deep vein thrombosis (DVT) be delayed for 24 h in case of a bloody tap [60]. Another risk factor for the development of epidural haematoma is difficulty in identifying the epidural space [61].

Difficulty in identification of the epidural space can often be encountered in patients who are obese. Other risk factors include advanced age, female gender and bony spinal pathology [50].
The usual clinical presentation of an epidural haematoma is radicular back pain with rapidly progressive neurological (motor and sensory) deficit and sphincter dysfunction [56]. The symptoms usually develop within 24 hours of either epidural insertion or removal, but sometimes the onset of symptoms may be delayed [50].

An MRI scan of the spine is the investigation of choice in patients suspected of having an epidural haematoma. Often the neurological deficit is attributed to the epidural infusion and the back pain to a musculoskeletal cause and this leads to a delay in diagnosis [62]. Early diagnosis is of paramount importance since a favourable outcome is dependent on early spinal decompression within 8 hours of the onset of symptoms [56]. Neurological outcome depends on the extent of the neurological deficit, the size of the haematoma and the time between haematoma formation and surgical decompression [56].

Leg strength monitoring is essential in assessment of spinal cord health
in patients receiving epidural analgesia [41]. The Bromage scale is commonly used to measure motor block [63].

Grade Criteria                                                                  Degree of block

I          Free movement of legs and feet                            Nil (0%)

II        Just able to flex knees with free movement
           of feet                                                                   Partial (33%)

III       Unable to flex knees, but with free movement     Almost complete
          of feet                                                                    (66%)

IV        Unable to move legs and feet                             Complete (100%)   


Table 1. Bromage scale

The perfect analgesic technique would provide complete pain relief with no motor block. Leg weakness during epidural analgesia must be treated with suspicion until proven to be reversible. [42].  Patients who have significant weakness of the leg should have epidural infusion stopped and if no motor recovery occurs within 4 hours, an urgent MRI scan should be performed [45] .

Direct penetration of the spinal cord during epidural catheterisation and subsequent injection of fluid into the substance of the cord, leading to localised hydromyelia has been proposed as one of the mechanisms for severe neurological complications resulting from epidural anaesthesia and analgesia [64]. Examination shows segmental levels of motor and sensory impairment which corresponds to the level of spinal cord injury. MRI shows tubular, clearly demarcated lesions which are hyperintense on T2 weighted images and hypointense on T1.

Air bubbles in the cord has been identified in patients who have become paraplegic after epidural anesthesia [65].

Local anesthetic drugs have been found to be potentially neurotoxic in experimental studies [66]. Polyethylene glycol found in methylprednisolone acetate is known to cause necrosis of neuronal tissue [67]. Injection of these neurotoxic drugs into the cord can cause damage to the cord.
Intravenous high dose methylprednisolone may be of value in these patients with cord damage.

Arachnoiditis and subarachnoid cyst

Arachnoiditis as a complication of epidural anesthesia has been reported.  Torres et al [68] reported 7 cases where patients developed arachnoiditis following epidural anesthesia. Subarachnoid cysts developed in all patients and in 5 cord cavitation developed. MRI was found to be useful in the detection of the arachnoiditis and the intramedullary cysts, as well as to monitor the extent of the lesion and progression of the lesions. In one case a tethered cord was present and in another there was spinal cord atrophy.

Possible etiology of these complications include scars from meningeal inflammation which induce ischemia leading to cavitation. CSF circulation blockade can also cause dilation of the central spinal canal which results in ischemia from compression followed by myelomalacia and cavitation.
Although progressive inflammation of the arachnoid due to trauma, infection, or hydrocortisone has been reported since the early 1970s,  coexistence of extensive syringomyelia (ES) and a giant anterior arachnoid spinal cyst (AASC) had not been reported until 2012. In 2012 Hirai et al [69] reported a case of adhesive arachnoiditis with extensive syringomyelia and a giant arachnoid cyst after spinal and epidural anesthesia. They had a  29 years old woman who presented with sudden anuresis 5 months after spinal/epidural anesthesia for cesarean section. She subsequently developed paraplegia with numbness below the chest. An MRI showed a giant AASC compressing the spinal cord at T1-T6 and there was an adhesive lesion at T7. Slight improvement in motor function occurred after
posterior laminectomy at T6-T7 and adhesiolysis at T7. Three years after the surgery motor function deteriorated further and posterior laminectomy at T5-T6 with insertion of a cyst-peritoneal shunt into the AASC was carried out.

Nogués et al [70] published a report where 3 women who had epidural anesthesia for gynecological surgery developed spinal arachnoiditis which led to subarachnoid cysts and cord cavitation. They found that MRI is useful for making a diagnosis and monitoring the extent and progress of the lesion.

Conclusion

Epidural anesthesia and analgesia (EAA) are extensively used in clinical practice for surgery and postoperative analgesia. Epidural anesthesia and analgesia reduces surgical complications and improve clinical outcomes.

Studies show a significant reduction in perioperative cardiac morbidity, pulmonary infections, deep vein thrombosis, pulmonary embolism, ileus, acute renal failure, blood loss and need for transfusion with EAA. The length of hospital stay and the 30 day mortality is also reduced with EAA. The incidence of postoperative infections is significantly reduced in patients treated with EAA. Though EAA is generally regarded as safe and effective, serious devastating neurological complications can occur following EAA.

Epidural abscess, meningitis, epidural haematomas, hydromyelia, cord cavitation, arachnoiditis and arachnoid spinal cysts are known complications of EAA which can produce serious and sometimes permanent neurological deficit including paraplegia. Prompt diagnosis and early aggressive treatment is essential for a good clinical outcome.

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Anterior dislocation of the shoulder

                  Anterior dislocation of the shoulder     

                                          Dr KS Dhillon

Anatomy of the shoulder Joint

Glenohumeral joint 

The shoulder joint also known as the glenohumeral joint is formed by the articulation of the head of the humerus with the glenoid cavity of the scapula. The head of the humerus is much larger than the glenoid fossa (only 25–30% of the humeral head is covered by the glenoid surface). To reduce the disproportion in the size of the surfaces, the glenoid fossa is deepened by a fibrocartilage rim, called the glenoid labrum. The articular margins are covered with hyaline cartilage. The joint capsule extends from the anatomical neck of the humerus to the rim of the glenoid. The shoulder capsule is large, loose and redundant to allow greater mobility at the joint. The inner surface of the capsule is lined with synovial membrane.

Ligaments of the joint

At the anterior portion of the capsule is reinforced by the glenohumeral ligaments including the superior, medial and inferior glenohumeral ligaments. These ligaments provide anterior stability to the shoulder. Superior stability is provided by the coracohumeral ligament which extends from the base of the coracoid process to the greater tubercle of the humerus. A transverse humeral ligament which spans the distance between the two tubercles of the humerus holds the tendon of the long head of the biceps in the intertubercular groove. Another ligament, the coracoacromial ligament runs between the acromion and coracoid process of the scapula and it forms the coracoacromial arch.  This ligament lies superior to the shoulder joint and prevents superior displacement of the humeral head.

Muscles and tendons

The clinically important contractile structures of the shoulder joint are the supraspinatus, infraspinatus, subscapularis and, of less importance, the teres minor. They form the rotator cuff and these muscles arise from the scapula and attach to the tuberosities of the humerus. Superficially these muscles are separate but in the deeper region they merge with each other as well as with the capsule and the tendon of the long head of the biceps.

Movements of the shoulder joint

The glenohumeral joint is the most mobile joint in the human body. The movements at the shoulder joint include abduction, adduction, flexion, extension, internal and external rotation.

Abduction

The supraspinatus muscle and the deltoid muscle are responsible for this movement. The muscle plays an important role in initiation of abduction. When this tendon is completely torn the patient can no longer lift the arm actively and must make a swinging movement of the whole body in order
to start the movement. Once the arm has moved through 30° of abduction, the deltoid takes over to complete abduction. During full elevation of the limb to 180 degrees only 90 degrees takes place at the glenohumeral joint and the rest occurs at the scapulothoracic region. The deltoid is the prime mover and the supraspinatus is the accessory muscle.

Adduction

Adduction of the arm is performed by the teres minor and major, pectoralis major, latissimus dorsi and the long head of the triceps brachii. The pectoralis major and latissimus dorsi are the prime movers while the
teres major and long head of triceps brachii are the accessory muscles.

Flexion

Flexion of the arm is carried out by the pectoralis major, deltoid, coracobrachialis and the biceps brachii. The pectoralis major and deltoid are the prime movers while coracobrachialis and the biceps brachii are the accessory muscles.

Extension

Extension of the arm is performed by the deltoid, teres major, latissimus dorsi and the long head of the biceps brachii. The deltoid is the prime mover and the teres major, latissimus dorsi and the long head of biceps brachii are the accessory muscles.

Medial Rotation

Medial or internal rotation is carried out by the subscapularis, pectoralis major, deltoid, latissimus dorsi and teres major. The subscapularis is the prime mover and the pectoralis major, deltoid, latissimus dorsi and teres major are the accessory muscles.

Lateral Rotation

Lateral or external rotation is performed by the infraspinatus, teres major and the deltoid. The infraspinatus is the prime mover and teres major and deltoid are the accessory muscles.

Dislocation of the Shoulder Joint

Dislocations of the shoulder are described by the position of the humeral head in relation to the glenoid fossa after a dislocation has occurred. Anterior dislocations are the most common with prevalence rate of 95%. The prevalence rate for posterior is 4% and for inferior dislocations is 1%. The presence of the coraco-acromial arch superiorly prevents superior dislocation of the femoral head.

Anterior shoulder dislocation

Anterior shoulder dislocation has a bimodal age distribution. The first and the largest group are young adult men who sustained high-energy injuries to the shoulder. The second peak occurs in patients over the age of 60 years. This older group of patients are those who have a dislocation from a much lower level of violence. In the older group of patients early reduction and early mobilization to prevent joint stiffness is the management priority.

In the younger group of patients the risk of recurrent dislocation strongly correlates with the severity of initial injury the age of the patient. The risk is particularly high in the 16–30 year old group.
In anterior dislocation of the shoulder, violent external rotation in abduction  causes the humeral head to lever out of the glenoid socket. This is sometimes associated with avulsion of anterior bony and soft tissue structures. When a portion of the anterior labrum is detached from the glenoid and the anterior glenoid periosteum is torn, the lesion is referred to as a Bankart's lesion. Magnetic resonance arthrography shows that the prevalence of these lesions after first time anterior dislocation is about 23% [1]. When the posterior part of the humeral head exits the joint, the head collides with the anterior rim of the glenoid, creating a bony indentation at the back of the humeral head. This bony defect are known as a Hill Sachs lesions, the prevalence of which is as high as 71% after an anterior dislocation [1].

Clinical presentation

Following an anterior dislocation of the shoulder, the patient presents with severe pain and the arm is held in an abducted and externally rotated position. The normal counter of the shoulder is lost and a defect is palpable anterior, lateral and inferior to the acromion. The humeral head is usually palpable anteriorly in the region of the coracoid process.

Bony injury

Carrying out X rays of the shoulder including an AP and axillary view is mandatory for the diagnose an anterior dislocation of the shoulder as well as to exclude associated fractures. Hill Sachs lesions can be seen in 54% of the patients[2]. In older patients an associated greater tuberosity fracture is quite common.

Vascular injury

Stayner et al [3] reported two cases of axillary artery injury in 95 cases of shoulder dislocation which amounts to a prevalence rate of about 2%. This injury occurs more frequently in the elderly whose arteries are artherosclerotic.

In patients with axillary artery injury the pathognomonic triad consisting of anterior shoulder dislocation, absent or diminished distal pulses and protruding axillary haematoma is present [4]. Since the upper limb has an excellent collateral circulation, the radial pulse can be palpable and good capillary filling present despite the presence of major arterial injury [4]. The presence of reduced pulse pressure and coolness in the hand warrants an urgent angiography. Upper limb ischemia may be due to arterial spasm which does not need surgery. An angiogram can distinguish transient spasm from a tear which requires surgery.

Nerve injury

Nerve injuries are common after anterior dislocation of the shoulder. Visser et al [5] carried out a prospective clinical and electrophysiological examination in 77 patients with anterior dislocation of the shoulder. They found axonal loss in 48% of the patients. The axillary nerve was most frequently involved (42%). Function of the shoulder was significantly impaired in patients with axillary and suprascapular nerves injuries. They found that increasing age and presence of haematoma are unfavourable prognostic factors.

Te Slaa et al [6] reported a 21% incidence of nerve injuries in patients with primary glenohumeral dislocation. Atef et al [7] reported a much lower incidence of nerve injury in patients with anterior dislocation of the shoulder. They report isolated axillary nerve injury in 3.33% of the patients and combined nerve injuries in 12.5% of the patients. Most of the nerve injuries recover fully without intervention. There are some more severe injuries which do not recovery.
Brachial plexus injury can be associated with shoulder dislocation. These injuries are usually postganglionic, infraclavicular and in continuity. Hence the prognosis for recovery is excellent [8,9].

Rotator cuff tears

As with nerve injuries, the incidence of rotator cuff tears also vary widely. The incidence of rotator cuff tears in patients with anterior dislocation varies between 14%–65%.  The incidence of this complication increases with increasing age [10].

Treatment of anterior dislocation shoulder

There is no consensus in the literature on the best technique for reduction of a dislocated shoulder. Success of any technique would depend on the surgeon's familiarity and analgesia used [11].
The easiest way to reduce the dislocation is by manipulation under general anesthesia. However most of the dislocation are usually reduced in the emergency department.

Chitgopkar and Khan  [12] were able to reduce 10 out of 12 anterior dislocation of the shoulder by using the original Kocher's technique without any sedation or anesthesia. The original Kocher’s method is apparently gentle and  painless. The patient initiates the movements, the surgeon just guides the patient through the manoeuvre. In 2 patients the humeral head had to be guided proximally and laterally using an index finger in the axilla. The patients can  go home immediately after the procedure.

Uglow [13] carried out a prospective randomised trial involving 45 patients with an anterior dislocation of the shoulder who were randomised into one of two treatment groups and manipulation was performed using Kocher's  method. In one group entonox was used and in the other intravenous sedation was used. A successful reduction was achieved in 80.9% of Entonox group and in 100% of intravenous sedation group.

Kosnik et al [14] carried out a prospective, randomized, non blinded clinical trial involving 49 patients who had anterior dislocation of the shoulder to evaluate whether local intraarticular lidocaine injection is as effective as effective as intravenous analgesia/sedation in facilitating shoulder dislocation. They found that intravenous analgesia/sedation had a higher success rate (100%) as compared to intraarticular lidocaine injection (86%), the differences, however, were not statistically significant (P = 0.16).

Wakai et al [15] carried out a Cochrane systematic review to compare the clinical efficacy and safety of intra-articular lignocaine (IAL) and intravenous analgesia (with or without sedation) (IVAS) for reduction of acute anterior shoulder dislocation. They found no significant difference between IAL and IVAS with regard to the success rate of reduction, pain during reduction, post-reduction pain relief. IAL is apparently less expensive and associated with fewer adverse effects and the recovery time is also shorter with IAL.

Taylor et al [16] carried out a multicenter, randomized, clinical trial to compare propofol and midazolam/fentanyl for reduction of anterior shoulder dislocations using the modified Kocher's maneuver. They found propofol to be as effective as midazolam/fentanyl for reduction of anterior shoulder dislocation. They cautioned that the advantage of shorter wakening times with propofol should be weighed against possible adverse events such as respiratory depression and vomiting.
Gleeson et al [17] carried out a study to compare the use of supra-scapular nerve block with intra-articular lignocaine for reduction of anterior dislocation of the shoulder. They found that intra-articular lidocaine injection was easier to perform and also was more effective for pain relief.
Gleeson et al [18] in another study compared the effectiveness of Entonox to intra-articular local anaesthetic for shoulder reduction and found that Entonox was more effective then intraarticular local anesthetic for pain relief.

Management post reduction

Traditionally after the shoulder has been relocated it is immobilised in an arm sling in a position of internal rotation for about 3 weeks. Some have, however, challenged this tradition.

Hoveliu et al [19] carried out a study involving 245 patients with 247 primary anterior dislocations of the shoulder who were followed up for 10 years after the dislocation had been reduced. Post reduction patients were assigned to one of three treatment groups: immobilization with arm sling which was discontinued once the patient was comfortable, immobilization with arm tied to torso with a bandage for 3 to 4 weeks or immobilization for various duration. They found that the type and duration of the initial treatment had no effect on the shoulder dislocation recurrence rates.

Itoi et al [20] carried out a magnetic resonance imaging (MRI) study in patients who had had a dislocation of the shoulder to assess the degree of coaptation of the Bankart lesion with the arm in internal rotation and  external rotation. They found that the degree of separation of the torn labrum was significantly less in external rotation than in internal rotation. This would mean that immobilisation in a sling with the arm in an external rotation position would reduce the incidence of recurrent dislocation.

In 2003, Itoi et al [21] published the outcome of a prospective study involving 40 patients with anterior dislocation, where post reduction, 20 patients had conventional immobilization in internal rotation and the other 20 patients had their arm immobilized in external rotation. They found that the dislocation recurrence rate was 0% in the external rotation group and the recurrence rate was 30% in the internal rotation group at a mean follow up of 15.5 months. The difference in recurrence rate was even greater in patients less than 30 years of age, with a recurrence rate of 45% in the internal rotation group and 0% in the external rotation group.

Whelan et al [22] carried out a meta-analysis of randomized controlled trials to assess the effectiveness of internal rotation versus external rotation immobilization on the rate of recurrence after primary anterior dislocation of the shoulder. They found that immobilization in external rotation was not significantly more effective in reducing the recurrence rate.

Hanchard et al [23] carried out a Chochrane systematic review to assess the effects of conservative treatment after closed reduction of anterior dislocation of the shoulder. Their review showed that evidence from randomised controlled trials existed only for a single approach i.e immobilisation in external rotation versus immobilisation in internal rotation. The evidence available was insufficient to demonstrate whether immobilisation in external rotation was any better then immobilisation in internal rotation.

Paterson et al [24] carried out a systematic review and meta-analysis of the literature to determine the optimum duration and position of immobilization of the shoulder after anterior dislocation to prevent recurrent dislocation.

They found that there is no benefit of conventional sling immobilization for
longer than one week for the treatment of primary anterior shoulder dislocation in younger patients. They also found that an age of less than
thirty years at the time of injury was significantly predictive of recurrence.

Recurrent dislocation

The risk factors for recurrent dislocation of the shoulder are young age, participation in contact sporting activities, presence of Hill-Sachs or osseous Bankart lesion, ipsilateral rotator cuff or deltoid muscle insufficiency, and underlying ligamentous laxity.

Hoveliu et al [19] carried out a study involving 245 patients with 247 primary anterior dislocations of the shoulder who were followed up for 10 years after the dislocation had been reduced.They found a recurrence rate of 48%. The recurrence rate in the 12 to 22 year age group was 34%, 28% in the 23 to 29 year age group and 9% in the 30 to 40 year age group. Twenty three percent of the patients with recurrent dislocation needed surgery.

Twenty-two per cent of the shoulders that had at least two recurrences in the first two to five years stabilized spontaneously without operative intervention at ten years follow up.
Simonet and Cofield [25] carried out a study involving 116 patients with anterior dislocation of the shoulder. Their study showed a 33% recurrence rate. The incidence of recurrent dislocation was 66% in those less then 20 years old and 40% in those between 20 and 40 years of age. There were no recurrent dislocations in those who were older than 40 years of age. The recurrence rate was 82% in young athletes and 30% in non athletes of the same age.

Some patients do not experience repeat dislocation but may suffer from recurrent subluxation of the joint which limits their overall activity levels.

Treatment of recurrent anterior dislocation

There are numerous surgical procedures available for treatment of recurrent shoulder dislocation. These include open Bankart, arthroscopic Bankart, Latarjet, Bristow, and older techniques, such as Putti-Platt and Magnuson-Stack. Arthroscopic and open Bankart operations to repair the labral tear are usually performed on patients with glenoid labral tears. In patients with glenoid bone loss the Latarjet or Bristow procedure is usually carried out. In both the Latarjet and Bristow procedures the coracoid process is osteotomized and transferred with the conjoined tendons through a horizontal split in the subscapularis tendon and fixed to the scapular neck near the glenoid with a screw. The Putti-Platt and Magnuson-Stack procedures are nonanatomic historical procedures where shortening and tightening of the subscapularis tendon is carried out.

Glazebrook et al [26] carried out a systematic review of the literature to assess the quantity and quality of scientific evidence available for surgical procedures used in the treatment of anterior shoulder dislocations.

They allocated a grade of recommendation for each surgical procedure based on the quality of the studies. Grade A recommendations were based  on consistent level 1 studies, grade B recommendations on level 2 or 3  studies and grade C recommendations were based on level 4 or 5 evidence. Grade I articles have insufficient evidence to recommend a treatment.

They found evidence for grade A recommendation for four surgical procedures. The arthroscopic Bankart, open Bankart, and Latarjet procedures were given grade A for recommendation and the Putti-Platt procedure was given a grade A against recommendation.

Six surgical procedures were given a grade B recommendation. Arthroscopic remplissage, remplissage, and arthroscopic lavage were given grade B in favour of recommendation. Bristow, open capsular shift and thermal capsulorrhaphy were given a grade B against recommendation.

There were 11 grade C surgical procedures with 7 against and 4 in favour of recommendation. The 7 against recommendation procedures included Magnuson-Stack, Bankart and remplissage, Boytchev, Eden-Hybbinette, arthroscopic staple capsulorrhaphy, stapling operation, and Caspari technique. The 4 in favour of grade C recommendation included J graft, arthroscopic Latarjet, Latarjet-Patte, and iliac crest bone graft.

The Putti-Platt procedure is not recommended any more. It is an old procedure and the literature on the subject is outdated. Limitation of range of motion is common and the redislocation rates are very high. The most extensively studied procedure is the Bankart’s procedure. Most published studies report superior outcome with open Bankart as compared to arthroscopic Bankart, with a lower recurrence rate and no significant difference in complication rate [27,28]. There are also studies which suggest that the arthroscopic Bankart and open Bankart show comparable postoperative results in terms of stability, range of motion, and complications [29,30]. There are other level 1 studies which suggest that both surgical procedures are adequate but arthroscopic Bankart offers better postoperative results with greater stability, fewer complications, and better range of motion [31]. The Latarjet procedure has been reported to give promising results with low recurrence rates, high graft union rates, satisfactory clinical outcome scores, and few complications [32-34].

Historically, open repair remains the gold standard treatment against which other treatment options are compared. The open repair is associated with a 95% reduction in re-dislocation[2].

Long-term prognosis

Hovelius et al [2] reported an 8.7% incidence of moderate to severe osteoarthritis in patients who had their first dislocation when they were below the age of 40 years.

Ogawa et al [35] reported a higher incidence of osteoarthritis in patients with traumatic anterior shoulder instability who were due for surgery. Plain X-rays showed osteoarthritis in 11.3% of cases whereas CT scans showed osteoarthritis in 31.2% of the cases.
It would appear that osteoarthritis is not an uncommon complication of  anterior dislocation of the shoulder.

Conclusion

Anterior dislocation of the shoulder is the most common dislocation in the human body. There is a bimodal age distribution in patients with anterior dislocation. The first and the largest group are young adult men who sustained high-energy injuries to the shoulder. The second peak occurs in patients over the age of 60 where the level of violence is low. In the younger age group the incidence of recurrent dislocation can be very high. Anterior dislocation of the shoulder can be associated with rotator cuff tears, vascular injury, nerve injury and bony injury.

There is no consensus in the literature on the best technique for reduction of a dislocated shoulder. Several techniques have been described and there is no one technique which is more superior to another. There is also no consensus in the literature as to the method and duration of shoulder  immobilization after the dislocation has been reduced.

The incidence of recurrent dislocation varies between 9% to 82%. It is the highest (82%) in young athletes. The incidence of recurrent dislocation reduces as we age.

There are a large number of procedures which can be used to treat recurrent dislocation. The most commonly used techniques include Bankart’s repair and the Latarjet procedure. Not all patients with recurrent dislocation would require surgery. Some stabilize spontaneously with time.

Osteoarthritis is not an uncommon long term complication of shoulder dislocation.

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