Carpal Tunnel Syndrome--Revisited

                   Carpal Tunnel Syndrome--Revisited

                       

                                                    DR KS Dhillon

Chronic carpal tunnel syndrome was first described by James Jackson Putnam in 1880. Other medical luminaries have shed more light on the subject in the subsequent years including Paget, Marie, Ramsay Hunt, Phalen and Osler [1]. Carpal tunnel syndrome is probably the most common peripheral compression neuropathy and is defined by compression of the median nerve at wrist level.

Anatomy of the carpal tunnel

The carpal tunnel is a rigid non expendable osteofibrous tunnel situated on the front of the wrist. Anteriorly it is bound by the flexor retinaculum and posteriorly lies the carpal sulcus. Medially lies the hamate hook,triquetral bone and pisiform bone, and laterally lies the scaphoid bone, trapezoid bone and tendon of the flexor carpi radialis (FCR) muscle. The sulus is formed by the capsule, and the anterior radiocarpal ligaments which cover the proximal row of carpal bones.

Besides the median nerve there are four superficial and four deep flexor tendons of the fingers in the tunnel. On the radial side there is the long flexor of the thumb.
The location of the median nerve in relation to other structures changes as it traverses the tunnel. At the entrance the nerve lies deep to the palmaris or between the palmaris and the flexor carpi radialis.
In neutral wrist position, it usually lies anterior to the superficial flexor of the index or the middle finger with the long thumb flexor on the radial side.

More distally in the palm the nerve divides into six branches: the thenar motor branch; three specific palmar digital nerves to the radial and ulnar side of the thumb and radial side of the index finger and two common palmar digital nerves of the second and third web spaces.

Anatomical variations of the carpal tunnel structures

There are several anatomical variations in and around the carpal tunnel which affect the nerves, tendons and arteries. These variation are responsible for variation in the clinical presentation and may lead to intraoperative complication during surgery.

Some of the variations include the following [2]:

A. Nerve anomalies

• High bifurcation of median nerve (1% to 3.3% of patients undergoing surgery). The radial median branch may have its own tunnel.
• Aberrant origin of motor branch of median nerve. There can be 5 variation. Most often the branch arises distal to the carpal tunnel which is the norm. In about a third of the cases it arises within the canal and in about a quarter of the cases the branch pierces the transverse carpal ligament and courses to the thenar muscles. Rarely the branch arises on the ulna and anterior side of the median nerve and crosses anterior to the median nerve on its way to the thenar area. In some patients it enters the palm superficial to the transverse carpal ligament.
• Variations in path of palmar cutaneous branch of median nerve. Normally the palmar cutaneous branch arises proximal to the carpal tunnel and enters the palm superficial to the carpal ligament. There are two other variations, one where it pierces the carpal ligament on its way to the palm and second where it courses on the ulna side of the median nerve.
• Anomalous course of ulnar nerve. The ulnar nerve usually enters the palm through the Guyon’s canal, a depression between the pisiform bone and the hook of the hamate. Occasionally the ulnar nerve has been found to traverse the carpal tunnel and the patients can present with carpal tunnel syndrome associated with symptoms of ulnar nerve compression.
• Median nerve (MN) and ulnar nerve (UN) anomalous anastomoses. There are four commonly described anomalous connections between the MN and UN. The most common anomalous anastomosis is between the connection from MN to UN in the forearm which is known as the Martin Gruber anastomosis (MGA). The interneural connections from UN to the MN is known as the Marinacci anastomosis. When there is an interneural connection between common digital nerves of UN and MN nerves in the palm of the hand it is called the Barrettini anastomosis.  An anomalous connection from the UN to the MN in the hand is known as the Riche–Cannieu anastomosis where there is a crossover in the palm, between the deep branch of the UN and the recurrent branch of the MN. 

 B.Tendon anomalies

• Conjoint FPL and FDP II (Linburg-Comstock syndrome). In some individuals there is an anomalous tendinous connection between the FPL and the FDP tendons to the index and sometimes the middle finger. In such circumstance the individual is unable to flex the DIP joint of the thumb without concomitant flexion of the dip joint of the the finger. This can lead to tendonitis which can mimic symptoms of carpal tunnel syndrome.

C. Vascular anomalies

• Persistent median artery. A persistent median artery is sometimes seen traversing the carpal tunnel. It can significantly contribute to vascularity of the hand. Sometimes it is present with bifurcated median nerve. The presence of this artery does not produce any symptoms but may get severed during a carpal tunnel release.
• Superficial ulnar artery.The ulnar artery sometimes takes a superficial course within the forearm and travels superficial to the muscles but deep to the antebrachial fascia where it risks being severed during an extended carpal tunnel release.

D.Muscle anomalies

• Palmaris longus. The palmaris longus muscle is one of the most variable muscles in the human body. Two variations of palmaris longus are related to the anatomy of the carpal tunnel. In some individuals the tendon of the palmaris longus traverses the carpal tunnel and inserts into the palmar fascia distally. In other individuals the muscle belly of the palmaris longus may be situated in the carpal tunnel.
• Index lumbrical. The lumbrical muscle to the index finger may arise  proximally on the FDS within the carpal tunnel and can cause carpal tunnel compression syndrome.
• Flexor digitorum superficialis indicis. In some individuals the FDS muscle may be present in the carpal tunnel along the index finger tendon and cause carpal tunnel syndrome.

Etiology of carpal tunnel syndrome(CTS)

In most of the patients there is no known cause for the CTS and it is than referred to as idiopathic CTS. In some case it is due to factors around the canal or within the canal and than it is referred to as secondary CTS.

Idiopathic carpal tunnel syndrome

Idiopathic CTS is usually seen in females (65–80%), between the ages of 40 and 60 years. In about 50–60% of the patients it is bilateral [3]. Anthropometric factors such as size of the canal, sex, age and genetic factors are the most important predisposing factors. Repetitive manual
activities, exposure to vibrations, cold temperatures, obesity and smoking have also been implicated as predisposing factors for carpal tunnel syndrome [4,5].

Secondary carpal tunnel syndrome [6]

A. Abnormalities of the wall of the carpal tunnel

Conditions that alter the condition of the walls of the canal can cause compression of the median nerve. These include:

• Carpal bone subluxation or dislocation
• Distal radius fractures and implants used for fixation of fractures can reduce the carpal tunnel space
• Wrist joint arthritis, degenerative and inflammatory
• Acromegaly.   

 B. Abnormalities of content of the tunnel [6]

• Tenosynovial hypertrophy 
• Inflammatory tenosynovitis due to rheumatism, lupus and infection
• Metabolic tenosynovitis due to diabetes mellitus, amyloidosis, gout and chondrocalcinosis
• Abnormalities of fluid distribution due to pregnancy, hypothyroidism and chronic kidney failure  
• Intratunnel tumors such as lipoma, synovial cyst, synovial sarcoma, schwannoma, neurofibroma or lipofibroma
• Hematoma due to hemophilia, anticoagulant accident or trauma
• Obesity

Repetitive flexion and extension of the wrist, flexion of the fingers and forearm supination has been implicated in an increase of pressure within the canal which can predispose an individual to CTS. An increase in prevalence of CTS has been seen in individuals who work more than 20 hours per week on the computer [7]. Exposure to vibration causes injury of the myelin and axons leading to ultrastructural microcirculatory compression problems and intraneural edema which can sometimes produce CTS [8] .

Diagnosis of carpal tunnel syndrome

The typical symptoms are nocturnal acroparesthesias comprising of tingling, numbness, swelling or hypoesthesia, with or without pain reaching at least two of the first three fingers and the palm. Night pain is the most  sensitive symptom predictor (96%) in patients with CTS [9].

The Durkan's compression test [10] which is performed by compression of the median nerve in the carpal tunnel for as long as thirty seconds has a 89% sensitivity [9].

Semmes-Weinstein Monofilament Testing and Phalen's maneuver has a 83% sensitivity and hand diagram scores have a 76% [9] to 80% sensitivity [11]. The Tinel's sign has a 71% sensitivity. Some have found that the Tinel’s sign has no diagnostic value in patients with CTS [12].

Electroneuromyography (ENMG) examination

An ENMG examination is used to study the sensory and motor nerve conduction of the median nerve through the wrist. Analysis of the amplitude and duration of the sensory and motor responses is done.
Bilateral ulna and median nerve studies are carried out.

In CTS focal demyelination occurs, hence nerve conduction study (NCS) is usually more valuable than needle electromyography (EMG) study. Meticulous attention has to be paid to ‘electrode placement, distance measurements, stimulation intensity, skin temperature, and many others factors are important to prevent misdiagnosis of CTS’ [13]. The skin temperature should be maintained at about 32C for NCS.

Sensory Conduction Studies

In patients with mild or early CTS there is a mild sensory nerve conduction slowing across the carpal tunnel. A delayed or prolonged peak latency of the median sensory nerve action potential (SNAP) is typically seen.

The peak latency is usually used, instead of onset latency, for detecting CTS because of difficulty in identifying the onset of the SNAP in the presence of a large stimulus artifact [13]. With progress of the CTS the  sensory peak latency gets further delayed with the amplitude becoming smaller. In severe CTS, there usually is no recordable SNAP despite signal averaging and enhancement.
The most commonly used protocol (antidromic technique), for median nerve sensory conduction study, is the one where stimulation is applied at the wrist and median SNAPs are recorded at the thumb, the index, the middle and ring fingers [13].

Motor Conduction Studies

Motor nerve conduction of the median nerve is usually measured by obtaining recordings over the abductor pollicis brevis (APB) muscle. A delay of the distal motor latency (DML) usually supports the diagnosis of CTS. A mild prolongation of the median DML, however does not suggest focal demyelination of the median nerve [13].

Sensitivity of electroneuromyography (ENMG) examination

ENMG examination may be positive in 0–46% of asymptomatic subjects and negative in 16–24% of patients with a clinical diagnosis of CTS [14,15,16,17].

The sensitivity of motor distal latency in the diagnosis of CTS is about 54% [18]. ENMG examination does not provide extra evidence in diagnosis of CTS when the clinical diagnosis is obvious [19]. Anatomical variations such as the Martin–Gruber and Riche–Cannieu types can affect the interpretation of the ENMG examination.

Treatment of carpal tunnel syndrome

Conservative Treatment

In patients with medical causes for CTS, the underlying medical condition is treated such as ‘diuretics for fluid retention, thyroid supplementation for hypothyroidism, insulin for diabetes, and immune modulating agents for rheumatoid arthritis’ [13].

Nighttime splinting of the wrist in neutral position has been found to be useful in reducing nocturnal symptoms. Oral anti-inflammatory drugs do reduce synovitis and provide relief in some patients. The use of pyridoxine (vitamin B6) for treatment of CTS has been abandoned since it has been found to be of no value in the treatment of patients with CTS.

Though prospective studies [20,21] have shown effectiveness of the use of local steroid injections in the treatment of CTS, a Cochrane database  systematic review by Marshall et al [22] showed that local corticosteroid injection for carpal tunnel syndrome provides greater clinical improvement in symptoms for only one month after injection compared to placebo. They found that there was no significant symptom relief beyond one month. The clinical outcome was no better with steroid injection as compared to NSAIDs and splinting after 8 weeks. Steroid injections should probably not be used as an option in the treatment of CTS.

Patient education is useful in patients with work related CTS where they are advised to avoid activities which aggravate the symptoms and to do simple hand and wrist exercises. Evaluation of the workstation and redesigning the workstation along with ergonomic tool modification is often useful in work related CTS [9].

Surgical treatment for carpal tunnel syndrome

In patients with acute CTS due to trauma from fractures and dislocations around the wrist and due to bleeding, immediate surgical intervention to relieve the pressure on the nerve is usually mandatory.
In patients with subacute and chronic CTS where conservative treatment has not helped and in patients with moderate to severe symptoms, surgical release of the carpal tunnel is known to be effective [23].

Carpal tunnel release or carpal tunnel decompression surgery involves the division of the flexor retinaculum/transverse carpal ligament by open or endoscopic surgery. The existing literature shows that the long term outcome of open carpal tunnel release (OCTR) is generally good. There are wide variations in success and failure rates reported in literature, partly due to variations in patient selection and variations in the definition of success and failure. Clinical success has been reported in 75–90 % of the patients and recurrence rates of between 4–57 % have been reported [24].
The long term outcome with endoscopic surgery is indistinguishable from that of open carpal release. There are a small number of studies which suggest that there is a higher incidence of recurrence with techniques other than OCTR [24].

There is only one study by Pensy et al [25] which asserts that the functional outcome of surgical treatment is not significantly different from that of conservative treatment on long-term follow-up, though the improvement in symptom scores was greater in surgical patients.
Literature review shows that ENMG examination, the only objective data available, tends to suggest that there are long-term, persistent ENMG abnormalities in a high percentage of patients who had treatment for CTS [24].

Scholten et al [26] carried out systematic review, for the Cochrane Database, to compare the efficacy of the various surgical techniques in relieving symptoms and promoting return to work or activities of daily living in patients with CTS. They found no strong evidence to support the need for replacement of the standard open carpal tunnel release by other existing alternative surgical procedures for the treatment of carpal tunnel syndrome. They found that none of the existing alternatives including endoscopic release offered significantly better relief from symptoms in the short- or long-term.

Neurolysis

In the past many surgeons used to do internal neurolysis as an adjunctive
procedure in operative treatment of carpal tunnel syndrome. It is now, however, no longer recommended, since several clinical studies have now failed to demonstrate any benefit from neurolysis [27,28].

Release of Guyon’s canal

Patients with carpal tunnel symptoms sometimes have paresthesias in the little finger. Some surgeons used to recommend simultaneous release of Guyon’s canal. This, however, is no longer recommended because there is evidence now which shows that the dimensions of Guyon’s canal enlarges with carpal tunnel release [29].

References

1. Sternbach G. The carpal tunnel syndrome. J Emerg Med. 1999 May-Jun;17(3):519-23.
2. Mitchell R, Chesney A, Seal S, McKnight L, Thoma A. Anatomical variations of the carpal tunnel structures. Can J Plast Surg. 2009;17(1):e 3–7.
3. Michelsen H, Posner MA. Medical history of carpal tunnel syndrome. Hand Clin. 2002; 18(2):257–68.
4. Falkiner S, Myers S. When exactly can carpal tunnel syndrome be considered work-related? ANZ J Surg. 2002;72(3):204–9.
5. Lozano-Calderon S, Anthony S, Ring D. The quality and strength of evidence for etiology: example of carpal tunnel syndrome. J Hand Surg Am. 2008;33(4):525–38.
6. Chammas M, Boretto J, Burmann LM, Ramos RM, dos Santos Neto FC, Silva JB. Carpal tunnel syndrome – Part I (anatomy, physiology, etiology and diagnosis. ). Rev Bras Ortop. 2014; 49(5): 429–36.
7. Andersen JH, Fallentin N, Thomsen JF, Mikkelsen S. Risk factors for neck and upper extremity disorders among computers users and the effect of interventions: an overview of systematic reviews. PLoS ONE. 2011;6(5):e19691.
8. Mackinnon SE. Pathophysiology of nerve compression. Hand Clin. 2002; 18(2):231–41.
9. Szabo RM, Slater RR Jr, Farver TB, Stanton DB, Sharman WK. The value of diagnostic testing in carpal tunnel syndrome. J Hand Surg Am. 1999 Jul;24(4):704-14.
10. Durkan J. A new diagnostic test for carpal tunnel syndrome. J Bone Joint Surg Am. 1991;73:535-538.
11. Katz JN, Stirrat CR. A self-administered hand diagram for the diagnosis of carpal tunnel syndrome. J Hand Surg Am. 1990 Mar;15(2):360-3.
12. Kuschner SH, Ebramzadeh E, Johnson D, Brien WW, Sherman R. Tinel's sign and Phalen's test in carpal tunnel syndrome. Orthopedics. 1992 Nov;15(11):1297-302.
13. Wang L. Electrodiagnosis of Carpal Tunnel Syndrome. Phys Med Rehabil Clin N Am  2013;24: 67–77.
14. Jablecki CK, Andary MT, So YT, Wilkins DE, Williams FH. Literature review of the usefulness of nerve conduction studies and electromyography for the evaluation of patients with carpal tunnel syndrome. AAEM Quality Assurance Committee Muscle Nerve. 1993;16(12):1392–414.
15. Witt JC, Hentz JG, Stevens JC. Carpal tunnel syndrome with normal nerve conduction studies. Muscle Nerve. 2004;29(4):515–22.
16. Atroshi I, Gummesson C, Johnsson R, Ornstein E. Diagnostic properties of nerve conduction tests in population-based carpal tunnel syndrome. BMC Musculoskelet Disord. 2003;4:9.
17. Redmond MD, Rivner MH. False positive electrodiagnostic tests in carpal tunnel syndrome. Muscle Nerve. 1988;11(5):511–8.
18. Seror P. Sonography and electrodiagnosis in carpal tunnel syndrome diagnosis, an analysis of the literature. Eur J Radiol. 2008;67(1):146–52.
19. Graham B. The value added by electrodiagnostic testing in the diagnosis of carpal tunnel syndrome. J Bone Joint Surg Am. 2008; 90(12):2587–93.
20. Girlanda P, Venuto C, Mangiapane R, et al. Local steroid treatment in idiopathic carpal tunnel syndrome: short and long–term efficacy. J Neurol 1993;240:187–90.
21. Dammers JW, Vermeulen M. Injections with methylprednisolone proximal to the carpal tunnel: randomized double blind trial. BMJ 1999;319:884–6.
22. Marshall  SC, Tardif  G, Ashworth  NL. Local corticosteroid injection for carpal tunnel syndrome. Cochrane Database of Systematic Reviews 2007, Issue 2. Art. No.: CD001554. DOI: 10.1002/14651858.CD001554.pub2.
23. Bland JD. Carpal tunnel syndrome. BMJ. 2007;335 (7615): 343–346.  doi: 10.1136/bmj. 39282.623553.AD.
24. Louie D, Earp B, Blazar P. Long-term outcomes of carpal tunnel release: a critical review of the literature. Hand (New York, NY). 2012; 7(3):242-246. 
25. Pensy RA, Burke FD, Bradley MJ, Dubin NH, Wilgis EF. A 6-year outcome of patients who cancelled carpal tunnel surgery. J Hand Surg Eur Vol. 2011 Oct;36(8):642-7.
26. Scholten RJ, Mink van der Molen A, Uitdehaag BM, Bouter LM, de Vet HC. Surgical treatment options for carpal tunnel syndrome. Cochrane Database Syst Rev. 2007 Oct 17;(4):CD003905. 
27. Lowry WE Jr, Follender AB: Interfascicular neurolysis in the severe carpal tunnel syndrome: A prospective, randomized, double-blind, controlled study. Clin Orthop 1988;227:251-254.
28. Mackinnon SE, McCabe S, Murray JF, et al: Internal neurolysis fails to improve the results of primary carpal tunnel decompression. J Hand Surg [Am] 1991;16:211-218.
29. Richman JA, Gelberman RH, Rydevik BL, et al: Carpal tunnel syndrome: Morphologic changes after release of the transverse carpal ligament. J Hand Surg [Am] 1989;14: 852-857.

Impingement syndromes of the ankle

                 Impingement syndromes of the ankle

                                         DR KS DHILLON

Introduction

A painful mechanical limitation of ankle movements caused by an osseous or soft-tissue abnormality is known as ankle impingement. Patients often present with chronic ankle pain of varying etiology. Ankle impingement syndrome, though rare, is one of the cause of chronic ankle pain [1]. 
There is no official classification for ankle impingement syndromes. The syndromes are described, depending on their location, as anterior, anterolateral, anteromedial, posterior, posteromedial, hindfoot extra-articular, and syndesmotic impingements [2].

Anterior ankle impingement

Anterior ankle impingement is usually seen in athletes such as football and soccer players, ballet dancers, gymnasts, and runners who are involved in activities that require repetitive ankle dorsiflexion.

Osseous anterior bony impingement occurs from osteophyte impingement of the anterior rim of the tibia and the talar sulcus. Repetitive forces are believed to lead to impaction-related microtrauma of the anterior chondral margin of the tibiotalar joint which over time leads to osteophyte formation from attempted repair with fibrosis and fibrocartilage proliferation [3]. The contact between opposing bone or the entrapment of soft tissues between the bones may produce pain. These osteophytes are located inside the joint and away from the capsular attachment.

Others believe that repetitive traction injury to the anterior joint capsule due to hyper plantar flexion leads to the formation of these osteophytes [4,5].

Although the anterior tibiotalar osteophytes are often referred to as “kissing osteophytes”, they do not actually overlap and abut. CT scan studies show that talar spurs usually lie medial to the midline of the talar dome and tibial spurs are usually located lateral to the midline [6]. There is a trough in the articular talar dome which usually “accepts” the tibial osteophyte during ankle dorsiflexion. Some refer to it as a “tram-track lesion” [7], and others refer to it as a “divot sign” [8]. Other studies have shown a high rate of  talar cartilage lesions (80.7 %) which correspond to the distal tibial osteophytes and also the presences of multiple loose bodies in these patients [9].

There is a triangular soft tissue mass which is composed of adipose and synovial tissues in the joint space in front of the ankle joint. This soft tissue mass can be compressed when dorsiflexion of the ankle exceeds 15° [10].

The presence of anterior osteophytes may further limit the space available for this soft tissue mass and cause entrapment, leading to chronic inflammation and synovitis[2]. Some of the other causes of anterior ankle pain include post-traumatic fibrous bands [11], thickened anterior tibiofibular ligaments [12,13], and synovial plica [14]. Although various types of lesions have been described, their exact etiology is not well understood.

Asymptomatic anterior tibiotalar spurs on lateral view x rays of the ankle may be present in 45% to 59% of professional athletes[15].

The clinical symptoms of anterior ankle impingement include pain and a subjective feeling of blocking on dorsiflexion. On examination, the dorsiflexion movements are painful and limited and occasionally a soft tissue swelling may be palpable [16]. The symptoms are usually due to degeneration of the joint rather than the spurs.

Usually plain x rays of the ankle are sufficient to detect the spurs. MRI of the ankle may show synovitis, effusion and bone marrow edema. However MRI is usually not necessary for anterior ankle impingement.

The mainstay of treatment is conservative with NSAIDs and rehabilitative  physiotherapy(16-18), but in resistant cases surgery appears to show  long-term benefit (16). Usually arthroscopic debridement of the spurs and soft tissues with a washout is carried out [16]. The prognosis depends on the severity of the degeneration of the joint [16]. A hundred percent to 77% excellent function after surgery at 6.5 years has been reported [16]. The evidence however remains weak.

Anterolateral Impingement

The anterolateral recess of the ankle is formed by the tibia posteromedially and the fibula laterally. Anteriorly and laterally lies the tibiotalar joint capsule, the anterior tibiofibular, anterior talofibular and the calcaneofibular ligaments.

Supination injuries, recurrent lateral ligament sprains and chronic lateral ligament instability can predispose a patient to anterolateral soft tissue impingement of the ankle. Chronic inflammation and hypertrophic changes of the synovial tissue occurs between the talus and the tibia [19]. Thickened synovial and scar tissue get entrapped in the anterolateral gutter  leading to pain and swelling after activity as well as limitation of ankle dorsiflexion and supination [20,21].

Rarely hypertrophy of the inferior portion of the anterior tibiofibular ligament and occasionally osseous spurs can cause anterolateral impingement [22,23].

Symptoms of anterolateral impingement include focal anterolateral pain
which is aggravated by supination or pronation of the foot. Examination usually shows anterolateral tenderness, swelling, pain on single-leg squatting, and pain on ankle dorsiflexion and eversion [22,23].
X rays of the ankle are usually of not much value in the diagnosis of anterolateral impingement. The role of MRI in the diagnosis is also controversial. MR arthrography has been able to detect abnormalities such irregular or nodular contour of the anterolateral soft tissues which correlated with anterolateral scarring or synovitis in the anterolateral recess of the ankle. However such finding are also seen in asymptomatic individuals [24]. Chondral defects, spurs, and laxity or rupture of the anterior talofibular ligament may also be seen in patients with anterolateral impingement.

Rehabilitative physiotherapy and NSAIDs usually relieve symptoms in most patients. Those who do not respond to conservative treatment are often treated with arthroscopic debridement of the joint. The published reports on the outcome of arthroscopic surgery for treatment of anterolateral impingement are level 4 retrospective studies[25 ] or involve small numbers of cases [26,27].

Anteromedial Impingement

The exact cause of anteromedial impingement is not know but it is believed to be caused by inversion or eversion injury leading to tearing of the anteromedial capsule and the tibiotalar ligament. Repeated microtrauma leads to synovitis and capsular thickening. Bony injury and cartilage damage may lead to spur formation with synovial and capsular thickening [1].

The clinical features include chronic anteromedial pain which is aggravated by ankle dorsiflexion. Examination shows anteromedial tenderness and limitation of ankle dorsiflexion and foot inversion [28,29].

MR arthrographic would show focal capsular and synovial thickening in
tibiotalar joint anterior to the tibiotalar ligament [29]. Bone spurs with anteromedial synovitis may also be seen.

There are no studies which document the effectiveness of conservative treatment in the treatment of anteromedial impingement syndrome. Neither has the outcome of steroid injections been well studied. Some authors recommend surgery (arthroscopic debridement) as the first line of treatment. Level 4 evidence (case series) shows excellent functional outcomes at a minimum of 2 years follow up [30].

Posterior Impingement

Posterior impingement is also known as the os trigonum syndrome and posterior tibiotalar compression syndrome [31]. Posterior impingement results from compression of soft tissues between posterior process of the calcaneus and the posterior tibia on plantar flexion of the ankle. The posterior talus contributes significantly to posterior impingement due to the presences of os trigonum or Stieda’s process in some patients.

Besides bony structures at the back of the ankle there are several ligamentous structures at the back of the ankle which include, the posteroinferior talofibular ligament, the transverse tibiofibular ligament, the tibial slip or the posterior intermalleolar ligament, and the posterior talofibular ligament [32].
Patients with posterior impingement syndrome usually present with pain at the back of the ankle on activities which involve extreme plantar flexion such as soccer, football, ballet and running downhill [31].

An acute plantar hyperflexion injury and chronic repetitive microtrauma are believed to lead to posterior impingement syndrome. Hypertrophy of the posterior tissue with compression leads to chronic pain at the back of the ankle. There may be damage to regional ligaments and tendon. Flexor hallucis tenosynovitis is often present in many patients [33].

Presence of a Stieda's process or an os trigonum is not diagnostic of impingement because these bony abnormalities are also present in asymptomatic individuals. A MRI can be useful in detecting bone marrow oedema within the talus, calcaneus or an os trigonum. It will also show synovitis and thickening of the posterior ligaments [32].

The first line of treatment is conservative, as with other impingement syndromes, and surgery can be carried out if conservative treatment fails. Surgery consists of arthroscopic debridement.

Posteromedial impingement 

The posteromedial joint space is bound by the medial malleolus and posterior tibiotalar ligament (PTTL) anteriorly and talar dome and posterior process of the talus laterally. Posteriorly it is bound by the posteromedial joint capsule, neurovascular bundle and flexor hallucis longus tendon.
The precipitating injury usually is plantar flexion, inversion and internal rotation trauma which leads to PTTL damage and synovitis ensues affecting the tibialis posterior, flexor hallucis longus and/or the flexor digitorum longus tendons [34].

It is one of the least common ankle impingement syndromes. Patients usually present with pain over the posteromedial aspect of the ankle with movements of the ankle.

Plain radiographs are of not much value in diagnosis of posteromedial impingement. A MRI would show abnormal pathology in the PTTL consisting of thickening and loss of the normal fibrillar pattern. Fluid collection, synovitis and irregular soft tissue may be seen in the posteromedial recess [35].
Treatment is usually conservatively, but surgical treatment may be contemplated in patients not responding to conservative treatment.

Extra-articular lateral hindfoot impingement syndrome (ELHIS)

The extra-articular lateral hindfoot impingement syndrome is not caused by trauma but results from a pathological tibialis posterior tendon which produces a flatfoot and hindfoot valgus deformity [36]. Commonly  impingement is seen between the lateral talus and calcaneus (talocalcaneal impingement) and also between the calcaneus and fibula (subfibular impingement) [36].

 Accessory anterolateral talar facet is also known to cause ELHIS. The accessory anterolateral facet can cause pathological impingement of the neck of the calcaneus in patient with flatfoot/hindfoot valgus deformity [37].

Repeated talocalcaneal and fibulocalcaneal impingement will lead to arthrosis at the contact points. Patients usually present with pain in the region of the sinus tarsi. Conventional radiography is useful in the diagnosis. Oblique x rays and valgus stress views are useful. Coronal oblique CT scans will also show the site of impingement. An MRI is useful for evaluating the degree of tibialis posterior tendon pathology. The MRI will also show cystic changes and bone marrow oedema within the lateral talus in addition to soft-tissue thickening between the fibula and the calcaneus and also show fibula tip oedema [36].

Initially treatment includes physical therapy, a period of immobilization, orthotics, and non-steroidal anti-inflammatory medications. In the event of failure of conservative treatment surgical intervention with preservation of the subtalar joint is carried out. Resection of the accessory anterolateral talar facet is carried out with correction of the hindfoot deformity. In patients with advanced arthritis subtalar arthrodesis is carried out [37].

Conclusion

Ankle impingement syndromes are an uncommon cause of chronic ankle pain. There is no classification for ankle impingement syndromes but they are named according to the location of the impingement around the ankle both anterior and posterior to the ankle. There are soft tissue and bony abnormalities involved in the pathology of impingement syndromes.
Symptoms with anterior impingement occur with terminal dorsiflexion and with posterior impingement on hyper plantar flexion.
The mainstay of diagnosis is history and physical examination. Imaging helps to confirm the diagnosis in most cases. Initially treatment is conservative, failing which open or arthroscopic surgery is carried out for treatment of impingement syndromes.
Although most authors claim good to excellent outcomes with arthroscopic surgery, the level of evidence however is low (level 4). Currently there is a lack of good quality outcome studies (level 1) in the literature for the treatment of impingement syndromes of the ankle.

References

1.  Robinson P, White LM. Soft-Tissue and Osseous Impingement Syndromes of the Ankle: Role of Imaging in Diagnosis and Management. RadioGraphics 2002; 22:1457–1471.
2. Lavery KP, McHale KJ, Rossy WH, Theodore G. Ankle impingement. Journal of Orthopaedic Surgery and Research. 2016;11(1):97. doi:10.1186/s13018-016-0430-x.
3. McMurray TP. Footballer’s ankle. J Bone Joint Surg Br. 1950; 32B(1): 68–9.
4. Tol JL, Verheyen CP, Dijk CN. Arthroscopic treatment of anterior impingement in the ankle. J Bone Joint Surg Br. 2001;83(1):9–13.
5. Dijk CN, Tol JL, Verheyen CC. A prospective study of prognostic factors concerning the outcome of arthroscopic surgery for anterior ankle impingement. Am J Sports Med. 1997;25(6):737–45. 
6. Berberian WS, et al. Morphology of tibiotalar osteophytes in anterior ankle impingement. Foot Ankle Int. 2001;22(4):313–7.
7. Kim SH, Ha KI, Ahn JH. Tram track lesion of the talar dome. Arthroscopy. 1999;15(2):203–6. doi: 10.1053/ar.1999.v15.015020. 
8. Raikin SM, Cooke PH. Divot sign: a new observation in anterior impingement of the ankle. Foot Ankle Int. 1999;20(8):532–3. doi: 10.1177/107110079902000812.
9. Moon JS, et al. Cartilage lesions in anterior bony impingement of the ankle. Arthroscopy. 2010;26(7):984–9.
10. Tol JL, van Dijk CN. Etiology of the anterior ankle impingement syndrome: a descriptive anatomical study. Foot Ankle Int. 2004;25(6): 382–6.
11. Valkering KP, et al. “Web impingement” of the ankle: a case report. Knee Surg Sports Traumatol Arthrosc. 2013;21(6):1289–92.
12. Bassett FH, et al. Talar impingement by the anteroinferior tibiofibular ligament. A cause of chronic pain in the ankle after inversion sprain. J Bone Joint Surg Am. 1990;72(1):55–9.
13. Akseki D, et al. The distal fascicle of the anterior inferior tibio-fibular ligament as a cause of anterolateral ankle impingement: results of arthroscopic resection. Acta Orthop Scand. 1999;70(5): 478–82.
14. Rosenbaum AJ, et al. Ankle impingement caused by an intra-articular plica: a report of 2 cases. Foot Ankle Spec. 2016;9(1): 79–82.
15. Cheng JC, Ferkel RD. The role of arthroscopy in ankle and subtalar degenerative joint disease. Clin Orthop 1998; 349:65–72.
16. Tol JL, Verheyen CPPM, Van Dijk CN. Arthroscopic treatment of anterior impingement in the ankle: a prospective study with a five-to-eight year follow-up. J Bone Joint Surg Br 2001; 83: 9–13.
17. Martin DF, Baker CL, Curl WW, Andrews JR, Robie DB, Haas AF. Operative ankle arthroscopy: long-term followup. Am J Sports Med 1989; 17: 6–23.
18. Ogilvie-Harris DJ, Mahomed N, Demaziere A. Anterior impingement of the ankle treated by arthroscopic removal of bony spurs. J Bone Joint Surg Br 1993; 75:437–440.
19. Wolin I. Internal derangement of the talofibular component of the ankle. Surg Gynecol Obstet. 1950;91(2):193–200.
20. Ferkel RD, Karzel RP, Pizzo W, et al. Arthroscopic treatment of anterolateral impingement of the ankle. Am J Sports Med. 1991;19(5):440–6.
21. Cutsuries AM. Arthroscopic arthroplasty of the ankle joint. Clin Podiatr Med Surg. 1994;11(3):449–67.
22. Lui HL, Raskin A, Osti L, et al. Arthroscopic treatment of anterolateral ankle impingement. Arthroscopy 1994; 10:215–218.
23. Lui HL, Nuccion SL, Finerman G. Diagnosis of anterolateral ankle impingement: comparison between MRI and clinical examination. Am J Sports Med 1997; 25:389–393.
24. Robinson P, White LM, Salonen DC, Daniels TR, Ogilvie-Harris D. Anterolateral impingement of the ankle: MR arthrographic assessment of the anterolateral recess. Radiology 2001; 221:186–190.
25. Urgüden M1, Söyüncü Y, Ozdemir H, Sekban H, Akyildiz FF, Aydin AT. Arthroscopic treatment of anterolateral soft tissue impingement of the ankle: evaluation of factors affecting outcome. Arthroscopy. 2005 Mar;21(3):317-22.
26. Moustafa El-Sayed AM. Arthroscopic treatment of anterolateral impingement of the ankle. J Foot Ankle Surg. 2010 May-Jun; 49(3): 219-23.
27. Koczy B, Pyda M, Stołtny T, Mielnik M, Pająk J, Hermanson J, Pasek J, Widuchowski J. Arthroscopy for anterolateral soft tissue impingement of the ankle joint. Ortop Traumatol Rehabil. 2009 Jul-Aug;11(4):339-45.
28. Mosier-La Clair SM, Monroe MT, Manoli A. Medial impingement syndrome of the anterior tibiotalar fascicle of the deltoid ligament on the talus. Foot Ankle Int 2000; 21:385–391.
29. Robinson P, White LM, Salonen D, Ogilvie-Harris D. Anteromedial impingement of the ankle: MR arthrography assessment of the anteromedial recess. AJR Am J Roentgenol 2002; 178:601–604.
30. Murawski CD, Kennedy JG. Anteromedial impingement in the ankle joint: outcomes following arthroscopy. Am J Sports Med. 2010 Oct;38(10):2017-24. 
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33. Hedrick MR, McBryde AM. Posterior ankle impingement. Foot Ankle Int 1994; 15: 2–8.
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37. Martus JE, Femino JE, Caird MS, Kuhns LR, Craig CL, Farley FA. Accessory anterolateral talar facet as an etiology of painful talocalcaneal impingement in the rigid flatfoot: a new diagnosis. Iowa Orthop J 2008; 28: 1–8.

Radiofrequency denervation for chronic axial back pain.

Radiofrequency denervation for chronic axial back pain.

                                   DR KS Dhillon 

What is radiofrequency denervation?

Radiofrequency denervation, radiofrequency neurotomy, and radiofrequency ablation are often used interchangeably. They all refer to a procedure that destroys the functionality of the nerve using radiofrequency energy.

There are primarily two types of radiofrequency ablation used in the treatment of axial back pain:

• A medial branch neurotomy which is used for treatment of spinal facet joint pain. 
• A lateral branch neurotomy which is used to treat pain from  the sacroiliac joints.

The facet joint is innervated by the medial branch of the dorsal rami from 2 adjacent spinal segments. The nerve supply of the SI joint is a contentious issue. The information is sparse and variable. For radiofrequency ablation (RFA) of the SI joint, the medial branch of L4, dorsal rami of L5, and lateral branches S1 and S2, are targeted.

The procedure involves setting up of an IV line, sedation, skin preparation, local anesthetic injection, fluoroscopic guided insertion of radiofrequency needle to the required site and passage of a small current to confirm the targeted nerve, numbing of the target nerve with local anesthetic, passage of radiofrequency waves to heat the tip of the needle and creating a heat lesion to denervate the nerve.

Efficacy of radiofrequency denervation for facet joint pain

Radiofrequency facet joint denervation procedures for the treatment of chronic low back pain have been in common use for more than 3 decades.  The efficacy of the procedure, however, has never been conclusively established.

van Wijk et al [1], in 2005, published the outcome of a multicenter, randomized, double-blind, sham treatment controlled trial to determine the efficacy of radiofrequency facet joint denervation. They had a total of 81 patients who were randomized to undergo radiofrequency facet joint denervation or sham treatment. A twice weekly recording of VAS, physical activity and analgesic intake determined the primary outcome. The secondary outcome measure included the global perceived effect (complete relief, >50% relief, no effect, pain increase), and the SF-36 Quality of Life Questionnaire.They carried out the first evaluation 3 months after treatment. There were no dropouts in the first evaluation. They found that the combined outcome measure showed no differences between radio- frequency facet joint denervation and the sham group.The VAS improved in both groups. Only the global perceived effect improved after radiofrequency facet joint denervation. They concluded that only in selected patients, radiofrequency facet joint denervation appears to be more effective than sham treatment but overall there is no benefits from radiofrequency denervation in treatment of chronic low back pain.

Gofeld et al [2] did a prospective clinical audit for quality in 209 patients with chronic back pain who were treated with radiofrequency denervation of the lumbar zygapophysial joints. The patients were screened and those with multiple unrelated painful sites, significant psychopathology and those with unrealistic goals were not included in the study. One hundred and seventy four patients (83%) completed the study. The patients were asked to complete a questionnaire at 6 weeks, 6 months and at 12, and 24 months following the procedure. They were asked to estimate the total perceived pain reduction on a scale of 0% to 100%. Improvement of pain more than 80% was graded as excellent and between 80% to 50% was graded as good. Pain improvement less than  50% and pain relief lasting less than 6 months were considered as treatment failure.

In 55 (31.6%) patients, the treatment was a failure. One hundred and nineteen (68.4%) patients had good to excellent pain relief at 6 months follow up. Of the 119 patients, 81 (96.4%) reported pain relief for 6–12 months, 36 (42.8%) for 12–24 months, and 2 (2.4%) for more than 24 months. The median pain relief among all eligible 174 patient was 9 month.

All the 119 patients with a positive response were able to increase their physical activities, and 99 (83.2%) of these also decreased their consumption of analgesics (not stopped use of analgesics) and in 20 other patients with a positive response the use of analgesics remained unchanged.
These figures do, however, raises doubts about the efficacy of the procedure which can be associated with complication, because the procedure did not eliminate the use of analgesics and only 2.4% of patients had relief after 24 months.

Lakemeier et al [3] carried out a randomized, controlled, double-blind trial, to compare intraarticular lumbar facet joint steroid injections and lumbar facet joint radiofrequency denervation in the treatment of low back pain. The Roland-Morris Questionnaire was the primary endpoint and the secondary endpoints were the visual analog scale and the Oswestry Disability Index. The outcome assessments were performed at baseline and at 6 months. The study involved fifty-six patients where 24 of 29 patients in the steroid injection group and 26 of 27 patients in the denervation group completed the 6-month follow-up. There was pain relief and functional improvement in both groups and there were no significant differences between the 2 groups for both the primary endpoint and secondary endpoints.

This study, if valid, would encourage the use of intraarticular lumbar facet joint steroid injections rather than joint radiofrequency denervation for treatment of lumbar facet pain, and in doing so, resources can be saved.

Maas et al [4] did Cochrane Database Systematic Review in 2015 to assess the effectiveness of RF denervation procedures for the treatment of patients with chronic low back pain.The authors found that there is no high-quality evidence which suggests that RF denervation provides pain relief for patients with chronic low back pain. They also found no convincing evidence to show that such treatment improves function. They concluded that the current evidence for RF denervation for chronic low back pain is very low to moderate in quality and high-quality evidence does not exist.

Juch et al [5] conducted three pragmatic multicenter, non blinded randomized clinical trials to assess the effectiveness of radiofrequency denervation in patients with chronic low back pain originating from the facet joints, sacroiliac (SI) joints and or the disc. They found that radiofrequency denervation combined with a standardized exercise program resulted in either no improvement or no clinically important improvement in chronic low back pain compared with a standardized exercise program alone. They concluded that their findings do not support the use of radiofrequency denervation to treat chronic low back pain from the facet and SI joints and the disc.

Lee et al [6] in 2017 carried out a meta-analysis of 7 RCT for a total of 454 patients with low back pain due to facet joint disease of the lumbar spine. Comparison was made between patients who had radiofrequency denervation and those who had control/sham treatments. The follow up was upto 1 year. Two hundred and thirty one patients had radiofrequency ablation and 223 patients had control treatments such as sham or epidural block procedures. At 1 year follow up, there was a greater improvement in the radiofrequency denervation group and the mean difference for VAS scores between the two groups was 3.55.The authors concluded that radiofrequency denervation produced significant reduction in low back pain originating from the facet joints compared with sham procedures or epidural nerve blocks.

The systematic reviews (SRs) indicate that there is conflicting evidence regarding the benefits of radiofrequency denervation for facet joint pain, which makes it difficult to recommend it for treatment of chronic low back pain. Most of the studies included in the  SRs were usually small with a mix of randomized and non-randomized studies. The studies did not document well the adverse events and complications related to the radiofrequency denervation procedure. The primary studies had small population size and were of short duration which makes it difficult to determine the long term benefits associated with the procedure.

Since there is no long term outcome data available to determine the benefits of the procedure, the literature does not support the use of the procedure to treat chronic low back pain.

References

1. van Wijk RM, Geurts JW, Wynne HJ, Hammink E, Buskens E, Lousberg R, Knape JT, Groen GJ. Radiofrequency denervation of lumbar facet joints in the treatment of chronic low back pain: a randomized, double-blind, sham lesion-controlled trial. Clin J Pain. 2005 Jul-Aug;21(4):335-44.
2. Gofeld M, Jitendra J, Faclier G. Radiofrequency denervation of the lumbar zygapophysial joints: 10-year prospective clinical audit. Pain Physician. 2007 Mar;10(2):291-300.
3. Lakemeier S, Lind M, Schultz W, Fuchs-Winkelmann S, Timmesfeld N, Foelsch C, Peterlein CD. A comparison of intraarticular lumbar facet joint steroid injections and lumbar facet joint radiofrequency denervation in the treatment of low back pain: a randomized, controlled, double-blind trial. Anesth Analg. 2013 Jul;117(1):228-35.
4. Maas ET, Ostelo RW, Niemisto L, Jousimaa J, Hurri H, Malmivaara A, van Tulder MW. Radiofrequency denervation for chronic low back pain. Cochrane Database Syst Rev. 2015 Oct 23;(10):CD008572.
5. Juch JNS, Maas ET, Ostelo RWJG, Groeneweg JG, Kallewaard JW, Koes BW, Verhagen AP, van Dongen JM, Huygen FJPM, van Tulder MW. Effect of Radiofrequency Denervation on Pain Intensity Among Patients With Chronic Low Back Pain: The Mint Randomized Clinical Trials. JAMA. 2017 Jul 4;318(1):68-81.
6. Lee CH, Chung CK, Kim CH. The efficacy of conventional radiofrequency denervation in patients with chronic low back pain originating from the facet joints: a meta-analysis of randomized controlled trials. Spine J. 2017 Nov;17(11):1770-1780.

Sacroiliac joint Pain and Osteoarthritis - An Update

       Sacroiliac joint Pain and Osteoarthritis - An Update

                                        Dr KS Dhillon

Introduction

The sacroiliac (SI) joint is the largest axial joint in the body. The anterior third is a diarthrodial synovial joint and rest of it is a syndesmosis, hence it is often referred to as a  diarthroamphiathrodial joint. There are multiple causes of SI joint pain but the cause of pain in most patient remains unknown. In 15% to 25% of patients with axial low back pain the SI joint is believed to be the cause of the pain. Osteoarthritis is probably the least common cause of SI joint pain. History, physical examination and radiological imaging are usually insufficient to diagnose SI joint pain. Small volume local anesthetic blocks are usually used to confirm that SI joint is the cause of pain but the validity of this test remains unproven. Though there are several invasive and non-invasive methods of treating SI joint pain, there is limited evidence of long term effectiveness of any of them. This review will outline the anatomy of the SI joint, the causes and prevalence of SI joint pain, as well as provide updates on the diagnosis and treatment of SI joint pain.

Anatomy of the sacroiliac (SI) joint

The sacroiliac joint is formed by the first three segment of the sacrum and the iliac bone. It is one of the largest axial joint in the body, with an average surface area of 17.5 cm2 [1]. It is an auricular-shaped (C-shaped), diarthrodial synovial joint where the sacral articular cartilage is hyaline and the iliac cartilage is fibrous [2]. The hyaline cartilage is replaced by fibrocartilage later in life. In reality only the anterior third of the joint is a synovial joint and the rest of the SI joint consists of ligamentous structures (interosseous sacroiliac ligament) which convert it into a syndesmosis. Hence some authors call it an amphiarthrodial or diarthroamphiathrodial joint [3]. The main part of the joint which connects the sacrum to the ilium is the posterior ligamentous structures which stabilise the joint and prevents movements in all planes. In women these ligaments are weaker which allows the mobility that is necessary for parturition [4].

Stability to the joint is conferred by the irregular articular surfaces and the the ligaments around the joint. These include the anterior, posterior and interosseous sacroiliac ligaments; iliolumbar, sacrotuberous and sacrospinous ligaments [5].

Besides the configuration of the joint and the ligaments, the latissimus dorsi via the thoracolumbar fascia, the gluteus maximus, and the piriformis also influence the movements and stability of the SI joint [6,7].

The nerve supply of the SI joint is a contentious issue. The information is sparse and variable. The Gray’s anatomy text makes no mention of it.
Solonen’s collection of data from past studies showed that the innervation is by branches from the lumbosacral plexus, superior gluteal nerve, dorsal rami of S1 and S2, and obturator nerve [3]. Cunningham’s Textbook of Anatomy on the other hand states that, “The sacroiliac joint is supplied: (1) by twigs directly from the sacral plexus and the dorsal ramus of the first two sacral nerves; and (2) by branches from the superior gluteal and obturator nerves” [2].

Nagakawa [8] reported that the SI joint innervation is by nerve filaments which are derived from the the ventral rami of L4 and L5, the superior gluteal nerve, and also from the dorsal rami of L5, S1, and S2.

Grob et al [9] found that the innervation of the SI joint is almost exclusively derived from the sacral dorsal rami.
There is a widely held belief that there are no movements at the SI joints but studies, however, show that there is  screw-axis motion of simultaneous sagittal plane rotation and translation at the joints [10,11]. The joint apparently fuses after the age 50 years [5,12].

A loss of SI joint synovial cavity and adhesion formation has been reported in both sexes. Sashin [13] concluded that the SI joints remain diarthrodial until the mid-adult years, and then motion progressively decreases. His conclusions were based on 257 postmortem examinations. He found that there was sacroiliac osteophyte formation in 85 percent of the males and 50 percent of the females, in individuals aged between 40 to 49 years. One hundred percent of the males aged between 50 to 59 years had osteophyte formation and in 60 percent of the individuals there was sacroiliac joint ankylosis.

Degenerative Sacroiliac Joint disease

The prevalence of abnormalities of the sacroiliac (SI) joint in the population remains unresolved [14]. O'Shea et al [14] studied the radiographic prevalence of SI joint abnormalities in patients with low back pain. Their cohort included 315 (173 men, 142 women) patients with age ranging from 18 – 60 years. Of the 315 patients, 100 (31.7%) had radiographic abnormalities of the SI joint. Possible degenerative changes were seen in 17 (male 8, female 9) patients (5.4%) and definite degenerative changes were seen in 56 (male 15, female 41) patients (17.7%). Twenty five (7.9%) had radiographic evidence of inflammatory disease of the SI joint. Two women had radiographic evidence of Osteitis condensans ilii. Degenerative changes were predominantly seen in women (68%) and inflammatory were predominantly seen in men (63%). In women, the authors found no correlation between degenerative SI joint abnormalities and degenerative changes in the lumbar spine. They also found a poor correlation between radiographic changes and symptoms.

Hodge and Bessette [15] retrospectively review 64 lower lumbar spine CT scans performed in patients with low back pain. The scans were of 29 women and 35 men, with a mean age 52 years. They evaluated the SI joint for osteoarthritic changes and they found that 16 SI joints (25%) were normal. In 48 cases (75%), there was evidence of osteoarthritis. In 8 cases (16%) there was some disagreement between the two readers but a consensus diagnosis of osteoarthritis was made.

Degenerative changes in the sacroiliac joint has been demonstrated pathologically in cadavers less than 30 years of age [16,17,18]. Pathologic abnormalities, however, become prominent in middle aged and elderly patients and usually involve the ilium. These changes include fibrillation of the cartilage and erosion with sloughing and denudation of cartilaginous surfaces. Subchondral eburnation and osteophytes become obvious. A   partial or complete fibrous ankylosis of the joint cavity occurs [16,17].

On radiographs of the SI joint the joint space in young adults is between 2-5 mm. A reduction of joint space between sacrum and ilium is common in patients over the age of 40 years and thereafter it increases in frequency [18]. Subchondral sclerosis and osteophytes are often present. The osteophytes may completely or partially bridge the joint. In the elderly, the incidence of complete bony ankylosis, which occurs by fusion of the osteophytes, varies between 20% to greater than 80% [16,17,18]. Focal calcification and ossification of the ligaments may occasionally be seen [19].

Prevalence of sacroiliac Joint Pain

Dysfunctional SI joints are known to cause low back pain. The prevalence of back pain due to SI joint dysfunction has not been well studied. The earlier studies used means that are not so reliable to make a diagnosis of SI joint pain. They used physical examination findings and/or radiological imaging to make the diagnosis of SI joint pain. One such large study was conducted by Bernard and Kirkaldy-Willis [20]. They found a prevalence rate of 22.5% in 1293 adult patients who presented with LBP. Their diagnoses was  predominantly based on physical examination.

Schwarzer et al [21] used fluoroscopically guided local anesthetic SI joint injections to diagnose SI joint pain.They found a 30% prevalence rate using the local anesthetic injections.
Maigne et al [22] conducted a prevalence study in 54 patients with unilateral LBP using a local anesthetic injections into the SI joint. They found a prevalence rate of 18.5%.

Etiologies of SI joint pain

The cause of SI joint pain can be intraarticular or extraarticular. Extraarticular sources are more common and include enthesopathy, fractures, ligamentous injury, and myofascial pain. Intraarticular sources of pain include arthritis and infection.

There are numerous predisposing risk factors for SI joint pain and these include, true and apparent leg length discrepancy, gait abnormalities, prolonged vigorous exercise, scoliosis, and spinal fusion to the sacrum [4].

These factors increase the risk by increasing the stress across the SI joint.
Arthritis including spondyloarthropathies and osteoarthritis can be one of the sources of the pain in the low back.

Diagnosis of SI joint pain

Physical examination

Diagnosis of SI joint pain is difficult and complex. There are dozens of physical examination tests available to diagnose such pain but none of them are of much value. The two most widely used tests tests are the Patrick’s  and Gaenslen’s  distraction tests. Clinical studies show that neither a medical history nor physical findings are consistently able to identify the SI joint as the source of pain [21,23,24]. In fact Dreyfuss et al. [25] found a 20% incidence of asymptomatic adults having positive findings on 3 commonly performed SI joint provocation tests.

Radiological examination

Studies examining radiologic findings in patients with SI joint pain have not lived up to expectation either. Maigne et al [26] and Slipman et al [27],
found sensitivities of 46% and 13% respectively for the diagnosis of SI joint pain with the use of radionuclide bone scanning. The low sensitivities indicate that bone scanning is a poor screening test for SI joint pain.The  correlation between diagnostic injections and symptoms with CT and radiographic stereophotogrammetry has also been found to be poor [28,29]. Elgafy et al [29] in a retrospective analysis found that CT imaging had a 57.5% sensitivity and 69% specificity in diagnosing SI joint pain.

Diagnostic Blocks

Pain relief after properly performed local anesthetic block of the SI joint is usually referred to as the most reliable test for diagnosing SI joint pain.

The validity of this assumption has, however, never been proven. Several factors affect the sensitivity and specificity of this test. These include ‘ the placebo effect, convergence and referred pain, neuroplasticity and central sensitization, expectation bias, unintentional sympathetic blockade, systemic absorption of LA, and psychosocial issues’ [4]. Furthermore obtaining a satisfactory SI joint block is very challenging. Extravasation of the local anesthetic (LA) into the surrounding pain generating structures can give false-positive blocks and failure to get adequate spread of the LA in the SI joint can produce false negative blocks.

North et al [30] did a randomized prospective study of 33 patients with sciatica due to lumbosacral spine disease. They found that the specificity of all blocks wa exceedingly low. For sciatic nerve blocks, the specificity was only between 24% and 36%. They however did not study blocks for the SI joint.

SI joints injections are difficult and can be associated with significant complications. Fortin et al [31] found extravasation of contrast in 9 out 10 volunteers who had SI joint injections for SI joint referral patterns mapping. Forty percent of the subjects had lower extremity numbness after LA injections which indicates inadvertent anesthetization of the lumbosacral nerve roots.
In a study by Maigne et al [22] 3 out 67 patients who had SI joint injections developed sciatic palsy and in 7 other patients penetration of the joint was not possible. Other investigators have reported a less than 5% failure rates with fluoroscopically guided SI joint injections [21,24,32]. There apparently is ‘no infallible, universally accepted method for diagnosing pain originating in the SI joint(s)’ [4].

Treatment of SI joint pain.

Sacroiliac joint is an uncommon source of low back pain [22] and OA of the SI joint is an uncommon cause of SI joint pain. Just as it is difficult to diagnose SI joint pain, similarly it is difficult to treat SI joint pain. The treatment can either be symptomatic or involve treating the underlying cause. There are a wide variety of treatments available for treating SI joint pain but there is a lack controlled outcome studies to guide treatment.

Psychosocial Issues

More and more evidence is becoming available to show that psychogenic syndromes play an important role not only in the genesis of low back pain but also in its treatment.
Polatin et al [33] studied 200 patients with chronic low back pain and they found that 77% of the patients met the lifetime diagnostic criteria for psychiatric illness. Fifty nine percent of the patients showed current symptoms for least one psychiatric diagnosis, with the most common being depression, substance abuse, and anxiety disorders. In more than 50% of the patients with depression and in more than 90% of the patients with anxiety disorder (95%) and substance abuse (94%) had psychopathological symptoms before the onset of back pain. Most of the studies, though not all, have reported that untreated psychopathology has a negative effect on the outcome of treatment of low back pain [34].

Besides psychiatric illness, social factors also have a role to play in the prognosis of low back pain. These include ‘return-to-work decisions, medication use issues, ….. negative environmental factors, codependency issues, secondary gains and their impact, presence of pain games, negatively acting financial considerations,.... presence of poor role models, impact of pain on general functioning, and the patient's future plans’ [35].

A multidisciplinary approach which identifies and treats concomitant psychosocial issues will have a better outcome in treatment of patients with SI joint pain.

Conservative management

There is a dearth of literature on the conservative management of SI joint pain. The principles of treatment of low back pain would apply to SI joint pain. The role of NSAIDs in the treatment of acute low back pain has been well established [36]. The use of NSAIDs and relative rest during the acute phase, along with application of cold compresses or hot packs can help relieve the pain.

Once the acute phase is over function can improve with therapeutic exercises and physical therapy [37]. The aim of the therapy would include  increasing mobility, stretching, strengthening, and correcting of asymmetries and correction hyperactivity of muscle groups.

High-velocity low-amplitude (HVLA) manipulation of the SIJ and spine has been used for the treatment of SI joint with some success [38]. Other modalities that have used in the treatment of SI joint pain include, ultrasound, diathermy, moist heat or cold, and TENS (transcutaneous electrical nerve stimulation) [39]. Stabilization of the SI joint with a compression belt has been used by some to treat pain in patient with SIJ dysfunction [40].

Injection therapy

Whenever a decision to undertake interventional treatment is taken, it is important to have sufficient clinical evidence to support the diagnosis and sufficient evidence to support the type of treatment to be undertaken. The source of pain whether intra or extra articular must be known. In patients with pain due to arthritis the source of pain would likely be intraarticular. SI joint injections have been shown to have some efficacy in treatment of SI joint pain, though the evidence is not overwhelming.
Most of the studies which support the use intraarticular steroid injections are observational studies [41-44].

There is a randomized controlled study, with a small patient population and short follow up, which studied the use intraarticular steroids. Maugers et al [45] performed a double-blind study in 10 patients (13 articulations) who had painful sacroiliitis. At 1 month follow up they found that 5 of the 6 joints injected with corticosteroids showed a pain relief of more than 70% and there was no pain relief in the placebo group. There was relapse of pain in one patient who had an injection of steroid. Six SI joints in the placebo group and two patients with failure and relapse of the corticosteroid group were reinjected with corticosteroid. At 3 and 6 months, success rates declined to 62 and 58%, respectively.

Systematic review of evidence for the effectiveness of intra-articular injections for SI joint pain shows that there is limited evidence of long term effectiveness [47,48].

Radiofrequency denervation

Radiofrequency denervation procedures have been used for pain relief from SIJ dysfunction.The innervation and target nerves for radiofrequency denervation (RFD) of the SIJ remain unclear. Radiofrequency denervation involves the use of radiofrequency (RF) to ablate the lateral branch nerves that innervate the SI joint. The lateral branch RF denervation is usually effective in alleviating extraarticular SIJ pain rather than intraarticular pain. Hence it is effective in younger patients who are more likely to have extra articular pathology in the ligaments which are innervated by the lateral branches [49].

There are controlled and uncontrolled studies that have demonstrated benefits of RF denervation, but none have compared RF denervation to more conservative therapy. Patient who have obtained effective but short term relief with SI joint block are the best candidates for SIJ denervation.
Vallejo et al [50] carried out a prospective case series in 22 patients with refractory sacroiliac pain who received pulsed radiofrequency denervation of the medial branch of L4, posterior primary rami of L5, and lateral branches S1 and S2. Sixteen patients (72.7%) experienced good to excellent pain relief following PRFD. The duration of pain relief was 6-9 weeks in four patients, 10-16 weeks in five patients, and 17-32 weeks in seven patients. Six patients (26.1%) did not respond to PRFD and had less than 50% reduction in VAS and were considered failures.

Ferrante et al. [51] carried out a prospective study where intra-articular RF ablation was carried out in 50 SI joint in 33 patients. The outcome was measured using visual analog scale (VAS), physical examination findings, pain diagrams, and opioid usage. A successful RF ablation was defined as a 50 % reduction in SIJ pain for more than 6 months, and only 36.4 % of subjects met the criteria. A positive response was found to be associated with an atraumatic inciting event.
Burnham and Yasui [52] carried out an uncontrolled, prospective, cohort study of 9 patients with SI joint pain who had RF ablation of the SI joint.

The subjects were asked to answer questionnaires which evaluated pain intensity and frequency, analgesic intake, disability, satisfaction with current pain level and the RF procedure. They found that 8 of the 9 subjects were satisfied with the procedure.

Cohen et al [53] carried out a randomized placebo-controlled study in 28 patients with injection-diagnosed sacroiliac joint pain. Fourteen patients received L4-L5 primary dorsal rami and S1-S3 lateral branch radiofrequency denervation using cooling-probe technology and 14 patients had placebo denervation. At one month follow up 79% in the denervation group and 14% in the placebo group had significant pain relief (i.e relief of 50% and more). At 8 months only 57% of the denervation group had significant pain relief and at 1 year only 2 patients (14%) in the treatment group continued to demonstrate persistent pain relief.

Hansen et al [54] carried out a systematic review of the literature in 2007 of the therapeutic sacroiliac joint interventions in the management of sacroiliac joint pain. They found that ‘there is limited evidence for short-term and long-term relief with intraarticular sacroiliac joint injections and radiofrequency thermoneurolysis’.

Rupert et al [55] in 2009 did a systematic appraisal of literature which evaluated SI joint interventions. They found that the indicated evidence for radiofrequency neurotomy of the SI joint is limited at Level II-3 for short-term (less than 6 months) and long-term relief (more than 6 months).
RF ablation can be associated with complications.  RF ablation can be associated with postprocedure numbness and tingling in about 20% of the patient  due to severing of cutaneous sensory branches. Bleeding and infection can occur after the procedure. Accidental ablation of the sacral spinal nerves can lead to incontinence, worsening pain or lower extremity weakness.

McKenzie-Brown et al [47] carried a systematic review of the effectiveness sacroiliac joint interventions in the treatment of SIJ pain. They found 4 relevant reports, one was prospective and three were retrospective. They found that the evidence for radiofrequency neurotomy in managing chronic sacroiliac joint pain was limited.

Hansen et al [48] in systematic review of the literature also found that the evidence for the use of RF ablation in the treatment of SIJ pain is limited.

Surgical intervention for SIJ pain

Buchowski et al [56] reported the functional and radiographic outcome of sacroiliac arthrodesis for the disorders of the sacroiliac joint. Twenty patients had SI joint arthrodesis for sacroiliac symptoms which were due to sacroiliac joint dysfunction (13 patients), osteoarthritis (5 patients), and spondyloarthropathy and sacroiliac joint instability (1 each). There was solid fusion in seventeen patients (85%). Only fifteen patients (75%) completed preoperative and postoperative SF-36 forms. Significant  improvement occurred in the physical functioning, bodily pain, vitality, social functioning, and in the neurogenic and pain indices.

Schütz and Grob [57] carried out a retrospective study in 17 patients with chronic SI joint syndrome who had a bilateral SI joint fusion. All the patients had positive response to local anesthetic block.The indication for SI joint fusion was chronic SI joint syndrome due to posttraumatic (5 patients) or idiopathic (12 patients) SI joint degeneration. Eighty two percent of the patients were dissatisfied with the procedure and 65% of the patients required reoperation.

Waisbrod et al [58] retrospectively reviewed 22 SI joint arthrodesis in patients with OA of the SI joint. The review was at between 12 and 55 months follow up. The outcome was defined as satisfactory, if there was at least 50% reduction of pain,no need for analgesics, and the patient continued with the same occupation as before the surgery. They found the the outcome was satisfactory in only 50% of the patients. After excluding patients with psychosomatic pain, the authors said that there was a 70% success rate.

Wise and Dall [59] reported the outcome of minimally invasive sacroiliac arthrodesis in 13 patient. Six of the patients had a bilateral fusion (total 19 joints). The follow up was between between 24 months to 35 months (mean 29.5 months). They had an overall fusion rate of 89% (17/19 joints).
On the average there was an improvement of 4.9 in the visual analog scale. The leg pain improved an average of 2.4 points and dyspareunia improved an average of 2.6 points on the visual analog scale.
Zaidi et al [60] did a systematic review of the literature to access the surgical and clinical efficacy of sacroiliac joint fusion. They reviewed a total of 16 peer-reviewed journal articles. There were 5 consecutive case series, 8 retrospective studies, and 3 prospective cohort studies with a total of 430 patients. One hundred and thirty one underwent open surgery and 299 underwent minimally invasive surgery (MIS) for SIJ fusion. The mean follow-up for open surgery was 60 months and for MIS it was 21 months. The underlying pathology in these patients was:

• SIJ degeneration/arthrosis  in 257 patients [59.8%]
• SIJ dysfunction 79 patients [18.4%]
• Postpartum instability 31 patients [7.2%]
• Posttraumatic 28 patients [6.5%]
• Idiopathic 25 patients [5.8%]
• Pathological fractures 6 [1.4%]
• HLA-B27+/rheumatoid arthritis 4 patients [0.9%]

The radiographically confirmed fusion rates for open surgery were between  20%-90% and for MIS between 13%-100%. Rates of excellent satisfaction, as determined by pain reduction, function, and quality of life, in patient with open surgery ranged from 18% to 100% with a mean of 54%. For patients who had MIS, an excellent outcome as judged by patients' stated satisfaction with the surgery, ranged from 56% to 100% with a mean of mean 84%. The reoperation rate after open surgery ranged from 0% to 65% with a mean of 15% whereas with MIS the reoperation rates varied from 0% to 17% with a mean of 6%. Major complication rates were high and ranged from 5% to 20%. A study which addressed safety reported a 56% adverse event rate.

The authors concluded that surgical intervention for SIJ pain may be beneficial in a subset of patients but keeping in mind the difficulty in making an accurate diagnosis and the fact that the evidence for the efficacy of SIJ fusion is lacking, serious consideration should be given to alternative treatments before considering a fusion of the SI joint.

Conclusions

The SI joint is a complex diarthroamphiathrodial joint. SI joint is believed to be the source of pain in 15% to 25% of patients with axial low back pain. Clinical presentation is usually nonspecific and physical examination maneuvers have little or no diagnostic value. Radiological investigations have low diagnostic sensitivity and specificity. Pain relief after properly performed local anesthetic block of the SI joint is usually referred to as the most reliable test (gold standard) for diagnosing SI joint pain. The validity of this assumption has, however, never been proven. Of the many treatment options such as activity modification, physical therapy modalities, orthosis, manipulation, injections, radiofrequency procedures, and surgery, none have stood the test of time. Treatment has to be tailored to the individual patient and treating patients with SIJ pain will continue to remain a challenge.

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Multiligamentous injury/Dislocation of the knee

          Multiligamentous injury/Dislocation of the knee
                                                           

                                                  Dr KS Dhillon

Introduction

There are 4 main ligaments which stabilize the knee, namely the extra-articular collateral ligament and the intra articular cruciate ligaments. The structures in the posterolateral and posteromedial corner also contribute joint stability.

When two or more of these are disrupted, the term multiligament injury is used. With such disruptions a knee dislocation or a substantial subluxation will occur.

Multiligament knee injuries are potentially devastating. Fortunately these injuries are uncommon. The estimated prevalence of multiligamentous knee injuries is about 0.02% to 0.2% of all orthopaedic injuries. The most common type of dislocation is anterior and/or posterior dislocation.
Knee dislocations are often associated with vascular and nerve injuries besides soft tissue injuries and fractures.

There are no guidelines and consensus regarding the best way to treat these injuries. The outcome of treatment is getting better over the years and the number of devastating complications is getting less.
This article will review the anatomy of the knee stabilizer, classification of knee dislocation, diagnosis, treatment and complications associated with knee dislocation and multiligamentous injury to the knee.

Anatomy of knee ligaments

There are 4 main ligaments that stabilize the knee. Two of them are intra-articular and two are extra-articular. The extra-articular ligaments include the medial and lateral collateral ligaments and the intra-articular include the anterior and posterior cruciate ligaments.

The anterior cruciate ligament (ACL) is an intracapsular but extrasynovial structure that consists of 2 bundles, the posterolateral (PL) and the anterolateral (AL) bundle. It arises from the lateral femoral condyle in the intercondylar notch with the PL bundle originating posterior and distal to the AL bundle. The insertion on the tibia is broad and irregular, anterior to and between the intercondylar eminence. The AL fibres are tight in flexion and extension while th PL fibres are tight in extension and loose in flexion. The Pl fibres prevent pivot shift of the tibia. The blood supply is from the middle geniculate artery and the innervation is from the posterior articular branches of tibial nerve. Its function is to prevent anterior translation of the tibia on the the femur.

 The posterior cruciate ligament is also intra-articular and extrasynovial. It arise from the medial femoral condyle and inserts on the  tibial sulcus and consists of two bundles.  The shorter, thicker and stronger anterolateral and the longer, thinner and weaker posteromedial bundle. Its blood supply is  middle geniculate artery. It prevents posterior translation of the tibia on the femur. 

The medial collateral ligament (MCL) arises from the medial femoral condyle and inserts on the medial side of the tibia. It consists of two components, the superficial and deep components. The superficial component arises from the medial femoral epicondyle and lies deep to gracilis and semitendinosus and inserts into the periosteum of the medial proximal tibia deep to the Pes Anserinus. The deep portion (medial capsular ligament) attaches to the medial meniscus and divides into the meniscofemoral and meniscotibial portions. It is separated from the superficial ligament by a bursa. The posterior fibres blend with the posterior capsule.

The MCL resists valgus angulation and the superficial portion contributes 57% and 78% of medial stability at 5 degrees and 25 degrees of knee flexion, respectively.

The lateral collateral ligament (LCL) also known as the fibular collateral ligament originates at the lateral femoral condyle posterior and superior to insertion of popliteus, runs superficial to the popliteus and inserts on the fibula anterior to the popliteofibular ligament on the fibula.
It resists varus angulation and is tight in extension and lax in flexion.                           

Structures in the Posterolateral corner (PLC) and the Posteromedial corner (PMC) also contribute to stability of the knee. The components of PLC include the LCL, Popliteus muscle and tendon, popliteofibular ligament and the lateral capsule. There is variable contribution from the arcuate ligament, iliotibial band and the fabellofibular ligament. The PLC works synergistically with the PCL to control external rotation and posterior translation.

The Posteromedial corner structures lie deep to the MCL and include the
insertion of semimembranosus, posterior oblique ligament, oblique popliteal ligament and the posterior capsule. They provide important rotatory stability.
The MCL has the strongest tensile strength at 4000N, followed by PCL 2500 N, the ACL 2200 N, and the LCL at 750 N.

Multiligament knee injury

The main ligamentous structures that stabilize the knee are the anterior cruciate ligament (ACL), posterior cruciate ligament (PCL), lateral collateral ligament and posterolateral corner, and medial collateral ligament and posteromedial corner. When two or more of these are disrupted, the term multiligament injury is used. With such disruptions a knee dislocation or a substantial subluxation will occur.

Often the terms multiligamentous knee injury and knee dislocation are interchangeably used. In some knee dislocation spontaneous reduction occur and the injury gets labelled as multiligamentous injury. One of the most frequently used anatomical classification of knee dislocation is the one by Schenck [1] which was modified by Wascher [2].

Schenck classification of knee dislocation

         KD I          Injury to single cruciate + collaterals
         KD II         Injury to ACL and PCL with intact collaterals
         KD III M    Injury to ACL, PCL, MCL
         KD III L     Injury to ACL, PCL, FCL
         KD IV        Injury to ACL, PCL, MCL, FCL
         KD V         Dislocation + fracture

“C” and “N” caps are used for associated injuries. “C” = arterial injury.
“N”=  neural injury, either tibial or the peroneal nerve. ACL= anterior cruciate ligament; FCL= fibular collateral ligament; KD= Knee Dislocation, Classification I–V; MCL= medial collateral ligament.

Prevalence of multiligamentous injuries

Multiligament knee injuries are potentially devastating. Fortunately these injuries are uncommon. The estimated prevalence of multiligamentous knee injuries is about 0.02% to 0.2% of all orthopaedic injuries [3,4].

The most common type of dislocation is anterior and/or posterior dislocation. Green and Allen [5] reported a 31% incidence of anterior dislocation, 25% posterior, and 3% rotatory dislocation. Frassica et al [6] reported a 70% incidence of posterior dislocation, 25% anterior, and 5% rotatory dislocations. Rotatory dislocations are least common and of the rotatory dislocation, posterolateral dislocation is the most common. Frequently this type of dislocation is irreducible by close means because the medial femoral condyle button-holes through the anteromedial capsule.
Most of the knee dislocations are close dislocations. The incidence of open dislocation varies between 19% and 35% of all dislocations [7,8]. Open dislocations usually carry a worse prognosis.

Associated injuries

1.Vascular injury

The incidence of vascular injury with knee dislocations has been estimated to be around 32% [5]. The incidence is about 50% with anterior and posterior dislocation [9]. There are two mechanisms of injury to the popliteal artery. One is stretching leading to rupture due to hyperextension of the knee. Stretching leading to rupture occurs because the artery is relatively fixed, proximally at the adductor hiatus and distally at tendinous arch of the gastrocnemius-soleus complex. Such injury is usually seen in anterior dislocation of the knee.

The other mechanism of injury is a direct contusion of the artery by the posterior tibial plateau in patients with posterior dislocation of the knee. Direct contusion leads to intimal damage with thrombus formation hours or days after the dislocation. Hence the initially examination may be normal [10]. In patients with bicruciate ligament ruptures the dislocation can reduce spontaneously but the incidence of arterial injury can be high [11].

Prolonged obstruction of the popliteal artery, which is an “end-artery” to the leg, with minimal collateral circulation through the genicular arteries, can lead to ischemia and eventual amputation of the limb [12].

Injury to the popliteal vein is less common. Any obstruction to blood flow in the vein is treated by surgical repair of the vein. Lacerations can be be closed successfully by lateral suture. If a repair will cause stenosis, then autogenous venous tissue can be used as a patch graft in the lateral suture repair.  A transected vein where adequate length remains, an end-to-end venous anastomosis can be carried out [13].



2.Nerve injury

Knee dislocations can be associated with an injury to the peroneal nerve or the tibial nerve. The incidence of nerve injury is about 20% to 30% [14] which is lower than the incidence of vascular injury. This is probably because the nerves are not as tightly anchored around the knee as the blood vessels.The peroneal nerve is more often injured than the tibial nerve. Posterior dislocation is more commonly associated nerve injuries [15].

3.Associated fractures

Since dislocations of the knee are often due to high energy trauma, fractures around the knee are commonly seen with knee dislocation. The incidence of associated fracture is around 60% [16]. Fractures of the tibial plateau and ligament avulsion fractures of the proximal tibia and distal femur are commonly seen.

4. Soft tissue injury

Besides the ligament injury, a dislocation of the knee can cause injuries to the menisci. Forty-one to 44% of patients with knee dislocation have been found to have a medial meniscal tear [17,18].

Diagnosis of multiligamentous injury

The clinical presentation would include a history of knee trauma and knee pain with or without deformity. About 50% of the dislocations reduce spontaneously, hence there maybe no deformity on presentation.In the other 50% there will be an obvious deformity of the knee. When there is a deformity an immediate reduction is carried out except when there is a ‘dimple sign’ present. A ‘dimple sign’ indicates buttonholing of medial femoral condyle through medial capsule seen in posterolateral dislocations. Close reduction in such a situation will lead to skin necrosis and is a contraindication to closed reduction.

Clinical examination will show anteroposterior, mediolateral or rotatory instability. Neurovascular examination is important with vascular examination receiving the top priority. After reduction, if the pulses are absent or diminished an immediate exploration and vascular repair is indicated. Ischemia time of more than 8 hours is associated with amputation rates of about 86% [19].
If the pulses are present and normal than the Ankle-Brachial Index (ABI) should be measured. If the ABI is more than 0.9, then monitor with serial examination. If the ABI is less than 0.9, an arterial duplex ultrasound or CT angiography is done. If arterial injury is present vascular surgery would be indicated.

Imaging studies

Before close reduction of the knee dislocation, plain anterior posterior and lateral radiographs of the knee are taken which will show the direction of the dislocation and also show associated fracture. The radiographs will aid in close manipulation and reduction of the knee dislocation. If there is evidence of arterial injury, an angiogram would be indicated. Any obstruction to venous outflow would mean the need for venography. After stabilization of the patient and after initially treatment of the dislocation, a MRI of the knee has to be done for further management of the injuries to the knee. MRI is useful in detecting damage to the ligaments and to assess meniscal as well as cartilage injury.
It is however a static study which cannot demonstrate the functional status of the injured ligament. A stress radiograph is more useful to assess the functional status of the ligaments of the knee [20].

Treatment of knee dislocation

Close reduction

A dislocated knee is an orthopaedic emergency and close reduction should be carried out in the emergency department after x rays have been done. The manipulation of the knee is done under conscious sedation and analgesia, by slow gradual leg traction applied at the ankle, while appropriate manipulation of the proximal tibia is carried. Once the dislocation has been reduced, neurovascular examination has to carried out. The limb is than placed in either a long leg splint or knee immobilizer. Post-reduction x rays are than performed to ensure that the reduction has been achieved. The presences of a ‘dimple sign’ would be a contraindication for a close reduction, because close reduction may lead to skin necrosis.

Urgent operative intervention

Urgent surgical intervention with external fixation is indicated, in patients where vascular repair has been undertaken and in patients with open dislocation, open fracture dislocation, irreducible dislocation, compartment syndrome, in patients with multiple trauma and also in patients where the reduction cannot be maintained.
Four-compartment fasciotomy is usually carried out when the ischemia time is more than 2.5 hours and when there is a compartment syndrome [14].

Definitive treatment of knee dislocation

Historically, knee dislocations were treated conservatively with a plaster cast or a brace for varying periods of time [21]. Favourable results with non-operative treatment have been reported in the past [22-25]. The trend nowadays favours surgical stabilization of the dislocated knee [26-30]. There, however, are no high-quality studies to guide treatment. There are no prospective randomized trials comparing nonoperative with operative treatment of patients with dislocation of the knee.

Levy et al [28] did a systematic review of the literature to compare the outcome of nonoperative versus operative treatment of knee dislocations. Their review suggests that ‘early operative treatment of the multiligament-injured knee yields improved functional and clinical outcomes compared with nonoperative management or delayed surgery’. There were only 4 studies comparing operative versus nonoperative treatment. The review had limitation, which included a lack of uniform outcome measures which made comparisons difficult.

Almekinders and Logan [31] did a comparison between patients treated conservatively and those treated surgically and found that the outcome was comparable. Although the outcome was comparable, the conservatively treated knees had gross ligament instability compared to the surgically stabilize knees. This is the basis on which most surgeons recommend surgical stabilization of the knee in patients with knee dislocation.

Dedmond and Almekinders [32]  carried out a meta-analysis to determine whether operative or nonoperative treatment had better outcomes after knee dislocation. Their analysis evaluated 132 knee dislocations treated surgically and 74 treated nonsurgically. They found no significant difference in the patients ‘ability to return to preinjury employment or athletic activity or in the amount of instability between the two groups’. They also found that significant disability is still possible after successful surgical treatment.

There are several authors who have showed improved ability to return
to sporting activities among patients who had surgical repair or reconstruction [33,34].
Although the the outcomes of surgically treated knee dislocations have improved, persistent pain, postoperative stiffness and the inability to return to the preoperative activity level continue to be a serious concern [35].

Timing of surgical intervention

There are some controversies about when to do surgical intervention after a knee dislocation. When intervention is in the first 3 weeks it is usually referred to as acute intervention and delayed intervention when it is after 3 weeks [36]. The presences of open injuries, vascular injuries, life threatening injuries and knee instability after close reduction would demand acute intervention. Despite the concerns about joint stiffness and loss of motion after acute intervention, many authors have reported good subjective and objective outcomes after acute repair and reconstruction of ligaments [27,28,37,38,39].

Harner et al [27] reported better subjective outcome scores and improved stability in patients with acute surgical reconstruction as compared to patients who had delayed surgical intervention.
Mook et al [40] did a systematic review of the literature to determine whether early, late, or staged operative treatment produced better outcomes. They found that delayed surgical intervention could potentially lead to stability equivalent to acute surgical management. Acute surgery is often associated with range of motion deficits. Early mobility after acute surgery produces fewer range-of-motion deficits but did not reduce the rate of follow-up manipulation or arthrolysis. Staged procedures may produce better subjective outcome and less range of motion deficits but did not reduce the need for follow up surgery for joint stiffness. Patients who had delayed surgical intervention did not need further intervention for knee stiffness.

Spontaneous healing periarticular ligaments and other soft tissues is well known. The medial and lateral collateral ligaments can heal spontaneously. Spontaneous healing of the PCL [41] and the ACL [42] has been reported. There may be a case for initially conservative treatment of multi-ligamentous injuries and a delayed repair/reconstruction of ligaments if there remains persistent symptomatic ligament laxity.

There are no standard guidelines for treatment of ligament injury after knee dislocation. Treatment has to be tailored to the requirements for an individual patient.

Complications

Complications associated with knee dislocation includes:

• Arthrofibrosis (stiffness) is the most common complication (38%), often seen delayed with delayed mobilization
• Laxity and instability (37%)
• Peroneal nerve injury (25%) which is most often with posterolateral dislocations. The results are poor with acute, subacute, and even delayed (>3 months) nerve exploration. Neurolysis and tendon transfers are the usual mode of treatment.
• Vascular compromise. Beside damage to the vessel, claudication, skin changes, and muscle atrophy can also be seen. Limb amputation and death are less common now with prompt recognition and treatment of complication.
• Deep venous thrombosis has also been associated with knee dislocations [43] .
• Acute compartment syndrome, which often necessitates a fasciotomy [44].
• Posttraumatic osteoarthritis is reported in 29.6% to 53% of knees [45]
• Postoperative infections range from 0% to 17.4% [45].

Conclusions

Dislocations of the knee are rare injuries and an orthopaedic surgeon would see a very limited number of cases in his career. They represent a complex and challenging clinical problem. Failure to recognize and treat the injuries which occur with knee dislocation can have devastating outcome especially if vascular injury is missed or there is a delay in detecting it.

There is no consensus regarding the best way to treat the ligament injuries in patients with knee dislocations. This is due to the fact that there are no prospective randomized controlled trials comparing nonoperative with operative treatment of patients with dislocation of the knee. This may in part be due to the rarity of such injuries. Treatment has to be tailored to the needs of the individual patient. On a positive note the outcome of treatment appears to be improving over the years. The number of devastating complications such as death and amputations are also getting rarer.

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