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.

References

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Continuing Professional Development (CPD): Does it help improve the safety and quality of care provided for patients and the public?

Continuing Professional Development (CPD): Does it help improve the safety and quality of care provided for patients and the public? 

                                               Dr KS Dhillon

CPD and CME

How did the concept of continuing medical education (CME) come about? Through the 1960’s many believed that drug advertising was educational and many physicians relied on information provided by the pharmaceutical industry. Industry funders were choosing the subjects offered in the talks provided and the drug firms provided commercially biased prescribing information which led to inappropriate drug use. Policy makers decided to provide an alternative which saw the birth of the concept of CME in the USA [1]. In USA they started granting CME recognition awards to doctors in the 1960s.
The European Union of Medical Specialists (UEMS) first made the move from CME to CPD. UEMS defined the term CPD thus ‘(t)he term CPD acknowledges the wide-ranging competencies needed to practice high quality medicine, including medical, managerial, ethical, social and personal skills. CPD therefore incorporates the concept of CME, which generally is taken to refer only to expanding the knowledge and skill
base required by doctors’ [2].
The CPD subcommittee of Academy of Medical Royal Colleges (AoMRC) has put forth a succinct definition of CPD. They defined CPD as ‘a continuing process, outside formal undergraduate and postgraduate training, that enables individual doctors to maintain and improve standards of medical practice through the development of knowledge, skills, attitudes and behaviour, CPD should also support specific changes in practice’ [3].
This definition emphasizes two important aspects of CPD i.e gaining knowledge and improving patient care.
Although CPD and CME are frequently used interchangeably the current literature considers CME as an ingredient of CPD. Many countries are moving from skill and knowledge based CME system to a CPD system which promotes competencies in a wide range of areas resulting in high quality medical practice [4].

International perspective of CPD

Murgatroyd (4) in 2011 did a study to evaluate the international perspective of CPD programmes and requirements for doctors. The study involved 25 countries from around the world to form an overview of CPD. The countries studied were from Europe, North America, Africa, Australasia and Asia. Out of the 25 countries as of 2011, France had no CPD requirement, in 7 countries CPD was voluntary (including Malaysia) and in 17 countries (including Singapore) CPD requirements were compulsory. In Canada the yearly credit requirements were the highest at 80 credits and it was the lowest in Kenya at 5 points. In Singapore the requirement was 25 credits per year.
Regulatory bodies in countries where CPD is mandatory have developed standards and have guidelines on the use of CPD, although these standards and guidelines vary from country to country. Each country has its own minimum numbers of credit requirement per year to fulfill the regulatory body’s requirements. In majority of the countries it is between 40 to 50 points. There is no international, standardised system for obtaining CPD credits, though in most countries 1 credit point is given for 1 hour of CPD activity [4].
The CPD scheme is delivered by different bodies in different countries and these include accredited providers, universities, specialist societies, specialist boards, specialist colleges, professional societies and medical associations.
In countries with compulsory CPD requirement, failure to obtain the required credits would result in sanctions ranging from suspension from register, fine, reprimand, removal from register, removal of licence, retake examinations, licence loss /fees reduced and loss of status plus fees [4].

Effectiveness of continuing professional development

CPD is suppose to keep the doctor up to date in clinical knowledge and in practice so that he/she can provide high quality care to the patients. CPD is suppose to keep the doctor safe to practice and it is suppose to improve the quality of service provided. Hence CPD and high quality of care are supposed to be irretrievably intertwined. Having said that it is also known that new knowledge does not always translate into a change in behaviour [5].
Knowledge translation is an interesting concept. It ‘describes any activity or process that facilitates the transfer of high-quality evidence from research into effective changes in health policy, clinical practice, or products’ [5].
There is obviously a need to amalgamate elements of education, research and quality improvement in daily clinical practice to improve patient outcomes.
There are however obstacles to this knowledge translation. In orthopaedic surgery for example there is level I evidence that arthroscopic knee joint debridement and arthroscopic partial meniscectomy serves no purpose in the treatment of patients with knee OA and patients with partial tear of the meniscus respectively, yet these are the most common operations performed in clinical orthopaedic practice around the world. This is an example of an instance where validated evidence has failed to achieve widespread implementation. More research in knowledge translation is needed where the discrepancies between what is known and what is done can be determined.
Schostaka et al [3] studied the effectiveness of continuing professional development (CPD). They found that that the effectiveness of CPD is related to the impact it has on knowledge, skills, values, attitudes, behaviours and changes in practice it produces in the workplace. The quality of CPD will dictate the improvements which will occur in the quality of the professional practice which is required for delivery of service. Learning in the professional setting was found to be most useful. There is a definite need for an ‘in-dept identification of learning needs’ both within and external to the place of work [3].
There is some consensus that CPD is useful when it addresses the needs of the clinicians, the patients they serve and the organization where they work. However, the effectiveness of CPD programs which are very diverse and not uniform, remains uncertain. The assessment of outcome of CPD activities remains difficult.

CPD in Malaysia

In Malaysia CPD is and has been voluntary. However, on 1st July 2017, the
Medical (Amendment) Act  2012, which is the amendment to the Medical Act 1971, and the Medical Regulations 2017 which replaces the Medical Regulation 1974, came into force.
Section 28(2)(b) of the Medical Regulations 2017 makes it mandatory for  registered medical practitioners to obtain a stipulated number of CPD points to make them eligible for the Annual Practising Certificate (APC).
This requirement will take effect for submissions received on or after 1 January 2019. The present requirement for the APC is 20 CPD points which are accumulated in a year. The collection of CPD points for the application of APC for a CPD year will be from 1st July to 30th June.
The medical practitioner is expected to take responsibility for his/her own  learning and professional development. The medical practitioner is expected to identify his/her educational needs and plan the CPD activities to be undertaken.
The practitioner is ‘encouraged’ to undertake CPD activities that are relevant to his/her field of practice and which will support his/her professional development. There is however no compulsion to undertake CPD activities in one’s own medical field or speciality. The doctor is advised to attend CPD activities that have been approved by the CPD review committees [6].
The Malaysian Medical Council – Continuing Professional Development  (MMC-CPD) grading system scoring schedule 2018,  is divided into 9 categories from A1 to A9.

A1- Medical congress (Local/International) - Attendance for 3 full days allows participant to earn a maximum of 20 points. A full day is 5 to 8 hours. Points for 1 day is 8, two days is 16 and three or more days is 20 points. The speakers at the congress must be of international standing. The guidelines however does not state what is speaker of international standing. The congress should contain plenary lectures /symposia. Presentation of free communication /poster (sic), etc should be allowed at the congress.

A2--Scientific Meetings of Academy / Universities /Colleges / Association / Institutions. Maximum points per meeting is 20 points.
a. 1- 2 hours 2 points
b. 2-4 hours (½ day) 4 points
c. 5-8 hours (full day) 8 points
d. 2 Full days 16 points
e. 3 or more full days 20 points

A3--Workshops/Course/ study tour which includes hands-on & skills
courses.
a. Half day (2-4 hours) 4 points
b. Full day (5-8 hours) 6 points
c. Two full days 10 points
d. Three or more full days 15 points
e. Skills accredited courses by specific disciplines (e.g. ALS, PALS, NRP, MTLS) 20 points.
f. Study tour 5 points

A4--CME session/ other professional activities. This include topic seminar, forum, lectures, formal ward rounds (teaching rounds), clinic attendance, hospital clinical meeting, video presentation, medical video conferencing, morbidity and mortality reviews, epidemiological reviews.
         a.Organising chairman for a scientific meeting gets 5 pts/ meeting
         b. Topic seminar 1 point/hr
         c. Forum 1 point/hr
         d.Lectures 1 point/hr (postgraduate lectures are not eligible for points)     
         e. Ward rounds 1 point/hr
         f. Clinic attendance 1 point/hr
         g. Hospital clinical meeting 1 point/hr
         h. Video presentation 1 point/hr
         i. Medical video conferencing 1 point/hr
         j. Morbidity and mortality  reviews 1 point/hr
         k. Epidemiological reviews 1 point/hr

A5 --  Presentation at meetings.
Plenary lecture/long paper/free paper/short paper/poster/other lectures, hospital clinical meeting, CME sessions, public medical talks
a. Free paper/ short paper/poster 10 points
b. Plenary lecture / long paper 10 points
c. Lecture presentation 5 points
d. Hospital clinical meeting 5 points
e. CME session 5 points
f. Public medical talk 5 points

A6 ---Publications of original articles in journal/ chapters in book / reports & important role in journal.
Publication of original articles in journal /chapters in books/reports
a. Indexed/peer reviewed journal (authors) 20 points
b. Non-indexed journal (authors) 10 points
c. Chapters in book (authors) 10 points per chapter
d. Reports e.g. Technical reports, working papers etc. 10 points
e. Editor 10 points,
         F. Member of Editorial Board 5 points
         G. Referee/reviewer (per article) 5 points

A7-- Self-study/group study/distance learning.
Reading scientific papers from indexed journals, organised
group discussion under accredited co-coordinator 1point per
paper or session. There needs to be documented evidence of the activity in the form of self administered MCQ  or documented evidence in the form of synopsis / evidence table.

A8-- CME Online. One point  per article or session. It requires accreditation of the providers by the CPD board.

A9--Special interest training courses (Short training courses/ Fellowship / Attachment).
These should be conducted by relevant recognised authorities - local or international which have been verified by the CPD committee.
Points are given only once, on completion of studies.
a. >3 - 6 months 20 points
b. >6 months - 1 year 30 points

The introduction to the guidelines for CPD, for medical practitioners in Malaysia by the Malaysian medical Council states that ‘the medical profession has not only a legal but a moral duty to promote high standards of patient care. Medical practitioners must be updated and competent throughout their working life by regularly participating in continuing professional development activities. The amendments to Medical Act and the Regulations were made to ensure that this objective is realised.

Does obtaining 20 CPD points ensure that the medical practitioner is uptodate and competent?The answer would probably be no.
The guideline encourage the medical practitioners to undertake CPD activities that are relevant to their field of practice and will support their professional development but there is no compulsion to undertake CPD activities relevant to their field of practice. Hence a medical practitioner may accumulate 20 points from an activity which is unrelated to his practice and still be eligible for renewal of his APC.

Lets analyse the MMC-CPD grading system.

Let's take category ‘A1- Medical congress (Local/International)’. A medical practitioner may register for the congress and not attend any of the session during the 3 days and still obtain 20 points. Most of the so called speakers of ‘international standing’ invited for these congresses are sponsored by pharmaceutical and or medical devices companies. How can they impart information which is not biased? Surely they cannot be expected to keep us updated and competent!

Category A 2 --Scientific Meetings of Academy / Universities /Colleges / Association / Institutions. Here too a practitioner may register and not attend any of the sessions and still receive the 20 points. Many of the conferences organised by medical associations and  academies cater for many medical disciplines and are not focused on a particular medical discipline and hence cannot update doctor from several disciplines. The needs of a general practitioner, a neurosurgeon, cardiac and orthopaedic surgeon are very different and cannot be fulfilled by meetings organised by medical associations and academies. Here too many of the speakers are sponsored by pharmaceutical and medical devices companies, who are biased and will not impart knowledge which is necessary to keep us updated and competent.

Category A3--Workshops/Course/ study tour which includes hands-on & skills courses. Points from such courses can be obtained once only and cannot be a source of points every year. These courses will not keep a person uptodate on the latest developments in one's speciality. These courses are basically meant for horning skills which the practitioner already possess.

Category A4--CME session/ other professional activities. Opportunities to participate in these activities are grossly limited. However, the organizing chairman of a scientific meeting gets 5 points. How organising a meeting makes a person uptodate and competent in his/her field of expertise is difficult to fathom. Why giving undergraduate lectures makes one eligible for points and giving postgraduate lecture does not make one eligible for points remains a mystery. One would believe that more in depth knowledge is needed to give postgraduate lecture as compared to an undergraduate lecture.

Category A5--  Presentation at meetings.
Points allocated for plenary lecture/long paper/free paper/short paper/poster/other lectures, hospital clinical meeting, CME sessions and public medical talks are well deserved. Such activities do help the practitioner remain uptodate.

Category A6 ---Publications of original articles in journal/ chapters in book / reports & important role in journal.

Points for publication of original articles in journal /chapters in books/ report are well deserved since such activity keeps the practitioner uptodate and competent.
There is however, some uncertainty as to whether being an editor, member of editorial board, referee/reviewer, helps one remain updated and competent. Whether CPD points should be allocated for such activity will depend on the quality of the journal,its impact factor and the number of issues published in a year. For example, there is a Malaysian journal which publishes 3 issues per year. More than half of the articles are case reports. It has a panel of 100 reviewers and its yearly Impact Factor‎ is ‎0.011 and 5-year Impact Factor is 0.009. Surely the reviewers of this journal do not deserve CPD points.
Points from categories A7 to A9 are unlikely to play a significant role in the CPD activities of medical practitioners.
Medical practitioners keen on keeping themselves updated and competent
will not need to participate in any of the activities prescribed by the MMC-CPD schedule. They will read and write to keep themselves updated. Medical practitioners who are forced to accumulate CPD points for the APC and are not keen to update themselves will find ways to get the points without getting updated. There are limits to professional self-regulation. So what can be done to make sure medical practitioners get updated?

What is the way forward? “Recertification”/Revalidation!

Recertification in USA

The unique strength of American medicine is a voluntary physician-led, nongovernmental process of setting standards. In 1936 the American Board of Internal Medicine (ABIM) was founded and the board set the standards for internal medicine practice and the practice of its subspecialties. It is physician-run organization which is independent of any
physician societies or membership organizations. The standards set by the board which are  measured by the “certification” process, lets the public know that the internist has met the ‘knowledge and practice requirements that ensure a high level of quality of care’ [7]. Though participation in this certification process is voluntary, about 98% of internists attempt certification and about 96% of them achieve certification [7].
In 1990 ABIM instituted a significant change to the program when they limited the validity of the certification to 10 years and after 10 years to maintain their certification the internist had to undergo a Maintenance of Certification (MOC) program. Those who did not do so would no longer be “board certified” [7]. About 85% of Diplomates continue to participate in the MOC program.
Studies show that  the board certified internist have better patient outcomes as compared to those who are not [8-12]. Studies also show that physician knowledge and the quality-of-care outcomes diminish with time, after graduation, with increasing years in practice [13].
The American Board of Medical Specialties (ABMS) is an umbrella organization for 26 specialty board. Most of the specialist boards require recertification every 10 years to maintain board certified status. The ABMS 
require every MOC program to have 4 components i.e ‘evidence of professional standing (license to practice); participation in lifelong learning and self-assessment; evidence of cognitive expertise (examination); and assessment of practice performance’ [7].

Revalidation in UK

The General Medical Council (GMC) in UK introduced revalidation for doctors in December 2012, after several years of discussion and debate.  The doctors in UK need revalidation to show to the GMC that they are uptodate and fit to practice and thereby maintain their licence to practice.
The doctors have to take part in a robust appraisal process and collect evidence to show they meet the necessary standards set by GMC. The revalidation cycle runs for 5 years and they need to revalidate once every 5 years. The first cycle was from 2012 to 2016.

For revalidation the doctor has to fulfill the following requirements:

Take part in an annual appraisal process
Complete at least one appraisal per year based on good medical practice
Collect and reflect on six types of supporting information.
The six types of supporting information include
           1. continuing professional development (CPD)
           2. quality improvement activity
           3. significant events
           4. feedback from colleagues
           5. feedback from patients
           6. review of complaints and compliments.
The above information has to be provided and discussed at their appraisal at least once in each five–year cycle.

Recertification & continual professional development

New Zealand has very comprehensive guidelines on recertification and continual professional development. Doctors in New Zealand must meet recertification and continual professional development (CPD) requirements if they want to maintain the right to be issued with a practising certificate. The Medical Council of New Zealand, requires doctors to undertake 50 hours of professional activity each year, which is directed to the maintenance of professional competence. This includes participation in audit of medical practice, peer review and continuing medical education. There has to be at least one audit per year, which entails ‘a systematic, critical analysis of the quality of a doctor’s own practice and is used to improve clinical and/or health outcomes, or to confirm that current management is consistent with
current available evidence or accepted consensus guidelines’ [14].
 There has to be a minimum of 10 hours of peer review per year. The peer review could involve joint review of cases, review of charts, practice visits to review a doctor’s performance, 360° appraisals and feedback, critique of a video review of consultation and discussion group, inter-departmental meetings that may review cases and interpretations of finding and mortality and morbidity meetings.
Doctors would need a minimum of 20 hours per year of Continuing medical education (CME) which would include attendance at relevant educational conferences, courses and workshops, self-directed learning programmes and learning diaries, assessments designed to identify learning needs in areas such as procedural skills, diagnostic skills or knowledge and journal reading [14]. CME may also include:

• examining candidates for college examinations
• supervising or mentoring others
• Teaching
• publication in medical journals and texts
• Research
• committee meetings with an educational content, such as guideline development
• giving expert advice on clinical matters
• presentations to scientific meetings
• working as an assessor or reviewer for the Council. 

Doctors are subjected to an audit by the Medical Council to ensure that doctors are complying with their recertification. Failure to satisfy requirements can result in the Council proposing to place conditions on the scope of practice or limitations on the practice and in serious cases, the Council can propose to suspend the doctors registration.

References

1. Rodwin MA, ‘Drug Advertising, Continuing Medical Education, and Physician Prescribing: A Historical Review and Reform Proposal’, Conundrums and Controversies in Mental Health and Illnesses. 2010 807-815 (p.809).
2. Charter on continuing medical education/continuing professional development approved by the UEMS Specialist Section and European Board of Anaesthesiology. European Journal of Anaesthesiology 2007; 24: 483–485.
3. Schostak J, Davis M, Hanson J, Schostak J, Brown T, Driscoll P,  Starke I, Jenkins N. The Effectiveness of Continuing Professional Development. A report prepared on behalf of College of Emergency Medicine, Federation of Royal Colleges of Physicians and Manchester Metropolitan University. 2010 College of Emergency Medicine at http://www.aomrc.org.uk/wp-content/uploads/2016/04/Effectiveness_of_CPD_0610.pdf accessed on 20/6/2018.
4. Murgatroyd GB. Continuing professional development -- The international perspective. Intelligence Unit, General Medical Council, July 2011 at https://www.gmc-uk.org/static/documents/content/CPD___The_International_Perspective_Jul_11.pdf_44810902.pdf accessed on 19/6/2018.
5. Lang ES, Wyer PC & Haynes RB. Knowledge translation: closing the evidence to practice gap. Ann Emerg Med 2007; 49 (3): 353-366.
6. Guidelines on Continuing Professional Development (CPD) For Medical Practitioners In Malaysia. Malaysian Medical Council 17 April 2018 at http://www.mmc.gov.my/images/contents/CPD/MMC-CPD%20Guidelines%20(updated).pdf accessed on 26/6/2018.
7. Levison W, Holmboe E. Maintenance of certification: 20 years later. Am J Med 2011; 124: 180-185.
8.  Norcini JJ, Lipner RS, Kimball HR. Certifying examination performance and patient outcomes following acute myocardial infarction. Med Educ. 2002;36(9):853-859.
9. Norcini JJ, Kimball HR, Lipner RS. Certification and specialization: do they matter in the outcome of acute myocardial infarction? Acad Med. 2000;75(12):1193-1198.
10. Chen J, Rathore SS, Wang Y, Radford MJ, Krumholz HM. Physician board certification and the care and outcomes of elderly patients with acute myocardial infarction. J Gen Intern Med. 2006;21(3):238-244.
11. Pham HH, Schrag D, Hargraves JL, Bach PB. Delivery of preventive services to older adults by primary care physicians. JAMA. 2005;294(4):473-481.
12. Ramsey PG, Carline JD, Inui TS, Larson EB, LoGerfo JP, Wenrich MD. Predictive validity of certification by the American Board of Internal Medicine. Ann Intern Med. 1989;110(9):719-726.
13. Choudhry NK, Fletcher RH, Soumerai SB. Systematic review: the relationship between clinical experience and quality of health care. Ann Intern Med. 2005;142(4):260-273.
14. Recertification and continuing professional development. Medical Council of New Zealand, April 2018 at https://www.mcnz.org.nz/assets/News-and-Publications/Recertification-and-continuing-professional-development-30-4-2018-v7.pdf accessed on 4/7/18.