Evidence-based medicine in orthopaedic surgery and its legal implications

Evidence-based medicine in orthopaedic surgery and its legal implications


                                    Dr KS Dhillon FRCS

Introduction

In medical negligence claims the plaintiff (patient) has to prove that the doctor owed him a duty of care, the doctor breached the duty and the breach caused damage. In medical negligence, there is no doubt that the doctor owes the patient a duty of care. This duty is to ‘exercise reasonable care and skill in diagnosing, advising and treating the patient’ (1).

A patient with osteoarthritis of the knee presents to the surgeon with knee pain after having a short course of conservative treatment. Surgeon A tells the patient that he will need an arthroscopic joint debridement which is quite a straight forward procedure and that would take care of the problem. Surgeon B, on the other hand, has a discourse with the patient about the disease and tells him that arthroscopic surgery is of no proven value in the treatment of OA and that he should persist with conservative treatment and eventually the pain will settle. He also tells the patient that surgery can be associated with complications which sometimes can be very serious.

Is there is any doubt about which surgeon the patient will choose? Surgeon A is practicing opinion based medicine while surgeon B is practicing evidence-based medicine. Surgeon A relied on what he learnt in postgraduate medical school and from his mentors/peers in arriving at a management decision while surgeon B relied on evidence-based information in arriving at a decision. This decision making is taken into consideration in the standard of care analysis by the courts to assess whether the surgeon exercised reasonable care and skill.

What is evidence based medicine?

Many physicians have been and are still practicing medicine based on, what they learned in medical schools, on information from their peers and mentors, from individual experience and from occasional seminars and conferences.

However over last two decades the practice of medicine has changed from the traditional mould to what is now popularly known as evidence-based medical practice. One of the most widely used definition of evidence-based medicine (EBM) is that by Sackett et al (2). They have defined it as ‘evidence-based medicine is the conscientious, explicit, and judicious use of current best evidence in making decisions about the care of individual patients. The practice of evidence-based medicine means integrating individual clinical expertise with the best available external clinical evidence from systematic research’. Best external evidence would mean the most recent clinically relevant patient centred and basic sciences research (2). Previously accepted diagnostic tests and treatment modalities that have been invalidated by current research should be abandoned otherwise outdated practice can be detrimental to the patients. Opinion and experience-based practice in the past has proved to be ineffective and even harmful (3).

Often ‘clinicians are unaware of the available evidence or fail to apply it’ (4).  Lack of time is the most frequent reason given by busy clinicians for their inability to keep abreast with current research. However ‘studies show that busy clinicians who devote their scarce reading time to selective, efficient, patient driven searching, appraisal, and incorporation of the best available evidence can practice evidence-based medicine’ (2). Treatment should do more good than harm to patients and the gold standard for such decision making would be systematic reviews of several randomised trials (2). Besides Medline there are many other online resources available for rapid access to the latest best evidence. For orthopaedic surgery, there are many well-researched resources available from where information can be rapidly obtained (5). The Cochrane reviews and structured abstracts in most journals provide very useful information which can help in evidence-based decision making. The Journal of Bone & Joint Surgery, for example, has structured abstracts and has a section on evidence-based orthopaedic besides the scientific articles.

For busy clinicians, well-researched evidence-based guidelines can be a source of valuation information. The U.S. Institute of Medicine defines clinical practice guidelines as ‘the consensus statements that have been systematically developed to assist practitioners and patients in making appropriate health care decisions for specific clinical circumstance’ (6).
Unfortunately, opinion based practice in orthopaedics is rampant with many traditions and myths which are not evidence based.

Myths in orthopaedic surgery

Husted et al has debunked many of the traditions and myths associated with hip and knee arthroplasty (7). Pre-operative removal of hair, urine sampling and testing, use of plastic adhesive drapes and preoperative warming of the operation theatre are not necessary and these measures do not improve the outcome of knee and hip arthroplasty yet these practices are almost universal. The intra-operative use of Tranemic acid is believed to be associated with increased risk of thromboembolic events which is not true. In fact, its use reduces bleeding and decreases the need for blood transfusion. The use of the tourniquet to improve cementing in knee replacement, use of disposable knives, routine use of indwelling urinary catheters and the use of drains to reduce haematoma formation in joint replacement has no scientific basis. Postoperative recommendations, of leaving the dressing untouched for 24 hours, avoidance of NSAIDS, avoiding flying in the early postoperative period, antibiotic prophylaxis for dental procedures, use of CPM, use of cryotherapy, not discharging patient till knee flexion is 90 degrees, and haemoglobin trigger of 10g/dl or a drop of haematocrit of 30% for blood transfusion, though widely practiced, these recommendations have no scientific basis.

When conservative medical treatment for knee pain, in patients with osteoarthritis, fails, surgeons generally advocate arthroscopic debridement of the knee. There has never been any physiological basis for such treatment and why it is done remains an enigma. In 2002 Moseley et al (8) published an article in the New England Journal of Medicine to show the futility of such treatment but to date such procedures are still carried out.

Arthroscopic partial meniscectomy is the most common orthopaedic operation performed in the USA (9). About 700,000 arthroscopic partial meniscectomies are performed annually in the USA at an estimated cost of 4 billion dollars (10). There is good scientific evidence that partial meniscectomy for degenerative tears provides no benefit to the patients (10) yet this practice is rampant.

When a patient presents to the physician with low back pain, an MRI of the lumbar spine is often the diagnostic test of choice of many physicians (often without any clinical work-up), despite the fact that abnormalities of the disc in asymptomatic people is well known. This idolatry of imaging is widespread and often the cause of back pain is attributed to the abnormalities detected by the MRI although the findings may be coincidental.

Jansen et al (11) studied the prevalence of MRI abnormalities of the lumbar spine in 98 asymptomatic subjects (50 men and 48 women) with an average age of 42.3 years. They found that only 38% of the subjects had a normal disc at all levels and 62% had abnormalities of the disc at one or more levels. Strong evidence shows that routine back imaging does not improve patient outcomes, exposes patients to unnecessary harms, and increases costs (12). Unnecessary imaging is done not only due financial incentives but also due to an unsubstantiated belief that imaging can be an alternative to a good history and physical examination.

Many physicians believe that osteoarthritis (OA) is a progressive degenerative disease of diarthrodial (synovial) joints characterised by pain, limitation of joint movements and eventually deformity of joints. However, there is scientific evidence to show that OA does not progress in all patients. Most of the studies of the natural history primary OA have been done for OA of the knee and studies for OA of the hip are sparse. The progression of knee OA is usually slow and it can take many years for the disease to progress. It is also known that it can remain stable for many years (13). In patients with osteophytes alone on radiographic examination, only one-third will show radiographic progression (14).

It is a common belief that OA is a progressive disease which would eventually lead to end stage disease which would require reconstructive surgery. Leyland et al in a 14 year population-based cohort study of 1,122 knees found that the percentage of knees with radiographic OA that were replaced (TKR) at year 15 was 1.1% for grade 0 knees, 4.9% for grade1 knees, 5.3% for grade 2 knees and 6.7% for grade 3 knees (15).

Spinal fusion for chronic non-specific back has no scientific basis yet such operations are frequently carried out. Chronic low back pain represents a common disabling and costly health problem but unfortunately in 80% to 95% of the patients a pathoanatomical diagnosis cannot be made despite the existence of modern imaging techniques (16). For spinal fusion to be successful in the treatment of chronic or recurrent low back pain there has to be a pathoanatomical diagnosis which accounts for the pain. The role of spinal fusion in progressive or unstable spondylolisthesis, spinal trauma, tumours and spinal infections is well established. However in patients with non-specific chronic low back pain a pathoanatomical diagnosis is often impossible to establish and, therefore, spinal fusion cannot be of any use in the treatment of chronic non-specific back pain.

There is a general belief that all ACL injuries must be treated with a reconstruction to minimise symptoms, improve the quality of life and minimise the risk of future complication such as chondral and meniscal injury. Now there is level 1 scientific evidence that the mid-term (5years) patient reported and radiographic outcomes between those patients treated with rehabilitation plus early ACL reconstruction and those treated with rehabilitation and optional delayed ACL reconstruction are the same in young active individuals (17). Another study by Neuman et al (18) which excluded professionals and those not willing to reduce their activity level and were followed up for 15 years the incidence of delayed reconstruction was 23%. This translates to a 77% of the patients who modify their activity level will not require an ACL reconstruction. Despite this evidence, there has been a dramatic increase in the number of anterior cruciate ligament (ACL) reconstructions that are carried out here in Malaysia as well as around the world.

Anecdotal evidence suggests that many surgeons recommend posterior cruciate ligament (PCL) reconstruction for injuries of the PCL. However, a review of the literature shows that reconstruction of the PCL is not the treatment of choice for PCL rupture. The majority of PCL tears produce a moderate laxity (10mm or less) of the PCL. The recommended treatment for such injuries is conservative with quadriceps muscle strengthening exercises. The treatment of choice of avulsion fractures involving the PCL when the fragment is large enough to be fixed with a screw is a surgical fixation of the fragment. The treatment of choice for chronic PCL tears is also conservative (19).

There are many surgeons who recommend a repair of grade 3 injuries of the lateral ligament of the ankle, but there is no evidence that such surgery gives better results than conservative treatment (20).
Myths continue to be perpetuated partly due to failure on the part of the physicians to keep abreast with current evidence-based medicine and also partly due financial conflicts of interest. Whatever the reasons why doctors continue to perpetuate these myths, failure to keep abreast with current evidence-based practice can have medicolegal implications.

Standard of care in medical negligence

There are 4 components in medical negligence claims which include a duty of care, breach of this duty and the breach caused (causation) injury (damage). It is a trite law that a duty of care is owed by the doctor to the patient. Breach of the standard of care is usually the threshold question in negligence claims. The question that usually arises is whether the physician possessed reasonable skill and exercised the skill in the care of the patient, which another reasonable physician would have exercised in a similar situation (21).

What a reasonable physician would have done under a given situation is decided by the court based on the testimony of the medical expert witness. The expert is expected to testify as to what others in the same profession would commonly do in such a situation. The expert normally refers to the clinical literature and research findings to support his/her testimony. Invariably the courts would expect the testimony to be supported with scientific evidence (21).

 Determining what is a reasonable standard of care is a problem. Most of the experts will not know how the majority of the doctors practice medicine. They usually ‘rely on their personal experience or theoretical assumptions about what is reasonable or what they, as experts, would have done under the same circumstances’ (21). A reasonable standard of care can be determined by reference to current evidence-based literature which is easily available online rather than basing it on past experience and on what we have learnt from peers, mentors or from the occasional seminars and conferences. This would entail the need to stay abreast with current clinical and scientific literature.

Medicine and technology are rapidly evolving and it would be reasonable for the courts to expect that the standard of care evolves accordingly. Hence, there is a duty to stay abreast with current developments. In English law, there is an obligation on the part of the physician to make reasonable effort to stay abreast. Swanwick J in Stokes v Guest Keen & Nettlefold said that ‘where there is developing knowledge, [the defendant] must keep reasonably abreast of it and not be too slow to apply it’ (22). A medical practitioner cannot be expected to read every new article published in his field of speciality but in a situation where a particular risk has repeatedly been highlighted the physician will be ignoring it at his own risk (23). Though a practitioner cannot be expected to read every new article published, all practitioners have easy access to a wealth of concise information on evidence-based medicine and clinical practice guidelines on a vast range of topics.

Clinical guidelines and legal liability

Although science in medicine has made great strides in last few decades, yet much of what we practice remains unsupported by scientific evidence(3). Myths continue to be perpetuated because of our reluctance to embrace evidence-based practice. Our practice has been based largely on common sense, tradition and on information passed on by our mentors and peers. Evidence-based medicine is gaining momentum and hopefully it will reverse the past trends of customary medical practice. Evidence-based medicine distinguishes between the best relevant medical information from literature and what is known in legal terms as ‘junk science’ (24).

There is enormous information available in the scientific literature which is difficult for an average clinician to read and digest. To overcome this problem, clinical practice guidelines (CPGs) have been developed to aid clinicians in decision making. These guidelines are developed by multidisciplinary expert groups who systematically review all available data in the literature and reach a consensus as to what is the best way to approach a given clinical condition. The US Federal government in 1989 recognised the need for such guidelines and established the Agency for Health Care Policy and Research (AHCPR) which was later named as the Agency for Health Care Research and Quality (AHRQ). One of its functions is to do outcome research as well as to formulate and distribute clinical practice guidelines. AHRQ has a National Guideline Clearinghouse which makes publically available a database of thousands of evidence-based clinical practice guidelines and related documents and the contents are updated weekly (25).

Though many in the medical community have welcomed these guidelines as a valuable source of useful information, there are others who believe that these guidelines are an affront to professional autonomy and a challenge to clinical judgement (26). Despite the criticism by some that these guidelines is ‘cookbook medicine’, the emphasis on EBM and formulation of CPGs is gaining momentum.

CPGs are not a substitute for EBM but is an important component of EBM, the aim of both is to assist physicians in making clinical decisions. Some CPGs may not be updated regularly hence the need to remain abreast with EBM is vital.

Though in the USA and UK clinical guidelines are not applied in courts as a legal standard of care, in the Netherlands published guidelines for general practitioners are accepted by the court as a legal standard of care. In France, legislations are in place to make practice by the guidelines mandatory, and there are sanctions for practitioners who deviate from such practice (24).

In the USA and the UK, guidelines cannot be admitted as evidence of the standard of care because such evidence would be regarded as hearsay. However, the expert witness in his testimony can use the guidelines as evidence of the standard of care. The use of guidelines by an expert in his testimony could fulfil the requirements of the standards set in Bolam (27) as well as those in Bolitho (28). Clinical guidelines are prepared by multidisciplinary expert groups who systematically review all available data in the literature and reach a consensus hence the guidelines would conform to Bolam’s requirement of a similar body of responsible and skilled professionals. Without a doubt the guidelines weigh all benefits and risk and are logical conclusions arrived at by experts, hence they would fulfil the requirements of Bolitho.

Many legal academics believe that with the growing emphasis on EBM and CPGs, the CPGs will in future ‘define the requisite "standard of care" for medical treatment and impact medical malpractice litigation. They may even replace expert testimony’ (24).

Repair of ligaments, joint debridement for OA, spinal fusion for non-specific back and neck pain are by far the most common elective orthopaedic procedures performed by orthopaedic surgeons. The traditional orthopaedic practice of routine repair of ligaments, spinal fusion for non-specific back and neck pain, joint debridement for OA, and sometimes joint replacement for joint pain in the absence of moderate to severe osteoarthritis, is unlikely to fulfil the requirements which the courts will expect in the standard of care analysis.

Conclusion
There is no doubt that there has been a steep rise in the malpractice insurance premiums for orthopaedic surgery over last two decades and the premiums continue to rise every year. This is a reflection of the increase in the number of malpractice suits filed in the courts as well as a reflection of the number of successful claims with high payouts in recent years. The customary orthopaedic practice of yesteryears cannot continue and we have to embrace rapidly evolving evidence-based practice. Lack of time cannot be an excuse since valuable evidence-based information is easily available.

Evidence base medicine is making inroads in the standard of care analysis by the courts to assess whether the surgeon exercised reasonable care and skill in diagnosing, advising and treating the patient. If we continue to practice opinion based medicine and not embrace evidence based medicine we will be at risk of being a subject of a malpractice suit.








References
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Treatment of low back and neck pain: An evidence based approach

 Treatment of low back and neck pain: An evidence approach

                                    Dr KS Dhillon FRCS, LLM

It is well known that musculoskeletal symptoms are common in adult communities and the prevalence of these symptoms increase with age. The most common site of pain from musculoskeletal disorders is the low back (23%) followed by the knee (19%) and the shoulder (16%) (1). The global point prevalence of low back pain (LBP) is the highest at 9.4% (2) and for neck pain it is 4.9% (3). LBP ranks highest in term of disability as measured by years lived with disability (YLD) and its prevalence and burden increases with age (2). Low back pain and neck pain constitutes a high proportion of a GP’s and an orthopaedic surgeon’s patient load. The treatment of musculoskeletal pain is financial burden and this burden can be expected to get worse with increasing lifespan of individuals and a larger aging population. Can this financial burden be reduced by providing evidence based care to patients with musculoskeletal pain? This review will be confined to the management of back and neck pain because of the similarities in the etiopathogenesis and the treatment of both these disorder as well as due to space constraints.

Treatment of low back pain

Definition and pathogenesis of back pain

Uniformity of definitions is essential to study prevalence and management outcome of low back pain. There is a lack of uniform definitions of low back pain in the literature. Acute back pain is defined as back pain that last for less than 6 weeks and subacute back pain is that which last between 6 to 12 weeks. Chronic low back pain is persistent low back pain that is present for at least 12 weeks. There will be patients with a history of back pain for many years who have repeated bouts of acute or subacute back pain but will not be classified as having chronic low back pain unless the episode of pain last at least 12 weeks. A recurrence of an episode of low back pain is defined as a return of low back pain lasting at least 24 hours and recurrent low back pain is defined as low back pain which has occurred at least two times over the past year with each episode lasting at least 24 hours (4).

There are several classifications of low back pain; the most widely accepted is that proposed by Waddell. Waddell’s diagnostic triage divides low back pain into three categories;
• Specific spinal pathology such as tumour, infection, fractures, cauda equina syndrome ( ‘Red flags’) which occurs in about 1 to 2 % of the patients.
• Nerve root pain such as that caused by disc prolapse and spinal stenosis which occurs in about 5% of the patients.
• Non-specific low back pain which occurs in about 85 to 95% of the patients (5).

The first two categories fit into the classical disease model where the disease can be accurately diagnosed and appropriately treated. However, the third category does not fit into this model, where a proper clinical diagnosis can be made. Such a diagnosis of non-specific low back pain according to Waddell is ‘intellectually and scientifically inadequate and fails to provide any biological basis for real understanding’ which results in treatment remaining ‘empirical or based on unproven hypotheses’ (5). Claims of diagnoses such lumbar strain or degenerative spine disease as a cause of low back pain remain unfounded and leaves room for uncertainty about treatment, prognosis and clinical outcome (5).

The treatment of patients with specific spinal pathology such as tumour, infection, fractures and cauda equina syndrome (which occurs in about 1 to 2 % of the patients) and in patients with nerve root pain such as that caused by disc prolapse and spinal stenosis (which occurs in about 5% of the patients), is quite straight forward with good outcome. The major problem is the treatment of the 95% of the patients with non-specific back pain who make frequent visits to the medical practitioner and which poses a social and financial burden.

Treatment of non-specific back pain

A review of 15 national/international guidelines, which are based on publications of studies on management of low back pain, show that there is no role for routine imaging in the management of non-specific low back pain (6). The guidelines mention that psychosocial and occupational factors (‘yellow flags’) are associated with poor prognosis and these factors often produce chronicity of back pain.

One of the most important therapeutic interventional factors in the management of the back pain is effective communication using simple non-medical terminology. The patient need to be reassured that there is nothing seriously wrong with his/her back. The patient should be advised to stay active and avoid bed rest. Activity should be gradually increased and the patient should be advised to return to work early even with the back pain (6).

All guidelines recommend that the first line of medicinal treatment for the pain should be the use of Paracetamol/acetaminophen. This should be followed with NSAIDS as the second line of treatment. However there is no irrefutable evidence that NSAIDS are more effective than placebo or no treatment at all for treatment of acute low back pain. It is the same with the use of muscle relaxants where there is conflicting evidence on the effectiveness as compared to placebo. NSAIDS can have gastrointestinal complications while muscle relaxation can cause dizziness, drowsiness and dependency among other complications (7).

The effect of opioids and compound analgesics is similar to that of NSAIDS but opioids and compound analgesic can have substantially higher risk of side effects as compared to paracetamol. The evidence for the use of, spinal manipulation, acupuncture, back exercises, bed rest, lumbar support, spinal injections, TENS, massage, topical applications and traction in the treatment of acute back pain, is at best conflicting in nature and is no better than the standard treatment of back pain with analgesics. However the use of cognitive behavioural therapy has been shown to reduce general disability in the long term (7).

Routine use of muscle relaxants is not recommended because any benefit can be outweighed by the adverse effects. Adjuvant agents such as anticonvulsants (Gabapentin, Pregablin) and anti-depressants (Amitriptyline) are not recommended for the treatment of acute low back pain (7).
Acute low back pain is generally self-limiting. However it is important to exclude specific spinal pathology such as tumour, infection, fractures, cauda equina syndrome (‘Red flags’) which occurs in about 1 to 2 % of the patients and needs immediate specific treatment. Usually rapid improvement in ‘pain (mean reduction 58% of initial scores), disability (58%), and return to work (82% of those initially off work)’ occurs within a month. Further improvement can occur up to about three months. After 3 months improvements of these parameters usually remain relatively constant. About 73% of patients will have at least one recurrence within 12 months (8).

Acute neck pain

Acute neck pain is defined as pain that is present in the back of the neck in the region from the superior nuchal line to a transverse line running through the tip of the spinous process of the first thoracic vertebra, which has been present for less than 3 months. Chronic neck pain is defined as that which is present for 3 months or more (7).

As with the lumbar spine, serious causes of acute neck pain are rare but they should be promptly diagnosed and treated. The incidence of serious cause of acute neck pain is less than 1% and these include spinal tumours, spinal infections, epidural haematomas and aneurysms. Fractures are uncommon causes of acute neck pain and the incidence is less than 5%. In most of the patients the acute neck pain is idiopathic or is due to whiplash injury. There is level III evidence that degenerative cervical spondylosis is neither the cause nor a risk factor for idiopathic neck pain (7).

Various terminologies have been used to describe the degenerative changes in the cervical spine including cervical spondylosis; cervical osteoarthrosis, degenerative disc disease and degenerative joint disease, but all these changes constitute normal age changes of the cervical spine (9). There are studies that show that cervical spondylosis occurs slightly more frequently in symptomatic than asymptomatic individuals (10) (11). The prevalence of disc degeneration has been found be no different in symptomatic and asymptomatic individuals and the prevalence of uncovertebral osteophytes and osteoarthrosis of the synovial joints of the neck has been found to be less prevalent in symptomatic individuals (12). Hence finding of degenerative changes in the cervical spine on radiographs does not mean that these degenerative changes are the cause of neck pain.

Imaging of the cervical spine is not necessary in patients with acute neck pain in the absence of trauma and clinical evidence of serious underlying disorder. Level III evidence suggests that 40% of patients of patients recover fully from non-specific acute neck pain. About 30% will continue to have mild symptoms and 30% may continue to have moderate to severe symptoms (13,14).
Level III and level IV evidence shows that in patients with whiplash injury about 56% of them fully recover within three months and 80% recover fully within one or two years. However about 15–40% continue to have symptoms and 5% are severely affected (15, 16).

There is dearth of clinical studies on the treatment of acute neck pain. However, advice to remain active, resume normal activities and maintain neck movements has been found to be more effective than the use of rest or cervical collar in the treatment of acute neck pain (level I and II evidence). Gentle neck exercises are more effective than the use of collar and analgesic. There is insufficient evidence on the effectiveness of use of analgesic, opioids, muscle relaxants, acupuncture, cervical manipulation, traction and electrotherapy in the treatment of acute neck pain (7).

Chronic low back pain

Chronic low back pain (CLBP) is defined as pain in back, in the region from the lower costal margin to the inferior gluteal line, which last at least 12 weeks. According to Waddell’s diagnostic triage specific spinal pathology such as tumour, infection, fractures, cauda equina syndrome ( ‘Red flags’) occurs in about 1 to 2 % of the patients and nerve root pain such as that caused by disc prolapse and spinal stenosis occurs in about 5% of the patients. Majority of the patients with chronic low back pain fall into the category of non-specific low back pain which occurs in about 85 to 95% of the patients (5).

There is level II (moderate) evidence that imaging of the spine is not recommended for patients with non-specific CLBP and there is moderate evidence that MRI of the spine is useful in patients with radicular pain and in patients suspected to have discitis or neoplasm of the spine (17). Level II evidence suggests that facet joint injections, MRI and discography are not reliable procedures for the diagnosis of facet joint pain and discogenic pain. There is level III evidence that radioactive bone scans are useful for the diagnosis of pseudoarthodesis after spinal fusion and for the diagnosis of stress fractures and malignancies. The use of electromyography as a diagnostic procedure in chronic nonspecific low back pain is not recommended (17).

Physical treatment for CLBP

There is insufficient evidence of the usefulness of physical treatment modalities, such as interferential therapy, laser therapy, lumbar support, short wave diathermy, ultrasound, thermotherapy, traction and TENS, in the treatment of CLBP and hence these modalities are not recommended for the treatment of CLBP (17).

Exercise Therapy

There is level II evidence that exercise therapy helps to reduce pain and disability in the short term and there is strong evidence that exercise is more effective than  ‘GP care’ in reducing pain, disability and return to work in the mid-term (3-6 months) in patients with CLBP. Reconditioning and back strengthening exercises are not recommended.

 Hence supervised exercise therapy is the first line of treatment of CLBP. Expensive training machines are not required. Cognitive-behavioural approach with graded exercise using exercise quotas is recommended. Group exercise programs are useful and they cost less than individual exercise programs (17).

Cognitive-behavioural treatment 

There is strong level I evidence that behavioural treatment is more effective for pain, functional status and behavioural outcomes than placebo and or no treatment and there is also strong evidence that a graded activity programme using a behavioural approach is more effective than traditional care for returning patients to work (17). There is strong evidence that multidisciplinary biopsychosocial rehabilitation with functional restoration approach reduces pain and improves function in patients with chronic low back pain (17).

Drug treatment

The complexity of the mechanisms causing chronic pain and the greater role of social, psychological, and economic factors makes the efficacy of drug treatment less clear in patients with CLBP (17).
A survey of primary care patients shows that the most commonly prescribed drugs for back pain are non-steroidal medications (NSAIDS) (69%) followed by muscle relaxants (35%), narcotics (12%) and acetaminophen (4%) (18).

Antidepressants

Antidepressants block the reuptake of neurotransmitters (norepinephrine and serotonin) and modulate pain sensation. The most studied are the tricyclic antidepressants (such as Amitriptyline). There is strong evidence that such antidepressants are effective in relieving pain in patients with CLBP but they do not improve function or disability (moderate evidence). Antidepressants are usually used in combination with other drugs such as NSAIDS especially in patients with severe back pain. However antidepressants should not be used in patients with renal disease, glaucoma, chronic obstructive pulmonary disease, cardiac failure and in patients who are pregnant (17).

Muscle relaxants

Muscle relaxants such as benzodiazepines are effective in the treatment of back pain (strong evidence) but there is insufficient evidence that they reduce muscle spasm. Their use can be associated with severe adverse events such as dizziness, drowsiness and addiction and hence used be only used for short durations (17).

NSIADs

There is strong evidence that NSAIDs are effective for the relief of chronic low back pain (level A). The use of NSAIDs are recommended for the treatment of CLBP but these drugs should be used for the shortest duration possible and should not exceed 3 months because of possible side effects such as  gastrointestinal complications (irritation, ulcers and bleeding) and cardiovascular complications (17).

Opioids

There is strong evidence that weak opioids such as tramadol relieve pain and disability in the short term in patients with CLBP. Their use is recommended in patients with moderate and severe back pain who do not respond to analgesic/NSAIDs or are unable to take NSAIDS due to their side effects (17).

Antiepileptic drugs (Gabapentin)

There is no evidence that antiepileptic drugs such as Gabapentin are effective in relieving pain in patients with CLBP and their use for treatment of CLBP is not recommended (17).

Epidural steroid injections

Review of literature shows that there is no evidence for the effectiveness of epidural/perineural steroid injections for non-radicular, non-specific low back pain and there is conflicting evidence of the effectiveness of such injections in the treatment of radicular pain.

Epidural injections can be associated with complications though they are uncommon. These include Cushingnoid symptoms (with frequent use), post-dural puncture headaches, epidural abscess, chemical meningitis and Arachnoiditis.

The use of epidural injections is not recommended for the treatment of CLBP (17).

Facet block and Intradiscal Injections

There is no evidence for the effectiveness Facet block (joint and nerve) and for intradiscal corticosteroid injections in the treatment of chronic low back pain and the use of such injection for the treatment of CLBP is not recommended (17).

Sacroiliac Joint Injections

There is only limited evidence (level C) that injection of the sacroiliac joint with corticosteroids relieves sacroiliac pain of unknown origin for a short duration of time (one month). The use of sacroiliac joint steroid injections is not recommended for treatment of CLBP (17).

Surgery

Chronic back pain is a symptom and not a disease. Specific spinal pathology which fits into a classical disease model, where treatment can be effective, can be found in only about 6% to 7% of the patients. In about 85 to 95% of the patients with back pain no pathoanatomical diagnosis can be made and such pain gets labelled as non-specific back pain.

Imaging findings such as degenerated disc, facet arthritis, spondylosis, spondylolysis and spondylolisthesis has no causal relationship to the pain in these patients. In the vast majority of patients the degenerated disc is implicated as the cause of chronic low back pain while in others the facet joints and sacroiliac joint is believed to be the cause of the pain. Although MRI scans can accurately depict the anatomical changes seen in the spine as degeneration of the spine sets in, the clinical significance of these changes remain elusive and the scans cannot help in elucidating the cause of the pain. Provocative discography which was in the past touted as a valid diagnostic test, has also failed to stand up to its usefulness. To date there is no imaging technique or diagnostic test which can localise the source of pain in patients with non-specific back pain.

Despite the inability to make a diagnosis in patients with non-specific low back pain, there has been a sharp increase in the number of patient undergoing spinal fusion for low back pain over the last two decades. Spinal fusion in patients with non-specific back pain is akin to treating a symptom (not a disease) with surgery. Logic dictates that such an approach cannot be very successful.

There is a dearth of level 1 studies in the medical literature comparing spinal fusion to non-surgical treatment of chronic low back pain. There are two relatively good level 1 studies (19, 20) with two to four years follow up comparing surgical to non-surgical treatment published so far, but they do not show superiority of surgical treatment over nonsurgical treatment. Furthermore spinal fusion is associated with significant and sometimes serious medical complications including mortality (21, 22, and 23).

Chronic neck pain

There is a dearth of evidence based publications in the medical literature on the treatment of chronic neck pain which is also the case for the treatment of acute neck pain. The general guidelines for treatment chronic neck pain remain the same as for acute neck pain with an emphasis on exercises of the neck as the mainstay of treatment.

A randomised control trial in females with chronic neck pain by Ylinen et al showed that dynamic neck exercises and neck strengthening exercises, both, had beneficial effect in pain relief and disability as compared to a control group. The dynamic exercise group did neck lifts in the supine and prone position while the neck strengthening group did resistant exercises using an elastic band. The control group did aerobic and stretching exercises for half an hour, three times a week. All three groups were followed up after 12 months. The study found that both strength and endurance training for 12 months were effective in decreasing pain and disability in women with chronic, nonspecific neck pain and stretching and aerobic exercises were much less effective than strength training (24).
There is insufficient evidence to recommend the use of thermotherapy, therapeutic massage, EMG biofeedback, mechanical traction, therapeutic ultrasound, TENS and electrical stimulation in the treatment of chronic non-specific neck pain (25).

Conclusion

Non-specific neck and back pain is a symptom and not a disease entity and the findings on spinal imaging do not indicate that these findings are the source of pain since a large number of patients with no symptoms can have similar findings on imaging. There is no diagnostic test available to determine the source pain in patients with non-specific neck or back pain. Therefore logically surgery is not the answer to the treatment of such pain. Avoiding expensive surgery which can be associated with serious complications would be the best evidence based approach in the management of patients with non-specific neck or back pain.

The best approach in the management of such patients would be effective communication and explanation to the patient that nothing is seriously wrong with them. They should be advised to remain active and avoid rest and immobilisation of the spine as far as possible. Exercises of the neck and back have been found to reduce pain. Cognitive-behavioural therapy has been found to be effective in the treatment of chronic pain. Acute pain usually settles with time in a significant number of patients.

The use of simple analgesics and NSAIDS for short duration of time does help to reduce the pain though there is not much evidence that they are better than no treatment at all. Mild narcotics can be added to NSAIDs if the pain does not settle with NSAIDs. Routine use of Anti-depressants and Muscle relaxants is not recommended but may be used briefly in patients with severe pain. There is no role for the use of anti-convulsants in the treatment of these patients.

Epidural and facet injections are not recommended because there is no evidence of their effectiveness in the treatment of patients with non-specific neck or back pain.

Almost all physical treatment modalities have not been found to be effective in the treatment of neck or back pain. The use of collars, lumbar supports, thermotherapy, ultrasound, traction, TENS, acupuncture, electrical stimulation and massage are not recommended in the treatment of neck and back pain because of lack of evidence of their effectiveness.

It is therefore quite obvious that an evidence based approach to the management of patients with non-specific neck and back pain will go a long way in reducing the financial burden of treating patients with these common conditions.

References

1. Urwin M, Symmons D, Allison T, et al. Estimating the burden of musculoskeletal disorders in the community: the comparative prevalence of symptoms at different anatomical sites, and the relation to social deprivation. Ann Rheum Dis 1998; 57:649–655.

2. Hoy D, March L, Brooks P, et al. The global burden of low back pain: estimates from the Global Burden of Disease 2010 study. Ann Rheum Dis. 2014 Jun; 73(6):968-74. doi: 10.1136/annrheumdis-2013-204428. Epub 2014 Mar 24.

3. Hoy D, March L, Woolf A et al. The global burden of neck pain: estimates from the global burden of disease 2010 study. Ann Rheum Dis. 2014 Jul; 73(7):1309-15. doi: 10.1136/annrheumdis-2013-204431. Epub 2014 Jan 30.

4. Stanton TR, Latimer J, Maher CG, Hancock MJ. How do we define the condition ‘recurrent low back pain’? A systematic review. Eur Spine J. 2010; 19(4):533-9.

5. Waddell G. Subgroups within "nonspecific" low back pain. J Rheumatol 2005; 32; 395-396.

6. Bart W. Koes, Maurits van Tulder, Chung-Wei Christine Lin, Luciana G. Macedo, James McAuley, and Chris Maher. An updated overview of clinical guidelines for the management of non-specific low back pain in primary care. Eur Spine J. 2010 Dec; 19(12): 2075–2094.

7. Evidence-based management of acute musculoskeletal pain. Australian Acute Musculoskeletal Pain Guidelines Group. June 2003 at http://www.nhmrc.gov.au/_files_nhmrc/publications/attachments/cp94.pdf

8. Pengel LHM, Herbert RD, Maher CG and Refshauge KM. Acute low back pain: systematic review of its prognosis. BMJ. 2003 Aug 9; 327(7410): 323.

9. Gore DR, Sepic SB, Gardner GM (1986). Roentgenographic findings of the cervical spine in asymptomatic people. Spine, 1: 521–524.
10. Heller CA, Stanley P, Lewis-Jones B, Heller RF (1983). Value of x-ray examinations of the cervical spine. British Medical Journal, 287: 1276–1278.

11. van der Donk J, Schouten JSAG, Passchier J, van Romunde LKJ, Valkenburg HA (1991). The associations of neck pain with radiological abnormalities of the cervical spine and personality traits in a general population. Journal of Rheumatology, 18: 1884–1889.

12. Fridenberg ZB, Miller WT (1963). Degenerative disc disease of the cervical spine. A comparative study of asymptomatic and symptomatic patients. Journal of Bone and Joint Surgery 45A:1171–1178.

13. Gore DR, Sepic SB, Gardner GM, Murray MP (1987). Neck pain: a long-term follow-up of 205 patients. Spine, 12: 1–5.

14. Lees F, Turner JWA (1963). Natural history and prognosis of cervical spondylosis. British Medical Journal, 2: 1607–1610.

15. Radanov BP, Sturzenegger M, Di Stefano G (1995). Long-term outcome after whiplash injury: a 2-year follow-up considering features of injury mechanism and somatic, radiologic, and psychosocial findings. Medicine, 74: 281–297.

16. Kasch H, Bach FW, Jensen TS (2001). Handicap after acute whiplash injury: a 1-year prospective study of risk factors. Neurology, 56: 1637–1643.

17. Airaksinen O, Brox JI, Cedraschi C et al. European Guidelines for the Management of Chronic Non-specific Low Back Pain. Eur Spine J (2006) 15 (Suppl. 2): S192–S300. DOI 10.1007/s00586-006-1072-1.

18. Cherkin DC, Wheeler KJ, Barlow W, Deyo RA. Medication use for low back pain in primary care. Spine (Phila Pa 1976). 1998 Mar 1;23(5):607-14.

19. Fairbank J, Frost H, Wilson-MacDonald J, Yu l, Barker K, Collins R for the Spine Stabilisation Trial Group. Randomised controlled trial to compare stabilisation of the lumbar spine with an intensive rehabilitation programme for patients with chronic low back pain: MRC spine stabilisation trial. BMJ 2005;doi:10.1136/bmj.38441.620417.BF.

20. Brox JI, Nygaard OP, Holm I, Keller A, Ingebrigtsen T, Reikeras O. Four-year follow-up of surgical versus non-surgical therapy for chronic low back pain. Ann Rheum Dis 2010; 69:1643-1648.

21. Deyo RA, Mirza SK, Martin BJ, Kreuter W, Goodman DC, Jarvik JG. Trends, major medical complications, and charges associated with surgery for lumbar stenosis in older adults. JAMA 2010; 302(13):1259-1265.

22. Fritzell P, Ha¨gg O, Wessberg P, Nordwall A and the Swedish Lumbar Spine Study Group. Lumbar fusion versus nonsurgical treatment for chronic low back pain. A multicentre randomized controlled trial from the Swedish Lumbar Spine Study Group. SPINE 2001; 26(23): 2521–2534.

23. Brox JI, Sørensen R, Friis A, et al. Randomized clinical trial of lumbar instrumented fusion and cognitive intervention and exercises in patients with chronic low back pain and disc degeneration. SPINE 2003; 28 (17): 1913–1921.

24. Ylinen J, Takala E, Nykänen M, et al. Active neck muscle training in the treatment of chronic neck pain in women. JAMA. 2003; 289(19):2509-2516.

25. Abright J, Allman R, Bonfiglio et al. Philadelphia panel evidence-based clinical practice for neck pain guidelines on selected rehabilitation interventions. PHYS THER. 2001; 81:1701-1717.

Fever in adults a common but much misunderstood entity: A brief Note

Fever in adults a common but much misunderstood entity: A brief Note

                                     

                                       Dr KS Dhillon, FRCS, LLM

Introduction

Anecdotal evidence shows that when a person feels that he has fever, he treats himself with paracetamol and when he visits his family doctor for fever, the doctor also prescribes paracetamol. The nurses in the hospital start tepid sponging of the patient when the temperature is just over 37⁰C and sometimes they will call the doctor in the middle of the night for advice on whether to serve paracetamol to the patient. Such anecdotal experiences raise several questions which beg to be answered.

What is fever?

Fever, an elevation of body temperature, also known as hyperthermia, is an important sign of health and disease in medical care of patients. The detection of normal body temperature or the norm was established way back in the middle of the 19^th century by a German physician (Wunderlich) when the thermometer was first introduced. Although at that time the thermometers were not calibrated and axillary temperatures (which were 1.4 to 2.2 degrees higher than that obtained by present digital devices) were measured, the norm for body temperature was established as a body temperature of 37⁰C and any temperature of 38⁰ C or more was defined as fever. Although the present day devices are more accurate and we know that normal body temperature is a range rather than a fixed number, most medical practitioners regard a temperature of 37⁰ C as the norm and any temperature of 38⁰ C or more as fever.

There are variations in the temperatures recorded by different means at different sites. The core body temperature is accurately measured via catheters in the pulmonary artery and that is believed to be the gold standard. However in clinical practice the rectal temperature is believed to be the gold standard. There are variations in the temperature measured at the rectum, axilla, mouth and the ear. However the tympanic membrane temperature measurement by digital devices has become a norm due its convenience and speed with which the temperature can be taken especially in a busy medical setting.

Review of literature shows that there is no fixed figure for normal body temperature just as there is no fixed figure for pulse rate or blood pressure. The temperature will vary with the device used, site of measurement, age and sex of the individual and the time of day when the temperature is taken. The temperature is lower in the morning and higher in the afternoon/evening. The temperature also varies with the menstrual cycle in females. The temperature is lower in the elderly frail individuals (1).

In a healthy adult (18 to 40 years), studies show that the oral temperature can range from 35.6^o C to 38.2⁰ C with a mean of 36.8⁰C. The 6am maximum temperature is about 37.2⁰C and 4pm maximum temperature is about 37.7⁰C with a daily variation of 0.5⁰C (2). In practice a temperature of 37⁰C is considered as normal body temperature with a circadian variation of between 0.5⁰C to 1⁰C (3). Fever is defined as temperature of 38.3⁰C or more and unless there is other evidence of infection, temperature of below 38.3⁰C does not need any investigation (3).

What causes fever?

The hypothalamus regulates the body temperature based on, the signals received from peripheral cold/warmth receptors via the peripheral nerves and from the temperature of the blood that surrounds the neurons in the hypothalamus.

Fever results from the resetting to a higher level the hypothalamic temperature set point at which the body temperature is normally maintained. This results in activation of the vasomotor centre which produces peripheral vasoconstriction leading to shunting of the blood to internal organs and reduction of heat loss. At this point the patient feels cold and shivering occurs which generates more heat from muscular activity. When the patient feels cold he/she takes cover under warm clothes which further leads to a rise in body temperature. The shift of blood to internal organs increases metabolic activity which generates more heat especially in the liver. All these chain of events results in a rise in body temperature till the new hypothalamic set point is reached and after that the hypothalamus maintains the temperature till the set point is changed by further change in events within and around the patient.

The hypothalamic resetting of set point is mediated by cytokines which are released by monocytes in response to infection or trauma or other insults to the body. Sympathetic hyperactivity is also known to increase the production of heat.

What is the significance of fever?

Elevation of body temperature appears to be an evolutionary protective response against infection which exists in the animal kingdom. Elevation of body temperature has been shown to be protective against infection in animals. When the body temperature rises the immune function improves with production of antibodies and cytokines, t-cell activation, and increased neutrophil and monocyte function. A rise in body temperature has been shown to inhibit streptococcus pneumonia (3).

Studies in humans have found a positive correlation between high temperatures and improved survival in patients with certain bacterial infections (3). However in patients with limited cardio-respiratory reserves, high fever can have deleterious effects because high fever increases oxygen consumption, increases CO2 production, increases energy expenditure and increases cardiac output. For every 1⁰C rise in body temperature there is a 10% increase in oxygen consumption. In patients with CVA and traumatic brain injury moderate elevation of temperature can worsen the brain damage (3).

Invariably in clinical practice all patients with fever are treated with antipyretic medications and external cooling to reduce the temperature to normal. When we know that fever is body’s protective response to infection, it appears that these attempts to reduce the body temperature to normal, are illogical. Furthermore bringing the temperature to normal will prevent the physician from monitoring the response to treatment instituted. The use antipyretic pharmaceutical agents may cause acute hepatitis, in very ill patients (especially alcoholics and emaciated patients), and in patients who have been self-medicating themselves with acetaminophen for chronic pain. The use of cooling blankets have been shown to be no more effective than the use of anti-pyretic in bringing down the temperature and these cooling blanket can produce rebound hyperthermia.

The general recommendations are that fever should not be treated symptomatically with medication or external cooling except in patients with brain injury, patients with poor cardio-pulmonary reserve and in patients with temperatures of more than 40⁰C (3).

Most healthy individuals tolerate temperatures of up to 40.5⁰C well without ill-effects. Hyperthermia beyond 42.1⁰C can cause cellular damage affecting the brain, muscles and the heart. It can cause DIVC, hypoxia, acidosis, hyperkalaemia, coma, fits, arrhythmias, and hypotension and can sometimes be lethal (4).

There is no evidence to support the routine treatment of fever even in patients with septic shock. In fact studies of pharmacologic antipyretics in such patients have failed to show any clinical benefit and some have even suggested they do more harm (5). A study by Lee et al showed that in critically ill septic patients, administration of NSAIDs or acetaminophen was independently associated with 28-day mortality, and there was no association between fever with mortality (5).

Conclusion

There are no norms for body temperature but most medical practitioners regard a temperature of 37⁰C with a circadian variation of between 0.5⁰C to 1⁰C as normal. Fever is defined as temperature of 38.3⁰C or more. Temperature is an important vital sign which allows the physician to monitor the response to treatment. Fever should not be treated symptomatically with medication or external cooling except in patients with brain injury, patients with poor cardio-pulmonary reserve and in patients with temperatures of more than 40⁰C. Most patients tolerate temperatures of up to 40.5⁰C without any ill-effects. Elevated temperatures are body’s attempt at healing and it would be paradoxical to bring the temperature to the so called norms. Treating fever in critically ill septic patients has been associated with mortality.

References

1. Sund-Levander M, Grodzinsky E. Time for a change to assess and evaluate body temperature in clinical practice. International Journal of Nursing Practice 2009; 15: 241–249.

2. Mackowiak PA, Wasserman SS, Levine MM. A critical appraisal of 98.6 degrees F, the upper limit of the normal body temperature, and other legacies of Carl Reinhold August Wunderlich.  JAMA 1992; 268(12):1578.

3. Marik PE. Fever in the ICU. Chest 2000; 117(3):855.

4. Goroll AH, Muller AG (Editors). Primary care medicine: Office evaluation and management of adult patient. 2009, 6^th edition, Lippincott Williams & Wilkins.

5. Lee BH, Inui D, Suh GY, et al. Fever and Antipyretic in Critically ill patients Evaluation (FACE) Study Group.; Association of body temperature and antipyretic treatments with mortality of critically ill patients with and without sepsis: multi-centered prospective observational study. Crit Care. 2012; 16(1):R33.

Radiological errors in orthopaedics and its medico-legal implications

Radiological errors in orthopaedics and its medico-legal implications

                              Dr KS Dhillon FRCS, LLM

The work of a radiologist involves detecting and describing imaging abnormalities and coming up with an accurate diagnosis. Though errors are an inevitable part of medical practice, these errors however can lead to medical malpractice claims. Medical malpractice claims have been on the rise in USA since the early 1970’s (1) and in Malaysia anecdotal evidence shows that such claims are also on the rise in the last few decades. In the USA radiology is one of specialities which is most liable to negligence suits (1). However it is not common to hear of negligence claims against radiologist in Malaysia but it is matter time before such claims become common.

About 12% of all negligence suits filed in the USA is related to radiological procedures or the radiologist (2, 3). Missed radiological diagnosis accounts for about 40% to 47% of the law suits. About 30% of suits are related to failure to order radiological examination (3). The most common type of missed diagnosis involves fractures followed by missed malignancies (2). The most commonly missed fractures are that of the femur, navicular bone and the cervical spine and bone tumours on plain radiographs feature among the commonly missed malignancies (1). The average error rate among radiologist in the USA is around 30% (1). The common reasons why malpractice claims are brought against radiologist include ‘observer errors, errors in interpretation, failure to suggest the next appropriate procedure and failure to communicate in a timely and clinically appropriate manner’ (1).

Errors in radiology

There are three types of observer errors which are common and these include scanning, recognition and decision making errors. Scanning errors result from failure to fixate at the abnormal lesion and recognition errors result from ability to fixate at the correct site but fail to recognise the abnormality. Decision making errors result from interpreting an abnormality as a normal structure (4). The most common error is decision making error (45%) followed by scanning error (30%) and recognition error (25%) (4).

Errors in interpretation

Interpretation errors occur because of lack of clinical knowledge about the patient, failure to look for previous studies done, poor index of suspicion, low level of vigilance and distraction by the abnormality detected which leads to failure to look for other abnormalities (1).

Failure to suggest the next appropriate procedure

Following the reporting of any abnormality on radiological imaging, if there are follow-up studies needed to clarify or confirm the impression, then the radiologist is duty bound to communicate this to referring physician. Failure to do so may expose the radiologist to a possible negligence suit (1).

Failure to communicate in a timely and clinically appropriate manner

Where appropriate, the radiologist should communicate important findings of imaging to the referring physician, though the final imaging report has been written and signed. The communication should be documented with details of what was communicated. Errors in communication have been responsible for malpractice claims (1).

Missed fractures

Errors in diagnosis of fractures are very common in the Accident and Emergency department.  Guly (5) collected data of missed injuries in a district hospital in the UK between 1992 and 1996. There were 953 diagnostic errors in 934 patients. About 80% of the diagnostic errors were missed fractures. Seventy-eight percent of the errors were due to misreading of the radiographs. Complaints and legal actions resulted from 22 of the diagnostic errors and 3 patients with diagnostic error died.

A systematic analysis of missed extremity fractures in emergency medicine was carried out by Wei et al (6). They reviewed 2,407 new patients in the emergency department who had extremity fractures from Jan 2003 to June 2004. The images were independently reviewed by an emergency radiologist and a musculoskeletal radiologist. They found a 3.7% overall rate of missed fractures. The location of the most frequently missed fractures was the foot (7.6%), followed by the knee (6.3%), elbow (6.0%), hand (5.4%), wrist (4.1%), hip (3.9%), ankle (2.8%), and shoulder (1.9%). Of the initially missed fracture, 70% were identified and only 33% of the initially missed fractures were attributed to radiographically imperceptible lesions. The shaft fractures are less often missed since they are usually clinically evident as compared to periarticular fractures which often clinically less evident.
In a retrospective study of multiple trauma patients admitted to the intensive care unit of a major teaching hospital, Frawley (7) found that a delayed diagnosis of missed injuries was made in 40% of patients.

For a radiologist to accurately interpret the radiological images, the radiologist needs information about the circumstances of the injury, a good clinical history and clinical findings which is often not available to the radiologist. Another reason why fractures are often missed is called the satisfaction of search (SOS) phenomena. This occurs when the radiologist detects a fracture on one image and this detection interferes with detection of a more subtle fracture in other images of the same patient. The gaze on the detected fracture has been found to be longer compared to the gaze time on other images (8).

Renfrew et al (9) reviewed and classified errors in radiology after reviewing 182 cases that were presented at problem case conferences from 1986 to 1990. They found that the sources of errors had not changed over 20 years. They found that errors involved;

1. ‘failure to consult old radiologic studies or reports,
2. limitations in imaging technique,
3. acquisition of inaccurate or incomplete clinical history,
4. location of a lesion outside the area of interest on an image,
5. lack of knowledge,
6. failure to continue to search for abnormalities after the first abnormality was found,
7. failure to recognize a normal biologic variant’

One hundred and twenty six were perceptual errors (64 false-negative, 15 false-positive, and 47 misclassification errors) and 56 were mishaps which included 38 complications and 18 communication errors.

Value of radiologists’ interpretation of radiographs

Clark et al (10) studied the clinical value of radiologists’ interpretations of peri-operative radiographs in orthopaedic patients. Their aim was to find out whether the radiology reports provided sufficient information which is necessary to make clinical decision. They retrospectively reviewed 371 radiographs of 211 consecutive patients. The reports were generated by 3 Board-certified radiologists. They evaluated the accuracy of description and assessment of the fractures and the implants used for fracture stabilization.

They found that fracture descriptions were complete for 85% of reports and the assessment of alignment and displacement (necessary to determine fracture care) was complete in only 9% of the reports. Precision of description of orthopaedic implants was accurate in 12% of the reports and 7% of the descriptions were in error. The description of effect of the implants was precise in 27% and the description of the position of the implants was accurate in 25% of the cases. Implant stability was assessed precisely in only 4% of cases. In 61% of the pre-operative studies the radiologists report was not available till after the surgery had been completed. The authors concluded that ‘the attending orthopaedic surgeon has traditionally interpreted such radiographs and should continue to do so to provide patients with more immediate and complete clinical evaluation and management’.
Crockett et al (11) did a retrospective analysis of radiographic reports of 161 consecutive patients with idiopathic scoliosis to assess their clinical value in surgical decision making and the usefulness of the reports in assessing post-surgical outcome. The reports were prepared by one of seven Board-certified radiologists and one of two Board-certified orthopaedic surgeons.

The presence of scoliosis was mentioned in 95% of the radiologist reports and in 99.4% of the orthopaedist reports. The type of curve was described in only 5% of the radiologist reports whereas it was described in 99.4% of the orthopaedist reports. The progression of curve was recorded in 16.7% and magnitude of the curve in 12.6% of the radiologist reports as compared to 98.4 and 98.1% respectively in the orthopaedist reports. The level of curve was reported in 10.6% of the radiologist reports and in 95.6% of the orthopaedic reports. The radiologist reported kyphosis in 28% and lordosis in 26.5% of the reports while the orthopaedist reported kyphosis in 98.2% and lordosis in 79.45% of the reports.

The radiologist noted the presences of instrumentation in 77.8% and fusion in 68.3% of the reports while the orthopaedist noted instrumentation in 84.4% and fusion in 100% of the reports. The radiologist misreported fusion in 7% and misidentified the instrumentation in 20% of the reports.
The authors concluded that the orthopaedic spine surgeons did not gain anything useful from the radiologist’s reports.

Radiologist and malpractice suits

In the USA radiologists comprise 3.6% of all physicians but they ranked number 6 among specialist who had claims closed where they were defendants. They were sued more often than plastic surgeons, anaesthesiologist, cardiologist and gastroenterologist but less often than obstetricians, internist, general surgeons and orthopaedist (12).

Berlin and Berlin (13) reviewed all malpractice suits in Cook County, Illinois, USA between 1975 and 1994. Among the suits involving the radiologists, errors in interpretation was the main concern in 55% of the cases from 1975 to 1979 and it was up to 71% of the cases from 1990 to 1994. Misdiagnosis of bone abnormalities especially fractures topped the list.

More recently Whang et al (12) reviewed the credentialing data of 8,401 radiologists to determine the most frequent causes of malpractice suits among radiologists. They found that the most common general cause was error in diagnosis (14.83 claims per 1000 person-years). In the category of missed diagnosis, breast cancer was the leading cause of litigation followed by non-spinal fractures, spinal fractures, lung cancer and vascular disease.
The other leading cause of malpractice suits was procedural complications followed by inadequate communication with patient and the referring physician. Failure to order additional test was a rare cause of malpractice suits.

A study, by Baker et al (14), of the demography of medical malpractice suits against radiologists showed that 30.9% of radiologists in the USA are the subject of a malpractice suit at least once in their career. The likelihood of a radiologist being sued is 50% by the time the radiologist reaches the age 60. The study found that male radiologists are sued more often than female radiologist.

The most common injuries of the muscular skeletal system (excluding the spine) for which malpractice suits are brought against the radiologist are foot and hip injuries. The highest settlement in the USA for musculoskeletal injuries (excluding the spine) is for the ankle injuries (15).

Of the malpractice suits brought against radiologist in the USA 13.2 % are related to the bones and adjacent soft tissue and 32.9% involve the spine. The cervical spine was involved in 68.2 % cases followed by the lumbar spine in 16.5% and the thoracic spine in 15.3% of the cases. The highest settlement has been for the cervical spine (average settlement of $483,156) followed by thoracic spine (average settlement of $481,608) and the lumbar spine (average settlement of $119,272 (16).

Improving quality of diagnostic radiology reporting

In the USA, The Joint Commission (TJC) had in 2007 introduced the Ongoing professional Practice Evaluation (OPPE) and Focused Professional Practice Evaluation (FPPE) processes to help monitor the performance of all medical professionals granted privileges in a hospital. OPPE helps identify practitioners who may be delivering unacceptable quality of care and the FPPE is a follow-up process to determine the validity of the findings of the OPPE. The review, decision and follow-up process is developed and implemented at each department level.

The American Board of Medical Specialist (ABMS) has introduced a program for Maintenance of Certification (ABMS MOC) to address the problem of physicians losing knowledge and skills as the years pass after their training (this has been repeatedly shown by research). The American Board of Radiology requires all diplomates with 10-year, time-limited primary or subspecialty certificates to successfully complete the requirements of the appropriate ABR MOC program for their specialty or subspecialty to maintain their certification. The MOC addresses six competencies which include ‘medical knowledge, patient care, interpersonal and communication skills, professionalism, practice-based learning and improvement, and systems-based practice’ (17). The practice performance module includes peer review and double-reading assessment. One of the popular peer review programme is the RADPEER quality assurance program. This peer review system ‘adds minimally to workload, is confidential, uniform across practices’. The radiologist who ‘review previous images as part of a new interpretation record their ratings of the previous interpretations on 4 point scale’. The ratings are then reviewed by a peer review committee and the ‘final ratings are then sent for central data entry and analysis’ (18). Such a system of peer review can help reduce errors and improve performance of the radiologist.

Radiology reporting in Malaysian private hospitals

The causes of errors in radiological reporting have been identified to include the following (9):

• ‘failure to consult old radiologic studies or reports,
• limitations in imaging technique,
• acquisition of inaccurate or incomplete clinical history,
• location of a lesion outside the area of interest on an image,
• lack of knowledge,
• failure to continue to search for abnormalities after the first abnormality was found,
• failure to recognize a normal biologic variant’

The practice in Malaysian private hospitals is to return all radiological films to the patient when the patient leaves the hospital. A copy of the report is in the patient’s medical file which is not with the radiologist when they report on subsequent images. The images are obtained by the radiographers and invariably there is no contact between the patient and the radiologist. Most often even if the images are not up to the mark the radiologist invariable goes ahead and reports the findings on the images rather than take the trouble to order new imaging. The patient’s clinical history is invariably not available to the radiologist. Sometimes the radiologist is overwhelmed by the workload to spend a lot of time on the images to be interpreted. Of course there is no recertification of the radiologists to make sure that they have not lost the knowledge and skill since their training was completed.

Furthermore there is a lack of subspecialty radiologists and most hospitals have general radiologists who report all investigations done for all medical specialities. Communication between the radiologist and the referring physicians is almost non-existent. With all these drawbacks the error rates are expected to be high. To my knowledge the incidence of error rates for radiological reporting in Malaysia are not available. The interpretive value of reporting by orthopaedic surgeons for orthopaedic imaging has been reported to be high as compared to that by radiologist. Therefore it is incumbent on all orthopaedic surgeons to report all the imaging themselves although there is a report written and signed by the radiologist.

Conclusion

Malpractice claims are on the rise in most western nations and also on the rise in Malaysia. In the USA 40% to 47% of the malpractice claims against the radiologist are for missed diagnosis. Missed diagnosis involving fractures is one the most common cause of malpractice suits. The average rate of missed diagnosis in the USA has been reported to be as high as 30% and one study from Australia quoted a figure of 40% of initial missed diagnosis in patients admitted to the intensive care unit. The causes of errors in diagnosis has been studied and reported in the literature. In the USA several programs have been instituted to address these problems. However in Malaysia the rates of missed diagnosis in radiological reporting are not known. It is likely to be much higher than that in the west. To my knowledge there are no programs in place to improve the existing status of radiological reporting.

Finally, review of literature shows that the interpretive value of reporting, of orthopaedic imaging, by the orthopaedic surgeons is very much higher as compared to that by the radiologists. Therefore it is incumbent on orthopaedic surgeons to interpret and report all imaging carried out on their patients despite the existence of a report by a radiologist. This would be consistent with our duty to care for the patient to prevent foreseeable injury which may lead to tortious liability.

References

1.Antonio Pinto and Luca Brunese. Spectrum of diagnostic errors in radiology. World J Radiol. 2010 Oct 28; 2(10): 377–383.

2.Berlin L. Malpractice and radiologists, update 1986: an 11.5-year perspective. AJR Am J Roentgenol. 1986 Dec;147(6):1291-8.

3.Berlin L, Berlin JW. Malpractice and radiologists in Cook County, IL: trends in 20 years of litigation. AJR Am J Roentgenol. 1995 Oct;165(4):781-8.

4.Kundel HL, Nodine CF, Carmody D. Visual scanning, pattern recognition and decision-making in pulmonary nodule detection. Invest Radiol. 1978 May-Jun;13(3):175-81.

5.Guly HR. Diagnostic errors in an accident and emergency department. Emerg Med J. 2001 Jul;18(4):263-9.

6.Wei CJ, Tsai WC, Tiu CM, Wu HT, Chiou HJ, Chang CY. Systematic analysis of missed extremity fractures in emergency radiology. Acta Radiol. 2006 Sep;47(7):710-7.

7.Frawley PA. Missed injuries in the multiply traumatized. Aust N Z J Surg. 1993 Dec;63(12):935-9.

8.Berbaum KS, El-Khoury GY, Ohashi K, Schartz KM, Caldwell RT, Madsen M, Franken EA Jr. Satisfaction of search in multitrauma patients: severity of detected fractures. Acad Radiol. 2007 Jun;14(6):711-22.

9.Renfrew DL, Franken EA Jr, Berbaum KS, Weigelt FH, and Abu-Yousef MM. Error in radiology: classification and lessons in 182 cases presented at a problem case conference. Radiology. 1992 Apr; 183(1):145-50.

10.Clark R, Anderson MB, Johnson BH, Moore DE, Herbert FD. Clinical value of radiologists' interpretations of perioperative radiographs of orthopaedic patients. Orthopedics. 1996 Dec; 19(12):1003-7.

11.Crockett HC, Wright JM, Burke S, Boachie-Adjei O. Idiopathic scoliosis. The clinical value of radiologists' interpretation of pre- and postoperative radiographs with interobserver and interdisciplinary variability. Spine (Phila Pa 1976). 1999 Oct 1; 24(19):2007-9.

12.Whang JS, Baker SR, Patel R, Luk L, Castro A 3rd. The causes of medical malpractice suits against radiologists in the United States. Radiology. 2013 Feb;266(2):548-54.

13.Berlin L, Berlin JW. Malpractice and radiologists in Cook County, IL: trends in 20 years of litigation. AJR Am J Roentgenol 1995;165(4):781–788.

14.Baker SR, Whang JS, Luk L, Clarkin KS, Castro A 3rd, Patel R. The demography of medical malpractice suits against radiologists. Radiology. 2013 Feb;266(2):539-47.

15.Baker SR, Patel RH, Lelkes V, Castro A 3rd, Sarmast U, Whang J. Non-spinal musculoskeletal malpractice suits against radiologists in the USA--rates, anatomic locations, and payments in a survey of 8,265 radiologists. Emerg Radiol. 2014 Feb;21(1):29-34.

16.Baker SR, Lelkes V, Patel RH, Castro A 3rd, Sarmast U, Whang J. Spinal-related malpractice suits against radiologists in the USA-rates, anatomic location, percent of adverse judgments, and average payments. Emerg Radiol. 2013 Dec;20(6):513-6.

17.Madewell et al. American Board of Radiology: Maintenance of Certification. Radiology January 2005;Volume 234, Issue 1.

18.Borgstede JP, Lewis RS, Bhargavan M, Sunshine JH. RADPEER quality assurance program: a multifacility study of interpretive disagreement rates. J Am Coll Radiol. 2004 Jan;1(1):59-65.

Reconstruction of the posterior cruciate ligament for isolated injuries of the posterior cruciate ligament: A myth or reality?

Reconstruction of the posterior cruciate ligament for isolated injuries of the posterior cruciate ligament: A myth or reality?

                                         Dr KS Dhillon FRCS, LLM

Posterior cruciate ligament (PCL) injuries result from a posteriorly directed force applied to the proximal tibia, unlike anterior cruciate ligament (ACL) injuries which result from non-contact rotational forces. Injuries to the PCL are believed to be rare as compared to ACL injuries. The true incidence of PCL injuries is unknown partly because these injuries are easily missed and some patients may not seek treatment because symptoms associated with PCL injuries are less disabling as compared to symptoms associated with ACL injuries. However the incidence of PCL injuries has been reported to vary from 1% to 47% of all ligament injuries of the knee (1). There have been suggestions that only about 40% of PCL injuries are isolated injuries and rest are usually combined ligamentous injuries (2). The ideal treatment of PCL injuries according several authors remains controversial (2-4).

Is treatment of PCL injuries controversial or are there some conflicts of interest involved in the treatment of patients with PCL injuries which makes surgeons promote surgical reconstruction of the PCL for such injuries?

Treatment of isolated PCL injuries

There is no controversy about the treatment of PCL avulsion fractures, which are ideally treated by open reduction and internal fixation when the fragment is large enough to be fixed with a screw. Isolated injuries of the PCL usually produce a grade I to II posterior laxity of the knee while a grade III laxity is produced by a combined PCL and posterior lateral corner injuries. What is the best method of treatment of isolated PCL injuries?

An acute mid-substance tear of the PCL may heal (5) unlike ACL mid-substance injuries which do not heal. Logically such injuries should be treated conservatively. The long term natural history of isolated PCL injuries suggests that there is no indication for surgical treatment of such injuries because the outcome of conservative treatment is good. There are no studies to show that surgical treatment is better than conservative treatment for isolated tear of the PCL. Neither is there any evidence that surgical treatment reduces the incidence of osteoarthritis of the knee after PCL injuries (4).

Natural history of isolated PCL injuries

One of the earlier studies of the long term outcome of non-operatively treated isolated PCL injuries was done by Parolie and Bergfeld in 1986 (6). They studied 25 patients who were treated conservatively for isolated PCL injuries and followed-up for a mean of 6.2 years (2.2 to 16 years). They found that 80% of the patients were satisfied their knee and 84% had returned to their previous sport, with 68% at same level of performance and 16% at a reduced level of performance. Patients who were satisfied with their knee and had returned to sports had quadriceps strength of more than 100% of the contralateral uninvolved knee and those who were dissatisfied with their knee and not returned to sports had less than 100% strength of the quadriceps as compared to the contralateral knee.

Selbourne et al (7) prospectively studied the natural history of acute, isolated, non-operatively treated PCL injuries in athletically active patients. The study included 133 patients all of whom completed a yearly questionnaire for an average of 5.4 years (2.3 to 11.4 years) and 51% of the patients (68 out of 133) returned for long-term clinical and radiological examination. The functional outcome was good with a mean modified Noyes knee score of 84.2 points, a mean Lysholm score of 83.4 and a mean Tegner activity score of 5.7.The grade of laxity had no correlation with subjective functional outcome. Fifty percent of the patients returned to the same sport at the same or higher level of performance, one third (33.3%) returned to same sport at a lower level and one-sixth (16.6%) did not return to the same sport.

The authors concluded that ‘athletically active patients with acute isolated posterior cruciate ligament tears treated nonoperatively achieved a level of objective and subjective knee function that was independent of the grade of laxity’.

The longest follow-up study of patients with acute, isolated PCL injuries treated non-operatively was reported by Shelbourne et al in 2013 (8). The study included 68 patients who had a subjective follow-up at a mean of 17.6 years and 44 of the patients had a subjective and objective follow-up at a mean of 14.3 years (10-21 years). The mean quadriceps strength was 97% of the contralateral side and the range of knee motion was normal in all patients.

Fifty percent of the patients had no osteoarthritis (OA) of the knee, 30% had mild OA, 9% (4 patients) had moderate and 2% (1 patient) had severe OA of the knee at a mean follow-up 14.3 years. The mean IKDC (International Knee Documentation Committee) and modified CKRS (modified Cincinnati Knee Rating System) subjective scores were 73.4 ± 21.7 and 81.3 ± 17.4, respectively at 17 years follow-up and the subjective scores did not correlate with the degree of PCL laxity.
The authors concluded that long term follow-up of patients, with isolated PCL injuries treated non-operatively, shows that patients remain active, have good muscle strength, full range of knee motion and they report good subjective scores and that the incidence post-traumatic OA is low.

In 2007 Patel et al (1) published a study involving 57 patients with acute isolated PCL injuries who were treated non-operatively with a mean follow up of 6.9 years (2 to 19.3 years). Seventeen patients (29.8%) had a grade I and 41 patients (71.9%) had a grade II laxity of the PCL. The functional outcome at 7 years was good with a mean Lysholm-II knee score of 85.2 points (range 51 to 100 points) and a mean Tegner activity level of 6.6 (range 3 to 10). The Lysholm-II knee scoring system, showed excellent results in 40%, good in 52%, fair in 3%, and poor in 5% of the knees. The incidence of mild medial compartment OA was 12% and moderate medial compartment OA 5% and none of the patients had severe OA.

These medium and long term studies of the natural history of isolated PCL injuries reveal that the subjective functional outcome is good, without surgical intervention, with majority of the patients returning to their pre-injury activity level. Are the results of PCL reconstruction better than conservative treatment?

Surgical treatment of isolated PCL injuries

Most of the published studies reporting the outcome of PCL reconstruction for isolated PCL injuries are small case series with a short follow-up, and the heterogeneity of the patients studied and the technique used make it difficult to judge outcome in these patients(3).
However there are two studies that have reported the long term outcome of PCL reconstruction in patients with isolated PCL injuries.

Herman et al (9) studied 25 patients (22 male, 3 female) with an average age of 30.8 years who underwent single bundle PCL reconstruction for pain and functional instability of the knee. The mean follow-up was 9.1 years (6.5 to 12.6 years). Twenty two patients were evaluated clinically and 3 patients provided telephone interviews.

The final mean IKDC score was 65, Lysholm score was 75 and the VAS (visual analogue score) was 8. The functional scores were fair to good and were significantly better than the pre-operatively scores. The final Tegner score was 5.7. The functional results were significantly better in patients with no cartilage damage at the time of surgery and in those who underwent surgery within 1 year post injury.

Jackson et al (10) evaluated the long term outcome of PCL reconstruction in 26 patients after failed conservative treatment. At 10 years follow-up the IKDC score was 87 and the Lysholm score improved from 60 to 90 post-operatively. Twenty two patients had radiological examination and 18% of the patients had grade II OA changes and another 18% had grade III OA changes.
A careful analysis of the subjective outcome reported by Shelbourne (7) and Patel (1) for non-operative treatment and that by Herman (9) and Jackson (10) for surgical treatment of PCL injuries appears to be very similar.

Complications of PCL surgery

PCL injuries are rare and the indications for surgery of the PCL are limited since conservative treatment has good outcome, therefore the number of PCL surgeries carried out by surgeons per year are small. This limited experience with such complex surgery can lead to a higher incidence of complications especially when there are vital neurovascular structures at the back of the knee. Furthermore catastrophic complications usually never get reported which can give surgeons a false sense of relative risks involved when undertaking such procedures.

Besides the standard complications, such as those associated with anaesthesia and complication of surgery such as infections and thromboembolic complications which can occur with any orthopaedic procedure, there are specific complications associated with PCL surgery, some of which includes neurovascular injury, osteonecrosis, fractures, stiffness, residual laxity and anterior knee pain.
A survey of frequency of complications associated with arthroscopic surgical procedures of the knee reported by Salzler et al (11), where the data was obtained from the ABOS (American Board of Orthopaedic Surgery) data base, showed that the complication rate was the highest for PCL surgery as compared with other arthroscopic procedures. The complication rate for PCL surgery was 20.1%, ACL surgery 9.7%, meniscal repair 7.7%, menisectomy 2.8% and chondroplasty 3.5%. The overall pulmonary embolism rate was 0.11% and the infection rate 0.84%. These were self-reported complication rates and the authors believe that the actual rates may be higher.

Conclusion

The outcome of non-operative treatment for isolated mid-substance PCL injuries is good as has been revealed by long term studies of the natural history of such injuries. The results of surgical reconstruction of the PCL are not superior to that of non-operative treatment and PCL surgery can be associated with complications which would not be seen with conservative treatment. Hence there appears to be no indication for PCL reconstruction for intra-substance tears of the PCL.

References

1. Patel DV, Allen AA, Warren RF, Wickiewicz TL, Simonian PT. The Nonoperative Treatment of Acute, Isolated (Partial or Complete) Posterior Cruciate Ligament-Deficient Knees: An Intermediate-term Follow-up Study. HSS J. 2007 Sep; 3(2): 137–146.

2. Clancy WG Jr, Sutherland TB. Combined posterior cruciate ligament injuries. Clin Sports Med 1994; 13(3):629–647.

3. Montgomery SR, Johnson JS, McAllister DR, Petrigliano FA. Surgical management of PCL injuries: indications, techniques, and outcomes. Curr Rev Musculoskelet Med. 2013 Jun; 6(2): 115–123.

4. Dowd GSE. Reconstruction of the posterior cruciate ligament: Indications and results. J Bone Joint Surg [Br] 2004; 86-B: 480-91.

5. Shelbourne KD, Jennings RW, Vahey TN. Magnetic resonance imaging of posterior cruciate ligament injuries: assessment of healing. Am J Knee Surg 1999; 12:209-13.

6. Parolie JM, Bergfeld JA: Long-term results of nonoperative treatment of isolated posterior cruciate ligament injuries in the athlete. Am J Sports Med 1986; 14:35-38.

7. Shelbourne KD, Davis TJ, Patel DV. The natural history of acute, isolated, nonoperatively treated posterior cruciate ligament injuries. A prospective study. Am J Sports Med. 1999 May-Jun; 27(3):276-83.

8. Shelbourne KD, Clark M, and Gray T. Minimum 10-Year Follow-up of Patients after an Acute, Isolated Posterior Cruciate Ligament Injury Treated Nonoperatively. Am J Sports Med July 2013 vol. 41 no. 7 1526-1533.

9. Hermans S, Corten K, Bellemans J. Long-term results of isolated anterolateral bundle reconstructions of the posterior cruciate ligament: a 6- to 12-year follow-up study. Am J Sports Med. Aug 2009; 37(8):1499-507.

10. Jackson WF, van der Tempel WM, Salmon LJ, Williams HA, Pinczewski LA. Endoscopically-assisted single-bundle posterior cruciate ligament reconstruction: results at minimum ten-year follow-up. J Bone Joint Surg Br. 2008 Oct; 90(10):1328-33.

11. Salzler MJ, Miller CD, Lin A, Irrgang JJ, Harner CD. Complications Following Arthroscopic Knee Surgery. Orthopaedic Journal of Sports Medicine, September 2013 vol. 1 no. 4 suppl 2325967113S00044.