ACL Pathology & Functional Impairment

Recent media reports reminded me of the necessity for vigilance and clinical reasoning when assessing for potential ACL deficiency.  It was highlighted from a recent sporting event – the all Ireland hurling semi-final when star player Henry Shefflin suffered a suspected ACL rupture.  For those of you unfamiliar with Gaelic games there are two codes played in Ireland; Gaelic football and Hurling.  If you have never seen hurling played I would highly recommend you check it out on YouTube. We have discussed ACL rehabilitation protocols previously here.

Now back to the story.  The player collapsed following an incident in which he reported feeling a ‘popping’ and was unable to continue but walked from the field.  He had a prior history of ACL disruption on the contra-lateral side two years previously and had verbalised to the medical staff that it felt like the same injury.  The treating physiotherapist observed that the clinical signs were relatively modest but in view of the history an MRI scan was conducted confirming an ACL disruption.  However, as the patient’s clinical signs were very modest and his functional impairment at this stage post injury was very modest it begged the question of whether it would be possible to play in the All-Ireland Hurling final in three weeks time.  There is a historic element to this as the team in question – Kilkenny, are seeking five Titles in a row which would be an unprecedented achievement and this player has played all matches.

The events that unfolded were surprising to say the least.  Within ten days of the injury eight thousand people turned up to watch the Kilkenny hurling team train and  to watch Henry Shefflin participate fully in the training session without any supportive device – part-taking in all the skill elements required for a game situation.  Apparently there had been no adverse reaction subsequently.  With the final looming in one week’s time it remains to be seen whether the player will play active roll but the story reminds me of the constant surprises we observe clinically between known pathology, clinical signs and functional impairment.

The literature would have us believe that approximately 30% of ACL disruption cases can return to competitive field sports activity without requiring surgical intervention.  Unfortunately the clinical challenge is that we cannot detect which patients are in this 30% sub-group and therefore only know by taking them through a sequential rehabilitation regime and observing achievement of milestones.  What is particularly surprising in this case was the speed of return to high level function even if the deadline is ultimately lost.  We’ll watch with interest…

There were some parallels with this example and a case of a twenty-five year old lady I had seen six weeks previously.  She presented with a spontaneous collapse of the right knee, again playing Gaelic football but this time presented with significant signs of joint effusion and functional impairment.  However, apart from the ominous signs of joint effusion I could not detect demonstrable laxity on anterior drawer, Lachman’s or pivot-shift tests.  As her functional capacity steadily improved over a number of weeks she progressed to jogging which unfortunately exacerbated her effusion.  On this basis and my suspicion of significant trauma initially (despite the absence of a full spectrum of confirmatory clinical signs) we arranged for surgical evaluation and MRI.  Again the Orthopaedic Surgeon’s physical examination was inconclusive and MRI scan confirmed a complete tear.  Surgery has subsequently being scheduled.

So take home messages from today’s discussion is the necessity for clinical reasoning when evaluating suspected ACL pathology or indeed any intra-articular pathology.  All may not be as it seems from clinical examination. The observation of suspicious features in the absence of positive definitive tests cannot always be fully relied upon.  In reality “function is king”, suspected pathology is secondary unless it is sinister or life threatening.  That is what makes the work of physiotherapist so exciting. How frequently do you see patients who fit the classic descriptions? Are there many exceptions to the rule?  Let us know.

Enjoy the clinical challenge.

David.

GHTime Code(s): f5aa8 nc 

Negative Test Results

A wise old doctor once told me that there was no such thing as a negative test result.  At the time I didn’t quite understand the significance but I have since come to strongly agree.

Much of the contemporary evidence on psychosocial aspects of pain management and clinical guidelines for interventions in low back pain in primary care discuss the relevance of supplementary investigations. In musculoskeletal practise we are generally concerned about imaging, bloods and differential diagnosis. From the clinicians perspective the primary reason for requesting investigations is to assist with diagnosis and exclude “Red Flag” pathology.  What has come to is the routine request of a battery of investigations without linking the necessity of investigations to the clinical findings. This lazy approach is sometimes referred to as “defensive Medicine” and is driven by a desire to avoid mal-practise suits or is part of the personal injuries litigation process. This has subsequently increased patient’s expectation that investigations should be routinely conducted. Unfortunately there is frequently an erroneous belief that these tests will actually change management – the fundamental reason for any supplementary investigation.

We know as clinicians that any investigation should be done for the purposes of influencing/directing management.  This issue is clouded by the complexity of the clinical reasoning process and the reality that there is not 100% correlation between clinical findings and pathology.  This can work in two ways.  Firstly, that the clinician’s perception raises suspicion of serious pathology or alternatively relatively modest clinical signs in the presence of serious pathology.  The question is whether we leave decision making to clinical judgement or pursue a course of routine implementation of tests as advised in “Guidelines”.

With the advent of psychosocial profiling the role of supplemental clinical tests came more in focus. This was because of the observation that some patients “ believed” they have serious pathology which might be demonstrable on investigation and unless tests are conducted an element of doubt persists, preventing progress beyond a rehabilitation roadblock.  Therefore just because a guideline says that routine x-ray is not appropriate from a clinical perspective if a patient perceives that it is of particular relevance then it will be hard to convenience them otherwise and thus pose a barrier to progression. As clinicians we may feel content in the security that guidelines provide – allowing us adopt a certain position to guide the patient /therapist discussion. However, we need to ensure we bring the patient along and this cannot always be done with discussion alone in my experience.

This does of course raise the issue of cost and who underwrites expense associated with what might be perceived as clinically spurious tests. I would argue nonetheless they are relevant / useful if the patient perceives them to be provided they can be used as a springboard to lever beyond a clinical bottleneck.

I find it useful to manage these patients who have a need for supplementary tests in the absence of clinical signs by attempting to predict what the scan, x-ray or blood test is likely to show.  This of course does put the clinicians ‘head on the block’ but it does establish confidence and enhance the credibility of the clinician (provided the results were correctly predicted).  And what if I predict wrongly I hear you say?. The answer is that there is always a cohort of patients where the clinical signs don’t match the pathology and even this can become a positive by establishing a baseline or allowing the clinician to outline what the particular symptom characteristics are associated with degeneration, spondylosis, inflammation, osteophytes etc to “match” or refute the patients symptoms.

One significant barrier can be the delay in pursuing adjunctive tests particularly if this is through a public health system and this often becomes an impediment to committing to rehabilitation pending the outcome of the tests.  Sometimes patients perceive a negative test as a lack of vindication of the existence of their symptoms and often appear to be somewhat disappointed.  From a therapeutic perspective the tables can be turned to use this evidence in a positive way to deconstruct any distorted perceptions of imminent structural failure and coax the patient into a progressive rehabilitation regime.  So on this basis I think we can say there is no such thing as a negative test – it just depends on who’s perspective.

Enjoy the clinical challenge.

David.

GHTime Code(s): d96dd 

Physiotherapy Expert Witness – practical strategies

Physiotherapy expert witness evidence was the topic of last week’s discussion and is the continuing theme today. As discussed the term “simple soft tissue injury” has become a catchall phrase within the legal system as well as primary care. I think it is a lazy expression because it avoids the onus of specific differential diagnosis and allows clinicians to hide behind a superficial examination (or screening radiology) without attempting to quantify the nature of the pathology, the extent of  tissues involved, the factors which are provoking symptoms and of course the appropriate treatment strategies.

From a physiotherapy perspective one simple strategy for identifying symptomatic tissue and recording in both  legal document and clinical report is to qualify the limiting factor when assessing range of motion. For example in the whiplash case we discussed if Cervical rotation is limited to 70° then a qualifying statement outlining the nature of symptoms produced and their location at the time of limitation provides more clinically useful information. For example the extract below demonstrates this for a Cervical & shoulder case on initial clinical examination.

Cervical Spine

Flexion                           -           ¾ range limited by pulling and discomfort in the right  neck and scapular area.

Extension                      -           Clear – No pain.

Right side flexion       –           80% (limited by right-sided discomfort).

Left side flexion          –          80% (limited by pulling and discomfort on

the right side).

Right rotation              –          80% (limited by strain and discomfort on the

right side).

Left rotation                 –         90% (limited by mild discomfort and pulling

on the right side).

Right Shoulder

Flexion                          -           full range           -           no pain.

Abduction                    -           full range           -           no pain.

Horizontal flexion     -           full range           -           no pain

Hand behind back     -           full range           -           no pain

These descriptors are particularly useful in establishing the likely tissue pathology but importantly also differentiating physiotherapy evidence from the routine evidence delivered from Orthopedic & Neurosurgeons – which in my experience never quantify the limiting factor other then stating  Ranges of motion (ROM).

Range of Motion – Revevance?

This issue is particularly relevant here because I was cross examined on this issue in the case we discussed last week.

The patient’s functional limitations where:

Sustained use of the arms particularly in overhead positions

Prolonged driving

Carrying

Sustained anti-gravity positions

The barrister enquired as to how the range of motion could be so good and yet she still described such functional limitations?

My reply was that it was like comparing apples and oranges. The functional limitations reported did not relate to movement deficits – they related to impaired tolerance for loading and sustain positions Therefore assessing range of motion was a somewhat irrelevant measure on from a clinical perspective. It shifted down the priority list (applied clinical reasoning) relative to the functional impairment.

Unfortunately this issue is rarely discussed in detail in a court of law because the surgeon’s evidence is often heavily weighted to range of motion findings and therefore these are considered to be important variables. I believe it is only when barristers are fully briefed on the pertinent aspects of clinical examination will the reliance on Radiology and ROM be surpassed. To achieve this there needs to be pre-court discussions analysing the clinical evidence and the line of question to be developed.

As clinicians we know that ROM is only one of a number of clinical variables and often has limited or no relevance in some clinical presentations. How many hypermobile patients with traumatic neck injuries have you seen where ROM has absolutely nothing to do with symptoms? How many fibromyalgia patients have restricted range of motion (greater than 20%?) and yet repeatedly describe a sense of tightness or muscle tension.

It is important that the role of ROM in a particular pathology be established in order to ascertain its relevance. This brings us nicely into another clinical marker which we as manual therapist use – Palpation.  Again I would consider this as a skill exclusive to physiotherapists and other allied health professionals and it’s an area where we have a proven to have particularly adept skills.  As clinicians when we palpate we are looking for a number of features related to tissue sensitivity.

Muscle spasm

Resistance to movement

Characteristic End-feel

Correlation with functional deficits

Correlation with primary areas of symptoms

These palpatory findings essentially form of an algorithm from which physiotherapists form a judgment – gaining a far deeper understanding of the tissue status.  The term muscle spasm is so frequently thrown around both clinically and legally without discussion of the underlying mechanisms and quantification of it’s relevance in the overall clinical context.

So, in conclusion, as we attempt to remedy the situation which will undoubtedly be an ongoing challenge, I encourage you to quantify the limiting factors in any clinical test procedure and take responsibility to define responsible structure s on the basis of examination findings. I think this will go some way to improving professional credibility- raising our perceived value not just within the legal profession but amongst our medical colleagues in musculoskeletal management.

Enjoy the clinical challenge

David

GHTime Code(s): f5ea6 

Expert Witness – A Day in the Dock

An interesting whiplash case

Expert witness work is not a pastime I actively pursue but inevitably get involved as part of routine clinical work.  Needless to say the spectrum of cases ranges from those with significant disabilities unable to work to those with modest functional discrepancies where the glass is ‘half empty’ instead of ‘half full’ and of course the occasional malinger gets in the door – only to be rapidly ejected within 3 treatments when discrepancies between signs, symptoms and participation become apparent.

The vast majority of medico-legal reports I write do not get contested in court and therefore despite the usual demands to be available on a standby basis (which incidentally I don’t agree to do) from time to time one is compelled to attend court.  Over the years I have been repeatedly struck at the lack of detailed musculoskeletal evidence discussed and analysed either in evidence or under cross examination.  It is absolutely routine for radiology, orthopaedic or neuro-surgical opinions to be submitted largely unchallenged even when the patient’s condition does not warrant such opinion’s – it’s like asking a plumber to look at an electrical fault.

This has resulted in the rather trivial dismissal of musculoskeletal pain, which doesn’t involve surgery or fracture as being simple “soft tissue pain”.  As we all know pain clinics around the planet are filled with patients in this category.  As far as I am aware there is no hierarchy of neural sensitivity from nerve receptors in bone, muscle, tendon, skin or nerve tissue.  Therefore this argument of “simple soft tissue pain” is not a particularly potent one in my opinion.

I write today’s post on the basis of a recent High Court experience in which I did get a chance to spend an hour in the witness box discussing the various merits of a complex (but genuine) whiplash case. We have discussed aspects of whiplash and neck pain treatment in previous posts I had treated this patient over a 3 year period.  She had a complex whiplash syndrome (classified as GD III on the Quebec task force scale or GD IIC Sterling classification) and it was clear from the initial assessment that this was a complex case.

Without labouring details she had been….

Off work for the eight months prior to consultation

Non-responsive to previous multi-modal physiotherapy

On a cocktail of medication

Had significant sleep disturbance

Was unable to support the weight of the head

Had bilateral neuropathic upper limb symptoms

Dizziness

Was generally fairly miserable.

Her occupational health physician had referred her to me on the suggestion that a “couple of sessions” of physiotherapy would put her right to get back to work within a fortnight.  I am not sure whether we examined the same patient, but this was clearly unlikely to be the scenario no matter what miraculous techniques I performed, or Devine intervention occurred.  I wrote to inform the referring physician of my opinion, the basis for which it was made and the need to institute multi-disciplinary pain management.

Six treatments later I did indeed arrange for formal pain management assessment having worked through some selective medication recommendations.  The reason I outline the detail here, and referring back to my initial comments above about the lack of discussion regarding symptom analysis, is on the basis of the cross examination which I encountered in the witness box.

Under cross examination I was asked why did I feel it appropriate to refer this case to a pain management physician.  I duly outlined my reasons based on the duration of time off work, severity of symptoms, non-responsiveness to treatment and limited potential for structured rehabilitation based on the current findings.  As this point the judge interjected to ask if I had directly referred the patient to the pain physician.  I replied “certainly – based on clinical need”.  The judge was somewhat surprised that I had not referred back to the GP.  I explained my decision that I had spend a significant amount of time in pain societies & professional liaison groups with GP’s teaching appropriate selection of patients for pain management and that because physiotherapy is an autonomous profession (for the last 25 years) it dictated that we make decisions and stand over them.  This undoubtedly surprised the judge again!

On further cross examination I was challenged with the view that an A&E consultant had assessed this lady and determined her fit for work two weeks prior to my consultation.  I informed the barrister that I disagreed.  Both the barrister and the judge responded by seeking clarification that I “actually” disagreed with the A&E consultant who was a fellow of the society and a consultant in emergency medicine.  My response was that in my opinion the role of the emergency consultant was to rule out sinister pathology in the form of neurological or orthopaedic conditions, but that he had minimal (no) role in rehabilitation and structuring of return to work programs.

There were many other points of contention, which may provide useful points of discussion in future but it illustrated to me a systemic perception / misperception of physiotherapy within the legal profession and the unacceptable status quo of appropriate recognition of experts in musculoskeletal health – which I consider physiotherapists to be.

This lack of discussion was confounded by the fact that the legal representatives on our side had no prior consultation with me (or any of the other experts) regarding the content of our reports or the interpretation of the clinical issues presented.  Again, this seems fairly typical in my experience and perpetuates a norm that clinical issues and patient function do not get properly discussed because they are dismissed as “soft tissue problems”.

This is a battle we must continue to fight on behalf of the physiotherapy profession but at least some pertinent clinical issues were discussed within a court of law. End of round one!

Enjoy the clinical challenge.

David.

GHTime Code(s): nc 

MYOFASCIAL PAIN SYNDROMES – Unanswered Questions?

Developments in the field of Myofascial pain syndromes over the  last decade has seen  significant evolution from the initial classification of trigger points as taut bands with research seeking to identify physical lesions and define location. Most of this development has been in the field of:

Biochemistry

Radiographic imaging

Elastography

Microdialysis techniques

Integration with our current understanding of pain mechanisms

Debate has now moved beyond whether Myofascial taut bands as entities actually exist into a more refined analysis of:

Identifying patient subgroups

Alternative etiological mechanisms

Identifying optimal management strategies.

The first point to recognise is that the cause of trigger points is still a matter of speculation. Travelle and Simons originally described both active and latent trigger points – latent to describe the concept of the clinical recognition of a palpable nodule, which was not reproducing symptoms.  The working assumption is that latent trigger points can exist without pain but then become activated for some reason.  As Robert Gerwin has alluded to trigger point tenderness does not occur except in regions of muscle hardness.  But regions of muscle hardness occur without local or referred pain.

It is currently “assumed” that the muscle hardness or taut band that occurs in the absence of pain is the first abnormality and that active trigger point is a more developed or second stage of the trigger point.  However this still remains hypotheses at this point.

Jay Shah amongst others has contributed largely to our knowledge on the biochemistry of the trigger points using microdialysis techniques.  This has indicated that there is a local mechanism of nerve sensitisation involving release of local neurotransmitters, hydrogen ions, potassium and cytokines, which are all classically associated with a peripheral inflammatory response (peripheral sensitisation).  The activation of these pathways also feeds into a central sensitivity state, which can become self-sustaining and independent of the peripheral components or essentially be a mirror of the state of peripheral sensitivity.

If the mechanical hypotheses of inducing trigger points is extrapolated there is a potential cascade of events involving neurotransmitters as alluded to above and also the release of acetylcholine at the motor end plate which amplifies motor end plate discharge and is thought to be associated with the development of localised muscle contractions – however this is only one of a number of theories.

Studies many years ago by Professor Patrick Wall indicated that taut bands can be produced in muscles simply by persistent depravation of sleep over a forty-eight hour period.  Clearly this mechanism is not associated with a mechanical event.  This raises the tantalising question of the chronic persistent myofascial pain syndrome in which:

Fatigue

Sleep disturbance

Muscle pain

are part of an integrated triad which is often challenging to resolve clinically.  What does appear evident from clinical observation is that mechanical muscle overload can occur at different ends of the spectrum from an acute severe overload that doesn’t induce fibre disruption but initiates sustained physical overload of  muscle fiber with the presumption of initiating the biochemical responses alluded to earlier.

At the other end of the spectrum is a low load, sustained activity associated with postural, ergonomic or occupational factors which by its nature is a less severe mechanical effect but cumulative over a longer period of time.

Other factors associated with the development of trigger points are:

Weakness

Hypoxia

Ischaemia

Central sensitisation

Referred pain

Gender

Hypermobility

The Diagnostic challenge

According to Jay Shah regarding this particular issue “validation of clinical diagnosis by palpation with these and other objective tests e.g. magnetic resonance & elastography would help establish the reliability of the clinical examination not as interrater reliability but in terms of the reliability of the physical examination to identify those patients whose myofascial trigger points is verifiable by other mean.

Current laboratory studies that show abnormalities would have to be validated themselves by showing that they independently identify trigger points that can be treated resulting in pain relief and improved function”.

Robert Gerwin adds “ there remains a need to develop a consensus on the clinical features required to diagnose myofascial trigger points.  There is also a need to develop objective laboratory criteria that can be used to standardise a diagnosis for the purposes of research.  They may have clinical value if they can be used to confirm an examination made by physical examination.  Elastography needs to be studied in a variety of trigger point pain syndromes”.

Treatment

The current treatment spectrum encompasses:

Stretch & spray

Local soft tissue mobilisation

Direct trigger point pressure

Dry needling

Injection therapy

Comparison of these modalities is still in its infancy other than anecdotal clinical evidence.

So in summary still much to do in this area of myofascial pain syndromes.

Enjoy the clinical challenge.

David

GHTime Code(s): 3acb9 00a7c nc nc nc 

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