A common form of clinical reasoning within the

A 52-year-old
female accountant presented in clinic with
a 6-week history of
elbow and neck pain. The cause of onset is unknown,
however is aggravated whilst playing badminton. The pain has significantly
increased in the last week. Anti- inflammatory medication (NSAIDS) were taken
by the patient, which initially resolved the pain.

 

‘Clinical reasoning’
is the process by which a therapist works with a patient to gather
information to generate and test hypotheses and determine optimal diagnosis with
an effective treatment plan (Jones, 1995). The most common form of
clinical reasoning within the physiotherapy profession is hypothetico-deductive
reasoning. The clinician collects the necessary information regarding the patient’s problem
which forms an initial diagnosis (Doody & McAteer, 2002). Further
data is collected during an objective assessment
which may confirm or contradict the diagnosis. This process may continue to occur during management
and reassessment.

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Frequent reflection
during the assessment and monitoring phase is a valuable part of clinical
reasoning. It aids the therapist to recognise their strengths and weaknesses and
further develops their clinical reasoning skills (Jones,1995).

 

Miss Lionel presented with immediate pain along the extensor carpi
radialis brevis (ECRB) when turning a key in the lock, lifting and tipping a
kettle and playing badminton. The patient reported pain
in the ECRB when writing with a duration of longer than ten minutes.

 

In view of the
above, coupled with the subsequent failure of anti-inflammatory medication,
leads to the diagnosis of lateral epicondyalagia (LE). LE comprises of 3 mutually related components;
changes in the pain system, the local tendon pathology, and impairments in the
motor system (Coombes, Bisset and Vicenzino, 2009).

 

Luk, Tsang and Leung (2014)
reports that histological examination of LE shows:

–      
angiofibroblastic
hyperplasia,

–      
tenocyte
hyperplasia

–      
increased ground
substance ground substance.

 

The absence of inflammatory
cells indicates the process is non-inflammatory
in nature, although neurogenic inflammation may play a role (Coombes, Bisset and
Vicenzino, 2009). This is likely to be the cause of the
short-term symptom relief of NSAIDS. NSAIDS and corticosteroids are
found to have no medium or long-term role when treating LE.

 

Lateral
epicondyalagia is regarded as a
degenerative process with dysfunctional and immature
healing. Changes to the normal tendon architecture including neovessal ingrowth
has recently been linked with pain in LE. This
emphasises the involvement between neural structures,
microvascular and neurochemicals at the insertion of ECRB (Coombes, Bisset and
Vicenzino, 2009). Tendons adapt to mechanical forces by changing their
structure. Loading promotes both synthesis and degradation of collagen lead by the
former process, resulting in increased type 1 collagen (Luk, Tsang & Leung,
2014).

 

The patient reported
a 6-week history of pain, this suggests that the patient may be undergoing both
nociceptive and non-nociceptive processes in addition to neuronal and
non-neuronal tissues. Increased concentrations
of glutamate and substance P have been found in LE affected tendons in
association with small blood vessels. This illustrates how the disordered pain system
of this condition correlates with its pathophysiology (Coombes, Bisset and
Vicenzino, 2009). These
neurochemicals are potent modulators of pain and regulators of local tendon
circulation and neurogenic inflammation. The
cardinal features of LE are angiofibroblastic hyperplasia in response to a
noxious stimulus. Some patients with LE can develop different degrees of
central sensitisation resulting in mechanical pain hypersensitivity in the
contralateral elbow or other locations. These patients may require different
pain management strategies (Jespersen et
al., 2013). Central sensitisation begins with activity in peripheral
nociceptors and is sustained in the absence of peripheral nociceptor input. Further
supporting the involvement of this process in LE, is the evidence of
myelinated group A fibres mediating the reduced mechanical pain threshold
beyond that of the original site of tissue injury (Coombes, Bisset and
Vicenzino, 2009).

 

Evidence has shown that patients most likely to experience LE
are amongst the population of manual workers and athletes who repeatedly make
repetitive movements of the forearm muscles against resistance. Miss Lionel
plays recreational badminton twice a week. Playing at
an amateur level indicates that she may not employ correct technique and could
potentially be over extending. The grip strength balance activity
between the wrist agonist and antagonist muscles together
with muscle strength of upper limb extremities are effective evaluations
used to determine LE (Lee et al., 2016). This theory is
particularly prominent in Miss Lionel’s case as her job as an accountant
demands extensive use of a computer. Typing involves prolonged wrist extension,
whilst writing or over-gripping a mouse would generate continued contraction of
the wrist extensors. This all indicates that the ergonomics of her desk set up
may need to be reviewed. A poor desk set-up maybe another possible contributing
factor to her neck pain.

 

 

Miss Lionel did
not present with any contraindications
for physiotherapy treatment. Precautions need to be
taken in relation to the phase of LE.

A known family history of rheumatoid
arthritis predisposes a person to developing the condition (Toms, 2009). The patient has reported that her
sister was diagnoses with rheumatoid arthritis 8 years ago, therefore close monitoring is required. Precaution is required
secondary to her high Visual analogue scale (VAS) score
when doing manual therapy.