I recently delivered this presentation on 'MSK Masqueraders' at the National Exhibition Center (NEC) in Birmingham for the 2015 Therapy Expo conference.
Basically this was a brief insight and overview of MSK Masqueraders and the impact on clinical practice. The context of each slide was expanded during the conference session and hopefully the presentation below gives you a flavour of the topics I covered. Be mindful that this presentation is a snippet of what I would usually cover so, is not a complete overview of the topic of Masqueraders, which is a challenging area of clinical practice.
Having knowledge of conditions that can masquerade as MSK pathology is a key aspect of the physiotherapist’s clinical development. More and more roles and opportunities are arising where we are responsible for first line assessment and care, which means we must have an ability to screen effectively, systematically and understand when the patient is presenting with symptoms that don't quite fit with an MSK presentation.
Index of suspicion, pattern recognition and understanding when and how to streamline you assessment to ascertain clarity on the next steps for a patient that you are concerned about can be challenging but is vital.
Twitter Handle: @stevenawoor
3. Rolling the ‘Clinical Dice..’
#therapyexpo
‘Many diagnoses are missed as not considered to be likely or not considered at all..’ [Jackson, 2011]
4. • Imaging
• Injecting
• Prescribing
• Minor Surgery
• FCP Roles
Physiotherapy has moved on
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5. Safety in LARGE numbers..!
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• Leadership
• Accountability
• Risk
• Governance
• Education
‘The line between failure and success is so fine that we scarcely know when we pass it…’
Elbert Hubbard
6. Mistakes Happen
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Consider the impact on person, family,
clinician & service
‘The man of science has learned to believe in justification, not by
faith, but by verification…” [Thomas Henry Huxley]
7. Clinical Reasoning
‘Clinical reasoning is only as good as the
information on which it is based …’ [Jones 1992]
Three types of error can occur in clinical reasoning:
1.Faulty perception or elicitation of cues
2.Incomplete factual knowledge
3.Misapplication of known facts to a specific problem
[Scott, 2000]
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8. Terminology
Masquerader
‘Appears in disguise or
assumes a false
appearance…’
Red Herring
‘Misleading biomedical or
psychosocial factor that
can deflect clinical
reasoning..’
Red Flag
‘Possible indicator of
serious pathology…’
Serious Pathology
‘Fracture, Cancer,
Infection, CES,
Inflammatory disorder…’
[Greenhalgh & Selfe, 2006; Clinical Standards Advisory Group 1994, Sykes, 1978]
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9. Dear Team,
Thank you for the reviewing this 65 yr old male who has a history of LBP, however more recently he
has had some unilateral leg pain which I believe coincides with a groin injury following gardening.
Neurologically he is intact and I would be grateful of your physiotherapy assessment.
• Pain during gardening 3/52
• LBP now worse in sitting
• Lying on ® side causes rib pain
• Intermittent ® leg pain
• No neuro reported
• Hypertensive
Clinical Scenario
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• Alcohol 70 units per week
• Testicular, Hip & Groin Pain
• Syncope x 3 episodes 3/52
• Ribs feel bruised
• Leg feels heavy
• Family history of PVD
11. #therapyexpo
Abdominal Aortic Aneurysm (AAA)
• Syncope may be the chief complaint, however, ć pain
less prominent
• Expanding AAA causes sudden, severe, LBP, flank,
abdominal, or groin pain
• Normal vital signs (?) ć ruptured AAA as a consequence
of retroperitoneal containment of hematoma
• Common & life-threatening
• 65 years > (M)
• History of PVD
• Usually asymptomatic until they expand or rupture
• Grey Turners Sign
• Grey Turners sign can be associated ć Cullen’s Sign
‘62 %chance that an AAA is present with a popliteal aneurysm and an 85 % chance it is present with a femoral artery
aneurysm; 14 %of patients with a known AAA will have a femoral or popliteal artery aneurysm…’
[Bosmann et al, 2009; Von Allmen et al;2012]
12. Grey Turners Sign Cullens Sign
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Things to watch & tune into….!
13. Unusual but worth noting..!
‘73-year-old man with a ruptured AAA presenting with isolated acute
right hip pain without any classical features…’ [Validyanathan et al, 2008]
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14. Or….how about this…!
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‘Every physician seems to recall a case of a missed aneurysm with catastrophic
outcomes where, in retrospect, warnings may have been overlooked. Because
of frequent visits, she had been labeled as a “frequent flyer", and back pain is
an extremely common and nonspecific symptom…’
[Helliker & Burton, 2003]
16. Cauda Equina Syndrome
‘Narrowing of the spinal canal that
compresses the nerve roots below the level of
the spinal cord…’
[Todd, 2009]
‘Classic Triad - Saddle anesthesia, bowel and/or
bladder dysfunction, and lower extremity
weakness…’
[Gautschi et al. 2008]
‘Average compensation ć missed or delayed
diagnosis £336,000 UK. 1000 operations per
year ć 30-40 cases in UK…’
[Gardner et al, 2011]
‘Challenge of notes, under- recording of the actual
presentation, failure to examine properly, act on
red flags, refer on or investigate with sufficient
urgency…’
[The CSP 2014; Greenhalgh, Selfe, 2006; Macfarlane, 2014]
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‘The most common cause of CES is lumbar disc herniation at the L4-L5 and L5-S1 levels and then in decreasing order,
tumour, infection, stenosis, haematoma, inflammatory and vascular..’ [Fraser et al, 2009]
17. Bladder Confusion & CES
#therapyexpo
Not uncommon for patients with severe
back and leg pain to complain of difficulty
passing urine
• Severe back and leg pain can lead to
Inhibition of bladder functioning
• Opiates (Morphine based) - Affect the
bladder sphincters -
• Anxiety – Affect on bladder function
Urinary Retention…!
• Vaginal childbirth, Infections, Diabetes, Stroke,
MS, Prostrate
• Surgery- Post-Op anaesthetic nerve block
• Medication - Antihistamines & Tricyclic
antidepressants (e.g. Amitriptyline)
• Bladder Stone - urinary tract blockage
• Prolapse of anterior vaginal wall
• Constipation – Hard stool in the rectum can pinch
shut the urethra
18. CES (Incomplete)
• Uni or bilateral sciatica may be present & >
• Deteriorating neuro
• Uni or patchy perineal / perianal numbness
• Anal sphincter tone reduced
• < desire to void, poor stream flow, strain to
micturate but with sensation of a full bladder
CES (Complete)
• May have NO leg pain OR
• Uni/bi lateral sciatica
• Widespread perineal sensory deficit
• NO anal sphincter tone
• Painless urinary retention with full bladder and
overflow incontinence
Sexual Dysfunction Associated ć CES
• Vaginal anesthesia and numbness
• Incontinence during intercourse
• < intensity and/or inability to achieve orgasm
• Inability to achieve erection
• Inability to achieve ejaculation
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Cauda Equina Syndrome
21. #therapyexpo
• Qualify
• Quantify
• Index of suspicion
Go back in time &
understand the history
in more detail if
needed..!
‘History is a vast early warning system…’ Norman Cousin
22. ‘Dear Sir, I am now required to remove my
MSK Hat and I will need to change tact
during assessment to ensure we have clarity.
Please bear with me..!’
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Removing the MSK Hat
23. ‘Questions are great, but only if you know the answers’ Laurell Hamilton
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24. It just sounds and looks a bit odd…!
• Masqueraders are rare
• Coexistence of conditions
• Pattern recognition obscured
• Generally unwell
• Co morbidities
• Gut feeling
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25. Dear Team,
Thank you for reviewing this 72yr old female who describes a 6-month history of left sided hip
pain, which has progressively worsened in the last 8 weeks. The patient is now complaining of
what I presume is Greater Trochanteric Bursitis on the left hip, which is affecting her walking. I
wonder if they may benefit from an injection.
• Fall 8 months ago in garden
• > Hip and back pain since
• Weird walking 12months
• Clumsiness
• Legs feel funny
Clinical Scenario
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• Hyper-reflexia LL
• B&B, Saddle Anesthesia clear
• No Hx of Cancer
• Weight stable
• Cant lie on left hip due to pain
28. Myelopathy
‘Neurologic deficit related to the spinal cord,
usually due to compression of the spinal cord…’
• Osteophytes
• Discogenic
• Carcinoma
• Trauma
• Infection
• Cysts
[Kent; Rapport; Rothman; Tartaglino et al, 1994]
Basically we are looking at a Space Occupying Lesion
(SOL) to various degrees…!
#therapyexpo
29. Metastatic Spinal Cord Compression (MSCC)
‘Metastatic spinal cord compression is defined
radiographically as an epidural metastatic lesion
causing true displacement of the spinal cord from its
normal position in the spinal canal…’
[Loblaw et al, 2003]
#therapyexpo
63 year-old man with metastatic
melanoma to the C5 vertebral
body
30. 8 Item Identification Tool for MSCC
• Referred back pain that is multi segmental or Band Like
• Escalating pain which is poorly responsive to Rx (Including meds)
• Different character of site to previous symptoms
• Funny feelings, odd sensations or heavy legs (Multi Seg)
• Lying flat increase back pain
• Agonising pain causes anguish an despair
• Gait disturbance, unsteadiness, especially on stairs (not just a limp)
• Sleep grossly disturbed due to pain being worse at might
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[The Greater Manchester and Cheshire Network UK]
31. Vigilance and awareness can be helpful..!
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• Identify early
• Gain clarity
• Calm approach
• Methodical
•
32. •Altered facial sensation (L)
•Light-headedness ć (L) UL 90°
•Nausea ć (L) UL > 90 °
•Exercise induced ‘heaviness’ of (L) UL
•Recent > SOB ć UL activity & inclines
Clinical Scenario
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Dear Team,
Thank you for the reviewing this 52yr old female who describes cervical spine pain which radiates into
the left with an associated tension related headache. I wonder if some physiotherapy may be of some
benefit. I enclose a copy of a recent x-ray that highlighted Spondylosis at the C4-5, which wont be
helping symptoms.
•Handwriting <
•Hypotensive
•Temporal headache
•Intermittent blurred vision (L)
• Capsualr pattern – left shoulder
34. #therapyexpo
Clinically evident ć symptoms of the ‘Pancoast-Tobias Syndrome’
which includes ‘Claude-Bernard-Horner syndrome’
• <5% of Bronchogenic Cancer = Apex of the lung
• Severe pain in the shoulder radiating toward axilla and/or
scapula & along the ulnar distribution of the upper arm
• Atrophy of hand and arm muscles and obstruction of the
subclavian vein resulting in oedema of the upper arm
• Subclavian vein swelling
• Involvement of the Thoracic Outlet
• Horner Syndrome - Miosis (a constricted pupil), Ptosis (a weak,
droopy eyelid), Anhidrosis (decreased sweating) with or without
enophthalmus (inset eyeball).
T1W Coronal ć mass arising from
right lung apex , involving the 1st
2nd ribs and the lower
root & trunks
Pancoast Tumour
35. Giant Cell Arteritis (GCA) ‘ A headache not too miss..!
• >70yrs & rare <50yrs
• Most common form of Vasculitis in adults
• 3 x more common in (F)*
• Abrupt onset of headache ‘Head Pain’ (75%)
• Scalp pain (difficulty in combing hair)*
• Jaw & tongue claudication Cramping pain occurring after prolonged chewing or
talking (DD ć TMJ)
• Limb claudication – ? large-vessel GCA (i.e. outside the cranial vessels).
• Visual disturbance - Transient
• Systemic symptoms ( low-grade - fever, anorexia and fatigue – 50%)
• Appetite, depression, fatigue*
• Polymyalgia symptoms (40-60%)
• Upper Cranial Nerve Palsies
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Competency with Cranial & Haemodynamic Testing!
36. Differential Diagnosis in GCA
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• Shingles
• Migraine
• Orbital or base of skull lesions
• Ischaemic attack
• Cluster headache
• Cervical spondylosis
• TMJ
• Ear problems
37. GCA & Bloods
• C-reactive protein (CRP)
• Erythrocyte sedimentation
rate (ESR)
• ESR & CRP are no longer
routinely requested together for
most conditions, either marker
(or both) can be raised in GCA
• If both CRP and ESR are normal, the
likelihood of giant cell arteritis
being present is reduced, but
cannot be ruled out.
• Full blood count (FBC)
• Liver function tests (LFTs)
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38. Thoracic Outlet Syndrome (TOS)
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Neurogenic (TOS) Upper (C5-7)
• Radiating neck pain to ear, face & occiput causing
headaches
• Mimics a C5-6 nerve root can be caused by hypertrophies
scalene, elongated C7 TP, presence of Csx rib
• Paresthesias fingers & hands*
Neurogenic (TOS ) Lower (C8-T1)
• Median & ulnar distribution ć or without neck/shoulder
pain
• Overhead activity can cause weakness
• Loss of grip and fine motor control
• No limited to a specific dermatome
[Nichols, 2009 ; Brantigan & Roos, 2004]
Vascular (TOS)
• Paget-Schroetter syndrome or Effort
Thrombosis
• Underlying anatomical abnormality
• Concomitant repetitive arm raising
exercises, such as swimming or throwing a
ball
[De Leon et al, 2009]
39. Dear team,
Thank you for reviewing this 46 year old female who was very fit up until last year. Could you please advise for exercises due to
weakness in both feet. I have attached an MRI of the foot for your records which has come back negative, as have a recent set
of full bloods. I wonder whether an orthotic may be of use.
Clinical Scenario
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• No trauma
• Antalgic gait
• NO B&B, SA, night pain
• 2 hr ‘Siesta’ required to function
• No PMhx
• Memory
• Hyperreflexia LL
• No radicular S&S
• First line analgesia no effect
• Sub 4hr Marathon 18/12
• Weakness L4/5 L5/S1
• Hair loss
40. Family History of Myotonic Dystrophy
• Muscle weakness
• Inward & upward-turning foot
• Breathing
• Balding
• Cardiac
#therapyexpo
41. Dear team,
Thank you for reviewing this 61 yr old female who has a 3-month history of insidious right sided shoulder pain, which presents
more as stiffness and wonder whether they may benefit from some exercise advice and an injection. I enclose a copy of a
recent x-ray which is unremarkable.
Clinical Scenario
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• Diagnosed ć (L) Breast Ca Jan 2015
• Chemotherapy
• Breast Surgery
• Radiotherapy
• Hormone Therapy
• Still under Consultant
• No neuro, B&B or SA
• Mid thoracic night Pain
• Lateral rotation < AROM & PROM
• Sympathetic response on ROM
42. Consideration for the medication
‘The MSK system has a high metabolic rate
& blood flow, therefore high exposure to
circulating medications..’
• Muscle Pain
• B&B Dysfunction
• Osteoporosis
• Fractures
• Tendon Ruptures
#therapyexpo
43. Medication
Clinical Presentation Considered Medication
Mild Aches and Pains Oral contraceptive (e.g: Microgynon) and Statins (e.g: Atorvastatin)
Muscle Cramps Diuretics (e.g. Bendroflumethiazide- Calcium Channel Blockers (e.g.: Verapamil) - Beta Agonists
(e.g.: Salbutamol)
Proximal muscle weakness, atrophy Oral Corticosteroids (e.g. Prednisolone), >10mg dose, for at least 30 days
Severe Pain, myopathy, malaise, fever, dark urine statins, 0.1-0.2% of pets in clinical trials have side effects
Osteoporosis Fracture Oral corticosteroids, i.e.. Doses > 5mg daily lead to significant and rapid bone loss. A cumulative
dose of >30g associated with high incidence of fracture 53%.
Avascular Necrosis -Corticosteroids 5-40% of pets on long term therapy
#therapyexpo
Adapted ~ Grieves Modern MSK Physiotherapy 2015
44. Medication
Clinical Presentation Considered Medication
Tendinopathy, tendon rupture , myopathy Injected corticosteroids , oral corticosteroids Glucocorticoids, direct catabolic effect on skeletal
muscle tissue
Myalgia, arthralgia, arthritis, tendinitis Quinalones (synthetic broad spectrum antibiotics - e.g.: ciprofloxacin) World wide incidence of
side effects estimated as 15-20 per 100,000 patients treated
Bladder & Bowel Dysfunction Opioid salts; constipation (e.g.: Tramadol, codeine) Anticonvulsants: urinary incontinence
(Gabapentin, Pregablin). Antidepressants = retention, sexual dysfunction (Amitriptyline,
Nortriptyline)
Muscle Cramp, muscle weakness Thyroid hormones (e.g: levothyroxine sodium… at excessive dosage
Joint aches and pain (Arthralgia) Antithyroid drugs used to treat hyperthyroidism – e.g.: Carbimazole
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Adapted ~ Grieves Modern MSK Physiotherapy 2015
47. Light Bulb Moments..!
‘To know what you know and what you
do not know, that is true knowledge...’
[Confucius]
#therapyexpo
48. Brining it all together isn't easy..!
#therapyexpo
• Knowledge & exposure
• Ongoing competency
• Structure & support
• Qualify & quantify
• Index of suspicion
• Pathways
50. References
• Boden SD, et al. JBJS 1990; 72-A: 403-408
• Bosmann M, Schreiner O, Galle PR (April 2009). "Coexistence of Cullen's and Grey Turner's signs in acute pancreatitis". Am. J. Med. 122 (4): 333–4.
• Brantigan CO, Roos DB. Diagnosing thoracic outlet syndrome. Hand Clin. 2004;20:27–36.
• Fraser S, Roberts L, Murphy E. Cauda equina syndrome: a literature review of its definition and clinical presentation. Arch Phys Med Rehabil.
2009;90(11):1964–68
• Gautschi OP, Cadosch D, Hildebrandt G. Emergency scenario: cauda equina syndrome--assessment and management. Praxis (Bern 1994)
2008;97:305–12
• Gitelman A, Hishmeh S, Morelli BN, Joseph SA, Casden A, Kuflik P, et al. Cauda equina syndrome: a comprehensive review. Am J Orthop.
2008;37(11):556–62
• Greenhalgh S, Selfe J. Red flags: a guide to identifying serious pathology of the spine. Edinburgh: Churchill Livingstone; 2006.
• Gardner A, Gardner E, Morley T. Cauda equina syndrome: a review of the current clinical and medico-legal position. Eur Spine J. 2011
May;20(5):690-7
• Helliker K, Burton TM. Medical ignorance contributes to toll from aortic illness. Wall Street Journal; Nov 4, 2003.
51. References
• Jackson J . ‘ Musculoskeletal Pathway Information’. West Sussex NHS Trust (2011)
• Jones, M.A. Clinical reasoning in manual therapy. Phys. Ther. 1992; 72: 875–884
• Loblaw DA, Laperriere NJ, Mackillop WJ. A population based study of malignant spinal cord compression in Ontario. Clin Oncol 2003;14:472-80
• Mooney V. Differential diagnosis of low back disorders: principles of classification. In: Frymore JW, editor. The adult spine: principles and practice.
New York: Raven Press; 1991. pp. 1559–60.
• Macfarlane R. Cauda equina syndrome: key issues. London: Kennedys. 2014.
• Ma B, Wu H, Jia LS, Yuan W, Shi GD, Shi JG. Cauda equina syndrome: a review of clinical progress. Chin Med J. 2009;122(10):1214–22
• Nichols AW. Diagnosis and management of thoracic outlet syndrome.Curr Sports Med Rep. 2009;8:240–9.
• The Chartered Society of Physiotherapy. Professional and public liability insurance. London: The Chartered Society of Physiotherapy. [Accessed: 29
May 2014]
• Scott I. Teaching clinical reasoning: a case based approach. In: Jones MA, Higgs J, editors. Clinical reasoning in the healthprofessions, 2nd ed.
Oxford: Butterworth Heineman; 2000 [chapter 34]
• Todd NV. An algorithm for suspected cauda equina syndrome. Ann R Coll Surg Engl. 2009 May. 91(4):358-9; author reply 359-60.
• Von Allmen RS, Powell JT. The management of ruptured abdominal aortic aneurysms: screening for abdominal aortic aneurysm and incidence of
rupture. J Cardiovasc Surg (Torino). 2012 Feb. 53(1):69-76
Notas del editor
MSK Masqueraders…. For the netx 45 mins or so…..
SO… lots of different professions workig in lots of different settings….which ever profession were in we are involved in patient care and alongside that comes patients safety….
I think we have all been in situations that are confusing and as I said ‘seeing throguh that can be difficult….’
n MSK Masquerders
Why talk about MSK Masqueradrers...
Many diagnoses are missed because they are either not considered to be likely or are not considered at all. As diagnosticians we use the law of probability all the time. Most headaches are not brain tumours. Most pigmented skin lesions are not melanomas
For me there are several clinical scenarios that give us cause for concern that in clinical practice.
1) Relating a patient's symptoms to radiological findings, resulting in unnecessary onward referral
2) Failure to diagnose an unusual presentation of a common MSK disorder
3) Misdiagnosis of something as a surgically treatable spinal disorder that is instead a medical or neurological condition mimicking myelopathy or radiculopathy. In the present review, we provide an overview of some of the common conditions that masquerades as surgically treatable spinal disease.
The first thing I will say is that PHYSIO HAS MOVED ONE..!! I use this analogy a last week my 6 year old son asked me what one of these was for..!
The responsibility of physio has moved on SIGNIFICNATLY in the last decade with requesting imaging, injecting, prescribing, minor surgery and FCP roles etc…and with that comes responsibility for patient care at level that we probably couldn't have envisaged 20yrs ago….
I think it is absolutely critical to start with the fact that because of the extended roles we are now being exposed to the risks even higher than it was and with that comes an ABSOLUTE must for SAFETY..!!
And with physio moving on there are some CHALLENGES and with those challenges we need to be even safer in what we do, how we do it and that means being part of a team….SAFETY in LARGE
numbers means you need a team and framework around you that can support those difficult decisions both CLINICALLY & OERATIONALLY …
You know the patient need moving on – can u make that decision and be accountable for it or do u need support from a senior member of the team
Do you and your team know that process..!
Are you working in isolation..!!
(Its no good making a decision and not having a pathway or process in place that can facilitate that at a pace that is required form an OPERATIONAL perspecitve
MSK physios are more and more becoming FCP in different guises, therefore the ACCOUNTABILITY for decisions we make is becoming more and more apparent… the GOVERNANCE, COMPETENCE, DEVELOPMENT & LEADERSHIP Framework that underpins our clinical practice is critical to ensure safety for us and our patients…
We work in an area that presents of with clinical risk everyday so the ability to make a judgment on the correct clinical pathway for a patient lies with us…. Whether that be onward referral, requesting imaging, injecting, prescribing or seeking advice from a member of the team to ensure the right decision is made we need to be aware of all parameters
The one thing I will say is that all of us here are working in different guises and should NOT have to make these decisions without support from senior staff, pathways and medical professionals.
Its about working as a team to ensure that the patient is safe…. and you have the appropriate Governance in place to support your decision.!
BECAUSE if its not presenting as MSK as part of your work up you will need to know next steps
Masqueraders are
MISTAKES Happen and can be costly for the persons involved, patient, family, clinician and service…….
ESPECIALLY with MASQUERADERS….but even if you do get it wrong you need to be able to justify your thought processes to the point as to how you reached your decision…
The man of science has learned to believe in justification, not by faith, but by verification.” Thomas Henry Huxley, Collected Essays Of Thomas Henry Huxley
We should learn something from every patient we see and pattern recognition improves time on time again… providing we challenge ourselves to recognize and understand when something doesn't’t quite fit the MSK picture…. and knowing how and when to step back and reflect during the SUBJECTIVE …NEXT SLIDE
& with when considering the front line clinical situation we are now in we need to try and keep a clear mind on some of the factors that can mask judgment and I suppose understanding some BASIC terminology can help…..
Misattribution by Patient Referring doctor or allied health professional Treating physiotherapist
Inappropriate overt illness behaviour Inappropriate overt illness behaviour
Other conditions which complicate the Other conditions which complicate the
clinical scenario
clinical scenario
Biomedical Masqueraders Biomedical Masqueraders
NOT in any particular order…. But what would you be thinking …. JUST Subjective..!
What are we thinking and would the subjective be enough…?
What would you look for next..?
AAA
65 year old male
No history of trauma
Insidious onset of LBP 3 years
Acute Mid thoracic pain 4-weeks with lifting
Groin pain with associated testicular 3-weeks
Dyspagia
No neuro
Hx of hypertension
Tsx pain > with cough and Grey Turners Sign – if I add this… does that change your mind & would you IOS be ++ anyway and why..?
No history of trauma
Insidious onset of LBP
Mid thoracic pain aggravated by coughing
Hx of hypertension
Dysphagia (problems with swallowing) is a recognized symptom in up to 20% of patients with aneurysms of the descending thoracic aorta (LeRoux TB. Rogers MA, Gotsman MS: Aneurysms of the thoracic aorta. T/ioru.r 26. 638 1971)
Aneurysm of the abdominal aorta may present with severe low-back pain; the addition of testicular pain is ominous and often precedes fatal rupture (Richardson1960;Sokoloff& Bland 1975; Appenzeller 1978; Adams 1981). The onset of dissection of an aneurysm in the ascending aorta or aortic arch is characterized by a sudden, tearing chest pain; this often radiates into the neck, dorsal trunk, abdomen and legs (Mcleod, 1981). The suddenness, severity and spread of pain should be sufficient evidence of serious visceral disease as oppose to an acute Thoracic MSK presentation
What are the options here….
Common & ife-threatening
65 years > (M)
History of PVD
Usually asymptomatic until they expand or rupture
An expanding AAA causes sudden, severe, and constant low back, flank, abdominal, or groin pain
Syncope may be the chief complaint, however, with pain less prominent.
Normal vital signs in the presence of a ruptured AAA as a consequence of retroperitoneal containment of hematoma
Grey Turners Sign (Flank bruising) can be associated ć Cullen’s Sign (Bruising around the Umbilicus)
Cullen's sign is superficial edema and bruising in the subcutaneous fatty tissue around the umbilicus.
Von Allmen RS, Powell JT. The management of ruptured abdominal aortic aneurysms: screening for abdominal aortic aneurysm and incidence of rupture. J Cardiovasc Surg (Torino). 2012 Feb. 53(1):69-76.
Bosmann M, Schreiner O, Galle PR (April 2009). "Coexistence of Cullen's and Grey Turner's signs in acute pancreatitis". Am. J. Med. 122 (4): 333–4.
The presence of a prominent popliteal or femoral artery pulse warrants an abdominal ultrasound to rule out an AAA and a lower extremity arterial ultrasound to rule out peripheral artery aneurysm. There is a 62 percent chance that an AAA is present with a popliteal aneurysm and an 85 percent chance it is present with a femoral artery aneurysm; 14 percent of patients with a known AAA will have a femoral or popliteal artery aneurysm.16
Diwan A, Sarkar R, Stanley JC, Zelenock GB, Wakefield TW. Incidence of femoral and popliteal artery aneurysms in patients with abdominal aortic aneurysms. J Vasc Surg. 2000;31:863–9
Just putting it out there….
Every physician seems to recall a case of a missed aneurysm with catastrophic outcomes where, in retrospect, warnings may have been overlooked. A Wall Street Journal article recently won a Pulitzer Prize for publicizing such aneurysm cases. 58 Our patient's back pain was initially dismissed. Because of frequent visits, she had been labeled as a “frequent flyer”—and back pain is an extremely common and nonspecific symptom.
Understanding CES and the horse tail can be confusing but is very important if you don’t want to get into trouble..!
CES is a good example of where Masqueraders can be gihlighted as its NOT clear cut sometimes and the Hx of a pt anbe confusing
DO I have enoguh flagd…. Is that really a bladder or bowle issue…… is that saddle anesthesia…..!
do I have enough flags…etc… it’s a HUGE subject and once again HISTORY is critical..!!!
It’s the BIG one that a lot of us talk about on the shop floor and can cause a lot of confuison
It’s a detailed session on its own so have tried to pull some of the key points out….
Average compensation following missed or delayed diagnosis of CES is £336,000 per case in the United Kingdom
HES Data shows 1000 operations are done each year for CES, so it is not a rare condition
The number of cases coming to litigation each year in the UK is uncertain. Gardner et al estimated between 30-40 cases per year in UK
Patients may challenge what the clinical notes record, in particular that they under- record the actual presentation.(4)
The basis for the claim is that the practitioner failed to: examine the patient properly; act on ‘red flags’ present, refer on or investigate with sufficient urgency.(4)
This does not just affect doctors and surgeons. Physiotherapists have been found to be clinically negligent for failing to act and/or refer on when a patient presented with possible CES. (2)
The Chartered Society of Physiotherapy. Professional and public liability insurance. London: The Chartered Society of Physiotherapy. [Accessed: 29 May 2014]
Greenhalgh S, Selfe J. Red flags: a guide to identifying serious pathology of the spine. Edinburgh: Churchill Livingstone; 2006.
Macfarlane R. Cauda equina syndrome: key issues. London:
Challenge of clinical notes record, under- record the actual presentation, failure to examine properly; act on ‘red flags’ present, refer on or investigate with sufficient urgency
Found to be clinically negligent for failing to act and/or refer on when a patient presented with possible CES
CES is the obvious one that jumps to most peoples mind with a reported average being as at £300,00 mainly because most cases are preventable
Early diagnosis
Difficult questioning (Set context)
Recognition by patient
Your interpretation & next question are KEY
CES (incomplete) – 48hr window where surgery maybe helpful
*Uni or bilateral sciatica may be present and increasing
*Worsening neuro
*Uni or patchy perineal / perianal numbness
*Anal sphincter tone reduced
*< desire to void, poor stream flow, strain to micturate but with sensation of a full bladder
CES (Complete)
May have NO leg pain ~OR Uni/bi lateral sciatica
Widespread perineal sensory deficit
NO anal sphincter tone
Painless urinary retention with full bladder and overflow incontinence
Sexual Dys assoc with CES
Vaginal anesthesia and numbness
Incontinence during intercourse
< intensity and/or inability to achieve orgasm
Inability to achieve erection
….. Ejaculation
Differential Diagnoses and Confusing Scenarios
It is not uncommon for patients with severe back and leg pain to complain of difficulty passing urine due to the following possible causes:-
Severe pain. This can inhibit bladder functioning or disrupt normal function. Opiate analgesia. Strong pain killers are usually opiates (Morphine type drugs)
and these affect the bladder sphincters. Other genito-urinary problems are many.
Differential Clues:-
Normally the above causes of bladder dysfunction are temporary or intermittent short lasting few hours only.
Anxiety plays a part in bladder function problems usually with pain control and relaxation the patient can pass urine.
These patients usually do not have a significant complaint of sensory impairment in the saddle region.
NB: Often the bladder problem is in isolation in these cases.
Urinary Retention
There are many possible causes of urinary retention including obstruction of the urinary tract or problems of the nervous system. Consider the following:
Nerve Disease or Nerve / Spinal Cord Injury – E.g. vaginal childbirth, infections of brain or spinal cord, diabetes, stroke, injury to nervous system of spine or pelvis, Multiple Sclerosis, heavy metal poisoning.
Prostate Enlargement- The male prostate gland may enlarge with age (benign prostatic hyperplasia or consider malignancy). As the prostate enlarges it presses on the urethra resulting in the bladder wall becoming thicker and irritable. The bladder may then contract even when holding only small amount of urine = frequency. Eventually the bladder may weaken and loses the ability to empty itself, so urine remains.
Infection- A urinary tract infection (UTI) may cause retention if the urethra becomes inflamed and swells shut.
Surgery- Post –operative temporary urinary retention is not uncommon due to anaesthetic nerve block.
Medication- Many medications work by calming overactive nerve signals. Some of the following
groups of drugs that may cause urinary retention are:- Antihistamines ; Anticholinergics/antispasmodics to treat stomach cramps, muscle cramps and incontinence; Tricyclic antidepressants.
Bladder Stone - urinary tract blockage
Prolapse of anterior or posterior vaginal wall structures– could cause urinary incontinence or retention.
Constipation – Hard stool in the rectum can pinch shut the urethra – more likely in the presence of retrocele.
Urethral Stricture – narrowing or closure of urethra E.g. trauma or infection.
1. Cauda Equina Syndrome with retention (CESR). Back pain with unilateral or bilateral sciatica, motor weakness of the legs, sensory disturbance in the saddle region, loss of anal tone and established loss of urinary control i.e. painless retention and overflow.
2. Incomplete Cauda Equina Syndrome (CESI). As above but with altered urinary sensation e.g. loss of desire to void, diminished sensation, poor stream, and need to strain. Painful retention may precede painless retention in some cases.
3. Suspected Cauda Equina Syndrome (CESS) Cases of severe back and leg pains with variable neurological symptoms and signs, and a suggestion of sphincter disturbance.
CES is the obvious one that jumps to most peoples mind with a reported average being as at £300,00 mainly because most cases are preventable
Early diagnosis
Difficult questioning (Set context)
Recognition by patient
Your interpretation & next question are KEY
CES (incomplete) – 48hr window where surgery maybe helpful
*Uni or bilateral sciatica may be present and increasing
*Worsening neuro
*Uni or patchy perineal / perianal numbness
*Anal sphincter tone reduced
*< desire to void, poor stream flow, strain to micturate but with sensation of a full bladder
CES (Complete)
May have NO leg pain ~OR Uni/bi lateral sciatica
Widespread perineal sensory deficit
NO anal sphincter tone
Painless urinary retention with full bladder and overflow incontinence
Sexual Dys assoc with CES
Vaginal anesthesia and numbness
Incontinence during intercourse
< intensity and/or inability to achieve orgasm
Inability to achieve erection
….. Ejaculation
The most common
causes of CES in decreasing order are
Disc Herniation
•
Spinal dysraphism is a broad term given to a group of anomalies where there are malformations in the dorsum of the embryo. Neural tube defects come under this group as well. PathologyThere is often abnormal fusion of the midline embryonic neural, vertebral and mesenchymal structures.
The HISTORY is key….
Qulaify the questions … DOES the pt UNDERSTAND what you are asking… how many times have u bruehd over B&B..!
Quantify ……. When, where , how much, patter, severity etc….
Index of suspicion…. If it raises your IOP …. Don’t just carry on…. Go back in time and undesrand the history more if needed..!!
quantify its context and how does that imapct on your index of suspicion
WE CANT KNOW every diagnoiss…. And we don’t need to ….BUT we do need to now when its NOT MSK…. PATTERN RECOGNITION…
BECAUSE we need to be able to recognize at which point we remove our MSK hat and start to direct, facilitate and investigate to a point that we can have clarity on as to next steps…. NOW that doesn't’t mean you have to be able to diagnose everything that isn't MSK …This is about VIGIELENCE and AWARENESS…
The MSK HAT analogy being removed is a term I have used in the past and also was common theme in our last set of interviews for ESP Roles at IPOPS…!
I have no idea..!
Unwell
Accumulation of ‘Flags’
What do I ask next
Next patient is in reception
HOWEVER………. A lot of the time we may not have any idea wjhat they are talknig about or don’t know how to pull it all together….
We have all been in clinic when this happens…!!
You could say that you are only as good as your next question…. However the ability to interpret the information, synthesise and act is another skill set that requires some time….
How many times have you brushed over the question … ANY bladder or bowel issues, one leg OR both legs…. …..and they respond …Yes fine….. but they have S&S that are confusing...
DON’T ask the question if you cant act upon it... And this is smothime about support and sulture on the work lac…….WE don’t expect to know ALL that is medcial, MSK…or just an MUS…. We need to be able to discuss it with colleagues
We've all bee in risky situations and the one thing we do learn from those scenarios is how to manage that situation differently next time … and a lot of that can be said for Physio in relation to PATTERN RECOGNITION….. Have I been here before, what was the outcome, what did I ask to get the right next steps…. What went wrong last time, how did I manage the patient, how did they react to the conversation…
Lets try this one for a scenario…….
NOT in any particular order…. But what would you be thinking …. JUST Subjective..!
What are we thinking and would the subjective be enough…?
What would you look for next..?
AAA
65 year old male
No history of trauma
Insidious onset of LBP 3 years
Acute Mid thoracic pain 4-weeks with lifting
Groin pain with associated testicular 3-weeks
Dyspagia
No neuro
Hx of hypertension
Tsx pain > with cough and Grey Turners Sign – if I add this… does that change your mind & would you IOS be ++ anyway and why..?
No history of trauma
Insidious onset of LBP
Mid thoracic pain aggravated by coughing
Hx of hypertension
Dysphagia (problems with swallowing) is a recognized symptom in up to 20% of patients with aneurysms of the descending thoracic aorta (LeRoux TB. Rogers MA, Gotsman MS: Aneurysms of the thoracic aorta. T/ioru.r 26. 638 1971)
Aneurysm of the abdominal aorta may present with severe low-back pain; the addition of testicular pain is ominous and often precedes fatal rupture (Richardson1960;Sokoloff& Bland 1975; Appenzeller 1978; Adams 1981). The onset of dissection of an aneurysm in the ascending aorta or aortic arch is characterized by a sudden, tearing chest pain; this often radiates into the neck, dorsal trunk, abdomen and legs (Mcleod, 1981). The suddenness, severity and spread of pain should be sufficient evidence of serious visceral disease as oppose to an acute Thoracic MSK presentation
What are the options here….
Lets take MYELOPTAHY on this occasion…..!!!
Lets take MYELOPTAHY on this occasion…..!!!
Myelopathy describes any neurologic deficit related to the
spinal cord. Myelopathy is usually due to compression
of the spinal cord by osteophyte or extruded disk material in
the cervical spine. Osteophytic spurring and disk herniation
may also produce myelopathy localized to the thoracic spine,
though less commonly. Other common sources of myelopa-
thy are cord compression due to extradural mass caused by
carcinoma metastatic to bone, and blunt or penetrating
trauma. Many primary neoplastic, infectious, inflammatory,
neurodegenerative, vascular, nutritional, and idiopathic dis-
orders result in myelopathy, though these are very much less
common than discogenic disease, metastases, and trauma. A
variety of cysts and benign neoplasms may also compress the
cord; these tend to arise intradurally. The most common of
these are meningiomas, nerve sheath tumors, epidermoid
cysts, and arachnoid cyst
KentDL,HaynorDR,LongstrethWT,Jr.,etal.Theclinicalefficacyofmagnetic resonance imaging in neuroimaging. Ann Intern Med 1994;120:856 –71
RapoportRJ,FlandersAE,TartaglinoLM.Intraduralextramedullarycausesof myelopathy. Semin Ultrasound CT MR 1994;15:189 –225
RothmanMI,ZoarskiGH,AkhtarN.Extraduralcausesofmyelopathy.Semin Ultrasound CT MR 1994;15:226 – 49
TartaglinoLM,FlandersAE,RapoportRJ.Intramedullarycausesofmyelopa- thy. Semin Ultrasound CT MR 1994;15:158 – 88
Fell in garden onto right hip 6/12
Patient described clumsiness last 12 months
Increased bladder frequency
Weight stable
THREADS clear
No Hx of Cancer
It is an important source of morbidity (including paralysis and bowel and bladder disorders) in patients with systemic cancer
This is a 63 year-old man with metastatic melanoma to the C5 vertebral body. This slow growing tumor was compressing the spinal cord, which resulted in arm pain and numbness in the hands.
New Advances
New 8 item tool to help iD early signs of MSCC. This was pulled together in the form of a credit card size for non-specialist front line clinicians working PC settings )The Greater Manchester and Chesire Network UK brought together oncology expertise from the Regional Cancer Centre (Chrisite) and PC MSK physiotherapy
This is all about VIGILANCE and AWARENESS…
VIGILANCE we need to be able to look at things through lots of different angles because their are numerous systems to consider…!
Identification early on of NON MSK pathology is a good starting point…. Then STEP back to give you time to gain CLARITY…… don’t fluster and develop a CALM Approach and be MATHODICAL….
Eg…. ‘ Is it ok if we stop there for a moment…. There's a lot of information we discussed and I just need to clarify a few points if that’s ok with you….?’
Early ID (involves ???)
Get through the FOG quick
Clarity
MSK disorders often co-exist with other pathologies
However the clinical severity ranges from Life Threatening (AAA) to CTS
What actually turns up on Ax is ….!!
A 51-year-old female presented with a 2-year history of insidious left sided posterior peri-scapular shoulder pain (VAS 8) with progressive radicular symptoms through a C5-T1 distribution over the last 6 months with the following reported during questioning:
Altered sensation across the left side of the face
Intermittent left sided blurred vision
Light-headedness with left upper arm activity > 90 degrees ROM
Intermittent loss of fine motor control associated with picking up small objects and deterioration in their handwriting.
Nausea associated with shoulder movement above 90 degrees of abduction and/or flexion
‘Heaviness’ of the upper limb, particularly with exercise
Insidious and progressive, Shortness of breath (SOB) within the last 2- weeks
SOB on walking up inclines, as well as upper limb activity above 90 degrees (ROM)
Thank you for the reviewing this 52yr old female who describes cervical spine pain which radiates into both shoulders with an associated tension related headache. I wonder if some physiotherapy may be of some benefit. I enclose a copy of a recent x-ray that highlighted Spondylosis at the Cervical spine which wont be helping symptoms.
What are the options here….
Pancoast tumors account for less than 5% of all bronchogenic carcinomas. These tumors are located in the apex of the lung and involve through tissue contiguity the apical chest wall and/or the structures of the thoracic inlet. The tumors become clinically evident with the characteristic symptoms of the “Pancoast-Tobias syndrome” which includes Claude-Bernard-Horner syndrome, severe pain in the shoulder radiating toward the axilla and/or scapula and along the ulnar distribution of the upper arm, atrophy of hand and arm muscles and obstruction of the subclavian vein resulting in edema of the upper arm.
Pancoast Tumour ( Superior Sulcus tumour) T1W Coronal shows a lobulated hypointense mass (blue arrows)arising from the right lung apex , involving the 1st and 2nd ribs and the lower roots and trunks References: RADIOLOGY, MID YORKSHIRE HOSPITALS NHS TRUST, MID YORKSHIRE HOSPITALS NHS TRUST - WFI4SL/UK
Demographics of GCA [7, 8]
. Mean onset at age 70 years.
. Rare before age 50 years.
. More common in Caucasian people than in
Afro-Caribbean people.
. Three times more common in females than in males.
Symptoms
. Abrupt-onset headache (usually unilateral in the tem- poral area and occasionally diffuse or bilateral).
. Scalp pain (diffuse or localized), difficulty in combing hair.
. Jaw and tongue claudication. . Visual symptoms (amaurosis fugax, blurring and
diplopia). . Systemic symptoms of fever, weight loss, loss of
appetite, depression and tiredness. . Polymyalgic symptoms. . Limb claudication. . Fever, weight loss and other constitutional symptoms.
Examination may reveal
. Abnormal superficial temporal artery; tender, thick- ened or beaded with reduced or absent pulsation.
. Scalp tenderness.
. Transient or permanent reduction in visual acuity (par-
tial or complete).
. Visual field defect.
. Relative afferent papillary defect on the swinging flash-
light test.
. Pale, swollen optic disc with haemorrhages on fundo-
scopy (anterior ischaemic optic neuritis).
. Unilateral or bilateral central retinal artery occlusion.
. Upper cranial nerve palsies.
. Featuresoflarge-vesselGCA:asymmetryofpulsesand
blood pressure and bruits (usually of the upper limb).
ifferential diagnosis
. Herpes Zoster.
. Migraine.
. Serious intracranial pathology, such as infiltrative retro
orbital or base of skull lesions.
. Other causes of acute vision loss, e.g. transient
ischaemic attack.
. Cluster headache.
. Cervical spondylosis.
. Other upper cervical spine disease.
. Sinus disease.
. Temporo-mandibular joint pain.
. Ear problems.
. Other systemic vasculitides and CTDs.
Complications of GCA
Disease related Early. Neuro-ophthalmic complications, such as vision loss and stroke [7]. If one eye is affected there is high risk (2050%) of bilateral vision loss and total blindness with any delay or stoppage of treatment.
Late. Inflammatory aorto-arteritis—development of aortic aneurysm, aortic dissection [24].
Glucocorticosteroid related. Weight gain, bruising, osteo- porosis and fractures, diabetes, cataracts, glaucoma, hypertension,
Accelerated atherosclerosis and hyperlipidaemia.
Recommended investigations (minimum data set) in GCA
. Full-blood count, urea and electrolytes (U&E), liver function tests, CRP and ESR:
an acute-phase response is characteristic of GCA (raised ESR, CRP, anaemia and thrombocytosis, abnor- mal liver function tests, particularly raised alkaline phosphatase, raised a-1 and a-2 globulins on serum electrophoresis).
. Chest radiograph.
. Urinalysis.
. Other relevant investigations to exclude mimicking
conditions.
Pitfalls in the diagnosis of GCA
Cardinal ischaemic features of GCA, such as jaw and tongue claudication and visual symptoms, may go unrec- ognized or be attributed to other conditions especially if not accompanied by headaches. Patients at highest risk of neuro-ophthalmic complications do not always mount high-inflammatory responses [35]. PMR is also asso- ciated with GCA in 50% of the cases at presentation [7]. An acute-phase response can occur in other settings, such as other rheumatological conditions, neoplasia and infection.
(2) Urgent referral for specialist evaluation is suggested for all patients with GCA. We recommend that a TAB
should be considered whenever a diagnosis of GCA is suspected. This should not delay the prompt insti- tution of high-dose glucocorticosteroid therapy [11]. (Level of evidence 3, strength of recommendation C.)
Patients either fulfilling three or more of the five ACR criteria or historical features of impending neuro-opthalmic complications, e.g. jaw claudication, amaurosis fugax and other visual symptoms, should be urgently referred to a rheumatologist or ophthalmologist, and the laboratory investigations listed above should be performed.
Demographics of GCA [7, 8]
. Mean onset at age 70 years.
. Rare before age 50 years.
. More common in Caucasian people than in
Afro-Caribbean people.
. Three times more common in females than in males.
Symptoms
. Abrupt-onset headache (usually unilateral in the tem- poral area and occasionally diffuse or bilateral).
. Scalp pain (diffuse or localized), difficulty in combing hair.
. Jaw and tongue claudication. . Visual symptoms (amaurosis fugax, blurring and
diplopia). . Systemic symptoms of fever, weight loss, loss of
appetite, depression and tiredness. . Polymyalgic symptoms. . Limb claudication. . Fever, weight loss and other constitutional symptoms.
Examination may reveal
. Abnormal superficial temporal artery; tender, thick- ened or beaded with reduced or absent pulsation.
. Scalp tenderness.
. Transient or permanent reduction in visual acuity (par-
tial or complete).
. Visual field defect.
. Relative afferent papillary defect on the swinging flash-
light test.
. Pale, swollen optic disc with haemorrhages on fundo-
scopy (anterior ischaemic optic neuritis).
. Unilateral or bilateral central retinal artery occlusion.
. Upper cranial nerve palsies.
. Featuresoflarge-vesselGCA:asymmetryofpulsesand
blood pressure and bruits (usually of the upper limb).
ifferential diagnosis
. Herpes Zoster.
. Migraine.
. Serious intracranial pathology, such as infiltrative retro
orbital or base of skull lesions.
. Other causes of acute vision loss, e.g. transient
ischaemic attack.
. Cluster headache.
. Cervical spondylosis.
. Other upper cervical spine disease.
. Sinus disease.
. Temporo-mandibular joint pain.
. Ear problems.
. Other systemic vasculitides and CTDs.
Complications of GCA
Disease related Early. Neuro-ophthalmic complications, such as vision loss and stroke [7]. If one eye is affected there is high risk (2050%) of bilateral vision loss and total blindness with any delay or stoppage of treatment.
Late. Inflammatory aorto-arteritis—development of aortic aneurysm, aortic dissection [24].
Glucocorticosteroid related. Weight gain, bruising, osteo- porosis and fractures, diabetes, cataracts, glaucoma, hypertension,
Accelerated atherosclerosis and hyperlipidaemia.
Recommended investigations (minimum data set) in GCA
. Full-blood count, urea and electrolytes (U&E), liver function tests, CRP and ESR:
an acute-phase response is characteristic of GCA (raised ESR, CRP, anaemia and thrombocytosis, abnor- mal liver function tests, particularly raised alkaline phosphatase, raised a-1 and a-2 globulins on serum electrophoresis).
. Chest radiograph.
. Urinalysis.
. Other relevant investigations to exclude mimicking
conditions.
Pitfalls in the diagnosis of GCA
Cardinal ischaemic features of GCA, such as jaw and tongue claudication and visual symptoms, may go unrec- ognized or be attributed to other conditions especially if not accompanied by headaches. Patients at highest risk of neuro-ophthalmic complications do not always mount high-inflammatory responses [35]. PMR is also asso- ciated with GCA in 50% of the cases at presentation [7]. An acute-phase response can occur in other settings, such as other rheumatological conditions, neoplasia and infection.
(2) Urgent referral for specialist evaluation is suggested for all patients with GCA. We recommend that a TAB
should be considered whenever a diagnosis of GCA is suspected. This should not delay the prompt insti- tution of high-dose glucocorticosteroid therapy [11]. (Level of evidence 3, strength of recommendation C.)
Patients either fulfilling three or more of the five ACR criteria or historical features of impending neuro-opthalmic complications, e.g. jaw claudication, amaurosis fugax and other visual symptoms, should be urgently referred to a rheumatologist or ophthalmologist, and the laboratory investigations listed above should be performed.
ESR & CRP are no longer routinely requested together for most conditions, either marker (or both) can be raised in GCA & given significant potential for morbidity in GCA both are requested for increased sensitivity & specificity.
be ruled out.
Up to 20% of people with confirmed GCA have only mildly raised inflammatory markers and a small number of patients will have levels within normal ranges on at least one of the tests.
If both CRP and ESR are normal, the likelihood of giant cell arteritis being present is reduced, but cannot be ruled out.
Vascular TROS
Venous TOS, also called Paget-Schroetter syndrome or effort thrombosis, can usually be attributed to both an underlying anatomical abnormality and concomitant repetitive arm raising exercises, such as swimming or throwing a ball
De Leon RA, Chang DC, Hassoun HT, Black JH, Roseborough GS, Perler BA, et al. Multiple treatment algorithms for successful outcomes in venous thoracic outlet syndrome. Surgery. 2009;145:500–7
wo subtypes of neurogenic TOS exist.[5,13] Upper TOS involves the superior aspect of the brachial plexus (C5 through C7), with symptoms felt mostly in the arm and forearm, sparing the hand.[5,13] Additionally, the patient can experience neck pain on the affected side that radiates to the ear, face, and occiput, causing headaches.[13] The pain can also radiate across the rhomboids, clavicle, and trapezius/deltoid area. It can mimic a C5-C6 nerve root compression by a herniated nucleus pulposus.[5,13] Causes of upper TOS include hypertrophied scalene, passage of the brachial plexus through the anterior scalene, anterior pressure on the middle scalene by an elongated C7 transverse process, or the presence of a cervical rib.[13] Lower TOS involves the C8-T1 components of the brachial plexus.[5,13]. In these patients, the hand is affected, but the arm and forearm are spared. However, these patients can have neck and shoulder pain as well, with a variable intensity that can radiate down the medial brachial area of the arm into the forearm and hand. Paresthesias are usually felt in the 4th and 5th digits.[5,13] Most patients with NTOS experience paresthesias in the fingers and sometimes the entire hand, usually in the median or ulnar distribution as described above. Also, if the arm is held overhead for a length of time, weakness may develop in the specific arm, and this fatiguing of the arm in overhead positions is often the presenting symptom. Furthermore, when carrying objects with the arm by the side (e.g. shopping bags) the arm may become numb and a loss of grip may occur. In more advanced cases, muscle atrophy can be seen, along with loss of fine motor movement.[13] Sleeplessness and irritability are likely. Most symptoms manifest after exercise, which helps to distinguish it from orthopedic injuries, which usually occur during exercise.[14] In addition, TOS is not limited to a specific dermatome, in comparison to a cervical disc problem which is usually dermatomal in nature.[13]
Nichols AW. Diagnosis and management of thoracic outlet syndrome. Curr Sports Med Rep. 2009;8:240–9.
Brantigan CO, Roos DB. Diagnosing thoracic outlet syndrome. Hand Clin. 2004;20:27–36.
N Trauma
Antalgic gait
No radicular S&S
No B&B, SA, Back Pain, Weight Stable, Night Pain, Sweats
THREADS clear
No PMHx of note
Daytime fatigue – requiring a ‘2hr siesta..!’
Hyperelexia – lower limb only
First line analgesia titrated up and no improvement
GH excellent until last 12 months
Marathon runner last year (Sub 4hrs)
Now struggling to walk due to foot pain and weakness
Inward & upward turned foot in last 6-month
problems, delayed development, and intellectual disability. Some of these health problems can be life-threatening. A variation of type 1 myotonic dystrophy, called congenital myotonic dystrophy, is apparent at birth. Characteristic features include
weak muscle tone
Inward- and upward-turning foot (clubfoot)
Breathing
Cataracts Balding Cardiac arrhythmia
Medication
PTs injecting since 1995 SP in 2005 and IP in 2013 - now not all if us will be extending our roles to take up NMP, however understanding the side effects of common medications which Masquerade as MSK problems can facial or thought process
Big ONEs:
Muscle Pain
Bladder & Bowel Dysfunction
Osteoporosis
Fractures
Tendon Ruptures
Large proportion of structures within the MSK system have a high metabolic rate and blood flow and as a consequence the MSK system has high exposure to circulating medications (REF)
Did the symptoms start after the mediation started and stop once the mediation had ceased..! (light bulb moment…. stop and dig deeper:)
Within CR the chronological sequence of symptoms is important
MSK SIDE EFFECTS OF MEDs
MSK Side effects: S&S
1. Mild Aches and Pains = Oral contraceptive (e.g: Microgynon) and Statins (e.g: Atorvastatin)
2. Muscle Cramps = Diuretics (e.g: Bendroflurnethiazidel) - Calcium Channel Blockers (e.g: Verapemil) - Beta Agonists (e.g: Salbutamol)
3. Proximal muscle weakness, atrophy = Oral Cortocosteroids (e.g: Predinisolone), >10mg dose, for at least 30 days
4. Severe Pain, myopathy, malaise, fever, dark urine = statins, 0.1-0.2% of pets in clinical trials have side effects.
5. Osteoporosis Fracture = oral corticosteroids, ie. Doses > 5mg daily lead to significant and rapid bone loss. A cumulative dose of >30g associated with high incidence of fracture 53%. Excessive risk of fracture disappears within 1 yr of stopping therapy
Avascular Necrosis - Corticosteroids 5-40% of pets on long term therapy
Tendinopathy, tendon rupture , myopathy - Injected corticosteroids , oral corticosteroids Glucocorticoids have a direct catabolic effect on skeletal muscle tissue
Myalgia, arthralgia, arthritis, tendinitis - Quinalones (synthetic broad spectrum antibiotics - e.g: ciprofloxacin) World wide incidence of side effects estimated as 15-20 per 100,000 pts treated
Bladder & Bowel Dysfunction - opiod salts; constipation (e.g: Tramdol, codiene) Anticonvulsants: urinary incontinence (Gabapentin, pregablin). Antidepresssants = retention, sexual dysfunction (Amitriptiline, nortriptyline)
Muscle Cramp, muscle wekaness : (Thyroid hormones (e.g: levothyroxine sodium… at excessive dosage
Joint aches and pain (Arthralgia) – Antithyroid drugs used ot treat hyperthyroidism – e.g: carbienrazole
Adapted ~ Grieves Modern MSK Physiotherapy
Medication
PTs injecting since 1995 SP in 2005 and IP in 2013 - now not all if us will be extending our roles to take up NMP, however understanding the side effects of common medications which Masquerade as MSK problems can facial or thought process
Big ONEs:
Muscle Pain
Bladder & Bowel Dysfunction
Osteoporosis
Fractures
Tendon Ruptures
Large proportion of structures within the MSK system have a high metabolic rate and blood flow and as a consequence the MSK system has high exposure to circulating medications (REF)
Did the symptoms start after the mediation started and stop once the mediation had ceased..! (light bulb moment…. stop and dig deeper:)
Within CR the chronological sequence of symptoms is important
MSK SIDE EFFECTS OF MEDs
MSK Side effects: S&S
Mild Aches and Pains = Oral contraceptive (e.g: Microgynon) and Statins (e.g: Atorvastatin)
Muscle Cramps = Diuretics (e.g: Bendroflurnethiazidel) - Calcium Channel Blockers (e.g: Verapemil) - Beta Agonists (e.g: Salbutamol)
Proximal muscle weakness, atrophy = Oral Cortocosteroids (e.g: Predinisolone), >10mg dose, for at least 30 days
Severe Pain, myopathy, malaise, fever, dark urine = statins, 0.1-0.2% of pets in clinical trials have side effects.
Osteoporosis Fracture = oral corticosteroids, ie. Doses > 5mg daily lead to significant and rapid bone loss. A cumulative dose of >30g associated with high incidence of fracture 53%. Excessive risk of fracture disappears within 1 yr of stopping therapy
Avascular Necrosis - Corticosteroids 5-40% of pets on long term therapy
Tendinopathy, tendon rupture , myopathy - Injected corticosteroids , oral corticosteroids Glucocorticoids have a direct catabolic effect on skeletal muscle tissue
Myalgia, arthralgia, arthritis, tendinitis - Quinalones (synthetic broad spectrum antibiotics - e.g: ciprofloxacin) World wide incidence of side effects estimated as 15-20 per 100,000 pts treated
Bladder & Bowel Dysfunction - opiod salts; constipation (e.g: Tramdol, codiene) Anticonvulsants: urinary incontinence (Gabapentin, pregablin). Antidepresssants = retention, sexual dysfunction (Amitriptiline, nortriptyline)
Muscle Cramp, muscle wekaness : (Thyroid hormones (e.g: levothyroxine sodium… at excessive dosage
Joint aches and pain (Arthralgia) – Antithyroid drugs used ot treat hyperthyroidism – e.g: carbienrazole
Medication
PTs injecting since 1995 SP in 2005 and IP in 2013 - now not all if us will be extending our roles to take up NMP, however understanding the side effects of common medications which Masquerade as MSK problems can facial or thought process
Big ONEs:
Muscle Pain
Bladder & Bowel Dysfunction
Osteoporosis
Fractures
Tendon Ruptures
Large proportion of structures within the MSK system have a high metabolic rate and blood flow and as a consequence the MSK system has high exposure to circulating medications (REF)
Did the symptoms start after the mediation started and stop once the mediation had ceased..! (light bulb moment…. stop and dig deeper:)
Within CR the chronological sequence of symptoms is important
MSK SIDE EFFECTS OF MEDs
MSK Side effects: S&S
Mild Aches and Pains = Oral contraceptive (e.g: Microgynon) and Statins (e.g: Atorvastatin)
Muscle Cramps = Diuretics (e.g: Bendroflurnethiazidel) - Calcium Channel Blockers (e.g: Verapemil) - Beta Agonists (e.g: Salbutamol)
Proximal muscle weakness, atrophy = Oral Cortocosteroids (e.g: Predinisolone), >10mg dose, for at least 30 days
Severe Pain, myopathy, malaise, fever, dark urine = statins, 0.1-0.2% of pets in clinical trials have side effects.
Osteoporosis Fracture = oral corticosteroids, ie. Doses > 5mg daily lead to significant and rapid bone loss. A cumulative dose of >30g associated with high incidence of fracture 53%. Excessive risk of fracture disappears within 1 yr of stopping therapy
Avascular Necrosis - Corticosteroids 5-40% of pets on long term therapy
Tendinopathy, tendon rupture , myopathy - Injected corticosteroids , oral corticosteroids Glucocorticoids have a direct catabolic effect on skeletal muscle tissue
Myalgia, arthralgia, arthritis, tendinitis - Quinalones (synthetic broad spectrum antibiotics - e.g: ciprofloxacin) World wide incidence of side effects estimated as 15-20 per 100,000 pts treated
Bladder & Bowel Dysfunction - opiod salts; constipation (e.g: Tramdol, codiene) Anticonvulsants: urinary incontinence (Gabapentin, pregablin). Antidepresssants = retention, sexual dysfunction (Amitriptiline, nortriptyline)
Muscle Cramp, muscle wekaness : (Thyroid hormones (e.g: levothyroxine sodium… at excessive dosage
Joint aches and pain (Arthralgia) – Antithyroid drugs used ot treat hyperthyroidism – e.g: carbienrazole
However… we are generally contender with the normal clinical pattern that p[resents and too often we underestimate the value of the Subjective Ax and listing to the patients story….and that can happen for a number of reasons…
Typical Friday clinic… which you may of seen me jest about on Twitter… but the reality is that with complex patients comes complex needs and complex
AND for me theses are about LIGHT BULB Moments during the Subjective Ax where you check yourself and STEP BACK from the usual path…. We cant know everything , but we MUST recognize when we cant deal with the presentation in front of us and move the pt on in an appropriate and professional manner that keeps the pt informed as to why and next steps….!
that you can add to your clinical tool box and thought processes that facilitate your SUBJECTIVE Ax …..
and should resonate with all of us in relation to the REALITY of what we see in the clinical setting…
SO here we have an example…
Lets try this one for a scenario…….
Sykes JB, editor. Concise Oxford Dictionary, 6th ed, Oxford: Clarendon Press: 1978.
Clinical Standards Advisory Group. Reports of Clinical Standards Advisory Group on Back Pain. London: HMSO: 1994.
