Monday 9 March 2020

DVT / PE

What symptoms would a patient complain of if they had a DVT? 

Pain (usually unilateral calf) SIN = severe!
*When you see a lot of orthopaedic surgery like TKR, THR you get a good feel for what is the typical amount of pain. In my experience people with DVT have a profound level of pain.

S = Severe
I = High
N = Inflammatory (cardinal signs dolor, tumor, rubor,
Quality = Heavy ache

Clinical point: 
Always ask questions and examine a suspected DVT with suspicion of PE
e.g. Any SOB, chest pains, low SATS?

OBS: Dilated superficial veins, calf redness, discolouration, lower limb swelling
PALPATION: Pitting oedema, tenderness and firmness on palpation of the calf
SPECIAL TESTS: +ve Homan’s Sign

What would you do if a patient you were seeing presented with these symptoms?

Inpatient on the ward:
Escalate to nurse / RMO / consultant

Outpatient: 
Urgent GP referral for further Ix
A+E if suspected PE

Patients can be divided into “DVT unlikely” and “DVT likely” groups based on Wells score. An additional moderate risk group can be added based on the sensitivity of the d-dimer being used.
  • A score of 0 or lower is associated with DVT unlikely with a prevalence of DVT of 5%.
    • These patients should proceed to d-dimer testing:
      • A negative high or moderate sensitivity d-dimer results in a probability <1 and="" further="" imaging="" is="" li="" no="" required.="">
      • A positive d-dimer should proceed to US testing.
        • A negative US is sufficient for DVT rule out.
        • A positive US is concerning for DVT; strongly consider treatment with anticoagulation.
  • A score of 1-2 is considered moderate risk with a pretest probability of 17%.*
    • These patients should proceed to high-sensitivity d-dimer testing (moderate sensitivity d-dimer is not sufficient).
      • A negative high-sensitivity d-dimer is sufficient for rule out of DVT in a moderate risk patient with a probability of <1 li="">
      • A positive high sensitivity d-dimer should proceed to US testing.
        • A negative US is sufficient for ruling out DVT.
        • A positive US is concerning for DVT, strongly consider treatment with anticoagulation.
  • A score of 3 or higher suggests DVT is likely. Pretest probability 17-53%.
    • All DVT likely patients should receive a diagnostic US.
    • D-dimer testing should be utilized to help risk-stratify these DVT-likely patients.
      • In DVT likely patients with negative d-dimer:
        • A negative US is sufficient for ruling out DVT, consider discharge.
        • A positive US should be concerning for DVT, strongly consider treatment with anticoagulation.
      • In DVT likely patients with a positive d-dimer:
        • A positive US should be concerning for DVT, strongly consider treatment with anticoagulation.
        • A negative US is still concerning for DVT. A repeat US should be performed within 1 week for re-evaluation.


Tuesday 17 January 2017

Red Flags / Yellow Flags

Q. What are they? 

A. Signs and symptoms that indicate serious spinal pathology 


  • Age > 55 (above this age, particularly above 65) the chances of being diagnosed with serious pathologies such as cancer increases

  • PMHx or FHx of Ca  

  • Unexplained weight loss (5% within a 4 week period not related to change in diet or exercise) 

  • Constant / unremitting / progressive / non-mechanical pain (does not vary in a 24 hr period) 

  • Night pain (due to increase bony lysis at night) 

  • Generally unwell (fever / night sweats / signs of systemic illness) 

  • Bilateral neurological signs 

  • Ataxic gait (lack of muscle coordination / uncoordinated / jerky movements / poor balance) could indicate MS, stroke or TIA, head trauma, damage to cerebellum, spinal cord damage, brain tumour)

  • Major trauma (fall from a height / RTA) 

  • Minor trauma (in osteoporotic patients) 

  • Thoracic pain (most common region for metastases) 

  • Long term use of steroids 

Cauda Equina (require immediate referral to hospital for neurosurgical) 


  • Saddle anaesthesia (perianal sensory loss) 

  • Bladder or bowel dysfunction (urinary retention / incontinence or faecal incontinence) 

  • Bilateral leg pain / sciatica / neurological signs 

Yellow Flags 


Q. What are they? 

A. Bio-psychosocial factors that may risk increase likelihood of chronicity 

  • Pending compensation claim 
  • Off word 
  • Low work status 
  • Anxiety 
  • Depression 
  • Inappropriate coping strategies 
  • Passive dependent locus of control 

A - Attitudes 

Towards the current problem. Does the patient feel that with appropriate help and self management they will return to normal activities?

B - Beliefs 

The most common misguided belief is that the patient feels they have something serious causing their problem-usually cancer. 'Faulty' beliefs can lead to catastrophisation.

C - Compensation 

Is the patient awaiting payment for an accident/ injury at work/ RTA?

D - Diagnosis 

or more importantly Iatrogenesis. Inappropriate communication can lead to patients misunderstanding what is meant, the most common examples being 'your disc has popped out' or 'your spine is crumbling'.

E - Emotions

Patients with other emotional difficulties such as ongoing depression and/or anxietous states are at a high risk of developing chronic pain.

F - Family 

There tends to be two problems with families, either over bearing or under supportive.

W - Work

The worse the relationship, the more likely they are to develop chronic LBP.

Common Anterior Hip Complaints DDx / Assessment / Treatment

Credit to most of this goes to Nichole Hamilton with some additional thoughts from myself

"Carly Says Jacket Off"


Cartilage: Labral tear / articular cartilage wear

Soft tissue: Anterior capsule sprain, Iliopsoas tendinopathy, Iliopsoas bursa

Joint: OA / Synovitis

Other Dx: Stress # (NOF, Pubic Ramus), Osteitis Pubis, Hernia, Abdominal Pathology

"WHY is the anterior hip painful?"

Excessive load on the anterior hip can occur due to: 

1) Structural (bony) 


FAI:  CAM, PINCER or combined 

2) Biomechanical dysfunction 

Increased biomechanical load on the anterior hip with excessive anterior translation of femoral head (Sahrmann, 2003) 

1) Postural Alignment 

- Standing with hips in extension (watch out for sway back postures) 
- Genu recurvatum (knee hyperextension) 

"Want all the floors stacked on top of each other" 

Plumb line to align the femoral head in the roof of the acetabulum... 

Greater trochanter in line with...

Lateral femoral condyle and... 

Just anterior to lateral malleolus 

ASIS like car headlights facing dead ahead 

Manu-sternal junction over pubic symph 

2) Hypertonicity in deep posterior hip muscles / Tight Posterior Capsule 

Much like the shoulder if the posterior cuff is tight gets tight, develops trigger points, these muscles blend with the posterior capsule and prevent posterior glide (squeezes it anteriorly) 

Femoral head will follow the path of least resistance and if tight posteriorly will glide anteriorly and cause impingement 

Why do these posterior hip muscles get tight? Potentially more motor control strategies in LPHC, tightness compensating for poor stability somewhere else, poor lumbar-pelvic stability. 

3) Long / inhibited psoas 

A dynamic restraint that crosses the anterior aspect of the hip joint before it inserts into the lesser trochanter. Can protectively tighten to prevent / protect against shear and subluxation. 

Stretching in a hyperextended position with an anterior pelvic tilt can loosen the anterior capsule / iliofemoral ligament and cause this protective tightnening and can lead to labral stress. 

2 Pathways to Anterior Hip Impingement / Labral Tear 

Long inhibited psoas leads to... 
Reduced hip stability and motor control... 
Increased anterior translation of femoral head in extension (standing, running, wearing high heels)...
Increased load on anterior hip structures

OR 

Articular SIJ or lumbar dysfunction leads to...
Poor motor control strategies... 
Hypertonic posterior hip...
Restricted posterior glide during flexion (squatting for example)...
Anterior hip impingement with flexion

BOTH MAY RESULT IN... 

Anterior impingement / labral tear 

4) Hamstring Dominant Hip Extension 

Hamstrings being used as primary hip extensions mean that the axis of movement occurs at the origin (ischial tube) below acetabulum. The distal part of femur heads into extension but the femoral head anteriorly. Glutes cross the hip joint and don't produce that anterior translation. 

Watch out of hamstring synergistic dominance (performing movements in an anterior pelvic tilt e.g. squat or deadlift) alters length-tension relationship of glutes and puts them at a mechanical disadvantage, more likely for hammys to become primary hip extensor. 

5) Low Back 

Patients with CLBP...

Increased tonic activation of glutes in patients during low load tasks e.g. standing (glutes should be firing phasically) 

Also showed to have poor phasic strength, delayed firing (e.g. during an activity like climbing the stairs) 

Reduced cross-sectional area of psoas in patients with unilateral back pain 

During ASLR reduced activity of psoas results in increased anterior hip joint force (Lewis & Sahrmann, 2009) 

Also check ipsilateral SGIS 

6) Foot / ankle 

Inability to pronate (shock absorb) and supinate 

Excessive rigidity in forefoot, mid-foot, rear-foot can contribute to anterior hip load. 

Reduced ability to shock absorb. 

More likely to have hip in externally rotated position if stuck in supination 

Watch and listen to someone doing single leg hops (from one foot to the other) does it sound louder one side vs the other? i.e. poor pronation / shock absorption

7) Thorax  

One of the rotational centres (along with the hip) 

Asymmetry in thoracic rotation 

Should be equal range L vs R 

If limited L for example thorax will tend to sit in mid range (pointing slightly right) 

Hips with rotate left to have ASIS pointing forward and position right head of femur anteriorly in the acetabulum 

8) Anterior core control 

Able to prevent anterior tilt during hip flexion based activity e.g. squatting 

Assessment 

Subjective: When does the patient feel the symptoms? Flexion or extension? 

Flexion intolerant? 

Extension intolerant?

Labral tear: Insidious onset (rarely traumatic) groin pain related to hip movement usually reproduced with rotational movement e.g. pivoting / twisting, clicking/catching sensation often reported. 

Test: Does femoral head remained centered during the painful activity?

Special tests: Quadrant test / FADIR looking for reproduced of symptoms 

Observe: Are there any other areas in the chain that might be adding to the load on the anterior hip? 

Foot, thorax, SIJ? 

Palpate: Any local areas of the hip that are contributing to poor hip centering? 

Treatment 


Educate: Posture, daily habits, hip mechanics, pain education 

Manual therapy: Areas of hypertonicity that might be contributing to non-centering of femoral head (TFL, rec fem, piriformis, OI, posterior pelvic floor which has links to obturator internus). Foot, thorax, SIJ, lumbar. 

Exercises: Self release, correct core activation, functional hip centering, postural alignment, strengthening (lower fibres glute max, GMed, quadratus femoris, core stability, closed chain exercises e.g. bridge vs open chain hip extension. 

Avoid hip stretches (psoas, piriformis) can cause more harm than good 

Imagining: MRI or MR Arthrogram 

Surgery: Traumatic injury (20-30%) tend to be people who benefit best from surgery (not so much a biomechanical dysfunction causing labral tear), physio mx unsuccessful (3months no improvement), surgery often not essential for every patient.

Patients with OA signs in hip don't tend to do as well with hip arthroscopy



Thursday 31 October 2013

Predisposing factors to cervical instability

Factors that can predispose to cervical instability: 

Lax posterior transverse ligament (joining the dens to C1) thought to be a risk factor for atlantoaxial instability (Merrick et al, 2000) 



  • Main movement occurring at this level (atlantoaxial jt) is rotation of 35 degrees in each direction
  • Rotation is limited by the alar ligaments 





Pathologies 

Systemic inflammatory diseases (because the inflammation damages connective tissue, ligaments, joints etc) 


  • Lupus
  • RA (most common in cervical spine and MCP joints in the hands)
  • Ankylosing spondylitis (primarily affects c-spine)
  • Down Syndrome (laxity or congenital absence of transverse atlas ligament which can make minor traumas to the neck able to cause subluxation)



  • Degenerative changes of cervical spine (Andrews, 1981) 
  • Hypermobility 
  • Connective tissue disorders (Ehler's-Danlos syndrome, Marfan syndrome) 
  • Congenital bony abnormalities e.g. short dens, odontoid hypoplasia (basically geeky talk for the same thing!) 


PMH

Previous or recent RTAs (recurrent whiplash) 
OA 
General wear and tear 

DH (medications) 

Long term use of steroids 

Metastatic Disease 

Most prevalent in thoracic spine (1st) lung and breast primary tumors 

Lumbar (2nd) Prostate, colorectal, ovarian cancers 

Cervical (3rd) 


Red Flags of metastatic disease 

Non-mechanical picture (pain not affected by positional changes) 

Unremitting pain (no diurnal or nocturnal variation) 

Night pain and pain worse at night (this is due to more bony lysis occuring aka breaking down or erosion of the bone) 

References 

Merrick J, Ezra E, Josef B, Hendel D, Steinberg DM, Wientroub S. Musculoskeletal problems in Down Syndrome European Paediatric Orthopaedic Society Survey: the Israeli sample. J Pediatr Orthop B. Jun 2000;9(3):185-92.

Andrews LG. Myelopathy due to atlanto-axial dislocation in a patient with Down's syndrome and rheumatoid arthritis. Dev Med Child Neurol. Jun 1981;23(3):356-60.

Friday 11 October 2013

Morphine OD

I was watching the film "Prisoners" where at the end a little girl is given a lethal dosage of morphine. My flat mate Ed (a med student) told me that the first thing that would kill you from a morphine OD is respiratory failure. As your rate and depth of breathing reduces eventually it's not enough to keep you alive.

The medical fix is naloxone, a drug used to counter the effects of an opiate overdose. BUT the half life of naloxone is much shorter than morphine, it's broken down quicker so patients should be kept in for at least 24 hrs for observation.

Sunday 15 July 2012

Ehlers–Danlos syndrome

A group of inherited connective tissue disorders caused by a defect in the synthesis of type I or type III collagen.

S&S 

MSK


  • Hypermobile joints 
  • Hx of sprains, subluxation, dislocations 
  • Swan neck deformity 
  • Weak muscle tone 
  • Osteopenia

Wednesday 16 May 2012

Knee extension test in sitting

Testing if a patient can actively extend both knees and achieve at least a 3/5 grade knee extensor strength on Oxford scale is a basic way of assessing their capacity to attempt a sit to stand or gait.