Saturday 26 April 2014

Sprains

Early Management Aims during the first 72 hours
  • Reduce tissue temperature, pain and swelling
  • Reduce metabolic demands of the tissue
  • Prevent further injury
  • Promote collagen growth and realignment
  • Maintain cardiorespiratory and musculoskeletal activity

Acute Inflammatory Stage - PRICE

Protection - Prevents worsening of injury
Rest - Avoids pain from movement. Complete immobilisation is not indicated to prevent significant loss of ROM. Even for grade III injuries a functional splintage is strongly suggested.
Ice - Reduces pain. Application of ice should be for 10-30 minutes wrapped in cloth to avoid cold injury. Repetition can be as frequent as required, providing the affected part is fully warmed back to body temperature.
Compression - Provides comfort by limiting movement and reducing swelling, although should be applied so as to not reduce blood flow. 
Elevation - Helps to reduce swelling, especially with the affected part above heart level.

Sub-Acute Proliferation & Remodelling Stage

Active rehabilitation:
  • Electrotherapy (for example ultrasound for collagen synthesis)
  • Manual therapy (for joint pain)
  • Restore mobility and prevent joint deformity
  • Progressive loading to begin to restore strength and improve joint stability

In the remodelling stage:
  • Deep tissue frictions
  • Electrotherapy (for example ultrasound to enhance tensile strength and scare mobility)
  • Manual therapy (for joint stiffness)
  • Progressive mobilisation and strengthening exercises

Thursday 24 April 2014

Soft Tissue Healing

A soft tissue injury is the damage of muscles, ligaments and tendons throughout the body when their tensile strength is interrupted. They normally result in pain, swelling and bruising as well as loss of function.

Tissue healing compromises two essential components: regeneration and repair (dependant on the resultant tissue). In regeneration specialised tissues is replaced by the proliferation of surrounding undamaged specialised cells. In repair, lost tissue is replaced by granulated tissue which matures to form scar tissue.

The healing process is divided into 4 phases: bleeding, inflammation, proliferation and remodelling. These 4 phases hugely overlap and integrate during repair.

Bleeding is a relatively short phase that occurs following trauma or another similar insult. The normal time for bleeding to stop varies depending on the injury and the tissue type. Vascular tissue such as muscle will bleed for longer causing a greater escape of blood into the surrounding tissues whereas other tissues such as a ligament will bleed less and for a shorter amount of time. The average bleeding time is 6-8 hours although is heavily dependent on the patient and the nature of the injury, for example a crush injury to a vascular tissue could continue bleeding, admittedly minimally, for 24 hours post trauma.

Inflammation is a normal and necessary prerequisite to healing (Hardy 1989) and onsets after a few hours. It rapidly increases in magnitude over the following 1-3 days before gradually resolving over the following couple of weeks. Signs of inflammation include: swelling, pain, redness, heat and loss of function.

The cascade that is responsible for the initiation and control of inflammation can be due to trauma, mechanical irritation, thermal or chemical insult as well as immune responses. Fibrin and fibronectin form a substratum (underlying foundation layer) which is hospitable to the adhesion of various cells. The two essential elements to inflammation are the vascular and cellular cascades. They occur in parallel and are somewhat interlinked.

Vascular events are additional to the initial bleeding. Vasodilation follows an initial brief vasoconstriction and there is an initial increase in the velocity of the blood followed by a prolonged slowing. The white cells form a margin, platelets adhere to the vessel walls and the endothelial cells (lining the blood vessels) swell. The local vessels also become more permeable, which when combined with vasodilation, increases the flow of blood through the more permeable vessels and results in exudate (including protein rich plasma) passing into the tissue spaces. This can be at both the arterial and venous ends of the capillary network as the increase hydrostatic pressure overcomes the osmotic pressure of the plasma proteins.
The effect of the exudate is to dilute any irritant substances in the damaged area and form a fibrin clot with the high fibrinogen content of the fluid. This union between the surrounding intact tissues forms a mesh which can trap foreign particles and debris. Mast cells in the damaged area release hyaluronic acid and other proteoglycans which bing with the exudate and create a gel which limits local fluid flow and further traps various particles and debris (Hardy 1989).

The cellular events of inflammation include the early emigration of the phagocytes within minutes. They are followed out of the vessels by monocytes, lymphocytes, eosinophils and basophils (Lorena et al 2002). Once in the tissue spaces monocytes become macrophages (Forrest 1983). These cells exhibit a strong phagocytic activity and are responsible for the removal of damaged tissue and foreign objects. And to top it all off lactic acid, one of the end products of phagocytosis, is a stimulant for proliferation. Pretty clever, ‘ey? Increased hydrostatic pressure for the oedema can be detrimental as it can restrict blood flow if the injured tissue space is limited, increasing pain and limiting function.

Proliferation is the generation and deposition of granulation (repair) tissue, which in the majority of musculoskeletal injuries is collagen (scar) material. It has a rapid onset of 24-48 hours but takes 2-3 weeks to reach its peak reactivity, although the more vascular the tissue the shorter the time taken to reach this peak phase. The bulk of the scar production is completed during this time, but proliferation decreases thereafter through several months post injury. The key events in proliferation are: fibroplasia (production of fibrous tissue), angiogenesis (development of blood capillaries), increased extracellular collagen production, wound contraction (from myofibroblasts) to minimise the scar and a complex interactive response amongst cells and chemical mediators to ensure effective completion of the scar tissue.

Remodelling is the strengthening (type I collagen replaces type III) and alignment of collagen that results in an organised, quality, functional scar that allows movement in a similar way to the original tissue. This phase is widely reported to begin at the same time as the peak of the proliferative phase (2-3 weeks) however further research shows that it may begin at around 1-2 weeks post injury. During this phase movement is essential to ensure that the collagen aligns in the direction most suited to functional activities. Signs of the remodelling phase include reduced redness, oedema and pain.

Factors that are known to delay healing can be general or local. General factors include age, protein deficiency, low vitamin C levels, steroids and NSAIDs as well as cold temperatures. Local factors include ischaemia, adhesion to bone of other underlying tissue, continued inflammation, drying of the wound and excessive movement as it restarts inflammation.

Wednesday 23 April 2014

Leg Length Discrepancy

Having worked in a ski resort for the last 5 months, I have been in the unique position of only being able to see clients for the duration of their holiday. This means I have encountered a number of people who have been seeing the same therapist, at home, for a period of months to years. This has led me to one shocking revelation:
so many people don't know their own diagnosis

...and yet they continue to see their therapist. Does it not seem crazy that most of these clients cannot state what their therapist has been treating?! From these clients, the best I hear is nearly always 'My hips are out of alignment' or 'I've got one leg slightly shorter than the other.' Well... so what?

Gurney (2002) reviewed leg length discrepancy and suggested it does not need treating in all cases, with 20mm often used as the 'breakpoint'. Two centimetres! That's not a small amount. Furthermore, Gross (1978) conducted a survey in which all patients with a leg length discrepancy between 15 and 20mm 'did not consider their short leg to be a problem in any way.'

Based on a review published in 2005, 90% of the population has some anatomic leg length discrepancy (average 5.2mm), although this figure hugely varies between studies. Seven of the studies reviewed identified whether participants were symptomatic (LBP or knee/hip problems) or asymptomatic (varying from last 6 months to ever) ...and guess what? The mean leg length discrepancy between the two groups differed by 0.1mm (symptomatic mean 5.1mm, SD 3.9; asymptomatic mean 5.2mm, SD 4.2).

This isn't new information. The studies used in the above review were conducted between 1970 and 2005. Soukka et al (1991) measured leg length using radiographs in 247 participants between the ages of 35-54 years. 78 of these participants had disabling low back pain during the previous twelve months and a mean leg length discrepancy of 5.3mm (maximum 17mm). However, a further 53 participants also had a discrepancy (mean 5.5mm, maximum 20mm) but... wait for it... absolutely no history of low back pain.

Then, in 2006, 126 of 1,100 military cadets were identified to have lower limb discrepancy over 0.5cm. Over the following year there was no difference in incidence of injury between those with discrepancies and those without (Goss et al, 2006). Furthermore, gait asymmetry and effects on kinetics and kinematics are only present in discrepancies over 2cm (Kaufman et al, 1996).

Furthermore, accurate measurement of a leg length discrepancy requires the use of radiographic imaging.

However, amongst these studies, there is evidence that leg length discrepancies are linked to increasing your chances of some injuries. Lower limb stress fractures have been shown to be of higher incidence in those with discrepancies. This is also true of trochanteric bursitis, patellar apicitis, and patellofemoral syndrome amongst many others. However, there are also studies that state leg length discrepancies have little to no effect. And on an interesting side note, there are differing conclusions as to whether leg length discrepancies would predict or be the result of knee and hip OA (intriguingly this is predominantly in the longer leg, rather than the shorter).

Basically, there remains huge debate as to the effects and clinical relevance of leg length discrepancy. It is logical for there to be pelvic torsion when one leg is longer than the other, however there is inconclusive evidence to use leg length discrepancy and hip misalignment as a diagnosis for pain - especially for an acute issue. If using leg length discrepancy as a diagnosis, why not investigate whether there is piriformis malfunction, OA, plantar fasciitis or one of the many other questioned associated pathologies? With treatment for leg length discrepancy (such as foot lifts or surgery) recommended only for those with >2cm difference, manual therapies and exercise prescription are commonly looked to for those with <2cm difference. Clients should be questioning exactly how manual therapies are going to benefit their leg length discrepancy, or whether therapy is instead for an effect of their leg length discrepancy (that is, if the issue is related at all).

References

Goss, D. L., Moore, J.H., Slivka, E. M. and Hatler, B. S. (2006) 'Comparison of injury rates between cadets with limb length inequalities and matched control subjects over 1 year of military training and athletic participation' Military Medicine 171(6), pp. 522-525.

Gross, R. H. (1978) 'Leg length discrepancy: how much is too much?' Orthopedics 1(4) pp. 307-310.

Gurney, B. (2002) 'Leg length discrepancy' Gait & Posture 15 pp. 195-206.

Kaufman, K.R., Miller, L.S., Sutherland, D. H. (1996) 'Gait asymmetry in patients with limb-length inequality' Journal of Paediatric Orthopaedics 16 pp. 144-150.

Knutson, G. A. (2005) 'Anatomic and functional leg-length inequality: A review and recommendation for clinical decision-making. Part I, anatomic leg-length inequality: prevalence, magnitude, effects and clinical significance' Chiropractic & Osteopathy 13(11)

Soukka, A, Alaranta, H, Tallroth, K and Heliovaara, M (1991) 'Leg-Length Inequality in People of Working Age: The Association Between Mild Inequality and Low-Back Pain Is Questionable' Spine 16(4). 

Tuesday 22 April 2014

Wrist Fractures

Colles fractures (fracture of the distal radius) are the most common fracture in adults and are typically caused by a fall on an outstretched hand. The two categories that are most predominant are osteopenic females aged between 60-80 and males between 20-40. The former is typically a low-energy injury at a ratio of male:female 1:4. The latter is typically a high-energy fall to impact on the denser bone.

The angle of the wrist on impact (primarily ulnar/radial deviation and dorsiflexion) and the weight of the patient ultimately determine the fracture pattern, whether of the radius, scaphoid and the ulna.

Signs & Symptoms:
  • History of trauma or osteoporosis
  • Wrist pain
  • Tenderness over the fracture sight (distal radius/ulna or carpals)
  • Swelling
  • Deformity (for displaced fractures)
  • Tenderness in the anatomic snuff box (suggestive of a scaphoid fracture)
  • Finger numbness (high-energy injuries typically on the median nerve)

Other pathologies
with similar signs and symptoms include:
  • Wrist strains (no deformity or signs on x-ray)
  • Ligamentous carpal injury (pain with palpation on dorsum of wrist at the scapholunate interval)
  • Triangular fibrocartliage complex tear (ulnar sided wrist pain increasing on ulnar deviation)

The need for surgical intervention is determined from radiography. Surgery is indicated when there 
is radial length loss of 15mm or more or when there is a dorsal tilt of over 10 degrees.

Initial treatment is typically immobilisation by cast or splint. For undisplaced fractures, cast are normally maintained for 4-6 weeks. Undisplaced fractures may also result in spontaneous rupture of the extensor pollicis longus tendon; typically in the first 12-16 weeks after injury. Precisely why I don't know, however spontaneous EPL rupture also occurs in synovitis, tenosynovitis and RA. There's even the occasional case where the patient doesn't have any predisposing factors, but has a spontaneous EPL rupture none the less.

Interestingly, a HEP and application of ultrasound and ice has is supported by limited evidence (AAOS Treatment Guidelines), however patients perform active finger motion exercises following diagnosis. Furthermore there is moderate evidence to support that patients do not begin early wrist motion following stable fracture fixation. The prescription of Vitamin C also has moderate evidence to prevent disproportionate pain.

Friday 4 April 2014

Ankle Fractures

Ankle fractures typically refer to a break in either malleolus, although there are multiple possible fracture sites in the bony structure of the foot. Over the age of 65 they are more common in white women and present as an isolated fibular fracture. Under the age of 65 they are more common in males and present as a lateral malleolus fracture. The most common mechanism is usually a low-energy fall, with the next most common causes being: an inversion injury to the ankle, sporting injury, fall down the stairs, fall from a height or road traffic accident. There is increased risk of ankle fractures in those with a history of osteoporosis or frequent falls.

Diagnostic Factors
  • Recent trauma, typically from a low-energy fall
  • Pain and swelling, especially over the medial or lateral malleolus and on palpation
  • Inability to weight bear
  • 'Pop' or other sound heard on fall
  • Giving way on fall
  • Deformity - typically indicative of dislocation
  • Crepitus on range of motion
  • Tenderness of the proximal fibula
  • Tenting of the skin over the medial malleolus - typically indicative of dislocation

Ottawa Ankle Rules

A diagnostic tool to help decide the need for x-rays. If there is:
  • Posterior lateral or medial bony tenderness within 6cm of the distal aspect of the fibula or tibia
  • Inability to weight bear 4 steps at the scene or A&E
...then an x-ray should be ordered.

Imaging

Fracture --> X-ray
Comminuted fractures --> CT
Ligament or tendon damage --> MRI

Differential Diagnosis

ATFL or CFL ligament tear presents with minimal lateral malleolar posterior bony tenderness. There may be a positive anterior drawer test or increased talar tilt, but there is rarely significant deformity.

Achilles tendon rupture presents with no malleolar tenderness. There may be a gap in the Achilles tendon or a positive Thompson's test.

Talar fracture is unlikely to present with malleolar tenderness, but there may be a deformity to the ankle and hindfoot.

Syndesmotic disruption is unlikely to present with malleolar tenderness. Test with external rotation and calf squeeze test.