Managing Sports Injuries

426 Pages·2011·49.379 MB·English

For Hilde, Sophie and Max—two great girls and a great big dog
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MANAGING
SPORTS INJURIES
A guide for students and clinicians
Fourth Edition
Christopher M. Norris
PhD MSc MCSP
Director of Norris Associates,
Physiotherapists, Manchester and Congleton;
Visiting lecturer to Salford University and
Manchester Metropolitan University,
Manchester, UK
  Edinburgh London New York Oxford Philadelphia St Louis Sydney Toronto 2011
© 2011 Text: Christopher M. Norris. All rights reserved.
© 2011 Illustrations: Elsevier Ltd, unless otherwise noted. All rights reserved.
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First edition 1993
Second edition 1998
Third edition 2004
Fourth edition 2011
ISBN 978-0-7020-3473-2
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Notices
Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding,
changes in research methods, professional practices, or medical treatment may become necessary.
Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information,
methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their
own safety and the safety of others, including parties for whom they have a professional responsibility.
With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information
provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended
dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners,
relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best
treatment for each individual patient, and to take all appropriate safety precautions.
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Acknowledgements
Photography by Laura Scott-Burns and Nina Preece. Thanks to Amanda Bell, Lindsay Peacock, Jill Young and Helen Doyle, who modelled
for the photographs.
Preface to the 4th edition
The first edition of Sports Injuries appeared in 1993 and the book The techniques described for the treatment of sports injuries can
quickly became a regularly thumbed text for students and recently equally well be used to treat musculoskeletal (MSK) conditions seen
qualified therapists. Feedback from readers showed that the balance in everyday practice within any busy general department. Learning
between theoretical aspects and practical techniques supported the to apply the high standard of treatment used within top class sport
emerging move towards evidence-based practice within physio- gives the therapist knowledge which will benefit treatment across
therapy. The title has been changed for the fourth edition to reflect the board. Both the local plumber and the Sunday league player
these original strengths and Managing Sports Injures takes the deserve the same treatment standard as the top level soccer star.
book’s approach still further. Managing Sports Injuries aims to enable therapists to gain the knowl-
The new edition has an updated science base, expanded text, new edge to make this happen.
treatment notes and a greatly increased number of practical tech-
nique photographs, which, like the artwork, are now in full colour. Chris Norris
The book continues to be a practical guide to the evidence-based Manchester, 2011
treatment of soft tissue injuries affecting sports people.
Section One Principles
Healing 1
CHAPTER
Chapter contents
Injury 1 Synovial fluid 11
Inflammation 1 Bone 11
Heat and redness 2 Articular cartilage 17
Swelling 3 Arthritis 18
Pain 3 The joint capsule 19
Management of inflammation 8 Ligaments 19
Repair 8 Muscle 20
Tendons 22
Remodelling 9
Nerves 22
Matching treatment to the healing timescale 9
Skin 24
Individual tissue response to injury 9
Synovial membrane 9
The basic processes of soft tissue healing underlie all treatment Injury
techniques for sports injuries. We need to know what occurs in the
body tissues at each successive stage of healing to be able to select This stage represents the tissue effects at the time of injury, before
the treatment technique which is most appropriate for that time. A the inflammatory process is activated. With tissue damage, chemical
technique aimed at reducing the formation of swelling, for example, and mechanical changes are seen. Local blood vessels are disrupted
would be inappropriate when swelling had stopped forming and causing a cessation in oxygen to the cells they perfused. These cells
adhesions were the problem. Similarly, a manual treatment designed die and their lysosome membranes disintegrate, releasing the
to break up adhesions and mobilize soft tissue would not be helpful hydrolysing enzymes the lysosomes contained. The release of these
when inflammation is still forming and the tissues are highly enzymes has a twofold effect. First they begin to break down the
irritable. dead cells themselves, and second, they release histamines and
The stages of healing are, to a large extent, purely a convenience kinins which have an effect on both the live cells nearby and the
of description, since each stage runs into another. The term phasing local blood capillary network.
rather than separate stages may be more suitable. Traditionally, the The disruption of the blood vessels which caused cell death also
initial tissue response has been described as inflammation, but some causes local bleeding (extravasated blood). The red blood cells
authors see inflammation as a response separate to the processes break down, leaving cellular debris and free haemoglobin. The
occurring at the time of injury. Van der Meulen (1982) described blood platelets release the enzyme thrombin which changes fibrino-
both in terms of the ‘reaction phase’, arguing that the classical gen into fibrin. The fibrin in turn is deposited as a meshwork
inflammatory period is preceded by a short (10 minute) period around the area (a process known as walling off). The dead cells
before the inflammatory mechanism is activated. Others (Hunter, intertwine in the meshwork forming a blood clot. This network
1998), looking at the changes in strength of the healing tissue, have contains the damaged area.
termed the first stage the ‘lag phase’ because tissue strength does The changes occurring at injury are affected by age (Lachman,
not change. In any traumatic injury the initial stage is bleeding which 1988). Intramuscular bleeding, and therefore haemorrhage forma-
is the precursor for the inflammatory cascade seen as both a vascular tion, are more profuse in individuals over 30 years of age. The
and cellular response. amount of bleeding which occurs will be partially dependent on
The second stage of healing has been variously called repair, the vascularity of the injured tissues. A fitter individual is likely to
proliferation and regeneration. The tertiary stage has been termed have muscle tissue which is more highly vascularized, and therefore
remodelling (Van der Meulen, 1982; Kellett, 1986; Dyson, 1987). greater bleeding will occur with muscle injury. In addition, exercise
The terms injury, inflammation, repair and remodelling will be used itself will affect gross tissue responses. Muscle blood flow is greatly
in this text. increased through dilatation of the capillary bed, and again bleed-
When describing the stage of healing, the terms acute, subacute ing subsequent to injury will be greater.
and chronic are helpful. The acute stage (up to 48 hours following
injury) is the stage of inflammation. The subacute stage, occurring Keypoint
between 14 and 21 days after injury, is the stage of repair. The The tissues of an active athlete are more highly vascularized than
chronic stage (after 21 days) is the stage of remodelling. The term those of an inactive subject. The athlete’s tissues will therefore bleed
chronic is also sometimes used to describe self-perpetuating inflam- more during injury, and bruising will be more noticeable.
mation, where the inflammatory process has restarted due to dis-
ruption or persistent irritation of the healing tissues. The total
healing process occurs over a continuum, shown in Fig. 1.1.
Inflammation
Definition
The next stage in the healing sequence is that of inflammation sum-
Treatment must be adapted to the stages of healing, which are marized in Fig. 1.2. This may last from 10 minutes to several days,
injury, inflammation, repair and remodelling. depending on the amount of tissue damage which has occurred.
The inflammatory response to injury is the same regardless of the
© 2011 Elsevier Ltd
Section One – Principles
Acute Sub-Acute Chronic Inflammation
Inflammation
Injury Tissue Mast cells
Repair
damage and Platelets
bleeding Basinophils
e Remodelling
s
n
o
p
s
e
of r
y Chemical mediators
sit
n
e
nt
I
0 3 days 6 weeks 6 months Vascular Cellular
Time
response response
Figure 1.1 Timescale for healing. From Oakes, B.W. (1992) The classification
of injuries and mechanisms of injury, repair and healing. In Textbook of
Science and Medicine in Sport (eds J. Bloomfield, P.A. Fricker and K.D. Fitch).
Blackwell Scientific Publications, Melbourne. With permission. Chemical mediators
nature of the injuring agent or the location of the injury itself
Increased vasodilation Attraction of
(Hettinga, 1990). Various agents can give rise to injury, and
and vasopermeability phagocytes
Evans (1990a) listed physical, thermal, radiational, electrical and
chemical causes.
Inflammation is not simply a feature of soft tissue injuries. It
occurs when the body is infected, in immune reactions and when Increased phagocytosis
infarction stops blood flowing to an area. Some of the characteris- Increased flow volume
tics of the inflammatory response have even been described as Increased exudate
excessive (Cyriax, 1982) and better suited to dealing with infection,
Phagocytosis of debris
by preventing bacterial spread, than healing injury (Evans, 1990a).
The cardinal signs of inflammation are heat (calor), redness
(rubor), swelling (tumor) and pain (dolor). These in turn give rise to
the so-called fifth sign of inflammation disturbance of function of Tissue oedema Site clearance
the affected tissues (functio laesa).
Keypoint Release of mediators
Inflammation is often seen as undesirable. However, inflammation is Macrophages which stimulate
the first stage of healing and so is a vital step on the road to recovery. proliferative phase
The aim should be to prevent excessive inflammation and move the
athlete on through the stages of healing towards eventual full Figure 1.2 Inflammatory elements.
function.
Keypoint
Heat and redness
Aspirin is one of a group of drugs called non-steroidal anti-
Heat and redness take a number of hours to develop, and are due
inflammatory drugs (NSAIDs). These work by affecting prostaglandins,
to the opening of local blood capillaries and the resultant increased
which are also involved in action of the stomach. For this reason
blood flow. Chemical and mechanical changes, initiated by injury,
NSAIDs may cause gastric irritation and should not be given to those
are responsible for the changes in blood flow.
with a history of peptic ulcers.
Chemically, a number of substances act as mediators in the
inflammatory process. The amines, including histamine and
5-hydroxytryptamine (5-HT or serotonin) are released from mast The complement system, consisting of a number of serum pro-
cells, red blood cells and platelets in the damaged capillaries and teins circulating in an inactive form, is activated and has a direct
cause vessel dilatation and increased permeability lasting 10–15 effect on the cell membrane as well as helping to maintain vasodila-
minutes (Lachman, 1988). Kinins (physiologically active polypep- tation. Various complement products are involved, and these are
tides) cause an increase in vascular permeability and stimulate the activated in sequence. Finally, polymorphs produce leukotrienes,
contraction of smooth muscle. They are found normally in an inac- which are themselves derived from arachidonic acid. These help the
tive state as kininogens. These in turn are activated by the enzyme kinins maintain the vessel permeability.
plasmin, and degraded by kininases. Blood flow changes also occur through mechanical alterations
The initial vasodilatation is maintained by prostaglandins. These initiated by injury. Normally, the blood flow in the venules, in
are one of the arachidonic acid derivatives, formed from cell mem- particular, is axial. The large blood proteins stay in the centre of the
brane phospholipids when cell damage occurs, and released when vessel, and the plasmatic stream, which has a lower viscosity, is on
the kinin system is activated. The drugs aspirin and indometacin act the outside in contact with the vessel walls. This configuration
to inhibit this change—hence their use as anti-inflammatory agents reduces peripheral resistance and aids blood flow.
in sports injury treatment. The prostaglandins E1 and E2 are two of In a damaged capillary, however, fluid is lost and so the axial flow
the substances responsible for pain production, and they will also slows. Marginalization occurs as the slower flow rate allows white
promote vasodilatation, blood vessel permeability and lymph flow blood cells to move into the plasmatic zone and adhere to the vessel
(Oakes, 1992). walls. This, in turn, reduces the lubricating effect of this layer and
2
1
Healing
slows blood flow. The walls themselves become covered with a histamine, kinins and complement factors, have been shown to
gelatinous layer (Wilkinson and Lackie, 1979), as endothelium produce this effect (Fox, Galey and Wayland, 1980; Walter and
changes occur (Walter and Israel, 1987). Israel, 1987).
Some 4 hours after injury (Evans, 1980) diapedesis occurs as the
white cells pass through the vessel walls into the damaged tissue. Swelling
The endothelial cells of the vessel contract (Hettinga, 1990), pulling
The normal pressure gradients inside and outside the capillary
away from each other and leaving gaps through which fluids and
balance the flow of fluid leaving and entering the vessel (Fig. 1.4).
blood cells can escape (Fig. 1.3). Various substances, including
The capillary membrane is permeable to water, and so water will be
driven out into the interstitial fluid. However, because the tissue
fluids usually contain a small amount of protein, and the blood
Red blood cells Plasma White blood cells
contains a large amount, an osmotic pressure is created which tends
to suck water back from the tissue fluid and into the capillary once
more. The magnitude of this osmotic pressure is roughly 25 mmHg.
At the arteriole end of the capillary the blood pressure (32 mmHg)
exceeds the osmotic pressure and so tissue fluid is formed. At the
A venous end of the capillary the blood pressure has reduced
Basement membrane Endothelial cells (12 mmHg) and so, because the osmotic pressure now exceeds this
value, tissue fluid is reabsorbed back into the capillary.
Swollen and coated
During inflammation the capillary bed opens and blood flow
endothelial cells Platelets Fluid
increases (heat and redness). The larger blood volume causes a
parallel increase in blood pressure. Coupled with this, the tissue
fluid now contains a large amount of protein, which has poured
out from the more permeable blood vessels. This increased protein
concentration causes a substantial rise in osmotic pressure, and this,
together with the larger blood pressure in the capillary, forces fluid
out into the interstitium, causing swelling.
Protein exudation in mild inflammation occurs from the venules
B
only and is probably mediated by histamine (Evans, 1990a). More
Red cells forming rouleaux severe inflammation, as a result of trauma, results in protein exuda-
in central plasma stream tion from damaged capillaries as well.
During inflammation, lymphatic vessels open up and assist in the
Protein and removal of excess fluid and protein. The lymph vessels are blind-
fluid ending capillaries which have gaps in their endothelial walls
enabling protein molecules to move through easily. The lymph
vessels lie within the tissue spaces, and have valves preventing the
backward movement of fluid. Muscular contraction causes a
pumping action on the lymph vessels and the excess tissue fluid is
removed to the subclavian veins in the neck.
Pain
C
Pain is the result of both sensory and emotional experiences, and
is associated with tissue damage or the probability that damage will
occur. It serves as a warning which may cause us to withdraw from
Figure 1.3 Vascular changes which occur in inflammation. (A) Blood vessel
starts to dilate. (B) Dilated vessel showing marginalization. (C) White blood a painful stimulus and so protect an injured body part. Unfortu-
cells and fluid pass into tissue. From Evans, D.M.D. (1990a) Inflammation nately, pain often continues long after it has ceased to be a useful
and healing. In Cash’s Textbook of General Medical and Surgical Conditions form of protection. Associated muscle spasm, atrophy, habitual
for Physiotherapists (ed. P.A. Downie), 2nd edn. Faber and Faber, London. postures, guarding and psychological factors all combine to make
With permission. chronic pain almost a disease entity in itself.
Arteriole end
Venous end
(blood pressure (BP)
32 mmHg) Blood capillary (BP 12 mmHg)
Tissue space
Osmotic pressure (OP) OP>BP
BP>OP fluid formed
25 mmHg fluid reabsorbed
Lymphatic flow
Figure 1.4 Formation and reabsorption of tissue fluid.
3
Section One – Principles
Treatment note 1.1 Pain description in examination
During both the subjective examination and the objective examination persistent pain and is generally unwell, the indication is that a
(see Treatment note 1.5, p. 24) the patient will usually describe pain. pathology other than a musculoskeletal condition exists. In addition,
Both the type (nature) of pain and its behaviour are important factors changes in bladder and bowel habits, alteration in vision or gross
in making an accurate clinical diagnosis, and a number of factors changes in gait all require further investigation.
should be considered:
� When pain is decreasing the condition is generally resolving, while
No Mild Moderate Severe Very Worst
increasing pain suggests a worsening condition.
pain pain pain pain severe possible
� Constant pain which does not change with time, alteration of
pain pain
static posture or activities suggests a non-mechanical condition
such as chemical irritation, tumours or visceral lesions (Magee,
2002).
� Where pain changes (episodic pain), the therapist should try to 0 1 2 3 4 5 6 7 8 9 10
determine what activities make the pain worse (exacerbation) and No Moderate Worst
what make it better (remission). pain pain possible
� The therapist should try to determine if the pain is associated pain
with particular events (e.g. movements, visceral function),
or time of day.
� Pain with sporting activity which reduces with rest in general No Pain as bad
suggests a mechanical problem, irritating pain sensitive pain as it could
structures. Intensity of pain possibly be
� Morning pain which eases with movement indicates chronic Figure 1.5 Visual analogue scales (VAS) used in pain description.
inflammation which takes time to build up and reduces with From Petty and Moore (2001) with permission.
movement.
The description of pain itself may indicate the structure causing it
(see Table 1.1) and the behaviour of the pain on physical examination Table 1.2 Red flags in sport examination indicating
clarifies the picture. medical investigation
Recording pain System/possible
The intensity of pain may be recorded on a visual analogue scale pathology Pain behaviour
(VAS). The patient is asked to indicate the pain description or number
Cancer Persistent night pain
which best represents their pain. Where a 10 cm line is used the
Constant (25 hour) pain
distance from the left of the scale to the point marked by the patient
Unexplained weight loss (e.g. 4–6 kg in 10 days)
may be measured in millimetres and used as a numerical value
Loss of appetite
(Fig. 1.5).
Unusual lumps or growths
Red flags
Sudden persistent fatigue
It is important for the therapist to appreciate when pain and other
Past history of carcinoma
symptoms may suggest serious pathology which requires medical
Cardiovascular Shortness of breath
investigation—so called ‘red flags’ (Table 1.2). Where the patient has
Dizziness
Pain or feeling of heaviness in the chest
Pulsating sensations in the body
Discolouration in the feet
Persistent swelling with no history of injury
Table 1.1 Pain descriptions and related structures
Gastrointestinal/ Frequent or severe abdominal pain
Type of pain genitourinary Frequent heartburn or indigestion
Frequent nausea or vomiting
Cramping, dull, aching, worse with resisted Muscle
Change in bladder or bowel habits
movement
Unusual menstruation
Dull, aching, worse with passive movement Ligament, joint capsule
Neurological Changes in hearing
Sharp, shooting Nerve root Frequent or severe headache
Sharp, lightning-like, travelling Nerve Problems in swallowing or changes in speech
Burning, pressure-like, stinging, with skin Sympathetic nerve Gait disturbance, or problems with balance/
changes coordination
Drop attacks (fainting)
Deep, nagging, poorly localized Bone
Sudden weakness
Sharp, severe, unable to take weight Fracture
Source Magee (2002) and Waddell, G., Feder, G. and Lewis, M. (1997) Systematic
Throbbing, diffuse Vasculature
reviews of bed rest and advice to stay active for acute low back pain. British
Source Magee (2002) and Petty and Moore (2001) with permission. Journal of General Practice, 47, 647–652. With permission.
4
1
Healing
Types of pain Subchondral bone, tendons and ligaments are the next in line in
Pain may be classified as somatogenic (acute or chronic), neuro- terms of sensitivity, followed by muscle and cortical bone, the syn-
genic or psychogenic. Chronic pain may be considered as pain ovium and cartilage being largely insensitive.
which generally lasts for more than 6 weeks, while acute pain is The pain receptors are supplied by a variety of different nerve
pain of sudden onset which lasts for less than 6 weeks (Donley and fibres. Skin receptors are supplied by thinly myelinated (A delta)
Denegar, 1990). fibres which carry ‘fast’ pain and respond to strong mechanical
stimuli and heat above 45°C (Low and Reed, 1990). They give the
initial sharp well-localized pain feeling (pinprick). The function of
Definition fast pain is to help the body avoid tissue damage and it often pro-
Acute pain has a sudden onset and lasts for less than 6 weeks. vokes a flexor withdrawal reflex.
Chronic pain lasts in excess of 6 weeks. Impulses from free nerve endings found in deeper body tissues
are carried by non-myelinated C fibres. This is ‘slow’ pain, which
tends to be aching and throbbing in nature, and poorly defined.
Its onset is not immediate, and the sensation it produces persists
Musculoskeletal pain is not usually well localized—the surface
after the pain stimulus has gone. The function of slow pain seems
site where the pain is felt rarely correlates directly to injured subcu-
to be to enforce inactivity and allow healing to occur and it is
taneous tissue. Generally, the closer an injured tissue is to the skin
therefore often associated with muscle spasm. The C fibres respond
surface, the more accurate the athlete can be at localizing it.
to many different types of stimuli and, as such, are said to be
Deep pain is normally an aching, ill-defined sensation. It usually
‘polymodal’. However, they are most sensitive to chemicals released
radiates in a characteristic fashion, and may be associated with
as a result of tissue damage. Histamine, kinins, prostaglandins
autonomic responses such as sweating, nausea, pallor and lowered
E1 and E2, and 5-HT have all been implicated in this type of
blood pressure (Lynch and Kessler, 1990). Pain referral corresponds
pain production during inflammation (Walter and Israel, 1987;
to segmental pathways, most often dermatomes. The extent of radi-
Lachman 1988).
ation largely depends on the intensity of the stimulus, with pain
It can be seen that the pain experienced as a result of sporting
normally radiating distally, and rarely crossing the mid-line of the
injury will usually be either mechanical or chemical in nature.
body (Cyriax, 1982).
Mechanical pain is the result of forces which deform, or damage
Neurogenic pain is different again. Compression of a nerve root
the nociceptive nerve endings, and so may be caused by stretching
gives rise to ill-defined tingling, especially in the distal part of the
contracted tissue or by fluid pressure. This type of pain is influenced
dermatome supplied by the nerve. This is a pressure reaction, which
by movement. Chemical pain, on the other hand, results from irrita-
quickly disappears when the nerve root is released. Greater pressure
tion of the nerve endings, and is less affected by movement or joint
causes the tingling to give way to numbness. Compression or
position, but will respond to rest.
tension to the dural sleeve covering the nerve root gives severe pain,
generally over the whole dermatome. In contrast, pressure on a
nerve trunk usually causes little or no pain, but results in a shower
Keypoint
of ‘pins and needles’ as the nerve compression is released. Pressure
Fast pain helps the body avoid tissue damage by provoking a flexor
applied to a superficial nerve distally gives numbness and some
withdrawal reflex. Slow pain enforces inactivity (through muscle
tingling, with the edge of the affected region being well defined
spasm) to allow time for healing.
(Cyriax, 1982).
Irritability
Irritability may be defined as ‘the vigour of activity which causes Articular neurology
pain’ (Maitland, 1991). It is determined by the degree of pain which In addition to pain receptors (type IV), three other joint receptors
the patient experiences, and the time this takes to subside, in rela- are important. Type I receptors are located in the superficial layers
tion to the intensity of activity that brought the pain on in the first of the joint capsule. They are slow adapting, low-threshold mech-
place. The purpose of assessing irritability is to determine how anoreceptors, which respond to both static and dynamic stimula-
much activity (joint mobilization, exercise, etc.) may be prescribed tion. These receptors provide information about the static position
without exacerbating the patient’s symptoms. of a joint, and contribute to the regulation of muscle tone and
An assessment of irritability may be made at the second treatment movement (kinaesthetic) sense. The type I receptors sense both the
session. The amount of movement which the patient was subjected speed and direction of movement.
to in the previous session is known, as is the discomfort that he or Type II receptors are found mainly in the deeper capsular layers
she feels now. These subjective feelings are then used to determine and within fat pads. These are dynamic receptors with a high thresh-
the intensity of the second treatment session. Similarly, at the begin- old, and they adapt quickly. They respond to rapid changes of
ning of each subsequent treatment session the irritability is again direction of joint movement.
assessed. The type III fibres are found in the joint ligaments, and are again
high threshold dynamic mechanoreceptors, but are slow adapting.
Keypoint These receptors monitor the direction of movement, and have a
‘braking’ effect on muscle tone if the joint is moving too quickly or
Irritability is a measure of the amount of pain a patient experiences as
through too great a range of motion. The type IV receptor is the
a result of movement (including that of treatment). Irritability should
nociceptor described above. Table 1.3 provides a synopsis of the
be used to guide the type and intensity of treatment to avoid
various movement categories to which the receptors respond.
excessive post-treatment soreness.
Alteration in the feedback provided by joint receptors is of great
importance following sports injury, and is dealt with in the section
on proprioceptive training.
Pain production
Free or ‘bare’ nerve endings (type IV) respond to painful stimuli and Pain pathways
are termed nociceptors. They are largely unresponsive to normal Three categories or ‘orders’ of neurone make up the pain pathways.
stimuli, but have a low threshold to mechanical and thermal injury, First order neurones travel from the pain receptors to the spinal
anoxia and irritation from inflammatory products. Tissues vary in cord, second order neurones travel within the cord to the brainstem
the intensity of pain they will produce when stimulated. The joint and third order neurones travel from the brainstem to the higher
capsule and periosteum are the most sensitive to noxious stimuli. centres of the cerebral cortex.
5