Stroke
A stroke (also referred to as CVA – cerebrovascular accident) is an episode of acute
neurological dysfunction persisting ≥ 24 hours with acute infarction or hemorrhage. A
transient ischaemic attack (TIA) can present with similar symptoms but only last minutes
to hours and fully resolve in 24 hours.
Epidemiology (incidence, prevalence)
Demographic features (age, sex,
ethnicity etc)
Risk factors
Aetiology (cause)
After coronary heart disease and cancer,
stroke is the 3rd most common cause of
death in western countries. Approximately
9000 people per year have a stroke in NZ.
Risk increases with age
Maori & PI > NZ European
Hypertension, diabetes, heart disease, atrial
fibrillation, smoking, obesity, carotid artery
stenosis, history of TIA, high cholersterol,
excessive alcohol intake.
There are two types of stroke:
1) Ischamic (80%)
Caused by an interruption of the
blood supply.
2) Hamorrhagic (20%)
Caused by a ruptured blood vessel
The main causes of ischaemic stroke are:
 Thrombosis: obstruction of a blood
vessel by a blood clot formed locally
 Embolism: obstruction of a blood
vessel caused by a blood clot
(embolus) coming from somewhere
else in the body
 Systemic hypoperfusion
Pathological changes
Haemorrhagic strokes are most common in
small blood vessels and potential causes are
hypertension, trauma, bleeding disorders,
drug use and vascular malformations.
When an ischaemic stroke occurs, part of the
brain suffers from lack of blood. Without
blood the brain tissue is no longer supplied
with oxygen and irreversible injury is caused
due to cell death. Due to the organisation of
blood supply to the brain (Circle of Willis),
collateral circulation is possible so while part
of the brain tissue may die immediately,
other parts are potentially only injured and
may recover. The area of the brain where
tissue might recover is called the penumbra.
Ischaemia also triggers pathophysiological
processes which result in cellular injury and
death such as the release of glutamate or the
production of oxygen free radicals.
Clinical features (typical presentation)
Special tests and investigations
Medical management (if applicable)
A haemorrhagic stroke causes tissue injury by
compression of tissue from an expanding
haematoma. This can result in tissue injury
and, consequently the increased pressure
might lead to a decreased blood supply to
the surrounding tissue.
Sudden onset of neurological symptoms
which last more than 24 hours.
Presentation depends on part of brain
affected however typical presentation is a
sensory-motor hemiparesis or hemiplegia,
contralateral to the side of the lesion in the
brain.
(hemiparesis is defined as weakness on one
side of the body; hemiplegia is total paralysis
of the arm, leg and trunk on one side of the
body).
Neurological examination may also find:
 Muscle weakness affecting arm, leg or
face
 Aphasia
 Dysarthria
 Dysphagia
 Gait problems
 Spatial neglect
 Visual problems
Typically in haemorrhagic strokes, onset of
symptoms is more rapid and often associated
with headache and/or vomiting.
CT or MRI
ECG – to detect arrhythmias of the heart
which may send clots in the heart to the
brain
Ultrasound of the carotid arteries
Stroke is a medical emergency. In the case of
an ischaemic stroke, the more rapidly the
blood flow is restored to the brain, the fewer
brain cells die. Thrombolysis involves the
administration of a clot-dissolving
intravenous drug which can completely
reverse the damaging effects of an occluded
vessel if given within 3-4hours after stroke
onset.
Acute treatments focus on minimising
enlargement of the clot or preventing new
clots from forming by means of medications
such as:
 Aspirin
 Clopidogrel
 Dipyridamole
Clinical course/prognosis
20% of first ever stroke patients die within a
month.
Over 50% of people will be left with
significant disability
Over 10% will have a recurrent stroke within
the first year
Initial motor and functional ability is the most
important predictor of long-term motor and
functional performance after stroke. Most
significant motor and functional recovery is
observed in the first month after stroke.
Recovery after this initial period does
happen, sometimes long after stroke.
Further reading: Lennon S, Ramdharry G, Verheyden G, ProQuest. Physical management for
neurological conditions. Fourth edition. ed. Amsterdam]: Elsevier; 2018. Chapter 7 (available
as an e-book through library)
Parkinson’s disease
Epidemiology (incidence, prevalence)
Demographic features (age, sex,
ethnicity etc)
Risk factors
Aetiology (cause)
Pathological changes
Clinical features (typical presentation)
2nd most common neurodegenerative disorder
worldwide, affecting an estimated 10 million
people
Global incidence 12-230/100000 people
Prevalence increases with age
Most common in older adults (affects 1% of
adults over 60)
and in males
Increasing age
Family history
Head trauma
Exposure to environmental toxins
Idiopathic PD accounts for over 70% of all cases cause is unknown – likely due to an interaction
between infective or toxic environmental factors
and genetic mutations.
Secondary parkinsonism may result from a
variety of pathological processes including drugs,
toxins, trauma and vascular disease.
PD is considered predominantly as a disorder of
the basal ganglia. The basal ganglia have
connections with the cerebral cortex and
thalamus and are important for automatic and
voluntary motor control, procedural learning and
emotional functions.
The 2 recognised pathological findings in the
brains of people with PD are:
 Loss of pigmented dopaminergic neurons
in the substantia nigra. Approx 60-80% of
dopaminergic neurons are lost before
motor signs occur. As the available
dopamine reduces, compensatory
changes in the BG arise: the circuit from
thalamus to cortex suppress movement,
causing bradykinesia.
 The presence of Lewy bodies which are
an accumulation of an abnormal synaptic
protein.
Motor signs
 Bradykinesia (reduced movement speed
and amplitude)
 Akinesia (difficulty initiating movements)
 Episodes of freezing
 Rigidity (resistance to passive movement)


Special tests and investigations
Medical management (if applicable)
Clinical course/prognosis
Tremor
Impaired balance and postural control
Non-motor signs
 Neuropsychiatric symptoms: depression,
anxiety, hallucinations, cognitive changes
 Sleep disorders
 Autonomic symptoms
 Quiet speech
 Loss of facial expression
 Gastrointestinal symptoms: dribbling,
dysphagia, nausea and constipation
 Sensory impairments
Diagnosis is based primarily on motor
presentation and response to medication.
Pharmalogical management
 Dopaminergic drugs which increase the
amount of dopamine in the brain, or
stimulate the parts of the brain where
dopamine works or, block the action of
enzymes that break down dopamine.
 Anticholinrgic drugs can control tremor
PD is a progressive disorder with no cure
Age of onset, motor severity, cognitive
impairment and psychotic symptoms predict
increased mortality risk
Further reading:

Lennon S, Ramdharry G, Verheyden G, ProQuest. Physical management for
neurological conditions. Fourth edition. ed. Amsterdam]: Elsevier; 2018. Chapter 11
(available as an e-book through library)
Type 2 diabetes
Diabetes occurs when there is too much glucose in the blood. Blood-sugar levels are
normally controlled by a hormone called insulin, which is made in the pancreas. High blood
glucose levels may be caused by (a) insulin deficiency, when the pancreas is not able to
make enough insulin (as in Type I diabetes), or (b) insulin resistance, when your body is not
responding to insulin as it should (as in Type 2 diabetes).
Insulin is a hormone that helps glucose enter the body's cells where it is used for energy. If
there is insufficient insulin, or it is not working effectively to act as a key to open the
channel for glucose to enter the cells, glucose builds up in your bloodstream. The normal
level of glucose in the body is between 4 and 8 mmol/L. When you have diabetes, your
body is not able to control your blood glucose levels and keep it in the safe range. If not
well controlled, high blood glucose levels will eventually lead to damage to many parts of
the body.
Prediabetes is when the amount of glucose in the blood is higher than normal and it
increases the risk of getting type 2 diabetes. Prediabetes affects 1 in 4 adults. Making
healthy lifestyle at this point can delay or prevent the development of type 2 diabetes.
Useful resources
https://www.diabetes.org.nz/what-is-diabetes/
https://www.healthnavigator.org.nz/health-a-z/d/diabetes-type-2/
Epidemiology (incidence,
prevalence)
There are over 240,000 people in New Zealand who
have been diagnosed with diabetes. Of all those
with a diagnosis of diabetes, 10% have type 1
diabetes; it is typically diagnosed in childhood or
young adults. Type 2 diabetes is the most common
form and typically occurs in adulthood. However, it
is increasingly being diagnosed in younger people.
As a condition, diabetes is often undiagnosed, with
an estimated 100,000 people who have it but don’t
know.
Demographic features (age, sex,
ethnicity etc)
Type 2 diabetes is more common in Māori, Pacific
and Asian populations; Māori and Pacific Islanders
are three times more likely to develop diabetes than
other New Zealanders.
The incidence of onset of type 2 diabetes increased
with age.
Risk factors
There are some non-modifiable risk factors for the
development of type 2 diabetes:
 Age over 45
 Māori, Pacific or Asian and aged over 35
 Have a family member with diabetes
The following are modifiable risk factors:
 Obesity
 Hypertension
 Poor diet
 Physical inactivity
 Hyperlipidaemia
https://vimeo.com/99966777
Aetiology (cause)
Type 1 diabetes is believed to be caused by an autoimmune reaction.
Type 2 diabetes is considered a disease of lifestyle
and the modifiable risk factors listed above can
contribute to its development.
https://vimeo.com/99962828 (diabetes overview and
symptoms)
Pathological changes
Type 2 diabetes is a progressive disease, meaning it
slowly worsens over time. The cells that produce
insulin are damaged or die over time and our bodies
are less able to make enough insulin to maintain the
blood glucose levels within the healthy range. This
means people with type 2 diabetes may also
experience insulin deficiency and require insulin
injections.
Well controlled blood glucose levels help reduce the
risk of diabetes-related complications such as poor
vision, heart disease or stroke, kidney
damage (diabetes is the top cause of kidney
failure), erectile dysfunction and lower limb
numbness.
https://vimeo.com/99977335
Clinical features (typical
presentation)
Common symptoms:
 Feeling thirsty
 Tiredness
 Frequent urination
 Urinary and skin infections
 Blurred vision
 Delayed healing of cuts/grazes
About 50% of people with type 2 diabetes have no
symptoms.
To watch for:
 Hypoglycaemia
Hypoglycaemia, or low blood glucose, occurs when
the blood glucose level (BGL) is less than 4 mmol/l,
or where symptoms of hypoglycaemia are
experienced at a level close to this.
Symptoms include looking pale; feeling shaky or
sweaty; sudden hunger; tingling around mouth and
tongue; dizziness; confusion; blurred vision.
Management: one serving of a quick-acting
carbohydrate such as 6 large jelly beans or 3 Dextro
Energy tablets.
 Hyperglycaemia
Hyperglycaemia, or high blood glucose, occurs when
BGLs are higher than normal; greater than 8mmol/l.
A high of up to 16-20mmol/l is usually manageable
as long as it settles with 24 hours. The aim should
be to keep BGLs in the healthy range (4mmol/l –
8mmol/l) 80% of the time. It is not advisable to
exercise where blood glucose levels exceed
17mmol/l.
The main symptoms are feeling thirsty; dry mouth;
passing large amounts of urine; and extreme
tiredness.
Management: short-acting insulin; drink extra
unsweetened fluids; retest BGL 2 hourly until return
to normal levels; test for ketones in blood if
symptoms worsening.
Special tests and investigations
The gold standard test for both screening and
diagnosis of diabetes in the glycated haemoglobin
test or HbA1c, which measures your average blood
glucose over the previous 8 to 12 weeks and gives
an indication of your longer-term blood glucose
control.
An HbA1c of ≤40 mmol/mol is normal.
An HbA1c of 41-49mmol/mol indicates prediabetes.
An HbA1c of ≥50mmol/mol indicates diabetes.
Blood glucose levels may need to be checked and
recorded periodically or, if being treated with
insulin, multiple times a day using a blood glucose
monitor. Many factors can affect blood glucose
levels so careful monitoring is the best way to
ensure that blood sugar levels remain within their
normal range.
Medical management (if
applicable)
The main treatment for type 2 diabetes is
administered orally; medications include
metformin; gliclazide; and glipizide.
An insulin injection is required once or twice daily in
the management of type 1 diabetes and in some
people with type 2 diabetes over time.
https://vimeo.com/99977333 (insulin)
Role of physical activity
Exercise improves blood glucose control in type 2
diabetes, as well as reducing cardiovascular risk,
supporting weight loss, and promoting well-being.
Regular exercise can prevent or delay the onset of
type 2 diabetes. Regular exercise also benefits
people with type 1 diabetes through improved
cardiovascular fitness, muscle strength, and insulin
sensitivity.
https://vimeo.com/99970369
Self-management
https://vimeo.com/99970367
Bronchiectasis
Bronchiectasis is a respiratory condition caused by the abnormal, irreversible dilatation of
the bronchi, as a result of destruction of the elastic and muscular tissue due to acute or
chronic inflammation and infection. The damaged airways impair drainage of bronchial
secretions resulting in chronic infection and mild to moderate airway obstruction. Without
effective management, the combination of infection and chronic inflammation results in
progressive lung damage.
Useful resources
The Bronchiectasis Toolbox: http://bronchiectasis.com.au/
Main & Denehy (2016) Cardiorespiratory Physiotherapy. Adults and Paediatrics, p.170-172
The TSANZ Position Statement on bronchiectasis is also useful:
https://www.mja.com.au/system/files/issues/193_06_200910/cha10303_fm.pdf
Article on the ethnicity, socioeconomic status and severity of non-CF bronchiectasis which
identifies the higher burden on Māori and Pacific patients:
https://onlinelibrary.wiley.com/doi/full/10.1111/imj.13739
Epidemiology
(incidence,
prevalence)
Demographic
features (age,
sex, ethnicity
etc.)
Risk factors
The prevalence of bronchiectasis is 3.7 per 100,000 population in New
Zealand but there is considerable variation between ethnic groups.
The incidence of bronchiectasis in New Zealand children aged under
15 is highest in Pacific children (24.7 per 100,000); higher 16.7 per
100,000 in Māori and 5.6 per 100,000 in non- Māori or Pacific Island
children. The median age at diagnosis is 5.2 years.
Bronchiectasis is more common amongst Māori and Pacific
populations. It also more commonly affects females and the
elderly.



A diagnosis of cystic fibrosis
Acute lung infection
Being of non-European ethnicity
Socio-economic deprivation increase the risk of hospitalisation.
Aetiology
(cause)
There are two kinds of bronchiectasis: cystic fibrosis (CF)bronchiectasis and non-CF bronchiectasis. A diagnosis of cystic fibrosis
is, therefore, a risk factor for bronchiectasis.
Having an established lung disease, such as chronic obstructive
pulmonary disease (COPD), asthma or interstitial lung disease, is a risk
factor for the development of non-CF bronchiectasis.
The main causes of non-CF bronchiectasis are damage to lower
respiratory tract following an acute infection, such as pneumonia or
whooping cough. Non-CF bronchiectasis can also develop following
viral infection and is associated with immune-deficiency (such as HIV);
conditions of mucociliary dysfunction (such as Primary Ciliary
Dyskinesia); systemic inflammatory conditions (such as rheumatoid
arthritis); gastric aspiration; tuberculosis and allergic
bronchopulmonary aspergillosis.
Pathological
changes
The pathophysiology of bronchiectasis is commonly described as
distinct phases of infection and chronic inflammation; the interaction
between the two creating a vicious circle resulting in bronchial
destruction leading to impaired mucociliary clearance, hypersecretion
of mucus and resulting airway obstruction.
See diagram: http://bronchiectasis.com.au/wpcontent/uploads/2015/09/Physiology-Vicious-Cycle.png
Clinical features
(typical
presentation)
Most common symptoms:
 Chronic cough
 Sputum
Other symptoms that may be present:
 Recurrent chest infections
 Fatigue and lethargy
 Exercise limitation
 Chronic sinusitis
 Shortness of breath/wheeze
Some people are totally asymptomatic.
A high resolution CT scan (c-HRCT) is the diagnostic gold standard. It is
the most sensitive and specific non-invasive method for diagnosing
bronchiectasis.
Special tests and
investigations
Chest x-rays are no longer used in the diagnosis of bronchiectasis as
they are often normal or shows non-specific findings in affected
individuals.
Lung function tests are an important assessment tool in the diagnosis
and management of bronchiectasis. Airflow obstruction is the most
common ventilatory pattern seen in bronchiectasis. The British
Thoracic Society Guideline for non-CF bronchiectasis recommends
that adults and school age children should have spirometry measured
at initial assessment to determine baseline level of lung function.
Sputum samples should be collected at baseline followed by 3 to 6
monthly samples to allow for documentation of microbiology;
antibiotic treatment and monitoring of the condition.
Medical
management (if
applicable)
Medications may not be required when patients are well.
Medications that may be administered during an exacerbation are:
 Antibiotics – these may oral, intravenous or nebulised.
Macrolide antibiotics (such as erythromycin) target both
inflammation and infection and have been shown to have
beneficial clinical effects in patients with bronchiectasis.
 Mucoactive agents – assist with airway clearance by increasing
hydration of the airway surface. These include isotonic saline
(0.9%); hypertonic saline (3%-7%); and Mannitol. Note: they
are not currently routinely recommended for people with
bronchiectasis due to the lack of research evidence.
 Bronchodilators – may be prescribed if there is reversibility of
airflow obstruction.
 Inhaled corticosteroids
Physiotherapy
management
Physiotherapy has a vital role in supporting those with bronchiectasis
to manage their condition through airway clearance techniques for
excess bronchial secretions, such as active cycle of breathing
techniques (ACBT), PEP devices and postural drainage. Exercise should
be encouraged as it can improve exercise tolerance; reduce symptoms
of breathlessness (dyspnoea); fatigue; and improve quality of life.
Exercise may also be an adjunct to clearing secretions.
Clinical
Most people with bronchiectasis have a good prognosis. An
course/prognosis established airway clearance routine and timely antibiotics in
response to exacerbations helps to maintain good health. Lung
function and quality of life are more likely to decline in those who do
not look after themselves.
Where bronchiectasis is secondary to another condition (e.g. cystic
fibrosis) there may be a poorer prognosis.
Factors associated with poorer prognosis include:


Living with the
condition
smoking
gram negative organisms (Escherichia coli and Pseudomonas
aeruginosa)
 aspergillus in sputum
 poor FEV1 and FVC
 compromised immunity
Jeff’s story: https://www.youtube.com/watch?v=GnNgX40cBFI
Jude’s’ story: https://www.youtube.com/watch?v=VyGp12XbPzs
Ischaemic/Coronary Artery Disease
Reference: Reference: Main and Denehy. Cardiorespiratory Physiotherapy: Adults and
Paediatrics. 5th edition. Elsevier. 2016. Pages 126-132.
Epidemiology
(incidence,
prevalence)
Demographic
features (age,
sex, ethnicity
etc)
Risk factors
Coronary artery disease (CAD) is a subgroup of the wider group of
cardiovascular disease. CAD is one of the leading causes of death
worldwide. One in 20 New Zealanders have been diagnosed with CAD
and one New Zealander dies every 90 minutes from CAD.
As for all cardiovascular diseases, risk factors for CAD are either
modifiable or non-modifiable.
Demographic features that comprise the non-modifiable risk factors
are:
Age and sex (≥ 45 yr male and ≥55 yr female)
Family history (father or brother who died of stroke or heart attack
>55 yrs old or mother or sister < 65 yrs old)
Ethnicity: The prevalence of deaths from CAD is 40.2% in Maori
compared to 10.5% in Pakeha
(Ministry of Health (2015) Mortality and demographic data, 2012. In:
HEALTH, MO (ed.).Wellington: New Zealand Government.)
In addition to the non-modifiable risk factors above, modifiable risk
factors are:
Smoking
Hypertension
Dyslipidaemia (ie. too little high density lipoprotein (good cholesterol)
and too much low density lipoproteins and triglycerides (bad
cholesterol)
Diabetes
Obesity
Physical inactivity
See your PHTY254 lab manual (lab 13.1) for values for blood pressure,
cholesterol, obesity and blood sugar levels
Aetiology (cause) CAD is caused by a build-up of cholesterol and other material, called a
plaque, on the inner wall of the coronary arteries. Over time the
plaque grows which narrows the inner artery diameter and obstructs
blood flow. The resulting reduced blood flow results in less oxygen
being delivered to the myocardium (heart muscle) causing ischaemia.
This ischaemia of the myocardium is what results in the symptoms of
CAD – angina or a myocardial infarction (see below).
Pathological
changes
Clinical features
(typical
presentation)
Signs and symptoms of a myocardial infarction (MI) vary, but can
include:
Discomfort in the chest and arms
Neck and jaw pain
Upper back pain
Sweating, nausea or dizziness.
Angina is caused by intermittent ischaemia to the myocardium and is
usually felt by chest pain with exertion or (if more severe or unstable)
at rest. Sometimes there is no pain associated with angina or
myocardial infarction – called a “silent MI”.
Special tests and
investigations
For some people the only signs of CAD is breathlessness or fatigue on
exertion due to the myocardium not receiving enough oxygen.
In order to diagnose the presence of CAD, an exercise stress test is
commonly performed. In the test a standardised incrementally
increasing treadmill test (for example the Bruce Treadmill Test) is used
and the heart electrical conductivity is monitored via ECG for changes
that may indicate myocardial ischaemia.
The most prominent changes in the ECG with myocardial ischaemia is
in the ST segment and T wave, where the ST segment could be
elevated or depressed, or the T wave may appear flatter, inverted or
increased in amplitude.
Other diagnostic tests include echocardiography (ultrasound imaging
of the heart) and coronary angiogram (injection of dye into the blood
stream followed by ultrasound imaging of the coronary arteries in
order to look for stenosis (narrowing) or the coronary arteries.
Diagnosis of a myocardial infarction is done via the following:
1) Presence of signs and symptoms indicative of a MI
2) ECG changes – typically looking for ST segment elevation
3) Blood tests – looking for elevated levels of cardiac biomarkers that
are released into the blood stream when the myocardium is damaged.
The most common biomarker tested for is Troponin. Troponin blood
levels rise within several hours of a MI and remain elevated for up to
two weeks.
If someone has raised troponin levels but a normal ECG this is called a
non-ST elevated myocardial infarction (NSTEMI).
If someone has raised troponin levels AND ST elevation in their ECG
this is called an ST elevated myocardial infarction (STEMI)
Medical
management (if
applicable)
Angina is treated medically using glyceryl trinitrate sublingual spray
(GTN) – this is a nitric oxide donor. Nitric oxide is a vasodilator and its
role in angina is to vasodilate the coronary blood vessels to restore
blood supply to the myocardium. GTN is a spray that is squirted under
the tongue in order to get fast absorption into the blood stream.
The immediate medical management for a myocardial infarction is to
restore blood flow to the myocardium as fast as possible. Medications
administered may include aspirin (which reduces blood clotting),
thrombolytics (to dissolve the clot), antiplatelet agents (to reduce
further clotting) and beta blockers (to slow HR and blood pressure to
reduce the workload and oxygen requirements of the myocardium).
Depending on the severity and number of blockages in the coronary
arteries, further treatment may be required. One intervention is
coronary angioplasty (where a deflated balloon on the end of a
catheter is inserted into the femoral artery and guided up the aorta
and into the coronary arteries, the balloon is inflated in order to push
the thrombis and plaque back and restore the internal lumen of the
blood vessel. Often a mesh cage (stent) is put into the coronary artery
in order to maintain the lumen of the artery. Because the only
incision is in the groin this is what we call “minimally invasive surgery”
and people can recover quite quickly.
Clinical
course/prognosi
s
For severe blockages that cannot be treated via angioplasty, open
heart surgery called coronary artery bypass graft (CABG) surgery is
performed. In this surgery either the saphenous vein in the leg or
radial artery in the arm are surgically removed and grafted from the
aorta to the coronary artery in order to bypass the blocked section of
the blood vessel. This is a very invasive procedure, as the sternum has
to be cut in half in order to access the heart and it takes 3 months or
longer to physically recover from such an operation.
CAD is a progressive condition. Even after angioplasty or CABG
surgery, the stents or grafted blood vessels can block over the next 1 –
2 decades. Therefore both pharmacological management (to reduce
cholesterol and BP) and lifestyle changes (healthy diet, physical
activity and smoking cessation) are required to prevent or slow the
progression of CAD.
The role of physiotherapy for people with CAD is to support people in
making lifestyle changes and guide them with engaging in physical
activity and exercise.
Cardiac rehabilitation programmes are supervised exercise and
education sessions where people exercise under the guidance of a
physiotherapist (and often a cardiac nurse). These programmes
typically run for 8 – 12 weeks. Comprehensive cardiac rehabilitation
programmes include education about medications, diet, physical
activity and smoking cessation, as well as behaviour change
interventions in order to help support people to make and maintain
lifestyle changes. You will learn more about cardiac rehabilitation
programmes in year 3.
Videos
https://www.heartfoundation.org.nz/your-heart/post-heartattack/about-heart-attacks
https://www.youtube.com/watch?time_continue=107&v=2z5_BLltXn
k
Anterior cruciate ligament (ACL) injury
Epidemiology (incidence,
prevalence)
Demographic features (age,
sex, ethnicity etc)
Risk factors
Aetiology (cause)
Pathological changes
Clinical features (typical
presentation)
Annual incidence of ACL tears is 81 per 100,000 people
aged 10 – 64 years in Europe.
A genetic predisposition to ACL injury has been
proposed, however there is not enough evidence in the
literature to definitively support this.
There is some evidence for a higher ACL injury rate in
females, and incidence is generally higher in a younger
than older population.
ACL injuries occur most commonly in sports involving
pivoting and sudden deceleration, in particular when
performing a cutting manoeuvre or on single-leg landing.
The typical ACL injury occurs with the knee externally
rotated and in 10 – 30 degrees flexion when the knee is
placed in a valgus position as the person pushes off
through the planted foot and internally rotates their
upper body with the aim of rapidly changing direction.
Unfavourable body movements in landing and pivoting
where the knee “collapses” of falls medial to the hip and
foot has become recognised as a potential cause of ACL
injuries. As a result, intervention programme that teach
and facilitate safer neuromuscular patterns during
manoeuvres such as cutting and jump-landing activities
have now been implemented in many sporting codes for
example netball and football (soccer). See Brukner and
Kahn, Chapter 12 pg 178-181 for an example of such an
injury prevention programme (FIFA 11)
5 – 15% of ACL injuries are partial tears, with complete
rupture being more common.
Typical features of the history include:
An audible “pop”, “crack” or feeling of something going
out and then going back
Most complete ACL tears are extremely painful in the
first few minutes after injury.
Usually unable to continue their activity at the time of
injury, and if they do they often feel instability or a lack
of confidence in the knee.
Typical examination findings include:
Swelling in the first few days can make physical
examination difficult and may need to be delayed until
swelling and pain are less intense.
- Restricted knee movements
-
-
Special tests and
investigations
Widespread mild tenderness on palpation
May have lateral joint tenderness (from impact
of tibia and femur at time of injury from the
valgus positioning)
ACL injuries often occur in conjunction with
medial meniscus injuries, in which case there
may be medial joint tenderness.
The Lachman’s test is the most useful test for ACL injury
Pivot Shift test is also diagnostic of ACL deficiency, but
requires the patient to have an intact MCL and iliotibial
band and be able to extend the knee
Anterior draw test – least sensitive for ACL tear
diagnosis
A knee x-ray to check for avulsion of ACL from the tibia
should be performed if an ACL tear is suspected
Medical management (if
applicable)
MRI can be helpful if unsure of diagnosis, however MRI
should mainly be used to detect associated meniscal and
cartilage injuries
The two approaches to ACL rupture management is
surgical and conservative (non-surgical).
Surgical ACL reconstruction uses either a patellar tendon
or semitendinosis & gracilis tendon bundle graft that is
fixed onto the original tibial insertion site and in the
intercondylar notch of the femur in a position where the
graft is maximally taut during knee movement.
Post-operative rehabilitation is generally a similar
protocol to that of conservative management.
The key aims of ACL rehabilitation are: 1) reduction of
pain, swelling and inflammation; and 2) regaining ROM,
strength and neuromuscular control (including a focus
on core stability and
proprioceptive and balance exercises).
The management of partial ACL tears depends on the
degree of instability in the knee. A clinically and
functionally stable partial tear can be treated
conservatively, where unstable lesions may require
surgical treatment, especially in those who wish to
return to high-intensity sport.
Clinical course/prognosis
See Brukner and Kahn, chapter 35, pages 740 – 751 for
more information about surgical and conservative
management approaches, and a detailed outline for an
ACL rehabilitation program.
There is a wide variation in time to return to sport
following an ACL injury. Reported rates for return to
sport in the literature are 65 – 88% within a year, with
another study reporting 72% returning to pre-injury
activity levels within 2 years.
The rate of graft re-rupture after 10 years is
approximately 6%, with the highest risk being in the first
12 months after ACL injury.
A frequent long term consequence of ACL rupture is
increased risk of knee osteoarthritis, with rates
approximately 50% at 10 – 20 years post injury.
Medial Collateral Ligament Injury (of the knee)
Demographic features (age,
sex, ethnicity etc)
Aetiology (cause)
Pathological changes
Clinical features (typical
presentation)
There are no typical demographic features of people
who sustain MCL injuries.
MCL injuries usually occur as a result of a valgus stress to
a partially flexed knee.
MCL injuries are classified on the basis of their severity:
Grade I – mild, first degree
Grade II – moderate partial ruptures, second degree
Grade III – complete tear, third degree
Grade III MCL injuries are often associated with a torn
ACL. The lateral meniscus can also be injured as the
valgus strain at the time of injury opens the medial side
and compresses the lateral side of the knee joint.
Typical features on examination:
Grade I:
- Local tenderness over MCL but
usually
no swelling
- Pain on valgus strain applied at 30 degrees knee
flexion, but no increased laxity (the ligament
integrity is intact)
Grade II:
- Marked tenderness and sometimes
localised swelling
-
Valgus stress applied at 30 degrees
knee flexion causes pain and some
increased laxity, but a definite end feel
(ligament integrity is compromised but
intact)
Grade III:
- Patient complains of feelings of instability in the
knee
- Amount of pain is variable, and often not as
severe as would expect given the severity of the
injury
- Tenderness over the ligament
- Valgus stress at 30 degrees knee flexion reveals
gross laxity without a distinct end point/end feel
Medical management (if
applicable)
Surgical management offers no benefit over non-surgical
management, thus non-surgical treatment is
recommended.
See Brukner and Kahn, chapter 35 pg 730-731 for
rehabilitation programmes for mild and moderate to
severe MCL injuries.
Clinical course/prognosis
Distal MCL injuries tend to recover more slowly than
proximal MCL injuries.
Grade I MCL injuries – people can usually return to sport
within 4 – 6 weeks.
Grade II – III MCL injuries – people can usually return to
sport within 10 – 12 weeks.
Ankle lateral ligament injury
Risk factors
Aetiology (cause)
Pathological changes
These injuries most commonly occur during rapid
changes in direction, or walking over uneven surfaces,
or landing on another person’s foot when jumping.
The usual mechanism of injury for a lateral ankle
ligament sprain is inversion and plantarflexion.
Damage can occur to the anterior talofibular ligament
(ATFL), the calcaneofibular ligament (CFL), the posterior
talofibular ligament (PTFL). However isolated ruptures
of the CFL and the PTFL are rare.
The ATFL is usually damaged first because: 1) the ATFL is
taut in plantarflexion whereas the CFL is relatively loose
and 2) the ATFL is weaker than the CFL.
Complete rupture of the ATFL, CFL and PTFL results in
dislocation of the ankle.
As for MCL injuries, lateral ankle ligament sprain injuries
are graded I, II and III.
Clinical features (typical
presentation)
Patients who have sustained an ankle sprain usually
report an audible snap, crack or tear (as opposed to a
‘pop’ which can happen in knee ligament injuries).
Depending on the severity of the injury, the athlete may
be able to continue playing (eg. grade I/mild sprain) or
may have to stop immediately (eg. grade II or III/mod –
severe sprain).
All three grades are associated with pain and tenderness
and varying degrees of swelling, limitations in ROM and
varying ability to weight bear.
Special tests and investigations
Ligament laxity is assessed using the anterior drawer
and talar tilt test (see Brukner and Kahn, pg 897 and
898). Note that these manual stress tests are more valid
when performed 5-7 days post injury (keep in mind the
limitations with ‘special tests’ – see chapter 14 Brukner
and Kahn)
Grade I – normal ligament laxity (remember to compare
sides as there is a large individual variation in normal
ankle laxity)
Grade II – some laxity but a firm end feel
Grade III – gross laxity without a discernible end feel
Medical management (if
applicable)
Note: because ankle fractures can happen via the same
injury mechanism it can be difficult to differentiate a
fracture from a moderate to severe ankle sprain.
According to the Otawa ankle rules, tenderness on
palpation at the lower posterior 6cm of the medial or
lateral malleolus as well as the inability to weight bear
both immediately and at the time of clinical examination
indicates the need for an ankle x-ray in order to check
for the presence of an ankle fracture. (see Brukner and
Kahn, Chapter 41, Fig 41.4, pg 898)
Surgical interventions for Grade III injuries offer no
benefit over non-surgical rehabilitation.
Initial management of lateral ankle ligament injuries
follow the POLICE principles:
P – protection
OL – optimal loading
I- ice
C- compression
E- elevation
(see Brukner and Kahn chapter 17, pg 247)
Management or all grades of lateral ankle ligament
injuries follow the same principles:
Weight bearing as tolerated (may need crutches, but
aim to at least partial weight bear with a heel-toe gait as
soon as possible)
Reduction of pain and swelling
Restoration of range of motion (active and passive
ROM exercises; accessory movilisations of the ankle,
subtalar and midtarsal joints should begin early)
Muscle strengthening (DF, PF, Inv and Ev as soon as
pain allows)
Proprioception exercises
Functional exercises (eg. jumping, hopping, running)
can begin once pain free, has full ROM and adequate
strength and proprioception
Clinical course/prognosis
Return to sport when functional exercises can be
performed without pain during or after activity
There is an increased risk of reinjury for 6 – 12 months
following lateral ankle ligament sprains. Both
neuromuscular training and bracing or taping may help
prevent ankle injury recurrence. Note that it takes 8 –
10 weeks for intensive neuromuscular training
programmes to achieve an effect.
75% of people who sustain an ankle sprain have had a
previous ankle injury (often the old injury was not fully
rehabilitated).
Sprain of the Ulnar Collateral Ligament of the thumb (Skiers Thumb/Gamekeepers thumb)
References:
Ritting AW, Baldwin PC, Rodner CM. Ulnar Collateral Ligament Injury of the Thumb
Metacarpophalangeal Joint. Clin J Sport Med. 2010. 20(2):106-112.
Brukner et al. Brukner and Kahn’s Clinical Sports Medicine. 5th edition. McGraw Hill
Education. 2017. Pages 499-501.
Epidemiology (incidence,
prevalence)
Aetiology (cause)
Pathological changes
Estimated to account for 86% of all injuries of the base of the
thumb
Damage to the ULC can be caused by either chronic repetitive
valgus stress of the thumb or an acute hyperabduction trauma,
for example skier falling on abducted thumb with ski pole in
hand (hence “Skiers Thumb”), or in sports requiring holding a
stick.
The UCL comprises of a proper collateral ligament (which is
taut in flexion) and an accessory collateral ligament (which is
taut in extension of the thumb).
UCL injuries can be categorised into 3 grades:
Grade I: Stretched but intact ligament
Grade II: Partial tear of the ligament
Grade III: Complete rupture of the ligament.
Bony avulsion fractures at the distal attachment of the UCL
occur in 20 – 30% of ULC ruptures.
Clinical features (typical
presentation)
A Stener lesion may occur in 64 – 87% of Grade III UCL lesions.
This is where the proximal end of the UCL retracts and ends up
lying superficial to the adductor pollicis aponeurosis. The
interposition of the aponeurosis between the proximal and
distal ends of the UCL interferes with healing.
The patient usually describes a specific event of
hyperextension and radial deviation of the thumb.
Swelling and local tenderness at the base of the thumb may be
present.
They may have difficulty pinching objects between the thumb
and index finger due to instability of the first MCP joint.
The UCL integrity is evaluated by stress testing of the MCP
joint of the thumb, whereby a radial force is applied in neutral
(to test the accessory collateral ligament) and 30 degrees of
flexion (to test the proper collateral ligament). Laxity of
greater than 15 degrees with a soft end feel compared to the
Special tests and
investigations
Medical management (if
applicable)
Clinical course/prognosis
contralateral thumb is an indication of a complete rupture.
Laxity of less than 15 degrees indicates an incomplete tear.
An x-ray is required to rule out an avulsion fracture.
Surgical repair is usually required for complete tears of the
UCL, especially when a Stener lesion has occurred.
Incomplete tears are splinted for 6 weeks in a thumb spica
with the thumb MCP joint placed in slight radial deviation,
after which a splint weaning and active ROM exercises are
initiated with strengthening exercises being introduced at 8 –
10 weeks post injury.
Protective splinting or taping for 2-3 months is recommended
on return to play.
Post-surgical rehabilitation is similar to management for
incomplete tears.
Muscle Injuries: Muscle Tears
A muscle tear occurs where excessive tensile and/or shear forces within the muscle cause
the muscle fibres and the surrounding connective tissue to fail.
Historically, the grading of muscle tears has involved a three-tier system;
Grade 1 – Mild. No appreciable tissue tearing; no loss of function or strength; only a lowgrade inflammatory response
Grade 2 – Moderate. Tissue damage; strength of the musculotendinous unit reduced; some
residual function
Grade 3 – Severe. Complete tear of musculotendinous unit and complete loss of function
More recently, the British Athletics Classification system has been developed:
Injuries are graded 0–4 based on MRI features, with Grades 1–4 including an additional
suffix ‘a’, ‘b’ or ‘c’ if the injury is ‘myofascial’, ‘musculotendinous’ or ‘intratendinous.’
0a = focal neuromuscular injury with normal MRI features
0b = generalised muscle soreness (DOMS) with normal MRI features
1 = small injuries (tears)
2 = moderate injuries (tears)
3 = extensive tears
4 = complete tears
a = myofascial injury
b = within muscle, usually at musculotendinous junction (MTJ)
c = extends into tendon
Useful resources
Brukner & Khan's clinical sports medicine: injuries
Peter Brukner; Karim Khan
5th edition. North Ryde, N.S.W. McGraw-Hill Education Australia 2016 (on reserve)
Therapeutic Exercise Foundations and Techniques Foundations and Techniques
Carolyn Kisner; Lynn Allen Colby
6th ed. Philadelphia: F. A. Davis Company 2012 (on reserve and e-book) Chapter 10
British Journal of Sports Medicine 2014; 48 1335-1335 Published Online First: 20 Aug
2014. doi:10.1136/bjsports-2014-094005
Quadriceps tear
Epidemiology (incidence,
prevalence)
Demographic features (age, sex,
ethnicity etc.)
Risk factors
Aetiology (cause)
Pathological changes
Clinical features (typical
presentation)
Special tests and investigations
Most prevalent in males
Increased susceptibility over aged 40
Quadriceps tendon ruptures have a reported
incidence of 1.37/100,000
Most commonly occur in middle aged people who
participate in running or jumping activities.
Quadriceps tendon ruptures in non-athletes are
usually the direct result of a fall or other trauma in
individuals with predefined medical comorbidities
which cause pathologic tendon degeneration.
Age
Certain morbidities including obesity; diabetes;
rheumatoid arthritis; gout
A quadriceps tear typically occurs when there is a
heavy load on the leg with the foot planted and
the knee partially bent. E.g. landing awkwardly
from a jump or when decelerating during sprinting
or agility sports, such as hurdling.
Tears can also be caused by falls, direct force to
the front of the knee, and lacerations (cuts) or by
the presence of chronic disease which weakens the
tendon.
See the Stages of Tissue Healing table 10.1 p.317
Kisner and Colby
End-stage renal disease patients on dialysis have the
highest association with tendon degeneration
resulting in ruptures. As renal function declines,
there is a resulting homeostatic imbalance of calcium,
phosphorus, vitamin D, and parathyroid hormone.
The elevated parathyroid hormone results in
increased bone turnover. Over time, this is thought to
weaken myotendinous junctions, resulting in
increased potential for tendon rupture with minimal
tensile stress.
Pain
Bruising/swelling
Tenderness
Difficulty walking
Inability to actively extend the knee
The diagnosis may be confirmed by x-ray or MRI scan.
Medical management (if
applicable)
Clinical course/prognosis
Video





REST
Knee brace/immobiliser
Stretching/flexibility exs
ROM and strengthening exercises
Surgical repair will be necessary for a
complete, or large, partial tear
Most people are able to return to their previous
occupations and activities after recovering from a
quadriceps tendon tear. Approximately 50% of
people have persisting thigh weakness and
soreness at the site of the tear.
https://www.youtube.com/watch?v=yoyz5GFd00M
Hamstring tear
Epidemiology (incidence,
prevalence)
Demographic features (age, sex,
ethnicity etc.)
Risk factors
Aetiology (cause)
Typically occurs during sporting activities; in
particular, football, sprinting and hurdling.
The reported injury rate varies (due to differing injury
definitions and sporting populations); however, the
reported prevalence in the various types of football,
to which most literature pertains, is 8% to 25%.
Re-injury is common, with rates in excess of 30%.
More likely to affect those over 25; black athletes are
more affected.
 Poor running mechanics
 Inadequate warm-up
 Muscle tightness
 Muscle imbalance
 Muscle weakness
 Inappropriate training loads/muscle fatigue
 Type of activity
 Slippery playing surfaces
Muscle overload is the main cause of hamstring
muscle tear. This can occur when the muscle is
stretched beyond its capacity or challenged with a
sudden load.
Hamstring muscle strains (tears) often occur when
the muscle is contracting eccentrically, for
example, during sprinting. The hamstring muscles
contract eccentrically as the back leg is
straightened and the toes are used to push off and
move forward. At this point, the hamstring muscles
Pathological changes
Clinical features (typical
presentation)
are both lengthened and loaded — with body
weight as well as the force required for forward
motion.
See the Stages of Tissue Healing table 10.1 p.317
Kisner and Colby






Sudden sharp pain in the back of the thigh
Pain in the back of the thigh/lower buttock on
walking, bending over or straightening the leg.
Swelling
Bruising
Tenderness
Persistent weakness
Hamstring tears are categorised into 3 groups:
Grade 1 tear
-
Mild swelling and spasm
Tightness in the back of the thigh but will be
able to walk normally.
Awareness of some hamstring discomfort and
unable to run at full speed.
Minimal pain on resisted knee flexion
Grade 2 tear
-
Walking pattern affected with possible limp
Twinges of hamstring pain during activity.
Possible swelling and tenderness on palpation
Pain on resisted knee flexion
Grade 3 tear
-
-
Special tests and investigations
Medical management (if
applicable)
Severe pain and muscle weakness
May require crutches
Immediate swelling post-injury with the
appearance of bruising with 24 hours
Patient history and physical examination may be
sufficient to provide a diagnosis.
X-ray or MRI scan may be used to confirm diagnosis
and determine location and extent of tear.
 REST
 Knee brace/immobiliser
 Stretching/flexibility exs
 ROM and strengthening exercises

Clinical course/prognosis
Video
Surgical repair will be necessary for a
complete, or large, partial tear
Aims of management:
 Reduce hamstring pain and inflammation.
 Normalise your muscle ROM and
extensibility.
 Strengthen quads and hamstrings.
 Strengthen calves, hip and pelvis muscles.
 Normalise lumbo-pelvic control and stability
 Normalise neurodynamics to enable sciatic
nerve to pass freely without scar adhesions.
 Improve game speed, proprioception, agility
and balance.
 Improve technique and function e.g. running,
sprinting, jumping, hopping and landing.
 Minimise risk of re-injury.
The majority of people will make a full functional
recovery following rehabilitation .
Recovery times based on the extent of the tear:
Grade 1 - 1 to 3 weeks
Grade 2 - 4 to 8 weeks
Grade 3 - 3 to 6 months. These may also require
surgery.
https://www.youtube.com/watch?v=CubBXSt_NRw
Biceps tear
Biceps-related pathologies are a common cause of shoulder pain and loss of function; it can
result in work limitations and affect athletic performance.
There are three categories of biceps-related shoulder pain:
1) Inflammatory/degenerative conditions and partial tears of long head of biceps
2) Instability of biceps tendon into the bicipital groove
3) Superior labrum anterior to posterior (SLAP) lesions
Epidemiology
(incidence,
prevalence)
Demographic
features (age, sex,
ethnicity etc.)
Risk factors
Aetiology (cause)
The incidence of biceps tendon rupture is around 2.55 per 100,000
patient-years.
Most cases are in males (over 95%); likely due to vocational activities.
Rupture is most common in adults over 50 but can also occur in
younger athletes.
 Participation in overhead activities such as throwing
 Poor conditioning
 Age over 40
 Smoking
 Use of corticosteroids
 Overuse/recurrent tendonitis
 History of rotator cuff tear
 Contralateral biceps tendon rupture
 Rheumatoid arthritis
 Single traumatic events, such as a fall onto an outstretched
arm
Biceps tendon rupture is mainly attributed to a sudden eccentric load
on the flexed and supinated forearm, which can result in rupture of
the tendon proximal and distal attachments.
Most common mechanisms of injury to the superior labrum are
throwing injuries or carrying, dropping or caching heavy objects. The
late cocking and follow through phases of throwing place the
greatest forces on the shoulder.
https://orthoinfo.aaos.org/en/diseases--conditions/shoulderinjuries-in-the-throwing-athlete/
Pathological
changes
See the Stages of Tissue Healing table 10.1 p.317 Kisner and Colby
Age, overuse, smoking, and corticosteroid contribute to tendon
degeneration and later, tendinopathy. A sudden eccentric load may
break tendon structures, mostly involving the bony attachment or
tendon-labral junction.
Clinical features
(typical
presentation)
In SLAP lesions:
 Pain localised to posterior or postero-superior joint
line, especially in abduction.
 Pain exacerbated by overhead or behind-the-back
motion
 Tenderness over anterior aspect of shoulder
 Pain on resisted biceps contraction
In proximal biceps tendon rupture:



Special tests and
investigations
Bulbous mass in the upper arm with a visible gap proximal to
the mass (Popeye sign)
Pain on resisted flexion or supination.
Tenderness at the superior margin of the muscle belly.
Partial ruptures may present with similar, but more subtle,
symptoms. There may be delayed diagnosis due to less significant
weakness or obvious deficit on palpation.
Special tests:
Speed test
O’Brien test
Passive compression test
Biceps load II test
(see page 394 Brukner & Khan for more detail)
Hook test:
https://www.youtube.com/watch?time_continue=4&v=YsqdHsuLgC4
Yergason’s test - positive if pain is reproduced in the bicipital
groove during the test
Medical
management (if
applicable)
Ultrasound is an inexpensive, non-invasive diagnostic tool.
Diagnostic arthroscopy will confirm SLAP lesion.
Conservative management of long head of biceps rupture takes 4-6
weeks on average. Non-operative management is appropriate for
those who do not require a high level of supination strength, and
may also be considered for subacute or chronic tendon tears.
Rehabilitation should follow a phased progression of rotator cuff
exercises; scapular exercises; and stretching.
A progressive loading programme should be introduced from week 2.
Arthroscopic repair has excellent outcomes for those not involved in
sports.
In overhead athletes, surgical results are less predictable with rates
of return to previous level of play between 20% and 94%.
Clinical
course/prognosis
Timely diagnosis and successful operation are the keys to correct
muscle deformity and to regain strength or forearm supination and
flexion.
Gastrocnemius tear
Calf muscle tears usually occur during acceleration, when extending the knee from a
stationary position with the ankle dorsiflexed, or during a forward lunge, such as while
playing tennis or squash. There is a small percentage of the population who can tear their
calf muscle by just walking.
The most common calf muscle torn is the medial gastrocnemius; mid-belly calf muscle tears
are most common. The gastrocnemius muscle is more susceptible to injury as it is
extends over the knee and ankle.
Epidemiology (incidence, prevalence)
Demographic features (age, sex, ethnicity
etc.)
Risk factors
Aetiology (cause)
Calf muscle tears are relatively common
and most often seen in sports which
require quick acceleration and changes in
direction such as tennis, running, jumping
and football. A calf muscle tear is also
termed “tennis leg” due to the
prevalence amongst tennis players.
There are limited studies documenting
rates of calf muscle tears; a 5-year study of
European soccer players found that 12% of
total muscle injuries sustained were injuries
to the gastrocnemius.
Young athletes are commonly affected; as
are those over the age of 40 participating in
physically demanding activities.
Increasing age and previous calf tear are
the biggest predictors of future calf tear.
Running on hills
Forced push-off activities(jumping)
Tennis
Injury can be caused sudden bursts of
acceleration as well as a sudden eccentric
overstretch of the gastrocnemius. During
certain sports, the gastrocnemius is
subject to high internal forces, plus rapid
changes in muscle length and type of
contraction.
Pathological changes
Clinical features (typical presentation)
See the Stages of Tissue Healing table 10.1
p.317 Kisner and Colby
The typical presentation depends on the
extent of the muscle tear.
Grade I:
 Sharp pain in the back of the calf
muscle during or after activity
 Muscle tightness
 Ability to continue activity,
without pain or with
 mild discomfort
 Post activity tightness and/or
aching
 Reproduction of pain on unilateral
heel raise or hop
Grade II:
 Sharp pain in the back of the calf
muscle during activity
 Unable to continue activity
 Significant pain with walking
following activity
 Mild to moderate bruising/swelling
 Pain with active plantarflexion
 Pain and weakness with resisted
 plantarflexion
 Loss of dorsiflexion
 Reproduction of pain on bilateral
heel raise
Special tests and investigations
Medical management (if applicable)
Grade III (complete rupture):
 Sudden severe calf pain, often at
musculotendinous junction
 A ‘pop’ sound at the time of injury
 Unable to continue with activity
 Considerable bruising and swelling
within hours of injury
 Unable to contract calf muscle
 Palpable defect in medial belly of
the muscle and tenderness on
palpation
Diagnostic ultrasound imaging
Magnetic resonance imaging (MRI)
Treatment and rehabilitation depends on
the severity of the muscle strain.





Clinical course/prognosis
RICE
Regain ROM and flexibility
Restore concentric muscle strength
Restore eccentric muscle strength
Restore speed, power, agility and
proprioception
Return to sport – dependent on grade of
tear:
Grade 1 – 10-12 days
Grade 2 – 16-21 days
Grade 3 – 6 months post-surgery
There is a risk of re-injury and, additionally,
there may be ongoing pain and limited
function in the long term.
Tendon injuries
Tendonitis, tendinopathy and tendinosis are all tendon overuse injuries. They typically occur
in three areas: the musculo-tendinous junction; the mid-tendon (non-insertional
tendinopathy); or the tendon insertion (insertional tendinopathy).
Non-insertional tendinopathies tend to be caused by a cumulative microtrauma from
repetitive overloading e.g. overtraining.
The majority of tendon injuries occur near joints, such as the shoulder, elbow, knee, and
ankle. The may present as a sudden injury but are often the result of repetitive tendon
overloading.
Tendonitis is inflammation of the tendon. Tendonitis can become chronic if whatever the
cause of the inflammation is not addressed. Mostly, it is temporary and curable with a few
weeks’ treatment.
Tendinosis is a non-inflammatory degenerative condition that is characterised by collagen
degeneration in the tendon due to repetitive overloading. This type of injury does not
respond well to anti-inflammatory treatments and is best treated with functional
rehabilitation. Early diagnosis and intervention provides the best outcome in terms of
recovery.
Tendon tear or rupture is unusual in a healthy tendon. Where tear or rupture occurs there
is usually an underlying pathology (such as tendinosis), that may be asymptomatic. The two
most commonly ruptured tendons are the Achilles tendon and supraspinatus tendon.
Useful resources
Brukner & Khan's clinical sports medicine: injuries
Peter Brukner; Karim Khan
5th edition. North Ryde, N.S.W. McGraw-Hill Education Australia 2016 (on reserve) p.46-51
Therapeutic Exercise Foundations and Techniques Foundations and Techniques
Carolyn Kisner; Lynn Allen Colby
6th ed. Philadelphia: F. A. Davis Company 2012 (on reserve and e-book)
Epidemiology (incidence, prevalence)
Demographic features (age, sex, ethnicity
etc)
Risk factors
Aetiology (cause)
Pathological changes
Tendon injuries cost ACC more than $280
million a year.
Men are more affected than women.
Lower limb tendon ruptures occur more
frequently in middle-aged and older
athletes.
Age
Overtraining
Repetitive activities
Exercise/sports
Conditions that affect rate of healing/repair
process. E.g. diabetes
Most tendon overuse injuries result from
gradual wear and tear to the tendon from
overuse or ageing. Repetitive actions are
more likely to damage a tendon.
Tendon tissues are predominantly
extracellular and have a low metabolic rate.
Therefore the vascularity and healing
capability of tendons is much lower than
other tissues.
Tendons have great tensile strength and
are designed to withstand high, repetitive
loading. However, a rapid increase, or
sudden change, in load being applied to the
tendon can result in small micro tears, and
the cumulative microtrauma appears to
exceed the tendon’s capacity to heal and
remodel.
Clinical features (typical presentation)
The damage will progressively become
worse, causing pain and dysfunction. In the
long run this can result in tendinopathy or
tendinosis.
Tendon overuse injuries
 Increasing pain on using the
affected tendon (may be pain-free
at rest)
 Pain/stiffness at night or first thing
in the morning
 Ability to ‘run through’ the pain
 Local tenderness and/or thickening
 Swelling over the affected area
 Crepitus when moving the affected
tendon
Special tests and investigations
Medical management (if applicable)
Tendon rupture(partial or complete)
 Partial rupture = sudden onset of
pain; localised tenderness; loss of
tendon function relative to the size
of tear
 Complete rupture = acute pain
which often settles quickly; total
loss of tendon function
Degree of tendon rupture can be confirmed
by ultrasound or MRI scan.
Physiotherapy management of tendon
overuse injury:





PRICE (protection; rest; ice;
compression; elevation).
Stage 1: Isometric exercise
Stage 2: Isotonic exercise
Stage 3: Energy storage exercise
Stage 4: Sport-specific energy storage
and release exercise
Physiotherapy management of tendon
rupture:


Clinical course/prognosis
Partial ruptures may be managed
conservatively with graded
rehabilitation
Complete ruptures require surgical
repair
Depends on the degree of injury and
tendon involved (see below)
Achilles tendinopathy
Useful resources
https://www.physio-pedia.com/Achilles_Tendinopathy
https://www.physio-pedia.com/Achilles_Tendinopathy_Toolkit
Epidemiology (incidence, prevalence)
May be insertional (25% of cases) or noninsertional (75% of cases).
Insertional Achilles tendinopathy reported
in 7-18% of runners and 9% of dancers.
Most common amongst those participating
in sport or recreational activities.
More common in males than females.
Mean age affected in 30-50 years.
Risk factors include abnormal
biomechanics; obesity; poor training
technique
Exact cause is unknown but it believed to
be overuse combined with mechanical
overload and patient susceptibility.
Pain and tenderness over mid-portion of
Achilles tendon (non-insertional)
Pain and tenderness at Achilles tendon
insertion on calcaneus (insertional)
Clinical diagnosis usually established on
history and physical examination.
This may include the following tests:
Demographic features (age, sex, ethnicity
etc.)
Risk factors
Aetiology (cause)
Clinical features (typical presentation)
Special tests and investigations
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Achilles Tendon Palpation Test may
detect tenderness 2-6 cm above Achilles
insertion
Royal London Hospital test
1) positon the ankle at maximal
dorsiflexion, palpate area and classify as
positive or negative for tenderness
2) this may elicit tenderness 3 cm proximal
to calcaneus when the ankle is in slight
plantar flexion, with tenderness decreasing
as ankle is moved into dorsiflexion
X-ray, ultrasound or MRI may be used when
history and physical examination are
inconclusive.
Medical management (if applicable)
Conservative management in the form of
ice and non-steroidal anti-inflammatories
(NSAIDs).
For non-insertional Achilles tendinopathy,
rest and activity modification is advised,
with a strong recommendation for an
eccentric loading exercise programme.
For insertional Achilles tendinopathy, a
brief period of immobilisation is
recommended. Eccentric loading may not
be as effective in this presentation.
Clinical course/prognosis
Taping or orthoses may also be considered.
The majority of patients with Achilles
tendinopathy respond well to conservative
treatment with 71%-100% returning to
previous levels of activity with few or no
complaints.
Approximately 30% of patients with
Achilles tendinopathy who are initially
treated conservatively may require
surgery in the long-term.
4% of adults diagnosed with Achilles
tendinopathy may ultimately sustain an
Achilles tendon rupture.
Achilles tendon rupture (complete)
Useful resources
Brukner & Khan's clinical sports medicine: injuries
Peter Brukner; Karim Khan
5th edition. North Ryde, N.S.W. McGraw-Hill Education Australia 2016 (on reserve) p.889892
https://www.physio-pedia.com/Achilles_Rupture
Epidemiology (incidence, prevalence)
Demographic features (age, sex, ethnicity
etc.)
Risk factors
Aetiology (cause)
Clinical features (typical presentation)
Special tests and investigations
Incidence is 5-36 per 100,000.
60-90% of Achilles ruptures occur during
sports
Typically affects athletes in 30s-40s
Males 10 times more affected than females
Previous Achille’s rupture
Other major tendon rupture
Recent local corticosteroid injection
Type 2 diabetes
Typically occurs when a quick change in
direction is performed and the ankle is
forced into dorsiflexion while the calf
contracts.
 Sensation of being kicked in the
back of the leg
 Immediate and gross reduction in
function
 Difficulty walking initially
 Ability to resume walking but with
no power in push-off phase
 Pain may not be the key feature
Calf squeeze test (Simmond’s or
Thompson’s test) has high specificity and
sensitivity for diagnosis.
Other tests include Matle’s test; Copeland’s
test and palpation test for a gap in the
tendon.
Medical management (if applicable)
The Achilles tendon total rupture score
(ATRS) is a patient-reported outcome
measure for evaluating outcomes postAchille’s tendon rupture
Open surgical repair has a 10% lower risk of
re-rupture compared with conservative
management.
Clinical course/prognosis
Video
A short period of rigid cast followed by a
functional brace post-surgery indicates that
early mobilisation reduce re-rupture rates
without increased risk of other
complications when compared with rigid
cast immobilisation.
Only 30-40% of athletes return to pre-injury
level due to long term deficits in strength
and function.
Complications that persist include calfmuscle weakness; tendon elongation and
gait abnormalities.
For more information on Achilles tendon
repair:
https://www.physiopedia.com/Achilles_tendon_repair
Rotator cuff tears
Epidemiology (incidence,
prevalence)
Demographic features (age, sex,
ethnicity etc.)
Risk factors
Aetiology (cause)
Pathological changes
Rotator cuff injuries may be traumatic, for
example as result of sports injury, or degenerative.
The incidence of rotator cuff tears is 25% in people
over 60; and 50% in people over 80. The cost of
rotator cuff repairs in New Zealand in 2015/2016
including surgical and physiotherapy costs was
over $32 million. Tears many be partial-thickness
(incomplete) or full-thickness (complete).
The most commonly torn rotator cuff tendon is the
supraspinatus.
There is a great incidence of tears in older age
groups; the mean age is 58. Rotator cuff tears
tend to affect more females than males with 66%
occurring in females.
Risk factors include age, smoking, and
participation in repetitive overhead activities,
either recreational or occupational.
Cause may be traumatic or degenerative.
In the case of degenerative tears, age related
factors include reduced tissue vascularity; and the
presence of hypocellularity, fascicular thinning and
granulation tissue at microscopic level.
Clinical features (typical
presentation)
Special tests and investigations
Shoulder pain; in particular, pain localised to the
anterolateral aspect.
Night pain with inability to sleep on the affected
side.
Signs and symptoms include supraspinatus
weakness, with pain exacerbated when the arm is
abducted beyond 90o. There may also be
weakness into external rotation and impingement
in those over 60.
There are a number of diagnostic tests available.
The full can test and empty can test (Jobe’s test)
both have high specificity and sensitivity for
diagnosis of a supraspinatus tear.
The lag sign and Hornblower’s sign both have high
specificity but low sensitivity for diagnosis of an
infraspinatus tear; these are, therefore, of use
where the test yields a positive result, indicating a
high likelihood of a rotator cuff tear.
To view how these tests are carried out:
https://www.youtube.com/watch?v=cRWokjKttm8
Medical management (if applicable)
Clinical course/prognosis
X-rays and MRI scan may be used in assisting with
diagnosis.
Non-operative management includes:
 rest and activity modification or 1-2 weeks
but avoidance of shoulder immobilisation
 NSAIDs
 Exercise therapy to improve pain and
increase function
Tendon repair may be considered taking account
of the following factors:
 Size of tear
 Patient characteristics inc. age; occupation;
level of activity (e.g. elite athlete);
symptom severity
 Response to prior non-operative treatment
Typically, incomplete tears do not heal but
symptoms may settle.
The risk of tear progression is increased in those
who are older, had a larger tear initially and where
there was no traumatic mechanism of injury.
Re-tear occurs in about 19% of surgically repaired
tendons at 6 months.
85% of all athletes return to sport after repair of
rotator cuff tears, but only 50% of professional
and competitive athletes return to their preinjury level of play after 4-17 months.
Lateral elbow tendinopathy
Lateral elbow tendinopathy (commonly referred to as tennis elbow) is an acute or chronic
tendinopathy of the common extensor origin at the lateral epicondyle of the elbow. The
musculotendinous junction of extensor carpi radialis brevis is most commonly affected.
It can also be known as: lateral epicondylitis; lateral epicondylosis; lateral epicondylalgia;
tendonitis of the common extensor origin; extensor tendinosis at the elbow; peritendinitis
of the elbow; or rowing elbow.
Useful resources
Brukner & Khan's clinical sports medicine: injuries
Peter Brukner; Karim Khan
5th edition. North Ryde, N.S.W. McGraw-Hill Education Australia 2016 (on reserve) p. 443450
https://www.physio-pedia.com/Lateral_Epicondylitis
https://www.physio-pedia.com/Lateral_Epicondyle_Tendinopathy_(Tennis_Elbow)_Toolkit
Epidemiology (incidence, prevalence)
It occurs in approximately 1-3% of adults.
Demographic features (age, sex, ethnicity
etc.)
It most commonly occurs in middle age;
peak incidence being between 40 and 60
years of age.
Occupational or recreational activities
involving repetitive movement of the arm.
Examples include:
 Fine, repetitive hand and
wrist movements, such as using scissors
or typing.
 Repeatedly bending the elbow, such as
playing the violin, cutting with a knife or
using a paintbrush.
 Twisting or gripping movements such as
holding a pen or using a screwdriver.
 Playing racquet sports, such as tennis,
badminton or squash.
Risk factors

Aetiology (cause)
Pathological changes
Clinical features (typical presentation)
Special tests and investigations
Throwing sports, such as the javelin or
discus.
 Sudden overuse of upper extremity in
previously sedentary persons
Overexertion of the common extensor
tendon at the lateral epicondyle of the
elbow, often due to repetitive wrist
extension and supination
In chronic lateral elbow tendinopathy, the
persistent cycle of repetitive or excessive
tendon loading leads to tissue microtrauma and degenerative changes in the
origin of the common extensor tendon.
Histologic observations of the degenerative
tendon demonstrate non-inflammatory,
angio-fibroblastic hyperplasia; formation of
new blood vessels; and collagen scaffold
disruption by fibroblasts and vascular
granulation tissue.
 Pain, which is often sharp, in the
lateral aspect of the elbow. Onset is
usually insidious
 Pain with active extension of the
wrist or supination of the forearm
 Difficulty or discomfort when lifting
or holding objects
 Tenderness at lateral epicondyle
 Weakened hand grip on affected
side
Diagnosis is usually based on history and
physical findings, including:




insidious onset of pain over lateral
aspect of elbow that may impair
functional tasks
Pain on resisted wrist or third finger
extension with extended elbow and
forearm pronated
Pain on passive wrist flexion with
the elbow extended
Tenderness at or near lateral
epicondyle (maximum tenderness
usually observed just anterior and
distal to lateral epicondyle)


Medical management (if applicable)
A combination of treatments is usually
most effective.

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
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Clinical course/prognosis
Imaging is usually not required to make a
diagnosis. It may be considered to rule
out alternative diagnoses.
The extent of tendon pathology on MRI
does not appear to correlate with
patient-reported symptom severity or
functional impairment in adults with
lateral epicondylitis.
Rest and activity modification as first-line
management.
Electrotherapeutic modalities (e.g.
ultrasound; TENS)
Graduated exercise to improve strength
and endurance +/- stretching
Elbow mobilisation with movement
(MWM)
Acupuncture
Taping
Graduated return to activity
Approximately 70%-95% of patients will
have resolution of symptoms within 12
months with conservative treatment.
De Quervain’s tenosynovitis
Useful resources:
Brukner & Khan's clinical sports medicine: injuries
Peter Brukner; Karim Khan
5th edition. North Ryde, N.S.W. McGraw-Hill Education Australia 2016 (on reserve) p.476477
https://www.healthinfo.org.nz/index.htm?living-with-de-quervains-tenosynovitis.html
Epidemiology (incidence,
prevalence)
Demographic features
(age, sex, ethnicity etc)
Risk factors
Aetiology (cause)
Pathological changes
Clinical features (typical
presentation)
This is a common wrist tendon entrapment syndrome in
which gliding of the abductor pollicis longus and the
extensor pollicis brevis tendons is restricted within the first
dorsal compartment.
The estimated prevalence is 1.3% of females and 0.5% of
males.
It affects women more than men with middle aged women
most commonly affected.
Risk factors include:
 female
 aged over 40
 occupational or recreational activities involving
repetitive radioulnar deviation, such as golf and
racquet sports
 a previous wrist injury
 inflammatory arthritis
 pregnancy
 the post-partum period
 lifting up a baby
o The cause is unknown but factors that may contribute
include chronic trauma to the first dorsal compartment
tendons; anatomical abnormalities; increased frictional
forces; biomechanical compression; scarring; and
increased fluid volume (such as during pregnancy).
There is deposition of dense fibrous tissue with thickening
of tendon sheaths (up to 5 times that of normal thickness)
and increased vascularity of tendon sheaths.
 Pain centralised over radial aspect of wrist; may
radiate into forearm and thumb
 Swelling just proximal to radial styloid
 Tenderness on palpation over first dorsal
compartment
 Impaired function of the affected hand

Special tests and
investigations
Aggravating factors include gripping; wringing;
twisting; lifting
 Generally relieved by rest and immobilisation
History and physical examination assist with diagnosis.
Tests to assist include in diagnosis:
 Eichhoff test.
https://www.youtube.com/watch?v=l_9Suv0xhmY

Medical management (if
applicable)
Clinical course/prognosis
Finkelstein test.
https://www.youtube.com/watch?v=8WBVXBx34W0
Imaging is not routine but may be used if additional
pathology is suspected or to assist with differential
diagnosis if there is clinical uncertainty.
Physiotherapy treatment includes:
 Splinting including night splints
 NSAIDs
 Corticosteroid injection
 Localised electrotherapeutic modalities
 Stretching
 Graduated strengthening
 Use of pen build up/golf grip to reduce stretch on
extensor tendons
 Avoidance of aggravating activities/activity
modification during recovery phase
The majority of people experience complete resolution of
symptoms within a few months with corticosteroid injection
effective in settling symptoms in 70 to 80% of cases.
Osteoarthritis
See the attached document for an overview of OA and chapter 30 of Magee:
clinical conditions 255\Osteoarthritis.pdf