Thursday, August 30, 2007

Tendenopathy definition and incidence

Rotator Cuff Tendinopathy-RCT-is a common cuase of painful restriction of the shoulder at all ages and affects about 1 in 50 adults and is particularly common in athletes who throw repetitively, swimmer and laborers who work with their arms over their heads.
o third most common musculoskeletal disorder after back and neck pain
o increases in incidence in those 60 years and over.
o 8-15% of athletic injuries involve the shoulder, and shoulder instability is very common in young athletes, nto so much in older ones
o It follows trauma in 30% of cases and is bilateral in only 5%
o Prevalence of shoudler diseases reported to range from 7-36% in general population, and shoulder complaints account for 1.2% of all GP encounters in Australia

It is ultimately the repeated impingement of the coroacromial arch onto the supraspinatus tendon that has been implicated as the likley mechanism of tendon injury, as the supraspinatus complex occupies a narrow space with light contact between supraspinatus and the coroacromial arch during normal abduction.

Tendinopathy is infact a more technically correct term for shoulder injuries, not tendonitis, as, although true inflammatory tendinopathies exist, most patients that present to a GP have had prolonged symptoms. Thus by the time they do present, acute inflammation would probably have subsided and been supplanted by degeneration of the normally highly arranged collagen structure of the tendon. There are three classifications of tendinipathy:
1) acute tendonitis alone
2) chronic tendinosus + acute tendonitis
3) chronic tendinosus alone

Mangaement of Cataracts

Initial Mx:
• Glasses, strong bifocals, magnification, stronger lighting and other visual aids

Surgery:
• When cataracts begin to affect everyday life, most effective Rx is surgery, no medical Rx (usually when acuity is b/w 6/6 and 6/18)
• Cataract surgery proves effective in 95% of cases, with improvement in vision and no complications
• Day surgery/outpatient procedure: takes less than an hour
• If both eyes affected, surgery performed on one eye at a time, with 1-2 month gap b/w to let initial eye heal
• Can choose to postpone surgery if vision/lifestyle not affected significantly, but younger or diabetic patients have greater need for surgery-progress faster

Preparation:
o Ophthalmologist measure eye with ultrasound to determine power of lens to insert
o Local anaesthetic used, general used only if patient very distressed/anxious

Technique:
Basically crystalline lens with cataract removed during surgery, capsule remains, new artificial intraocular lens inserted
o 2 types:
Extra-Capsular Cataract Extraction (ECCE)-lens removed but majority of lens capsule remains to support the artificial lens.
-Can be via phacoemulsification, where a small incision is made-3mm long- where cornea meets conjunctiva, horizontal incision. Small needle like probe inserted via incision, and ultrasound waves emitted into eye via probe break up lens+cataract, and bits are suctioned out via probe
-If cataract is advanced stage, ultrasound waves may not be able to break it up, so larger incision required-10mm-where cornea meets sclera. Ophthalmologist opens lens capsule through incision, removes nucleus of lens in 1 piece followed by softer lens cortex, capsule remains in place
Intra-Capsular Cataract Extraction (ICCE)¬-lens and capsule removed b/c cataract has progressed into capsule (rarely performed)
o After cataract removed, a plastic intraocular lens-silicone/acrylic-folded when outside the eye is inserted through the incision
o Once in the eye, IOL unfolds and is position inside lens capsule, it’s 6mm in diameter
o Most IOLs are monofocal, multifocal lenses are being developed but problems exist with intermediate focus and glare with multifocals.

Recovery:
o Incision heals fast, b/c very small and made horizontally. No stitches.
o Swelling and redness should go down within few days- week and vision should improve almost immediately
o If larger incision may take up to 8 weeks to heal completely
o Can’t drive home, and ophthalmologist may restrict movement e.g. bending/lifting for a few days
o Need follow up next day, one week and one month after surgery
o Doctor may prescribe medication to prevent infection and to control eye pressure
o Contact Doctor if experience: Vision loss, pain despite use of over-the-counter drugs, increase in inflammation/redness, nausea/vomiting/excessive coughing, light flashes or spots in front of eyes
o Most people require glasses after surgery b/c artificial lens usually monofocal and astigmatism may arise from surgery (Px has difficulty focussing b/c cornea is not curved evenly in all directions, less common with smaller incisions)
o 2nd Cataract: about 25% of patients develop a second cataract where back of lens capsule-left in during surgery-becomes opaque b/c of build-up of cells. Also called Posterior Capsule Opacification (PCO)
-PCO can develop months/years after procedure
-Rx is YAG (yttrium-aluminium-garnet) laser capsulotomy where laser is used to make a small opening in capsule to let light shine through
-short procedure, less than 5 mins, but Px has to remain for about 1 hr to monitor eye pressure. Can cause glaucoma, or increase welling of macula and retinal detachment

PS. I've sent two pics of anatomy of eye+catract surgery to emails

Advertising in the Health-Care Sector

Advertising in the Healthcare Sector

Legislation regarding advertising in the health-care sector falls under the federal statutory Trades Practices Act 1974 and the Medical Practices Act 1994, and the regulatory body that enforces the act is the Australian Competition and Consumer Commission (ACCC).
The acts are designed to protect consumers and the community from false and misleading advertising.

The Medical Practice Act 1994 outlines the responsibilities of the Medical Practitioners Board of Victoria in relation to regulation of advertising by medical practitioners. It states that a person must not advertise a medical practice or medical services in a manner which:

➢ is or is intended to be false, misleading or deceptive
➢ offers a discount, gift or other inducement to attract patients to a medical practitioner unless the advertisement also sets out the terms and conditions of that offer
➢ refers to uses or quotes from testimonials or purported testimonials
➢ creates an unreasonable expectation of beneficial treatment.

There are risks that advertising which is false, misleading or deceptive can lead to the provision of unnecessary medical services, or create unrealistic expectations about the benefits of such services, with adverse consequences for consumers.
The TPA prohibits conduct that is unconscionable, misleading or deceptive, or is likely to mislead or deceive.
Forms of promotion that are subject to legislative regulation include:

➢ print and electronic advertisements;
➢ outdoor advertisements;
➢ patient information brochures;
➢ direct mail outs
➢ representations made on the Internet.
➢ oral statements made to patients by health care professionals and their employees
In addition, Health Complaints Offices exist in some states, and medical and other health practitioner registration associations also assist in providing guidance on appropriate advertising for health professionals. For example, the Australian Medical Association's Position Statement on Advertising and Endorsement states that information about medical services should:
➢ be demonstrably true in all respects;
➢ not be misleading, vulgar or sensational;
➢ seek to maintain the decorum and dignity of the profession;
➢ not contain any testimonial or endorsement of clinical skills;
➢ not claim that one doctor is superior to others, nor contain endorsements for any particular doctor;
➢ avoid aggressive forms of competitive persuasion.

In accordance with these general guidelines, the AMA Position Statement states that the chief purpose of any advertisement should be to present information that is reasonably needed by any patient to make an informed decision about the appropriateness and availability of the medical services offered.


Differences between receiving private and public cataract surgery:
Public hospital:
o No direct cost to patient
o No choice of treating doctor, and often no consistent doctor during course of treatment
o Waiting time for elective procedures.
Private hospital:
o Cost of insurance and out of pocket expenses
o Choice of specialist and continuity of care
o Minimal waiting time.

PCL Week 7 - Doctors and Drivers

When a patient’s health affects their ability to drive, a doctor must consider their duty to their patient’s privacy, but also to the public’s safety. For many aging citizens, particularly in rural or remote areas, their ability to drive is more than just an issue of convenience, but also represents a level of independence. Many people may have had their licence for up to fifty years and so are naturally reluctant to give up what they have managed to obtain and maintain for such significant proportion of their lives. It is for this reason that they often require support and encouragement to make lifestyle changes in anticipation of not being able to drive.

Visual standards:
• Visual acuity - The person’s visual acuity in the better eye or with both eyes together must not be worse than 6/12. However, a conditional licence may be granted taking into account the opinion of the treating doctor, and the nature of the driving task, and is subject to periodic review. Cataracts often cause a loss of contrast sensitivity and greater sensitivity to glare, so patients may have more difficulty seeing when driving than is indicated by their visual acuity.
• Visual fields - The criteria for an unconditional licence are that binocular visual field has a horizontal extent of at least 120 degrees, within 10 degrees above and below the horizontal midline and that the person is free from any significant visual field loss that is likely to impede driving performance.
• Diabetes - A person with diabetes controlled by diet alone may drive without licence restriction and without notification to the Driver Licensing Authority. They should be reviewed periodically.

Reporting process:
The laws require drivers to report VicRoads if they have any permanent or long-term illness that is likely to affect their ability to drive safely. As the relationship between patient and health professional is confidential, the doctor will not normally communicate directly with VicRoads. They will however provide the patient with advice about their ability to drive safely as well as a letter, or report, to take with them (except in South Australia and the Northern Territory, where reports are directly made to the relevant licensing authorities).

Penalties may be imposed on a driver that fails to report an impairment, and may be liable at common law if they continue to drive knowing that they have a condition that is likely to adversely affect safe driving.

Doctors also have an obligation to public safety, so if they believe a patient is not heeding advice to cease driving, they may report directly to VicRoads. The Victorian Road Safety Act (1986) provides statutory immunity to doctors who, in good faith, report that a patient has a medical condition which renders them unfit to hold a driver’s licence.

Week 7 - Aboriginal Health Issues

* Aboriginal people have higher rates of ill health than any other group in Australia
* The Victorian Koori people account for only 0.5% of the population (the lowest number of indigenous people) but report the highest rates of acute illness, chronic illness, and cigarette smoking in Australia
* Main health issues confronting Koori people include smoking, diet, diseases like cardiovascular disease, diabetes and high blood pressure, stress, drugs, alcohol and poor children's health

For these health issues, there's a range of causes:
* genetic susceptibility
- it has been suggested that Aboriginal people have a "thrify genotype", which helped to support their traditional hunter-gatherer lifestyle. This means that their bodies are genetically programmed for glucose intolerance and high blood cholesterol levels - protecting against starvation. As traditional diets were rich in nutrients and low in fat, this did not create an issue until the high-fat, high-sugar western diet was introduced. This in addition to poor access to healthy foods for Aboriginal populations causes higher incidences of obesity, diabetes and cardiovascular disease.
- As a result of this genetic susceptibility and also poor access to healthy food, around 6 out of 10 Aboriginal and Torres Strait Islander people are either overweight or obese. This multiplies the chances of developing Type II diabetes by 10.
* Lack of physical exercise
* Low birth weight
- An aboriginal woman is twice as likely to have a low birth weight baby than a non-aboriginal woman. some studies indicate that low birth weight is associated with an increased risk of developing Type II diabetes.
* Poor standard of living/Low socioeconomic status
- Research shows that a person who has a limited income, low level of education and few employment prospects is more likely to engage in behaviours that increase the odds of disease.
- Aboriginal and Torres Strait Islander people are among the most economically disadvantaged of all Australians
* Reduced Access to Medical Care
- Culturally sensitive medical care is limited, especially for Aboriginal Australians who live in remote or rural areas.
FOR MORE INFO, LOOK AT THESE FACT SHEETS:1. http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Aboriginal_health_issues_diabetes?OpenDocument
2.
http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Aboriginal_health_issues?open

Monday, August 27, 2007

practice exam answers from holly

1. C
2. B
3. FFTF
4. TTTT
5. TFFF
6. C
7. D
8. E
9. D
10. E
11. D
12. B
13. B
14. FFTF
15. FTFF
16. FTFT
17. TTTT
18. TTTF
19. FTFT
20. FFFT
21. FTTF
22. TTTT
23. FTTF
24. TTTF
25. TFTF
26. TFTF
27. TTTF
28. D
29. FTFT
30. E
31. C
32. TTFT

good luck for wednesday!!!!!!!!!!!!!

Thursday, August 23, 2007

Management of Shingles

• The main challenge in the management of shingles is the rapid treatment of the pain involved.
• Early and adequate antiviral treatment will help to reduce the severity and duration of the pain involved.
• The use of antiviral agents is to stop virus replication as quickly as possible and minimize nerve damage
o There are three antiviral compounds which have been assessed for their ability to speed the resolution of shingles
 Aciclovir
• Total Pain duration is greatly reduced
• 800 mg 5 times per day for 7 days
 Famciclovir
• 500 mg 3 times per day for 7 days
 Valaciclovir
• Speeds pain resolution significantly faster than acyclovir
• 1 g 3 times per day for 7 days
o Must be administered within 72 hours of rash onset
• These antiviral agents are appropriate for all patients presenting with shingles within 72 hours of rash onset
• Valaciclovir is probably the most effective agent available as it is the fastest at resolving the pain associated with shingles.
• Famciclovir and valaciclovir offer more convenient dosing than acyclovir.
• Complications can be reduced to 20% or less by early treatment, as well as reducing duration of lesion formation and time to healing

Wednesday, August 22, 2007

Cause of Shingles

Shingles is caused by the varicella-zoster virus, the virus that causes chicken pox. It affects mostly the elderly and those who are immunocompromised.

It only affects those who have previously had chicken pox. When the patient has recovered from CP the virus lies dormant in the base of some sensory nerve cells. After many years the virus may become active again. When activated the virus multiplies and spreads along the nerve it has been occupying, breaking out into a painful rash on the dermatome of the infected nerve.

Shingles can only be contracted from the dormant chicken pox virus – it is not contagious.

Tuesday, August 21, 2007

Prognosis and complications of shingles

The rash and pain usually subside within 3 to 5 weeks. There are numerous complications possible, many depending on which dermatome was affected.


Postherpetic neuralgia
Postherpetic neuralgia is pain in a previous shingles zone; this occurs in some 10% of patients (often elderly). Burning, continuous pain responds poorly to analgesics. Depression is almost universal. Treatment is unsatisfactory but there is a trend towards gradual recovery over 2 years. Amitryptyline is commonly used. Methyl-prednisolone intrathecally is sometimes helpful.


Ophtalmic complications
In cranial nerves, herpes zoster has a predilection for the fifth and seventh nerves. ‘Ophtalmic’ herpes is infection of the first division of the fifth cranial nerve. This can lead to corneal scarring and secondary panophthalmitis.


Ramsay Hunt syndrome
Geniculate herpes (geniculate ganglion of seventh cranial nerve) is also called Ramsay Hunt syndrome. There is a facial palsy with herpetic vesicles in the external auditory meatus (this receives a sensory twig from the facial nerve) and / or on the soft palate. Deafness, or a fifth nerve lesion may occur.


Local complications
Local complications are secondary bacterial infection, very rarely local purpura with necrosis (purpura fulminans), generalized zoster, and postherpetic neuralgia.

Monday, August 20, 2007

PCL Week 6 – “Angela has a pain in her arm”

Risk Factors for Shingles:
You can only get shingles if you have already had chickenpox (virus lies dormant)
· 20% of people who’ve had chickenpox develop shingles

Risk Factors:

  • Stress and fatigue
    o Excessive emotional and physical stress or extreme fatigue
  • Conditions that weaken your immune system
    o E.g. cancer, HIV/AIDS
  • Certain treatments
    o Radiation therapy
    o Immunosuppressants
    § Chemotherapy
    § Steroid medications
  • Age
    o >60y/o » 3 times more likely to develop shingles
  • Ethnic background
    o White people are 4 times more likely to develop shingles
  • Gender
    o Some studies suggests females are more susceptible

Angela appears to have all of these risk factors in some way.
She has become more stressed and fatigued than usual due to her daughter’s chronic pain which is requiring her assist a lot more around the house.
She has had breast cancer in the past and been on Tamoxifen which may have weakened her immune system.
She is an 88 year old, white female.

Thursday, August 16, 2007

Week 5 Topic 2 - Summary

How do we know that years of exposure to loud noises causes hearing impairment?

Basically – From studies!

Over the last 40 years various studies of large groups of people that have had exposure to noise at work have found that ongoing exposure to noise can cause hearing loss; even some sounds quieter than shouting can, over years, cause some damage to hearing.

It has been found that thirty years exposure will produce in half the exposed workers
-about 5 decibels of high-frequency hearing loss for an average exposure to 85 decibels of noise at work;
-over 10 decibels of high-frequency hearing loss for an average exposure to 90 decibels of noise at work;
-over 20 decibels of high-frequency hearing loss for an average exposure to 95 decibels of noise at work.





What happens to the ear itself?

Noise-induced hearing loss is a form of sensori-neural loss (i.e. due to disorder of the sound sensing mechanism within the cochlea or the nerve supplying it) that gradually worsens over a period of years.
Continuing loud noise causes the degeneration of the outer hair cells, especially in the basal turn of the cochlea (which is responsible for sensing high frequency noises). This damage can range from loss of some stereocilia up to complete death and loss of cells. The pathogenesis is not fully understood but is suspected to be partly vascular and partly biochemical.

This damage to the outer stereocilia means that the variable amplification function of the outer hair cells no longer operates effectively at certain frequencies – usually the higher frequencies. Therefore, the range of intensity at which sound is perceived is narrowed.





How does conductive hearing loss differ from noise-induced hearing loss?

N.B. Because noise damages only the outer hair cells, pure noise-related hearing loss cannot exceed the level of amplification afforded by those hair cells; it cannot exceed 65 decibels.
Also, noise-induced hearing loss starts at the frequency of 4000 hertz.

Noise-induced hearing loss is particularly related to resonance of the ear canal. Whereas conductive hearing loss occurs when there is pathology located between the entry to the ear canal and the cochlea. It prevents the auditory stimulus from reaching the cochlea. Because bone conduction occurs, conductive deafness is never complete; at worst it can cause a 60 decibel deficit.

Compensation & Prevention

Below is the summary for compensation and prevention (seriously contemplating transferring to law...)
I'll be away tomorrow, so apologies to everyone for missing their role plays.

COMPENSATION FOR HEARING LOSS

Compensation refers to a monetary provision made as payment for a service or reparation for some wrongdoing. In the case of this week’s PCL, the term most likely refers to Worker’s Compensation - commonly referred to as “Compo” – due to the fact that Des’ hearing was most likely damaged by his work as a mechanic.

The WorkCover Authority is the scheme in Victoria that manages compensation in Victoria. The Authority liaises between the employee, employer and the insurers. Any employee that has been injured may apply for compensation and there is no need to prove that the employer was negligent, simply that the injury sustained was a result of their employment. This makes the scheme a “no-fault” system. In order to claim compensation, Des must prove that he has “Industrial Deafness” as a result of his work.

Industrial Deafness is defined by the Victorian Accident Compensation Act 1985 as “any condition of deafness caused by exposure, continued exposure or periods of continuous exposure to industrial noise.” The employee must have also suffered a reasonable amount of hearing loss, that being a loss that “impacts upon the normal function and interaction” of the worker.

The provision of compensation is intended for the employee to use to pay for medical costs of assessing and maintaining the health of the employee’s ears/hearing and a lump sum of money proportional to the impairment caused. Such a lump sum is determined by standard tables as used by the Victorian WorkCover Authority as well as several private insurers. The payment of medical costs is subject to the medical treatment being reasonable, that is how efficient it is in reaching the aim of restoring as, much as possible, the hearing acuity, direction sense and social interaction of the employee to pre-damage level of function.

If the employee has been employed by several employers and hearing damage is believed to been the result of a gradual development over the course of such employment, so long as no previous claim has been made, then the current employer must bear the full costs of any compensation claim. Even if the employee has been non-compliant with safety regulations set down by the employer, e.g. refusing to wearing earplugs, etc. the employee still gets compensation as the scheme is no-blame scheme.

For further remittance (a LOT further!), the injured employee may also sue their employee for negligence. The PCL is not very clear in this aspect. Des appears to be the manager of the garage. Whether this means that he self-employed or he is employed by a corporation that owns a chain of garages is unclear. If Des was self-employed, it would be difficult to find a lawyer willing to bring charges against Des himself. However, if Des is the employee of a company, he may sue if there is a case for employer negligence. This may result in the court ordering the employer to pay further compensation or the two parties may reach an out-of-court settlement.

For negligence to be proved, the plaintiff must establish that the company has failed to meet its duty as an employer under the Occupational Health and Safety Act. In Des’ case, the regulations concerned involve those regarding noise in workplaces. These regulations require the employee to identify and control as much as possible noises in an area where the noise intensity exceeds 85 dB for 8 hours of each day. If the noise can not be controlled sufficiently, the employer must limit the duration of employee exposure to the noise and/or provide ear protection and audiometric tests every second year to monitor employees’ hearing. Any abnormal test must also be reported to the WorkCover Authority.

Aside from the regulations and ear protection, further simple preventative measures can be taken such as good maintenance of machinery to reduce noisy operation, rubber or spring mountings to reduce vibration, enclosures, screens or walls to contain noise, presses rather than hammers to straighten metal and the reduction of the use of compressed air.

Role-play 4

- Describe the features of a hearing aid and how things will be for Des when he gets one or a pair
- Empathise with Des and explain why treatment is necessary

The main advantage of having binaural hearing aids is that sound presented to both ears is interpreted to be louder than in just the one ear. So the hearing aids can be set at a lower volume, resulting in less background noise being audible.

Des’ hearing loss is most evident in higher frequencies. Development has resulted in hearing aids that have variable amplification i.e. they are frequency specific, and also mimic the function of the outer hair cells by reducing amplification in the presence of intense ambient sound.

‘In canal’ may preferable for the wearer for cosmetic reasons (as it is less visible), however ‘behind the pinna’ offers better direction sense, which assists the wearer to focus on what one person is saying when other people are talking near by.

Hearing aids cost several thousand dollars, however there is a maximum contribution of $6,900 (at April 2004) from the Victorian WorkCover Authority.

While adjusting the wearer is advised to stay at home or in familiar surrounds. The wearers own voice and the noises around them sound different and at first may be tiring and irritating. The wearer should not force or prolong conversations when they are tired and most importantly do their best to exercise patience as they adjust to their hearing aid.

Over the first few days the hearing aid feels like a foreign object. It may stimulate excess wax production and as the ear canal epithelium is thin, it may become inflamed or bleed – this is reduced as the epithelium thickens to adjust. Care must be taken to keep the hearing aid clean and protected from physical damage.

Others can assist in the transition by ensuring that they speak clearly (but not shout) and also be ensuring that they have the speaker’s attention (their lips may act as a visual cue) and by avoiding conversations in areas with high background noise.


Get it? FogHORN! ... like the original hearing HORNS!? ...Ahh screw you guys...

Friday, August 10, 2007

Pathophysiology: Rotator Cuff Tendinopathy

Physiology
- Rotator cuff is a group of 4 tendons (SITS) that stabilizes the shoulder joint.
- Allows movement: raise and rotate arms.
- When you raise your arm above your head:
o The supraspinatus tendon (upper) and the subacromial bursa will glide on the acromion of scapula.
o The undersurface of acromion may be rough/abnormally shaped. It rubs or scrapes the bursa and tendon.
- Repetitive activities (with overhead motion) can result in
o Bursitis  inflammation of bursa
o Tendinitis  inflammation of tendon

Pathology

Tendinopathy = Tendinitis (inflammation) @ tendinosis (tear)
- Normally, the rotator cuff moves within a confined space (subacromial space) with subacromial bursa (cushion between tendons and bone).
- When the subacromial space becomes smaller due to inflammation, bone spurs or fluid build-up, the rotator cuff tendons may be squeezed and rub against bone (impingement).
- As a result, the tendons may become damaged and irritated, causing bleeding and inflammation of the bursa or tendons.

- Over time, tendon may wear against the undersurface of acromion, causing TEAR & bleeding.
- Tears heal  replacement by scar tissue (weak/thickened/less flexible/fibrous)
- Gradual scarring of tendon  the entire rotator cuff weakens
- Finally, rotator cuff cannot balance the upward pull of the deltoid muscle
o This may further damage the tendon, renewing the cycle of tearing and scar formation
o The weaker the tendon becomes, the more susceptible it is to partial or complete tears

- Cycle of inflammation  tearing of tendons  scar formation
- This results in pain and loss of function
- May lead to other shoulder problems (e.g. frozen shoulder syndrome)
o Adhesive capsulitis  frozen shoulder
o Stiffness, pain, limited range of movement
o Tissues around the joint stiffen, scar tissue forms

- Rotator cuff tears occur when the tendons become weak from inflammation/scarring/fraying
- Tears result from slow, progressive damage over time.

A rotator cuff is more easily damaged or torn as age-related degeneration develops.

The factors below often occur together or overlap:
a. Bones are that irregularly shaped  affect cuff movement in subacromial space
b. Normal wear and tear lead to changes in rotator cuff, such as:
a. General degeneration of the tendon  thinning, fraying and tearing
b. Decreased blood supply to tendons
c. Arthritis of the acromioclavicular (AC) joint  results in bony growths that can damage rotator cuff
c. Joint looseness and muscle imbalance in the shoulder
a. Formation of scar tissue
b. Changes in the tissue itself
d. Repetitive activities, especially forceful overhead motions
a. Repetitive activity – tendons rub or scrape against the acromion (this can irritate the rotator cuff)
b. Repeated overhead motions – damage stabilizing ligaments and result in an imbalance of opposing shoulder muscles (cause tendons to rub against the bones – impingement)
e. Overuse
a. Young athletes – tendinitis (throwing/swimming/racquet sports)
b. Lead to functional overload (shoulder joint becomes unstable)
c. The ball of humerus (humeral head) moves upward, narrowing the subacromial space where rotator cuff moves.
d. In this narrowed space, the rotator cuff is squeezed, forcing the tendon to rub against bone (impingement).

Thursday, August 9, 2007

Medical Management of Rotator Cuff Injury

Initially, during the first 48-72 hours after the injury is sustained, use the ‘RICER’ treatment regime:
~ Rest – abstain from anything that aggravates the injury, or from the activity that may have caused it, i.e. swimming
~ Ice – apply ice to the shoulder for 20 minute periods at least three times a day
~ Compression – bandage the area
~ Elevation – perhaps not so necessary for shoulder region but maybe a sling if the pain is bad?
~ Refer – visit a medical practitioner ASAP

After two days of RICER have elapsed, apply heat to the area, e.g. a heat pack or heat lamp. This will help increase blood flow to the injured area. Massage also helps with this as well as helping to minimise the formation of scar tissue.

Take non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, which will reduce pain, fever and inflammation. Take daily over a period of 6 weeks.
NSAIDs work by inhibiting the enzyme cyclooxygenase, which catalyses the formation of messenger molecules involved in the inflammatory process, such as prostaglandins.

For continued pain and limited functionality due to persistent inflammation an injection of corticosteroid/cortisone (a steroid) into the subacromial space of the shoulder may be needed. This acts as a powerful anti-inflammatory agent by acting at the DNA level (ie binding directly to DNA) to down-regulate the production and function of immune/inflammatory cells and mediators such as macrophages and eicosanoids.
They do however have a number of side-effects, so must be used only if absolutely necessary.

Once the pain has been resolved, it is vital to perform specific strengthening exercises to ensure return to function.
Strengthening of the shoulder rotator cuff muscles is best performed by isolating each muscle group and selectively training that muscle. The subscapularis is the anterior stabilizer of the rotator cuff and responsible for internally rotating the shoulder. It is best strengthened by holding a hand weight in front of the body, with the arm flexed to 90 degrees, and rotating the hand to touch the belt. The exercise can be performed while lying on your back with the elbow close to your side and flexed ninety degrees. Lift the weight until it is pointing toward the ceiling and then lower it slowly.
The supraspinatus is strengthened by holding a light weight (initially 3-5 lbs) out straight in front of the body, with the thumbs pointed toward the floor. Slowly elevate the weight to above the head.
The infraspinatus is strengthened by holding the weight in the position of the ski pole just prior to planting the pole. By rotating the arm from the neutral straight ahead position, to the externally rotated (out to the side) position, the infraspinatus and teres minor are strengthened. Again, this exercise can also be performed while lying on your side with the elbow close to your hip, and flexed ninety degrees. Rotate the weight until it is pointing toward the ceiling. Shoulder exercises are best performed with relatively light weights and multiple repetitions.
The logic behind stretching and strengthening the inflamed rotator cuff in order to speed healing and functional performance is as follows: the inflamed tissue is characterized by increased fluid between the cells, increased numbers of new blood vessels and inflammatory type cells. As a result of this inflammatory reaction, new collagen tissue is laid down in an effort by the body to heal the injured tissue. If the shoulder is immobilized during this time, the new collagen is laid down in a disorganized fashion, creating scar. The goal of gentle stretching, strengthening and anti-inflammatory medication, is to stimulate the cells to lay down collagen along the lines of stress, forming normal strong tendons. The combination of a good warm up, gentle stretching, strengthening below the limits of pain, icing after working out and anti-inflammatory medication has been consistently shown to speed recovery time in the strongest possible fashion.

Investigations for RC Tendonopathy

Invesitgations for Rotator Cuff Tendonopathy:

Firstly physical examination along with symptoms
XRay:
-detect possible anatomical abnormalities eg variations in acromion may give a tendency towards tendonopathy
-detect calcific tendonitis; calcific deposits on supraspinatus tendon may cause pain (although may be present without being the cause of pain), generally found in elder patients (30-50 yrs)
-degenerative changes eg arthritis of AC or GH joint
-may order neck XRay (generally of cervical neck region) in case of suspected neck/nerve damage
All above tests are to rule out other differentials eg nerve damage, arthritis etc
Ultrasound:
-can detect Rotatot cuff tears
-good for assesing tendon of rotator cuff
-can detect fluid eg fluid in subdeltoid bursa is indicative of a full thickness rotator cuff tear
(is an inexpensive and non invasive technique)
MRI:
-can detect suspected tear
-may demonstrate inflammation
-can detect swelling
(not likely to be used in case of tendonopathy as expensive procedure)
Arthroscopy:
-can detect tears
-can fix smaller tears
(invasive procedure)
Arthrogram:
-injection of contrast dye into joint, can reveal tears and abnormalities

Psychosocial Consideration

Michelle is a young, highly competitive athlete who has already had success at a state level and now has her sights on a national and international career. She is currently swimming four hours of intensive training on a daily basis and so any rest or rehabilitation period is likely to represent a big challenge for her. It is for this reason that she is likely to be reluctant to comply, however, as she is already being handicapped by her injury sooner or later she will be forced to slow things down (that sounds a little conniving!).

However, the American College of Sports Medicine has some suggestions on what Michelle can do for a quick rehabilitation, so that she can hopefully (don’t know just how bad the injury is) jump back into the pool in no time.

• Education – education about the injury is crucial so that the athlete has realistic expectations about the rehabilitation process and how to avoid re-injury. It is important to note that athletes are often misinformed about their injury by coaches, team mates, parents, the internet, Dr Seuss etc. This is also believed to help alleviate any emotional upheaval.

• Stress management and coping mechanisms – emotional reaction plays a key role. Some studies have suggested the use of psychological strategies including goal setting, positive affirmations, cognitive restructuring and visualisation, which are all associated with faster recovery.

• There is also a need to redirect energy that is normally used in training:
o Work – Michelle already works in a public relations firm. Maybe this is an opportunity to concentrate or take a larger role in this area of her life
o Coach or mentor younger swimmers (allows to remain within the swimming environment)
o Many injured athletes look to career opportunities such as motivational speaking


- This picture serves no purpose... just wanted to see if it would work

Saturday, August 4, 2007

Hypothermia

Hypothermia is defined as the core temp being below 35 (rectal or oesophageal).

Causes:
  • Decreased oxygen consumption
  • slowed depolarisation of nerve cells in the PNS and muscles in the heart
  • Increase in RBC count (haemoconcentration)
  • Pancreatitis.
S+S:
Mild: weakness, lethargy, drowsiness, irritability, confusion, impaired coordination
Moderate: Delirious, drowsy, comatose, no apparant respiration or BP, and general failure of metabolic processes causing hyperkalaemia (high potassium in the blood), ventricular fibulation (waked out heart beat)
Severe: asystole (stopping of the heart's electric activity) causing death.

treatment:
change into warm clothes, heat up! warm area, waterproof clothing etc. Don't give alcohol cigarettes tea or coffee. Don't try and stimulate peripheral circulation.