ptp&m013 npte 5

PHYSICAL THERAPY PRINCIPALS & METHODS PTP&M013 NPTE-5/5 Revision: 02 Page: 1 of 110

NATIONAL PHYSIOTHERAPY EXAM PREP GUIDE

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Mullsons Health & Wellness, which shall be copied, reproduced, disclosed to others, published, and could be used in whole or part, for any purpose, without the express advance written permission of a duly authorized agent of the Company. This specification is subject to recall by Mullsons Health & Wellness at any time.

Medicine: it’s a noble profession, It serves humanity

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PASSAGE TO THE USA, VIA CAPE OF NPTE.

NATIONAL PHYSIOTHERAPY EXAMINATION-PART-5 SPEC. BY: Abdulrehman S. Mulla DATE: 03/21/2009 REVISION HISTORY REV.

DESCRIPTION

CN No.

BY

DATE

01 Initial Release PT0013 ASM 04/25/2009






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TABLE OF CONTENTS PAGE 7.0 OSTEOPOROSIS UPDATE INCLUDING WORLD HEALTH ORGANIZATION CRITERIA, BONE MINERAL DENSITY AND INTERVENTION: ....................................................................................................................................................................................................... 6

7.1 DIAGNOSING OSTEOPOROSIS:............................................................................................................................................................. 7 7.1.1 BMD TEST: ............................................................................................................................................................................... 8 7.1.2 RECIEPIENTS OF THE BMD Test: .......................................................................................................................................... 8 7.1.3 TYPES OF BONE DENSITY TESTS: ....................................................................................................................................... 9 7.1.4 OTHER TYPES OF TESTS: ................................................................................................................................................... 10 7.1.5 HOW OFTEN TO REPEAT A BMD TEST: ............................................................................................................................. 11

A. TESTS TO FIND BROKEN BONES:....................................................................................................................................... 11 7.1.6 UNDERSTANDING BMD TEST RESULTS: ........................................................................................................................... 11 7.1.7 WHAT YOUR T-SCORE MEANS: .......................................................................................................................................... 12 7.1.8 TREATMENT CONSIDERATIONS: ........................................................................................................................................ 12

7.2 PHYSIOTHERAPY INTERVENTIONS:................................................................................................................................................... 14 7.2.1 RISK FACTORS:..................................................................................................................................................................... 14 7.2.2 TARGET CLIENT GROUPS FOR TREATMENT BY PHYSIOTHERAPISTS:........................................................................ 14 7.2.3 PHYSIOTHERAPY ASSESSMENT: ....................................................................................................................................... 15 7.2.4 ANTHROPOMETRIC AND SPINAL MOBILITY ASSESSMENT: ........................................................................................... 16

A. HEIGHT:.................................................................................................................................................................................. 16 B. WEIGHT: ................................................................................................................................................................................. 16 C. CHEST EXPANSION MEASURED AT XIPHISTERNUM: ...................................................................................................... 16 D. CERVICAL/THORACIC DEFORMITY (TRAGUS TO WALL): ................................................................................................ 16 E. SHOULDER ELEVATION: ...................................................................................................................................................... 16 F. LUMBAR SPINE RANGE OF MOVEMENT (SCHOBER EXTENSION): ................................................................................ 16

7.2.5 STRENGTH/ENDURANCE ASSESSMENT: .......................................................................................................................... 16 7.2.6 AEROBIC CAPACITY ASSESSMENT:................................................................................................................................... 17 7.2.7 BALANCE ASSESSMENT: ..................................................................................................................................................... 17 7.2.8 FUNCTIONAL ASSESSMENT:............................................................................................................................................... 17 7.2.9 PAIN ASSESSMENT: ............................................................................................................................................................. 18 7.2.10 ANALYSIS OF ASSESSMENT AND OUTCOMES:................................................................................................................ 18

7.3 PHYSIOTHERAPY MANAGEMENT: ...................................................................................................................................................... 18 7.3.1 MANAGEMENT FOR THE OSTEOPENIC AND PREVENTION GROUP: ............................................................................. 18 7.3.2 EXERCISE MANAGEMENT FOR BONE HEALTH: ............................................................................................................... 19 7.3.3 PRECAUTIONS: ..................................................................................................................................................................... 21 7.3.4 THE OSTEOPOROTIC GROUP WHO HAVE NOT SUSTAINED FRACTURES: .................................................................. 21

A. EXERCISE MANAGEMENT FOR BONE HEALTH: ............................................................................................................... 21 B. PRECAUTIONS ...................................................................................................................................................................... 22

7.3.5 FRAILER GROUP WITH SEVERE CHANGES WHO HAVE OFTEN SUSTAINED FRACTURES:....................................... 22 A. EXERCISE MANAGEMENT: .................................................................................................................................................. 22 B. PRECAUTIONS: ..................................................................................................................................................................... 23 C. PAIN MANAGEMENT: ............................................................................................................................................................ 23

I. HYDROTHERAPY: ......................................................................................................................................................... 23 II. TRANSCUTANEOUS ELECTRICAL NERVE STIMULATION (TENS):.......................................................................... 23 III. INTERFERENTIAL THERAPY:....................................................................................................................................... 23 IV. HEAT: ........................................................................................................................................................................ 23 V. RELAXATION:................................................................................................................................................................. 24 VI. COMPLEMENTARY THERAPIES: ................................................................................................................................. 24

7.3.6 BALANCE AND FALLS MANAGEMENT: ............................................................................................................................... 24 7.3.7 POSTURE AND FLEXIBILITY: ............................................................................................................................................... 25 7.3.8 EXERCISE PRESCRIPTION: ................................................................................................................................................. 25 7.3.9 PSYCHOLOGY OF EXERCISE: ............................................................................................................................................. 26

A. ADHERENCE:......................................................................................................................................................................... 26 B. PROMOTING HABITUAL EXERCISE: ................................................................................................................................... 26

7.4 POTENTIAL HARMS AND RISKS: ......................................................................................................................................................... 27 7.5 EDUCATION: .......................................................................................................................................................................................... 27

7.5.1 PATIENT EDUCATION: .......................................................................................................................................................... 27 7.5.2 HEALTH EDUCATION: ........................................................................................................................................................... 27

8.0 MUSCULOSKELETAL DIFFERENTIAL DIAGNOSIS; KINEMATIC CHAIN TABLES: ........................................................................... 28 8.1 GENERAL PRINCIPLES: ........................................................................................................................................................................ 28

8.1.1 DIFFERENTIAL DIAGNOSIS IN ORDER OF PREVALENCE: ............................................................................................... 29






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8.1.2 DIFFERENTIAL DIAGNOSIS OF JAUNDICE:........................................................................................................................ 30 8.2 ARTHRITIS:............................................................................................................................................................................................. 31

8.2.1 APPENDICULAR ARTHRITIS: ............................................................................................................................................... 31 A SUTTON'S LAW:..................................................................................................................................................................... 31 B RADIOGRAPHIC HALLMARKS:............................................................................................................................................. 31 C PATTERN APPROACH: ......................................................................................................................................................... 35 D DEMOGRAPHICS:.................................................................................................................................................................. 36 E THE LAW OF PARSIMONY:................................................................................................................................................... 37 F. CONCLUSION: ....................................................................................................................................................................... 37

8.2.2 AXIAL ARTHRITIS: ................................................................................................................................................................. 38 A. DEGENERATIVE DISORDERS:............................................................................................................................................. 38

I. OSTEOARTHRITIS:........................................................................................................................................................ 38 II. DEGENERATIVE NUCLEAR DISEASE: ........................................................................................................................ 39 III. DEGENERATIVE ANNULAR DISEASE: ........................................................................................................................ 39 IV. DIFFUSE IDIOPATHIC SKELETAL HYPEROSTOSIS (DISH)....................................................................................... 40 V. INFLAMMATORY SPONDYLOARTHROPATHIES: ....................................................................................................... 40

1. RHEUMATOID ARTHRITIS: ................................................................................................................................... 40 2. ANKYLOSING SPONDYLITIS: ............................................................................................................................... 40

VI. CRYSTALLINE ARTHRITIS:........................................................................................................................................... 41 1. GOUT:..................................................................................................................................................................... 41 2. CALCIUM PYROPHOSPHATE CRYSTAL DEPOSITION DISEASE: .................................................................... 41

VII. PSORIATIC ARTHRITIS: ................................................................................................................................................ 41 VIII. PSORIATIC ARTHRITIS: ................................................................................................................................................ 41 IX. REITER'S SYNDROME: ................................................................................................................................................. 41 X. ENTEROPATHIC ARTHROPATHY: ............................................................................................................................... 42

B. RADIOGRAPHIC HALLMARKS:............................................................................................................................................. 42 I. OSTEOPHYTES: ............................................................................................................................................................ 42 II. SYNDESMOPHYTES: .................................................................................................................................................... 43 III. DISC SPACE NARROWING:.......................................................................................................................................... 43 IV. BONY PROLIFERATION: ............................................................................................................................................... 43 V. EROSIONS: .................................................................................................................................................................... 44 VI. CRYSTAL DEPOSITION:................................................................................................................................................ 44 VII. SCLEROSIS:................................................................................................................................................................... 44 VIII. ANKYLOSIS: ................................................................................................................................................................... 44 IX. SUBLUXATION: .............................................................................................................................................................. 44

C. PATTERN APPROACH: ......................................................................................................................................................... 44 I. OSTEOARTHRITIS:........................................................................................................................................................ 44 II. DEGENERATIVE DISC DISEASE:................................................................................................................................. 45 III. DISH: ........................................................................................................................................................................ 46 IV. ANKYLOSING SPONDYLITIS: ....................................................................................................................................... 47 V. RHEUMATOID ARTHRITIS: ........................................................................................................................................... 48 VI. CPPD CRYSTAL DEPOSITION DISEASE:.................................................................................................................... 48 VII. GOUT: ........................................................................................................................................................................ 49 VIII. HYDROXYAPATITE CRYSTAL DEPOSITION DISEASE: ............................................................................................. 49 IX. PSORIATIC ARTHRITIS: ................................................................................................................................................ 49 X. REITER'S SYNDROME: ................................................................................................................................................. 50 XI. ENTEROPATHIC ARTHROPATHY: ............................................................................................................................... 50

D. DEMOGRAPHICS:.................................................................................................................................................................. 51 I. ARTHROPATHIES WITH MALE PREDOMINANCE: ..................................................................................................... 51 II. ARTHROPATHIES WITH FEMALE PREDOMINANCE:................................................................................................. 51

E. THE LAW OF PARSIMONY:................................................................................................................................................... 51 8.3 LUCENT LESIONS OF BONE: ............................................................................................................................................................... 52

8.3.1 DIFFERENTIAL DIAGNOSIS OF SOLITARY LUCENT BONE LESIONS:............................................................................. 52 A. AGE:........................................................................................................................................................................................ 53 B. AGE VS. MALIGNANT TUMOR TYPE ................................................................................................................................... 53 C. SIZE: ....................................................................................................................................................................................... 53 D. MARGINS:............................................................................................................................................................................... 53 E. MATRIX:.................................................................................................................................................................................. 54 F. LOCATION: ............................................................................................................................................................................. 54 G. EPIPHYSIS: ............................................................................................................................................................................ 55 H. METAPHYSIS: ........................................................................................................................................................................ 55






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I. DIAPHYSIS: ............................................................................................................................................................................ 55 J. PERIOSTEAL REACTION: ..................................................................................................................................................... 55 K. MULTIPLICITY: ....................................................................................................................................................................... 56

8.3.2 DIFFERENTIAL DIAGNOSIS OF MULTIPLE LUCENT BONE LESIONS: ............................................................................. 56 A. WISE SAYINGS ABOUT SOLITARY LUCENT LESIONS: ..................................................................................................... 56

8.4 SCLEROTIC LESIONS OF BONE: ......................................................................................................................................................... 58 8.4.1 GENERIC DIFFERENTIAL DIAGNOSIS OF SCLEROTIC BONE LESIONS: ........................................................................ 58 8.4.2 DIFFERENTIAL DIAGNOSIS OF FOCAL OR MULTIFOCAL SCLEROTIC BONE LESIONS: .............................................. 59 8.4.3 DIFFERENTIAL DIAGNOSIS OF DIFFUSE SCLEROTIC BONE LESIONS: ......................................................................... 59 8.4.4 THINGS TO REMEMBER ABOUT SCLEROTIC LESIONS: .................................................................................................. 60

8.5 PERIOSTEAL REACTION: ..................................................................................................................................................................... 60 8.5.1 CAUSES OF SOLID PERIOSTEAL REACTION:.................................................................................................................... 62

8.6 SOFT TISSUE CALCIFICATIONS: ......................................................................................................................................................... 62 8.6.1 GENERIC DIFFERENTIAL DIAGNOSIS OF DYSTROPHIC SOFT TISSUE CALCIFICATIONS: ......................................... 63

8.6 FRACTURES WITHOUT SIGNIFICANT TRAUMA:................................................................................................................................ 66 8.7 FACIAL AND MANDIBULAR FRACTURES:........................................................................................................................................... 68

8.7.1 FACIAL FRACTURES:............................................................................................................................................................ 68 8.7.2 RADIOGRAPHIC SIGNS OF FACIAL FRACTURES:............................................................................................................. 69

A. WISE SAYINGS ABOUT FACIAL FRACTURES: ................................................................................................................... 72 8.7.3 MANDIBULAR FRACTURES:................................................................................................................................................. 72

A. THINGS TO REMEMBER ABOUT MANDIBULAR FRACTURES: ......................................................................................... 74 8.8 THE PAINFUL JOINT PROSTHESIS:..................................................................................................................................................... 75 8.9 SCOLIOSIS: ............................................................................................................................................................................................ 77

8.9.1 CLASSIFICATION OF SCOLIOSIS: ....................................................................................................................................... 79 8.9.2 RADIOGRAPHIC ASSESSMENT OF THE SCOLIOSIS PATIENT: ....................................................................................... 79

9.0 UPDATES ON BASIC LIFE SUPPORT AND CPR: ................................................................................................................................ 82 9.1 ADULT BASIC LIFE SUPPORT: ............................................................................................................................................................. 82

9.1.1 MAIN CHANGES IN ADULT BASIC LIFE SUPPORT (FIGURE 1). ....................................................................................... 84 9.1.2 MAIN CHANGES IN AUTOMATED EXTERNAL DEFIBRILLATION (AED). .......................................................................... 84 9.1.3 MAIN CHANGES IN ADULT ADVANCED LIFE SUPPORT (FIGURE 2). ............................................................................. 85

A. CPR BEFORE DEFIBRILLATION:.......................................................................................................................................... 85 B. DEFIBRILLATION STRATEGY:.............................................................................................................................................. 85 C. FINE VF:.................................................................................................................................................................................. 86 D. ADRENALINE: ........................................................................................................................................................................ 86 E. ANTI-ARRHYTHMIC DRUGS: ................................................................................................................................................ 86 F. THROMBOLYTIC THERAPY FOR CARDIAC ARREST: ....................................................................................................... 86 G. POST RESUSCITATION CARE - THERAPEUTIC HYPOTHERMIA: .................................................................................... 86 A. ADULT BLS SEQUENCE:....................................................................................................................................................... 87

9.1.4 EXPLANATORY NOTES: ....................................................................................................................................................... 89 A. RISK TO THE RESCUER: ...................................................................................................................................................... 89 B. JAW THRUST: ........................................................................................................................................................................ 89 C. AGONAL GASPS: ................................................................................................................................................................... 89 D. MOUTH-TO-NOSE VENTILATION: ........................................................................................................................................ 89 E. MOUTH-TO-TRACHEOSTOMY VENTILATION:.................................................................................................................... 89 F. BAG-MASK VENTILATION:.................................................................................................................................................... 89 G. CHEST COMPRESSION: ....................................................................................................................................................... 90 H. COMPRESSION-ONLY CPR:................................................................................................................................................. 90 I. OVER-THE-HEAD CPR: ......................................................................................................................................................... 90 J. RECOVERY POSITION: ......................................................................................................................................................... 90

9.1.5 CHOKING:............................................................................................................................................................................... 91 A. RECOGNITION: ...................................................................................................................................................................... 91 B. ADULT CHOKING SEQUENCE:............................................................................................................................................. 91

9.1.6 EXPLANATORY NOTES: ....................................................................................................................................................... 92 A. RESUSCITATION OF CHILDREN AND VICTIMS OF DROWNING: ..................................................................................... 92

9.2 ADULT ADVANCED LIFE SUPPORT:.................................................................................................................................................... 93 9.2.1 CPR BEFORE DEFIBRILLATION:.......................................................................................................................................... 93

A. DEFIBRILLATION STRATEGY:.............................................................................................................................................. 93 B. FINE VF:.................................................................................................................................................................................. 94 C. VF/VT: ..................................................................................................................................................................................... 94 D. PULSELESS ELECTRICAL ACTIVITY / ASYSTOLE: ............................................................................................................ 94 E. ALS TREATMENT ALGORITHM: ........................................................................................................................................... 94






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I. SHOCKABLE RHYTHMS (VF/VT): ................................................................................................................................. 94 a. Sequence of actions................................................................................................................................................ 94

F. PRECORDIAL THUMP: .......................................................................................................................................................... 95 G. EXPLANATION FOR THE CHANGES IN THE TREATMENT OF VF/VT:.............................................................................. 95

I. CPR BEFORE DEFIBRILLATION:.................................................................................................................................. 95 II. DEFIBRILLATION STRATEGY:...................................................................................................................................... 95

H. FINE VF:.................................................................................................................................................................................. 96 I. ADRENALINE: ........................................................................................................................................................................ 97 J. VASOPRESSIN:...................................................................................................................................................................... 97 K. ANTI-ARRHYTHMIC DRUGS: ................................................................................................................................................ 98

I. NON-SHOCKABLE RHYTHMS (PEA AND ASYSTOLE) ............................................................................................... 98 L. ASYSTOLE: ............................................................................................................................................................................ 99 M. DURING CPR:......................................................................................................................................................................... 99 N. POTENTIALLY REVERSIBLE CAUSES:................................................................................................................................ 99 O. THE FOUR ‘HS’: ..................................................................................................................................................................... 99 P. THE FOUR ‘TS’:.................................................................................................................................................................... 100 Q. INTRAVENOUS FLUIDS:...................................................................................................................................................... 100 R. OPEN-CHEST CARDIAC COMPRESSION:......................................................................................................................... 100 S. SIGNS OF LIFE:.................................................................................................................................................................... 100

9.2.2 DEFIBRILLATION: ................................................................................................................................................................ 100 A. STRATEGIES BEFORE DEFIBRILLATION:......................................................................................................................... 100

I. SAFE USE OF OXYGEN: ............................................................................................................................................. 100 II. CHEST HAIR:................................................................................................................................................................ 101 III. PADDLE FORCE: ......................................................................................................................................................... 101 IV. ELECTRODE POSITION: ............................................................................................................................................. 101 V. PADS VERSUS PADDLES: .......................................................................................................................................... 101

B. AIRWAY MANAGEMENT AND VENTILATION: ................................................................................................................... 101 I. BASIC AIRWAY MANOEUVRES AND AIRWAY ADJUNCTS:..................................................................................... 101

C. VENTILATION:...................................................................................................................................................................... 102 D. ALTERNATIVE AIRWAY DEVICES:..................................................................................................................................... 102

I. LARYNGEAL MASK AIRWAY (LMA):........................................................................................................................... 102 II. THE COMBITUBE:........................................................................................................................................................ 102 III. TRACHEAL INTUBATION: ........................................................................................................................................... 102 IV. CONFIRMATION OF CORRECT PLACEMENT OF THE TRACHEAL TUBE:............................................................. 103

E. CRICOTHYROIDOTOMY: .................................................................................................................................................... 103 F. ASSISTING THE CIRCULATION:......................................................................................................................................... 104

I. INTRAVENOUS ACCESS:............................................................................................................................................ 104 G. POST-RESUSCITATION CARE: .......................................................................................................................................... 105

I. AIRWAY AND BREATHING:......................................................................................................................................... 105 II. CIRCULATION: ............................................................................................................................................................. 105

H. DISABILITY (OPTIMISING NEUROLOGICAL RECOVERY):............................................................................................... 105 I. SEDATION: ................................................................................................................................................................... 105 II. CONTROL OF SEIZURES:........................................................................................................................................... 105 III. TEMPERATURE CONTROL:........................................................................................................................................ 105

10.0 DISASTER RESPONSE AND PLANNING INCLUDING PT ROLE: ..................................................................................................... 107 10.1 DISASTER PLANNING/PREPAREDNESS:.......................................................................................................................................... 107

10.1.1 DISASTER RECOVERY: ...................................................................................................................................................... 109 10.1.2 EVALUATING THE PLAN ANNUALLY. DISASTER RESPONSE........................................................................................ 109

10.2 PRINCIPLES OF HOSPITAL DISASTER PLANNING: ......................................................................................................................... 110

TOPICS COVERED: • Osteoporosis update including World Health Organization criteria, bone mineral density and

intervention • Musculoskeletal differential diagnosis; kinematic chain tables • Updates on basic life support and CPR • Disaster response and planning including PT role






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7.0 OSTEOPOROSIS UPDATE INCLUDING WORLD HEALTH ORGANIZATION CRITERIA, BONE MINERAL DENSITY AND INTERVENTION:

Osteoporosis is characterized by reduced bone strength, diminished bone density, and altered macrogeometry and microscopic architecture of bone. Although both men and women can have osteoporosis, the risk in men is often unrecognized and remains undiagnosed for years. The resultant morbidity, mortality, and healthcare costs could all be avoided with timely intervention. No clear-cut guidelines are available for the management of osteoporosis in men. A silent disease until the catastrophic end result, osteoporosis is underdiagnosed and undertreated in men and women but is even less managed in men. With appropriate therapy, the disease can be arrested before any fracture occurs.

Osteoporosis is generally considered a women’s health issue, as evidenced by a substantial body of literature on this topic. However, according to the National Osteoporosis Foundation, approximately one fifth of patients with symptomatic osteoporosis are men. Even though osteoporosis is more common in women, the associated morbidity and mortality are greater in men. This is because osteoporosis is unrecognized in men and therefore the resulting fractures in men are associated with more complications. It is high time that primary care physicians evaluate all men starting at age 70 or those at high risk. • About one fifth of all patients with symptomatic osteoporosis are men. • The morbidity and mortality associated with osteoporosis is greater in men than in women. • In men older than 70, osteoporosis results from decreases in calcium intake/ absorption, vitamin D

activation, sex hormone concentration, and declining functioning of osteoblasts. • Evaluate all men older than 70 regularly for osteoporosis using dual-energy x-ray absorptiometry

testing. • Treatment options for primary disease include bisphosphonates, parathyroid hormone, androgens, and

nonpharmacologic interventions, including diet and calcium and vitamin D supplementation.






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7.1 DIAGNOSING OSTEOPOROSIS: There is no method of determining the actual structure of bones without actually removing a

piece during a biopsy (which is not practical or necessary). Instead, the diagnosis of osteoporosis is based on special x-ray methods called densitometry. Densitometry will give accurate and precise measurements of the amount of bone (not their actual quality). This measurement is termed "bone mineral density" or BMD.

The World Health Organization "WHO" has established criteria for making the diagnosis of osteoporosis, as well as determining levels which predict higher chances of fractures. These criteria are based on comparing bone mineral density (BMD) in a particular patient with those of a 25 year old female. BMD values which fall well below the average for the 25 year old female (stated statistically as 2.5 standard deviations below the average) are diagnosed as "osteoporotic". If a patient has a BMD value less than the normal 25 year old female, but not 2.5 standard deviations below the average, the bone is said to be "osteopenic" (osteopenic means decreased bone mineral density, but not as sever as osteoporosis). Interestingly, although these criteria are widely used, they were devised in a Caucasian female so there will be some differences when these levels are applied to non Caucasian females or to males in general. Despite this flaw, measurement of BMD is used daily and has proven to be very helpful in all groups. Some men will be subject to increased fracture rates when they have significantly less BMD than the predicted fracture level for women. In other words, some men will be at increased risk for fracture even when they have osteopenia.

Osteoporosis is different from most other diseases or common illnesses in that there is no one single cause. The overall health of a person's bones is a function of many things ranging from how well the bones were formed as a youth, to the level of exercise the bones have seen over the years. During the first 20 years of life, the formation of bone is the most important factor, but after that point it is the prevention of bone loss which becomes most important. Anything which leads to decreased formation of bone early in life, or loss of bone structure later in life will lead to osteoporosis and fragile bones which are subject to fracture.






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7.1.1 BMD TEST:

A BMD test is the only way to detect low bone density and diagnose osteoporosis. The lower a person’s bone mineral density, the greater the risk of having a fracture. A BMD test is used to: • Detect low bone density before a person breaks a bone • Predict a person’s chances of breaking a bone in the future • Confirm a diagnosis of osteoporosis when a person has already broken a bone • Determine whether a person’s bone density is increasing, decreasing or remaining

stable (the same) • Monitor a person’s response to treatment

7.1.2 RECIEPIENTS OF THE BMD Test:

There are some reasons (called risk factors) that increase your likelihood of developing osteoporosis. The more risk factors you have, the more likely you are to get osteoporosis and broken bones. Some examples are being small and thin, older age, being female, a diet low in calcium, lack of enough vitamin D, smoking and drinking too much alcohol. Your healthcare provider may recommend a BMD test if you are: • A postmenopausal woman under age 65 with one or more risk factors for osteoporosis • A man age 50-70 with one or more risk factors for osteoporosis • A woman age 65 or older, even without any risk factors • A man age 70 or older, even without any risk factors • A woman or man after age 50 who has broken a bone • A woman going through menopause with certain risk factors • A postmenopausal woman who has stopped taking estrogen therapy (ET) or hormone

therapy (HT) Some other reasons your healthcare provider may recommend a BMD test:






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• Long-term use of certain medications including steroids (for example, prednisone and cortisone), some anti-seizure medications, Depo-Provera and aromatase inhibitors (for example, anastrozole, brand name Arimidex)

• A man receiving certain treatments for prostate cancer • A woman receiving certain treatments for breast cancer • Overactive thyroid gland (hyperthyroidism) or taking high doses of thyroid hormone

medication • Overactive parathyroid gland (hyperparathyroidism) • X-ray of the spine showing a fracture or bone loss • Back pain with a possible fracture • Significant loss of height • Loss of sex hormones at an early age, including early menopause • Having a disease or condition that can cause bone loss (such as rheumatoid arthritis or

anorexia nervosa)

7.1.3 TYPES OF BONE DENSITY TESTS:

Central DXA: The National Osteoporosis Foundation (NOF) recommends a BMD test of the hip and spine by a central DXA machine to diagnose osteoporosis. DXA stands for dual energy x-ray absorptiometry. When testing can’t be done on the hip and spine, NOF suggests a central DXA test of the radius bone in the forearm. In some cases, the type of bone density testing equipment used depends on what is available in your community.

Healthcare providers measure BMD in the hip and spine for several reasons. First, people with osteoporosis have a greater chance of fracturing these bones. Second, these fractures can cause more serious problems, including longer recovery time, greater pain and even disability. BMD test results in the hip and spine can predict the likelihood of future fractures in other bones.

With most types of BMD tests, a person remains fully dressed, and the test usually takes less than 15 minutes. BMD tests are non-invasive, meaning that no needles or instruments are placed through the skin or body. When repeating a BMD test, it is best to use the same testing equipment and have it done at the same place. This provides a more accurate comparison with your last test result.

Although it is not always possible to have your BMD test at the same place, it is still important to compare your current BMD test to your last one.

pDXA






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7.1.4 OTHER TYPES OF TESTS:

In addition to central DXA, there are other methods to measure bone density that can predict the risk of breaking a bone. However, the results from these other methods are not equivalent to the results from a central DXA machine. Below are other BMD testing methods: • pDXA (peripheral dual energy x-ray absorptiometry) • QUS (quantitative ultrasound) • QCT (quantitative computed tomography) • pQCT (peripheral quantitative computed tomography) The QUS method of BMD testing uses sound waves to measure bone density. The other types of equipment listed above use radiation. Except for QCT, the amount of radiation is very small. For comparison, you are exposed to 10–15 times more radiation flying in a plane round trip between New York and San Francisco.

Healthcare providers do not routinely use standard x-rays for BMD testing. While x-rays can identify broken bones, they are not sensi-tive enough to detect osteoporosis until 25 to 40 percent of bone density has been lost. By this time the disease is well advanced.

pQCT

QUS

QCT






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7.1.5 HOW OFTEN TO REPEAT A BMD TEST:

People taking an osteoporosis medication should repeat their BMD test by central DXA every two years, according to the National Osteoporosis Foundation (NOF). Some healthcare providers may have certain patients repeat their BMD test after one year. The peripheral tests (pDXA, QUS and pQCT) are not appropriate for monitoring response to treatment at this time.

A. TESTS TO FIND BROKEN BONES:

• If you have a loss of height, posture changes or back pain, your healthcare provider may order an x-ray to look for fractures in your spine. An x-ray is the most common way to tell if you have a broken bone in your spine or other bones. In some people, spine fractures don’t cause any pain.

• Once you have a fracture in the spine, you are at greater risk for more spine fractures in the future. If you have this type of fracture, that’s why you need to speak with your healthcare provider about steps to protect your spine. You should also consider treatment with an osteoporosis medication. When you have a fracture in the spine, you still need to have a BMD test if you haven’t had one.

• Another way to find fractures in the spine is with a vertebral fracture assessment (VFA) by a DXA machine. This method uses less radiation than a standard x-ray. VFAs can show breaks in the spine and can also show the difference between broken bones and abnormally shaped bones.

7.1.6 UNDERSTANDING BMD TEST RESULTS:

When you have a bone mineral density test, • It compares your bone density to a “young normal” healthy 30-year-old adult with peak

bone density (also called peak bone mass). Peak bone density is the point at which a person has the greatest amount of bone that she or he will ever have.

• You will get the result of your BMD test in a special number called a T-score. It stands for “standard deviations” or “SD.” It indicates how much your bone density is above or below normal.

• Healthcare providers use the T-score to diagnose osteoporosis. If more than one bone is tested, they use the lowest T-score to make a diagnosis of osteoporosis. The World Health Organization (WHO) has defined the T-scores and what they mean.






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7.1.7 WHAT YOUR T-SCORE MEANS:

• A T-score between +1 and -1 is normal bone density. Examples are 0.8, 0.2 and -0.5. • A T-score between -1 and -2.5 indicates low bone density or osteopenia. Examples are

T-scores of -1.2, -1.6 and -2.1. • A T-score of -2.5 or lower is a diagnosis of osteoporosis. Examples are T-scores of -

2.8, -3.3 and -3.9. • The lower a person’s T-score, the lower the bone density. A T-score of -1.0 is lower

than a T-score of 0.5; a T-score of -2.0 is lower than a T-score of -1.5; and a T-score of -3.5 is lower than a T-score of -3.0.

• For most BMD tests, 1 SD difference in a T-score equals a 10-15 percent decrease in bone density. For example, a person with a T-score of -2.5 has a 10-15 percent lower BMD than a person with a T-score of -1.5. Your BMD test result also includes a Z-score that compares your bone density to what

is normal in someone your age and body size. Healthcare providers do not use Z-scores to diagnose osteoporosis in postmenopausal women and men age 50 or older. Among older adults low bone mineral density is common, so Z-scores can be misleading. An older person might have a “normal” Z-score but still be at high risk for breaking a bone.

Most experts recommend using Z-scores rather than T-scores for younger men, premenopausal women and children. However, healthcare providers often use

T-scores for perimenopausal women. A Z-score above -2.0 is normal according to the International Society for Clinical Densitometry (ISCD). A diagnosis of osteoporosis in younger men, premenopausal women and children should not be based on a BMD test result alone. NOF does not recommend routine BMD testing in children, adolescents, healthy young men or premenopausal women.

7.1.8 TREATMENT CONSIDERATIONS:

The results of the BMD test help your healthcare provider make recommendations about either prevention or treatment of osteoporosis. When making a decision about treatment with an osteoporosis medication, your healthcare provider will also consider your risk factors for osteoporosis, your likelihood of having future fractures, your medical history and your current health. Below are treatment guidelines for postmenopausal women and men age 50 or older: • Most people with T-scores of -1 and above (normal bone density) do not need to take

an osteoporosis medication. • People with T-scores between -1 and -2.5 (osteopenia) should consider taking an

osteoporosis medication when they have certain risk factors. • All people with T-scores of -2.5 and below (osteoporosis) should consider taking an

osteoporosis medication. WORLD HEALTH ORGANIZATION DEFINITIONS OF OSTEOPOROSIS

BASED ON BONE DENSITY T-Scores BMD Category

Examples Range

1 -1 & above Normal BMD

0.5

0 osteopenia






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-0.5

-1

-1.5 Between Low BMD (Osteopenia)

-2 -1 and -2.5

-2.5 -2.5 and Osteoporosis

-3 below

-3.5

-4

A new method called absolute fracture risk helps healthcare providers and their patients age 40 and older make better decisions about when to take an osteoporosis medication. Absolute fracture risk estimates a person’s chance of breaking a bone over a period of 10 years. Postmenopausal women and older men with osteoporosis are at greatest risk of breaking a bone.

In the past, healthcare providers knew to treat people with osteoporosis, but were sometimes uncertain about when to treat patients with osteopenia. The absolute fracture risk method makes it easier for healthcare providers and their patients with osteopenia to decide when an osteoporosis medication is necessary. This method helps make sure that people with the greatest chance of breaking a bone get treated.

Healthcare providers can get a patient’s absolute fracture risk by using a special web-based tool on a computer in their office. The healthcare provider enters a patient’s hip T-score and certain risk factors for osteoporosis. The tool predicts the patient’s absolute fracture risk. Soon, some central DXA machines will be able to provide this information.

Osteoporosis medications either slow or stop bone loss or rebuild bone. They also reduce the chances of having a broken bone. NOF encourages you to discuss your treatment options with your healthcare provider. Always look at both the risks and benefits of taking a medication, including potential side effects.

For an osteoporosis medication to work, a person still needs to get enough calcium and vitamin D and to exercise. According to NOF recommendations, adults under age 50 need 1,000 mg of calcium and 400-800 IU of vitamin D daily. Adults 50 and over need 1,200 mg of calcium and 800-1,000 IU of vitamin D daily. There are two types of vitamin D supplements. They are vitamin D3 and vitamin D2. Previous research suggested that vitamin D3 was a better choice than vitamin D2. However, more recent studies show that vitamin D3 and vitamin D2 are equally good for bone health. Vitamin D3 is also called cholecalciferol. Vitamin D2 is also called ergocalciferol.






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7.2 PHYSIOTHERAPY INTERVENTIONS:

7.2.1 RISK FACTORS:

Physiotherapists need to be aware of the major risk factors for osteoporosis so that they can effectively participate in all aspects of the prevention and management of this condition. The two major risk factors are being female and elderly. In addition, there are a number of other well established risk factors listed below6: • Early menopause (age <45) • Hypogonadism • Physical inactivity • Thin body type • Major gynaecological surgery e.g. hysterectomy • Amenorrhea • Anorexia • Heredity • Rheumatological conditions e.g. rheumatoid arthritis, ankylosing spondylitis • Smoking • High alcohol • High caffeine intake • Insufficient dietary calcium and Vitamin D. • Secondary osteoporosis accounts for 20% of cases in women and 40% of cases in

men and may occur as a result of 11: • Endocrine disorders (including thyrotoxicosis, primary hyperparathyroidism, Cushing’s • Syndrome). • Rheumatological conditions • Gastro-intestinal disorders (malabsorption, partial gastrectomy, liver disease) • Malignancy (multiple myeloma, metatastic carcinoma) • Certain drugs (corticosteroids, heparin).

7.2.2 TARGET CLIENT GROUPS FOR TREATMENT BY PHYSIOTHERAPISTS:

For the purpose of these guidelines a pragmatic decision was made to separate the target client groups into 3 broad categories:

Amenorrhea

Endocrine disorders






15

1. Those with normal bone mass concerned with reducing the risk together with people with mild bone changes (osteopenia).

2. People with a clinical diagnosis of osteoporosis without any history of fracture (#). 3. A frailer group with advanced bone changes usually having sustained fractures (#).

All categories can include both men and women of all ages. However the frailer group do tend to be older. Physiotherapists must use all available clinical information to ensure that clients are correctly categorised. If in doubt a definitive diagnosis should be obtained from the referring specialist.

The following symbols denote each group and are used throughout the recommendations to assist in the correct choice of assessment techniques and effective interventions for each category.

• Men and women who have been diagnosed with mild bone changes (i.e. BMD more than 1 SD below young average) (osteopenia) and those concerned with reducing the risk (prevention).

• Men and women who have been diagnosed with osteoporosis (i.e. BMD 2.5 SD below young adult mean) but have not yet sustained any fractures.

• A much frailer group with more severe osteoporotic changes (i.e. BMD more than 2.5 SD). This group mainly but not always comprises a more elderly population (both men and women). These patients may or may not have sustained one or more fractures.

These symbols are printed at the foot of each page as a reminder to the reader.

7.2.3 PHYSIOTHERAPY ASSESSMENT:

Once patients with a diagnosis of osteoporosis have been referred for physiotherapy, they should be correctly categorised and a detailed, standard physiotherapy assessment carried out. This will help to ensure that important issues are not inadvertently omitted. Accurate assessment of all aspects of impairment, disability and handicap, using reliable and appropriate measuring tools, is the key to delivering successful and appropriate management programmes, and assessing effectiveness. Listed below are assessment procedures applicable to osteoporosis patients, which are reliable and considered good practice by the Guideline Developers. Most of the testing procedures do not require sophisticated equipment and can therefore be used by most physiotherapists. They should be used selectively, according to the disease severity at the time of referral. Measurement of cervical /thoracic deformity, balance, lumbar spine endurance, flexibility and effect on life style should always be carried out when assessing any osteoporotic patient.






16

7.2.4 ANTHROPOMETRIC AND SPINAL MOBILITY ASSESSMENT:

These measures should always be assessed and recorded. A. HEIGHT:

Measured in centimetres (cm), patient standing with back against the wall without shoes.

B. WEIGHT: In kilograms (kg) using calibrated scales.

C. CHEST EXPANSION MEASURED AT XIPHISTERNUM: Record chest excursion with the patient standing with their hands on their head. Maximal inhalation is followed by exhalation. Total change is measured as the value at maximal inhalation minus the value at maximal exhalation. The measuring tape is placed around the xiphisternum. One measure is taken to the nearest cm. A modified technique may have to be used for those osteoporotic patients who do not have sufficient range of movement to stand with their hands on their head.

D. CERVICAL/THORACIC DEFORMITY (TRAGUS TO WALL): Heels and buttocks touching the wall, the knees straight, pushing head back while still keeping the chin in neutral position. The distance between the tragus (mastoid process) and the wall is measured to the nearest 0.1 of a cm using an tape measure.

E. SHOULDER ELEVATION: Measurement is taken with the patient standing with their back against the wall. A goniometer is placed over the greater tuberosity. The patient is instructed to elevate their shoulder into flexion. Again modifications may have to be made to the starting position for those patients with kyphotic changes.

F. LUMBAR SPINE RANGE OF MOVEMENT (SCHOBER EXTENSION): Patient standing with knees straight and feet slightly apart. Three skin marks are made: the first at the lumbosacral junction, the second and third 5cm below and 10cm above this mark. The patient is then asked to extend their back. The approximation is measured and subtracted from 15cm. One measurement should be taken.

7.2.5 STRENGTH/ENDURANCE ASSESSMENT:

Some measure of strength/endurance should be assessed and recorded. Various methods of strength measurement are available: • The trunk extension endurance measurement is a simple method of measuring the trunk

extensors. The procedure is as follows: the patient lies prone and holds their sternum off the floor.

• A small pillow is placed under the abdomen to decrease lumbar lordosis and the patient is asked to maintain cervical flexion and to demonstrate this position15. This assessment should not be maintained for longer than 20 seconds. It is contra-indicated for patients with a history of heart complaints as blood pressure may become elevated. Patients with a marked kyphosis must also be excluded.

• These client groups can use various modalities of other strength testing equipment, e.g. isometric, isotonic, using the 1 Repetition Maximum (1RM) method or more sophisticated equipment, such as isokinetics.






17

• Measurement of 1RM can also be used in this group, but care should be taken to avoid using weights at the end of long levers.

7.2.6 AEROBIC CAPACITY ASSESSMENT:

Some measure of aerobic capacity should be assessed and recorded. Various methods of aerobic tolerance testing can be used, specific to the target group. • A submaximal progressive exercise test using either a treadmill or cycle ergometer

can be used to estimate aerobic capacity. • Where testing equipment is not available, the Adapted Shuttle Walking Test is a

useful test and very easy to carry out. This test can safely be used on patients with moderate osteoporotic changes depending on their level of disability. The procedure is as follows:

The patient is asked to walk up and down a 10m course. The speed is dictated by an audio signal played on a tape. The patient walks at the stated pace and aims to turn around when they hear the signal. The patient is asked to continue the test until they are unable to maintain the required speed, or a pre-determined endpoint is met e.g. 60% of age-adjusted predicted maximum heart rate. This is worked out by using the simple equation 220 minus the age of the patient. This gives predicted maximum heart rate. This figure is the multiplied by 0.60 to give the 60% maximum.

• Other walking tests may be appropriate for patients with more severe changes or those tested at home, for example, the Elderly Mobility Scale (EMS) and the ‘Timed Up and Go Test’ (TUAG).

• The Guideline Developers consider these two tests appropriate for this patient group. The EMS is a 20 point scale measuring functional abilities such as transfers, balance and walking speed. For the TUAG test the subject is asked to stand up from a standard height chair walk 3 metres, turn around, walk back and sit down. The whole process is timed from initiation of standing to the sitting position.

7.2.7 BALANCE ASSESSMENT:

This should always be assessed and recorded. • Assessment of balance is an important measurement, as one of the main aims of a

physiotherapy exercise programme is to reduce falls. A very simple test is the ‘one legged stand’. For this, the patient is asked to stand between a set of parallel bars on one leg without holding onto the bars.

• The subject is given a practice attempt and this is followed by a timed attempt. Testing can be carried out on both legs and can also be carried out with eyes closed. This should always be tested between parallel bars for safety.

7.2.8 FUNCTIONAL ASSESSMENT:

• Assessment of functional ability in the community should always be made. This will help to ensure the appropriate intervention for each individual.

• It is important to establish the extent of disability and handicap. This will help in the setting of treatment goals, plans for intervention, and so take the physiotherapy management effective for the patient; to reduce the chances of falling in the community. For an in-depth pain and activity record the Osteoporosis Functional Disability Questionnaire (OFDQ) is very useful.






18

• An appropriate functional test for this group should be used e.g. ‘timed sit to stand’, grip strength, stair climbing or 20 metre timed walk.

7.2.9 PAIN ASSESSMENT:

• There are various measurement tools applicable for these patient groups. For example: visual analogue scales, the McGill pain questionnaire, and the monitoring of daily analgesic intake.

• The QFDQ can also be used as a measurement of pain.

7.2.10 ANALYSIS OF ASSESSMENT AND OUTCOMES:

• It is not enough to merely record a standard assessment and use standardised outcome measures.

• The findings of the assessment and the results of the outcome measures should be routinely analysed by individual clinicians and the Service as a whole. This will help clinicians to consider the effects of intervention and attribute the reasons for changes appropriately.

7.3 PHYSIOTHERAPY MANAGEMENT:

The management section deals firstly with the unique exercise and lifestyle requirements for enhancing bone health and functional independence in each of the three target groups. This is followed by more general sections about balance, posture, education, psychological well-being and potential harms and risks which affect all three groups.

7.3.1 MANAGEMENT FOR THE OSTEOPENIC AND PREVENTION GROUP:

Aims • Increase the peak bone mass in the at risk/preventative group • Maintain or increase BMD in the osteopenic group and reduce the early rapid bone

loss after menopause • Improve muscle strength, balance, cardiovascular fitness • Improve posture • Improve psychological well-being • Provide education.






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7.3.2 EXERCISE MANAGEMENT FOR BONE HEALTH:

• Exercise therapy in the form of weight bearing aerobic training activity and or strength training activity is now recognised as a valid and important intervention in the management of bone health. It is thought that the mechanical stresses that are put through bone during exercise can affect bone density. Weight bearing activity stimulates bone remodelling. It has been hypothesised that bone hypertrophy occurs in response to microfractures at the level of the osteon. Microscopic damage occurs where the tendon attaches to the bone when the stress applied is in excess of the normal levels, e.g., during weight bearing physical activity.

• There is evidence that high impact exercise has the greatest potential to affect bone density in pre-menopausal women.

• High impact exercise is suitable for those who regularly exercise. A lower impact programme of exercise is also appropriate especially for those not used to exercise. To be effective all exercise programmes need to be progressive in terms of impact and intensity as fitness and strength levels improve. However it is essential that all programmes begin at a low level that is comfortable for the patient. The assessment will give the physiotherapist a reference point from which to start the exercise programme. Reference should be made to the ACSM on progression of exercise programmes. However it is generally accepted that microfracture is needed for an osteogenic response.






20

Many well-designed randomised controlled trials have investigated the effects of exercise on bone health in the postmenopausal osteopenic group. The aim of exercise in this group is to reduce the early rapid loss of bone density following the menopause and also maintain and sometimes increase bone mass. • High impact exercise, e.g. skipping and jogging, has the greatest potential to improve

BMD in premenopausal group. Grade A Level Ib

• Low to medium impact exercise, such as step aerobics, intermittent jogging is more appropriate for those not used to exercising and those over 50 years of age 30. Grade A Level 1b

• Integrate high impact with medium and or low impact activities for a well-designed and safe programme. People should be instructed in the use of rebound techniques, i.e. give or bend in the knees on take off and landing.

• Strength training is useful in sedentary young individuals provided it is of a high enough intensity i.e. 70–80% 1RM. It not only improves strength, but also is accompanied by improvements in BMD. Grade A Level 1b

• All exercise programmes should start at an easy level and be progressive in terms of intensity and impact. Grade C, Level III






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7.3.3 PRECAUTIONS:

Although high impact exercise is recommended for improvements in bone health, prolonged periods of high impact exercise are not necessary and can cause soft tissue injuries and pelvic floor stress. Optimum benefits will only be achieved by ensuring safe design of programmes and correct performance that incorporates a balance of high/low impact exercise. All high impact exercise is inappropriate and unsafe if: • People suffer from joint conditions • People cannot perform exercise with correct technique i.e. unable to rebound

effectively • People with pelvic floor problems • The design of the programme is unsafe, e.g. all of the exercise occurs on the spot, and

if the programme does not incorporate medium and low impact exercise.

7.3.4 THE OSTEOPOROTIC GROUP WHO HAVE NOT SUSTAINED FRACTURES:

Aims • Maintain bone strength • Prevent fractures • Improve muscle strength, balance, cardiovascular fitness • Improve posture • Improve psychological well-being • Provide education • Aim to reduce falls A. EXERCISE MANAGEMENT FOR BONE HEALTH:

• The evidence of the effects of exercise on the skeleton is not as conclusive for those with an actual diagnosis of osteoporosis. Most of the studies have been carried out on postmenopausal sedentary women who are not actually osteoporotic. The conclusions from these studies are that exercise regimes are beneficial in promoting bone health. It has been inferred from these studies and others that these regimes could be used effectively for those with osteoporosis.

• One study, which has investigated those patients with an actual diagnosis of osteoporosis, found improvements in bone mineral density of the distal forearm following high rates of dynamic loading. This reinforces the hypothesis that exercise training is required to be site specific.

• One study carried out concluded that post-menopausal bone mass can be significantly increased by a strength regimen that uses high load, low repetitions but not by an endurance regimen that uses low load, high repetitions. This suggests that peak load is more important than the number of loading cycles in increasing bone mass in early post-menopausal women.

• Some of the principles also apply to the postmenopausal osteopenic group and in these cases the symbol will also be shown.

• It is advised that the overload principle is applied through a high load and low repetitions regime.

• Any form of strength training does require to be site specific i.e. targeting areas such as the muscle groups around the hip, quadriceps, dorsi/plantar flexors, rhomboids, wrist extensors and back extensors. Grade A, Level 1b






22

• Weight bearing exercises should be targeted to loading bone sites predominantly affected by osteoporotic change i.e. hip, vertebrae and wrist. Grade B, Level 2a

• The most recent meta-analysis concluded that exercise (aerobic and strength) helps to slow the rate of post-menopausal bone loss in postmenopausal women.

• Exercise should be used in combination with both adequate calcium intake and some type of hormone replacement therapy for maintaining and/or increasing bone mineral density in postmenopausal women at risk from osteoporosis 38. Grade A, Level 1a

• All exercise programmes should start at an easy level and be progressive in terms of intensity and impact.

B. PRECAUTIONS The following activities should be avoided: • High impact exercise • Trunk flexion • Trunk rotational torsion movements with any loading • Lifting • The pelvic floor precautions listed in the 7.3.3 section also apply.

7.3.5 FRAILER GROUP WITH SEVERE CHANGES WHO HAVE OFTEN SUSTAINED FRACTURES:

Aims • Falls reduction • Prevention of further fractures • Balance/co-ordination • Improvements in muscle strength, flexibility, aerobic capacity, posture • Gait re-education • Psychological well-being and increased confidence • Reduce/control pain

A. EXERCISE MANAGEMENT:

• The aim of exercise therapy in this frailer group is predominantly to minimise the risk of falling and thereby risk of fracture, as opposed to affecting bone density. However, studies of this generally elderly group have found that improvements in muscle strength can be achieved.

• The exercise tolerance of this group may be poor. Therefore any form of training must start with a very low intensity.

• Exercise training must start at a very low intensity using low impact exercises. • For strength training initially use very short levers or body resistance. • Exercises in warm water (hydrotherapy) are assisted by the physical properties of

water, namely buoyancy and temperature. The weight relieving property of water immersion allows easier movement with less pain. There is no evidence to suggest that hydrotherapy has any effect on bone mineral density. However, there is evidence that other physiological parameters can be affected, such as muscle strength, aerobic capacity and pain control. There may also be an increase in psychological well being.






23

• Exercises that patients find difficult on dry land may be more easily carried out in water. For example, trunk extension will be impossible for some of these patients on dry land but can be achieved in water and resistance can gradually be increased.

• All exercise programmes should be progressive in terms of intensity and impact. A very gentle low impact programme using gravity and body resistance exercise is recommended. Grade C, Level III

B. PRECAUTIONS:

• No high intensity exercise • All the precautions listed in the previous sections apply to this frail group.

C. PAIN MANAGEMENT:

Pain management in this group is a major part of the therapeutic intervention. These patients are often referred for physiotherapy following painful vertebral compression fractures. Pain management therefore becomes a priority before the patient can be introduced to any exercise programme. However, it should be noted that only 50% of patients with a vertebral fracture complain of pain 45. Other causes of pain can be abnormal stress on joints and soft tissues due to postural changes, resulting in muscle spasms and imbalances. Another complaint is pain arising from the lower ribs pressing down onto the pelvis, due to reduction in height and kyphotic changes. The following modalities may be effective for osteoporosis and apply to all those with associated pain in any of the target groups. I. HYDROTHERAPY:

Hydrotherapy should be considered as a treatment modality where the patient has pain from recent vertebral fractures, and/or postural and balance problems. Hydrotherapy is also a very useful modality to build confidence in very disabled people and those afraid of further falls.

II. TRANSCUTANEOUS ELECTRICAL NERVE STIMULATION (TENS):

• TENS has been shown to be effective in some patients with chronic pain conditions. The rationale for use is based on the activation of the pain gate mechanism.

• TENS should be considered as a modality for the osteoporotic patient with intractable pain, especially those with chronic back pain and recent vertebral fractures. Grade A, Level Ib

III. INTERFERENTIAL THERAPY:

The mechanism for pain relief is the same as for TENS.

IV. HEAT: • Applied heat has several possible physiological benefits, such as reducing

muscle spasm, increasing local blood flow and stimulating an analgesic effect. • Patients should be instructed on how to use heat therapy safely at home to

relieve pain symptoms






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V. RELAXATION: Relaxation has long been advocated for reducing muscle tension and anxiety 49. The two most widely accepted methods are the Jacobsen progressive relaxation and the Mitchell simple physiological technique. The use of relaxation should be discussed with/offered to osteoporotic patients with intractable pain.

VI. COMPLEMENTARY THERAPIES:

Recently other forms of pain management such as reflex therapy; aromatherapy and acupuncture have become more popular as alternative ways of managing pain by physiotherapists. For more detailed information reference should be made to the specific literature and the appropriate CSP Clinical Interest Group.

7.3.6 BALANCE AND FALLS MANAGEMENT:

• Exercise for all age groups has the potential to improve dynamic stability and co- ordination and therefore could have a protective role in preventing falls in later life. The activity needs to be weight bearing.

• A study carried out on pre-menopausal women found that high impact loading exercise carried out once a week improved both balance and co-ordination.

• The diagnosis of osteoporosis becomes of clinical importance following fractures, which are generally the result of trauma from falls. Causes of falls are known to be multi-factorial. They include deficiencies in eyesight, footwear, balance, co-ordination, strength, home environment and general health, including diet and medication.

• Tai Chi is an ancient exercise and martial art that has been practised in China for centuries by all age groups. There are various forms of Tai Chi. One particular form of Tai Chi is Chuan, which is especially useful for older people. It includes slow, controlled dimensional movements and has been shown to improve balance, muscle strength and to reduce significantly the fear of falling.

• It is important particularly with the fragile groups to aim for a sensible balance between providing people with protective means, i.e. walking frames, hip protection pads, and enough exercise to obtain potential improvements in bone health, strength and balance. Physiotherapists, through their training, experience of exercise with other vulnerable groups, and skills in observation, are well placed to facilitate progress in these groups and should be encouraged to do so.

• A thorough falls risk assessment should be made and risk factors eliminated as far as possible.

• Some elements of Tai Chi could be incorporated into any exercise class but are especially effective for those elderly people where balance is a problem.

• Any activity that promotes co-ordination and balance appropriate to the severity of the disease should be encouraged, i.e. simple balance exercises such as supported one leg stands can be effective.

• The use of hydrotherapy is frequently indicated to reduce pain, and to provide a safe environment for balance exercises.






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7.3.7 POSTURE AND FLEXIBILITY:

• Thoracic kyphosis, due to vertebral fractures, is often a clinical sign of osteoporosis and is often associated with pain. Postural education and awareness are important in preventing/minimising respiratory problems, neck pain and balance disorders.

• Severe kyphotic changes may be a problem for subjects in this group, possibly limiting their ability to exercise due to a compromised respiratory system and causing pain. It is especially important for those with postural deformities to maintain maximum range of movement of the shoulder girdle, spine and hips and prevent further postural changes. Stretching exercises should focus on the thoracic and cervical spine for these patients.

• Back extension exercises are very important for this group55. Kyphosis can often be improved as it is not totally dictated by the shape of the bones but also by muscle weakness and/or pain. Grade B, Level IIa

• Back extension exercises can also be taught in the seated position for those unable to lie on their front.

• Exercises should concentrate on encouraging chest excursion, rhomboid exercises and balance.

• Gait re-education and appropriate walking aids may also be necessary. • Stretching to improve flexibility should be part of every exercise programme for all of

the client groups. Stretching of all the major upper and lower limb muscle groups should be carried out.

• Stretching should always be carried out following a warm-up period. • Ballistic stretching should always be avoided.

7.3.8 EXERCISE PRESCRIPTION:

• It is important to consider the roles of Frequency/Intensity and Duration of Exercise Prescription in maximising the positive effects on bone health.

• Studies have shown that weight-bearing exercise, with progressive increases in intensity, needs to be continued for more than nine months in order to achieve positive effects on bone density. Once exercise programmes are discontinued the positive effects will be reversed.

• There is now evidence of a dose response relationship between exercise and bone mineral accretion following a study by Korht et al. She found a significant relationship between increases of whole body BMD and the net increase in energy expenditure (i.e. physical activity). She indicated that vigorous exercise training can induce significant increases in BMD in older postmenopausal women. However, more work needs to be done to determine whether single parameters of the amount of exercise, such as frequency, duration and intensity, can be predictive of changes in BMD.

• In the absence of other specific literature on intensity of exercise needed to impact directly on bone health, it is suggested that the recommendations from the American College of Sports

• Medicine on dosage in connection with cardiovascular health might be applied. In 1990 it recommended a weekly minimum of at least three x 20-minute sessions of vigorous intensity exercise. However, in 1993 the Centre for Disease Control in conjunction with the American

• College of Sports Medicine recommended a general more active living approach with more frequent bouts of moderate intensity exercise 17. Five x 30 minutes per week of moderate exercise is a general guideline.






26

• As bone density changes due to weight-bearing exercise will not normally be detected before nine months, exercise programmes should be designed and structured to enable and motivate clients to continue indefinitely and exercise with moderate intensity five x per week. Once exerciseprogrammes are discontinued the positive effects will be reversed. Grade A Level 1b

7.3.9 PSYCHOLOGY OF EXERCISE:

• Habitual exercise, particularly aerobic type activity, is well known to have beneficial psychological effects in all age groups. These effects have been well researched in a number of clinical populations. There are guidelines on constructing sessions to improve well-being in cardiac rehabilitation and chronic low back pain which could be adapted for the osteoporotic population. A recent study by Bravo et al found an improvement in self-perceived health in subjects who had exercised for one year, compared to their non-exercising counterparts.

• Encourage habitual aerobic type exercise (dry land or water) for psychological health benefits. Grade A, Level 1b

A. ADHERENCE:

• It is generally accepted that neither initial motivation nor sustained compliance to exercise are easy to achieve. Factors such as the enjoyment, convenience and intensity of prescribed exercise can have a significant impact on participation and adherence. Group exercise has a number of potential advantages, including a large professional-to-subject ratio, on site supervision, visual modelling on the instructor, a set structure with regard to location, exercise format and duration, time and face-to-face encouragement.

• Gaining advice and information from fellow participants and group support is also helpful. Music in an exercise class is a useful way to create a positive atmosphere. Self-management techniques to use in conjunction with or following participation in exercise classes should be encouraged.

• A successful exercise programme, especially for an older population, should build on individuals’ previous habits, tapping any skills that have been acquired. Above all, exercise must be seen to be personally rewarding. A skilled class leader can present participation as a means of escape from physical dependency, of earning the respect of significant others and of personal fulfilment.

B. PROMOTING HABITUAL EXERCISE:

• The target groups will have to form a lifelong habit of exercising regularly. Once individuals can exercise safely and have an awareness of how to avoid potential risks they should start to participate in appropriate exercise groups in leisure facilities and sports centres. It should be recognised, however, that some individuals do not like exercising in a group. If this is the case individuals should be encouraged to enjoy an active lifestyle including exercises at home.

• Physiotherapists should forge links with local institutions (leisure and sports facilities) and possibly contribute to the training of fitness instructors in order to facilitate continuing safe and effective exercise provision for these subject groups outside the healthcare setting.






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7.4 POTENTIAL HARMS AND RISKS: • The physiotherapist must be aware that there are potential risks for those undertaking exercise

and special care should be taken with the osteoporotic and frailer group. • Fracture is the main risk factor for all the client groups. • Exercises should not be high impact. Excessive rotational movements should be avoided as

well as flexion exercises, as these have been shown to increase vertebral fractures. • Care should be taken with the exercise tolerance of the individual. If the individual has a poor

exercise tolerance test result (See Section 7.2.6), exercises should be gentle but still progressive.

• Forceful joint manipulation is contra-indicated when osteoporosis has been diagnosed.

7.5 EDUCATION:

7.5.1 PATIENT EDUCATION:

Patient education is an important part of physiotherapy management, both in obtaining adherence to an exercise programme and in helping to relieve pain, fear and anxiety when pain is a major symptom. It is the role of the physiotherapist therefore to: • Guide patients to understand the implications and risk factors associated with

osteoporosis and to motivate them to become active participants in all aspects of the management of their condition.

• Give lifestyle advice on lifting and handling, diet, posture and safe exercise/activity • Encourage patients to achieve the correct balance between activity and rest and to set

realistic individual goals, which will be dependent on the severity of their condition. • Make available to people additional information with regard to local self help groups,

exercise classes in the community and the National Osteoporosis Society. • Liaise with other health care professionals such as dietitians, doctors, occupational

therapists and specialist nurses.

7.5.2 HEALTH EDUCATION:

• Physiotherapists have a professional responsibility to promote exercise strategies for bone health for all age groups.

• Physiotherapists should especially involve themselves in promoting the benefits of exercise to raise physical activity levels for young people and therefore achieve a high peak bone mass. They should aim to highlight the importance of prevention to all age groups.

• Lists of useful local information for sufferers should be available in physiotherapy departments.






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8.0 MUSCULOSKELETAL DIFFERENTIAL DIAGNOSIS; KINEMATIC CHAIN TABLES:

8.1 GENERAL PRINCIPLES: • Vascular • Infection • Neoplasm • Drugs • Inflammatory/Idiopathic • Congenital • Autoimmune • Trauma • Endocrine/Metabolic

Let's try VINDICATE with diffuse sclerotic bone disease. We want to start by considering that diffuse disease is most often caused by entities that are generalized or systemic in action. Put these entities at the top of your differential. Below them on the list should be the entities that usually are more focal in nature, but which can occasionally spread diffusely throughout the musculoskeletal system. Omit any entities that don't make any sense or don't cause bony sclerosis. So, here's the raw differential one might come up with: • Vascular

o Hemangiomas o Infarcts (sickle cell)

• Infection o Chronic osteomyelitis

• Neoplasm o Primary

Osteoma Osteosarcoma

o Metastatic Prostate Breast Other

• Drugs o Vitamin D o Fluoride

• Congenital o Bone islands o Osteopoikilosis o Osteopetrosis o Pyknodysostosis

• Trauma o Fracture (stress)

• Endocrine/Metabolic o Hyperparathyroidism o Paget's disease

The next thing to do is to reorder these entities so that they are now arranged in order of their likelihood. Here's how that list might look if rearranged this way for a particular patient:






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8.1.1 DIFFERENTIAL DIAGNOSIS IN ORDER OF PREVALENCE:

• Generalized or systemic processes o Hyperparathyroidism o Diffuse skeletal infarcts (sickle cell) o Drugs (vitamin D, fluoride) o Congenital (osteopetrosis, pyknodysostosis)

• Usually focal processes presenting as diffuse disease o Metastatic tumor (prostate, breast, other)

• Entities that are pretty darned unlikely to present as a diffuse process o Primary neoplasms (osteoma, osteosarcoma) o Congenital (bone islands, osteopoikilosis) o Metabolic (Paget's) o Trauma o Chronic osteomyelitis o Hemangiomas

If a disorder or finding has its own special differential, use it Sometimes, a specific category of disease will have its own intrinsic logic that dictates the easiest way to approach disorders in that category. Examples of this will be presented for each major finding in this syllabus. For now, I'll present two examples of this: one for vertebra plana (a vertebral body that is as flat as a pancake) and one for jaundice. First, let's look at what the universal differential diagnosis gives us for vertebra plana. • Infection

o Vertebral osteomyelitis (bacterial, TB, etc.) • Neoplasm

o Metastasis o Myeloma o Lymphoma o Eosinophilic granuloma

• Trauma o Fracture

For vertebra plana, the differential diagnosis I like to use is: MELT. I likethis differential not only because it is useful and succinct, but also because it actually spells out a real word! • Metastasis / Myeloma • Eosinophilic granuloma • Lymphoma • Trauma / TB

With a specific differential diagnosis like this, you don't waste your time considering a lot of unlikely causes of disease.

This shorter and more specific differential diagnosis came up with the same list of possibilities, as the longer and more comprehensive one, just in a different order. The down side of using the longer universal differential diagnosis is that it forces one to consider lots of possible etiologies that just don't make that much sense as causes for vertebra plana.

Sometimes, though, it does make more sense to lengthen the differential diagnosis, rather than shorten it. A good example of this is in the workup of jaundice, which has jillions of causes. Just as an exercise, shut the syllabus for a moment and see how many causes of jaundice that you can






30

think of off the top of your head. Go ahead, dig around up there, and when you finish racking your brain, come back here and we'll look at a way to expand VINDICATE to look at jaundice.

8.1.2 DIFFERENTIAL DIAGNOSIS OF JAUNDICE:

Prehepatic Hepatic Posthepatic

V Pulmonary embolism with infarction

hemobilia

I generalized sepsis, malaria viral hepatitis cholangitis

N neoplastic syndromes hepatoma & hepatic metastases

pancreatic carcinoma & cholangiocarcinoma

D alcohol, solvent exposure, contraceptives

I pancreatitis

C hereditary spherocytosis & other causes of hemolysis

Gilbert, Rotor, Dubin-Johnson & Crigler-Najar syndromes

biliary atresia

A hemolytic-uremic syndrome

T soft tissue injury with large hematomas

hepatic trauma

E parenteral hyperalimentation Hopefully, VINDICATE helped you to dredge up a few more entities in your differential

diagnosis that you might have otherwise missed. It certainly helps me to dredge them up. One last thing about mnemonics: sometimes they are appropriate and helpful and sometimes

they're not. I offer the following two examples as a reductio ad absurdum proof of this point. 1. OMONTETE I learned this one on a pediatric rotation while I was in med school. It was given to

me as a memory aid for use in newborn physical examinations. 2. " Frank sings those fine, fine songs -- sings even new tunes ever tunefully." I learned this one

sometime during my radiology residency, just in time for boards..... Wise sayings in musculoskeletal radiology As Captain James T. Kirk keeps saying, "Spock, sometimes logic is not enough!" Once one has applied all of the logical rules, one still may not have a definite diagnosis. In such cases, it is helpful to apply various empirical rules that have been noted and collected over the years by various wise and venerable musculoskeletal radiologists. These are the radiological equivalent of some of the wise sayings from other walks of life shown below.

WISE SAYING USERS USAGE Red sky in morning, sailors take warning -- Red sky at night, sailor's delight. Sailors Weather prediction

Beer and whiskey, mighty risky -- whiskey and beer, never fear. Drunkards

Estimation of the a priori probability of big time yorfing given excessive consumption of short chain hydrocarbons

Red and yellow, kill a fellow -- red and black, OK, Jack. Boy Scouts

Distinguishing the highly poisonous coral snake from the similar but nonpoisonous king snake

A long lesion in a long bone. Radiologists A finding suggestive of fibrous dysplasia






31

There is an awful lot more that one should know about fibrous dysplasia besides the fact that it often presents as a long lesion in a long bone, but this can still be a very helpful little rule at times. Therefore, in each chapter, after I have laid a logical framework for approaching a radiologic problem, I will then try to list as many "wise sayings" about that problem that I can remember.

8.2 ARTHRITIS: Arthritis may, at times, present a mystifying appearance to the radiologist. However, even complex cases will usually yield to a logical and systematic approach. My personal approach involves consideration of each of the following five principles in turn: 1. Sutton's law 2. Radiographic hallmarks 3. Pattern approach 4. Demographics 5. The law of parsimony I find it helpful to separately consider the arthropathies that affect the appendicular and axial skeleton. In the next two sections, I will apply each of the five principles above to these two categories of arthritis.

8.2.1 APPENDICULAR ARTHRITIS:

A SUTTON'S LAW: This law has been ascribed to Willie Sutton, a famous bank robber. When asked why he robbed banks, he reportedly said, "Because that's where the money is." In the radiographic evaluation of appendicular arthropathies, the "money" is generally in a relatively small handful of disorders. Even though over 90 different rheumatic diseases are recognized by the American College of Rheumatology, only three entities are commonly seen in most clinical radiology practices, even including those located in large tertiary medical centers. Osteoarthritis (a.k.a. degenerative joint disease) is the most commonly seen form of appendicular arthritis. The other two commonly seen arthropathies are rheumatoid arthritis and calcium pyrophosphate dihydrate (CPPD) deposition disease. Less common arthropathies that may manifest radiographic findings in the appendicular skeleton include septic arthritis, and gout. Most other appendicular arthropathies are seen only rarely.

B RADIOGRAPHIC HALLMARKS:

In George Orwell's Animal Farm, it is stated that "All animals are equal. But some animals are more equal than others." This principle is manifested in the appendicular arthropathies, where some radiographic findings are quite specific and can quickly lead one to the correct diagnosis. Other findings are less specific and are usually unhelpful in ordering one's differential diagnosis.






32

In a diarthrodial joint, osteophytes are the sine qua non of osteoarthritis. Osteophytes can be seen in both primary and secondary osteoarthritis.

• Osteophytes can also be seen at various entheses (sites of tendinous or ligamentous attachment to bone), often due to altered or increased stress there.

• In general, the presence of erosions bespeaks some type of inflammatory disease, whether the erosions are due to synovial hypertrophy, crystalline deposits, or infection.

• In rheumatoid arthritis, the erosions follow the development of an inflammatory proliferation of the synovium, called pannus. As this pannus increases in amount, it begins to cause erosions of the chondral surface.

Marked osteophytosis (arrows) is seen in the DIP and PIP joints in these fingers

Osteophytosis (arrow) is noted at the articular margin of the femoral head






33

• As the pannus increases further in amount, one begins to see erosions at the periarticular "bare" areas. These "bare" areas refer to bone within the synovial space which is not covered by articular cartilage. The articular cartilage tends to protect the bone that it covers. The marginal "bare" areas are not covered by cartilage, and the earliest erosions of rheumatoid arthritis are seen here.

If the inflammation proceeds unchecked, the erosions of the bone and the cartilage may become profound, and the joint may finally undergo fibrous ankylosis.

The presence of crystal deposits (chondrocalcinosis or tophi) indicates one of the crystalline arthropathies. In calcium pyrophosphate dyhidrate depostition (CPPD) disease, the most common site of radiographic calcifications is in fibrocartilage and hyaline articular cartilage (chondrocalcinosis). However, calcifications may also be seen in the joint capsule or synovial membrane.

Erosions (arrows) are noted in the periarticular areas of the toes in this patient with rheumatoid

arthritis

Multiple erosions and marked joint space narrowing are noted in a pancarpal

distribution in this patient with rheumatoid arthritis

Erosions (arrows) are noted at the articular margins of

the tibia in this patient with juvenile chronic arthritis






34

Calcification may be seen at several sites about a joint in CPPD

Chondrocalcinosis is seen in the triangular fibrocartilage of this wrist

Chondrocalcinosis is seen in both the fibrocartilage of the menisci and in the hyaline articular cartilage of this

knee

A gouty erosion (arrow) is noted along the medial margin of the first metatarsal head in

this patient with gout -- relative sparing of the articular cartilage is also noted






35

In gout, erosions are caused by tophi. These tophi may be either intra- or extra-articular in location. Calcifications are occasionally seen in tophi. The erosions of gout may appear very similar to those seen in rheumatoid arthritis. However, in gout, there tends to be early sparing of the articular cartilage between the erosions, while the cartilage is thinned much earlier in the course of rheumatoid arthritis.

C PATTERN APPROACH: It would be nice if one could start with a few basic pathophysiological axioms, and from these first principles go on to deduce the characteristic sites of joint involvement of the various appendicular arthropathies. Unfortunately, such principles remain obscure, forcing one to memorize empirical patterns. However, once learned, these patterns can be helpful in ordering the differential diagnosis. Although such patterns have been described for most of the appendicular joints (Resnick, 1995), the most specific of these patterns of joint involvement are seen in the hands and wrists. Less specific patterns are seen in the hips and knees.

Typical distribution of arthritis in the hands Joint compartments of the wrist -- CMC (first carpometacarpal), CCMC (common

carpometacarpal), ST (scaphotrapezial), MC (midcarpal), RC (radiocarpal), and DRUJ (distal

radioulnar joint)

Typical distribution of arthritis in the wrists






36

Any joint in the body can be affected by secondary osteoarthritis due to trauma, infection or another arthropathy. However, the findings of primary (idiopathic) osteoarthritis are usually seen in the distal interphalangeal (DIP) joints of the hand, and the first carpometacarpal joint and scaphotrapezial joint of the wrist. The proximal interphalangeal (PIP) joints may occasionally be affected. Rheumatoid arthritis(RA)tends to involve the PIP and metacarpophalangeal (MCP) joints of the hand and all of the major joint compartments of the wrist (pancarpal involvement). CPPD deposition disease usually initially affects the radiocarpal (RC) joint in the wrist, but may also involve the MCP joints of the hand.

D DEMOGRAPHICS: • Age and gender may occasionally be useful in narrowing the differential diagnosis

of the appendicular arthropathies. For example, the most common arthropathies in children are juvenile chronic arthritis and septic arthritis, while entities such as rheumatoid arthritis, osteoarthritis and CPPD arthropathy are generally seen in older adults. CPPD arthropathy affects both genders equally. Rheumatoid arthritis has a moderate female predominance, as does osteoarthritis in the older age group. Gout, on the other hand, has a moderate to strong male predominance.

• Other demographic factors, such as home location, occupation and even ethnic subtype can occasionally be helpful in steering the differential toward or away from certain disease entities.

Typical distribution of arthritis in the knees

Typical distribution of arthritis in the hips






37

E THE LAW OF PARSIMONY: • In the first two years of medical school, one is taught to take historical points and

physical findings and to put them together into one diagnosis which explains everything (the law of parsimony). However, once one reaches the ward rotations and opens a patient's chart to the problem list, one sees that most real patients have several disorders going on simultaneously.

• By the time one gets out of medical school, into radiology, and begins to interpret joint films, this lesson often seems to have been lost. In real life, patients often have more than one arthropathy. This is most commonly seen in patients with secondary osteoarthritis superimposed upon some other arthropathy.

• Virtually any arthropathy which causes cartilage loss can lead to secondary osteoarthritis, with all of the classic signs of osteoarthritis, including osteophytosis. In fact, in certain patients, the changes from the primary arthropathy may be significantly obscured by the secondary osteoarthritic changes. A clue that this is happening is that the most distinctive sign of osteoarthritis, osteophytosis, is often fairly minimal compared to other findings such as joint space narrowing or subchondral sclerosis. In fact, this is a very common presentation of rheumatoid arthritis of the knee: marked joint space narrowing and subchondral sclerosis, but no evident erosions, and only minimal osteophytosis. In primary osteoarthritis, on the other hand, marked joint space narrowing is usually accompanied by moderate or marked osteophytosis.

• Other combinations of arthropathies are possible, such as gout and CPPD, gout and RA, RA and DISH (RADISH), etc. Therefore, when apparently contradictory findings are noted, remember that the law of parsimony is often broken.

F. CONCLUSION:

The five simple principles listed above are neither absolute nor comprehensive, and they should not be followed dogmatically. Relying solely on them for the diagnosis of arthritis would be like using only the rule "buy low, sell high" to seek wealth. However, these principles form an effective framework for the diagnosis of most of the cases of appendicular arthropathy which one actually sees in a clinical radiology practice, and can be very helpful in elucidating the cause of even radiographically complex arthropathies.






38

8.2.2 AXIAL ARTHRITIS:

In the appendicular skeleton, one is mostly concerned with the diarthrodial synovial joints. While this type of joint is also found in the axial skeleton (the facet (a.k.a. aphophyseal) joints and portions of the sacroiliac joints), there are also many amphiarthrodial joints which are not synovial (the intervertebral disc joints). However, there are several structures in the intervertebral disc joint which are analogous to structures found in a true synovial joint. The cartilaginous endplate, the annulus fibrosus, and the nucleus pulposus are analogous to the articular cartilage, the joint capsule and the synovial fluid of the synovial joint. The different anatomy and physiology of these joints means that we will see different disorders affecting this part of the skeleton. However, the same basic logical principles mentioned in the last chapter also apply here. A. DEGENERATIVE DISORDERS:

I. OSTEOARTHRITIS: This is, by far, the most common type of arthritis seen in humans. By definition, osteoarthritis occurs in a synovial joint. In the spine, therefore, osteoarthritis occurs in the apophyseal (facet) joints, the uncovertebral joints (cervical spine), the costovertebral joints, and the sacroiliac joints. Osteoarthritis may be primary or secondary.

Marked osteophytosis and joint space narrowing is noted in the facet joints in this patient with severe osteoarthritis of the lumbar spine -- the osteophytosis is causing significant encroachment on the lateral

recesses bilaterally






39

II. DEGENERATIVE NUCLEAR DISEASE:

Another very common disorder is degeneration of the nucleus pulposus. With age, the nucleus tends to become more and more dehydrated, and gradually begins to degenerate. As this happens, the intervertebral disc height begins to decrease. When this happens, the altered pattern of stresses may lead to marginal osteophytosis adjacent to the affected endplates. As the disc space decreases in height, increased stress is also placed on the facet joints, leading to the frequent association of osteoarthritis of the facets at the same level.

III. DEGENERATIVE ANNULAR DISEASE:

Yet another extremely common degenerative disorder involves degeneration of the annulus fibrosus. This leads to marginal osteophytosis at the endplates, especially in the thoracolumbar spine in many persons over 50 years of age. In the literature, this entity has been termed "spondylosis deformans" or "senile ankylosis". However, both of these terms tend to make the disease sound a lot worse than it really is. Using these terms in a film report can lead to calls from clinicians wondering just what horrible disease their patients have. Therefore, I prefer to state "marginal osteophytes are noted at multiple disc spaces in the spine" in my dictations. The clinicians know what I'm describing and they and their patients are not unduly frightened by the unfamiliar terminology used for this very familiar process.

with increasing age (arrow), progressive degeneration of the nucleus leads to decreasing disk space height

With increasing age (arrow), progressive degeneration of the annulus leads to increasing osteophytosis at the disk space margins -- the height of the disk space is largely preserved






40

In practice, one often sees evidence of degeneration of both the annulus and the nucleus. It usually doesn't make a lot of difference to the referring clinician which component of the disk has degenerated. Therefore, I suggest using the term "degenerative disk disease" in one's dictations to refer to these entities.

IV. DIFFUSE IDIOPATHIC SKELETAL HYPEROSTOSIS (DISH) DISH is an extremely common entity of unknown etiology, which manifests itself by ossification of the anterior longitudinal ligament, which produces large flowing bony excrescences along the spine, especially the anterior aspect.

V. INFLAMMATORY SPONDYLOARTHROPATHIES: 1. RHEUMATOID ARTHRITIS:

This is a disorder of unknown etiology characterized by synovial inflammation, pannus formation, and then destruction of bone and cartilage.

2. ANKYLOSING SPONDYLITIS:

This chronic inflammatory disorder of unknown etiology principally affects the axial skeleton. Alterations occur in synovial and cartilaginous articulations and in sites of tendon and ligament attachment to bone. Over 90 % of caucasian patients with ankylosing spondylitis are HLA-B27 positive.

Disk space narrowing is

noted at multiple levels in this patient

with degenerative

disk disease -- a thin linear

area of lucency in the L4-5 disk

space represents gas

in the degenerated

disk

Marked marginal

osteophytosis is noted at each disk space in

this patient with predominantly

annular degeneration






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VI. CRYSTALLINE ARTHRITIS: 1. GOUT:

This is the prototypic crystalline arthropathy, characterized by the deposition of monosodium urate crystals in the skin, subcutaneous tissues, and joints. This is most meaningfully classified as idiopathic gout, encompassing the vast majority of individuals, or gout associated with known disorders or enzymatic defects.

2. CALCIUM PYROPHOSPHATE CRYSTAL DEPOSITION DISEASE:

Calcium pyrophosphate crystal deposition disease: a general term for a disorder characterized by the deposition of calcium pyrophosphate dihydrate (CPPD) crystals in or around joints.

a. PSEUDOGOUT:

A term applied to one of the clinical patterns that may be associated with CPPD crystal deposition disease. This pattern, characterized by intermittent acute attacks of arthritis, simulates the findings of gout.

b. CHONDROCALCINOSIS:

A term reserved for pathologically or radiologically evident calcification of hyaline articular cartilage or fibrocartilage. In some cases, this calcification may not indicate deposits of CPPD crystals but rather accumulations of some other crystal.

c. PYROPHOSPHATE ARTHROPATHY:

A term used to describe a peculiar pattern of structural joint damage occurring in CPPD crystal deposition disease simulating, in many ways, degenerative joint disease but characterized by distinctive features.

VII. PSORIATIC ARTHRITIS:

This is a disorder characterized by recurrent painful periarticular calcium hydroxyapatite deposits in tendons and soft tissues.

VIII. PSORIATIC ARTHRITIS: This is a relatively uncommon arthropathy, which occurs in about 2 to 6 % of patients with psoriasis. Approximately 25 to 60 % of patients with psoriatic arthritis are HLA-B27 positive.

IX. REITER'S SYNDROME: Reiter's syndrome is a relatively uncommon arthropathy of uncertain etiology with the classic triad of urethritis, arthritis, and conjunctivitis. Of all of the rheumatic diseases, Reiter's syndrome is most suspects for an infectious etiology. It appears likely that the disease can be transmitted in association with either epidemic dysentery or sexual intercourse. The syndrome frequently follows an infection of the bowel or lower genitourinary tract, and it seems likely that these sites are the portals of entry for the causative agent. It has been suggested that the abnormalities of the vertebral column may be related to organisms extending directly to the sacroiliac joints and spine via the prostatic venous plexus or via the

PYROPHOSPHATE ARTHROPATHY






42

venous plexus of Batson. Implicated organisms include pleuropneumonia-like organisms (PPLO), the Bedsonia group of organisms, and viruses, although to date, no single agent has been definitely incriminated in this disease. Approximately 75 to 96 % of patients with Reiter's syndrome are HLA-B27 positive.

X. ENTEROPATHIC ARTHROPATHY: This arthropathy occurs in about 1 - 26 % of patients with ulcerative colitis or Crohn's disease. The relationship between inflammatory intestinal diseases and arthritis is not fully understood. Infectious, immunologic, and genetic etiologies have been advanced. Approximately 90 % of patients with ulcerative colitis or Crohn's disease who develop spondylitis or sacroiliitis are HLA-B27 positive.

B. RADIOGRAPHIC HALLMARKS:

I. OSTEOPHYTES: In a diarthrodial joint, this is the sine qua non of osteoarthritis. Osteophytes can be seen in both primary and secondary osteoarthritis. They can also be seen at various entheses, often due to altered or increased stress at the entheses (traction osteophytes). The traction osteophytes of degenerative annular disease begin several millimeters from the edge of the vertebral body, and tend to be initially oriented horizontally at their attachment to the vertebral bodies. They then often curve slightly and may even form a complete bony bridge across the disc space.

HYDROXYAPATITE DEPOSITION

DISEASE

ENTEROPATHIC ARTHROPATHY Bridging

osteophytes in the spine of a patient with

degenerative disk disease

REITER'S SYNDROME PSORIATIC

ARTHRITIS






43

II. SYNDESMOPHYTES: Syndesmophytes are generally seen only in the seronegative spondyloarthropathies. These are due to inflammation and ossification of the outer fibbers of the annulus fibrosis, known as the Sharpey's fibers. This is classically seen in ankylosing spondylitis. In the other seronegative spondyloarthropathies, one usually sees Para vertebral ossification which forms in the paravertebral connective tissue at some distance from the spine. In practice, it may be very difficult to distinguish osteophytes from Syndesmophytes or paravertebral ossification.

III. DISC SPACE NARROWING: This almost always means degenerative nuclear disease or infection. These can often be distinguished by looking at the adjacent endplates. In degenerative disc disease, the endplates are often dense, sclerotic, and associated with osteophytosis. In infection, the subchondral line of the endplate often becomes ill-defined and discontinuous.

IV. BONY PROLIFERATION: This is a striking feature of the seronegative spondyloarthropathies, particularly psoriatic arthritis. This bony proliferation occurs about erosions, and probably relates to an exaggerated healing response of the injured bone. This proliferation may take the form of irregular excrescences, subperiosteal deposition of bone, and intra-articular osseous fusion.






44

V. EROSIONS: In general, the presence of erosions bespeaks some type of inflammatory disease, whether the erosions are due to synovial hypertrophy, crystalline deposits, or infection.

VI. CRYSTAL DEPOSITION: In general, this is indicative of one of the crystalline arthropathies -- either CPPD or hydroxyapatite.

VII. SCLEROSIS: Not an especially specific finding in spinal arthropathy.

VIII. ANKYLOSIS: This may occur as a result of many degenerative and inflammatory processes in their later stages.

IX. SUBLUXATION: Stability of the spine is maintained by the spinal ligaments, articular capsules, and discs. Any arthropathy which causes degeneration or destruction of these structures may lead to instability of the spine and subluxation in several locations.

C. PATTERN APPROACH:

I. OSTEOARTHRITIS: Osteoarthritis of the spine looks much like osteoarthritis elsewhere in the body. Any of the spinal synovial joints can be affected, including the facet and uncovertebral joints, the costovertebral joints, and the SI joints. Findings include osteophytosis, joint space narrowing, subchondral sclerosis, and subchondral cyst formation. Besides causing local joint pain, facet osteoarthritis may cause nerve root impingement or compression if the osteophytes are large enough to extend into the lateral recess of the spinal canal, as shown below.






45

II. DEGENERATIVE DISC DISEASE: • Degeneration of the nucleus pulpous, the annulus fibrosis, or both may be

present. While these processes can often be distinguished from each other, overlap in findings will be seen in many patients who have both processes occurring in the same disc.

• The key distinguishing characteristic between these two processes is disc space narrowing. If present, this is strongly suggestive of degenerative nuclear disease. This is often accompanied by endplate sclerosis and mild to moderate osteophytosis.

On the other hand, degenerative annular disease is often not associated with significant disc space narrowing, and the marginal osteophytes seen with this entity are often much larger than those seen with degenerative nuclear disease.






46

III. DISH: With DISH, the flowing ossification seen is usually along the anterior longitudinal ligament. Although there has been recent speculation that DISH may be a disorder of vitamin A metabolism, DISH remains an idiopathic disorder. As such, it lacks not only a known specific cause but also a known specific disease marker (such as monosodium urate crystals in gout). Therefore, DISH is necessarily a diagnosis by exclusion. Since DISH is diagnosed on a morphologic basis alone, there will be of necessity some overlap between certain cases of DISH and other disorders with similar radiographic features, such as ankylosing spondylitis, and degenerative disc disease. To help minimize this overlap, certain arbitrary morphologic criteria have been proposed. Similar Disorders Finding That Distinguishes Them From DISH Ankylosing spondylitis SI and facet joints must be normal

Degenerative nuclear disease Disc spaces must be of normal height Degenerative annular disease Ossification must be seen along four contiguous vertebral bodies Since we often don't have any specific therapy for DISH, is there any reason to try to distinguish it from all of these other disorders? I feel that there is. If for no other reason, knowing the name of a disease allows one to be much more precise in giving a prognosis to a patient. Knowledge of the presence of DISH may alter therapy for other disorders. For example, DISH patients are prone to heterotopic bone formation in surgical sites. Because of this, some orthopedic surgeons will prophylactically treat DISH patients with radiation or drug therapy prior to performing a total joint arthroplasty, in an attempt to prevent or diminish the development of heterotopic bone formation after surgery.

Prominent, flowing ossification is noted along the anterior margin of the

cervical spine in this patient with DISH -- it is easy to see why such patients

often complain of dysphagia






47

IV. ANKYLOSING SPONDYLITIS:

Ankylosing spondylitis affects synovial and cartilaginous joints as well as sites of tendon and ligament attachment to bone (entheses). An overwhelming predilection exists for involvement of the axial skeleton, especially the sacroiliac, apophyseal, discovertebral, and costovertebral articulations. Classically, changes are initially noted in the sacroiliac joints and next appear at the thoracolumbar and lumbosacral junctions. With disease chronicity, the remainder of the vertebrae may become involved. However, this characteristic pattern of spinal ascent is by no means invariable; it may occur slowly or rapidly, and is less frequent in spondylitis accompanying psoriasis and Reiter's disease.

Sacroiliitis is the hallmark of ankylosing spondylitis. It occurs early in the course of the disease. Although an asymmetric or unilateral distribution can be evident on initial radiographic examination, roentgenographic changes at later stages of the disease are almost invariably bilateral and symmetric in distribution. This symmetric pattern is an important diagnostic clue in this disease and may permit it differentiation from other disorders that affect the sacroiliac articulation, such as RA, psoriasis, Reiter's syndrome, and infection. Changes in the SI joint occur in both the synovial and ligamentous (superior) portions, and predominate on the iliac side, for reasons that are obscure.

The classic histologic descriptions of synovial joint alterations in ankylosing spondylitis stress that the synovitis is similar or identical to that in rheumatoid arthritis. Indeed, ankylosing spondylitis was once called rheumatoid spondylitis, under the impression that ankylosing spondylitis was just a variant of rheumatoid arthritis. Further research into this entity revealed enough clinical and immunological differences between the two entities to warrant calling it a disease of its own. In general, the inflammatory process in ankylosing spondylitis is more discrete and of lower intensity that in rheumatoid arthritis.

The characteristic radiographic features of ankylosing spondylitis include erosions, sclerosis, syndesmophytosis, and ankylosis.

Bilateral erosions and sclerosis are noted in the SI joints of this patient with

ankylosing spondylitis

Erosions are noted in the lumbar facet joints of this patient with

ankylosing spondylitis






48

V. RHEUMATOID ARTHRITIS: As mentioned above, the histological changes noted classically in rheumatoid

arthritis are similar or identical to those of ankylosing spondylitis. However, the general pattern of distribution of these changes are usually quite distinct from that of ankylosing spondylitis. For example, rheumatoid arthritis predominantly involves the cervical spine, with apophyseal joint erosion and malalignment, intervertebral disc space narrowing with endplate sclerosis and without osteophytes, and with multiple subluxations, especially at the atlanto-axial junction. Abnormalities of the thoracolumbar spine and sacroiliac joints are infrequent and less prominent than those of ankylosing spondylitis. Other helpful differential findings are the absence of osteoporosis and the presence of bony proliferation and intraarticular bony ankylosis in the seronegative spondyloarthropathies.

VI. CPPD CRYSTAL DEPOSITION DISEASE: The spine is frequently involved in CPPD crystal deposition disease. Intervertebral discal calcifications are frequent in the outer annular fibers, and may mimic early syndesmophytes of ankylosing spondylitis, because of their vertical orientation and slender appearance. These annular calcifications may be associated with back pain. Disc space narrowing is common in CPPD crystal deposition disease, and may be extensive, widespread, and associated with considerable vertebral sclerosis. However, the nucleus pulposus is not commonly calcified. Calcification of ligamentum flavum may also be noted. Occasionally, destructive abnormalities of cervical spine are present. Chondrocalcinosis is only infrequently seen in the sacroiliac joints, but is very common in the fibrocartilaginous joint of the pubic symphysis.

The dens is eroded in this patient with rheumatoid arthritis -- a

mass of pannus is

noted behind the dens and impinging on

the thecal sac and cord






49

VII. GOUT: Spinal manifestations of gout are extremely uncommon, and documented urate

deposition in the spine is exceedingly rare. When seen, spinal gout may manifest as erosions of the synovial joints or endplates, and disc space narrowing may be present.

The incidence of gout in the sacroiliac joint has been reported at 7 - 17 %, although many of the changes ascribed to gout in the earlier literature were probably mimicked in these reports by the changes of osteoarthritis. Sacroiliac joint involvement is seen more frequently with early onset disease, and large cystic areas of erosion in ilium and sacrum are the most specific findings of gout in these joints.

VIII. HYDROXYAPATITE CRYSTAL DEPOSITION DISEASE: Hydroxyapatite crystal deposition disease is most commonly seen about the shoulder. However, it may also occur within the longus colli muscle, which is the principal flexor of the cervical spine. Tendinitis in this region may result in acute neck and occipital pain, rigidity, and dysphagia. Calcifications tend to occur particularly in the superolateral group of the longus colli. The typical radiographic findings of this disorder consist of prevertebral soft tissue swelling in upper cervical region, as well as amorphous calcification, usually anterior to C-2, and just below the anterior arch of C-1. Resorption of this calcification and soft tissue swelling is common, and it may disappear completely in 1 to 2 weeks.

IX. PSORIATIC ARTHRITIS: About 30 to 50 % of patients with psoriatic arthritis develop sacroiliac joint

changes radiographically. Bilateral sacroiliac joint abnormalities are much more frequent than unilateral changes, and although asymmetric findings may be apparent, symmetric abnormalities predominate. Radiographic sacroiliac joint changes include erosions and sclerosis, predominantly on the iliac side, and widening of the articular space. Although significant joint space diminution and bony ankylosis can occur, the incidence of these findings, particularly ankylosis, is less than that of classic ankylosing spondylitis or the spondylitis associated with inflammatory bowel disease. Sacroiliitis may appear without spondylitis, just as spondylitis may appear without sacroiliitis.

As in Reiter's syndrome, paravertebral ossification about the lower thoracic and upper lumbar segments can occur in psoriatic arthritis, and it may represent an early manifestation of the disease. Such ossification appears as a thick and fluffy or thin and curvilinear radiodense region on one side of the spine, paralleling the lateral surface of the vertebral bodies and the intervertebral discs. Occasionally, slender, centrally located, and symmetric spinal outgrowths in psoriasis are identical in appearance to the syndesmophytes of ankylosing spondylitis. However, the greater size, the unilateral or asymmetric distribution, and the location farther away from the vertebral column are features that distinguish paravertebral ossification from the typical syndesmophytosis of ankylosing spondylitis or the spondylitis of inflammatory bowel disease.

In addition to the pattern and distribution of bony outgrowths, there are other features of psoriatic spondylitis that differ from those in classic ankylosing spondylitis. Osteitis and squaring of the anterior surfaces of the vertebral bodies are relatively infrequent in psoriasis. Although apophyseal joint space narrowing,

sclerosis and ill-definition of both SI joints is noted in this patient

with Reiter's syndrome






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sclerosis and bony ankylosis may be seen, the prevalence of these findings is much less than that in ankylosing spondylitis.

Cervical spine abnormalities may be striking in psoriatic arthritis, including apophyseal joint space narrowing and sclerosis, osseous irregularity at the discovertebral joint, and extensive proliferation along the anterior surface of the spine. Atlanto-axial subluxation can also be evident (in one series up to 45 % of patients with psoriatic spondylitis).

X. REITER'S SYNDROME: Reiter's syndrome is associated with an asymmetric arthritis of the lower

extremity, sacroiliitis, and, less commonly, spondylitis. Although its general features resemble those of ankylosing spondylitis and psoriatic arthritis, Reiter's syndrome possess a sufficiently characteristic articular distribution to allow accurate diagnosis.

Ankylosing spondylitis has a similar axial skeletal distribution (although cervical changes are more frequent in ankylosing spondylitis), but significant peripheral articular changes are more frequent.

Psoriatic arthritis may lead to considerable alterations in the articulations of both the appendicular and the axial skeleton. However, in psoriasis, widespread involvement of the upper extremity may be apparent, and distal interphalangeal joint abnormalities in both upper and lower extremities are common. The sacroiliac and spinal changes of Reiter's syndrome are virtually identical to those of psoriasis, although the incidence and severity of these abnormalities and the tendency to involve the cervical spine are greater in psoriasis.

XI. ENTEROPATHIC ARTHROPATHY: The spondylitis and sacroiliitis of inflammatory bowel disease are identical to

those of classic ankylosing spondylitis. The history of inflammatory bowel disease can sometimes help to distinguish these entities, although spondylitis in ulcerative colitis is poorly correlated with activity of the bowel disease. In ulcerative colitis, spinal abnormalities may become manifest prior to, at the same time as, or following the onset of intestinal changes. In fact, spondylitis most commonly precedes the onset of colitis and may progress relentlessly without relation to exacerbation, remission, or treatment of the bowel disease. In Crohn's disease, the joint abnormalities tend to occur simultaneously with the bowel disease.

Peripheral joint abnormalities tend to occur much more frequently with enteropathic arthropathy than with ankylosing spondylitis. When they do occur, they are usually self limited, and rarely cause lasting deformity of the joint. However, in ankylosing spondylitis, the peripheral joint findings typically include joint space narrowing, osseous erosions, cysts, and bony proliferation, which may help in distinguishing these entities.

Bony proliferation (arrows) is noted along the anterior margin

of the lumbar spine in this patient with Reiter's syndrome






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D. DEMOGRAPHICS: All of the entities described in this section on axial arthropathies can occur in the young or the old, and in men or women. However, just as in the appendicular arthropathies, there are certain trends in the distribution of these disorders that may sometimes be helpful in refining one's differential diagnosis. The following tables show some of these trends. As with the appendicular arthropathies, other demographic features such as home location, occupation, and ethnic subtype may occasionally be of help.

Age Age Group Age of Onset Disorder Young (< 20 years) < 20 years Juvenile chronic arthritis

Septic arthritis Middle (> 20 years) onset 15 - 35 years Ankylosing spondylitis

Reiter's Young adults

Enteropathic arthropathies 25 - 55 years Rheumatoid arthritis

Psoriatic arthritis Older patients (> 55 years) > 55 years Osteoarthritis DISH CPPD I. ARTHROPATHIES WITH MALE PREDOMINANCE:

Disorder male:female ratio Ankylosing spondylitis 4:1 to 10:1 Psoriatic 2:1 to 3:1, but controversial Reiter's 5:1 to 50:1 Gout 20:1 DISH 3:2 CPPD 1:1 Primary osteoarthritis (< 45 years) Enteropathic arthropathy Ulcerative colitis 4:1 Crohn's disease 1:1

II. ARTHROPATHIES WITH FEMALE PREDOMINANCE:

Disorder female:male ratio Rheumatoid Arthritis 2:1 to 3:1 Primary osteoarthritis (> 45 years) CPPD 1:1

E. THE LAW OF PARSIMONY:

As in the appendicular arthropathies, a patient may have more than one arthropathy going on in a given joint. Again, this is most commonly due to secondary osteoarthritis due to some other arthropathy, although other unusual combinations of arthropathies may be seen. This principle can sometimes help to clarify what otherwise might be a confusing radiographic picture.






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8.3 LUCENT LESIONS OF BONE: Where, oh where does one start in the workup of this type of lesion? In my opinion, the first order of

business is to learn the names of all of the tumors and tumor-like processes that involve bone. Richard Moser, former registrar of the AFIP, has said that among the thousands of radiology residents he taught there, there was one major cause for residents blowing unknown tumor cases: they didn't know the names of all of the tumors. This makes sense. If you have never heard of a non-ossifying fibroma, it is unlikely that you will ever put it in your differential diagnosis. If you would cast out the demon, you must first know its name. If you don't know Rumplestiltskin's name.... So get busy and first learn at least the names of all of these tumors. I know what a glutealgia it is to learn all of these names. When I was a first-year resident, I thought it was ludicrous to have to do this. To me, it was as if someone had taken a bunch of histological prefixes, shaken them up in a bag, and then drawn out a few at random, stuck them together, and then added "-oma" to it to get most of the types of bone tumors. How else do you explain entities like hemangiopericytoma, angiomyolipoma, chondromyxoid fibroma, or ossifying non-ossifying fibroma? Sooooooo.... go ahead and learn the names of all of these entities. Yes, Right Now! I'll be waiting right here when you get back.

A widely used mnemonic for this is: FEGNOMASHIC. However, I find it a lot easier to remember a mnemonic if it actually forms a real word. As it turns out, one can rearrange the letters of FEGNOMASHIC to form: FOGMACHINES. Take your choice -- either works just the same. The entities considered in this mnemonic are: Mnemonic = FOGMACHINES

8.3.1 DIFFERENTIAL DIAGNOSIS OF SOLITARY LUCENT BONE LESIONS:

• Fibrous Dysplasia • Osteoblastoma • Giant Cell Tumor • Metastasis / Myeloma • Aneurysmal Bone Cyst • Chondroblastoma / Chondromyxoid Fibroma • Hyperparathyroidism (brown tumors) / Hemangioma • Infection • Non-ossifying Fibroma • Eosinophilic Granuloma / Enchondroma • Solitary Bone Cyst

This is a fairly long differential diagnosis. However, it is one that you must learn. I still

run through it every time I see one of these lesions, just to make sure that I consider all of the important possibilities.

The discussion that follows will dwell almost totally on the plain radiographic findings of these lesions. CT and MRI are wonderful tools for tumor workups, but they are fairly non-specific. Their place in the workup is to tell us where the lesion is: what its extent is; whether there are any metastases (either in the same bone or elsewhere); and whether an adjacent joint, nerve or blood vessel is involved. However, to tell us what a lesion is, the plain radiograph is still supreme. We've been looking at the darned things for almost a century now, and the plain film findings of most bone tumors are fairly well known. Plain films are not terribly sensitive, but they do have a decent specificity. Therefore, any workup of a bone tumor should start with a good set of plain films.






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A. AGE: Patient age is a very important bit of knowledge to have in the workup of a tumor. According to Edeiken, about 80% of malignant tumors can be correctly diagnosed on the basis of age alone. From a study of the age prevalence of 4,000 malignant bone tumors, he gives the following table.

B. AGE VS. MALIGNANT TUMOR TYPE AGE (years) TUMOR 1 neuroblastoma 1 - 10 Ewing's of tubular bones 10 - 30 osteosarcoma, Ewing's of flat bones 30 - 40 reticulum cell sarcoma (Primary histiocytic lymphoma),

fibrosarcoma, parosteal osteosarcoma, malignant giant cell tumor, lymphoma

40 + metastatic carcinoma, multiple myeloma, chondrosarcoma

C. SIZE: What does the size of a lesion tell us? Unfortunately, not a whole lot about the histological type of lesion that we are dealing with. However, describing the size of a lesion is part of another important aspect of tumor management: pretreatment staging of the extent of the lesion. Surgery is the preferred treatment for many lesions in this category. The surgeon wants to know where to cut so as to remove all of the lesion, along with an area of normal tissue on all margins of the tumor. Lesion size as measured on plain films will not tell us this accurately -- if anything, it tends to greatly underestimate the extent of the lesion. However, it provides a convenient first-order approximation of the extent (a lower bound on its size) while the early workup is being arranged. Definitive assessment of the pretreatment extent of a lesion will require MR or CT.

D. MARGINS: This is one of the most important things that you can determine about a solitary,

lucent, expansile lesion of bone. Why is this? Because, this is the finding that will give you your best shot at determining the biological activity of the lesion (how fast is it growing?). This is important, because in general, the faster a process grows, the more likely it is to be malignant.

So, how can we determine biological activity from the margin of the lesion? The answer is bone response. Bone is sensitive to a variety of stimuli, and generally responds to one of the processes in FOGMACHINES by either removing bone or creating bone. That's right! The bone itself does the removing or creating of bone - not the disorder involving the bone. At the AFIP, they are fond of saying that the only things that can remove bone are osteoclasts and orthopedic surgeons. I agree with this rule, but would also add talented amateurs to the list (lawnmower and saw accidents, auto crashes, blast injuries, and animal bites are favored mechanisms of bone removal by amateurs -- professionals prefer saws, drills, and osteotomes and confine their efforts to operating rooms). For this reason, the term "expansile lesion" is a bit of a misnomer, since the lesion itself is not expanding the bone. The bone is remodeling itself in response to the stimulus of the lesion.

The other thing to know about bone response is that while it is certain, it is rather slow. If a lesion is growing slowly, then the bone will have plenty of time to retreat from






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the lesion, removing some bone around the lesion, but also laying down new bone around the margins of the lesion. This generally has the effect of producing a sclerotic and usually distinct margin around the lesion. If process grows more rapidly, the bone may only have time to retreat before the lesion, and not have time to lay down this sclerotic rim. Solitary lucent lesions in bone with a distinct margin are generally called "geographic" lesions, whether or not they have a sclerotic rim.

If the lesion grows more rapidly still, there may not be time for the bone to retreat in an orderly manner, and the margin may become ill-defined. Rather than a single discrete lesion, we may see several ill-defined foci of lucency. This has been termed a "moth-eaten" pattern.

If, alas, the process grows more rapidly still, then the bone's retreat may become disorderly indeed. Continuing this battlefield analogy, the boundary between normal and abnormal bone may be lost altogether, with only a very ill-defined pattern of lucency seen, caused by many small, irregular holes in the bone, left behind by osteoclasts. This is an extremely aggressive pattern, sometimes called a "permeative" pattern.

The presence of a permeative pattern usually means that the patient either has an aggressive infection or a malignant tumor. The most common malignancies that give this pattern are metastases, myeloma, primary histiocytic lymphoma, and Ewing's sarcoma. These lesions are sometimes referred to as "round cell lesions" due to the small, dark, round cells that they display to the pathologist.

E. MATRIX: What is matrix, anyway? It is stuff produced by osteoblasts and chondroblasts that eventually becomes, respectively, normal bone and cartilage. Bone tumors form matrix just as a normal bone does, but sometimes in greater quantity. Also, matrix produced by tumors is usually quite abnormal, and does not ossify properly. Why do we look for tumor matrix? Because, it helps us to give a bone tumor a rough histological classification into one of three categories: cartilage-producing, bone-producing or other. Cartilaginous tumors (enchondroma, chondrosarcoma, chondromyxoid fibroma, etc.) will tend to produce cartilaginous matrix, while tumors from the osteoid series (osteoma, osteoblastoma, osteosarcoma, etc.) will tend to produce osseous matrix. In order to see matrix on plain radiographs, it has to calcify. Chondroid matrix, for example tends to produce small punctate or swirled areas of calcification. Adjectives applied to this cartilaginous matrix include "popcorn-like", "curvilinear", or "speckled". Osseous matrix tends to be dense and confluent, and invokes descriptive terms like "cloud-like" or "mashed potatoes". Other lesions tend to produce little or no calcification in their matrix (fibrous dysplasia, fibrosarcoma, malignant fibrous histiocytoma, solitary bone cyst, etc.). Although the term "ground-glass" has been applied to this appearance of matrix, I think that it is a bit confusing, since a fogged film with no diagnostic information on it has a ground-glass appearance also. If I don't see any definite calcified matrix in a lesion, I prefer to just say that instead.

F. LOCATION: Most expansile, lucent lesions are located in the medullary space of the bone. However, we can further define the location of the lesion by noting its relationship to the physis. Many lesions tend to occur in a "favorite" part of the bone. The favored locations are listed in the figure below.






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G. EPIPHYSIS: Very few lesions tend to arise in the epiphysis. Chondroblastoma is one of the very

few tumors that arise here before the physis closes. Osteomyelitis can also arise in the epiphysis.

Several entities can spread across the physis. Osteomyelitis is a classic example of this. Although the dogma for years has been that malignancies such as osteosarcoma and Ewing's tumor rarely cross the physis, more recent experience with MRI has shown this to be untrue. With very sensitive pulse sequences such as STIR (short-tau inversion recovery), subtle extension across the physeal plate may be seen not uncommonly.

After the plate closes, the physis ceases to be an anatomic barrier to disease, and a variety of lesions can be seen involving the epiphyseal area, such as giant cell tumor, enchondroma or aneurysmal bone cyst. Helpful tips in steering the differential diagnosis among these entities include the facts that most enchondromas will exhibit chondroid matrix, most giant cell tumors will abut an articular margin, and most aneurysmal bone cysts appear, well, "aneurysmal" or expansile. It was once thought that aggressive tumors, such as Ewing's tumor and osteosarcoma tended to "respect" the physeal plate and only rarely cross it. However, more recent studies (Panuel, Norton) of the behavior of such tumors with sensitive MR pulse sequences show that osteosarcomas may cross the plate into the epiphysis in 70 - 80 % of cases and Ewing's tumor in about 20 %.

H. METAPHYSIS: This is the fastest growing area of a bone, and also the most likely area for a primary neoplasm to arise. This is especially true in the distal femur and proximal tibia, which are the fastest growing metaphyseal areas in the skeleton. The metaphysis also has the best blood supply of the bone, so entities such as infection or metastasis will commonly be seen in this area as well. In general, most of the entities in FOGMACHINES (with the exception of chondroblastoma) will be most commonly seen in the metaphyseal area of a given bone.

I. DIAPHYSIS: Most of the entities in FOGMACHINES can also appear in the diaphysis, although with less frequency. Notable exceptions are: chondroblastoma, which almost always occurs in an epiphysis or epiphyseal equivalent (most apophyses, the patella and the calcaneus); giant cell tumor, which almost always occurs in an apophysis or in the bone adjacent to a join space; osteoblastoma, which usually occurs in the posterior elements of the spine; and aneurysmal bone cyst, which is usually metaphyseal in location.

J. PERIOSTEAL REACTION: Periosteal reaction is an important finding to note in the workup of bone tumors. However, it also occurs due to several other processes besides tumors. Therefore, I have given periosteal reaction a chapter all to itself. Please refer to this chapter on periosteal reaction for a discussion of how it relates to bone tumors.






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K. MULTIPLICITY: So, what do you do if the patient has multiple lucent lesions? Well, you go through pretty much the same thought processes that you went through for a solitary lesion. The main thing that is different is the differential diagnosis that you use. A lot of the entities in FOGMACHINES don't really make sense as a cause of multiple lucent lesions. However, some of them do. It turns out that one can simply trim out the entities that don't make sense and what's left works just fine for multiple lesions. Thus, our differential reduces like this:

8.3.2 DIFFERENTIAL DIAGNOSIS OF MULTIPLE LUCENT BONE LESIONS:

Mnemonic = FOGMACHINES --> FEMHI • Fibrous Dysplasia • Metastasis / Myeloma • Hyperparathyroidism (brown tumors) / Hemangioma • Infection • Eosinophilic Granuloma / Enchondroma This leaves the letters FMHIE as our differential for multiple lucent lesions. Try as I might, I still haven't been able to come up with any kind of decent word out of these letters. Clyde Helms orders them as FEMHI, and you can make up your own order if you like. If you do come up with a real word in English or some other language out of these five letters, tell me what it is and I will buy you a taco.

A. WISE SAYINGS ABOUT SOLITARY LUCENT LESIONS:

Sometimes, all the logical principles that you have at your disposal don't seem to help very much, and one must fall back on some of the empirical maxims that musculoskeletal radiologists have accumulated over the years. Here are a few of the ones I have used over the years. 1. With a long lesion in a long bone, think of fibrous dysplasia. 2. Simple cyst, enchondroma, and fibrous dysplasia can mimic each other and can be

hard to distinguish. Thus, when you think of one of these three entities, also think of the other two.

3. Giant cell tumors nearly always occur near a joint surface. 4. Certain bones in the body can be considered "epiphyseal equivalents" for purposes of

differential diagnosis. These include the patella, the calcaneus, and most apophyses. Therefore, for lucent lesions in these areas, one should include the classic epiphyseal entities such as chondroblastoma, giant cell tumors and aneurysmal bone cysts.

5. Lucent lesions of the sternum should be considered malignant until proven otherwise (Helms CA, personal communication, 1983).

6. Keep in mind that the classic descriptions of bone tumors that you spend so much time studying are for untreated lesions. What kind of lesions do radiologists spend most of their time looking at? Treatedlesions -- treated with surgery, chemotherapy, cryotherapy and radiation therapy. In surgically treated lesions, besides simple resection of the lesion, one may also see replacement by a metal prosthesis, an allograft, or other forms of bone grafting. In short, you won't see the "classic" appearance of a lesion for very long in a given patient. When the patient first presents to you, you may not even have any history of these prior interventions, so you will just have to remember this phenomenon. Also, any given film that you see of a patient is just one frame out of a long documentary movie about that patient -- movies change. Remember this.






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Fibrous Dysplasia Hyperparathyroidism leads to

Enchondroma Eosinophilic Granuloma






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8.4 SCLEROTIC LESIONS OF BONE: What does it mean that a lesion is sclerotic? Well, generally, it means that it is due to a fairly

slow-growing process. Bone reacts to its environment in two ways -- either by removing some of itself or by creating more of itself. If the disorder it is reacting to is rapidly progressive, there may only be time for retreat (defense). If the process is slower growing, then the bone may have time to mount an offense and try to form a sclerotic area around the offender.

How should one approach sclerotic bone disease? I think that the best way is to start with a good differential diagnosis for sclerotic bones. One can then apply various features of the lesions to this differential, and exclude some things, elevate some things, and downgrade others in the differential.

Let's apply the good old universal differential diagnosis to sclerotic bone lesions. Mnemonic = VINDICATE

8.4.1 GENERIC DIFFERENTIAL DIAGNOSIS OF SCLEROTIC BONE LESIONS:

• Vascular o Hemangiomas o Infarct






• Inflammatory/Idiopathic • Congenital

o Bone islands o Osteopoikilosis o Osteopetrosis o Pyknodysostosis

• Autoimmune • Trauma

o Fracture (stress) • Endocrine/Metabolic

o Hyperparathyroidism o Paget's disease

One of the first things you should notice about sclerotic bone lesions is whether they are single and focal, multifocal, or diffuse. You can then customize the above differential for whichever pattern of sclerosis that you see. Generally, this just follows common sense -- some lesions should logically be expected to be focal, others multifocal, and yet others diffuse or systemic. For example:






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8.4.2 DIFFERENTIAL DIAGNOSIS OF FOCAL OR MULTIFOCAL SCLEROTIC BONE LESIONS:

• Vascular o Hemangiomas o Infarct





• Congenital o Bone islands o Osteopoikilosis

• Trauma o Fracture (stress)

• Endocrine/Metabolic o Paget's disease

As you can see, by just dropping the items that tend to cause generalized sclerosis, we have generated a fairly good differential for focal lesions. The differential for multifocal lesions happens to be identical to that for focal lesions.

8.4.3 DIFFERENTIAL DIAGNOSIS OF DIFFUSE SCLEROTIC BONE LESIONS:

• Vascular o Infarct (e.g. sickle cell)

• Neoplasm o Metastatic

Prostate Breast Other


• Congenital o Osteopetrosis o Pyknodysostosis

• Endocrine/Metabolic o Hyperparathyroidism

You may have been surprised to see metastatic disease listed as a leading cause for diffuse sclerotic bones. It is true that the usual appearance of skeletal metastases is that of focal lesions -- diffuse sclerosis occurs in only a small fraction of cases of skeletal metastases. However, cancers that metastasize to bone are very common. The lesson here is that when we are dealing with a very common disorder, even its less common presentations will be seen commonly.

Diffuse sclerotic metastases to the pelvis, sacrum and femurs






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8.4.4 THINGS TO REMEMBER ABOUT SCLEROTIC LESIONS:

There are a number of other helpful findings you can look for that can help you to cone in on or away from specific entities in one of these differential lists. 1. Most cases of chronic osteomyelitis look pretty nonspecific. However, if one sees

sinus tracts associated with a sclerotic area, one should strongly consider osteomyelitis.

2. Diffuse skeletal infarcts can be a common cause of diffuse skeletal sclerosis. In fact, in areas where sickle cell disease is common, this may be the leading cause of diffuse sclerotic bones. When you are considering osteonecrosis in your differential diagnosis, look at the joints carefully. If you can find evidence of subchondral collapse or the typical lucent/sclerotic appearance of the necrotic bone in the weight-bearing bone, then osteonecrosis becomes a much more likely diagnosis.

3. Patients with sclerotic lesions due to metastasis often have a history of prior malignant disease. Ask the patient or the clinician about this.

4. Likewise patients with sclerotic lesions due to various drugs or minerals will tell you what they are taking if you ask them.

5. When considering congenital causes of sclerotic lesions, benign causes such as bone islands or osteopoikilosis usually have a fairly typical appearance and are hard to mistake. Osteopetrosis and pyknodysostosis are likewise hard to mistake for other entities since the bones are denser than in any other disorder, and the long bones tend to have very tiny medullary canals.

6. When considering trauma as a cause for sclerotic lesions, remember to check and see if the areas involved are areas in the typical distribution for stress fractures.

7. When considering hyperparathyroidism, look for evidence of subperiosteal bone resorption.

8. When considering Paget's disease, it is extremely helpful to note whether there is associated bony enlargement. This is extremely common in Paget's disease but extremely uncommon with a blastic metastasis. Another finding classic for Paget's disease is that it almost always starts at one end of a bone and then spreads toward the other end of the bone.

8.5 PERIOSTEAL REACTION:

The periosteum is a membrane several cell layers thick that covers almost all of every bone. About the only parts not covered by this membrane are the parts covered by cartilage. Besides covering the bone and sharing some of its blood supply with the bone, it also produces bone when it is stimulated appropriately. What does it take to make this happen? Practically anything that breaks, tears, stretches, inflames, or even touches the periosteum. So, when some anonymous process stimulates this reactive bone formation, eventually we see evidence of it on some imaging study.

Once we spot this reactive new bone, how do we deal with it? In the best of all possible worlds, one would be able to look at the pattern of periosteal reaction and then give a precise histological diagnosis. Alas, this is not that kind of world. We can't give a precise histological diagnosis. But wait -- it gets worse! We can't even tell for sure if the underlying process is benign or malignant! As it turns out, about all we can do is say with some confidence whether the process is a benign or an aggressive one. Why is this? Well, the periosteum is a fairly promiscuous tissue, and puts on a similar response to all comers. The main determinant of how the new bone formation looks is how fast the abnormal process grows, and has little to do with any intrinsic properties of the periosteum. Therefore, any differences in the pattern of periosteal reaction must arise in the disease process itself -- not in the periosteum. Again, evidence of the speed at which these processes are growing






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is the main thing we look for when assessing periosteal reaction. Knowledge of this speed will help us to differentiate these processes into two broad categories.

With slow-growing processes, the periosteum has plenty of time to respond to the process. That is, it can produce new bone just as fast as the lesion is growing. Therefore, one would expect to see solid, uninterrupted periosteal new bone along the margin of the affected bone.

However, with rapidly growing processes, the periosteum cannot produce new bone as fast as the lesion is growing. Therefore, rather than a solid pattern of new bone formation, we see an interrupted pattern. This interrupted pattern can manifest itself in several ways, depending on just how steadily the lesion grows. If the lesion grows unevenly in fits and starts, then the periosteum may have time to lay down a thin shell of calcified new bone before the lesion takes off again on its next growth spurt. This may result in a pattern of one or more concentric shells of new bone over the lesion. This pattern is sometimes called lamellated or "onion-skin" periosteal reaction.

If the lesion grows rapidly but steadily, the periosteum will not have enough time to lay down even a thin shell of bone, and the pattern may appear quite different. In such cases, the tiny fibers that connect the periosteum to the bone (Sharpey's fibers) become stretched out perpendicular to the bone. When these fibers ossify, they produce a pattern sometimes called "sunburst" or "hair-on-end" periosteal reaction, depending of how much of the bone is involved by the process.

Another pattern seen in rapidly growing processes is called the Codman's triangle. This is a bit of a misnomer, since there really is not a complete triangle. When a process is growing too fast for the periosteum to respond with even thin shells of new bone, sometimes only the edges of the raised periosteum will ossify. When this little bit of ossification is seen tangentially on a radiograph, it forms a small angle with the surface of the bone, but not a complete triangle. So, when a process is growing too fast for even the Sharpey's fibers to ossify, one may only see a soft tissue mass arising from the bone, perhaps with small Codman's triangles at its margins.

So what is the significance of all of these patterns? Well, we can usually differentiate lesions into one of two categories: benign vs. aggressive processes. If we see a solid pattern of periosteal reaction, we can be fairly confident that we are dealing with a benign process. How confident? In normal everyday practice, my estimate is that you can be about 90 - 95 % confident in this rule(9), but your mileage may vary. As with many rules in medicine, there are some caveats associated with the use of this rule. The main caveat with this rule is that benign processes and malignant processes may coexist. The usual way that this may manifest is when there is a fracture or infection in the same area as a tumor. In this case, you may see a fairly complex pattern of

Solid periosteal reaction along the cortex of a

bone

lamellated periosteal reaction

"sunburst" and "hair-on-end" periosteal

reaction

a Codman's triangle

Osteosarcoma of the distal

femur, demonstrating dense tumor

bone formation and a sunburst

pattern of periosteal reaction.

a complex pattern of periosteal reaction






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periosteal reaction that demonstrates some elements that look benign and some that look very aggressive.

The take home point here is that complex patterns like this may be very misleading, and should be interpreted with caution. In general, though, the more aggressive the pattern of periosteal reaction, the greater the chance that you are dealing with a malignancy. Here are partial lists of causes of both solid and aggressive periosteal reaction:

8.5.1 CAUSES OF SOLID PERIOSTEAL REACTION:

• Infection • Benign neoplasms

o Asteroid osteoma • Eosinophilic granuloma • Hypertrophic pulmonary osteoarthropathy • Deep venous thrombosis (lower extremity)

Causes of Aggressive Periosteal Reaction • Osteomyelitis • Malignant neoplasms

o Osteosarcoma o Chondrosarcoma o Fibrosarcoma o Lymphoma o leukaemia o Metastasis

8.6 SOFT TISSUE CALCIFICATIONS: Soft tissue calcifications pop up all of the time, and it behooves the radiologist to say something intelligent about them. Fortunately the differential diagnosis for this finding is not too difficult. Soft tissue calcifications are usually caused by one of the following six entities. These are listed below in order of prevalence. Differential Diagnosis of Soft Tissue Calcifications Cause Typical Appearance Prevalence

Dystrophic

Small to large amorphous Ca++ in the damaged tissue – may progress to ossification (formation of cortex and medullary space are then seen) 95 - 98 %

CPPD Chondrocalcinosis; occasionally associated with calcifications in the soft tissues of the spine 1 - 2 %

Metastatic calcification Finely speckled Ca++ throughout soft tissues 1 - 2 %

Tumoral calcinosis Big globs of Ca++, usually near a joint << 1 %

Metastatic osteosarcoma Amorphous, fluffy, confluent collection of Ca++ <<< 1 %

Primary soft tissue osteosarcoma Amorphous, fluffy, confluent collection of Ca++ <<<< 1 % As you can see, almost every calcification that one sees in the soft tissues in actual radiographic practice is due to dystrophic calcification. What does this mean? Simply this: when tissue is






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damaged, the body responds to this injury in a nonspecific manner by invoking the generic inflammatory response reaction. This sometimes ends with calcification of the damaged tissue. This calcification is probably usually only microscopic, but is occasionally enough to be seen radiographically.

Again, dystrophic calcification means damaged tissue. Any kind of damage will do. Going through the universal differential diagnosis, we come up with the following possible causes: Mnemonic = VINDICATE

8.6.1 GENERIC DIFFERENTIAL DIAGNOSIS OF DYSTROPHIC SOFT TISSUE CALCIFICATIONS:

• Vascular o Venous insufficiency

• Infection o Parasitic infestation

Cysticercosis Dracunculiasis Armillifer armillatus etc.

• Neoplasm o Primary bone-forming tumor

Osteosarcoma

o Tumor necrosis • Drugs

o Vitamin D • Autoimmune

o Dermatomyositis o scleroderma

• Trauma o Heterotopic ossification o Injection granulomas

Some foci of dystrophic calcification will go on to actually ossify. The best name for this process

(in my humble opinion) is heterotopic ossification (bone formation outside of its usual location). The

Patient with dystrophic calcification in the Achilles tendon due to recurrent trauma and

tendonitis.






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term myositis ossificans is inaccurate and outdated and should no longer be used. This old term would have one believe that it occurs in muscle (myo-) and is a primary inflammatory process (-itis). In fact, this process occurs not only in muscle, but also in connective tissue. Likewise, any sort of tissue injury can cause heterotopic ossification, not just inflammation.

So, you have just found some white (radiopaque) stuff in a patient's soft tissue. Now what? Well, before you go too much further, it is nice (in the interests of precision) to decide whether you are dealing with calcification or ossification. If the process of ossification has progressed far enough, this distinction can be made, although this is not always possible. How, then, can one tell them apart? Two key words form the crux of this distinction: order and organization. In bone, calcium is not just randomly deposited all over the place. Instead, it is laid down in a certain orderly pattern. Look for a surrounding shell of dense cortical bone, which surrounds a central medullary space.

Since most calcifications are dystrophic, your biggest job now is to pick the most likely causes of it. The actual morphology of the calcification can help here. For example, consider venous thrombosis. When this occurs around a venous valve, the resulting calcification (or even ossification) is round, dense, and sometimes lamellated, and is called a phlebolith. These are commonly seen in the complex venous plexi in the pelvis. They can also be seen in peripheral veins, especially in the lower extremities. Rarely, one may see them in soft tissue hemangiomas. While parasitic infestations are not exceedingly common, they are around for those who would see them. In our county hospital last year, we saw two patients with cysticercosis just passing across the regular orthopedic trauma board. With parasitic infestations, the morphology of the calcifications can be quite specific. With cysticercosis, the classic findings are multiple elongated foci of calcification just about the shape and size of grains of rice. These "rice grain" calcifications are usually oriented along the direction of the muscle fibers. Dracunculiasis, on the other hand, forms small crescentic calcifications.

Following chemotherapy or radiation therapy, a soft tissue tumor may calcify, due to tumor

necrosis. In this case, a good history from the clinician will usually provide the answer. Injection granulomas tend to be focal and densely calcified. They are typically located in

common intramuscular injection sites, such as the gluteus maximus. Autoimmune disorders such as the CREST syndrome or dermatomyositis can also cause soft

tissue calcifications. The CREST syndrome consists of calcinosis cutis (usually seen under the skin of the hands or wrists), Raynaud's phenomenon, esophageal disorders, sclerodactyly, and

Patient with multiple bilateral phleboliths in the pelvic veins.

Patient with multiple "rice-grain" calcifications in muscles about knees due to cysticercosis.






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telangiectasia. In dermatomyositis, the most prominent calcifications are in the muscles of the upper arms and legs.

Heterotopic ossification can occur almost anywhere in the musculoskeletal system. It is usually

seen following focal injury to an area. However, it is also a common complication of closed head injury, paraplegia or quadriplegia. In this patient group, the ossification usually occurs about the shoulders, elbows, or hips.

Certain patients, such as those with ankylosing spondylitis or DISH (diffuse idiopathic skeletal hyperostosis), have a predilection to form bone around surgical sites. A rare cause of heterotopic ossification is known as myositis ossificans congenita universalis. As the name implies, this entity is congenital and hereditary. It is characterized by profound ossification of the soft tissues throughout the body. This ossification interferes with motion and respiration, and is usually lethal at an early age.

What about those patients in the other few percent who don't have dystrophic calcifications. When should you consider these diagnoses? This is not an easy question to answer, but I'll try.

Metastatic calcifications can result from any process with an elevated calcium-phosphate product. Entities such as renal failure, hyperparathyroidism, sarcoidosis, milk-alkali syndrome, etc. can lead to metastatic calcifications. These are often fine and diffuse throughout the soft tissues.

Calcium pyrophosphate dihydrate deposition disease (CPPD) is usually associated with chondrocalcinosis. This typically appears as a fine white line overlying the hyaline articular cartilage. CPPD is also associated with calcifications in the soft tissues of the spine.

Tumoral calcinosis is a rare, weird entity of unknown etiology. Fifty percent of these patients may have some associated abnormalities in their renal lab work. The calcifications are usually large, globular, and located in the soft tissues over joints. Not much else looks like this.

66 year old male with scleroderma, exhibiting

acroosteolysis, skin atrophy over fingertips and calcinosis

cutis.

46 year old female with dermatomyositis and extensive soft tissue

calcifications about the knee.

33 year old female with limited range of motion about shoulder, elbow and knee after closed head injury. Heterotopic ossificiation is noted at all three

sites.

31 year old female with lupus erythematosus and

renal disease, with metastatic calcifications in

soft tissues around shoulder and early

subchondral collapse of humeral head from early

osteonecrosis.






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Calcific tendenitis is commonly seen about the shoulder. The typical appearance is that of

small focal globs of amorphous calcification, usually seen around the supraspinatus tendon. These calcifications are in the form of a thick paste of hydroxyapatite crystals.

Calcific tendenitis is commonly seen about the shoulder. The typical appearance is that of small focal globs of amorphous calcification, usually seen around the supraspinatus tendon. These calcifications are in the form of a thick paste of hydroxyapatite crystals.

Osteosarcoma may occasionally metastasize to soft tissue. This is uncommon, and can mimic heterotopic ossification. An even rarer variety of osteosarcoma arises primarily in the soft tissue.

Child with conventional intramedullary osteosarcoma of distal femur with large soft tissue mass exhibiting classic osteoid matrix. However, an osteosarcoma arising from the soft tissues or metastatic to soft tissue would appear much the same as this mass.

8.6 FRACTURES WITHOUT SIGNIFICANT TRAUMA:

The circumstance of fracture without any history of significant trauma is not uncommon. Whenever you get this history, a red flag should pop up in your visual cortex and a bell should go off in your auditory tracts.

Generally, the differential diagnosis here is fairly logical. The thing to remember is that a bone needs a reason to break. Usually, that reason is that a substantial force has been applied to the bone. If there is no evidence of such a force, we must look for some other reason. To do this, you must first answer two questions: 1) did the fracture occur through normal or abnormal bone; 2) is there normal or decreased amount of bone present? Once you have answered these two questions, you can use the following handy-dandy flowchart to arrive at the most likely mechanism for the fracture.

Patient with CPPD and

chondrocalcinosis of hyaline

articular cartilage and

meniscal fibrocartilage of

knee.

Elderly female with tumoral calcinosis about hand and wrist.

Patient with a large focus of calcific tendinitis in the

supraspinatus tendon.wrist.






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Fractures through abnormal bone are called "pathological" fractures. Probably the most

common cause of this is an underlying tumor, either benign or malignant. However, almost any underlying process of bone that weakens the bone can lead to a pathological fracture. Therefore, one should also consider infection, osteomalacia, and Paget's disease, among other causes.

When there is normal bone but just not enough of it, we call it osteoporosis. This is by far the most common reason for a fracture without significant trauma.

Osteoporosis lies in wait for every living human, if only they live long enough to develop it. This is especially true of postmenopausal women, who may lose up to 20 % of their bone mass in a year in extreme cases. Other risk factors for osteoporosis include Caucasian heritage, smoking, lack of antigravity exercise, low dietary calcium intake, and various amenorrheic states.

Now, how do you go about diagnosing osteoporosis? Well, if it is early osteoporosis, looking at radiographs won't help you much, because plain films are hideously insensitive to osteopenia. In order to see a lesion in bone, an estimated 30 to 50 % of the bone must first be lost. If the osteoporosis is really bad, the bones may look washed out, and only the primary weight-bearing trabeculae may be visible. If less that 30 - 50 % of the bone is gone, then you may have trouble being sure that osteoporosis exists at all.

To definitively diagnose osteoporosis, one must perform some type of quantitative imaging study on the bone in question. The current state of the art in quantitative bone assessment is dual energy X-ray absorptiometry (DEXA). This is done with a dedicated device about the size of a conventional radiographic examination table. A scanning arm then passes over the patient and scans the area of interest. As this scanning arm moves about, a beam of X-rays at primarily two different energies are transmitted through the patient, and their respective amounts of absorption by the tissues of the patient's body are measured by a sensing probe on the other side of the patient. If a patient has more bone, then less X-rays make it through the patient into the X-ray detector. If less bone is present, then more X-rays make it through. A computer attached to the device then takes this data, and uses it to create a transmission image of the bones of interest, and then compares this data with normative standards so that one can decide if the patient indeed has osteoporosis.

With chronic repetitive stress, one can break any bone in the body. However, this is more likely in certain bones, such as the tibial shaft, the metatarsal shafts, the femur, and the bones of the pelvis. If the fracture is fairly new, then there may be no plain film evidence of it. Later, once the fracture has been around long enough, periosteal reaction is often seen adjacent to the fracture site. A radionuclide bone scan or MRI can be used to screen for stress fractures. The bone scan will show a stress fracture as an area of increased uptake of tracer, while MRI will show focal or diffuse marrow edema at the fracture site.

The main reason prompting the early diagnosis of stress fracture is so that the patient can be advised to rest the affected part. If the affected part continues to be loaded sufficiently, then a stress fracture may develop into a completed fracture through the bone.






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8.7 FACIAL AND MANDIBULAR FRACTURES:

8.7.1 FACIAL FRACTURES:

The bones of the skull and face collectively make up the most complex area of skeletal real estate in the body. Analysis of the fractured face requires a knowledge of not only normal anatomy, but also of common fracture patterns in the face.

Although they represent serious injuries, the workup and treatment of facial fractures is often properly delayed until more pressing problems have been addressed, such as the establishment of an adequate airway, hemodynamic stabilization, and the evaluation and treatment of other more serious injuries of the head, chest and skeleton. Once these problems have been managed, it is time to work up facial fractures.

At our institution, high resolution CT is currently the imaging procedure of choice for most facial fractures. The complex anatomy and fractures of the facial bones are shown extremely well by CT, and soft tissue complications can be evaluated to a far greater degree with CT. Therefore, the plain film facial series has taken a back seat to CT in the past few years, and is now used only in certain situations, such as when the facial trauma is very focal (nasal fracture), or when CT is unavailable. However I find it easier to initially teach the anatomy and fracture patterns of the face with plain films. Once these concepts have been grasped by the resident, one can then move on to the axial and coronal anatomy shown by CT.

A basic facial series consists of three or four films: a Waters view (PA view with cephalad angulation), a Caldwell view (PA view), a lateral view, and occasionally a submentovertex view. If a nasal fracture is suspected, then a lateral view of the nasal bone with special nasal technique may be done. Of these views, the most consistently helpful view in facial trauma is the Waters view. It tends to show all of the major facial structures at least as well and often better than other radiographic views of the face.

It can initially be a bit daunting to think about ruling out fractures of the complex collection of bones that make up the face. However, here are several simplifying rules that can make life a lot easier: 1. Look at the orbits carefully, since 60 - 70 % of all facial fractures involve the orbit in

some way. The exceptions: a local nasal bone fracture, a zygomatic arch fracture, and the LeFort I fracture. It is especially important to examine the orbital borders and apex, as well as the optic canal.

2. Know the most common patterns of facial fractures and look for them. 3. Bilateral symmetry can be very helpful. Normal radiopacities are usually bilateral, while

abnormal ones are usually unilateral. 4. Carefully trace along the lines of Dolan when examining the Waters view in a facial

series. What are the lines of Dolan? They are three anatomic contours best seen on the

Waters view of the face, and they were first popularized by Dolan et al. As you can see, the 3 lines of Dolan lead the eye along some facially important structures. Lee Rogers pointed out that the 2nd and 3rd lines together form the profile of an elephant.

When you search for a fracture, you are really searching for one or more of the following radiographic signs.

The lines of Dolan and the

elephants of Rogers






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8.7.2 RADIOGRAPHIC SIGNS OF FACIAL FRACTURES:

• Direct Signs Nonanatomic linear lucencies Cortical defect or diastatic suture Bone fragments overlapping causing a "double-density" Asymmetry of face

• Indirect Signs Soft tissue swelling Periorbital or intracranial air Fluid in a paranasal sinus

The most common mechanism producing facial fractures is auto accidents. About 70 %

of auto accidents produce some type of facial injury, although most are limited to soft tissue. The face seems to be a favorite target in fights or assaults, which are the next most common mechanism. The remainder of facial fractures are produced by falls, sports, industrial accidents and gunshot wounds. Less than 10 % of all facial fractures occur in children, perhaps because of the increased resiliency of a child's facial skeleton. The most common patterns of midfacial fractures are summarized in the table below.

Fracture Type Prevalence

Zygomaticomaxillary complex (tripod fracture) 40%

I 15%

II 10%LeFort III 10%

Zygomatic arch 10%

Alveolar process of maxilla 5%

Smash fractures 5%

Other 5%Probably the most common facial fracture is the tripod or zygomaticomaxillary complex

fracture, so called because it involves separation of all three major attachments of the zygoma to the rest of the face.

Frontal view of a zygomaticomaxillary

complex fracture

submentovertex view of a

zygomaticomaxillary complex fracture






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Although it may be fractured, the separation of the frontal process of the zygoma from the frontal bone usually occurs in the form of a diastasis of the zygomaticofrontal suture. This fracture is usually due to a direct blow to the body of the zygoma. This fracture will generally cause contour abnormalities of all three of the lines of Dolan. Occasionally, extraocular muscles may become entrapped in the zygomaticomaxillary component of the fracture complex. The displaced tripod fragment may physically restrict motion of the mandible. In some cases, force may propagate along the long axis of the lateral orbital wall and involve the orbital apex or optic canal, resulting in diminished vision. CT is extremely helpful in evaluating these fractures.

Fractures may be isolated to the zygomatic arch. Clinically, these injuries are usually due to a blow from the side of the face. Patients with this injury often present with flatness of the lateral cheek area and inability to open their mouth, due to impingement of the zygomatic arch fragment upon the coronoid process of the mandible or the temporalis muscle. Adequate visualization of this fracture may require a submentovertex view or CT.

Another focal fracture type is a fracture of the alveolar process of the maxilla, which involves a small piece of the maxilla, associated with several fractured teeth. The main treatment goal here is to maintain viability of the teeth. If all of the fractured teeth cannot be accounted for, a chest film should be carefully examined to look for evidence of aspirated tooth fragments.

Another common fracture is the orbital floor fracture, or "blowout" fracture. The usual mechanism is a blow to the eye, with the forces being transmitted by the soft tissues of the orbit downward to the thin floor of the orbit. The floor is usually the path of least resistance, and fractures downward into the maxillary sinus. Common clinical signs are enophthalmos and diplopia (especially on upward gaze), and one should remember that about 24 % of these fractures are associated with ocular injury as well. On a Waters view, one may see a soft tissue mass on the superior margin of the maxillary sinus, representing the herniated periorbital tissues into the sinus. One may also see a "trapdoor" fragment of bone protruding down into the sinus, often hinged on the ethmoidal side. CT will, of course, show these fractures and soft tissue mass much better.

"blowout fracture" -- the arrows point to the fracture fragments and periorbital tissue which have herniated into the maxillary

sinus






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The nose is the most frequently injured facial structure, undoubtedly because of its

prominent position on the face. Likewise, the most commonly missed facial fracture of the face is a fracture of the nasal bone. Although one can occasionally see a nasal bone fracture well on a standard lateral skull film, these fractures are much better seen when the film is shot with special low kVp nasal bone technique (essentially soft tissue technique). One should always look at the inferior nasal spine (part of the maxilla) as well for subtle fractures. Common pitfalls in viewing the nasal bone are the normal sutures lining the nasal bone, as well as the linear channel for the nasociliary nerve, which may all be mistaken for a fracture. A helpful rule is that this channel runs parallel to the bridge of the nose, while most nasal bone fractures will run perpendicular to the bridge. It is well to remember that the humble nasal bone fracture may be associated with more extensive injuries, such as the orbital rim or floor and the ethmoid or frontal sinuses.

Normal nasal bone anatomy

Frontal views of LeFort complex fractures I - III lateral views of LeFort complex fractures I - III






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The LeFort I, or transmaxillary fracture runs between the maxillary floor and the orbital floor. It may involve the medial and lateral walls of the maxillary sinuses and invariably involves the pterygoid processes of the sphenoid. Clinically, the floating fragment will be the lower maxilla with the maxillary teeth.

The LeFort II occurs along yet another weak zone in the face, and is sometimes called a pyramidal fracture because of its shape. A common mechanism is a downward blow to the nasal area.

The most severe of the classic LeFort fracture complexes is the LeFort III. I suppose that this is pretty obvious, given a three-part grading system. In this case, the large unstable (floating) fragment is virtually the entire face! Thus, this fracture is also referred to as craniofacial disassociation. This is a very severe injury, and is often associated with significant injury to many of the soft tissue structures along the fracture lines. Generally, considerable force is necessary to produce this injury, and it is uncommon as an isolated injury. It may also occur in association with severe skull and brain injuries.

With the exception of the LeFort I injury, "pure" LeFort injuries are not commonly seen. More commonly seen are variants of the LeFort classification. One of the most common of these is the LeFort II - tripod fracture complex. This complex is usually due to the large forces encountered in a motor vehicle accident. LeFort was probably unable to apply this much force to the cadaver faces in his study, and it is therefore not too mysterious why he didn't describe these more complex injuries. When describing these injuries, one should probably give a separate diagnosis to each half of the face. Even more complex patterns may be encountered, such as a mixed LeFort II/LeFort III complex or a LeFort III/LeFort II/tripod complex.

Besides the classic LeFort patterns and the mixed LeFort variants, there is another common pattern which is called, for obvious reasons, a "smash" fracture. In these injuries, severe comminution of the face is present, and underlying skull injury is likely. These patients are often in unstable condition with associated axial and appendicular skeletal injuries as well. This category includes several varieties of otherwise unclassifiable fractures, which are named for the portion of the face primarily involved. Subclassifications of smash fractures include the frontal, naso-frontal (naso-ethmoid) or central facial smash syndromes. CT is mandatory for adequately displaying all of the bony and soft tissue components of these injuries.

A. WISE SAYINGS ABOUT FACIAL FRACTURES:

1. Look at the orbits carefully, since 60 - 70 % of all facial fractures involve the orbit in some way.

2. Bilateral symmetry can be very helpful. 3. Carefully trace along the lines of Dolan. 4. Use CT liberally in working up facial fractures.

8.7.3 MANDIBULAR FRACTURES:

The mandible is another commonly fractured bone in the head, and most of these fractures are obvious on clinical exam. Clinical findings include facial distortion, malocclusion of the teeth, or abnormal mobility of portions of the mandible or teeth.

The mandible is one of those bones covered by the "ring bone rule", which may be stated thusly: if you see a fracture or dislocation in a ring bone or ring bone equivalent, look for another fracture or dislocation. You can experiment with this tendency of ring bones to break in more than one place by going through a bag of pretzels and trying to break one of them in just one place. Then try it with a bag of bagels. You should now have a good






73

appreciation for Lee Rogers' corollary to the ring bone rule, which he calls the "pretzel-bagel spectrum". To wit, the stiffer a ring bone is, the more likely it is to break in more than one place. The more flexible it is, the more likely it is to break in just one place. The mandible has some flexibility, due not only to the mobility around the temporomandibular joints (TMJ's) but also to the tendency of the TMJ's to absorb some forces during trauma. What this boils down to is that one sees an average of 1.5 to 1.8 mandibular fractures per customer, depending on whether the mechanism is blue collar (fist or other anonymous blunt object) or white collar (automobile crash) respectively. Like the nose, the mandible also has a prominent position on the face, making it a favorite target for either of these mechanisms. Mandibular fractures have traditionally occurred at twice the prevalence of facial fractures, but this ratio has been decreasing with the increasing prevalence of high-speed auto accidents. Only 5 % of all mandibular fractures occur in children, and most of these are also caused by auto accidents, with about 1/3 due to bicycle accidents.

Mandibular fractures can occur at any of the following sites.

Common sites of mandibular fractures

Fracture Type Prevalence

Body 30 - 40 %

Angle 25 - 31 %

Condyle 15 - 17 %

Symphysis 07 - 15 %

Ramus 03 - 09 %

Alveolar 02 - 04 %

Coronoid process 01 - 02 %

When double fractures occur, they are usually on contralateral sides of the symphysis. Common combinations include the angle plus the contralateral body or condyle. Triple fractures occasionally occur, and the most common type is fracture of both condyles plus the symphysis.

Common sites of mandibular fractures






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The mandible may also be dislocated without fracture, sometimes spontaneously during a large yawn. The patient usually presents with considerable pain. Spasm in the masseter and pterygoid muscles tend to force the condyles up the anterior slope of the articular eminence and prevent normal mouth closure.

A. THINGS TO REMEMBER ABOUT MANDIBULAR FRACTURES: 1. Remember the ring bone rule. 2. Symphyseal fractures can be diabolically hard to see, even on a well-exposed AP

film 3. Remember the Panorex view -- this can usually only be taken by a special

machine in the oral surgery department, but it provides the best single view of the mandible and will show you fractures that cannot be seen by any other method short of CT.

4. Look carefully along the cortical margin of the whole mandible for discontinuities. This may be the only sign of a fracture that you will see.

5. Also carefully examine the mandibular canal for discontinuities. 6. A fracture line entering the root of a tooth is considered an open fracture by

definition. 7. Pathologic fractures can occur in the mandible. Look carefully for evidence of a

periapical abscess or a mandibular tumor, especially if there doesn't seem to be enough trauma to match the injury.

Mandibular dislocation -- the condyle (c) is anterior to the articular eminence (e)






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8.8 THE PAINFUL JOINT PROSTHESIS:

The development of prosthetic joints is a Good Thing. The alternatives include chronic,

debilitating joint pain, loss of mobility and function, and even life in a wheelchair. Surgery has provided other possibilities. To paraphrase the Old Testament: "If thine joint offends thee, cast it out!" This might be the Biblical rationale for an archaic procedure called the Girdlestone procedure, in which the articular surface of an end stage, painful joint is resected. The resulting articulation can be surprisingly pain-free. Nowadays, about the only time one sees this appearance is after removal of an infected joint prosthesis or occasionally in the treatment of claw-toe deformities.

Even though prosthetic joints are a Good Thing, they are not a source of unalloyed joy to their recipients. Loosening and infection are two reasons why. There are other causes for a painful prosthetic joint, but these two items are always uppermost in the minds of orthopedists.

Why does a good prosthesis go bad? Largely because they are composed of foreign stuff that acts differently from the original bone. First of all, consider Wolfe's Law of Bone, which is that bone is formed and retained along the lines of stress in that bone. Another way of putting it is: "Form follows function." Look at the trabecular pattern in a calcaneus or a proximal femur -- it's easy to see where the lines of stress are here, because that's where the trabeculae are. Another way to express this rule is: "Use it or lose it." Bone is an amazingly dynamic tissue in this respect. Something as innocuous as spending the night in bed causes a definite but small degree of calcium loss from the bones. If one underuses a body part for a longer period, a striking amount of bone loss can be seen. A good example of this is the disuse osteoporosis seen following casting of an injured extremity. This can easily be seen on follow-up radiographs. In order to see any bone loss






76

whatsoever on plain radiographs, one must first lose 30 - 50 % of one's bone mass. When one considers this, the disuse osteoporosis seen after casting seems even more impressive.

What does this have to do with patients with prosthetic joints? Well, in an ideal world, a prosthetic joint component would carry stress and distribute it to the underlying bone in a manner identical to the original bone. Alas, this does not happen in real life. Prosthetic components react to stresses a lot differently than the original bone that they replaced, and tend to distribute it to the remaining bone much differently. For example, in a hip prosthesis, much of the load applied to the femoral component tends to be transmitted to the bone near its distal tip. The bone near the proximal part of the component tends to have less force transmitted through to it. What happens to the native bone that is now no longer receiving its usual loading? Bone loss occurs here. This phenomenon is called "stress shielding". Since one can get quite a bit of stress shielding around a prosthesis, it's no mystery why one sees progressive bone loss around prosthetic components over the years on follow-up radiographs.

The concept of stress shielding helps to explain the usual life course of a joint prosthesis. A hip prosthesis, for example, may last for 5 - 10 years before sufficient stress shielding occurs that the prosthesis loosens enough to be symptomatic. The loose prosthesis is then removed by the orthopedist, and a new one is put in. However, the native bone around the original femoral component now generally has substantially diminished bone stock. Therefore, the new one has to have a longer stem so that it will reach down far enough to seat in normal bone. This new prosthesis works for another 5 - 10 years, until stress shielding has caused enough bone resorption around this new prosthesis for it too to become symptomatically loosened. Then, a newer, even longer prosthesis is placed, and the cycle continues. Obviously, this process can't go on forever, since you eventually run out of undisturbed bone in which to seat the prosthesis. Therefore, 20 - 30 years is about as long as one can expect to keep a series of prostheses going with a patient's native bone stock. After that, one has to consider bone grafting. This also explains why orthopedists prefer not to put prosthetic joints into patients before they are in their 50's or 60's. Ideally, the last prosthesis placed should wear out about the same time that the patient does.

Life for the patient and the orthopedist would be a lot better if loosening were the only major cause of painful prostheses. Alas, life for both is much complicated by the presence of infection. For various reasons, foreign objects within the body tend to be great places to harbor infections, sort of like all of the tiny creatures living around a coral reef. One complication of infection is subsequent loosening of the prosthesis.

Unfortunately, osteomyelitis is a hard infection to treat. Despite optimal medical and surgical care, it may recur again and again over many years. This is especially true if foreign material or a devitalized fragment of bone remains in the body. This unfortunately means that an infected prosthesis must be removed. It also means that the infection must be cured before a replacement prosthesis can be inserted.

Therefore, it makes a big difference to an orthopedist whether or not a prosthetic joint is merely loosened or loosened and infected. With no infection, the prothesis will be replaced in the same operation in which the old one is removed. With infection, a new prosthesis may not be placed until several months later, once the infection has been eradicated.

The radiologist can play an important role in this decision-making. To help settle an important question like this, one needs to try to get a piece of the patient's disease. In other words, the patient needs an aspiration-arthrogram -- an aspiration of joint contents to send for cultures, and a limited arthrogram to prove intraarticular placement of the aspiration needle. In some cases, if no fluid can be aspirated, it is helpful to inject nonbacteriostatic saline into the joint to lavage the joint and then be reaspirated for culture. In my opinion, it is very important to inject at least a small amount of contrast into the joint space to prove one's intraarticular position. In my experience, it is






77

only too easy to inject great quantities of contrast or air into a variety of soft tissue structures (such as joint capsules, fat pads, etc.) without feeling much resistance with the injecting syringe.

Another cause of pain about a prosthetic joint is stress fracture in one of the rami of the obturator rings of the pelvis. This association is probably due to altered biomechanics following prosthesis placement. This is one of those good news/bad news findings on post prosthesis followup films. The bad news is that the patient has a stress fracture. The good news is that the patient's pain is most likely not due to a loose prosthesis. Bursitis may also cause pain about a prosthetic joint and can clinically mimic a loosened or infected joint.

8.9 SCOLIOSIS:

Scoliosis occurs relatively frequently in the general population, and its frequency depends upon the magnitude of the curve being described. Scoliosis of greater than 25 degrees has been reported in about 1.5/1000 persons in the United States. Most curves can be treated nonoperatively if they are detected before they become too severe. However, 60 % of curvatures in rapidly growing prepubertal children will progress. Therefore, scoliosis screening is done in schools across America and several other countries. This screening is probably not necessary until the fifth grade. Beyond that point, boys and girls should be examined every 6 - 9 months. Generally, curvatures less than 30 degrees will not progress after the child is skeletally mature. Once this has been established, scoliosis screening and monitoring can usually be stopped. However, with greater curvatures, the curvature may progress at about 1 degree per year in adults. In this population, monitoring should be continued.

If scoliosis is neglected, the curves may progress dramatically, creating significant physical

deformity and even cardiopulmonary problems with especially severe curves. Currently, scoliosis is treated successfully by special braces, electrical stimulation, surgery, or by combinations of these three techniques.

Generally, scoliosis is treated by orthopedic surgeons with special training in spinal problems. However, radiographic scoliosis examinations are ordered by a wide variety of other physicians, most of whom look toward the radiologist as the local musculoskeletal expert, after the orthopedist. Therefore, one must know how to read these films and how to dictate a coherent and helpful interpretation of them.






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A sample dictation of a typical examination is shown below: Standing AP and lateral views of the entire spine demonstrate an arcuate thoracolumbar

scoliosis with a rightward convexity. No associated vertebral abnormalities are noted. Using the Cobb technique, and measuring from the top of the T9 and the bottom of the L3 vertebral bodies, this angle measures approximately 27 degrees. The apex of the curve is at the T12 vertebral body and demonstrates grade 3 out of 4 rotation to the right. Lateral bending films show persistence of the curvature with bending to the right and increased curvature with bending to the left. This indicates that the thoracolumbar curve is structural and major. The iliac apophyses are complete along the iliac crests, but have not yet fused with the ilium, indicating that the patient has not yet reached skeletal maturity.

The remainder of this chapter will discuss the rationale behind each of the parts of this sample dictation.

The normal thoracolumbar spine is relatively straight in the sagittal plane and has a double curve in the coronal plane. As shown below, the thoracic spine in convex posteriorly (kyphosis) and the lumbar spine is convex anteriorly (lordosis). Normally there should be no lateral curvature of the spine.

Scoliosis is a complicated deformity that is characterized by both lateral curvature and vertebral rotation. As the disease progresses, the vertebrae and spinous processes in the area of the major curve rotate toward the concavity of the curve. On the concave side of the curve, the ribs are close together. On the convex side, they are widely separated.

As the vertebral bodies rotate, the spinous processes deviate more and more to the concave side and the ribs follow the rotation of the vertebrae. The posterior ribs on the convex side are pushed posteriorly, causing the characteristic rib hump seen in thoracic scoliosis. The anterior ribs on the concave side are pushed anteriorly.

Scoliosis also causes pathologic changes in the vertebral bodies and intervertebral discs, as

shown above.

Normal spine demonstrating the

normal thoracic kyphosis and

lumbar lordosis

Typical distortion of vertebra and ribs in thoracic scoliosis as seen from below






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8.9.1 CLASSIFICATION OF SCOLIOSIS:

• Nonstructural scoliosis • postural scoliosis • compensatory scoliosis

• Transient structural scoliosis • sciatic scoliosis • hysterical scoliosis> • inflammatory scoliosis

• Structural scoliosis o idiopathic (70 - 80 % of all cases) o congenital o neuromuscular

poliomyelitis cerebral palsy syringomyelia muscular dystrophy amyotonia congenita Friedreich's ataxia

• neurofibromatosis • mesenchymal disorders

o Marfan's syndrome o Morquio's syndrome o rheumatoid arthritis o osteogenesis imperfecta o certain dwarves

• trauma o fractures o irradiation o surgery

Idiopathic genetic scoliosis accounts for about 80 % of all cases of the disorder, and has a strong female predilection (7:1). It can be subclassified into infantile, juvenile and adolescent types, depending upon the age of onset. The most common of these is adolescent scoliosis, which by itself is by far the most common type of idiopathic scoliosis in the United States.

Scoliosis can result from congenital vertebral anomalies, as shown below. Discovery of these anomalies should prompt a workup for other associated cardiac, genitourinary or vertebral anomalies.

8.9.2 RADIOGRAPHIC ASSESSMENT OF THE SCOLIOSIS PATIENT:

The radiographic assessment of the scoliosis patient begins with erect anteroposterior and lateral views of the entire spine (occiput to sacrum). In addition, the examination should include a lateral view of the lumbar spine to look for the presence of spondylolysis or spondylolisthesis (prevalence in the general population is about 5 %). The scoliotic curve is then measured from the AP view. The most commonly used method (used by the Scoliosis Research Society, the U. S. Air Force, and everyone I've ever worked with) is the Cobb method. The Cobb method has several advantages over other methods, including the fact that it is more likely to be consistent even when the patient is measured by several

vertebral anomalies causing scoliosis Other causes of scoliosis are occasionally seen, especially due to trauma, neurofibromatosis or

associated with one of the neuromuscular disorders.






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different examiners. An alternative system, known as the Risser-Ferguson method, is used far less commonly.

One must first determine what type of curvature is present. The curvature may be acute, such as seen with a fracture or hemivertebra. More often, it is smooth and arcuate, as shown below. The presence of any vertebral or rib anomalies should be reported. Scoliosis is generally described as to the location of the curve or curves, as shown below.

One should also describe whether the convexity of the curve points to the right or left. If there is a double curve, each curve must be described and measured.

To use the Cobb method, one must first decide which vertebrae are the end-vertebrae of the curve. These end-vertebrae are the vertebrae at the upper and lower limits of the curve which tilt most severely toward the concavity of the curve. Once these vertebrae have been selected, one then draws a line along the upper endplate of the upper body and along the lower endplate of the lower body as shown below.

If the endplates cannot be easily seen, these lines can be drawn along the top or bottom or the pedicles. The angle of interest is simply the angle between these two lines. However, with minor degrees of scoliosis, these two lines will probably intersect off the film somewhere, like downtown Seattle. Therefore, a useful theorem from high school geometry is used to help measure this angle. If one constructs perpendicular lines to these first two lines, these perpendicular lines will intersect on the film and will have the same angle between them as exists between the first two lines. When reporting this angle, it is important to mention that one is using the Cobb method and also which end vertebrae were chosen for the measurement. This latter data is especially important, since once chosen, the same levels should be used from then on to measure curvature on follow-up films. This information should be in the radiographic report, since it becomes part of the patient's chart and therefore lasts far longer than the radiographs, which are often recycled after 5 years or so.

Once one has measured the angle of curvature, one may then estimate the degree of rotation of the vertebra at the apex of the curve by looking at the relation of the pedicles to midline.

Cobb method for measurement of scoliosis

Patterns of scoliosis

measurement of rotational component of scoliosis






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Prior to surgery, a set of lateral bending films are often taken to assess the rigidity or flexibility of the curves. In the illustration below, the thoracic curve is the major curve and the lumbar curve is simply a compensatory curvature. This is shown by the lateral bending films.

One can also look for evidence of maturation in the vertebral bodies themselves at the

endplates, as shown below. When the plates blend in with the vertebral bodies to form a solid union, maturation is complete.

Bending films may help to differentiate structural from nonstructural curves

Determination of skeletal maturity

Determination of vertebral maturity






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9.0 UPDATES ON BASIC LIFE SUPPORT AND CPR:

9.1 ADULT BASIC LIFE SUPPORT:

Basic life support (BLS) includes recognition of signs of sudden cardiac arrest (SCA), heart attack, stroke, and foreign-body airway obstruction (FBAO); cardiopulmonary resuscitation (CPR); and defibrillation with an automated external defibrillator (AED). This section summarizes BLS guidelines for lay rescuers and healthcare providers.

Many SCA victims can survive if bystanders act immediately while VF is still present, but successful

resuscitation is unlikely once the rhythm deteriorates to asystole.8 Treatment for VF SCA is immediate bystander CPR plus delivery of a shock with a defibrillator. The mechanism of cardiac arrest in victims of trauma, drug overdose, drowning, and in many children is asphyxia. CPR with both compressions and rescue breaths is critical for resuscitation of these victims.

It is five years now since the last European resuscitation guidelines were published(1). The science of resuscitation has been enriched with further significant scientific evidence that has led to new evidence-based guidelines. These guidelines were released in November 2005 and published in the international Journal of Resuscitation, November 2005(2).

There are major changes to the previous guidelines, emphasizing that clinical guidelines must be updated regularly in order to advise health care providers on best practice. Nevertheless, guidelines in general do not define the only way that resuscitation should be achieved; they merely represent a widely accepted view of how resuscitation can be undertaken both safely and effectively.

The new guidelines aim not only at applying the best evidence available in the science of resuscitation but also focus on an easier approach for lay people and health care professionals. They pay much attention to the early recognition of very ill patients and the early prevention and treatment of cardiac arrest. The importance of recognizing critical illness and preventing cardiac arrest (in- or out-of-hospital) and post-resuscitation care has been highlighted by the inclusion of these elements in a new four-ring chain of survival.

According to the new guidelines, rescuers begin cardiopulmonary resuscitation if the victim is unconscious or unresponsive and not breathing normally. Checking for a carotid pulse has been omitted as it is an inaccurate method of confirming the presence or absence of circulation.

During the first few minutes after non-asphyxial cardiac arrest the blood oxygen content remains high and myocardial and cerebral oxygen delivery is limited more by diminished cardiac output than by a lack of oxygen in the lungs; therefore initial rescue breaths are less important than chest compression. This has led to the removal of the initial two rescue breaths from the BLS new guidelines.

During CPR, the new recommendation is to give each rescue breath over about 1 second, with enough volume to make the victim’s chest rise, but to avoid rapid and forceful breaths. This recommendation applies to all forms of ventilation during CPR, including mouth to mouth and Bag-Valve-Mask.

Adult Chain of Survival.






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This is based on the following evidence: 1. During CPR blood flow to the lungs is substantially reduced so an adequate ventilation-perfusion ratio

can be maintained with tidal volumes and respiratory rates lower than normal. 2. Not only is hyperventilation (too many breaths or too large volumes) unnecessary but it is harmful

because it increases intra-thoracic pressure thus decreasing venous return to the heart and diminishing cardiac output; survival is consequently reduced.

3. When the airway is unprotected a tidal volume of 1 L produces significantly more gastric distention than a tidal volume of 500 ml.

4. Low minute ventilation (lower than normal tidal volume and respiratory rate) can maintain effective oxygenation and ventilation during CPR. During CPR a tidal volume of approximately 500 - 600 ml should be adequate.

5. Interruptions in chest compressions (for example to give rescue breaths) have a detrimental effect on survival. Giving rescue breaths over a shorter time will help to reduce the duration of essential interruptions.

A major change in the new guidelines is the emphasis on minimizing the interruptions of chest

compressions. The new recommendation is to give 30 compression and 2 rescue breaths rather than the 15 and 2 in the guidelines of 2000. The reason behind this recommendation is that coronary blood flow decreases substantially when chest compressions are stopped and several compressions are then necessary before the coronary flow recovers its previous level.

There is insufficient evidence to support a specific hand position for chest compression during CPR in adults. The new guidelines recommend placing the heel of the hand in the center of the chest with the other hand on top.

The previous guideline of finding the middle of the lower half of the sternum by placing one finger on the lower end of the sternum and sliding the other hand down to it has been omitted.

Another major change from the previous guidelines is related to defibrillation. The new guidelines emphasize the importance of early defibrillation as the ability to deliver early defibrillation is one of the most important factors in determining survival from cardiac arrest. However these guidelines recommend, for out-of-hospital but not in-hospital VF or VT, to give a period of CPR for two minutes before defibrillation despite the evidence supporting this being weak and coming only from animal studies.

The recent guidelines recommend giving only one shock wave of 150-360 J of bi-phasic or 360 J of mono-phasic defibrillators, followed immediately by CPR for two minutes without the need to check for the rhythm or pulse after delivering the shock wave. The reason is to prevent interruptions of CPR during defibrillation as this is associated with post-resuscitation myocardial dysfunction and reduced survival as well as reducing the chances of converting VF to another rhythm. Furthermore the first shock efficacy of biphasic wave forms exceeds 90% and failure to convert VF successfully is more likely to suggest the need for a period of CPR rather than a further shock.

Even if the defibrillation attempt is successful in restoring a perfusing rhythm, it is very rare for the pulse to be palpable immediately after defibrillation. Moreover, even if a perfusing rhythm has been restored, giving chest compressions does not increase the chances of VF recurring.






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9.1.1 MAIN CHANGES IN ADULT BASIC LIFE SUPPORT (FIGURE 1).

The decision to start CPR is made if the victim is unresponsive and is not breathing normally. Rescuers should be taught to place the hands on the center of the chest instead of wasting time by using the “rib margin” method. Each rescue breath is given over 1 second rather than 2 seconds. The ratio of compression to ventilations is 30:2 for adult victims of cardiac arrest. For an adult victim the first two rescue breaths are omitted, with 30 compressions being given immediately after cardiac arrest is established.

9.1.2 MAIN CHANGES IN AUTOMATED EXTERNAL DEFIBRILLATION (AED).

Public access defibrillation (PAD) programs are recom mended for locations where the expected use of an AED for witnessed cardiac arrest exceeds once in two years. A single defibrillatory shock (at least 150 J biphasic or 360 J monophasic) is delivered, followed immediately by 2 minutes of uninterrupted CPR without a check for termination of VF or a check for signs of life or a pulse.






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9.1.3 MAIN CHANGES IN ADULT ADVANCED LIFE SUPPORT (FIGURE 2).

A. CPR BEFORE DEFIBRILLATION: • In an out-of-hospital cardiac arrest attended but not witnessed by health care

professionals equipped with manual defibrillators, give CPR for 2 minutes (i.e. about 5 cycles at 30:2) before defibrillation.

• Don’t delay defibrillation if an out-of-hospital arrest is witnessed by a health care professional.

• Don’t delay defibrillation for in-hospital cardiac arrest.

B. DEFIBRILLATION STRATEGY: • Treat VF/pulseless VT with a single shock, followed by immediate resumption of CPR (30

compressions to 2 ventilations). Do not reassess the rhythm or feel for a pulse. After 2 minutes of CPR check the rhythm and give another shock (if indicated).

• The recommended initial energy for biphasic defibrillators is 150-200 J. Give second and subsequent shocks at 150-360 J.

• The recommended energy when using a monophasic defibrillator is 360 J for both the initial and subsequent shocks.

Figure 2: Adult Basic Life Support Cardiac Arrest Algorithm






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C. FINE VF: If there is doubt about whether the rhythm is asystole or fine VF, do not attempt defibrillation, instead continue chest compressions and ventilation.

D. ADRENALINE: • VF/VT: Give adrenaline 1 mg IV if VF/VT persists after a second shock. Repeat the

adrenaline every 3-5 min thereafter if VF/VT persists. • PEA/Asystole: Give adrenaline 1mg IV as soon as intravenous access is obtained, and

repeat every 3-5 min thereafter until return of spontaneous circulation (ROSC) is achieved.

E. ANTI-ARRHYTHMIC DRUGS: • If VF/VT persists after three shocks, give amiodarone 300 mg by bolus injection. A further

dose of 150 mg may be given for recurrent or refractory VF/VT, followed by an infusion of 900 mg over 24 hours.

• If amiodarone is not available lidocaine 1mg/kg can be used as an alternative but do not give lidocaine if amiodarone has been given already. Do not exceed a total of 3 mg/kg of lidocaine during the first hour.

F. THROMBOLYTIC THERAPY FOR CARDIAC ARREST:

• Consider thrombolytic therapy when cardiac arrest is thought to be due to proven or suspected pulmonary embolus. Thrombolysis may be considered in adult cardiac arrest on a case-by-case basis following initial failure of standard resuscitation in patients in whom an acute thrombotic etiology for the arrest is suspected. Ongoing CPR is not a contra-indication to thrombolysis.

• Consider performing CPR for up to 60-90 min when thrombolytic agents have been given during CPR.

G. POST RESUSCITATION CARE - THERAPEUTIC HYPOTHERMIA:

Unconscious adult patients, with spontaneous circulation, after an out-of-hospital VF cardiac arrest should be cooled to 32-3 ؛4 C for 12-24 h.






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Mild hypothermia may also benefit adult patients after an out-of-hospital arrest, with spontaneous circulation, from a non-shock able rhythm or after a cardiac arrest in hospital.

A. ADULT BLS SEQUENCE: Basic life support consists of the following sequence of actions: 1. Make sure the victim, any bystanders, and you are safe. 2. Check the victim for a response.

• Gently shake his shoulders and ask loudly, ‘Are you all right?’ 3A. If he responds:

• Leave him in the position in which you find him provided there is no further danger. • Try to find out what is wrong with him and get help if needed. • Reassess him regularly.

3B. If he does not respond: • Shout for help. • Turn the victim onto his back and then open the airway using head tilt and chin lift:

• Place your hand on his forehead and gently tilt his head back. • With your fingertips under the point of the victim's chin, lift the chin to open the

airway. 4. Keeping the airway open, look, listen, and feel for normal breathing.

• Look for chest movement. • Listen at the victim's mouth for breath sounds. • Feel for air on your cheek. In the first few minutes after cardiac arrest, a victim may be barely breathing, or taking infrequent, noisy, gasps. Do not confuse this with normal breathing. Look, listen, and feel for no more than 10 sec to determine if the victim is breathing normally. If you have any doubt whether breathing is normal, act as if it is not normal.

5A. If he is breathing normally: • Turn him into the recovery position (see below). • Send or go for help, or call for an ambulance. • Check for continued breathing.

5B. If he is not breathing normally: • Ask someone to call for an ambulance or, if you are on your own, do this yourself; you

may need to leave the victim. Start chest compression as follows: o Kneel by the side of the victim. o Place the heel of one hand in the centre of the victim’s chest. o Place the heel of your other hand on top of the first hand. o Interlock the fingers of your hands and ensure that pressure is not applied

over the victim's ribs. Do not apply any pressure over the upper abdomen or the bottom end of the bony sternum (breastbone).

o Position yourself vertically above the victim's chest and, with your arms straight, press down on the sternum 4 - 5 cm.

o After each compression, release all the pressure on the chest without losing contact between your hands and the sternum.

o Repeat at a rate of about 100 times a minute (a little less than 2 compressions a second).

o Compression and release should take an equal amount of time. 6A. Combine chest compression with rescue breaths.

• After 30 compressions open the airway again using head tilt and chin lift.






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• Pinch the soft part of the victim’s nose closed, using the index finger and thumb of your hand on his forehead.

• Allow his mouth to open, but maintain chin lift. • Take a normal breath and place your lips around his mouth, making sure that you

have a good seal. • Blow steadily into his mouth whilst watching for his chest to rise; take about one

second to make his chest rise as in normal breathing; this is an effective rescue breath.

• Maintaining head tilt and chin lift, take your mouth away from the victim and watch for his chest to fall as air comes out.

• Take another normal breath and blow into the victim’s mouth once more to give a total of two effective rescue breaths. Then return your hands without delay to the correct position on the sternum and give a further 30 chest compressions.

• Continue with chest compressions and rescue breaths in a ratio of 30:2. • Stop to recheck the victim only if he starts breathing normally; otherwise do not

interrupt resuscitation. • If your rescue breaths do not make the chest rise as in normal breathing, then before

your next attempt: • Check the victim's mouth and remove any visible obstruction. • Recheck that there is adequate head tilt and chin lift. • Do not attempt more than two breaths each time before returning to chest

compressions. • If there is more than one rescuer present, another should take over CPR about every

2 min to prevent fatigue. Ensure the minimum of delay during the changeover of rescuers.

• 6B. Chest-compression-only CPR. • If you are not able, or are unwilling, to give rescue breaths, give chest compressions

only. • If chest compressions only are given, these should be continuous at a rate of 100 a

minute. • Stop to recheck the victim only if he starts breathing normally; otherwise do not

interrupt resuscitation. 7. Continue resuscitation until:

• Qualified help arrives and takes over, • The victim starts breathing normally, or • You become exhausted.

"Adult BLS2005.ppt"






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9.1.4 EXPLANATORY NOTES:

A. RISK TO THE RESCUER: • The safety of both the rescuer and victim are paramount during a resuscitation attempt.

There have been few incidents of rescuers suffering adverse effects from undertaking CPR, with only isolated reports of infections such as tuberculosis (TB) and severe acute respiratory distress syndrome (SARS). Transmission of HIV during CPR has never been reported. There have been no human studies to address the effectiveness of barrier devices during CPR; however, laboratory studies have shown that certain filters, or barrier devices with one-way valves, prevent oral bacteria transmission from the victim to the rescuer during mouth-to-mouth ventilation. Rescuers should take appropriate safety precautions where feasible, especially if the victim is known to have a serious infection, such as TB. Initial rescue breaths

• During the first few minutes after non-asphyxial cardiac arrest the blood oxygen content remains high. Ventilation is, therefore, less important than chest compression at this time.

• It is well recognised that skill acquisition and retention are aided by simplification of the BLS sequence of actions. It is also recognised that rescuers are frequently unwilling to carry out mouth-to-mouth ventilation for a variety of reasons, including fear of infection and distaste for the procedure. For these reasons, and to emphasise the priority of chest compressions, it is recommended that, in most adults, CPR should start with chest compressions rather than initial ventilations.

B. JAW THRUST:

The jaw thrust technique is not recommended for lay rescuers because it is difficult to learn and perform. Therefore, the lay rescuer should open the airway using a head-tilt-chin-lift manoeuvre.

C. AGONAL GASPS:

Agonal gasps are present in up to 40% of cardiac arrest victims. Laypeople should, therefore, be taught to begin CPR if the victim is unconscious (unresponsive) and not breathing normally. It should be emphasised during training that agonal gasps occur commonly in the first few minutes after sudden cardiac arrest. They are an indication for starting CPR immediately and should not be confused with normal breathing.

D. MOUTH-TO-NOSE VENTILATION:

Mouth-to-nose ventilation is an effective alternative to mouth-to-mouth ventilation. It may be considered if the victim’s mouth is seriously injured or cannot be opened, the rescuer is assisting a victim in the water, or a mouth-to-mouth seal is difficult to achieve.

E. MOUTH-TO-TRACHEOSTOMY VENTILATION:

Mouth-to-tracheostomy ventilation may be used for a victim with a tracheostomy tube or tracheal stoma who requires rescue breathing.

F. BAG-MASK VENTILATION:

• Considerable practice and skill are required to use a bag and mask for ventilation. The lone rescuer has to be able to open the airway with a jaw thrust whilst simultaneously holding the mask to the victim’s face. It is a technique that is appropriate only for lay rescuers who work in highly specialised areas, such as where there is a risk of cyanide poisoning or exposure to other toxic agents.






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• There are other specific circumstances in which non-healthcare providers receive extended training in first aid which could include training, and retraining, in the use of bag-mask ventilation. The same strict training that applies to healthcare professionals should be followed and the two-person technique is preferable.

G. CHEST COMPRESSION:

In most circumstances it will be possible to identify the correct hand position for chest compression without removing the victim’s clothes. If in any doubt, remove outer clothing. In Guidelines 2000 a method was recommended for finding the correct hand position by placing one finger on the lower end of the sternum and sliding the other hand down to it. It has been shown that the same hand position can be found more quickly if rescuers are taught to ‘place the heel of your hand in the centre of the chest with the other hand on top’, provided the teaching includes a demonstration of placing the hands in the middle of the lower half of the sternum. Whilst performing chest compression: I. Each time compressions are resumed, the rescuer should place his hands without delay

‘in the centre of the chest’. II. Compress the chest at a rate of about 100 a minute. III. Pay attention to achieving the full compression depth of 4-5 cm (for an adult). IV. Allow the chest to recoil completely after each compression. V. Take approximately the same amount of time for compression and relaxation. VI. Minimise interruptions in chest compression. VI. Do not rely on a palpable carotid or femoral pulse as a gauge of effective arterial flow. VIII. Compression rate’ refers to the speed at which compressions are given, not the total

number delivered in each minute. The number delivered is determined not only by the rate, but also by the number of interruptions to open the airway, deliver rescue breaths, and allow AED analysis.

H. COMPRESSION-ONLY CPR:

Studies have shown that chest-compression-only CPR may be as effective as combined ventilation and compression in the first few minutes after non-asphyxial arrest. Laypeople should, therefore, be encouraged to do compression-only CPR if they are unable or unwilling to provide rescue breaths, although combined chest compression and ventilation is the better method of CPR.

I. OVER-THE-HEAD CPR:

Over-the-head CPR for a single rescuer and straddle CPR for two rescuers may be considered for resuscitation in confined spaces.

J. RECOVERY POSITION:

• There are several variations of the recovery position, each with its own advantages. No single position is perfect for all victims. The position should be stable, near a true lateral position with the head dependent, and with no pressure on the chest to impair breathing.

• It is recommended that the below sequence of actions must be adopted to place a victim in the recovery position:

o Remove the victim’s spectacles. o Kneel beside the victim and make sure that both his legs are straight. o Place the arm nearest to you out at right angles to his body, elbow bent with the

hand palm uppermost.






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o Bring the far arm across the chest, and hold the back of the hand against the victim’s cheek nearest to you.

o With your other hand, grasp the far leg just above the knee and pull it up, keeping the foot on the ground.

o Keeping his hand pressed against his cheek, pull on the far leg to roll the victim towards you onto his side.

o Adjust the upper leg so that both the hip and knee are bent at right angles. o Tilt the head back to make sure the airway remains open. o Adjust the hand under the cheek, if necessary, to keep the head tilted. o Check breathing regularly. o If the victim has to be kept in the recovery position for more than 30 min turn him

to the opposite side to relieve the pressure on the lower arm.

9.1.5 CHOKING:

A. RECOGNITION: Because recognition of choking (airway obstruction by a foreign body) is the key to successful outcome, it is important not to confuse this emergency with fainting, heart attack, seizure, or other conditions that may cause sudden respiratory distress, cyanosis, or loss of consciousness. Foreign bodies may cause either mild or severe airway obstruction. The signs and symptoms enabling differentiation between mild and severe airway obstruction are summarised in the table below. It is important to ask the conscious victim ‘Are you choking?’

General signs of choking Attack occurs while eating

Victim may clutch his neck

Signs of mild airway obstruction Signs of severe airway obstruction

Response to question ‘Are you choking?’ Response to question ‘Are you choking?’

Victim speaks and answers yes Victim unable to speak

Other signs Victim may respond by nodding

Other signs

Victim unable to breathe

Breathing sounds wheezy

Attempts at coughing are silent

Victim is able to speak, cough, and breathe

Victim may be unconscious

B. ADULT CHOKING SEQUENCE: (This sequence is also suitable for use in children over the age of 1 year) 1. If the victim shows signs of mild airway obstruction:

• Encourage him to continue coughing, but do nothing else. 2. If the victim shows signs of severe airway obstruction and is conscious:

o Give up to five back blows. o Stand to the side and slightly behind the victim. o Support the chest with one hand and lean the victim well forwards so that

when the obstructing object is dislodged it comes out of the mouth rather than goes further down the airway.

heimlich.jpg






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o Give up to five sharp blows between the shoulder blades with the heel of your other hand.

• Check to see if each back blow has relieved the airway obstruction. • The aim is to relieve the obstruction with each blow rather than necessarily to give all

five. o If five back blows fail to relieve the airway obstruction give up to five

abdominal thrusts. o Stand behind the victim and put both arms round the upper part of his

abdomen. o Lean the victim forwards. o Clench your fist and place it between the umbilicus (navel) and the bottom

end of the sternum (breastbone). o Grasp this hand with your other hand and pull sharply inwards and upwards. o Repeat up to five times.

• If the obstruction is still not relieved, continue alternating five back blows with five abdominal thrusts.

3. If the victim becomes unconscious: • Support the victim carefully to the ground. • Immediately call an ambulance. • Begin CPR (from 5B of the Adult BLS Sequence). Healthcare providers, trained and

experienced in feeling for a carotid pulse, should initiate chest compressions even if a pulse is present in the unconscious choking victim.

9.1.6 EXPLANATORY NOTES:

• Following successful treatment for choking, foreign material may nevertheless remain in the upper or lower respiratory tract and cause complications later.

• Victims with a persistent cough, difficulty swallowing, or with the sensation of an object being still stuck in the throat should therefore be referred for a medical opinion. Abdominal thrusts can cause serious internal injuries and a doctor should examine all victims receiving abdominal thrusts for injury.

A. RESUSCITATION OF CHILDREN AND VICTIMS OF DROWNING:

• Both ventilation and compression are important for victims of cardiac arrest when the oxygen stores become depleted – about 4-6 min after collapse from ventricular fibrillation (VF), and immediately after collapse for victims of asphyxial arrest. Previous guidelines tried to take into account the difference in causation, and recommended that victims of identifiable asphyxia (drowning; trauma; intoxication) and children should receive 1 min of CPR before the lone rescuer left the victim to get help. The majority of cases of sudden cardiac arrest out of hospital, however, occur in adults and are of cardiac origin due to VF. These additional recommendations, therefore, added to the complexity of the guidelines whilst affecting only a minority of victims.

• Also important is that many children do not receive resuscitation because potential rescuers fear causing harm. This fear is unfounded; it is far better to use the adult BLS sequence for resuscitation of a child than to do nothing.

• For ease of teaching and retention, therefore, laypeople should be taught that the adult sequence may also be used for children who are not responsive and not breathing.

• The following minor modifications to the adult sequence will, however, make it even more suitable for use in children:






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• Give five initial rescue breaths before starting chest compressions (adult sequence of actions 5B).

• If you are on your own perform CPR for approximately 1 min before going for help. • Compress the chest by approximately one-third of its depth. Use two fingers for an infant

under 1 year; use one or two hands for a child over 1 year as needed to achieve an adequate depth of compression.

• The same modifications of five initial breaths, and 1 min of CPR by the lone rescuer before getting help, may improve outcome for victims of drowning. This modification should be taught only to those who have a specific duty of care to potential drowning victims (e.g. lifeguards).

• Drowning is easily identified. It can be difficult, on the other hand, for a layperson to determine whether cardiorespiratory arrest has been caused by trauma or intoxication. These victims should, therefore, be managed according to the standard protocol.

9.2 ADULT ADVANCED LIFE SUPPORT:

This section on adult advanced life support (ALS) adheres to the same general principles as in Guidelines 2000, but incorporates some important changes. The guidelines in this section apply to healthcare professionals trained in ALS techniques. Laypeople, first responders, and automated external defibrillator (AED) users are referred to the basic life support (BLS) and AED sections.

9.2.1 CPR BEFORE DEFIBRILLATION:

• In the case of out-of-hospital cardiac arrest attended, but unwitnessed, by healthcare professionals equipped with manual defibrillators, give CPR for 2 min (i.e. about 5 cycles at 30:2) before defibrillation.

• Do not delay defibrillation if an out-of-hospital arrest is witnessed by a healthcare professional. • Do not delay defibrillation for in-hospital cardiac arrest.

A. DEFIBRILLATION STRATEGY:

• Treat ventricular fibrillation/pulseless ventricular tachycardia (VF/VT) with a single shock, followed by immediate resumption of CPR (30 compressions to 2 ventilations). Do not reassess the rhythm or feel for a pulse. After 2 min of CPR, check the rhythm and give another shock (if indicated).

• The recommended initial energy for biphasic defibrillators is 150-200 J. Give second and subsequent shocks at 150-360 J.

• The recommended energy when using a monophasic defibrillator is 360 J for both the initial and subsequent shocks.






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B. FINE VF:

If there is doubt about whether the rhythm is asystole or fine VF, do NOT attempt defibrillation; instead, continue chest compression and ventilation. Adrenaline (epinephrine)

C. VF/VT:

• Give adrenaline 1 mg IV if VF/VT persists after a second shock. • Repeat the adrenaline every 3-5 min thereafter if VF/VT persists.

D. PULSELESS ELECTRICAL ACTIVITY / ASYSTOLE:

• Give adrenaline 1 mg IV as soon as intravenous access is achieved and repeat every 3-5 min.

• Anti-arrhythmic drugs • If VF/VT persists after three shocks, give amiodarone 300 mg by bolus injection. A further

dose of 150 mg may be given for recurrent or refractory VF/VT, followed by an infusion of 900 mg over 24 h.

• If amiodarone is not available, lidocaine 1 mg kg-1 may be used as an alternative, but do not give lidocaine if amiodarone has already been given. Do not exceed a total dose of 3 mg kg-1 during the first hour.

• Post resuscitation care – therapeutic hypothermia • Unconscious adult patients with spontaneous circulation after out-ofhospital • VF cardiac arrest should be cooled to 32-34°C for 12-24 h. • Mild hypothermia may also benefit unconscious patients with spontaneous circulation after

out-of-hospital cardiac arrest due to a non-shockable rhythm, or after cardiac arrest in hospital.

E. ALS TREATMENT ALGORITHM:

• Arrhythmias associated with cardiac arrest are divided into two groups: shockable rhythms (VF/VT) and non-shockable rhythms (asystole and PEA). The principle difference in management is the need for attempted defibrillation in patients with

• VF/VT. Subsequent actions, including chest compression, airway management and ventilation, venous access, administration of adrenaline, and the identification and correction of reversible factors, are common to both groups.

• The ALS treatment algorithm provides a standardised approach to the management of adult patients in cardiac arrest.

I. SHOCKABLE RHYTHMS (VF/VT):

a. Sequence of actions • Attempt defibrillation (one shock - 150-200 J biphasic or 360 J monophasic). • Immediately resume chest compressions (30:2) without reassessing the rhythm or

feeling for a pulse. • Continue CPR for 2 min, then pause briefly to check the monitor: • If VF/VT persists:

o Give a further (2nd) shock (150-360 J biphasic or 360 J monophasic). o Resume CPR immediately and continue for 2 min. o Pause briefly to check the monitor.






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• If VF/VT persists give adrenaline 1 mg IV followed immediately by a (3rd) shock (150-360 J biphasic or 360 J monophasic).

• Resume CPR immediately and continue for 2 min. • Pause briefly to check the monitor. • If VF/VT persists give amiodarone 300 mg IV followed immediately by a (4th)

shock (150-360 J biphasic or 360 J monophasic). • Resume CPR immediately and continue for 2 min. • Give adrenaline 1 mg IV immediately before alternate shocks (i.e. approximately

every 3-5 min). • Give a further shock after each 2 min period of CPR and after confirming that

VF/VT persists. o If organised electrical activity is seen during this brief pause in

compressions, check for a pulse. o If a pulse is present, start post-resuscitation care. o If no pulse is present, continue CPR and switch to the nonshockable

algorithm. o If asystole is seen, continue CPR and switch to the nonshockable

algorithm.

F. PRECORDIAL THUMP: Consider giving a single precordial thump when cardiac arrest is confirmed rapidly after a witnessed and monitored sudden collapse, and a defibrillator is not immediately to hand. A precordial thump should be undertaken immediately after confirmation of cardiac arrest but only by healthcare professionals trained in the technique. Using the ulnar edge of a tightly clenched fist, deliver a sharp impact to the lower half of the sternum from a height of about 20 cm, then retract the fist immediately to create an impulse-like stimulus. A precordial thump is most likely to be successful in converting VT to sinus rhythm. Successful treatment of VF by precordial thump is much less likely: in all the reported successful cases the precordial thump was given within the first 10 seconds of VF. There are very rare reports of a precordial thump converting a perfusing to a non-perfusing rhythm.

G. EXPLANATION FOR THE CHANGES IN THE TREATMENT OF VF/VT:

I. CPR BEFORE DEFIBRILLATION: • Although Guidelines 2000 recommended immediate defibrillation for all shockable

rhythms, recent evidence indicates that a period of CPR before defibrillation may improve survival after prolonged collapse (> 5 min). The duration of collapse is frequently difficult to estimate accurately, so give CPR before attempted defibrillation outside hospital, unless the arrest is witnessed by a healthcare professional or an AED is being used. This advice does NOT apply to lay responders using an AED outside hospital, who should apply the AED as soon as it is available.

• In contrast, there is no evidence to support or refute CPR before defibrillation for in-hospital cardiac arrest. For this reason after in-hospital VF/VT cardiac arrest, give a shock as soon as possible.

II. DEFIBRILLATION STRATEGY:

• There are no published human or experimental studies comparing a single shock protocol with a three-stacked shock protocol for the treatment of VF/VT cardiac arrest. Experimental studies show that relatively short interruptions in chest compression to






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deliver rescue breaths or perform rhythm analysis are associated with reduced survival. Interruptions in chest compression also reduce the chances of converting VF to another rhythm. Significant interruptions in chest compression are common during out-of-hospital and in-hospital cardiac arrest.

• When using a three-shock protocol, the time taken to deliver shocks and analyse the rhythm causes significant interruptions in CPR. This fact, combined with the improved first shock efficacy (for termination of VF/VT) of biphasic defibrillators, has prompted the recommendation of a single-shock strategy.

• With first shock efficacy of biphasic waveforms exceeding 90%, failure to terminate VF/VT successfully implies the need for a period of CPR (to improve myocardial oxygenation) rather than a further shock. Even if defibrillation is successful in restoring a perfusing rhythm, it is very rare for a pulse to be palpable immediately afterwards, and the delay in trying to palpate a pulse will further compromise the myocardium if a perfusing rhythm has not been restored.7

• If a perfusing rhythm has been restored, giving chest compression does not increase the chance of VF recurring. In the presence of post-shock asystole, however, chest compressions may induce VF.

• The initial shock from a biphasic defibrillator should be no lower than 120 J for rectilinear biphasic waveforms, and 150 J for biphasic truncated exponential waveforms. For uniformity, it is recommended that the initial biphasic shock should be at least 150 J. If an initial shock has been unsuccessful it may be worth attempting the second and subsequent shocks with a higher energy level.

• However, there is no evidence to support either a fixed or escalating energy protocol. Both strategies are acceptable. Manufacturers should display the effective waveform energy range on the face of the biphasic device. If you are unaware of the effective energy range of the device, use 200 J for the first shock.

• This 200 J default has been chosen because it falls within the reported range of selected energy levels that are effective for first and subsequent biphasic shocks, and can be provided by every biphasic manual defibrillator available today. It is a consensus default and not a recommended ideal. If biphasic devices are clearly labelled, and providers are familiar with the devices they use in clinical care, there will be no need for the default 200 J. Ongoing research is necessary to establish the most appropriate initial settings for both monophasic and biphasic defibrillators.

• Because of the lower efficacy of monophasic defibrillators for terminating VF/VT, and the change to a single-shock strategy, the recommended initial energy level for the first shock using a monophasic defibrillator is 360 J. If needed, second and subsequent shocks should be given at 360 J. A monophasic waveform is less efficient than a biphasic waveform at terminating VF/VT, and most manufacturers now sell only biphasic devices. The urgency with which monophasic defibrillators are replaced must be determined locally, taking into consideration available resources and competing healthcare demands.

H. FINE VF:

Fine VF that is difficult to distinguish from asystole is very unlikely to be shocked successfully into a perfusing rhythm. Continuing good quality CPR may improve the amplitude and frequency of the VF and improve the chance of successful defibrillation to a perfusing rhythm. Delivering repeated shocks in an attempt to defibrillate what is thought to be fine VF will increase myocardial injury, both directly from the electric current and indirectly from the interruptions in coronary blood flow.






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I. ADRENALINE:

• There is no placebo-controlled study that shows that the routine use of any vasopressor at any stage during human cardiac arrest increases survival to hospital discharge. Current evidence is insufficient to support or refute the routine use of any particular drug or sequence of drugs. Despite the lack of human data the use of adrenaline is still recommended, based largely on experimental data. The alpha-adrenergic actions of adrenaline cause vasoconstriction, which increases myocardial and cerebral perfusion pressure during cardiac arrest.

• Immediate resumption of CPR after shock delivery, along with the elimination of a rhythm check at this stage, makes it difficult to select an ideal point in the ALS algorithm at which to give adrenaline. The consensus recommendation is to give adrenaline immediately after confirmation of the rhythm and just before shock delivery (drug–shock–CPR–rhythm check sequence). Have the adrenaline ready to give so that the delay between stopping chest compression and delivery of the shock is minimised. The adrenaline that is given immediately before the shock will be circulated by the CPR that follows the shock.

• When the rhythm is checked 2 min after giving a shock, if a non-shockable rhythm is present and the rhythm is organised (complexes appear regular or narrow), try to palpate a pulse. Rhythm checks must be brief, and pulse checks undertaken only if an organised rhythm is observed. If an organised rhythm is seen during a 2-min period of CPR, do not interrupt chest compressions to palpate a pulse unless the patient shows signs of life suggesting return of spontaneous circulation (ROSC). If there is any doubt about the existence of a pulse in the presence of an organised rhythm, resume CPR. If the patient has

• ROSC, begin post-resuscitation care. • If the patient’s rhythm changes to asystole or PEA see non-shockable rhythms below. In

patients in asystole or PEA, give adrenaline 1 mg IV immediately intravenous access is achieved.

• In both VF/VT and PEA / asystole, give adrenaline 1 mg IV every 3-5 min (approximately every other two-minute loop).

• In patients with a spontaneous circulation, doses considerably smaller than 1 mg IV may be required to maintain an adequate blood pressure.

J. VASOPRESSIN:

A recent meta-analysis of five randomised trials showed no statistically significant difference between vasopressin and adrenaline for ROSC, death within 24 h, or death before hospital discharge. A subgroup analysis, based on initial cardiac rhythm, did not show any statistically significant difference in the rate of death before hospital discharge. Despite the absence of placebo-controlled trials, adrenaline has been the standard vasopressor in cardiac arrest. There is insufficient evidence to support or refute the use of vasopressin as an alternative to, or in combination with, adrenaline in any cardiac arrest rhythm. Thus, adrenaline remains the primary vasopressor for the treatment of cardiac arrest in all rhythms.






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K. ANTI-ARRHYTHMIC DRUGS: There is no evidence that giving any anti-arrhythmic drug routinely during human cardiac arrest increases survival to hospital discharge. In comparison with placebo and lidocaine, the use of amiodarone in shock-refractory VF improves survival to hospital admission.9,10 There are no data on the use of amiodarone for shock-refractory VF/VT when single shocks are used. On the basis of expert consensus, if VF/VT persists after three shocks, give amiodarone 300 mg by bolus injection during the brief rhythm analysis before delivery of the fourth shock. A further dose of 150 mg may be given for recurrent or refractory VF/VT, followed by an infusion of 900 mg over 24 h. Lidocaine 1 mg kg-1 may be used as an alternative if amiodarone is not available, but do not give lidocaine if amiodarone has been given already. I. NON-SHOCKABLE RHYTHMS (PEA AND ASYSTOLE)

Pulseless electrical activity (PEA) is defined as cardiac electrical activity in the absence of any palpable pulse. These patients often have some mechanical myocardial contractions but they are too weak to produce a detectable pulse or blood pressure. PEA may be caused by reversible conditions that can be treated if they are identified and corrected (see below). Survival following cardiac arrest with asystole or PEA is unlikely unless a reversible cause can be found and treated effectively. • Sequence of actions for PEA • Start CPR 30:2. • Give adrenaline 1 mg IV as soon as intravascular access is achieved. • Continue CPR 30:2 until the airway is secured, then continue chest compressions

without pausing during ventilation. • Recheck the rhythm after 2 min.

o If there is no change in the ECG appearance: Continue CPR. Recheck the rhythm after 2 min and proceed accordingly. Give further adrenaline 1 mg IV every 3-5 min (alternate loops).

o If the ECG changes and organised electrical activity is seen, check for a pulse.

• If a pulse is present, start post-resuscitation care. • If no pulse is present: • Continue CPR. • Recheck the rhythm after 2 min and proceed accordingly. • Give further adrenaline 1 mg IV every 3-5 min (alternate loops).

Sequence of actions for asystole and slow PEA (rate < 60 min-1) • Start CPR 30:2. • Without stopping CPR, check that the leads are attached correctly. • Give adrenaline 1 mg IV as soon as intravascular access is achieved. • Give atropine 3 mg IV (once only). • Continue CPR 30:2 until the airway is secured, then continue chest compression

without pausing during ventilation. • Recheck the rhythm after 2 min and proceed accordingly. • If VF/VT recurs, change to the shockable rhythm algorithm. • Give adrenaline 1 mg IV every 3-5 min (alternate loops).

"tachy algorithm.jpg"






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L. ASYSTOLE: Asystole is a condition that can be precipitated or exacerbated by excessive vagal tone. Theoretically, this can be reversed by a vagolytic drug; therefore, give atropine 3 mg (the dose that will provide maximum vagal blockade) for asystole or slow PEA (rate < 60 min-1). Whenever a diagnosis of asystole is made, check the ECG carefully for the presence of P waves because the patient may respond to cardiac pacing. There is no value in attempting to pace true asystole.

M. DURING CPR:

During the treatment of persistent VF/VT or PEA / asystole, there should be an emphasis on giving good quality chest compression between defibrillation attempts, recognising and treating reversible causes (4 Hs and 4 Ts), and obtaining a secure airway and intravenous access. Healthcare providers must practise efficient coordination between CPR and shock delivery. The shorter the interval between cessation of chest compression and shock delivery, the more likely it is that the shock will be successful. Reduction in the interval from compression to shock delivery by even a few seconds can increase the probability of shock success. Providing CPR with a CV ratio of 30:2 is tiring; change the individual undertaking compressions every 2 min.

N. POTENTIALLY REVERSIBLE CAUSES:

Potential causes or aggravating factors for which specific treatment exists must be sought during any cardiac arrest. For ease of memory, these are divided into two groups of four, based upon their initial letter, either H or T: • Hypoxia • Hypovolaemia • Hyperkalaemia, hypokalaemia, hypocalcaemia, acidaemia, and other metabolic disorders • Hypothermia • Tension pneumothorax • Tamponade • Toxic substances • Thromboembolism (pulmonary embolus/coronary thrombosis)

O. THE FOUR ‘HS’:

• Minimise the risk of hypoxia by ensuring that the patient’s lungs are ventilated adequately with 100% oxygen. Make sure there is adequate chest rise and bilateral breath sounds. Using the techniques described below, check carefully that the tracheal tube is not misplaced in a bronchus or the oesophagus.

• Pulseless electrical activity caused by hypovolaemia is usually due to severe haemorrhage. This may be precipitated by trauma, gastrointestinal bleeding, or rupture of an aortic aneurysm. Restore intravascular volume rapidly with fluid, coupled with urgent surgery to stop the haemorrhage.

• Hyperkalaemia, hypokalaemia, hypocalcaemia, acidaemia, and other metabolic disorders are detected by biochemical tests or suggested by the patient’s medical history, e.g. renal failure. A 12-lead ECG may be diagnostic. Intravenous calcium chloride is indicated in the presence of hyperkalaemia, hypocalcaemia, and calcium-channel-blocking drug overdose.

• Suspect hypothermia in any drowning incident; use a low-reading thermometer.






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P. THE FOUR ‘TS’: • A tension pneumothorax may be the primary cause of PEA and may follow attempts at

central venous catheter insertion. The diagnosis is made clinically. Decompress rapidly by needle thoracocentesis, and then insert a chest drain.

• Cardiac tamponade is difficult to diagnose because the typical signs of distended neck veins and hypotension are usually obscured by the arrest itself. Cardiacarrest after penetrating chest trauma is highly suggestive of tamponade and is an indication for needle pericardiocentesis or resuscitative thoracotomy.

• In the absence of a specific history, the accidental or deliberate ingestion of therapeutic or toxic substances may be revealed only by laboratory investigations. Where available, the appropriate antidotes should be used, but most often treatment is supportive.

• The commonest cause of thromboembolic or mechanical circulatory obstruction is massive pulmonary embolus. If cardiac arrest is thought to be caused by pulmonary embolism, consider giving a thrombolytic drug immediately.

Thrombolysis may be considered in adult cardiac arrest, on a case-by-case basis, following initial failure of standard resuscitation in patients in whom an acute thrombotic aetiology for the arrest is suspected. Ongoing CPR is not a contraindication to thrombolysis.

Q. INTRAVENOUS FLUIDS:

• Hypovolaemia is a potentially reversible cause of cardiac arrest: infuse fluids rapidly if hypovolaemia is suspected. In the initial stages of resuscitation there are no clear advantages to using colloid: use saline or Hartmann’s solution.

• Avoid dextrose; this is redistributed away from the intravascular space rapidly, and causes hyperglycaemia, which may worsen neurological outcome after cardiac arrest.

R. OPEN-CHEST CARDIAC COMPRESSION:

Open-chest cardiac compression may be indicated for patients with cardiac arrest caused by trauma, in the early postoperative phase after cardiothoracic surgery, or when the chest or abdomen is already open, for example during surgery following trauma.

S. SIGNS OF LIFE:

If signs of life (such as regular respiratory effort or movement) reappear during CPR, or readings from the patient’s monitors (e.g. exhaled carbon dioxide or arterial blood pressure) are compatible with a return of spontaneous circulation, stop CPR and check the monitors briefly. If an organised cardiac rhythm is present, check for a pulse. If a pulse is palpable, continue post-resuscitation care, treatment of peri-arrest arrhythmias, or both. If no pulse is present, continue CPR.

9.2.2 DEFIBRILLATION:

A. STRATEGIES BEFORE DEFIBRILLATION: I. SAFE USE OF OXYGEN:

In an oxygen-enriched atmosphere, sparks from poorly-applied defibrillator paddles can cause a fire. Taking the following precautions can minimise this risk: • Remove any oxygen mask or nasal cannulae and place them at least 1 m away from

the patient’s chest. • Leave the ventilation bag connected to the tracheal tube or other airway adjunct.

Alternatively, disconnect the ventilation bag from the tracheal tube and move it at least 1 m from the patient’s chest during defibrillation.

Thoracocentesis

tamponade






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• The use of self-adhesive defibrillation pads, rather than manual paddles, may minimise the risk of sparks occurring.

II. CHEST HAIR:

It may be necessary rapidly to shave the area intended for electrode placement, but do not delay defibrillation if a razor is not immediately available.

III. PADDLE FORCE:

If using paddles, apply them firmly to the chest wall. The optimal force is 8 kg in adults, and 5 kg in children 1-8 years using adult paddles. Place water-based gel pads between the paddles and the patient’s skin.

IV. ELECTRODE POSITION:

• Place the right (sternal) electrode to the right of the sternum, below the clavicle. • Place the apical paddle vertically in the mid-axillary line, approximately level with the

V6 ECG electrode position or the female breast. This position should be clear of any breast tissue. It is important that this electrode is placed sufficiently laterally.

• Antero-posterior electrode placement may be more effective than the traditional antero-apical position in cardioversion of atrial fibrillation. Either position is acceptable.

• An implantable medical device (e.g. permanent pacemaker or automatic implantable cardioverter defibrillator (AICD)) may be damaged during defibrillation if current is discharged through electrodes placed directly over the device. Place the electrode away from the device or use an alternative electrode position. Remove any transdermal drug patches on the chest wall before defibrillation.

V. PADS VERSUS PADDLES:

Self-adhesive defibrillation pads are safe and effective and are an acceptable alternative to standard defibrillation paddles. They enable the operator to defibrillate from a safe distance, rather than leaning over the patient as occurs with paddles. When used for initial monitoring of a rhythm, both pads and paddles enable quicker delivery of the first shock compared with standard ECG electrodes, but pads are quicker than paddles.

B. AIRWAY MANAGEMENT AND VENTILATION:

• The principles of airway and ventilation management remain unchanged from Guidelines 2000.

• Patients requiring resuscitation often have an obstructed airway. Prompt assessment, with control of the airway and ventilation of the lungs, is essential.

• Without adequate oxygenation it may be impossible to restore a spontaneous cardiac output. In a witnessed cardiac arrest in the vicinity of a defibrillator, attempted defibrillation should take precedence over opening the airway.

• Give high-flow oxygen. In the spontaneously breathing patient, masks with non re breathing reservoir bags are more effective than standard masks.

I. BASIC AIRWAY MANOEUVRES AND AIRWAY ADJUNCTS:

Assess the airway. Use head tilt and chin lift, or jaw thrust to open the airway. Simple airway adjuncts (oropharyngeal or nasopharyngeal airways) are often helpful, and sometimes essential, to maintain an open airway.






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C. VENTILATION: • Provide artificial ventilation as soon as possible in any patient in whom spontaneous

ventilation is inadequate or absent. Expired air ventilation (rescue breathing) is effective but the rescuer’s expired oxygen concentration is only 16-17%, so it must be replaced as soon as possible by ventilation with oxygen enriched air. A pocket resuscitation mask enables mouth-to-mask ventilation.

• Some enable supplemental oxygen to be given. Use a two-hand technique to maximise the seal with the patient’s face. A self-inflating bag can be connected to a facemask, tracheal tube, or alternative airway device. The two-person technique for bag-mask ventilation is preferable. Deliver each breath over approximately 1 sec and give a volume that corresponds to normal chest movement; this represents a compromise between giving an adequate volume, minimising the risk of gastric inflation, and allowing adequate time for chest compression. During CPR with an unprotected airway, give two ventilations after each sequence of 30 chest compressions.

• Once an airway device has been inserted, ventilate the lungs at a rate of about 10 breaths min-1 and continue chest compression without pausing during ventilation.

D. ALTERNATIVE AIRWAY DEVICES:

I. LARYNGEAL MASK AIRWAY (LMA): • A laryngeal mask airway is relatively easy to insert, and ventilation using an LMA is

more efficient and easier than with a bag-mask. If gas leakage is excessive, chest compression will have to be interrupted to enable ventilation. Although an

• LMA does not protect the airway as reliably as a tracheal tube, pulmonary aspiration is uncommon when using an LMA during cardiac arrest.

II. THE COMBITUBE: A Combitube is relatively easy to insert and ventilation using this device is more efficient and easier than with a bag-mask. Great care must be taken to avoid attempting to ventilate the lungs through the wrong port of the Combitube.

III. TRACHEAL INTUBATION:

There is insufficient evidence to support or refute the use of any specific technique to maintain an airway and provide ventilation in adults with cardiopulmonary arrest. Despite this, tracheal intubation is perceived as the optimal method of providing and maintaining a clear and secure airway. It should be used only when trained personnel are available to carry out the procedure with a high level of skill and confidence. The perceived advantages of tracheal intubation over bag-mask ventilation include: • Maintenance of a patent airway, which is protected from aspiration of gastric contents

or blood from the oropharynx; • Ability to provide an adequate tidal volume reliably even when chest compressions are

uninterrupted; • The potential to free the rescuer’s hands for other tasks; • The ability to suction airway secretions; • The provision of a route for giving drugs. Use of the bag-mask is more likely to cause gastric distension which, theoretically, is more likely to cause regurgitation and aspiration. However, there are no reliable data to indicate that the incidence of aspiration is any higher in cardiac arrest patients ventilated using a bag-mask compared with those ventilated via a tracheal tube. • The perceived disadvantages of tracheal intubation over bag-mask ventilation include:






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• The risk of an unrecognised, misplaced tracheal tube; • A prolonged time without chest compression while intubation is attempted; • A comparatively high failure rate. • Intubation success rates correlate with the intubation experience of the individual. • Healthcare professionals who undertake intubation should do so only within a

structured, monitored programme, which should include comprehensive competency-based training and regular opportunities to refresh skills.

Rescuers must weigh the risks and benefits of intubation against the need to provide effective chest compression. The intubation attempt will require interruption of chest compression, but once an advanced airway is in place ventilation can continue uninterrupted. Those skilled in advanced airway management should be able to undertake laryngoscopy without stopping chest compression; a brief pause in chest compression will be required as the tube is passed through the vocal cords. Alternatively, to avoid any interruption, the intubation attempt may be deferred until ROSC. No intubation attempt should take longer than 30 sec. If intubation has not been achieved by then, recommence bag-mask ventilation. AfteR intubation, tube placement must be confirmed and the tube secured adequately.

IV. CONFIRMATION OF CORRECT PLACEMENT OF THE TRACHEAL TUBE: Unrecognised oesophageal intubation is the most serious complication of attempted tracheal intubation. Routine use of primary and secondary techniques to confirm correct placement of the tracheal tube should reduce this risk. Primary assessment should include bilateral observation of chest expansion, bilateral auscultation in the axillae (breath sounds should be equal and adequate), and auscultation over the epigastrium (breath sounds should not be heard). Clinical signs of correct tube placement (condensation in the tube, chest rise, breath sounds on auscultation of lungs, and inability to hear gas entering the stomach) are not completely reliable. Secondary confirmation of tracheal tube placement by an exhaled CO2 or oesophageal detector device should reduce the risk of unrecognised oesophageal intubation. If there is doubt about correct tube placement, use the laryngoscope and look directly to see if the tube passes through the vocal cords. None of the secondary confirmation techniques will differentiate between a tube placed in a main bronchus and one placed correctly in the trachea. There are inadequate data to identify the optimal method of confirming tube placement during cardiac arrest, and all devices should be considered as adjuncts to other confirmatory techniques. During cardiac arrest pulmonary blood flow may be so low that there is insufficient exhaled CO2, so the CO2 detector does not identify a correctly placed tracheal tube. When exhaled CO2 is detected during cardiac arrest it indicates reliably that the tube is in the trachea or main bronchus, but when it is absent tracheal tube placement is best confirmed with an oesophageal detector device. A variety of electronic as well as simple, inexpensive, colorimetric CO2 detectors are available for both in-hospital and out-of-hospital use.

E. CRICOTHYROIDOTOMY:

If it is impossible to ventilate an apnoeic patient with a bag-mask, or to pass a tracheal tube or alternative airway device, delivery of oxygen through a cannula or surgical cricothyroidotomy may be life saving.






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F. ASSISTING THE CIRCULATION: I. INTRAVENOUS ACCESS:

a. Peripheral versus central venous drug delivery: Peripheral venous cannulation is quicker, easier to perform, and safer. Drugs injected peripherally must be followed by a flush of at least 20 ml of fluid. Central venous line insertion must cause minimal interruption of chest compression.

b. Intraosseous route: If intravenous access is difficult or impossible, consider the intraosseous route for both children and adults. The intraosseous route also enables withdrawal of marrow for venous blood gas analysis and measurement of electrolytes and haemoglobin concentration.

c. Tracheal route: If intravenous or intraosseous access cannot be established, the tracheal route can give some drugs. The dose of adrenaline is 3 mg diluted to at least 10 ml with sterile water.

d. Drugs: The use of adrenaline and anti-arrhythmic drugs has been discussed above.

e. Magnesium Give magnesium sulphate 8 mmol (4 ml of a 50% solution) for refractory VF if there is any suspicion of hypomagnesaemia (e.g. patients on potassium-losing diuretics). Other indications are: o Ventricular tachyarrhythmias in the presence of possible hypomagnesaemia; o Torsade de pointes; o Digoxin toxicity.

f. Bicarbonate Giving sodium bicarbonate routinely during cardiac arrest and CPR (especially in out-of-hospital cardiac arrest), or after ROSC, is not recommended. Give sodium bicarbonate (50 mmol) if cardiac arrest is associated with hyperkalaemia or tricyclic antidepressant overdose. Repeat the dose according to the clinical condition of the patient and the results of repeated blood gas analysis.

g. Atropine: Blockade of parasympathetic activity at both the sinoatrial (SA) node and the atrioventricular (AV) node may increase sinus automaticity and facilitate AV node conduction. The adult dose of atropine for asystole, or PEA with a rate < 60 min-1, is 3 mg IV.

h. Calcium: Calcium is indicated during resuscitation from PEA if this is thought to be caused by:

• Hyperkalaemia; • Hypocalcaemia; • Overdose of calcium-channel-blocking drugs; • Overdose of magnesium (e.g. during treatment of pre-eclampsia).

The initial dose of 10 ml 10% calcium chloride (6.8 mmol Ca2+) may be repeated if necessary. Remember that calcium can slow the heart rate and precipitate arrhythmias. In cardiac arrest, calcium may be given by rapid intravenous injection. In the presence of a spontaneous circulation it should be given slowly. Do not give calcium solutions and sodium bicarbonate simultaneously by the same venous access.






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G. POST-RESUSCITATION CARE: Return of spontaneous circulation is just the first step towards the goal of complete recovery from cardiac arrest. Interventions in the post-resuscitation period influence the final outcome significantly. The post-resuscitation phase starts when ROSC is achieved. Once stabilised, the patient should be transferred to the most appropriate high-care area (e.g. intensive care unit or cardiac care unit) for continued monitoring and treatment. I. AIRWAY AND BREATHING:

Consider tracheal intubation, sedation, and controlled ventilation in any patient with obtunded cerebral function. Adjust ventilation to achieve normocarbia and monitor this using the end-tidal CO2 and arterial blood gas values. Adjust the inspired oxygen concentrations to achieve adequate arterial oxygen saturation. Insert a gastric tube to decompress the stomach; gastric distension caused by mouth-to-mouth or bag-mask ventilation will splint the diaphragm and impair ventilation. Obtain a chest radiograph to check the position of the tracheal tube and central venous lines and exclude a pneumothorax associated with rib fractures from CPR.

II. CIRCULATION: Haemodynamic instability is common after cardiac arrest. An arterial line for continuous blood pressure monitoring is essential, and the use of a non-invasive cardiac output monitor may be helpful. Infusion of fluids may be required to optimise filling. Conversely, diuretics and vasodilators may be needed to treat left ventricular failure. Infusion of an inotrope may be required to maintain a mean arterial blood pressure that is no lower than the normal pressure for the patient, and achieves an adequate urine output. Maintain the serum potassium concentration between 4.0-4.5 mmol l-1. If there is evidence of coronary occlusion, consider the need for immediate revascularisation by thrombolytic therapy or percutaneous coronary intervention.

H. DISABILITY (OPTIMISING NEUROLOGICAL RECOVERY): I. SEDATION:

If sedation is required, short-acting drugs (e.g. propofol, alfentanil, remifentanil) will enable earlier neurological assessment.

II. CONTROL OF SEIZURES: Seizures are relatively common in the post-resuscitation period and may cause cerebral injury. Control seizures with benzodiazepines, phenytoin, propofol, or a barbiturate as appropriate.

III. TEMPERATURE CONTROL: a. Treatment of hyperpyrexia

A period of hyperthermia is common in the first 48 h after cardiac arrest. The risk of a poor neurological outcome increases for each degree of body temperature above 37°C. Treat hyperthermia occurring in the first 72 h after cardiac arrest with antipyretics or active cooling.

b. Therapeutic hypothermia: • Mild hypothermia is thought to suppress many of the chemical reactions

associated with reperfusion injury. Two randomised clinical trials showed improved outcome in adults, remaining comatose after initial resuscitation from out-of-hospital VF cardiac arrest, who were cooled within minutes to hours after ROSC.11,12 Unconscious adult patients with spontaneous circulation after out-of-

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hospital VF cardiac arrest should be cooled to 32-34°C.13 Cooling should be started as soon as possible and continued for at least 12-24 h. Induced hypothermia may also benefit unconscious adult patients with spontaneous circulation after out-of hospital cardiac arrest from a non-shock able rhythm, or cardiac arrest in hospital.

• Treat shivering by ensuring adequate sedation and giving neuromuscular blocking drugs. Bolus doses of neuromuscular blockers are usually adequate but infusions are occasionally necessary. Re-warm the patient slowly (0.25-0.5oC h-1) and avoid hyperthermia. The optimum target temperature, rate of cooling, duration of hypothermia, and rate of rewarming have yet to be determined; further studies are essential.

• External or internal cooling techniques or both can be used to initiate treatment. • An infusion of 30 ml kg-1 saline at 4oC decreases core temperature by 1.5oC. • Intravascular cooling enables more precise control of core temperature than

external methods, but it is unknown whether this improves outcome. • Complications of mild therapeutic hypothermia include increased infection,

cardiovascular instability, coagulopathy, hyperglycaemia, and electrolyte abnormalities such as hypophosphataemia and hypomagnesaemia.

c. Blood glucose control: There is a strong association between high blood glucose levels after resuscitation from cardiac arrest and poor neurological outcome. Tight control of blood glucose (4.4 - 6.1 mmol l-1) using insulin reduces hospital mortality in critically ill adults, but this has not been demonstrated in post-cardiac-arrest patients specifically. The optimal blood glucose target level in critically ill patients has not been determined. Comatose patients are at particular risk from unrecognised hypoglycaemia, and the risk of this complication occurring increases as the target blood glucose concentration is lowered. In common with all critically ill patients, patients admitted to a critical-care environment after cardiac arrest should have their blood glucose monitored frequently and hyperglycaemia treated with an insulin infusion. The blood glucose concentration that triggers insulin therapy and the target range of blood glucose concentrations should be determined by local policy. There is a need for studies of glucose control after cardiac arrest.

d. Prognostication: There are no neurological signs that can predict outcome in the comatose patient in the first hours after ROSC. By three days after the onset of coma related to cardiac arrest, 50% of patients with no chance of ultimate recovery have died. In the remaining patients, the absence of pupil light reflexes on day three, and an absent motor response to pain on day three, are both independently predictive of a poor outcome (death or vegetative state) with very high specificity.






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10.0 DISASTER RESPONSE AND PLANNING INCLUDING PT ROLE:

Natural disasters have a major and long lasting impact on people of the countries affected. Physiotherapists as experts in physical rehabilitation should be involved in planning policy for disasters as well as disaster management. To achieve this it is necessary to develop effective strategies to sensitise and educate Physiotherapists to be able to work as first responders in the face of a disaster and to help rehabilitate the people affected to achieve the highest attainable level of health. 10.1 DISASTER PLANNING/PREPAREDNESS:

• Assist in creating a resource list that is community-specific. • Make arrangements for Physical therapists to be part of the local disaster response team. Establish occupational

therapy's role. • Educate families/clients about creating a family disaster plan. • Talk with families about integrating purposeful activities, especially for children, into a family disaster plan. • Talk with clients with disabilities/special needs about evacuation plans. • Work with local disaster planning groups, including people with disabilities. • Educate teams about shelter accessibility, creating environments with purposeful occupations, establishment of

routines and adapting environments for independence. Getting caught in a disaster without a safety plan is not a good idea for anybody, but for people with chronic illnesses, lack of planning can lead to unnecessary tragedy and preventable loss of life. Don’t wait for imminent disaster to start thinking about how you’ll stay safe. Follow these steps and make sure you’re ready before disaster strikes. 1. Know your risks:

The first thing you must do when making a disaster plan is to know what and when you are planning for. Fires? Floods? Earthquakes? Tornadoes? Hurricanes? Something else? Is your threat seasonal or year round? Get to know your geographical area and the types of threats you are most likely to encounter.

2. Know Your Resources: Don't try to figure everything out on your own. Draw on the expertise of those who know what to do in your situation. To get you started, try some of these resources: • County Emergency Management Offices: Find out what your county has to offer in the way of

shelters, transportation, and assistance programs. Also find out what type of early warning systems your county has in place.






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• Cystic Fibrosis Treatment Centers:Talk to your health care team at the CF center to find out what resources they have or can refer you to that will help you meet your medical needs.

• National Resources: No matter where you live, you will find a wealth of information and services from agencies like the Red Cross and Ready America.

3. Make a List of Things You Need: Take an inventory of everything that you will need to make it through the day. Don’t leave anything out. Think about things like: • Medicine and nutrition supplements • Refrigeration • Electricity Equipment Supplies • Access to doctors • Communication • Transportation

4. Assemble a Kit: Now that you know what you’ll need, start to gather the things on your list. Make sure you include: Medicine: • 2 week supply of medicines that come from your local pharmacy • 4 week supply of medicines that come by mail order, because the post office may

experience delivery delays in the midst of a disaster. Supplies: • Batteries • Oxygen tanks Important phone numbers: • Doctors • Pharmacy • CF Foundation • Family and emergency contacts A list of your: • Medicines and allergies • Diagnoses • Treatments • Providers

5. Prepare for Utility Outages: What will you do if you lose power or water? You'll need: • An alternate power source: If you can, consider purchasing a portable generator to provide

electricity for your equipment. If you can’t get a hold of a generator, talk to your equipment vendors to find out if battery operated versions are available. Bottled water: At least a two week supply

o A cooler: For storing medications, especially Pulmozyme and Tobi o A knowledge of manual chest physiotherapy: Brush up on manual airway clearance

techniques, in case you can’t use your vest. 6. Plan Your Escape:

Draft a map of your house, and then use it to plot your escape route. Be sure to consider how you will get your equipment out. Plan a backup escape route in case you are unable to follow your original plan. Know your neighborhood evacuation route so you are familiar with where to go once you get out of your house.

7. Know Where You’ll Go: Some options to consider:






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• Special needs shelter: Most counties have at least one shelter designated for people with special health care needs. Often, these shelters are staffed with medical personnel and usually they have generators to ensure refrigeration and power.

• Regular shelter: If you just need a place to go without all the bells and whistles, a standard emergency shelter may be an appropriate choice. Before choosing any shelter, be sure to talk to your doctor about your risks for exposure to infection in crowded places.

• Out of town: If you are planning to seek shelter out of town, be sure to find local health care providers ahead of time. The Cystic Fibrosis Foundation or your CF Care center team can help you with that.

8. Build a Disaster Network: • Disaster tree: Create a phone list with your family and friends. When a disaster hits, the person at

the top of the list should call the next in line to make sure they are okay. • Helpers: Arrange in advance for people who can be available to help you, if needed.

9. Write Your Plan Down: • Make sure the people in your network know what you intend to do. Write your plan

down. Keep it in a safe place and give a copy to the people in your network. 10. Practice Makes Perfect:

At least once a year, stage a mock emergency and practice your plan. Check your disaster kit to make sure everything is there and replace expired items. Escape from your house and drive your evacuation route to wherever you plan to go in a real disaster. Be sure to include the people in your network and test out the disaster tree.

10.1.1 DISASTER RECOVERY:

• Help people re-establish routines, adapt lifestyles and reengage in occupations, especially when moving from shelters.

• Assist directing people to community resources, especially related to disability issues. • Facilitate support groups to decrease stress and anxiety and increase coping skills.

10.1.2 EVALUATING THE PLAN ANNUALLY. DISASTER RESPONSE

• Assist in the evacuation of vulnerable populations including people with disabilities. • Help create shelters that support people's occupations. • Establish routines. • Develop meaningful daily physical activities. • Create environments that facilitate independence. • Organize developmentally appropriate activities for children. • Facilitate fun activities to take place in the shelter. • Attend to the needs of people with disabilities (obtain adaptive equipment such as communication

devices, walkers or devices to assist activities of daily living). • Connect people in shelters that lived close to each other prior to the disaster. • Assess key elements of life before disaster to assist in after-shelter planning (What did you do

yesterday?). • Decrease anxiety/stress. • Create support groups in shelters. • Assist first responders in coping with stress.

Help develop systems for efficient shelter management.






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10.2 PRINCIPLES OF HOSPITAL DISASTER PLANNING: This chapter will address primarily domestic, peacetime disasters because these are the types of events most likely to be faced by United States hospitals. This chapter points out more problems than solutions, which might prove somewhat frustrating to the disaster medical planner. Nevertheless, one hopes that, where no definitive answers are presented, an accurate perception of the problems will bring the solutions closer. In the meantime, some of the proposed solutions must be treated like hypotheses that still require testing.

"Disaster Response Planning and Coordin

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