BPK 241 Week 1

Injury Prevention

Injury Prevention

• Reduction of Force

• Strengthening of Body Parts

• Screening of Participants

Goal of Preventative Medicine

To promote health and well-being and prevent disease, disability and death

Preventative Medicine

• Primary prevention

• Secondary Prevention

• Tertiary Prevention

Primary Prevention

Things we do to prevent injury/ illness

• Warm-up

• Stretching

• Training

Secondary Prevention

Once and injury or illness has occurred

• Anitbiotics/ antiinflammators

• Rehab to return to original function

• Braces/ Taping on return to sport

Tertiary Prevention

Things we do when original function cannot be restored

• Reduce long-term impairment

• Improve quality of life

Importance of Preparation

• Decrease incidence of injuries

• Decrease severity of injuries

Forms of Preparation for Physical Activity

• General Conditioning (Endurance, Strength, Power, Flexibility)

• Specific Training (Sport specific, Individual specific, Skills)

• Protective Measures (Equipment, Nutrition, Hydration)

General Conditioning

C.O. = H.R. x S.V.

• Fitness is proportional to your resting H.R. over 1 minute

• 20 to 60 minute exercise, HR > 150 bpm, at least 3 times per week

Strength and Power Training

• Resistance (weight) training (PRE)

• Isometric (muscle contract but no length moved) vs Isotonic (eccentric, concentric)

• Plyometrics

• Who, when, why, how

Flexibility Training

who, what, where, how

Sport Specific

• Skating, Batting, Pitching, Shooting, Golf swing, Swim stroke

Individual Specific

• Foot Speed, Strength, Power, Flexibility

Skills

• Gross vs fine motor skills

• Open vs closed skills

Equipment

• Absorbs energy

• Disperses energy

• Deflects a blow

• Limit excess movement

Nutrition Six Classes

• Protein

• Carbohydrates

• Fats

• Vitamins (ADEK vs BC)

• Minerals

• Water/ Electrolytes

Nutrition Role

• Growth, repair, and maintenance of all tissues

• Regulate body processes

• Provide Energy

Protein (20-25%)

• Protein on own does not increase muscle mass

• Complex process, related to hormones

• Protein necessary, but not primary source of fuel

• Extra protein consumed is burned as energy or stored as fat

Carbohydrates (55-60%)

• The most efficiently broken down and metabolized form energy (glucose) for the body

• Broken down and stored as glycogen in the liver and muscles

• Average 150 lbs athletes carries 1500-2000 calories in form of carbs

Fats (15-20%)

• Types: Saturated & unsaturated

• Not the enemy and the primary fuel for light to moderate intensity exercise

• More likely to burn fat than carbs for athletes that maintain low to mod intensity

• Avg 150 lbs athletes carries up to 80,000 calories in fat

• Consume more unsaturated than saturated fat (eliminates unnecessary calories, but not nutrients)

Vitamins and Minerals

• Play key roles in the metabolism of carbs and fats which are your primary muscle fuels during exercise

• Involved in the repair and building of muscle protein in response to training

Vitamins ADEK

Fat soluble, excess is stored in body fat, increased risk of toxicity, need to be careful

Vitamins BC

Water soluble, excess is excreted in urine, therefore needs to be replenished

Minerals

• Dietary elements found naturally in the earth’s crust, has 20 different types in the body, mostly stored in liver and bones

• Some are essential to our health and can only be obtained from what you eat and drink

• Major minerals like Na, K, Cl, C, P, Mg, S need 100 mg or more daily

• Trace minerals like Fe, Z, I, Cu, Ma, F, Se are needed in smaller amounts, usually less than 20 mg daily

Anemia

Iron deficiency

Water/ Hydration

Essential for survival - used for digestion, temperature control, eliminating waste products, prevent dehydration

Approx 60% of body weight

Dehydration

Not enough water

• Amount of blood pumped with each heartbeat decreases

• Exercising muscle do not receive enough oxygen

• By-products of exercise are not flushed out of the body as regularly as they should be

• Exhaustion sets in and the athlete’s performance suffers

Hyper hydration (hyponatremia)

Too much water

Signs of dehydration

• Early Symptoms include: Thirst, Headache, Fatigue, Weakness, Dry mouth, Loss of appetite, Muscle cramps

• Late Symptoms include: Nausea, Hot to touch, Dizziness, Lack of coordination, Confusion, Fainting

• Water loss of > 10 to 20% body weight may = death

Electrolyte Minerals & Hydration

• Ingestion of sodium during exercise may help with maintaining or restoring plasma volume during exercise and recovery

• Consumption of sports drink helps retain water in the body and aids in hydration by increasing the absorption of fluid from the intestines into the muscles

• Researchers suggest 6-8% carb sport drink with at least 110 mg of sodium per 8 ounce serve as a fuel of energy that water can’t provide

Cramping

Excessive sweating with sodium/mineral loss, muscle twitching & cramps

Heat exhaustion

Prolonged period of fluid loss via activity in high temperatures

Heat stroke

Failure of thermoregulatory system

• Sudden collapse, loss of consciousness, flushed, hot skin, shallow breathing and rapid pulse, core temp of 106 F or higher

Heat stroke prevention

• Fluid and electrolyte replacement

• Gradual acclimization

• monitor temp and humidity

• identify susceptible individuals

• weight records

• uniforms

ABCDs

• Airway

• Breathing

• Circulation

• Disability

Emergency Care General Points

• Keep head and neck stable

• Keep warm

• N.P.O nil per os (nothing by mouth)

• Get help

• Serial repetition of ABCDs- record status

Shock Definition

• The state of insufficient blood flow to the tissues of the body as a result of problems with the circulatory system

Neurogenic Shock

General dilation of blood vessels

Psychologic Shock

Temporary dilation of blood vessels to brain

Cardiogenic Shock

Reduced C.O leads to reduced B.P

Septic Shock

System vasodilation - dilated veins leads to reduced B.P

Hypovolemic

Reduced blood volume leads to reduced C.O./ B. P.

Anaphylactic

System Vasodilation - leads to reduced B.P.

Shock Signs and Symptoms

Result of decreased amount of blood for the circulatory system

• Reduced B.P

• Hypoxia

• Reflexive increase HR (tachycardia, rapid pulse)

• Skin cool and clammy (warm and dry if septic shock)

• Anxiety, thirst, impaired consciousness

Shock Treatment

• N.P.O

• ABCDs

• Maintain body temp ,elevate legs

• Transport to medical center ASAP

Bone structue

• Diaphysis (Shaft)

• Metaphysis

• Epiphysis

• Epiphyseal plate

• Periosteum

Joint Structure

• Bones (which articulate)

• Joint capsule/ connective tissue

• Synovial membrane and fluid

• Cartilage (hyaline vs fibrocartilage)

• Bursae

• Nerves, blood vessels

• Ligaments

• Muscle tendons

Joint Types

• Hinge (elbow)

• Saddle (thumb)

• Facet (spine)

• Pivot (upper C1)

• Gliding (wrist carpal)

• Ball-and-Socket (hip)

Fracture types

Open (compound) vs Closed (simple)

• Varieties (Transverse, Oblique, Comminuted, Spiral, Greenstick, Epiphyseal plate, Segmental, Avulsed, Impacted, Torus)

• Acute vs Stress (elastic vs plastic range)

Bone Fracture Continuum

• Normal Bone → Stress reaction → Stress Fracture → Full (Acute) Fracture

• Osteoclastic activity > Osteoblastic activity

• Decreased bone mass perpetuates the problem

Response of bone to stress

• Structure (strength and stiffness)

• Load (magnitude, duration, direction, repetitions)

• Support (muscle activation, equipment)

• Past history

Response of joints to stress

• Structure (bone stability, flexibility, capsule, ligaments)

• Load (magnitude, duration, direction, repetitions)

• Support (muscle activity, braces, tape)

• Past history

Response of Tissues to Stress

The stronger the tissue, the greater magnitude of load it can withstand:

• Load = outside or internal forces acting on body

• Mechanical stress = tissue responses to forces

• Viscoelastic properties = amount of resistance to stress

• Yield Point = elasticity of tissue can no longer hold back stress = mechanical strain (strain or sprain)

Soft Tissue Injury Repair

• Acute Inflammatory Phase (0-72 hours)

• Proliferation/ Repair Phase (2 days- 6 weeks)

• Remodelling/ Maturation Phase (4 weeks - 6 months, longer?)

Inflammation

• Protective tissue reaction

• “Clinical” if causes pain or disability

• Usually a localized, beneficial response to tissue injury

Cardinal Signs of Inflammation

• Rubor: increased blood flow

• Calor: Increased blood flow

• Tumor: fluid accumulation

• Dolor: local tissue pressure

• Functio laesa: swelling and tenderness

Acute Inflammatory Phase

Consists of two primary events:

• Vascular evnets

• Cellular events

Vascular and cellular reactions are mediated by chemical mediators, derived from plasma proteins or cells (cytokines) and are produced in response to OR activated by stimuli

Vascular events (minutes to several hours)

Changes in vascular flow (Vasoconstriction and Stasis)

Tissue damage activates the coagulation cascade: Thromboplastin → prothrombin → thrombin → Fibrinogen → Insoluble clot (Quickly followed by Vasodilation → increased blood flow AND increased vascular permeability)

Increased Vascular permeability - Hallmark of acute inflammation and protein and fluid leakage from artery

Vasoconstriction

Blood vessels constrict for a brief period

Stasis

Increased blood viscosity

Cellular Events

Initiated by chemical mediators:

• Release from invading organism, damaged tissue, WBC’s involved in inflammatory response

• Margination

• Rolling

• Adhesion

• Migration (diapedesis/extravasation

• Migration → chemotaxis

Inflammation Benefits

Supplies things to injury site

• Clotting factors

• Anti-infection materials & processes:

  • Leukocytes

  • Phagocytes (macrophages) - eat damaged/destroyed cells

  • Antibodies

  • Stick micro-organisms to phagocytes

  • Attack foreign cells (e.g., put holes in their membranes)

  • Nutrients (O2, amino acids, glucose)

• Stimulates proliferation of endothelial cells (neovascularization) & fibroblasts (cells that synthesize collagen and extracellular matrix)

Edema

• Restrict blood flow if no room for swelling

• Produce pain, which can limit movement

• Excessive or chronic inflammation may → tissue destruction, fibrosis, and necrosis (death)

Acute vs Chronic inflammation

Acute: immediate, few days and resolution, abscess formation

Chronic: delayed, up to many months or years, tissue destruction, fibrosis, necrosis

Systemic Manifestations

• Fever

• Leukocytosis

• Myalgia

• Arthralgia

• Malaise

• Chills

Inflammation Treatment

Remove underlying cause

• Incise and drain abscess

• Antibiotics

• Remove foreign body

• Remove Mechanical stress

Treat local effects

• POLICE, then heat

• NSAID drugs

• Physio, Chiro, RMT, Acupuncture, Naturopath

Treat systemic effects

• Antipyretics (ASA, acetaminophen)

• Analgesics (NSAIDS, narcotics)

• Antibiotics

Inflammation types

• Myositis

• Arthritis

• Tendonitis

• Bursitis

• Vasculitis

• Dermatitis

Proliferation/Repair Phase (2 days- 6 weeks)

• Characterized by proliferation of capillaries (neovascularization) and fibroblasts which synthesize granulation tissue aka scar tissue (a collagen and extracellular matrix with cross-linking)

• Collagen initially is laid down in random fashion and is predominantly Type III collagen

• As the quantity of collagen at the injury site increases, the number of fibroblasts decrease

• More Type III, less Type I collagen. Weak (H-bonds), rather than covalent bonds, between collagen fibres) and susceptible to re-injury

• Poorly vascularized and Disorganized

Remodelling/Maturation Phase (4 weeks - 12-24 months)

• Starts 1 to 2 weeks post injury

• Long term process that involves realignment & maturation of collagen fibres that make up scar tissue

• Myofibroblasts re-orient collagen fibrils in the direction of loading

  • Increased stress and strain causes collagen fibres to realign to position of maximum efficiency

  • Parallel to lines of tension

  • Gradually assumes more normal appearance and function

• Lasts 10-12 months, total maturation phase may take years to be fully complete

Remodelling/ Maturation Phase Movement

• Increases synthesis

• Increases lysis

• Reorganizes - decrease in weaker type III collagen, increase in stronger type I collagen

• Importance of this stage overlooked since patients stop doing rehab exercises once acute pain and disability are gone

• Rehab isn’t done for a year or more; stopping before complete increases risk of re-injury

Phases of Soft Tissue Injury Repair

1. Inflammation (days to several weeks)

2. Proliferation (several weeks to month)

3. Remodelling aka Maturation (a year+)

Wound Healing Mechanisms

Scar tissue formation and Regeneration

Wound Healing Tissue Types

• Labile

• Stable (smooth muscle, glands, connective tissue)

• Permanent (cardiac and skeletal muscle, neurons)

Primary Union

• Clean incision

• Edges well - approximated

• Smaller scar, rapid healing

Secondary union

• Large, irregular wound

• Contamination

• Larger scar, slower healing, dysfunction

Factors that influence Healing

Local:

• Location of wound, Extent of Injury, Edema, Hemorrhage, Poor Vascular Supply, Separation of Tissue, Muscle Spasm, Atrophy, Infection

Systemic:

• Blood Supply

• Corticosteroids

• Health/Age/Nutrition

Ice

• Vasoconstriction (Hunting Response)

• Decreased bleeding into injured tissue

• Decrease in inflammatory response

• Decreased swelling

• Decrease pain - decreases excitability of free nerve endings (nociceptors)

• Decreased muscle spasm

• Decreased cellular damage - low secondary tissue hypoxia

Implications of Cold on Performance

• Decreased pain sensation

• Golgi Tendon organs less sensitive

• Muscle spindles less sensitive

• Increase stiffness at myotendinous junction

• Muscle more susceptible to fatigue if cooled below 25 C

Heat

• Vasodilation - increased blood flow

• Increase in inflammatory response

• Increased swelling

• Decreased pain

• Decreased muscle spasm

• Decreased stiffness of soft tissues

• Increased metabolism within cells that are warned

• Critical temp threshold for beneficial effects is 39 C

• Can be achieved by 15 min of general exercise

Types of vascular events

1. Vasoconstriction (seconds)

2. Vasodilation (minutes)

3. Permeability Increase - oedema formation