Chapter 2: Understanding

1
Chapter 2 Understanding Managing the Healing
Process Through Rehabilitation
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Understanding the Healing Process

• Programs must be based on healing process
  framework
• Phases
• Inflammatory
• Fibroblastic-repair
• Maturation-remodeling
• No definitive beginning or end

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The Primary Injury

• Described as either chronic or acute
• Macrotraumatic injuries
• Result of acute trauma
• Produce immediate pain and disability
• Fractures, dislocations, sprains, strains
• Macrotraumatic injuries
• Overuse injuries, resulting from repetitive
  overload, incorrect mechanics
• Tendinitis, tenosynovitis bursitis
• Secondary injury
• Inflammatory or secondary hypoxic injury

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Inflammatory ResponsePhase I

• Injury results in altered cellular metabolism and
  chemical mediators
• Macroscopic characteristics
• Swelling
• Tenderness
• Redness
• Increased temperature
• Initial response is critical in healing process
• An injury must cause the Inflammatory Response

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• Vascular Reaction
• Involves vascular spasm, formation of clot and
  fibrous tissue growth
• Vasoconstriction occurs 5-10 minutes following
  injury
• Causes anemia followed by hyperemia due to
  dilation
• Ultimately a slowing of blood flow occurs
  progressing to stasis and stagnation
• Initial response lasts 24-48 hours

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• Chemical Mediators
• Histamine
• Vasodilation and increased cell permeability
• Leukotaxin
• Margination
• Increased permeability
• Necrosin
• Phagocytic activity
• Swelling is directly related to extent of vessel
  damage

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• Clot Formation
• Disrupted vessel walls expose collagen within
  endothelium walls
• Platlets adhere to vascular wall in conjunction
  with leukocytes forming a plug
• Plug obstructs local lymphatic fluid drainage
• Results in localization of the injury
• Precipitated by fibrinogen ? fibrin conversion
• Cascade of events involving thromboplastin,
  prothrombin, and thrombin
• Clot formation begins 12 hours after injury and
  is complete within 48 hours
• Clot vs. Scab

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• Chronic inflammation
• Occurs when acute inflammation does not eliminate
  injuring agents and restore normal physiological
  state
• Leukocytes are replaced with macrophages,
  lymphocytes and plasma cells
• Specific mechanism is unknown
• Overuse and overload related
• No specific time frame in which acute becomes
  chronic inflammation
• Resistant to physical and pharmacological agents
• Introduction of non-steroidal anti-inflammatory
  drugs (NSAIDs) some research indicates impedance
  of healing

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Fibroblastic-Repair Phase II

• Fibroplasia
• Active scar formation
• May last 4-6 weeks
• Signs and symptoms will subside
• Endothelial capillary buds develop allowing for
  aerobic healing
• Increased blood flow for nutrient delivery

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• Fibroblastic-Repair (continued)
• Granulation tissue develops with breakdown of
  fibrin clot
• Granulation tissue composed of fibroblasts,
  collagen and capillaries
• Fibroblasts synthesize extracellular matrix
  containing collagen and elastin
• Proteoglycans
• Glycosaminoglycans
• Fluid
• Collagen is deposited randomly at day 6 or 7
• Results in increased scar tensile strength
• Persistent inflammatory response promotes
  extended fibroplasia, resulting in increased
  scarring

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Maturation-Remodeling Phase III

• Realignment of collagen
• Continued breakdown and synthesis of collagen
• Increased stress and strain results in increased
  collagen realignment
• Nonvascular, contracted, strong, firm scar
  present after 3 weeks
• Maturation may require several years to complete

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Role of Progressive Controlled Mobility

• Wolffs Law
• Bone and soft tissue will respond to physical
  demands placed upon them
• Remodeling and realignment
• Initial immobilization is necessary what
  happens to ligaments, tendons, bone?
• Controlled mobilization enhances
• Scar formation
• Revascularization
• Muscle regeneration and fiber reorientation
• Tensile properties
• Controlled activity allows for gradual return to
  normal levels of function

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Factors that Impede Healing

• Extent of Injury
• Edema
• Hemorrhage
• Poor Vascular Supply
• Separation of tissue
• Muscle spasm
• Atrophy

• Corticosteroids
• Keloids and hypertrophic scars
• Infection
• Humidity, climate, and oxygen tension
• Health, age, and nutrition

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Pathophysiology of Injury to Various Tissues

• Epithelial Tissue
• Covers internal and external surfaces
• Skin, outer layer of organs, inner lining of
  blood vessels, glands
• Purposes
• to protect and form structure for other tissues
• Function in absorption and secretion
• Relies on diffusion for fluid, oxygen, waste and
  nutrient transport
• Injuries
• Abrasions, lacerations, punctures, avulsions
• Infection, inflammation or disease

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• Connective Tissue
• Functions
• Provides body framework, fill space, stores fat
• Helps repair tissue, produces blood cells,
  protects against infection
• Cell types
• Defined by extracellular matrix (fibers, ground
  substance)
• Macrophages, mast cells, fibroblasts
• Collagen
• Strong, flexible inelastic structure that holds
  connective tissue together
• Enables tissue to resist mechanical deformation
  oriented in direction of tensile stress
• Mechanical properties
• Elasticity, viscoelasticity, plasticity
• Physical properties
• Force-relaxation, creep response, hysteresis

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• Types of Connective Tissue
• Fibrous
• Dense tendon, aponeurosis, fascia, ligaments,
  joint capsule
• Loose adipose
• Cartilage
• Rigid connective tissue composed of chondrocytes
  within a collagen, elastin, ground substance
  matrix
• Poor blood supply slows healing
• Hyaline, fibrocartilage and elastic
• Reticular connective tissue
• Composed of collagen and supports structural
  walls of organs
• Elastic connective tissue
• Composed of elastic fibers and found in blood
  vessels, airways and hollow organs

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• Bone
• Consists of living cells and mineral deposits
• Cancellous spongy bone
• Cortical bone solid
• Rich blood supply
• Functions to provide support, movement and
  protection

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• Blood
• Compose of various cells suspended in fluid
  intracellular matrix (plasma)
• Plasma contains red blood cells, white blood
  cells and platelets
• Essential for nutrition, cleansing, and
  physiology of the body

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Ligament Sprains

• Sprains involve damage to a ligament
• Ligaments
• Inelastic band of tissue
• Provides joint stability, controls bone position
  during joint motion, provides proprioceptive input

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• Grades of Ligament Sprains
• Grade I - some pain, minimal loss of function, no
  abnormal motion, and mild point tenderness
• Grade II - pain, moderate loss of function,
  swelling, and instability
• Grade III - extremely painful, inevitable loss of
  function, severe instability and swelling, and
  may also represent subluxation

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Ligament Healing

• Follows same course of repair events as with
  other vascular tissues
• Ligaments sprained extra-articularly result in
  bleeding in the subcutaneous space
• Intra-articular ligament sprains result in
  bleeding within the capsule
• Vascular proliferation, fibroblastic activity and
  clot formation occur during the initial 6 weeks
  of recovery
• Collagen and ground substance work to bridge torn
  ends of ligaments via scarring
• Scar maturation will gradually occur and collagen
  tensile strength will increase

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Factors Affecting Ligament Healing

• Surgically repaired extra-articular ligaments
• Heal with less scarring
• Stronger than un-repaired ligaments
• Non-surgically repaired ligaments
• Heal via fibrous scarring resulting in ligament
  lengthening and increased joint instability
• Intra-articular ligament damage
• Results in synovial fluid presence, diluting
  hematoma, disrupting clot and healing
• Ligament healing and immobilization
• Muscle strength training can enhance joint
  stability

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Fractures of Bone

• Acute bone fractures - partial or complete
  disruption that can be either closed or open
  (through skin) serious musculoskeletal condition
• Risk of infection is increased with open
  fractures
• Type of fractures include
• greenstick, impacted, longitudinal, oblique,
  serrated, spiral, transverse, comminuted,
  blowout, and avulsion

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A Greenstick B Transverse C Oblique D Spiral
E Comminuted F Impacted G Avulsion
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• Stress fractures- no specific cause but with a
  number of possible causes
• Overload due to muscle contraction
• Altered stress distribution due to muscle
  fatigue, changes in surface
• Rhythmic repetitive stress vibrations
• Signs and symptoms
• Focal tenderness and pain
• Pain with activity
• Pain becomes constant and more intense,
• Does not show up on X-ray until osteoblastic
  activity begins callus formation
• Treatment
• Removal from activity for at least 14 days
• Does not usually require casting unless normal
  fracture occurs

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Bone Healing

• Significantly different from soft tissue healing
• Additional functional elements associated with
  healing
• Torsion
• Bending
• Compression
• Trauma results in disruption of blood vessels,
  periosteal damage and clot formation
• Fibrous collagen network is constructed after 1
  week -serves as framework for chondroblasts

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• Cartilage begins to infiltrate callus
• Osteoblasts begin to proliferate, forming
  cancellous and trabeculae
• Callus crystallizes remodeling begins
• Osteoclasts appear to resorb bone fragments and
  clean debris
• Bone transition during remodeling
• Fibrous cartilage ? fibrous bone ? lamellar bone
• Osteoblasts and osteoclasts respond to stresses
  placed on bone
• Immobilization is required for 3-8 weeks
• Dependent on bone, severity, location, patient age

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Cartilage Damage

• Osteoarthritis
• Arthritis is an inflammatory condition with
  secondary destruction
• Arthrosis degenerative process with cartilage
  destruction, bone remodeling and secondary
  inflammation
• Cartilage fibrillates
• Release of fibers and ground substance into joint
• Often occurs in peripheral cartilage
• Fibrillation degenerative process associated
  with poor nutrition and disuse
• Can extend to stressed areas and increase
  proportionally to stress applied

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• Osteophytosis
• Attempt at increasing surface area to decrease
  contact force
• Chondromalacia
• Non-progressive cartilage transformation with
  areas of irregularity and softening
• Begins in non-weight bearing areas and progresses
  to areas of stress
• Use patterns, external force application, altered
  joint mechanics (laxity or trauma related) can
  serve as predisposing factors

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• Injuries conducive to osteoarthritic changes
• Dislocations and subluxations
• Osteochondritis dissecans
• Recurrent synovial effusion and hemarthrosis
• Ligament damage resulting in altered mechanics
  and cartilage damage
• Additional factors
• Loss of ROM, strength, power
• Altered mechanics

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Cartilage Healing

• Limited healing capacity
• Variable healing depending on damage to cartilage
  and or subchondral bone
• Articular cartilage fails to undergo clot
  formation or cellular response
• Defective region remains defective
• When subchondral bone is involved the
  inflammatory process proceeds as normal

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Injuries to Musculotendinous Structures

• Skeletal muscle exhibits 4 traits
• Elasticity
• Extensibility
• Irritability
• Contractility
• Muscle size and architecture often contribute to
  type and magnitude of motion (gross vs. fine,
  powerful vs. coordinated)

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Muscle Strains

• Strains occur when the musculotendinous unit is
• Overstretched
• Forced to contract against too great a resistance
• Damage occurs
• Muscle
• Tendon
• Musculotendinous junction
• Tendon-bone interface

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Muscle Strain Classifications

• Grade I
• some fibers have been stretched or actually torn
  resulting in tenderness and pain on active ROM,
  movement painful but full range present
• Grade II
• number of fibers have been torn and active
  contraction is painful, usually a depression or
  divot is palpable, some swelling and
  discoloration result
• Grade III
• Complete rupture of muscle or musculotendinous
  junction, significant impairment, with initially
  a great deal of pain that diminishes due to nerve
  damage

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Muscle Healing

• Similar healing to other soft tissues
• Hemorrhaging and edema lead to phagocytosis
• Fibroblasts and ground substance produce a
  gel-like matrix leading to fibrosis and scarring
• Myoblastic cell infiltrate the region promoting
  myofibril regeneration
• Collagen undergoes maturation with active
  contractions being critical to apply tensile
  stress
• Lengthy recovery for each grade
• Patience is a must

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Tendinitis

• Term used to describe multiple pathological
  tendon conditions
• Inflammation of tendon, with no involvement of
  paratenon
• Paratenonitis
• Inflammation of tendon outer layer
• Friction injury
• Tendinosis
• Degenerative tendon changes with no clinical or
  histological signs of inflammation

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• Chronic Tendinitis
• Tendon degeneration
• Loss of normal collagen and cellularity
• No inflammatory cellular response
• Signs and symptoms
• Pain with movement
• Swelling
• Crepitus
• Key treatment rest
• Additional treatment options
• NSAIDs and modalities
• Alternative activities

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Tenosynovitis

• Due to friction and decreased space for sliding
  synovial sheaths are necessary in tendons
• Overuse results in inflammation and development
  of sticky adhesions within the sheath
• Signs and symptoms
• Similar to tendinitis
• Movement may be more limited with tenosynovitis
• Treatment is the same as if the athletic trainer
  were treating tendinitis

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Tenosynovitis
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Tendon Healing

• Large amounts of collagen are required for
  adequate healing
• However, collagen synthesis can become excessive
  resulting in fibrosis and interfering with tendon
  sliding action
• Scar tissue will gradually elongate allowing for
  appropriate tendon motion
• If a synovial sheath surrounds an injured tendon
  the injury could be devastating
• Typical tendon healing may require 4-5 weeks
  before strong contractions can be imparted on
  tendon

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Injury to Nerve Tissue

• Generally involve contusion or inflammation
• More severe injuries involve crushing or severing
• Causes life-long disability
• Paraplegia or quadriplegia

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• Peripheral nerves can regenerate if injury does
  not impact cell body
• Slower regeneration with proximity to cell body
• Regeneration requires an optimal environment
• Degenerative changes occur
• Increased metabolism and protein production for
  regeneration
• While cell body contains genetic material
  necessary to maintain axon is does not transmit
  to distal segments of axon
• Schwann cells
• If cut contacts Schwann cells re-innervation of
  distal segments is more likely

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• New axon buds will develop on the proximal axon
• One sprout will form new axon
• Contact with Schwann cells will allow for Schwann
  cell proliferation new myelin
• Regeneration is slow
• Occurs at a rate of 3-4 mm per day
• Can be obstructed by scar formation
• CNS nerves regenerate poorly due to lack of
  connective tissue support

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Additional Musculoskeletal Injuries

• Dislocations and Subluxations
• Dislocations present with total disunion of bone
  apposition between articular surfaces- requiring
  manual or surgical realignment
• High level of incidence in fingers and shoulder
• Subluxations are partial dislocations causing
  incomplete separation of two bones
• Reduction should not occur without and X-ray
  (necessary to rule out fractures)
• Inappropriate reduction may complicate the injury
• Return to play is largely governed by the degree
  of soft tissue injury

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Bursitis

• Result of excessive movement or trauma to bursa
• Causes irritation, inflammation and increased
  synovial fluid production
• May continue to become inflamed with repeat
  irritation with increasingly more pain
• Commonly impacted bursa
• Pre-patellar
• Olecranon
• Subacromial

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Muscle Soreness

• Overexertion in strenuous exercise resulting in
  muscular pain
• Two types of soreness
• Acute-onset muscle soreness
• accompanies fatigue, muscle pain experienced
  immediately after exercise
• Delayed-onset muscle soreness (DOMS)
• pain that occurs 24-48 hours following activity
  that gradually subsides
• Caused by slight microtrauma to muscle or
  connective tissue structures
• Prevention and treatment
• Gradual build-up of intensity
• Some form of stretching

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Contusions

• Result of sudden blow to body
• Can be both deep and superficial
• Hematoma results from blood and lymph flow into
  surrounding tissue
• Localization of extravasated blood into clot,
  encapsulated by connective tissue
• Speed of healing dependent on the extent of
  damage
• If muscle damage occurs ROM will be impacted
• Incidents of repeated blows may result in
  myositis ossificans development
• Prevention rest and protection
• Allow for calcium re-absorption

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Managing the Healing Process Through
Rehabilitation

• Pre-Surgical Phase
• Involves only those athletes requiring surgery
• If surgery can be delayed, exercise may help to
  improve outcome
• Maintaining or increasing strength, ROM,
  cardiorespiratory fitness, neuromuscular control
  may enhance the athletes ability to perform
  rehabilitation after surgery

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Phase I Acute Injury Phase

• Initial swelling management and pain control are
  crucial
• PRICE
• If the athletic trainer is too aggressive during
  the first 48 hour the inflammatory process may
  not have time to accomplish what it needs to
• Immobilization for 24-48 hours is a must
• By days 3-4 the athlete should be engaged in some
  mobility exercises and should be encouraged to
  gradually bear weight if it is a lower extremity
  injury
• Use of NSAIDs

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Phase 2 Repair Phase

• As the inflammatory process has subsided and pain
  decreases with passive ROM exercises should be
  added
• Increase cardiorespiratory fitness
• Restore full ROM
• Restore or increase strength
• Re-establish neuromuscular control
• Continued modality use for pain modulation and
  swelling control
• Cryotherapy
• Electrical stimulation

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Phase 3 Remodeling Phase

• Longest phase with the ultimate goal being return
  to play
• Continued collagen realignment
• Pain continues to decrease with activity
• Regain sports-specific skills
• Dynamic functional activities
• Sports-directed strengthening activities
• Plyometric strengthening
• Functional testing
• Determine specific skill weakness

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• Heating modalities
• Ultrasound, diathermy
• Increase circulation in deeper tissue
• Manual therapy
• Massage
• Reduce guarding, spasm, pain
• Enhanced and lymphatic flow will deliver
  essential nutrients and increase
  breakdown/removal of waste, respectively

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Using Medication to Effect the Healing Process

• Used primarily for pain modulation
• Non-steroidal anti-inflammatory drugs (NSAIDs)
• Aspirin, acetaminophen, ibuprofen, naproxen
  sodium, ketoprofen
• Aspirin
• Aspirin interferes with pain signal transmission
  from thalamus
• Tissue damage results in release of arachidonic
  acid from phospholipid walls
• Results in production of prostaglandins,
  thromboxane, prostacyclin
• Mediate inflammatory response

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• Effects
• NSAIDs block pain and inflammation by inhibiting
  prostaglandin synthesis
• Modulate lysosomal membrane destruction (enzymes)
• Aspirin (only NSAID) that irreversibly inhibits
  cyclooxygenase (other NSAIDs reversible)
• Alters sympathetic outflow of hypothalamus for
  fever reduction
• Side effects
• Gastric distress, heartburn, nausea, tinnitus,
  headache, diarrhea
• Cautions
• Impairs clotting, irreversible inhibition of
  cyclooxygenase
• Prolonged bleed risk

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• Ibuprofen
• Analgesic and antipyretic effects
• Similar side effects
• No impact on platelet aggregation
• Dose of 400mg serves as analgesic and
  anti-inflammatory agent
• Acetaminophen
• Analgesic and antipyretic effects
• Limited anti-inflammatory capabilities
• Used to somatic pain and fever reduction
• No gastric irritation or bleeding
• No impact on clotting factors

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• NSAIDs
• Anti-inflammatory, analgesic and antipyretic
  agents
• Should not be used if suffer from aspirin allergy
  triad
• Use cautiously if athlete is exposed to
  dehydration
• Inhibits prostaglandin synthesis, compromising
  elaboration of prostaglandins in kidney
• Ischemia within kidneys occurs
• Fewer side effects and longer lasting than
  aspirin
• May require liver function monitoring
• While medications can be effective, irritating
  agent causing inflammation must also be
  eliminated

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• Oral muscle relaxants
• Reduce spasm and guarding
• Facilitate rehabilitation programs
• No evidence of superiority over analgesics or
  sedatives
• Many analgesics and anti-inflammatory products
  are available over the counter (OTC)
• Combination of products
• Chronic aspirin, phenacetin or acetaminophen use
  can result in papillary necrosis or
  analgesic-associated nephropathy
• Caffeine dependence

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Sports Medicine Approach to the Healing Process

• Assist/manipulate the natural process of the body
  while doing no harm
• Primary goals
• Have a positive influence on inflammation and
  repair process
• Expedite recovery of function
• ROM, strength, cardiorespiratory fitness,
  neuromuscular control
• Minimize early effects of inflammatory process
• Pain, spasm, edema accumulation, decreased motion
• Prevent recurrence of injury
• Resist future periods of tissue overload through
  strengthening