Title:  Bone Fractures – Information Sheet                             Team-Lead Name: ____________________

Etiology:  load exceeds strength of bone resulting in bone break

Risk Factors:

• Trauma, Vehicle accident, Workplace Accident, Domestic Violence, Sports
• Osteoporosis/Osteopenia, Osteomalacia, Rickett’s,
• Age (e.g., due slowing of organ maintenance, as well as menopause, decreased levels of estrogen, testosterone, growth hormone, and thyroid hormone),
• Bone disease (e.g., bone infection=osteomyelitis),
• Bone cancer such as osteosarcoma,
• Osteonecrosis = bone death perhaps due to impaired blood supply),
• Nutrition deficiencies (or starvation, lack of protein, lack of essential vitamins A, B₁₂, D, C, and K, lack of calcium phosphate),
• Endocrine diseases (e.g., hyperparathyroidism),
• Autoimmune disease (e.g., pernicious anemia, which leads to vitamin B12 deficiency),
• Sedentary behaviour due to loss of bone density,
• Obesity, impaired vision,
• Intoxication (alcohol, drugs), risky behaviours,
• Smoking
• Medications (glucocorticoids, antidepressants, anticonvulsants, androgen deprivation therapy)

Prevalence & Incidence:

• From our textbook notes: Most common fractures at each of these risk factors (e.g., age, biological sex, setting)
  • o Males 15-24yrs (tibia, clavicle, lower humerus)
  • o Elderly 65+yrs (hip)
  • o Workplace (hands and feet)
  • o Osteoporosis (upper femur, upper humerus, vertebrae, & pelvis)
• From: https://www.canada.ca/en/public-health/services/publications/diseases-conditions/osteoporosis-related-fractures-canada-2021.html
  • o “In 2019–2020, there were: 156 hip fractures per 100,000 Canadians aged 40+
  • o Females are 2x more likely to fracture their hip compared to males”
• And from: https://www.canada.ca/en/public-health/services/publications/diseases-conditions/osteoporosis-related-fractures-2020.html
  • o “In 2015–2016 alone, there were a total of 130,000 fractures. Fractures of the forearm were the most common followed by fractures of the hip, spine, humerus and pelvis. Fracture rates were higher among women than men and increased with age among both sexes. Forearm fractures were the most common among adults between 40 and 79 years old, whereas hip fractures were the most common among those aged 80 years and older.”
• From https://www.who.int/news-room/fact-sheets/detail/fragility-fractures
  • o “In 2019, there were 178 million new fractures globally, an increase of 33.4% of the absolute number of new fractures since 1990, partly driven by population growth and ageing.
  • o The same year, there were 455 million prevalent cases of acute or long-term symptoms of a fracture, an increase of 70.1% of the absolute prevalence since 1990.
  • o Globally in 2019, fractures accounted for 25.8 million years lived with disability (YLDs), an increase of 65.3% of the absolute YLDs since 1990.
  • o Fractures are more likely to occur in older people, especially older women.
  • o Most fractures in older people are due to bone fragility (fragility fractures) and result from mechanical forces quantified as equivalent to a fall from standing height or less (known as low energy trauma).”
  • o World-wide, “The most common sites of fragility fractures are the: spine, hip, distal forearm (wrist), proximal humerus (upper arm). Other fragility fracture sites include the pelvis, ribs, and proximal tibia. Hip and vertebral (spine) fractures are considered the most serious fragility fractures.”

Difference between Types of Fractures:

• Oblique = fracture is at an angle to the shaft of the bone,
• Comminuted = fracture involves many small fragments at site of break
• Simple = fracture involves single break to bone,
• Open = fracture results in bone fragment piercing through skin,
• Closed = fracture does not involve bone piercing through skin,
• Pathologic = fracture is at a site in the bone that has been weakened by disease (e.g., osteoporosis/osteomyelitis)
• Segmented = fracture involves at least 2 breaks creating an inner segment,
• Spiral = fracture is at a spiraled angle to the shaft of the bone due to excessive rotational force,
• Transverse = fracture is at a perpendicular angle to the shaft of the bone
• Greenstick = fracture is at an angle to the shaft of the bone
• Impacted (telescoped)= one bone is jammed (pushed hard) into another bone
• Colle’s, at the wrist = usually a fracture of the radius due to falling
• Pott’s, at the ankle = usually the tibia or fibula due to rolling ankle
• Compression (buckle), many fragments, . In adults, commonly found in vertebrae
• Stress (fatigue & insufficiency), Stress: due to repetitive activities such as running (particularly in unconditioned person)….an incomplete fracture
  • Fatigue Stress fracture due to overuse (e.g., professional dancer’s foot fracture),
  • Insufficiency Stress Fracture due to normal stresses on bone, but bone is weakened by osteoporosis, or due to load higher due to pregnancy, often occurs in sacrum
• Avulsion: Fragment of bone connected to a ligament or tendon detaches from main bone.

Steps of Fracture Healing:   

1. Hematoma Formation & Inflammatory Response:  Bleeding at broken ends of the bone with subsequent hematoma (swelling of clotted blood) formation
   • with hemostasis and platelet activation, involving vasoconstriction of broken blood vessels to reduce bleeding, formation of platelet plugs to seal capillary wall leakages and activation of pro-Thrombin Activator otherwise known as Factor X to activate thrombin enzyme which converts inactive fibrinogen to fibrin, a long ropy protein that creates mesh to stabilize platelet plugs and help seal broken blood vessels and stop bleeding, in a process called coagulation.
   • The size of the hematoma depends on the amount of damage.
   • The hematoma stabilizes the fracture ends. (1-3d)
   • Fibrin meshwork serves as framework for ingrowth of fibroblasts.
   • The dead tissue & debris stimulate an intense inflammatory response (characterized by vasodilation, exudation of plasma & leukocytes, and infiltration by inflammatory leukocytes, growth factors).  Mast cells are responsible for releasing histamine that triggers this inflammatory response which is necessary for bringing in WBCs, such macrophages to phagocytose cellular debris and set the stage for healing. Inflammation results in redness, warmth, swelling and pain.
2. Organization of Hematoma into fibrous network with fibrin securing platelet plugs and sealing of broken blood vessels.
   • Mitosis and regeneration of blood vessels occurs involving mitosis of blood vessel cell wall components and phagocytic removal of dead blood, debris.
   • Lysis of fibrin with plasmin enzyme activity and dissolution of platelet plugs, as vessel damage is repaired.
   • Capillary buds & neovascularization is occurring.
3. Procallus Formation: Fibrocartilage formation.
   • Chondrocytes create cartilage bridge between broken ends of bone.
   • Vascular & mechanical forces influence this stage (3d- 2wk)
   • Invasion of osteoblasts into the cartilage callus, lengthening of collagen strands, and deposition of osteoid and calcium phosphate salts into the cartilage gel-like matrix. (2-6wk)
   • Not strong enough to bear weight.
4. Bony Callus formation: new bone is built up and osteoclasts destroy dead bone. (3wk-6mo)
5. Remodeling is accomplished as excess callus is reabsorbed and trabecular bone is laid down.
   • The callus is slowly replaced by trabecular bone along the lines of stress and medullary canal is re-established. (6wk – 1yr).
   • The initial “woven bone” is converted to “lamellar bone”.
   • Fracture is considered healed when: fracture is stable, free of pain, no movement in fracture is detected and radiograph shows bone crossing fracture site

Diagnostic Tools:

1. Imaging – eg. X-ray, CT scan

Treatment:

1. RICE (Rest, Ice, Compression, Elevate)
2. Check for signs of shock (diaphoresis=excess sweating, low Blood Pressure, high Heart Rate, loss of consciousness, anxiety, nausea, vomiting, pallor=paleness),
3. Keep patient warm
4. Clean wound, treat with antibiotics if open wound
5. Realign (traction, pins, screws, plates, wire), immobilize (splint, cast).
   • Traction (apply force to maintain alignment & limit muscle spasms)
   • Possibly need bone graft bridging, bone cement, or electrical or ultrasound stimulation
6. Monitor for development of Fat emboli, Compartment syndrome (monitor 5Ps as well as tonometer pressure readings within any damaged muscle compartment, and pulse oximetry), and/or DIC
7. Monitor healing of fracture – follow up imaging, and assessment of wound
8. Strengthening and Stretching Exercises: limit muscle atrophy, maintain good circulation & joint mobility
9. Nutrition, stop smoking, reduce corticosteroid use

Potential Complications (Osteomyelitis, Fat emboli, Exuberant callus, Mal-union, Non-union, Nerve damage, Stunted growth):

1. Osteomyelitis:  infection of the bone due to open fracture and bone ends becoming contaminated with microorganisms (most often bacteria), leading to further osteonecrosis through infection and possible release of toxins by bacteria (depending on what bacteria is present)
2. Fat emboli:  due to fat from yellow marrow in medullary cavity entering leaking/broken blood vessels within fracture site and travelling through the bloodstream to lodge in smaller capillaries, causing regions of ischemia and hypoxia – leading to signs and symptoms that are dependent on which organ/tissue becomes oxygen-deprived. (e.g., could cause stroke, heart attack, be pulmonary embolism, leading to more systemic loss of blood flow and oxygen distribution, and organ failure)
3. Exuberant callus:  is a temporary overproduction of bony callus during bone fracture healing that is gradually remodelled over time,
4. Mal-union:  healing of bone in incorrect position due to improper alignment of bone fragment ends
5. Non-union:  failure of bone ends to grow together within 4-6mo due to infection, repetitive stress, improper alignment or poor circulation. Instead, gap fills with dense fibrous fibrocartilage tissue or fluid-filled space.
6. Nerve damage:  due to bone being innervated and nerves being damaged through trauma or ensuing hypoxia. Can result in abnormal sensations, loss of sensations, loss of motor nerves can result in muscle weakness
7. Stunted growth:  due to fracture through epiphyseal growth plate – which then ossifies during healing meaning that the bone can no longer grow longer – so a child could end up with one leg longer than the other for example.

Compartment Syndrome – List steps that occur, with 5Ps, explaining each one (use more than 5 steps if you need to):

Summary: Damage to surrounding muscles, can lead to inflammation building up within those muscle compartments.   High pressure in a muscle compartment that is enclosed in fascia reduces blood flow leading to hypoxia (& therefore damage).  Plasma protein & fluid leak into tissue causing more swelling.  Necrosis of muscle & nerves can occur (within 4-8hr).  Acute Compartment Syndrome requires immediate surgery (Fasciotomy) to reduce pressure accompanied by skin grafts.

1. When skeletal muscles are damaged and rupture, this is called rhabdomyolysis.
   • The skeletal muscle cells release their intracellular components (e.g., potassium and skeletal muscle specific proteins such as: myoglobin, troponin, tropomyosin, myosin, and actin).
   • The cellular damage itself triggers the WBC Mast Cells and Basophils to release pro-inflammatory cytokines (e.g., histamine, prostaglandin, leukotriene, bradykinin) which cause vasodilation and increased capillary permeability.
   • The 4 cardinal signs of inflammation will therefore be present in that region (redness, warmth, pain and swelling).
   • The solutes released from the muscle cells also cause an osmotic ECF shift (i.e. pulling more water into the compartment).
   • The fluid leaking out of the blood vessels is called exudate and as it fills the interstitial spaces, this is called an ECF (extracellular fluid) shift and leads to swelling/edema and an increase of volume within the muscle compartment.
   • The fascia is made of dense regular connective tissue and contains a lot of long ropy collagen protein that does not expand.
   • Therefore, the pressure within the muscle compartment increases, which pinches off blood flow into the compartment (compartment tamponade), leading to more hypoxia and more cell death (muscle and nerve necrosis).
2. As myoglobin enters the bloodstream (myoglobinemia) it damages the nephrons of the kidney leading to nephron tubular necrosis and renal failure.
   • (Initially, patient may have myoglobinuria (which colours urine a tea colour). When nephrons fail completely, patient will not be forming any urine (anuria) leading to the build up of toxins in the blood which can contribute to the dysfunction of the brain and heart as well as the failure of other organs.
3. As potassium enters the bloodstream (hyperkalemia) contributes to cardiac dysrhythmias. As muscle cell perform anaerobic cellular respiration, lactate is produced and acidosis can develop which also can lead to organ dysfunction.
4. Shock can develop = not enough blood flow to tissues in this case due to low blood pressure (due to systemic vasodilation due to large amount proinflammatory cytokines, released due to extensive damage).  Shock signs = Pallor, Diaphoresis, Hypotension, Reflex Tachycardia, Nausea/vomiting
5. Monitoring for 5Ps all of which are occurring in the compartment and distally as well, are due to poor blood flow (pulselessness, pallor, paralysis (dysfunction of motor nerves), paresthesia (dysfunction of sensory nerves and pain). Pain is due to proinflammatory cytokines as well as other cellular components triggering nociceptors (pain nerves).  Bleeding also triggers pain nerves
6. Volkmann’s contractures occur due to tendon and/or muscle damage – both tissues do not regenerate well, leading to scarring in those tissues when damaged – scars are made of a lot of collagen which shrinks and can pull joints into deformed positions and cause loss of range of movement.

Word Bank: Possible Lesson 4 Terms to use:

ecchymosis, contusion, bruise, trabecular/spongy bone, woven bone, compact/cortical bone, epiphyseal/growth plate, inflammation, hematoma, platelets, fibrin, RBCs, WBCs, procallus, internal & external cartilage callus, bony callus, remodeling, osteoporosis, osteonecrosis, bleeding, realignment/reduction, traction, pins, screws, plates, wire, splint, cast, bone cement, nutrition, calcium, vitamin D, ultrasound, electrical stimulation, bone graft, x-ray, Volkmann’s ischemic contracture, muscle compartment, fascia, fasciotomy, rhabdomyolysis, myoglobinemia, myoglobinuria, disseminated intravascular coagulation (DIC), shock, pallor, pulselessness, paresthesia, paralysis, pain, diaphoresis, hypotension, reflex tachycardia, nausea, vomiting, edema, compartment tamponade, muscle ischemia, muscle infarction, ECF shift, acidosis, hyperkalemia, cardiac dysrhythmia, reperfusion injury, tonometer, capillary refill time.