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76 Cards in this Set
- Front
- Back
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what is an open fracture |
fractured tissue/bone have penetrated through the skin, exposing deep tissue and bone to microbial invasion |
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how do you know theres an open fracture |
-bone sticking out -continuous bleeding -some you need imaging |
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complications associated with open fractures |
1. microbial infection 2. severe blood loss |
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what is a closed fracture |
skin integrity maintained over fracture site |
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what is a complication associated with closed fracture |
compartment syndrome- veins and arteries covered in fascia- swelling in area constricted- causing pressure and circulation is unable to happen |
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what classification is used when there is fracture at the epiphyses |
Salter Harris system |
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how does the salter harris system work |
Type 1- Straight Across Type 2- Above Type 3- Lower or below Type 4- Two or Through (true) Type 5- ERasure of growth plate |
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what are the different types of fracture shape/line |
transverse oblique segmental spiral |
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what is a transverse fracture line |
fracture line perpendicular to long axis of bone, result of direct high energy force in the direction of the fracture line |
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what is an oblique fracture line |
angular fracture line, result of angular or rotational force |
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what is a segmental fracture line |
separate segment of bone bordered by fracture lines, results of high energy force |
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what is a spiral fracture line |
complex, multi-planar fracture, result of rotational force "around" long axis of bone, low energy |
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what is a intra-articular FL |
fracture line crosses articular cartilage and enters joint |
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what is a avulsion FL |
tendon or ligament tears/pulls off bone fragment |
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what is a compressin/impacted FL |
impaction of bone, typical sites are vertebrae or proximal tibia |
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what is a torus FL |
buckle fracture of one cortex, often in children |
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what is a greenstick fracture |
incomplete fracture of one cortex, often in children |
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what is a comminuted FL |
>2 fragments |
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what is nondisplaced |
fracture fragments are aligned |
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what is dispalced |
fracture fragments not aligned |
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what is distracted |
fracture fragments are separated by a gap (opposite of impacted) |
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impacted |
fracture fragments are compressed |
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angulated |
direction of fracture apex (ex varus/vagus, describes the angle of displacement in degrees) |
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what is translated/shifted |
percentage of overlapping bone at the fracture site |
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what is rotated |
fracture fragment rotated about long axis |
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what types of fractures cause significant hemorrhage |
high energy long bone fractures (femur, humerus, tibia, fibula) pelvic fractures |
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hw do you asses a patients neurovascular status |
vascular- pulse, capillary refill, pallor neuro- sensory and motor function distal to the fracture |
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what are the 5 P's to fracture |
pain pallor pulse paralysis paresthesia |
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what does reduction do to a fracture |
-decreases pain and bleeding -facilitates transport -makes it less likely to convert a closed to an open fracture **rarely will reduction compromise nerve or vascular integrity** |
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how do you deal with an orthopedic emergency |
-control hemorrhage--> make sure patient isn't in shock -neruo exam -splinting +/- reduction -copious irrigation with sterile fluid (saline) and cover with a sterile (ideal) or clean dressing -antibiotics |
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when do we do an open reduction (operation) |
-non-union (bones aren't coming together) -failed open reduction -open fracture -neurovascular compromise (5 P's) -displaced fracture within the joint -salter harris 3,4,5 -many fragments (multiple areas of trauma) -cant cast (i.e. hip fracture) or pathologic fracture |
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when are vascular injuries common |
more common in open fractures, fracture and dislocation, widely displaced fractures, in sites where vessel close to bone |
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what do you do pre and post reduction |
asses neurovascular status and take a note |
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what is compartment syndrome |
increased pressure in a compartment where muscle and tissue are surrounded by fascia and bone (can't expand in this area) -pressure becomes so high, capillaries can no longer perfuse tissue -->necrosis |
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what are some signs of compartment syndrome |
5 P's of vascular injury EXTREME pain pain that worsens on passive stretch |
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what causes nerve injuries |
fracture fragments, direct trauma, stretching, ischemia |
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where are nerves at an increased risk of injury? |
superficial to skin, lie close to bone, or span a joint |
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whats more common nerve or vascular injuries |
nerve |
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whats the most common form of non-thrombotic embolism` |
fat emboli |
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where can emboli travel |
-usually lungs- systemic veins -brain- causes ischemic stroke |
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what is fat emboli syndrome (FES) |
single or multiple long bone fracture in young or pelvic/hip fractures in elderly predispose to FES -multi-system inflammation and schema due to widespread blockage of many small vessels |
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what are the clinical findings for FES |
single or multiple long bone fractures in young or pelvic/hip fractures in elderly predispose to FES -->multisystem inflammation and ischema due to widespread blockage of many small vessels dyspnea- when in pulmonary system petechiae- when in small vessels of skin cognitive dysfunction- trapped in superficial part of brain |
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what is the prognosis for FES |
acute respiratory failure and permanent widespread neurological damage |
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what is patent foramen ovale |
abnormal communication between right and left atria -fat embolism enters arterial system and this can lead to ischemia |
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whats the first step to fracture healing |
1.Hematoma fills the fracture gap, surrounding injured area –Inflammatory cells, fibroblasts, and new vessels penetrate the fibrin mesh and release avariety of cytokines (PDGF, TGF, FGF) --> increased osteoprogenitor, osteoblastic and osteoclastic activity –Hematoma is organized after the first week and the ends of the bones undergo remodelling –New soft tissue/cartilage that has developed is called the pro callus – very weak, no value for weight bearing formation of fracture hematoma |
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whats the second step to fracture healing |
2.Osteoprogenitor cells deposit subperiostealwoven bone perpendicular to the cortical axis and within the medullary cavity –activated mesenchymal cells also form hyaline and fibrocartilage to bridge the gap –After 2-3 weeks, repair tissue reaches its maximal thickness, and cartilage begins to ossify =bony callus. After it mineralizes, weight bearing is possible fibrocartilaginous callus formation |
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whats the third step to fracture healing |
3.Early callus formation results in an excess of cartilage and woven bone –If the ends of the bone are poorly-aligned, callus increases along the concave surface of the bone –Weight-bearing forces cause remodelling along lines of stress –Eventually woven bone is replaced by lamellar bone bone remodelling |
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what can fracture healing be impaired by |
1.movement before the callus has fully ossified resulting in delayed or non-union-->continual non-union can form a pseudoarthrosis- with a cyst taking up the centre of the defective callus 2. infection-->constant inflammation will undermine the repair process 3. strong anti-inflammatories-->you need inflammation to mediate repair |
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what does continuous non-union cause |
formation of pseudoarthrosis -cyst will take up the centre of the defective callus- the cyst can be lined by synovial like cells |
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12% of arthritis cases are what |
post-traumatic arthritis -complicates 20-50% of traumatic joint injury |
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what are the characteristics of early onset osteoarthritis |
late fracture complication -limited inflammation, accentuated loss of cartilage and subchondral bone with use -ankle and knee most common sites -can occur early after the trauma and resolve, or can result in development or arthritis a decade or more after the injury |
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what is another name for osteonecrosis |
avascular necrosis |
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what is osteonecrosis |
ischemic necrosis of the bone (bone infarct) |
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where does osteonecrosis occur |
-in the medullary cavity of metaphysics or diaphysis -or in subchondral portion of epiphysis |
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what are the most common reasons for osteonecrosis |
-fracture -post-steroid administration -idiopathic |
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conditions associated with osteonecrosis are thought to cause what |
1. mechanical injury to blood vessels 2. thromboembolism 3. external pressure on vessels 4. venous occlusion |
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what are some conditions associated with osteonecrosis |
alcohol abuse gaucher disease infection pregnancy tumors sickle cell crisis (when RBC not in proper shape) |
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why is osteonecrosis not usually in the cortex? |
it has collateral circulation (periosteal vessels and nutrient vessels) |
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what is osteomyelitis |
inflammation of bone and marrow- refers to infectious (not autoimmune) etiologies of inflammation |
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what are the three major types of osteomyelitis |
1. pyogenic osteomyelitis- almost always cause by bacteria, vast majority staphylococcal 2. tuberculous osteomyelitis 3.skeletal syphillis |
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how can organisms reach the bone |
-hematogenous seeding -extension from nearby soft tissue -direct implantation |
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what is bacteremia |
bacteria in the blood |
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what are the clinical features of pyogenic osteomyelitis |
-acute--> malaise, fever, chills, throbbing pain over infected area -young children-->fever and a limp or refusal to use fractured limb -biopsy with bone cultures |
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how is pyogenic osteomyelitis treated |
antibiotics and surgical drainage |
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what are the common bacteria in neonatal pyogenic osteomyelitis |
haemophilia influenzae and group B streptococci |
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people with sickle cell disease are predisposed towhat infection in the bone |
salmonella |
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what are some complications of chronic osteomyelitis? |
1. pathologic fracture 2. secondary amyloidosis 3. endocarditis 4. sepsis 5. development of squamous cell carcinoma in the sinus tract (where pus leaks out through the skin) 6. rarely sarcoma in infected bone |
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why can osteomyelitis cause secondary amyloidosis |
due to the long term production of antibodies |
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whats the difference between subchondral and medullary infarcts? |
subchondral (below a joint)- overlying cartilage may slough off, and the joint may be destroyed medullary- usually heal and may even be clinically silent unless they are large |
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what do infarcts look like in cancellous bone? |
wedge-shaped with death of osteocytes and rupture of adipocytes -osteoclasts resorb dead trabecular and osteoblasts try to rebuild the trabeculae, the necrotic bone can collapse and fail to regenerate if nutrient supply insufficient |
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in pyogenic osteomyelitis what happens during acute infection? |
inflammatory reaction- bone becomes necrotic within 48 hours and bacteria can extend through osteons -abscesses form and can lift the periosteum off the cortisol bone, impeding blood flow- abscess can form a draining sinus -after a week or so, inflammatory cells can wall off the abscess and new bone may develop around the necrotic area- new bone development can be impressive |
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what are se frequent pathogens during the neonatal period |
haemophilia influenza and group B streptococci |
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in sickle cells disease what is a common infection seen |
salmonella |
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what does an osseous infection look like in those with active tuberculosis |
blood-borne -tends to infect lumbar and thoracic vertebrae (Pott disease) -very destructive -can break though IVD and involve multiple vertebrae, leading to abscess formation -can lead to neurological deficits as well as destruction of bone |
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what does a skeletal syphilis infection look like? |
uncommon- usually recognized and treated before skeletal involvement -bones involved tend to be: nose, palate, skull, long bones -granulomatous inflammation (gummae)found among edematous granulation tissue and necrotic bone -reactive bone deposition can result in large bony deformities |
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what is syphilitic saber shin? |
produced by massive reactive periosteal bone deposition on the medial and anterior surfaces of the tibia |
