Pathophysiology of Tibial Fracture

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    I had a pt with a tibial shaft fracture and I have no idea what to do for the pathophysiology on my care plan. Any help is appreciated. Thank you
  2. 5 Comments so far...

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    in looking at the pathophysiology of a fracture you are, in essence, looking at bone that has been broken apart by trauma. there are a number of ways the trauma happens. then, there is the "what" that is going on at the cellular level. do you know the specific type of force that caused the fracture in this patient? where a force and stress was applied to the limb will often determine the type of fracture that results (compound, simple, greensick, displaced, comminuted, segmental spiral, hairline) [we're getting into a little physics here.]

    here's the information i'm getting from my copy of pathophysiology: the biologic basis for disease in adults and children, third edition, by kathryn l. mccance and sue e. heuther:

    a fracture in bone occurs when a force has gone beyond the tensile or compressive strength of the bone. this varies for the individual bones. in younger people these fractures tend to be a result of trauma, particularly in the tibia, clavicle and lower humerus. fractures in the upper femur, upper humerus, vertebrae and pelvis tend to be associated with osteoporosis in older individuals. fractures are classified as complete (broken all the way through) or incomplete (damaged, but still in one piece) and open (also known as compound where the skin is broken and the bone may be exposed) or closed (also known as simple where the skin has not been broken). when bone has broken into two or more segments it is called a comminuted fracture. linear fractures run parallel to the long axis of the bone. oblique fractures run at a 45-degree angle to the shaft of the bone. a spiral fracture encircles the bone. a transverse fracture is a straight across perpendicular fracture of a bone.

    (page 1438) "pathophysiology
    when a bone is broken, the periosteum and blood vessels in the cortex, marrow, and surrounding soft tissues are disrupted. bleeding occurs from the damaged ends of the bone and from the neighboring soft tissue. a clot (hematoma) forms within the medullary canal, between the fractured ends of the bone, and beneath the periosteum. bone tissue immediately adjacent to the fracture dies. this necrotic tissue along with any debris in the fracture area stimulates an intense inflammatory response characterized by vasodilation, exudation of plasma and leukocytes, and infiltration by inflammatory leukocytes and mast cells. [for information on the pathophysiology of the immune response, see http://allnurses.com/forums/f50/hist...ct-244836.html]". within 48 hours after the injury, vascular tissue invades the fracture area from surrounding soft tissue and the marrow cavity, and blood flow to the entire bone is increased. bone-forming cells in the periosteum, endosteum, and marrow are activated to produce subperiosteal procallus along the outer surface of the shaft and over the broken ends of the bone. osteoblasts within the procallus synthesize collagen and matrix, which becomes mineralized to form callus (woven bone). as the repair process continues, remodeling occurs, during which unnecessary callus is resorbed and trabeculae are formed along lines of stress. except for the liver, bone is unique among all body tissues in that it will form new bone, not scar tissue, when it heals after a fracture."

    from pathophysiology: a 2-in-1 reference for nurses by springhouse, springhouse publishing company staff, page 399)
    "bone growth
    bone formation is ongoing and is determined by hormonal stimulation, dietary factors, and the amount of stress put on the bone. it's accomplished by the continual actions of bone-forming osteoblasts and bone-reabsorbing cells called osteoclasts. osteoblasts are present on the outer surface of and within bones. they respond to various stimuli to produce the bony matrix, or osteoid. as calcium salts precipitate on the organic matrix, the bone hardens. as the bone forms, a system of microscopic canals forms around the osteocytes (mature bone cells). osteoclasts are phagocytic cells that digest old, weakened bone section by section. as they finish, osteoblasts simultaneously replace the cleared section with new, stronger bone.

    vitamin d supports bone calcification by stimulating osteoblast activity and calcium absorption from the gut to make it available for bone building. when serum calcium levels fall, the parathyroid gland releases parathyroid hormone, which then stimulates osteoclast activity and bone breakdown, freeing calcium into the blood. parathyroid hormone also increases serum calcium by decreasing renal excretion of calcium and increasing renal excretion of phosphate ions

    phosphates are essential to bone formation; about 85% of the body's phosphates are found in bone. the intestine absorbs many phosphates from dietary sources, but adequate levels of vitamin d are necessary for their absorption. because calcium and phosphates interact in a reciprocal relationship, renal excretion of phosphates increases or decreases in inverse proportion to serum calcium levels. alkaline phosphatase (alp) influences bone calcification and lipid and metabolite transport. osteoblasts contain an abundance of alp. a rise in serum alp levels can identify skeletal diseases, primarily those characterized by marked osteoblastic activity such as bone metastasis of paget's disease. it can also identify biliary obstruction or hyperparathyroidism, or excessive ingestion of vitamin d.

    in children and young adults, bone growth occurs in the epiphyseal plate, a layer of cartilage between the diaphysis and epiphysis of long bones.

    osteoblasts deposit new bone in the area just beneath the epiphysis, making the bone longer; osteoclasts model the new bone's shape by reabsorbing previously deposited bone. these remodeling activities promote longitudinal bone growth, which continues until the epiphyseal growth plates, located at both ends, close during adolescence. in adults, bone growth is complete, and this cartilage is replaced by bone, becoming the epiphyseal line."

    this information will help you to determine the related factors in forming your 3-part nursing diagnostic statements. it also helps you to understand some of the signs and symptoms the patient is having (pain, swelling) and why they may be at risk for things like fat or pulmonary embolism, neurovascular impairment. some of this information should also give you some ideas of some of the nursing interventions you should be including in your care plan, particularly regarding dietary replacement of calcium and magnesium.
    Last edit by Daytonite on Jan 31, '08
    shescoolie, mozzgirl01, DC5, and 3 others like this.
  4. 0
    Thank you so much for this post!!! I have revised my concept map so many times! and this will do. Thank you Daytonite. I know its an old post
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    The local separation of a bone into two or more pieces under the action of stress. Strong force is required to produce a fractured tibia. As a result, soft tissue damage, devascularization, and open fracture are frequent. The tibia is one of the more common sites of a stress fracture. Complications are compartment syndrome, fat embolism, problems associated with bony union, and possible infection associated with open fracture.

    Thats what I put, hope it helps
  6. 0
    this is what i put for tibial fracture pathophysiology
  7. 0
    Thank you for the info


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