Musculoskeletal System - Essay Example

Musculoskeletal System Q1a The lower leg has 2 bones, the tibia and the fibula. Of these two, tibia is the only weight bearing bone and is the most commonly fractured long bone in the body (Konowalchuk, 2005). The bone lies longitunially in the medial side of the leg. The diaphyses of the bone is the most commonly fractured part of the bone. The most common fracture pattern is transverse AO Type 42A3 (Chang et al, 2007). Most of the times, fracture of tibia is associated with fibula fracture also, because; the force from tibia is transmitted along the interosseous membrane to the fibula (Norvell, 2006). In Julia, fibular fracture did not occur. Over the anterior and medial aspect of tibia, the skin and subcutaneous tissue are very thin and thus fractures in this region of shaft are open. Also, even if the fracture is closed, the skin and subcutaneous tissue which is thin can become compromised (Norvell, 2009). Q1b The main causes of pain in Julia are fracture and damage to the subcutaneous tissue and skin over the fracture. However, other causes of pain also must be looked at because tibial fracture can be associated with several complications. These include neurovascular compromise, compartment syndrome, peroneal nerve injury, wound infection, fat embolism and gangrenous changes (Norvell, 2009). Q2a Specific cells which have a role in the healing process of the fracture are inflammatory cells, fibroplasts and osteoprogenitor cells. There are basically 3 stages of healing following fracture. They are stages of inflammation, stage of repair and stage of regeneration. Immediately after fracture, there is hematoma formation due to rupture of blood vessels. This hematoma fills the fracture gap and surrounds the area of bone injury (Rosenberg, 2007). A fibrin mesh is provided by the clotted blood which helps seal off the fracture site and creates a frame work for inflammation and repair. There is influx of inflammatory cells, ingrowth of fibroblasts and development of new capillary vessels. There is also release of some cytokines by the degranulated platelets and migrated inflammatory cells (Rosenberg, 2007). The cytokines activate the osteoprogenitor cells in the periosteum, medullary cavity, and surrounding soft tissues and stimulate the production of osteoclastic and osteoblastic activity. By the end of the first week, the hematoma is organized, the adjacent tissue is prepared for further matrix production and the fractured ends of the bones are being modelled, which is mainly uncalcified tissue (Rosenberg, 2007). The activated osteoprogenitor cells start depositing subperiosteal trabaculae of woven bone. During fracture healing, the woven bone containing type III collagen is replaced by regular type I collagen containing lamellar bone (Stoffel, 2007). The repair of the tissue reaches its maximal girth at the end of second week. Around this time, though there is stabilization of the fracture site, the bone is not yet ready for weight bearing. The newly formed cartilage along the fracture line undergoes endochondral ossification and bridges the gap between fracture ends with bony callus. The stiffness and the strength of the callus gradually increase to the point of weight bearing as it mineralizes (Rosenberg, 2007). Initially, excess of fibrous tissue, cartilage and bone are produced and as the callus matures and transmits weight bearing forces, the instress portions are reabsorbed. The medullary cavity also is restored (Rosenberg, 2007). Q2b Four important factors affecting wound healing are presence of soft tissue injury and local blood supply, presence of infection, Vitamin C and corticosteroids (South Australian Orthopedic Registrars Notebook, 2010). Soft tissue injury and derangements in local blood supply delays wound healing because of inappropriate supply of oxygen and nutrients essential for the healing process. Removal of metabolic waste also is affected causing accumulation of toxic substances which delay wound healing. Infection delays wound healing because of accumulation of pus and delay in the process of healing. Vitamin C is very essential for the formation of normal collagen matrix necessary for establishment of normal bone matrix. Corticosteroids cause inhibition of differentiation of osteoblast and thus slow down the process of healing. Q2c Fractures in children heal very well even if the injury has occured to growth plate (Center for Orthopedics and Sports Medicine, 2003). However, long-term damage in terms of growth of the leg depends on certain factors like the age of the child, severity of injury, portion of the growth plate injured and type of the growth plate fracture (Center for Orthopedics and Sports Medicine, 2003). Growth can be stunted if the injury has damaged the blood supply to the epiphysis. Also, if the injury has caused either a shift in the growth plate or a damage, crushing or shattering of the same, then retardation of the growth of the leg is likely to occur (Center for Orthopedics and Sports Medicine, 2003). Open injury increases the risk of infection and thus retards healing process and growth. In Julia, there is no open wound. Complications of the fracture like injury to blood supply or nerve supply, compartment syndrome, mal-union, delayed union and others can lead to premature growth arrest and aberrations in growth. Q2d Fracture healing is excellent in children and recovery is very fast (Center for Orthopedics and Sports Medicine, 2003). The chances of development of complications like delayed union and malunion are uncommon (Center for Orthopedics and Sports Medicine, 2003). Unlike in older people like Julias grandmother who have several factors which delay wound healing like osteoporosis, poor nutrition, anemia and poor wound healing due to oldage and poor mobilisation (Norvell, 2009), Julia is a young girl and has good chances of recovery. Return to playing depends not only on fracture healing but also on muscle recovery. Gaston et al (2000) studied muscle recovery following tibial diaphysis fracture and they found that the knee extensors and flexors have about 40% of normal power two weeks after fracture, rising to between 75% and 85% of normal at one year, with the return of power of the flexors being better than that of the extensors. Also, while plantar flexion is weak two weeks after injury but improves quickly, the power of plantar flexion and dorsiflexion is between 90% and 100% of normal by one year. They opined that this probably is the reason why most patients take a considerable time to return to sporting and other strenuous activities. A study by Shaw et al (1997) concluded that young men take a mean of 26 weeks to return to football training and 40 weeks for competitive football. Thus it can be said that Mr. X will take atleast 9-10 months to resume active foot ball playing. This is further supported by the study by Chang et al (2007) wherein the researchers reported that the average time to return to activity was 23.3 weeks. Thus returning to playing within 3 months may not be possible for Julia. References Chang, W.R., Kapasi, Z., Daisley, S., Leach, W.J. (2007). Tibial shaft fractures in football players. Journal of Orthopaedic Surgery and Research, 2,11 Center for Orthopedics and Sports Medicine (2003). Growth Plate Injuries. Retrieved on 19th march, 2010 from http://www.arthroscopy.com/sp22000.htm Gaston, P., Will, E., McQueen, M.M., Elton, R.A., & brown, C.M. (2000). Analysis of muscle function in the lower limb after fracture of the diaphysis of the tibia in adults. J Bone Joint Surg (Br), 82-B:326-31 Konowalchuk, B.K., 2005. Tibial Shaft Fractures. eMedicine from WebMD. Retrieved on 19th March, 2010 from: http://www.emedicine.com/orthoped/topic340.htm Norvell, J.G. (2009). Fractures, Tibia and Fibula. eMedicine from WebMD. Retrieved on 19th March, 2010 from: http://www.emedicine.com/emerg/topic207.htm Rosenberg, A. E.(2007). Bones, Joints, and Soft Tissues. Robbins and Cotran Pathologic Basis of Disease. 7th edition. Philadelphia: Saunders. Shaw, A.D., Gustilo, T., Court-Brown, C.M. (1997). Epidemiology and outcome of tibial diaphyseal fractures in footballers. Injury, 28, 365-7. Stofell, K., Engler, H., Kuster, M., & Riesen, W. (2007). Changes in Biochemical Markers after Lower Limb Fractures. Clinical Chemistry, 53, 131-134. South Australian Orthopedic Registrars Notebook. (2010). Fracture Principles. Retrieved on 19th March, 2010 from http://som.flinders.edu.au/FUSA/ORTHOWEB/notebook/trauma/fractures.html Read More