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Books on the topic 'Bone fracture treatment'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 February 2022

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1

Practical fracture treatment. 2nd ed. Edinburgh: Churchill Livingstone, 1989.

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2

Practical fracture treatment. 3rd ed. Edinburgh: Churchill Livingstone, 1994.

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3

Esser, Max, FRCS Ed ORTH FRACS., ed. Practical fracture treatment. 4th ed. Edinburgh: Churchill Livingstone, 2003.

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4

McRae, Ronald. Practical fracture treatment. 2nd ed. Edinburgh: Churchill Livingstone, 1989.

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5

McRae, Ronald. Practical fracture treatment. 3rd ed. Edinburgh: Churchill Livingstone, 1994.

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6

Esser, Max, FRCS Ed ORTH FRACS., ed. Practical fracture treatment. 5th ed. Edinburgh: Churchill Livingstone, 2008.

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7

Charnley, John. The Closed treatment of common fractures. 4th ed. Cambridge: Colt Books in association with The John Charnley Trust, 1999.

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8

Scherl, Susan A. Surgical management of pediatric long bone fractures. Rosemont, IL: American Academy of Orthopaedic Surgeons, 2009.

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9

External fixation: Joint deformities and bone fractures. New York, N.Y: International Universities Press, 1987.

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10

(Matthias), Rapp M., and SpringerLink (Online service), eds. The Double Dynamic Martin Screw (DMS): Adjustable Implant System for Proximal and Distal Femur Fractures. Heidelberg: Steinkopff, 2008.

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11

1930-, Boyd Robert J., and McCabe Charles J, eds. Trauma management: Early management of visceral, nervous system, and musculoskeletal injuries. Chicago: Year Book Medical Publishers, 1988.

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12

Herbert, Timothy J. The fractured scaphoid. Saint Louis, Mo: Quality Medical Pub., 1990.

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13

Muckle, David Sutherland. An outline of fractures and dislocations. Bristol: Wright, 1985.

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14

DeVries, Wilma J. The effect of volume variations on the osteogenic capabilities of autogenous cancellous bone graft in the dog. Charlottetown: University of Prince Edward Island, 1991.

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15

(Fabrizio), Annocaro F., and Centre hospitalier universitaire de Nancy, eds. Flexible intramedullary nailing in children: The Nancy University manual. Heidelberg: Springer, 2010.

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16

Office orthopedics for primary care: Treatment. 3rd ed. Philadelphia, PA: Saunders Elsevier, 2006.

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17

Anderson, Bruce Carl. Office orthopedics for primary care: A treatment manual. Portland, OR (8007 SE 140th Dr., Portland, Oregon 97236): JJ&R Publishing, 1992.

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18

Office orthopedics for primary care: Diagnosis and treatment. Philadelphia: W.B. Saunders, 1995.

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19

Anderson, Bruce Carl. Office orthopedics for primary care: Diagnosis and treatment. 2nd ed. Philadelphia: W.B. Saunders Co., 1999.

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20

Ali, Abbassian, and Langdon Ilana, eds. A practical guide to hand and carpal fracture management. London: Imperial College Press, 2009.

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21

1917-, Bonfiglio Michael, and Campbell Crawford J, eds. Orthopedic pathophysiology in diagnosis and treatment. New York: Churchill Livingstone, 1990.

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22

M, McQueen Margaret, and Tornetta Paul, eds. Trauma. Philadelphia: Lippincott Williams & Willkins, 2006.

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23

D, Ringe J., ed. Treatment of metabolic bone disease: Management strategy and drug therapy. London: Martin Dunitz, 2000.

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24

Fardon, David F. Osteoporosis: Your head start on the prevention & treatment of brittle bones. Tucson, Ariz: Body Press, 1987.

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25

Hamilton, Frank Hastings. A practical treatise on fractures and dislocations. San Francisco: Norman Pub., 1991.

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26

Osteoporosis: Your head start on the prevention and treatment of brittle bones. New York: Macmillan, 1985.

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27

Fractures in the elderly: A guide to practical management. New York: Humana, 2011.

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28

Trúc, Thưvong. Truat đka crot khoa: Khoa trị gnay xương, bong gân ... Los Alamitos, Calif: Xuân Thu, 1987.

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29

Zhongguo gu shang zhi liao cai se tu pu. Beijing: Beijing ke xue ji shu chu ban she, 2002.

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30

The Closed Treatment of Common Fractures. 4th ed. Greenwich Medical Media, 2004.

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31

The Closed Treatment of Common Fractures. 4th ed. Cambridge University Press, 2004.

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32

Charnley, John. The Closed Treatment of Common Fractures. 4th ed. Greenwich Medical Media Ltd, 1999.

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33

The Magic School Bus: Bus Fixes a Bone. Scholastic, 2010.

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34

W, Virkus Walter, ed. Curbside consultation in fracture management: 49 clinical questions. Thorofare, NJ: SLACK, 2008.

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35

A, Bianchi-Maiocchi, Aronson J, and Association for the Study and Application of Ilizarov's Method., eds. Operative principles of Ilizarov: Fracture treatment, nonunion, osteomyelitis, lengthening, deformity correction. Baltimore: Williams & Wilkins, 1991.

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36

Surgical Management of Pediatric Long Bone Fractures. Amer Academy of Orthopaedic, 2008.

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37

McRae's Orthopaedic Trauma and Emergency Fracture Management. Elsevier - Health Sciences Division, 2015.

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38

Naqui, Zaf, and David Warwick. Bone and joint injuries of the wrist and forearm. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757689.003.0004.

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The forearm is a complex quadrilateral structure linked by the proximal and distal radioulnar joints, ligaments, which include the interosseous membrane and triangular cartilage, and several obliquely orientated muscles. A displaced fracture or ligament rupture within this forearm is likely to involve other structures. Treatment requires anatomic recovery of stable function. The ulnar corner can sustain fractures or ligament ruptures which affect stable, pain-free, congruous forearm rotation. The distal radius may fracture after high- or low-energy trauma; anatomic reduction may not be essential in all; inaccuracy may lead to loss of rotation and ulnocarpal abutment but long-term arthritis is unusual. Children’s fractures are managed with consideration of remodeling potential. The scaphoid is vulnerable to non-union; plaster immobilization, early percutaneous fixation, and later bone-grafting all have roles. Salvage for osteoarthritic non-union may reduce pain but compromises function. Rupture of the carpal ligaments may cause substantial disruption and require complex reconstruction.
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39

1944-, Regazzoni P., ed. The Dynamic hip screw implant system. Berlin: Springer-Verlag, 1985.

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40

R, Tucker Myron, ed. Rigid fixation for maxillofacial surgery. Philadelphia: J.B. Lippincott Co., 1991.

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41

Haddad, F. S., and F. Rayan. Management of total hip replacement periprosthetic fractures. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.007012.

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♦ Periprosthetic fractures: intraoperative or postoperative femoral or acetabular fractures♦ Third commonest reason for reoperation after THA♦ Vancouver classification Type A, B, and C♦ Three most important factors that determine treatment are:• Site of the fracture• Stability of the implant• Quality of the surrounding bone stock.
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42

Jadon, Deepak R., Tehseen Ahmed, and Ashok K. Bhalla. Disorders of bone mineralization—osteomalacia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0146_update_001.

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Disorders of bone mineralization cause rickets in children and osteomalacia in adults. Both remain common in developing countries. Incidence in Western countries had declined since the fortification of foodstuffs, but appears to be increasing again. Calcium and inorganic phosphate are the key precursors for bone mineralization and growth. The commonest aetiology of osteomalacia is vitamin D deficiency, primarily due to low dietary intake and inadequate sun exposure. In the last decade gene mutations have been identified that are responsible for inherited rickets and osteomalacia, particularly those that result in phosphate deficiency, hypophosphatasia, and vitamin D receptor or metabolizing enzyme mutations. Additionally, the pathogenesis of tumour-induced osteomalacia is becoming better understood. Osteomalacia may present as bone pain and tenderness, muscle pain and weakness, and skeletal deformity or fracture. Key investigations include biochemical assessment and plain radiographs. Radioisotope bone scans and bone biopsy may be considered in selected cases. Differential diagnoses include osteoporosis, seronegative arthritides, and localized soft tissue disorders. Treatment, guided by the underlying aetiology, aims to reduce symptoms, fracture risk, bone deformity and sequelae. Vitamin D deficient patients require vitamin D and calcium replacement.
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43

Jadon, Deepak R., Tehseen Ahmed, and Ashok K. Bhalla. Disorders of bone mineralization—osteomalacia. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0146.

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Disorders of bone mineralization cause rickets in children and osteomalacia in adults. Both remain common in developing countries. Incidence in Western countries had declined since the fortification of foodstuffs, but appears to be increasing again. Calcium and inorganic phosphate are the key precursors for bone mineralization and growth. The commonest aetiology of osteomalacia is vitamin D deficiency, primarily due to low dietary intake and inadequate sun exposure. In the last decade gene mutations have been identified that are responsible for inherited rickets and osteomalacia, particularly those that result in phosphate deficiency, hypophosphatasia, and vitamin D receptor or metabolizing enzyme mutations. Additionally, the pathogenesis of tumour-induced osteomalacia is becoming better understood. Osteomalacia may present as bone pain and tenderness, muscle pain and weakness, and skeletal deformity or fracture. Key investigations include biochemical assessment and plain radiographs. Radioisotope bone scans and bone biopsy may be considered in selected cases. Differential diagnoses include osteoporosis, seronegative arthritides, and localized soft tissue disorders. Treatment, guided by the underlying aetiology, aims to reduce symptoms, fracture risk, bone deformity and sequelae. Vitamin D deficient patients require vitamin D and calcium replacement.
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44

Sukhtankar, Priya, Julia Clark, and Saul N. Faust. Bone and joint infections in children. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0099.

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Bone and joint infections in children are uncommon, but they affect all ages and there is a wide range of disease. The mode of infection may be haematogenous or by direct inoculation from a wound. The child may present acutely unwell or with a chronic infection. Clinical features include fever, reluctance to move the affected limb, pain, and swelling. Laboratory tests and medical imaging are used to confirm diagnosis. Medical treatment is with initial intravenous antibiotic therapy, usually followed by oral treatment. Surgical treatment may be necessary if abscess or joint collection is present. In general prognosis is good with timely initiation of treatment, although complications such as pathological fracture are occasionally seen.
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45

Ralston, Stuart H. Paget’s disease of bone. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0144_update_001.

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Paget’s disease of bone (PDB) affects up to 1% of people of European origin aged 55 years and above. It is characterized by focal abnormalities of bone remodelling which disrupt normal bone architecture, leading to expansion and reduced mechanical strength of affected bones. This can lead to various complications including deformity, fracture, nerve compression syndromes, and osteoarthritis, although many patients are asymptomatic. Genetic factors play a key role in the pathogenesis of PDB. This seems to be mediated by a combination of rare genetic variants which cause familial forms of the disease and common variants which increase susceptibility to environmental triggers. Environmental factors which have been suggested to predispose to PDB include viral infections, calcium and vitamin D deficiency, and excessive mechanical loading of affected bones. The diagnosis can be made by the characteristic changes seen on radiographs, but isotope bone scans are helpful in defining disease extent. Serum alkaline phosphatase levels can be used as a measure of disease activity. Inhibitors of bone resorption are the mainstay of medical management for PDB and bisphosphonates are regarded as the treatment of choice. Bisphosphonates are highly effective at reducing bone turnover in PDB and have been found to heal osteolytic lesions, and normalize bone histology. Although bisphosphonates can improving bone pain caused by elevated bone turnover, most patients require additional therapy to deal with symptoms associated with disease complications. It is currently unclear whether bisphosphonate therapy is effective at preventing complications of PDB.
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46

Ralston, Stuart H. Paget’s disease of bone. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0144.

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Paget's disease of bone (PDB) affects up to 1% of people of European origin aged 55 years and above. It is characterized by focal abnormalities of bone remodelling which disrupt normal bone architecture, leading to expansion and reduced mechanical strength of affected bones. This can lead to various complications including deformity, fracture, nerve compression syndromes, and osteoarthritis, although many patients are asymptomatic. Genetic factors play a key role in the pathogenesis of PDB. This seems to be mediated by a combination of rare genetic variants which cause familial forms of the disease and common variants which increase susceptibility to environmental triggers. Environmental factors which have been suggested to predispose to PDB include viral infections, calcium and vitamin D deficiency, and excessive mechanical loading of affected bones. The diagnosis can be made by the characteristic changes seen on radiographs, but isotope bone scans are helpful in defining disease extent. Serum alkaline phosphatase levels can be used as a measure of disease activity. Inhibitors of bone resorption are the mainstay of medical management for PDB and bisphosphonates are regarded as the treatment of choice. Bisphosphonates are highly effective at reducing bone turnover in PDB and have been found to heal osteolytic lesions, and normalize bone histology. Although bisphosphonates can improving bone pain caused by elevated bone turnover, most patients require additional therapy to deal with symptoms associated with disease complications. It is currently unclear whether bisphosphonate therapy is effective at preventing complications of PDB.
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47

Magliano, Malgorzata. Osteoporosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.010006.

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♦ Osteoporotic fractures affect one in two women and one in five men over the age of 50♦ Previous fragility fracture increases future fracture risk and should prompt further assessment and treatment♦ Clinical risk factors in combination with bone mineral density measurement allow identifying patients at risk♦ Screening for secondary causes of osteoporosis is important, particularly in men and younger women♦ Patients at high risk for future fracture should be offered appropriate treatment. Bisphosphonates together with adequate calcium and vitamin D supplementation constitute first-line therapy♦ Compliance with treatment and clinical response need to be monitored.
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48

Shepherd, Angela J., and Juliet M. Mckee. Osteoporosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190466268.003.0015.

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Osteoporotic fractures are major causes of suffering and death. Dual-energy x-ray absorptiometry (DEXA) is the standard of care for diagnosis (T-score ≤ –2.5) of osteoporosis. Prevention of fractures requires addressing bone and muscle strength and balance. Physical exercise, good nutrition (fruits, vegetables, adequate calcium), adequate vitamin intake (C, D, and K), tobacco cessation, and no more than moderate alcohol intake enhance bone health and decrease fracture risk. Long-term treatment with glucocorticoids, certain drugs used in breast or prostate cancer treatment, and proton pump inhibitors used for gastroesophageal reflux disease may increase the risk for osteoporosis. Pharmacologically, bisphosphonates are the mainstay of osteoporosis treatment.
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49

Hutchison, Alastair J., and Michael L. Picton. Fractures in patients with chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0121.

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Patients with any degree of chronic kidney disease (CKD) have a much higher risk of fractures than the general population, and the risk of death at 1 year post hip fracture in a dialysis patient is over 60%, compared to less than 20% for a non-CKD patient. The assessment of fracture risk and diagnosis of the underlying skeletal pathology in CKD patients is a significant clinical challenge. Non-invasive imaging techniques are not totally reliable in the general population, and the presence of advanced CKD (stages 4, 5, and 5D) renders them largely useless. Bone strength is not determined only by quantity of bone, and renal osteodystrophy can significantly affect bone quality, rendering it liable to fracture even in the presence of a normal bone density measurement. Currently, the only reliable method of assessing both quantity and quality of bone is the examination of trans-iliac bone biopsy, which is generally, but probably incorrectly, perceived to be overly invasive. However, identifying the cause of reduced bone strength and fractures may influence the choice of therapy. For example, in the presence of low-turnover states such as adynamic bone, antiresorptive agents may be ineffective. Pharmaceuticals licensed for the treatment of osteoporosis in the general population can be used similarly in patients with CKD 1–3 without dosage alteration. In CKD 4, post-hoc analyses suggest denosumab is effective and safe, based on a 3-year study that included 73 such patients. In CKD 5 and 5D no dependable data exists to guide therapy, and it should probably be reserved for patients who have already suffered and survived a fracture, and are therefore at high risk of death from a second event.
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50

Henry, M. Stress fractures. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.012017.

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♦ Stress fractures are fractures occurring as the result of repetitive, submaximal loads, in the absence of a specific precipitating traumatic event.♦ These fractures can be subdivided into two groups on the basis of aetiology. Whereas ‘fatigue fractures’ result from the excessive repetitive (i.e. abnormal) loading of normal bone, ‘insufficiency fractures’ are fractures resulting from normal forces acting on abnormal bone.♦ Early diagnosis allows the initiation of effective treatment that can prevent prolonged pain and disability, as well as avoiding the progression to displacement or a non-union.♦ While management decisions are generally focused on activity modification, protection of weight bearing, and immobilization, there is a subset of fractures at high risk for progression to complete fracture, non-union, or delayed union. These high-risk stress fractures, including tension-side femoral neck fractures and anterior tibial cortex fractures, require aggressive treatment to prevent the sequelae of poor healing.
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