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Ear Trauma
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
Caustic injuries to the external canal and drum perforation from button batteries require emergency treatment. Eardrops must not be used. Extensive soft tissue and bone necrosis is possible. Emergency removal, irrigation and debridement should be performed, but repair or grafting should be delayed.
Osteonecrosis of the Jaws Associated with the Use of Bisphosphonates: A Review of 63 Cases
Published in Niall MH McLeod, Peter A Brennan, 50 Landmark Papers every Oral & Maxillofacial Surgeon Should Know, 2020
Most patients required surgical procedures to remove all of the involved bone, and 75% had a sequestrectomy; other procedures involved marginal mandibular resection, segmental mandibular resection, and partial or complete maxillectomy. Two patients received hyperbaric oxygen therapy (30 one-hour sessions) before undergoing a marginal mandibular resection of necrotic bone, and despite having vascularised bone at the resection margins, there was progressive necrosis most likely requiring a segmental resection. Two asymptomatic patients with regions of exposed and necrotic bone were followed and treated conservatively with local wound care and irrigations. One patient with metastatic uterine leiomyosarcoma presented with a large sequestered segment of the right maxilla that had spontaneously exfoliated, resulting in a large oroantral communication. Stopping bisphosphonate treatment did not have a major impact on the progression of this process. Five patients had persistent bone necrosis and even developed new regions of exposed bone despite being removed from bisphosphonate therapy by their oncologists.
Effects of treatment on bone and bone marrow
Published in Anju Sahdev, Sarah J. Vinnicombe, Husband & Reznek's Imaging in Oncology, 2020
Lia A Moulopoulos, Vassilis Koutoulidis
The effect of radiation therapy on bone has been documented by pathological studies (3–5). The changes that occur in irradiated bone are due to destruction of the cellular bony matrix and the fine vasculature that supplies the bone. Radiation therapy induces an immediate inflammatory reaction in the bone marrow. All cellular elements die within a few days after the initiation of treatment and, as early as in the first week of therapy, the marrow becomes hypocellular with oedema and haemorrhage. Endarteritis occurs later in the post-radiation period and is responsible for the late post-radiation manifestations observed on radiographic examinations. Destruction of the microvasculature of the bone prevents the migration of haematopoietic elements from contiguous healthy bone marrow. Vascular compromise leads to bone necrosis. Necrotic bone is gradually removed by ‘creeping substitution’ and new bone is deposited over a period of years.
Pain, impaired functioning, poor satisfaction and diminished health status eight years following perilunate (fracture) dislocations
Published in Disability and Rehabilitation, 2020
Charlotte M. Lameijer, Caren K. Niezen, Mostafa El Moumni, Corry K. van der Sluis
Perilunate dislocations and perilunate fracture dislocations (PLD/PLFDs) are rare injuries of the wrist and comprise only 7% of all carpal injuries [1–5]. PLFDs occur more frequently than PLDs (ratio 2:1), in which the scaphoid bone is most often fractured [6]. Most PLD/PLFDs are seen following injury with high energy transmission. Twenty percent of all PLD/PLFDs are associated with polytrauma [7]. Diminished range of motion of 59–82% and grip strength measurements ranging from 59–87% in comparison to the uninjured wrist were reported 6-months to 5 years following PLD/PLFDs [3,8–11]. In addition, poor outcomes regarding PROs have been reported with Disability of Arm Shoulder Hand (DASH) scores ranging from 14–40 and Patient Rated Wrist Evaluation (PRWE) scores ranging from 13–41 [3,8–13]. Complicated PLD/PLFD is thought to result in poorer outcomes due to extensive soft tissue damage [7]. Late identification of PLD/PLFDs ligament ruptures or accompanying fractures also lead to worse outcomes [2,7,14–16]. Bone necrosis and posttraumatic arthritis is known to develop following this injury [17]. Prevalence of posttraumatic arthritis following PLD/PLFDs of up to 56% has been reported 6 years post-injury [7]. The development of posttraumatic arthritis of the wrist increases with direct or indirect impact load on the joint, soft tissue contusion, joint dislocation, and intra-articular fractures (most often scaphoid bone fractures) [18–20]. Posttraumatic arthritis can result in severe functional impairment with regard to range of motion and grip strength [18].
Uncemented monoblock trabecular metal posterior stabilized high-flex total knee arthroplasty: similar pattern of migration to the cruciate-retaining design — a prospective radiostereometric analysis (RSA) and clinical evaluation of 40 patients (49 knees) 60 years or younger with 9 years’ follow-up
Published in Acta Orthopaedica, 2019
Radoslaw Wojtowicz, Anders Henricson, Kjell G Nilsson, Sead Crnalic
1 patient (female, 55 years) with bilateral operations staged 6 months apart had her second (right) operated knee revised 3 months postoperatively. Postoperative knee alignment was 3° varus and tibial component alignment 4° varus. The tibial implant subsided 9 mm medially within the first weeks postoperatively, resulting in a severe varus malalignment. There were no signs of infection. At revision 3 months after the index operation, the tibial implant was firmly fixed to bone and had to be cut out with saw and chisels. Bone underneath and adjacent to the implant showed signs of bone necrosis on microscopic analysis. A stemmed revision tibial component was inserted. The first (left) knee operated on this patient had postoperative HKA angle 180° and tibial component alignment of 1° varus, and functioned very well during the follow-up.
The role of Iloprost on bone edema and osteonecrosis: Safety and clinical results
Published in Expert Opinion on Drug Safety, 2018
Ippokratis Pountos, Peter V Giannoudis
Avascular necrosis is a common and multifactorial disease with an annual incidence of approximately 15,000 new cases per year in the USA [16,17]. It is estimated that it accounts for 10% of all total hip replacement operations [16,17]. The exact pathophysiology of AVN remains unclear but multiple etiological risk factors have been implicated (Table 2). Several authors have proposed theoretical models to describe the events that take place during the progression of the disease. An excessive localized accumulation of interstitial fluid leads to the aggravation of the edema and to bone necrosis [18–20]. This bone necrosis possible occurs due to alterations of bone vascular network that promotes ischemia, venous stasis, and microembolisms. It must be said that the term ‘avascular’ is rather misleading as the blood flow is interrupted in the presence of the feeding vessels [21]. Evidence includes suppression of the osteoblasts, apoptosis of the osteocytes, fat hypertrophy with proliferation of fat cells [16,17,22–24]. Subsequently, if involvement of the overlying cartilage occurs, flattening of the head surface followed by collapse and eventually development of secondary osteoarthritis can follow. Other contributing factors are a genetic predisposition and/with alterations in bone homeostasis not allowing healing and remodeling of the affected bone [16,17,22–24].