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Dermal filler complications and management
Published in Michael Parker, Charlie James, Fundamentals for Cosmetic Practice, 2022
Avascular necrosis is the term used to describe cell death secondary to a lack of oxygenated blood. In the context of dermal filler augmentation, there are two main mechanisms in which avascular necrosis can occur: first, it may be caused by direct injection of dermal filler into an artery, and second, it may due to a local pressure effect of the filler itself pressing on an artery from the outside. Regardless of the underlying cause, avascular necrosis can confer devastating long-term sequelae on your patients and therefore mandates swift identification and definitive management.
Orthopaedics
Published in Kaji Sritharan, Jonathan Rohrer, Alexandra C Rankin, Sachi Sivananthan, Essential Notes for Medical and Surgical Finals, 2021
Kaji Sritharan, Jonathan Rohrer, Alexandra C Rankin, Sachi Sivananthan
Aseptic necrosis of all or part of the femoral head due to impairment of the blood supply by recurrent infarction; aetiology unknown. Can progress to avascular necrosis. Associated with long-term risk of developing early OA (in 30s) of the hip joint. Peak age: 3–9 years; 3–5 times more common in males; both hips affected in <10%.
Orthopaedics
Published in Kristen Davies, Shadaba Ahmed, Core Conditions for Medical and Surgical Finals, 2020
The main blood supply to the head of the femur comes from vessels that travel underneath the capsule along the femoral neck. This blood supply is mainly from the trochanteric anastomosis, which has contributions from the lateral and medial circumflex femoral arteries as well as the superior and inferior gluteal artery (Figure 11.2.1). If the hip fracture occurs within the femoral capsule (e.g. an intracapsular fracture), the blood supply to the head of the femur is often compromised, especially if it is a displaced fracture. If the blood supply to the head of the femur is compromised, avascular necrosis can occur.
Variations and characteristics of the various clinical phenotypes in a cohort of Nigerian sickle cell patients
Published in Hematology, 2021
Augustine Duru, Anazoeze Jude Madu, Helen Okoye, Charles Nonyelu, Onochie Obodo, Kelechi Okereke, Kenechi Madu
We had a total of 42 (24 males and 18 females) study participants who had avascular necrosis (AVN) with a prevalence of 15.6% (males 14.5% and females 17.1%). This was not significantly associated with sex (1.852, p = 0.058), SLU (0.312, p = 0.589), nephropathy (2.376, p = 0.164), osteomyelitis (1.016, p = 0.418), pulmonary hypertension (0.024, p = 1.00) or cholelithiasis (3.8, p = 0.071). The median age was 26 years, Hb was 8.2 g/dL, leucocyte count 9.9 × 109/L, platelet count of 368 × 109/L, frequency of crisis was 4 episodes/year and direct bilirubin was 8.6 IU/L. The frequency of other chronic complication in patients who had AVN were 31.7% (13/41) SLU, 4.9% (2/41) priapism, 9.8% (4/41) nephropathy, 17.1% (7/41) osteomyelitis, 9.8% (4/41) osteoarthritis and 4.9% (2/41) neurological complications. There was no significant relationship between the occurrence of AVN and the measured indicators of severe disease in this cohort.
Hip preserving surgery for avascular hip necrosis: does terminating exposure to known risk factors improve survival?
Published in The Physician and Sportsmedicine, 2020
Roger Erivan, Hicham Riouach, Guillaume Villatte, Bruno Pereira, Stéphane Descamps, Stéphane Boisgard
The present study was single-center, retrospective, and small scale, but this kind of pathology is rare, with 4.7 cases per 10,000 person-years in the Swedish population [27]. Moreover, there was no loss to follow-up, and all patients were included, reducing selection and attrition bias. Double reading was not implemented for X-rays [28], which may have biased the assessment of stages. Patient’s non-surgical treatments, if any were not taken into account, which again may have affected our findings [10]. Immunohistochemical factors affecting the progression of avascular necrosis were not analyzed [29]. Risk factors were categorized as avoidable or not, although in some cases there is room for discussion: e.g., does a diabetic patient who is under treatment still present a risk factor? – we decided that ‘yes’, but this may introduce bias. No differences were found preoperatively, but that may just have been due to small sample size.
Multifocal avascular necrosis in a patient with refractory immune thrombocytopenia and antiphospholipid antibodies; case report and review of literature
Published in Platelets, 2019
Hala El-Gendy, Rasmia M. El-Gohary, Safaa Mahfouz, Hamdy M.A. Ahmed, Doaa M. El Demerdash, Gaafar Ragab
Dear editor(s), as you know, avascular necrosis (AVN), also known as ischemic necrosis, osteonecrosis and aseptic necrosis, was first described in 1738 by Alexander Munro and is defined as necrosis of a localized area of bone [1]. Immune thrombocytopenia (ITP) and antiphospholipid syndrome (APS) are two different autoimmune diseases that are rarely associated with AVN. ITP is characterized by low peripheral blood platelet count (< 100 × 109/L) and may present with petechiae and bleeding. It may occur in isolation (primary) or in association with other disorders (secondary) [2]. In ITP, anti-platelet antibodies directed against single or multiple platelet membrane glycoproteins (GP) lead to acceleration of platelet destruction and inhibition of their production [3]. Secondary causes include autoimmune disorders such as systemic lupus erythematosus (SLE) and APS; viral infections including hepatitis C virus (HCV) and human immunodeficiency virus (HIV); and certain drugs [4]. APS is caused by antiphospholipid antibodies (aPLs) and results in a hypercoagulable state which can clinically present with arterial, venous, or small vessel thrombosis and/or pregnancy morbidities [5].