World Journal of Pharmaceutical
and Medical Research

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An International Peer Reviewed Journal for Pharmaceutical and Medical Research and Technology
An Official Publication of Society for Advance Healthcare Research (Reg. No. : 01/01/01/31674/16)
ISSN 2455-3301
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Abstract

A NARRATIVE REVIEW ON AVASCULAR NECROSIS OF FEMORAL HEAD IN SICKLE CELL PATIENTS IN TRIBAL BELTS OF MAHARASHTRA

*Bhandari Prasad S., Patond K. R. and Badole C. M.

ABSTRACT

Avascular necrosis (AVN), is also known as osteonecrosis. Avascular necrosis is a disease that results from the temporary or permanent loss of blood supply to the bone. When blood supply is cut off, and ischemia of bone tissue has taken place, leading to infarction, ultimately the bone tissue dies and the bone collapses.[1] If avascular necrosis happens near a joint, the joint surface may collapse. More than 20,000 people each year enter hospitals for treatment of osteonecrosis of the hip. In this disease, bilateral involvement is found in many cases. The prevalence of AVN is around 20,000–30.000 new diagnoses per year. This condition may happen in any bone. This can result from trauma such as femoral neck fracture or because of the atraumatic associated etiologies [2] such as excessive alcohol, glucocorticoid use, Sickle Cell anemia, systemic lupus erythematous (SLE), radiation therapy, and coagulopathy. In these conditions there occurs an ischemic consequence because of the compromised blood flow to the femoral head. Most living tissues need oxygen, without which there is inefficient metabolic functioning. Once infarction takes place, oxidative phosphorylation cannot take place and necrosis ensues. AVN is multifactorial but can begin with interruption of blood and oxygen supply to vasculature in and around the bone. It progresses to trabecular thinning (seen in osteoporosis also) and it results in the collapse of the bone. In the case of sickle cell disease, this infarction results from occlusion of the vasculature by red blood cells (RBCs) which have changed their form from biconcave or round to crescent or sickle shape and flow less smoothly in the blood vessels. Their shape allows them to adhere to other RBCs as well as the endothelial walls, worsening vaso-occlusion. This leads to occlusion of bone marrow, ischemia, and progression to AVN. It is common in sickle cell disease. As much as 50% of sickle cell patients can develop AVN by the time they reach the age of 35. However, it is very rare in sickle cell trait (SCT), a much milder form of sickle cell disease in which patients are usually asymptomatic.

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