Impact of Anemia on Outcomes Following Total Hip Replacement Surgery and Patient Prognosis

TL;DR

Anemia affects outcomes in total hip replacement surgery, and managing it preoperatively can improve recovery and patient satisfaction.

Contribution

This review links cellular mechanisms of anemia to clinical management strategies in total hip replacement surgery.

Findings

Anemia increases risks of transfusion, infection, and prolonged hospital stays after THR.

Preoperative anemia management may enhance surgical outcomes and quality of life.

Hepcidin regulates iron levels and contributes to anemia in chronic diseases.

Abstract

Anemia is a prevalent comorbidity among patients undergoing total hip replacement (THR) surgery, significantly affecting surgical outcomes and patient prognosis. This review synthesizes current literature on the relationship between anemia and THR, with a focus on postoperative complications, recovery times, and overall patient satisfaction. While several recent meta‐analyses have quantified the risks associated with anemia, our review offers a novel perspective by linking cellular mechanisms to clinical management strategies. We analyze various studies that highlight the prevalence of anemia in this patient population and its potential impact on surgical risks, including increased rates of transfusion, infection, and prolonged hospital stays. Furthermore, we explore the implications of anemia on functional recovery and long‐term outcomes, emphasizing the necessity for preoperative screening and management strategies. Our findings suggest that addressing anemia before THR may improve surgical outcomes and enhance patients' quality of life. This review underscores the importance of a multidisciplinary approach in the preoperative assessment and management of patients with anemia undergoing total hip replacement surgery.

The processes involved in iron acquisition are closely controlled by hepcidin‐based regulatory mechanisms. Hepcidin is a peptide hormone mainly produced in the liver, acting as an acute‐phase reactant that responds to changes in plasma iron levels. It does this by binding to ferroportin, a protein responsible for exporting iron from cells, leading to its degradation. The expression of hepcidin rises when there are elevated levels of iron in the bloodstream and tissues, as well as during systemic inflammation or infections. Conversely, factors such as increased red blood cell production, iron deficiency, and low tissue oxygen levels can suppress its production, influenced by signals from the bone marrow, liver, and possibly muscle and fat cells. The rise in hepcidin levels triggered by inflammatory cytokines, particularly interleukin‐6, accounts for the sequestration of iron and the decreased availability of iron for erythropoiesis seen in anemia associated with chronic diseases.

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