The Bone Cement Hypercoagulation Syndrome: Pathophysiology, Mortality, and Prevention

Area of Science:

• Biomaterials Science
• Orthopedic Surgery
• Cardiovascular Physiology

Background:

• Acrylic bone cement, introduced in the 1950s for hip prostheses, has been linked to perioperative cardiorespiratory and vascular complications.
• Surgical procedures involving bone marrow damage and methyl methacrylate release trigger neurogenic stimulation and coagulation activation.

Purpose of the Study:

• To elucidate the pathophysiologic mechanisms underlying fatal cardiorespiratory and vascular dysfunctions associated with bone cement implantation.
• To identify the role of toxic substances and vasoactive compounds in cement-induced complications.

Main Methods:

• Review of human and animal studies investigating the effects of bone cement.
• Analysis of cell fragments and activated cells in pulmonary microcirculation.
• Assessment of coagulation activation and vasoactive substance release.

Main Results:

• Bone cement constituents cause cell destruction and activate coagulation, leading to pulmonary microcirculation sequestration.
• A hypercoagulable state in pulmonary circulation can result in arterial thromboembolism and organ damage (brain, heart, kidneys).
• Release of vasoactive substances contributes to hemodynamic imbalances and potentially fatal outcomes.

Conclusions:

• The primary drivers of devastating outcomes are substantial coagulation activation and cell destruction from curing bone cement and released vasoactive substances.
• Susceptible populations, like elderly patients with hip fractures, are at higher risk for these complications.
• Understanding these mechanisms is crucial for mitigating risks associated with bone cement use in orthopedic surgery.