The Bone Cement Hypercoagulation Syndrome: Pathophysiology, Mortality, and Prevention.
Ola E DahlAre Hugo PrippMark JaradehJawed FareedPublished in: Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis (2023)
Since Charnley introduced acrylic cement to seal metallic hip prostheses in the 1950s, reports of perioperative fatal cardiorespiratory and vascular dysfunctions have been published. Studies on humans and animals have shown neurogenic stimulation and substantial local and systemic activation of coagulation are caused by surgical bone marrow damage and chemical cell destruction by toxic monomeric methyl methacrylate from the implanted cement and other tissue-released substances. Venous blood-borne cell fragments and conjugates of activated cells from the surgical site are sequestered and trapped in the pulmonary microcirculation. A substantial hypercoagulation occurs in the lung circulation. Hypercoagulable blood is passed over to the arterial side and may cause vessel obliteration and organ damage. This process may affect the brain, heart, and kidneys and, through the release of vasoactive substances, introduce hemodynamic imbalances that can lead to fatal outcomes in susceptible populations such as elderly patients with hip fractures. The main underlying pathophysiologic processes leading to these occasionally devastating outcomes are a substantial activation of coagulation and cell destruction caused by the toxic substance released by curing bone cement and several vasoactive substances.
Keyphrases
- single cell
- bone marrow
- cell therapy
- drinking water
- oxidative stress
- heart failure
- mesenchymal stem cells
- bone mineral density
- randomized controlled trial
- spinal cord injury
- patients undergoing
- emergency department
- cardiac surgery
- type diabetes
- stem cells
- middle aged
- body composition
- multiple sclerosis
- cardiovascular disease
- blood brain barrier
- adipose tissue
- case report
- bone loss
- resting state
- subarachnoid hemorrhage
- functional connectivity
- meta analyses