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OK - Modul Ortho - Bone Cement Implantation Syndrome
OK - Modul Ortho - Bone Cement Implantation Syndrome
SYNDROME (BCIS)
MODUL ORTHOPEDI – 2 R3
FUD – PAM – VIK – DRI – WIT – PIL – KIS – AYO – GAR – NAD
INTRODUCTION
There have been multiple reports of this phenomenon since the approval of
MMA cement by the FDA in 1971 for orthopedic procedures
Additional proposed
theories focus on the role Nearly all the studies and
of histamine release, models used to explain
complement activation, BCIS are based on research
and multimodal involving hip arthroplasties
possibilities
PATHOPHYSIOLOGY
Multimodal Model
Embolic model (Histamine release, hypersensitivity and
complement activation)
• The cement then expands in the space • Anaphylaxis and BCIS share many
between the bone and the prosthesis features (significant increase in plasma
pressurising air and the medullary histamine concentration)
contents forcing into the circulation • Surgeon contact with Methyl
• These embolic contents include fat, Methacrylate (MMA) increase in
marrow, cement, air, bone particles, and blood levels of C3a and C5a
aggregates of platelets and fibrin (anaphylactoid complements and are
• They may reach the lungs, heart, and potent mediators of vasoconstriction and
coronary circulation bronchoconstriction)
• Showers of pulmonary emboli hypoxia • These mediators yield an increase in
and right ventricular dysfunction pulmonary vascular resistance, causing
leading to hypotension V/Q disturbances, hypoxia, right
ventricular failure, and cardiogenic shock
PATHOPHYSIOLOGY
This exothermic reaction leads to hardening of the cement and expansion against the prosthetic
components
The resultant canintramedullary hypertension (>500 mm Hg) cause embolization of fat, bone
marrow, cement, and air into venous channels
The release of tissue thromboplastin may trigger platelet aggregation, microthrombus formation in
the lungs, and cardiovascular instability as a result of the circulation of vasoactive substances
RISK FACTOR
CLINICAL FEATURES
Clinical signs of BCIS plus the sudden reduction in ETCO2 are strong
indicators of BCIS; however, a definitive diagnosis is made by computed
tomographic scan
CLINICAL FEATURES
Even with large embolic loads, healthy hearts may recover in seconds to minutes
The underlying mechanism – acute pulmonary hypertension and secondary right ventricular
failure – should be considered reversible
Aggressive stabilisation and supportive therapy are the cornerstones in managing BCIS
For patients who have not met the criteria for severe BCIS but who have a suspicious clinical
picture, they should be monitored closely in a high-dependency unit for at least the first 24 hours
after the operation
TERIMA KASIH