Partially controllable: canal prep to minimise blood and fat inclusion; broach to leave 2mm cancellous bone proximally; pulsatile lavage; brush and dry; adrenaline gauze/H2O2; suction
Monomer leakage on pressurisation -> vasodilatation and cardiosuppression
Triad: desaturation, hypotension, arrythmia
Donaldson classification: Grade 1: SpO2 <94%/fall in SBP 20%; Grade 2: SpO2 <88%/fall in SBP 40%/unconsciousness; Grade 3: requiring CPR
Prevention: increase O2 at cementation, medullary lavage, meticulous haemostasis, do not inject before dough time
Q7How does cement viscosity affect its use?▸
Viscosity = internal friction of the fluid; mainly a concern in THR (TKR is pressurised easily)
Low viscosity: better interdigitation into cancellous bone but cannot stop bleeding; poorer clinical result in THR (less effective marrow displacement, haemodynamic backflow)
High viscosity: may not be usable in a cement gun for medullary insertion
Medium viscosity: usable with cement gun pressurisation and can stop bleeding; modified by temperature, humidity, mixing conditions; Simplex-P is medium viscosity
Q8What are the local and systemic complications of bone cement?▸
Systemic: cardiopulmonary suppression, emboli
Local: bone necrosis
Systemic syndrome: bone cement implantation syndrome
Q9What is the pathophysiology of bone cement implantation syndrome?▸
Monomer leakage into the bloodstream upon pressurisation -> vasodilatation and cardiosuppression
Release of endothelial mediators, histamine and complement activation
Mechanical blockage / multiple embolisation theory: high pressure during insertion + exothermic cement reaction -> cement expands; air and marrow contents embolise
Q10What are the risk factors and prevention of bone cement implantation syndrome?▸
Patient: ASA 3-4, known pHT/IHD, osteoporosis; pathological fracture/fracture TOF, long stem
Anaesthetic prevention: close monitoring and increase O2 at cementation; avoid volume depletion