- BCIS occurs in 20% of cemented arthroplasties
- Only 0.5 - 1.7% of these are Grade 3
- The highest incidence is in cemented hemiarthroplasty, but can occur in other cemented procedures including TKR and THR
Bone Cement Implantation Syndrome
Bone Cement Implantation Syndrome
This topic appeared as part of a CRQ on intra-operative cardiac arrest in September 2024.
Resources
- BCIS is a potentially fatal complication of orthopaedic surgery involving pressurised bone cement
| Patients at high risk |
| ASA III or IV |
| Pulmonary hypertension or systemic hypertension |
| Significant cardiac or pulmonary disease |
| Male gender |
| Increasing age |
| Drugs: diuretics, warfarin |
| Bone disease: osteoporosis or bony metastases |
- Cardiovascular disease such as atherosclerosis, angina, heart failure or use of ACE-I/β-blockers are not predictive of Grade 2 or 3 BCIS
Theoretical models
- The embolic model describes embolization of medullary contents into the circulation by the presence of expanding cement in the intramedullary space
- Such emboli include air, fat, marrow, cement, bone particles and fibrin/platelet aggregates
- These contents are embolised to the pulmonary and/or coronary circulations, leading to:
- Mechanical effects of emboli
- Local mediator release increasing PVR
- The multimodal model is used to account for the fact that the degree of embolisation:
- Correlates poorly with the extent of hypoxia and hypotension
- Cannot alone account for all the features of BCIS
- It describes increased complement (C3a and C5a) levels and raised plasma histamine concentrations in response to the methyl methacrylate cement
- These mediators cause increased PVR, V/Q mismatch, hypoxia, RV failure and cardiogenic shock
Pathophysiolgoical effects
- The main pathophysiological effects of BCIS are:
- Hypoxia
- Increased PA pressure (increased PVR)
- V/Q mismatch
- Hypotension
- RV dilation occurs
- Causes shifting of interventricular septum into LV
- This reduces LV compliance, LV filling and thus cardiac output
Timing
- Features of BCIS typically occur at the time of bone cementation and prosthesis insertion
- It can, however, occur:
- Before cementation e.g. during femoral reaming
- After cementation e.g. during joint reduction and limb tourniquet deflation
Features
- Classically results in a combination of:
- Arterial hypoxaemia
- Cardiovascular disturbance, typically:
- Hypotension
- Raised PVR and resultant reduction in RV ejection fraction
- Also arrhythmias, cardiogenic shock or cardiac arrest
- Loss of consciousness
Classification
| Feature | Grade 1 | Grade 2 | Grade 3 |
| Incidence | ~20% | 3-5% | ~1% |
| SpO2 | <94% | <88% | - |
| Systolic BP fall | >20% | >40% | CV collapse |
| Loss of consciousness | No | Yes | Cardiac arrest |
| 30-day mortality | 9.3% | 35% | 88% |
| 1-year mortality | 30% | 48% | 94% |
General
- Identify high-risk patients during team brief
- Discuss alternate surgical strategies
- Use of a 'Cement Curfew', which starts at cement mixing and ends when the hip is relocated
Anaesthetic
- Euvolaemia; avoid intravascular volume depletion
- Ensure good cardiac output prior to cement insertion with SBP within 20% of pre-operative value
- Increase FiO2 at the time of cementation
- Measure BP every 2.5mins during cement curfew (if no invasive BP monitoring)
Surgical technique
| Femoral intramedullary canal | Cement-associated |
| Lavage before cementing (High-pressure, high-volume, pulsatile) |
Bone - vacuum cementing technique |
| Depressurising via suction catheter | Retrograde insertion |
| Brushing and drying of canal | Use of low-viscosity cement |
- BCIS is a time-limited phenomenon and therefore treatment is supportive and aggressive
- PA pressures usually normalise within 24hrs
- Secure airway
- Administer 100% oxygen
- Support cardiovascular physiology with:
- Invasive monitoring e.g. arterial line, central line, CO monitoring
- Volume resuscitation e.g. crystalloid bolus to maintain RV preload
- Vasopressors
- Positive inotropy e.g. β1 agonists
- Standard ALS if cardiac arrest