Bone cement implantation syndrome

Figure 22.1

(A) Normal circulation. (B) Proposed combined model with peripheral vasodilatation, reduced venous return, increased pulmonary vascular resistance and pulmonary embolization, reduced cardiac output, reduced systemic vascular resistance (allowing some counter increase in cardiac output due to reduced afterload) and hypoxia from both the emboli and the pulmonary effects of histamine. (IVC: inferior vena cava; LA: left atrium; LV: left ventricle; PA: pulmonary artery; PV: pulmonary vein; RA: right atrium; RV: right ventricle; SVC: superior vena cava)


(Adapted from: A. J. Donaldson, H. E. Thomson, N. J. Harper, N. W. Kenny. Bone cement implantation syndrome. Br J Anaesth 2009; 102:12–22. Used with permission).


Other etiologic models of BCIS have been presented. Circulating cement monomers may cause vasodilation that may contribute to hypotension during BCIS [9, 11]. This has been shown in vitro, but does not account for all the signs and symptoms of BCIS. Histamine release causing an anaphylactoid reaction has been demonstrated in some studies, but not in others. Further, histamine-blocking agents have not altered morbidity or mortality [15]. A postmortem study involving autopsy of BCIS patients revealed neither elevated histamine nor elevated tryptase levels, casting doubt on histamine-mediated anaphylactoid or anaphylactic etiologies [11]. Additional theories include increased levels of potentially vasoactive endogenous cannabinoids [16] and morphine-induced histamine release as potential contributors to BCIS [11]. Finally, the contribution of a complement activation model involving the vaso- and bronchoactive mediators C3a and C5a has been both confirmed and denied in various studies [9, 17].




4. Review the differential diagnosis for BCIS and compare and contrast diseases with similar presentations


Other conditions may mimic the presentation of BCIS. An anaphylactoid or anaphylactic reaction would give a similar presentation with hemodynamic compromise, shock, and death [18]. Most reactions, however, respond to aggressive resuscitation with fluids and vasoactive agents. Cardiogenic shock, specifically right ventricular failure, would present very similarly to BCIS. In patients with pre-existing right ventricular dysfunction and/or advanced pulmonary hypertension, anesthetic or surgical factors may cause worsening of right heart failure. An example is monitored anesthesia care where excess anesthesia causes hypercarbia, acidosis, and potentially hypoxia secondary to hypoventilation. This perturbation, though tolerated well by most, may cause right heart failure in someone with pre-existing right heart dysfunction and/or pulmonary hypertension.



5. Describe and explain patient management


Preoperatively, several classes of patients seem to be at higher risk for BCIS (Table 22.2) [7, 19]. As a result, it is of paramount importance to risk stratify patients to aid in preoperative optimization, surgical planning, and perioperative management. Those most at risk are patients with a history of heart disease (specifically right ventricular dysfunction), coronary artery disease, or pulmonary hypertension [9–10, 12, 18]. In addition, postmortem evaluation of patients who died from BCIS revealed severe coronary atherosclerosis and myocardial fibrosis in all individuals [11]. These patients have little reserve for the hemodynamic perturbations of BCIS, likely increasing their susceptibility. Other markers of underlying cardiac disease have also been associated with BCIS (e.g., diuretic or warfarin use) [20]. A patent foramen ovale may also enhance the lethality of BCIS by escalating the impact of an embolic event [9]. Interestingly, osteoporosis may enhance embolization due to increased bone pore cavity size and a previously non-instrumented femoral canal is thought to have more tissue available for embolization [18]. The highest risk patients are those receiving a long stem femoral prosthesis for metastatic disease [21, 23].



Table 22.2

Patient risk factors for developing BCIS [8–9, 17, 19].































ASA physical status score of 3 or higher
Pre-existing COPD
Age >85
Male gender
Congestive heart failure
Diuretic or warfarin use
Underlying cardiovascular disease (esp. RV dysfunction, CAD, and/or pHTN)
Fracture type (esp. intratrochanteric or malignancy related)
Metastatic bone disease
Femoral canal diameter of more than 21 mm
Previously non-instrumented femoral canal
Patent foramen ovale
Osteoporosis


CAD: coronary artery disease; COPD: chronic obstructive pulmonary disease; pHTN: pulmonary hypertension; RV: right ventricular.


There are multiple surgical factors that may decrease the chance of BCIS (Table 22.3). The largest impact is by avoiding cemented procedures in the highest-risk patients. Similarly, avoiding bilateral cemented procedures may also be warranted in high-risk individuals. Removal of tissue and lavage of the femoral or other canal prior to cementation has been shown to reduce the chances of BCIS, likely by decreasing the available tissue for embolization [14]. Venting of the distal femoral canal also decreases the medullary pressure experienced by the tissues and cement, thus minimizing the forces pushing emboli into vascular spaces [9, 14].



Table 22.3

Surgical considerations to reduce BCIS [8, 13, 22].



















Avoidance of bilateral cemented procedures
Lavage of the femoral canal
Removal of tissues before cementation
Venting the femur
Minimizing prosthesis length
Use of low-viscosity cement
Preparation of cement in a vacuum

In patients undergoing hemiarthroplasty for pathologic or impending fractures one must expect a longer prosthesis to be placed into the femur. The longer implant allows for stabilization of the bone distal to the metastatic lesion preventing a future fracture. Insertion of a long stem cemented prosthesis requires a larger cement burden and more instrumentation of the femoral canal, therefore making these patients extremely high risk for developing BCIS [21]. Intraoperative mortality in this patient population has been described at 4.3% in the setting of a pathologic fracture [8]. Even non-cemented long stem intramedullary nails have been associated with hypotension or hypoxia in 25% of patients.


Patients at high risk of developing BCIS should receive more aggressive preoperative preparation than that done for low risk ones [9, 20]. This may involve large-bore intravenous access, invasive blood pressure monitoring, and the consideration of central venous access. General endotracheal intubation is the anesthetic of choice to permit high FiO2 concentrations and the use of positive-end expiratory pressure should BCIS occur. Adequate intravascular volumes should be administered throughout the procedure, especially at the time of cementation, to help with blood pressure control. The use of neuraxial anesthesic should be approached with caution in the high-risk patient. The vasodilatation and sympathectomy often achieved with neuraxial anesthesia can make management of an episode of BCIS extremely difficult. The use of an epidural for postoperative analgesia can be considered and has been shown to provide superior analgesia in lower extremity tumor surgery [24].


Should BCIS occur, the patient should be placed on 100% FiO2 and the airway secured, if not already done. Invasive arterial monitoring and possibly central venous access should be established but should not interfere with the resuscitation effort. Inotropic support for right ventricular failure and cardiogenic shock should be initiated. Afterload should be supported to ensure coronary and cerebral perfusion. Transesophageal echocardiography may help to guide management.

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Jan 24, 2017 | Posted by in ANESTHESIA | Comments Off on Bone cement implantation syndrome

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