Bone cement implantation syndrome

Overview

 

Aim:
The aim of the work is to inform the readers about the bone cement implantation syndrome, and to remind them about various risk factors and recommended procedures.

Type of work:
Review article with a case report.

Materials and results:
The author illustrates a fatal course of bone cement implantation syndrome on a case report. In the following discussion, the author deals with the aetiology of origin and procedures, which may be applied as a prevention of bone cement implantation syndrome.

Conclusion:
Bone cement implantation syndrome is a reaction, which may occur with the use of bone cement. It is manifested with hypotension, hypoxia, and may result in cardiac arrest and death of the patient. The cause of BCIS is not precisely known, and is most probably multifactorial. It is advisable for the operating surgeons to bear this threat in mind and take preventive measures, in order to decrease the risk of BCIS development.

Keywords:
Bone cement implantation syndrome, femoral neck fractures, hemiarthroplasty

INTRODUCTION

Bone cement implantation syndrome (BCIS) occurs suddenly, during the implantation of bone cement or shortly afterwards, and is characterized with hypotension, hypoxia, arrhythmia, and may result in cardiac arrest. This syndrome is observed in up to 28% of patients [6].

The first reported case of patient death due to BCIS comes from 1970 [7]. In 2009, Donaldson divided BCIS into three categories:

1^st  degree is characterized with a drop of saturation below 94% or a decrease of systolic blood pressure by more than 20%.

2^nd degree includes drop of saturation below 88% or a decrease of systolic blood pressure by more than 40% or sudden loss of consciousness.

3^rd degree is characterized with circulatory failure, requiring cardiopulmonary resuscitation [1, 5].

In 2009, National Patient Safety Agency in the United Kingdom informed the general public about the problems of BCIS, and requested a definition of guidelines, which should result in decreasing the risk of BCIS. The first concise guideline, which was prepared in cooperation with anaesthesiologists, orthopaedists and geriatrists, was published in 2015. This guideline consists of three basic points [3]. The first one describes assessment of risk factors in the individual patient. The risk factors listed here include high age, serious heart or pulmonary disease and use of diuretics. Higher incidence is reported in men. The second point describes preparation of the surgical team for the procedure, namely identification of the patient and prevention of wrong-side surgery. The third point describes the work of the surgeon and anaesthesiologist during bone cement implantation. The surgeon should flush thoroughly the canal prepared for insertion of the stem, and inform the anaesthesiologist about the use of cement; furthermore, he should use injector gun for correct administration and avoid too strong pressure in the canal during cement administration. The anaesthesiologist should maintain normovolemia during the surgery, confirm the surgeon the information regarding cement administration and have vasopressors ready for cases of sudden circulatory collapse [3].

CASE REPORT

Woman, 90 years of age, fell at home in the morning on her way to the toilet, discovered by family members in the afternoon. The patient was transported by ambulance to emergency department with pains in her right hip. The performed radiograph of the pelvis and hip (Fig. 1) revealed a femoral neck fracture on the right side.

The patient was admitted to traumatology, and was prepared for the surgical procedure. The patient was indicated for cervico-capital prosthesis of the femoral head. Upon admission, the patient was dehydrated, laboratory examination revealed hyperkalaemia, decreased function of the thyroid gland and high blood pressure. Infusion and analgesic therapy was started at the department. Pre-anaesthesia and internal medicine assessment was performed two days after the injury. The patient was able to undergo the surgical procedure, with ASA 3-4 risk. Control laboratory examination was performed on the third day in the morning, with correction of the internal environment. The procedure was performed under routine spinal anaesthesia. The patient was circulatory stable during the whole procedure. Blood pressure 120/60, saturation 98%. Cement was mixed in the open air, and administered manually. Approximately four minutes after cement administration, the patient’s circulatory stability suddenly worsened, blood pressure dropped to 70/30, saturation to 60%, with subsequent cardiac arrest. The anaesthesiologist initiated resuscitation, with administration of 1 mg of Adrenalin. The circulation was restored after approximately one minute. However, the patient was further circulatory unstable, and required support with continuous administration of Noradrenalin at 3 mg/hr. The surgery was quickly finalized, with blood loss of 200 ml. The patient was transferred to intensive care unit, nevertheless, with progreding circulatory instability. The dose of Noradrenalin was increased to up to 6 mg/hr. The patient died approximately one hour after the end of the surgical procedure. Autopsy of the patient was not performed.

DISCUSSION

In differential diagnostics of a sudden drop of blood pressure and saturation during surgery, the following factors may be considered: large blood loss, pulmonary embolism, deepening of the general anaesthesia, total subarachnoid anaesthesia, allergic reaction or infarction. In the presented case report, no large blood loss was observed. The procedure was performed in spinal anaesthesia, the anaesthesiologist ruled out a total subarachnoid anaesthesia. The performed electrocardiogram did not reveal any acute myocardial ischemia. No exanthema was observed on the skin, which would point towards a possible allergic reaction. Pulmonary embolism caused with releasing of a venous thrombus may have been the cause of circulatory failure. The bone cement implantation syndrome may be detected during autopsy as microembolization of numerous organs, with the emboli consisting of a mixture of bone marrow and cement [9]. In our presented case report, the autopsy was not required or performed, that is why it is not possible to confirm, whether the patient sustained a pulmonary embolism or BCIS. However, as the circulatory failure followed shortly after cement administration, it is possible to assume the presence of BCIS. Chart 1 shows the development of systolic arterial blood pressure values in time during surgery in four patients, in whom cemented cervico-capital endoprosthesis of the hip joint was implanted. The values of systolic arterial blood pressure dropped in all patients following bone cement administration, in two patients (patient No. 1 and patient No. 4) by more than 20%. Such decrease of blood pressure may be considered as 1^st degree of BCIS.

The exact mechanism of BCIS onset is not known, and is most probably multifactorial. At present, there exist several theories attempting to explain the cause of BCIS. All theories are subject of further research and testing. The most frequently mentioned theories include monomer, microembolization, histamine, hypersensitive or the theory of complement activation [1].

Monomer theory

The basic composition of bone cement are methyl methacrylate monomers (MMA), which polymerize and stiffen during exothermic reaction. This theory presumes infiltration of individual MMA monomers into blood circulation. It has been proven in vitro, that these monomers cause vasodilatation. Animal studies have shown that the concentration of MMA in blood is significantly lower than minimal value, which would be able to influence blood circulation. That is why this theory is gradually being abandoned [1].

Microembolization theory

The role of microembolization is the most probable cause of BCIS. Emboli were proved with transoesophageal echocardiography in the right atrium, ventricle and pulmonary artery. Autopsies confirmed microembolization in the area of pulmonary circulation in animals and adults [9]. Microembolization does not cause only mechanical obstruction of the respiratory passageways, also the endothelium is damaged and mediators activated, which leads to vasoconstriction and increase of pulmonary vascular resistance [2]. However, the microembolization by itself cannot explain all possible manifestations of BCIS, that is why also other mechanisms are presumed to participate upon the manifestation of BCIS [1].

Hypersensitivity

This theory was inspired by the demonstrable increase of plasma concentrations of histamine in patients with hypotension during cementing. There has been only one clinical trial conducted based upon this theory, dealing with the use of blockers of histamine receptors. The results of the study were inconclusive, that is why this theory has been gradually abandoned [1, 12].

Theory of complement activation

Increased levels of complement components, more precisely C3a and C5a were observed during surgical procedures with bone cement administration. These components potentiate vasoconstriction and bronchoconstriction. However, a clinical trial studying administration of high doses of Methylprednisone did not confirm any clinical effect. Other performed studies aimed at complement activation were inconclusive [1].

Multifactorial theory

Various opinions have emerged lately, which define the onset and course of BCIS as multifactorial. All the above-presented theories have their share upon influencing BCIS occurrence. The multifactorial effect results in increase of pulmonary vascular resistance, microembolization into the right heart, decrease of the cardiac output and hypoxia. This model seems to be most probable, and also is able to explain all symptoms which may appear. Nevertheless, no clinical trial aimed at confirming this theory has been conducted so far [1].

RISK FACTORS

A large clinical trial was performed in Sweden in 2014, which concentrated upon the incidence and risk factors of BCIS. A total of 1,016 study subjects were enrolled in the clinical trial. The incidence was 21%, 5,1%, and 1,7% of the first, second and third degrees of BCIS, respectively.

Statistically significant risk factors, as defined by this study, include ischemic heart disease with syndrome of angina pectoris, chronic heart failure, and chronic obstructive pulmonary disease. Furthermore the use of beta-blockers, diuretics, ACE inhibitors and Warfarin. The study also proved that there exists no statistically significant difference in long-term survival of patients undergoing surgical procedures without BCIS occurrence, when compared to patients who experienced the 1^st degree of BCIS only. However, as far as the second and third degree of BCIS is concerned, these were associated with a significantly shorter long-term survival [6]. The patient from our case report suffered from several significant risk factors, which may have contributed to the onset and more serious course of BCIS.

PREVENTION

Decreasing the risk of BCIS onset is an important part of preoperative preparation in individual patients, correct selection of the surgical procedure is equally important. Furthermore, it is important to obtain personal history of the patient during pre-operative assessment, in order to be able to evaluate the risk factors. It is also crucial to maintain normovolemia and sufficient saturation with oxygen, prior to the surgical procedure and also during its course [11]. Implantation of Swan-Ganz catheter in patients with a high risk, as recommended by some authors, is very questionable, due to the high invasiveness of the procedure itself. New animal study has been prepared, with vena cava filter implantation into vena cava inferior as a prevention of microembolization [4]. Among the surgical techniques reducing the risk of BCIS belong namely thorough medullary lavage following rasping and preparation of the marrow cavity in order to remove remnants of bone marrow, consistent haemostasis in order to reduce blood loss, vacuum mixing of the cement and use of injector gun [10]. Another discussed technique is drilling a hole in the lower part of the diaphysis intended for decreasing the pressure during cement administration. In the presented case report, injector gun was not used, nor vacuum mixing of the cement. The use of these tools and procedures would have been advantageous, as it would certainly have reduced the risk of BCIS occurrence. Another alternative of reducing BCIS is the use of uncemented endoprostheses [2, 8]. The use of uncemented endoprostheses is associated with a higher risk of periprosthetic fractures; however, the occurrence of BCIS is excluded. Clinical studies performed lately did not prove a statistically significant difference in long-term survival of patients with uncemented endoprosthesis when compared with patients, in whom cemented endoprosthesis was used [8]. Yet another important component of the surgical procedure is the communication and cooperation between the operating surgeon and the anaesthesiologist at the operating theatre, and notifying the anaesthesiologist about administration of cement.

CONCLUSION

Bone cement implantation syndrome is a relatively unexplored phenomenon, which may become manifested, to a certain degree, in up to one third of patients. Despite its so-far unexplained aetiology and pathophysiology, it is necessary to bear this possible complication in mind. In the presented case report, all clinical manifestations pointing towards BCIS were present: sudden drop of blood pressure and saturation occurred shortly after bone cement administration, with subsequent circulatory failure. Unfortunately, the patient did not undergo autopsy, which would have confirmed the diagnosis of bone cement implantation syndrome. The recommended procedure of preparing the patient for surgery with administration of bone cement could be divided into three stages. The first stage consists of precise collection of the patient history, information regarding permanent medication and evaluation of risk factors. The second stage includes a thorough pre-operative preparation, i.e. maintaining homeostasis, sufficient hydration and oxygen saturation. The third stage is the surgical procedure as such. The operating surgeon should perform adequate haemostasis of the surgical wound, in order to eliminate the blood loss. Vacuum mixing of bone cement is recommended, together with using an injector gun, in order to eliminate the passage of cement monomers into blood circulation. The operating surgeon should notify the anaesthesiologist about administration of cement. The use of uncemented cervico-capital endoprostheses is a treatment of choice, which is not widely used in our country, though. Implantations of Swan-Ganz catheter or drilling a hole in the lower part of the femoral diaphysis remain among debatable techniques, which cannot be strongly recommended.

It is clear that bone cement implantation syndrome will require further studies and exploration which would help us fully understand the essence of all processes occurring in the organism during cement administration.

Used abbreviations: ASA – American Society of Anaesthesiologists

Filip Čechlovský, MD

cechlovskyfif@gmail.com