|LETTER TO EDITOR
|Year : 2011 | Volume
| Issue : 2 | Page : 240-242
Bone cement implantation syndrome: A rare catastrophe
Nikhil Mudgalkar, KV Ramesh
Department of Anesthesia, Prathima Institute of Medical Sciences, Karimnagar, Andhra Pradesh, India
|Date of Web Publication||9-Apr-2012|
D 101, PIMS Campus, Nugnur, Karimnagar, Andhra Pradesh
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Mudgalkar N, Ramesh K V. Bone cement implantation syndrome: A rare catastrophe. Anesth Essays Res 2011;5:240-2
Bone cement implantation syndrome (BCIS) is characterized by hypoxia, hypotension or both and/or unexpected loss of consciousness occurring around the time of cementation, prosthesis insertion, reduction of the joint or, occasionally, limb tourniquet deflation in a patient undergoing cemented bone surgery. 
The following case report describes a cardiac arrest in a patient undergoing a cemented hemiarthroplasty. This report provides further clinical evidence of the risks and consequences of fat embolization during hip arthroplasty surgery. Data concerning the fatalities of BCIS is sporadic and rare, so more and more reporting of data may help in understanding the condition better.
A 68-year-old male patient was admitted to our hospital with history of fracture neck of femur left. He had history of fall one day ago. Patient was dyspnoeic at rest (Grade IV) on admission. On evaluation, he was found to have fibrosis of the left upper lung with collapse of the left lower zone. He was a chronic smoker. Other medical history included hypertension since six years and bronchial asthma since six years, on irregular medication; old Pulmonary Koch's which was irregularly treated 20 years ago. ECG Electrocardiogram showed premature ventricular ectopics. On admission, patient was stabilized with anti-hypertensive medications, anti-asthma medications and oxygen. Active Koch's was ruled out. After five days of treatment the patient felt symptomatically better, and it was decided to operate the patient for Austin Moore prosthesis (hemiarthroplasty).
On the day of surgery, the patient was conscious and coherent, with a pulse rate of 92/ min, blood pressure of 150/90 mm hg in supine position, respiratory rate was 22 and patient was not dyspnoeic. His cardiac examination was normal while respiratory examination showed decreased breath sounds on the left side; there were no adventitious sounds on either side. His investigation revealed hemoglobin of 9.8 g%, blood sugar of 117 mg/dl, blood urea of 50 mg/dl and serum creatinine of 1.9 mg/dl.
Patient was taken onto the operation table and monitors (pulse oximetry, NIBP non invasive blood pressure and electrocardiogram monitors) were applied. In view of the respiratory condition of the patient, it was decided to proceed with regional anesthesia (epidural). Under all aseptic precautions, epidural space was identified with loss of resistance technique with 16-gauge tuhoy needle at 6 cm from the skin, 18-gauge epidural catheters were inserted and fixed at 9 cm from the skin at the L2- L3 level. Injection Ropivacaine 0.75% 10 ml was given in titrated doses. After 15 min, adequate anesthesia (T10) level was obtained. The patient's blood pressure dropped to 130/80 mm of hg with NIBP and pulse rate was 84/ min and respiratory rate was 20/min. Patient was put on oxygen supplementation of 5 lit/min with face mask. Lateral position was given. Blood pressure was 130/84 mm hg and pulse rate 82/ min, respiratory rate was 20/ min after painting and draping procedure was started. The hemodynamics and respiration was normal during the procedure. After 45 min of surgery, medullary reaming was completed and bone cement (surgical simplex P, stryker) was applied. On application of bone cement, patient developed sudden bradycardia, with a heart rate of 20/ min, peripheral pulses were not felt, blood pressure was not recordable with NIBP. Patient became apnoeic and unconscious. Immediately, endotracheal intubation was done in lateral position with 7.5-mm portex endotracheal tube. Wound was packed and patient was shifted to supine position. Patient was ventilated with 100% oxygen, and effective cardiac compression started. Intravenousfluids were started; injection adrenaline 1 mg (1:1000) was given Intravenous, injection atropine 0.6 mg (1:1000) given and external cardiac compression started. After five cycles of cardiopulmonary resuscitation pulses were palpable and heart rate was 130/min, it was a sinus rhythm. Systolic blood pressure was recorded as 90 mm Hg. Intravenous fluids were continued to maintain preload along with inj dopamine 10 mcg/kg/min. Surgical closure was done and patient was shifted to acute medical care unit with life support.
In AMC, patient was put on ventilator, with dopamine support (10 mcg/kg/min) to maintain blood pressure around 100 mm Hg systolic and internal jugular catheterization was done to assess central venous pressure (CVP), which was around 12 cm throughout the period. Fluids were guided by CVP. Arterial blood gases and chest X-ray revealed no additional findings. Patient did not regain consciousness.
After eight hours of surgery, patient developed sudden pulseless electric activity, CPR was initiated including external cardiac compressions and injection atropine 0.6 mg IV and injection adrenaline 1 mg (1:1000); they were repeated every 3 min till three doses. Patient could not be revived after one hour of resuscitation.
Patient's relatives did not consent for necropsy.
| Discussion|| |
Bone cement is an acrylic substance used to secure implants to bone or to fill joint cavity. Bone cement is a filler and not an adhesive. The contents include methylmethacrylate monomer, a colorless flammable liquid, barium sulphate added to make cement radio-opaque, and polymer component - a white powder and benzyl peroxide.
Bone cement implantation syndrome is now an established entity, though there is no widely accepted definition to it. The cases range from a mild form like transient hypoxemia to a fatal form including death.
Severity classification of BCIS is as under: 
Grade 1: moderate hypoxia (SpO 2 <94%) or hypotension [fall in systolic blood pressure (SBP) >20%]
Grade 2: severe hypoxia (SpO 2 <88%) or hypotension (fall in SBP >40%) or unexpected loss of consciousness.
Grade 3: cardiovascular collapse requiring CPR.
The incidence of BCIS varies widely in the literature and fatalities have been rare. In India two fatalities have been reported from Max Hospital, Delhi.  The etiology and pathophysiology of BCIS has not been completely understood. Various theories have been proposed including release of polymethyl methacrylate monomer into circulation during cementation.; recent studies focus on emboli formed during cementation and resultant right ventricular failure.
Embolization occurs as a result of high intramedullary pressures developing between cement and prosthesis insertion. The cement undergoes an exothermic reaction and expands between the space of the bone and prosthesis trapping air and medullary contents under pressure. The temperature of cement can increase up to 96 degrees centigrade. When prosthesis is put, the contents escape into the interstices of bone because of already developed intramedullary hypertension. This leads to embolization. Knowing that the extent of embolization is proportional to the intramedullary pressure.
The debris from the medulla can embolize to the lungs and heart. It is the shower of pulmonary emboli that result in characteristic circulatory changes leading to hypoxia and right ventricular dysfunction, though the degree of cardiovascular collapse is not proportional to the degree of embolization.
Numerous patient-related risk factors have been implicated in the genesis of BCIS including old age, poor preexisting physical reserve, impaired cardiopulmonary function, preexisting pulmonary hypertension, osteoporosis, bony metastases, and concomitant hip fractures, particularly pathological or intertrochanteric fractures. 
Surgical risk factors include previous uninstrumented femoral canal, and use of long-stem femoral component. 
Anesthetic risk for BCIS can be reduced by meticulous preoperative examination to rule out significant cardiac, pulmonary or metastatic bone diseases, complete investigation of the patient's co-morbid diseases and careful pre-optimization of the patients. Increasing the inspired concentration of oxygen should be considered at the time of cementation.  Hemodynamic monitoring should be considered for all cases that are particularly at risk for BCIS. 
Surgical risk reduction strategies for BCIS include medullary lavage, good hemostasis before cement insertion, minimizing length of prosthesis, using non-cemented prosthesis and venting the medulla.  Venting the medulla permits air to escape from the end of the cement plug and reduces the air embolus.
A fall in end-tidal carbon dioxide concentration can be the first sign of the embolism and should alert the anesthesiologist. In awake patients, first symptoms may include dyspnoea and altered sensorium.  If there is an evidence of BCIS, inspired oxygen concentration should be 100%, and it should be continued in the postoperative period. The hemodynamic collapse of the BCIS should be treated on the lines of right ventricular failure.  Aggressive resuscitation with IV fluids has been recommended. 
Choice of vasopressor is generally sympathetic alpha 1 agonist in view of the right heart failure and vasodilatation.
In our case as mentioned above, the patient was a high-risk candidate for BCIS as he was an elderly patient having severe cardiopulmonary disease with decreased functional reserve (age 68 years, pulmonary fibrosis, bronchial asthma and systemic hypertension, old pulmonary Koch's). Immediately after putting bone cement, patient developed sudden bradycardia hypotension, and unconsciousness. Patient was resuscitated with endotracheal intubation and ventilation with 100% oxygen supplementation, effective cardiac compression, and injection adrenaline. Patient revived after five cycles of CPR, fluids were loaded and patient was treated on the lines of right ventricular failure. Patient developed pulseless electric activity after eight hours of surgery and could not be revived. This was Grade III bone cement implantation syndrome, despite our best efforts we could not revive the patient.
So, in conclusion, we should take extra precaution while using bone cement in patients with co-morbid diseases, increase inspired oxygen concentration while using bone cement, and keep a close vigil on the patient's hemodynamic status during and after use of bone cement to prevent unexpected fatalities; "detect early and act fast" to save the patient.
| References|| |
|1.||Donaldson AJ, Thomson HE, Harper NJ and Kenny NW. Bone cement implantation syndrome. Br J Anaesth 2009;102:18. |
|2.||Govil P, Kakar PN, Arora D, Das S, Gupta N, Govil D, et al. Bone cement implantation syndrome: A report of four cases. Indian J Anaesth 2009;53:214-8. |
|3.||Byrick RJ, Forbes D, Waddell JP. A monitored cardiovascular collapse during cemented total knee replacement. Anesthesiology 1986;65:213-6. |
|4.||British Orthopaedic Associations. Primary total hip replacement: A guide to good practice. 2006. Available from: http://www.boa.ac.uk/site/showpublications.aspx?ID=59 [Last accessed on 2011 June 30]. |
|5.||Duncan JA. Intra-operative collapse or death related to the use of acrylic cement in hip surgery. Anaesthesia 1989;44:149-53 |
|6.||Byrick RJ. Cement implantation syndrome: A time limited embolic phenomenon. Can J Anaesth 1997;44:107-11. |
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