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Bone cement implantation syndrome

Bone cement implantation syndrome. Dr Alyani HSNZ. Table of content. case illustration introduction definition incidence clinical features aetiology and pathophysiology risk factors risk reduction and management. CASE ILLUSTRATION.

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Bone cement implantation syndrome

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  1. Bone cement implantation syndrome Dr Alyani HSNZ

  2. Table of content • case illustration • introduction • definition • incidence • clinical features • aetiology and pathophysiology • risk factors • risk reduction and management

  3. CASE ILLUSTRATION

  4. Case illustration 1Indian Journal of Dental and Medical Sciences, December 2013 • 51 years old malay male involved with motor vehicle accident. He complaint of pain over right hip and unable to ambulate after that. • He is a chronic smoker and did not have any medical illness before. • Right hip radiograph showed comminuted fracture neck of right femur extending to lesser tubercle.

  5. He was planned for bipolar hemiarthroplasty and posted for operation on day 3 of admission • Spinal anaesthesia was performed at spinal level of L3,L4 • One and half hour of surgery,during reaming of medulary cavity, the surgeon noted hairline fracture extending to midshaft of the femur hence planned to attach the implant with bone cement

  6. One minute after cement implantation, there was severe bradycardia, hypotension and desaturation until 78% and he went into cardiac arrest. • The surgery was stop, he was repositioned and CPR was commenced. He was intubated with ETT size 8.0mm. • After 2cycles of chest compression his conscious level improving and bradycardia and hypotension also improved. • The surgery then proceed uneventfuly

  7. Case illustration 2Malaysian Journal of Pathology, December 2013 • A 59-year-old Indian lady had allegedly slipped and fallen in a sitting position in the bathroom of her house. • She was admitted to hospital and was subsequently diagnosed to have a closed fracture of the neck of her left femur. • She underwent total hip replacement surgery under combined spinal epidural anaesthesia. • During the operation, upon completion of bone cementing, her heart rate suddenly dropped from 100 to 55 per minute, oxygen saturation fell to 76% and she became unresponsive.

  8. Intravenous adrenaline and atropine were immediately given, however, her blood pressure and heart rate continued to fall • The patient was immediately sedated and intubated. • After completion of the surgery, she was transferred to the intensive care unit (ICU). • However despite full inotropic support, she did not respond and passed away approximately twelve hours post procedure • An autopsy examination was subsequently performed

  9. INTRODUCTION

  10. introduction • Bone cement was introduced in 1970 • Bone cement is a surgical material used in joint arthroplasty surgery, filling of a bone defect, use in orthopeadic tumour surgery etc • contain 'pearls' that has pre polymerized PMMA (polymethyl metacrylate) in a powder form + liquid monomer of methyl metacrylate (MMA) = mixed with addition of catalyst that initiate polymerization of monomer --> paste. • BCIS is firstly reported after 10years of introduction of bone cement

  11. Under reported • Usually described with hip arthroplasty, however it can occur in any procedure that use cement • May occur at any stage of bone surgery: • femoral reaming • acetabular or femoral cement implantation • insertion of prosthesis • joint reduction • limb tourniquet deflation

  12. DEFINITION AND GRADING

  13. Definition • No agreed definition • Confluent of clinical features that includes: • Hypoxia • Hypotension • cardiac arrythmias • increased pulmonary vascular resistence (PVR) • cardiac arrest

  14. GRADING

  15. incidence

  16. Clinical features

  17. significant transient reduced in O2 saturation and SBP profound CVS changes (arythmia/ shock/arrest) • Spectrum of severity • Increased PVR • increased pulmonary arterial pressure • RV EF reduced (further distended RV pushing septum to LV, further reducing filling) • reduce SV • reduce CO • reduced MAP • transient but may persists up to 48hours

  18. Features suggestive of cerebral vessel embolisation such as delirium or focal neurological deficit • emboli from the canal that escape pulm circulation or thru a potent foramen ovale • evidence by demonstrated cerebral emboli by doppler USG in 40-60% of patient undergoing joint arthroplasty

  19. Aetiology and pathophysiology

  20. The pathophysiology and pathogenesis of BCIS is not fully understood • Suggested model: • monomer mediated model • embolic model • histamine release and hypersensitivity • multimodal model

  21. Monomer mediated model • MMA monomer in circulation causing vasodilatation • but not supported as plasma MMA level after cemented arthroplasty < required level to cause CVS effect • Hence, it is suggested that BCIS is due to increase intramedullary pressure during cementation causing the cement to become embol

  22. Embolic model • Evidence: emboli detected in RA, RV, pulmonary artery by echo, pulmonary embolization in post mortem study • Emboli content : fat, marrow, cement particles, air, bone particles, aggregates of fibrin and platelets

  23. Mechanism : • Increase intramedullary pressure as a result of: • cement packing in the medullary canal using finger packing or cement gun • cement undergoes exothermic reaction and expands in space between prosthesis and bone • prosthesis insertion with the cement inside • trapped air, medullary content under pressure forced into circulation.

  24. Presence of the emboli will cause: • Mechanical stimulation and damage of endothelium result in reflex vasoconctriction or release of endothelial mediators Embolic material may release vasoactive or proinflammatory substance that directly increased PVR, eg: thrombin / tissue thromboplastin • Release of chemical mediators systemically can cause reduction in SVR such as • PG 1alfa, tissue thromboplastin

  25. EMBOLI

  26. Cont’d case illustration • Case 2 : autopsy examination • Lungs : showed bone marrow elements in the blood vessels, composed of fat admixed with haemopoietic precursor cells. Fat was also observed in the pulmonary sinusoids. • Heart : showed marrow elements adherent to the endocardium • Fat, marrow elements and amorphous material were also seen within the blood vessels of the liver and kidneys. • Kidney : showed features of acute tubular necrosis.

  27. Fat cells in blood vessels • The cause of death was disseminated microembolization as a consequence of hybrid total hip replacement surgery Pancreas : showed acute inflammatory cell infiltrates, patchy areas of haemorrhage and necrosis and surrounding fat necrosis

  28. Histamine release and hypersensitivity • significant increased in plasma histamine concentration in hypotensive patient undergoing cementation (type 1 hypersensitivity) • unclear • increase in c3a and c5a level (complement activation) --> potent vasoconcstrictors and bronchoconcstriction

  29. Multimodal model • Combination of above process • Depends on patient's physiological responds

  30. Risk factors

  31. Old age • poor preexisting physical reserve • preexisting pulmonary hypertension • Osteoporosis* • bony metastasis* • concomittant hip fracture* *Abnormal or increased vascular channels in marrow • previously uninstrumented femoral canal (higher risk than a revision surgery) • use of long stem femoral component PATIENT FACTOR SURGICAL FACTOR

  32. Risk reduction and management

  33. Anaesthetic risk reduction • anaesthetic volatile agent may be assoc with greater haemodynamic changes for the same embolic load • avoidance of nitrous oxide to avoid exacerbating air embolism • avoiding intravascular volume depletion • high level intraoperative vital signs monitoring in high risk patient such as IABP,central venous catheter

  34. Surgical risk reduction • Do a medullary lavage • Good homeostasis before cement insertion • Minimizing the length of prosthesis • Using non cemented prosthesis • Venting the medullary canal • Mixed the cement in partial vacuum rather than at atmospheric pressure

  35. Management • Communication between surgeon and anaesthetist before the operation is performed especially in high risk patient • Fall in ET C02 is the first indicator of BCIS • In awake patient, early sign may include dyspnoea and altered sensorium • Management mainly empirical and according to the presentation • If BCIS is suspected, inspired oxygen should be increased to 100% • To treat CVS collapse as RV failure – aggressive recussitation with IV fluid is recommended • Inotropic support if needed • Administration of sympathetic alfa 1 agonist

  36. reference • Bone cement implantation syndrome, A.J. Donaldson, HE Thomson, NL Harper, NW Kenny, Manchester UK, British Journal of Anaesthesia, 2009 • BCIS – A Case Report, Anish KA, SuranjithSorake, S.Padmanabha, Mangalore India, IOSR Journal of Dental and Medical Sciences, December 2013 • Case report, Bone Cement Implantation Syndrome, Razuin R, Effat O, Shahidan MN, Shama DV, MFM Miswan, Faculty of medicine, UiTM, Hosp Sungai Buloh, Malaysian Journal of Pathology, 2013 • Bone Cement and Implication for anaesthesia, GautamKhanna, Jan Cemovsky, Oxford Journal , Feb 2012

  37. Special thanks to Dr Rohani Thanks

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