Bone cement implantation syn-drome (BCIS)

Department of Anaesthesia, University Hospital of South Manchester

Br J Anaesth 2009; 102: 12–22

전공의 3 년차 노지성

Background• BCIS cause of morbidity and mortality in cemented hip arthro-

plasty

• Increase in the number of ASA II and III patients undergoing a THR in recent years

Between April 2006 and March 2007 보고 : • length of stay

– 9.8 days (cemented primary THR) vs. 8.6 days(uncemented procedure)

• mortality after cemented and uncemented primary THR – 2.3% and 1.6%

2000~3 National Institute for Health and Clinical Excel-lence (NICE) guidelines• long-term viability (cemented prosthesis):better results

Search strategy

• Medline search for the phrases; bone cement, bone cement implantation syndrome,

arthroplasty, hip replacement, complications, methyl methacrylate (MMA), and monomer

Definition• No agreed definition

a number of clinical features: hypoxia, hypotension, cardiac arrhythmias, in-

creased pulmonary vascular resistance (PVR) and cardiac arrest-hip arthroplasty 에만 국한된 것은 아님

Occur at one of the five stages in the surgical proce-dure; ‘pericementation period’

Proposed definition of BCIS cemented bone surgery. occurring around the time of cementation, prosthesis

insertion, reduction of the joint or, occasionally, limb tourniquet deflation

1.hypoxia 2.hypotension 3.unexpected LOC

Proposed severity classification of BCIS

• Grade 1: moderate hypoxia (SpO2<94%) or hypotension (fall in SBP > 20%)

• Grade 2: severe hypoxia (SpO2<88%) or hypotension (fall in SBP > 40%) or unexpected

LOC

• Grade 3: cardiovascular collapse requiring CPR.

Incidence not possible to draw true incidence : under-

reported, lack of a standard definition• A study of 48 patients: 1 patient (2%) suffered

significant hypotension and 8 patients (17%) de-veloped significant desaturation

• A study of 55(cemented long-stem hip arthro-plasty): hypotension in 38%, desaturation in 25%.

mortality data • Only three large case during cemented THR :

0.11%• The largest study in 1999

– 23 in 23,077 : intra-operative deaths patients (ce-mented arthroplasty)» 11 deaths in 11,655 cemented total hip arthroplas-

ties, » 12 during 2,814 cemented hemiarthroplasties» Because of cardio-respiratory problems dur-

ing cementation

Clinical features

• Wide spectrum of severity in the peri-cementation period

• significant, transient reduction in SpO2 ,BP

• smaller proportion: profound intra-operative car-diovascular changes, which may proceed to ar-rhythmias, shock or cardiac arrest

embolization of femoral canal contents to the cerebral circulation post-operative delirium• A case report- BCIS during hemiarthroplasty

Intra-operative cardiac arrest 후 의식 회복이 안되어 MRI F/U:

suggestive of multiple cerebral fat emboli

Etiology and pathophysiology 1

• not fully understood

• Proposed several mechanisms

Initial theories: focused on the release into the circulation of MMA cement monomer

More recent research : the role of emboli formed during cementing and prosthesis insertion

histamine release, complement activation, and endogenous cannabinoid-mediated va-sodilatation

• Monomer-mediated model BCIS 에서 혈역학적 변동은 cementing 시 monomer 에 의해

일어난다는 이론 . 하지만 이는 monomer 의 직접적인 작용이라기 보다는 in-

tramedullary pressure(IMP) 결과로 인한 것이며 , 이로써 embolization 을 일으킨다 .

• Embolic model Echocardiography: Embolism 발견 Post-mortem studies: pulmonary embolization 물리적인 효과와 mediator 방출의 결과

• pulmonary vascular tone 을 증가 mechanical embolization

• Mechanism of emboli formation cementation 과 prosthesis insertion 때 IMP 증가 , ce-

ment 의 온도가 높아져 prosthesis 와 bone, trapping air 와 medullary contents 사이의 공간이 확장되어 혈류로 밀려 들어간다 .

Cementation 은 cement gun 이나 손으로 femoral canal을 packing pressures 가 생성된다 .(Table 3)

Etiology and pathophysiology 2

Etiology and pathophysiology 2

• Transosophageal echocardiography (TOE)

emboli in the heart using TOE and these vary greatly in size and number (Fig. 1)

A study• emboli in 47 out of the 48 patients.• appearance of multiple small emboli as a ‘snow

flurry’• Emboli greater than 10 mm: 1/3 에서 발견됨

most marked during reaming of both the femur and acetabulum, and during insertion of the femoral component and reduction of the hip joint

Etiology and pathophysiology 3

Fig. 1 (A) Small emboli ( <5 mm) filling less than half of the right atrium. (B) Medium-sized emboli (5–10 mm, arrowed) and small emboli filling

more than half of the right atrium. (C) Small emboli ( <5 mm) completely filling the right atrium, multiple

paradoxical emboli in left atrium. (D) Large emboli ( >10 mm) in the right atrium with delayed passage at the tricuspid valve.

• Evidence of emboli at autopsy

marrow, fat, bone emboli, and MMA microparti-cles in the lungs

fat emboli: brain, kidneys, and myocardium

• The link between IMP and embolization

embolization 은 IMP 와 비례한다 . 상한효과도 존재함

• 즉 , 이런 현상은 femoral canal 에 존재하고 있는 debris 양이 제한 때문이었다 . (Fig. 2).

Etiology and pathophysiology 4

• Fig 2 . Number of fat emboli in the lungs (area of 1200 mm2) and the maximum mean IMP over a 10-s interval. • Reproduced with permission from Waddell and Byrick

• The haemodynamic effects of embolization

embolize to the lungs, heart or paradoxically to the cerebral and coronary circulations hypoxia & hypotension (because of RV dysfunction)

• Mediator release from emboli

1. damage of endotheliumreflex vasoconstriction or release of endothelial mediators

2. embolic material may release vasoactive or pro-in-flammatory substances increase PVR

Etiology and pathophysiology 5

Fig 3. Pulmonary vessel with embolus comprising fat, platelets, fibrin & marrow debris. (1) Reflex vasoconstriction and endothelial production of endothelin 1.(2) Release of vasoconstriction mediators; platelet derived growth factor (PDGF),

serotonin (5-HT), thromboxane A2 (Tx-A2), platelet activating factor (PAF), adenosine diphosphate (ADP). (3) Vasoconstriction attributable to non-cellular components of embolus including thrombin.

• Problems with the embolic model1. Embolization 이 항상 혈역학적 변동과 연관된 것은 아니고 ,2. Embolism 의 정도가 hypotension 이나 hypoxemia 의

정도와 관련성이 부족3. 또한 TOE study 에서 보면 embolic event 는 보이나 , V/Q

mismatch 는 정상으로 유지된다 .

micro-embolism 은 BCIS 에서 기여인자 이긴 하나 , 아마도 다른 mechanisms 도 공존할 것으로 추측

• Histamine release and hypersensitivity

1972 년에 발표된 BCIS 의 치명적인 case 에서는 Anaphylaxis (Type 1 hypersensitivity) 가 복합적으로 관련되었을 가능성이 있었다 .

또한 cementation 을 받는 저혈압 환자에서는 plasma histamine concentration 이 증가

Etiology and pathophysiology 6

Complement activation• cemented hemiarthroplasty 에서 C3a 와 C5a 수치

증가가 증명

Multimodal model• clinical features may depend upon the individual’s

physiological response• patient’s pre-existing co-morbidities may alter the clin-

ical features of BCIS

Etiology and pathophysiology 7

Patient risk factors & Surgical fac-tors• old age• poor pre-existing physical reserve• impaired cardiopulmonary function• Osteoporosis, bony metastases• concomitant hip fractures• particularly pathological or intertrochanteric fractures• PFO or ASD emboli and neurological sequelae 증가

Anaesthetic risk reduction

• ASA score of three or over

14% of primary hip arthroplasty 26% of revision procedure full investigation of co-morbidity and pre-optimization 이

필요 .

• Depending on individual patient and the type of prosthesis

• Avoiding i.v. depletion-reduce the extent of the haemody-namic changes in BCIS

haemodynamic monitoring CVP: volume optimization, pulmonary artery catheter, TEE in high risk patients.

Surgical risk reduction

• several modifications in the surgical & anaesthetic technique

Medullary lavage good hemostasis before cement insertion minimizing the length of the prosthesis venting the medulla

• reduces the risk of an air embolus• But, risk of femoral fracture

Retrograde cement insertion mixed cement in a partial vacuum

Management• 마취의사와 수술의사와의 Communication 중요• the early indication of BCIS

A fall in ETCO2 Esophageal Doppler measurements Regional A. : dyspnea and altered sensorium

• Recommendations 경험과 case reports ,basic physiological principle 의해 판단 a cemented prosthesis should be avoided in patients at high

risk of BCIS

• BCIS 가 의심될 경우 ,1. oxygen concentration 100% 유지2. be treated as RV failure

• pure alpha agonist or a mixed alpha and beta receptor agonist• Hemodynamic instability

– Sympathetic a1 agonists (first-line agent)– if there is insufficient pre-load : aggressive resuscitation with

i.v. fluids 3. central venous catheter-CVP monitoring

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