15 Pulmonary Embolism in Cemented Total Hip Arthroplasty Michael Clarius, Christian Heisel, Steffen J. Breusch

Summary

Consequences of Pulmonary Embolism

Embolism is a well-known complication of cemented total hip arthroplasty (THA). As a result of manipulations of the medullary cavity, the intramedullary pressure rises and fat, bone marrow and air embolises into the venous system and to the lung. Clinically, this is seen as acute hypotension, which can go as far as cardiac failure. Although a fatal outcome is rare, fat embolism is a serious complication. The most effective prophylactic measure to reduce the risk is a thorough lavage of the femoral cavity. The use of pulsatile jet-lavage can be regarded as an obligatory preparatory procedure before cement application. Fat and bone marrow are removed as potential embolic sources and, further, the cement-bone interface is enhanced.

Pulmonary embolism leads to an increase in pulmonary vascular resistance. The blockage of the pulmonary vascular system results in an increased AV-shunt and in pulmonary hypoperfusion [49, 60, 95]. The acute pressure increase in the pulmonary arteries [16, 17] causes the functional and structural alteration of a cor pulmonale to occur resulting in left ventricular hypovolaemia and a reduced cardiac output [1, 91]. Clinically, this is seen as acute hypotension, which can go as far as cardiac failure.

Introduction Deep vein thrombosis (DVT) and pulmonary embolism (PE) are feared and well known complications of THA [54]. Fat embolism comprises an entity amongst the group of PE and usually occurs in the early perioperative phase and is unrelated to DVT. The incidence of postoperative DVT as assessed by phlebography is reported in literature to be as high as 77% [68], although, in clinical practice, it is frequently underestimated and consequently not diagnosed. An important and life-threatening complication of DVT is secondary PE with an incidence estimated to be between 6–33% [28, 43, 68] confirmed by lung perfusionand ventilation scans. Although effective anti-embolic and DVT prophylactic measures have been able to reduce these figures significantly, DVT and PE are still the most common causes of death after THA [54, 93].

Cardiopulmonary Complications and Death During Total Hip Arthroplasty Soon after introduction of methylmethacrylate (MMA) as bone cement towards the end of the 1960s, reports of adverse intraoperative complications were published and associated with the use of bone cement. Sir John Charnley [18] himself, who inaugurated MMA in orthopaedic surgery observed a drop in blood pressure immediately after implantation of the endoprosthesis in many of his patients for up to 5 minutes which was more pronounced during implantation of the stem than the cup. Some authors reported instances of intraoperative cardiac arrest [18, 25, 27, 66, 67, 69, 78, 88, 98], which were fortunately manageable with resuscitation. Such instances of so-called »cardiac arrest syndrome« [88] as a reaction to implantations of cemented implants was not, however, always reversible and a number of intraoperative deaths were reported in literature (⊡ Table 15.1), mostly in patients with hip fracture. At autopsy 15/49 cases showed extensive pulmonary fat embolisation. An exact microscopic examination of lung tissue revealed an additional bone marrow emboli-

321 Chapter 15 · Pulmonary Embolism in Cemented Total Hip Arthroplasty

⊡ Table 15.1. Intraoperative cardiac arrests and deaths during total hip replacement reported in literature Author

Diagnosis

Cardiac Arrest Syndrome

Death

Autopsy

Cause of Death

Charnley 1970

no information

4

2

–

–

Powell et al. 1970

hip fracture

3

–

–

–

Hyland, Robins 1970

hip fracture

1

1

1

air and fat embolism

Burgess 1970

hip fracture

1

1

1

fat embolism

Gresham et al. 1971

hip fracture

2

2

2

fat embolism

Schulitz et al. 1971

OA

3

2

1

fat embolism

Thomas et al. 1971

hip fracture

1

1

–

–

Cohen, Smith 1971

Revision

1

1

1

fat and bone marrow embolism

Phillips et al. 1971

hip fracture

1

1

1

fat and bone marrow embolism

Dandy 1971

hip fracture

4

2

2

fat embolism

Michelinakis et al. 1971

hip fracture

2

–

–

–

Sevitt 1972

hip fracture

2

2

2

fat embolism

Kepes et al. 1972

hip fracture

2

2

1

bone marrow embolism

Peebles et al. 1972

hip fracture

1

1

–

–

Newens, Volz 1972

hip fracture

1

–

–

–

De Angelis et al. 1973

Revision, OA

2

–

–

–

Nice 1973

hip fracture

1

1

–

–

Milne 1973

OA

1

–

–

–

Tronzo et al. 1974

no information

1

1

–

Jones 1975

no information

1

1

–

fat embolism

Hyderally, Miller 1976

path. hip fracture

1

1

–

–

Beckenbaugh, Ilstrup 1978

no information

1

1

–

–

Engsaeter 1984

no information

1

1

1

fat embolism

Zichner 1987

no information

10

3

Hochmeister et al. 1987

hip fracture

1

1

1

fat and bone marrow embolism

Maxeiner 1988

hip fracture

3

3

1

fat embolism

Egbert et al. 1989

path. hip fracture

1

1

1

fat and bone marrow embolism

Patterson et al. 1991

hip fracture

7

4

1

no evidence of embolism

Bogner, Landauer 1991

hip fracture

10

10

1

no evidence of embolism

Pietak et al. 1997

hip fracture

2

2

2

fat and bone marrow embolism

Tsujitou et al. 1998

no information

2

2

2

fat embolism

Parvizi et al. 1999

17 HF., 4 OA, 1 RA, 1 NU

23

23

13

11/13 bone marrow, 3/13 bone cement

Ortega et al. 2000

no information

5

1

1

fat embolism

Fallon et al. 2001

path. hip fracture

1

1

1

fat embolism

Leidinger 2002

hip fracture

12

12

12

1x fat embolism, 11x right heart failure

115

87

49

–

total

HF hip fracture, OA osteoarthritis, RA rheumatoid arthritis, NU non union.

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sation alongside fat embolisms in 18 patients whereby the particles were found to even contain cancellous bone fragments.

Intraoperative Mortality Intraoperative mortality during hip replacement was evaluated by Parvizi [77] in a large retrospective study involving 38,488 patients and found to be at around 0.06%. One particularly risk-laden group was the patient with fracture of the femoral neck with an intraoperative mortality of 0.18%, those with pertrochanteric fracture and cemented hip replacement suffered a 1.6% risk. Leidinger [61], though, published data in 2002 from 150 patients with fracture of the femoral neck for whom the intraoperative mortality was found to be much higher at 8%. Elective THA carries a risk well below 0.1%.

Diagnosis and Visualisation of Intraoperative Embolism

15

Frost [37] suspected the heat emission during polymerisation as the primary cause of the observed losses in pressure. Other authors postulated a connection between the acute onset of hypotension and the release of monomeric MMA, which was assumed to cause peripheral vasodilatation and bradycardia accompanied by a negative inotropic effect when released during the hardening process [34, 53, 58, 62, 66, 69, 72, 79, 97, 104]. Radioactive marking of the monomer proved the influx of methylmethacrylate into the blood circulation, which permitted in vivo MMA measurements [50, 65]. Hypotension could be reproduced in animal models after intravenous injection of the monomer with a dose dependent relationship. Intraoperative measurements in patients showed in vivo concentrations from 0.3–5.9 mg/100 ml [50, 58, 65, 103, 114], but Bright [14] found that a measurable hypotensive effect was only attained at concentrations around the tenfold of those achieved in humans. Death occurred in the animal model after injection of doses correlating with the hundredfold MMA concentrations (125 mg/100 ml) [50]. However, clinically a statistical correlation between measured MMA concentrations and pressure drop could not be demonstrated.

The intraoperative complications forced anaesthetists to monitor patients very carefully when hip replacement was undertaken. During intraoesophagal cardiac auscultation so-called »mill-wheel-murmurs« could be detected during prosthesis implantation [70]. These phenomena were accompanied by hypotensive episodes and blood aspiration via a Swan-Ganz catheter allowed Jones to establish the first diagnosis of fat embolism in 1975. Visualisation of intraoperative embolism was first achieved using echocardiography [20, 22, 44, 92, 109]. The development of transoesophageal echocardiography (TEE) allowed a continuous high-quality monitoring of the patient intraoperatively without complicating influences such as breathing movements, adipositas or emphysema, because it is benefited by the close proximity of the oesophagus to the target organ the heart (⊡ Fig. 15.1). Continuous echocardiographic monitoring during cemented hip replacement operations allowed an assessment of the relative frequency of intraoperative embolic events [22, 41]. Therefore TEE is regarded as the most sensitive method to detect intraoperative embolism [39], although the less invasive transcranial Doppler has been advocated.

Pathomechanism Cement »Toxicity« Many attempts were made to explain the implantation syndrome [90]. Initially, bone cement was seen as the prime culprit and cause of cardiovascular complications.

⊡ Fig. 15.1. Normal cross-sectional view of the heart as seen during transoesophageal echocardiography

323 Chapter 15 · Pulmonary Embolism in Cemented Total Hip Arthroplasty

Not just the monomers, but also initiators of the dimethyl-p-toluidin type were accused of causing acute hypotensive crises. But Schlag [96] was able to demonstrate that initiators of this type were totally depleted during the polymerisation process. It is therefore important to realise the cement itself is not the »toxic culprit«.

Intramedullary Pressure Another line of argument in the explanation of the implantation syndrome was the pathogenetic intravasation of air, fat and bone marrow components and the autopsy findings mentioned above appeared to support this. Causal in this argument is the increase in intramedullary pressure during implantation of the prosthesis [19, 26, 40, 80, 94]. Experiments involving femora from deceased donors were able to show very high intramedullary pressure peaks of up to 1447 kPa as can be seen in ⊡ Table 15.2. Values of up to 250 kPa were attained during intraoperative pressure measurement (⊡ Table 15.2).

⊡ Table 15.2. Intramedullary pressure during implantation of the femoral prosthesis Author

Pressure (kPa) Without Drill Hole

Ohnsorge 1971

455

Phillips et al. 1973

250

Hallin 1974

89

Breed 1974

114

Method

With Drill Hole 262

cadaver femur intraoperative intraoperative

13

animal model

Tronzo et al. 1974

75

Kallos et al. 1974

118

32

animal model

von Issendorff, Ritter 1977

504

96

cadaver femur

intraoperative

Indong et al. 1978

1282

cadaver femur

Drinker et al. 1981

1243

animal model

Engsaeter et al. 1984

76

4

intraoperative

Orsini et al. 1987

223

animal model

Wenda et al. 1988

131

intraoperative

Song et al. 1994

488

cadaver femur

1052

cadaver femur

McCaskie et al. 1997

157 667

intraoperative cadaver femur

Reading et al. 2000

131

cadaver femur

Yee et al. 1999

Dozier et al.2000 Churchill et al. 2001

The increase in intramedullary pressure during cement insertion and stem implantation causes an influx of air [2, 3, 5, 24], fat and bone marrow fragments via the linea aspera [31] into the venous system [45, 112]. A proportion of these particles embolise swiftly, the remainder adhere to vessel walls and initiate the development of a mixed thrombus [114]. It was Pelling and Butterworth [80], who finally proved the mechanism of fat displacement from the femur as the decisive mechanism. There was no difference in the extent of fat embolism between bone cement, bone wax and simple dough. Irrespective of the operative approach chosen, the femoral vein is subject to a significant torsion as a result of flexion and rotation of the leg and this can lead to temporary total occlusion of the vessel [101]. Intraoperative phlebography has been able to confirm this phenomenon [87]. Such occlusion implies a complete cessation of blood flow, torsion of the femoral vein leads to damage of the endothelial wall, the trauma of the operation itself causes a higher propensity for blood to coagulate and thus the triad of factors postulated by Virchow in 1856 for the development of venous thrombus is fulfilled. This shows that the high incidence of postoperative deep venous thrombosis of the leg after hip replacement as well as the subsequent pulmonary embolic events can be explained to a high degree by the operative method itself. A further consequence of the operative method is that the act of relocation of the hip implies also the re-canalisation of the femoral vein from which the newly formed thrombi are released into the venous system [22]. The danger of cardiopulmonary complications rises and it becomes apparent why this moment can be regarded as particularly dangerous, even more so, as it closely follows the most critical moment, that of cement and stem implantation.

486

cadaver femur

1447

cadaver femur

Multicentre Study Our own investigations within the framework of a multicentre study included 96 cemented THA patients, which were continuously monitored using TEE. We were able to identify several intraoperative steps that were followed by embolic events. ⊡ Figure 15.2 shows such a risk profile during a total hip replacement operation. Our studies revealed that femoral stem implantation and relocation of the hip (i.e. unkinking of the femoral vein) were the most embolism-prone operative steps. A so-called »snow flurry« (⊡ Fig. 15.3), which is the echocardiographic correlate for an air embolism, was seen in virtually all patients immediately after cement and stem implantation. Diagnostic signs such as these are then frequently followed by a manifest embolus (⊡ Fig. 15.4), which can then circulate in the right-side of the heart for up to 2 minutes before being swept out into the blood vessels of the lung (⊡ Fig. 15.5 and 15.6).

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embolic events during cemented total hip replacement 80 70 60 50 percentage 40 30 72,3

20 10

11,6 7,1 0 1,1 cupjet-lavage cup-trial preparation (n=14)

70,2

29,8 9,6 cupimplantation positioning of the leg

13,8 1,1 stempreparation

pluginsertion

3,2 stem-trial

⊡ Fig. 15.2. Time and operative step dependent embolic events during cemented THA (n = 96)

R1 stemimplantation

relocation

⊡ Fig. 15.3. »Snow flurry«, the echocardiographic correlate of air embolism

15

⊡ Fig. 15.5. Massive embolus circulating in the right heart for more than 40 seconds after trial reduction

⊡ Fig. 15.4. Filamentous embolus in the right atrium

325 Chapter 15 · Pulmonary Embolism in Cemented Total Hip Arthroplasty

»Snow flurries« were observed in 85% of stem implantations and emboli similarly, in 72%. Some very small emboli occurred during pulsatile lavage of the acetabulum in 1/14 patients [22]. At the moment of relocation of the implanted components, 93% of patients who were subject to echocardiographic monitoring displayed »snow flurries«, while embolic events could be found in 70%. It is, however, of note that no pulsatile lavage had been used in 82/96 patients in this multicentre study, hence representing a worse case scenario.

Cementing Techniques Influencing Intraoperative Embolism There are several factors influencing intramedullary pressure and therefore intraoperative embolism. In a new animal

model we were able to compare certain methods and operation/cementing techniques and it was possible to quantify the amount of fat and bone marrow intravasation.

Animal Model A new sheep model was developed (⊡ Fig. 15.6), which allowed for standardised bilateral, simultaneous cement pressurisation. The operative procedure involved bilateral placement of intravenous catheters into the external iliac veins via retroperitoneal approach (⊡ Fig. 15.7). A specially designed cementing apparatus was used to allow for bilateral simultaneous cement pressurisation. Venous blood from both iliac catheters was then collected during cementing (⊡ Fig. 15.8), anticoagulated and a quantitative and qualitative fat analysis was performed.

Catheters in the external iliac veins

Blood collection in aliquots with sodiumcitrate

Reducing valves and manometers Cement pressurization apparatus

⊡ Fig. 15.6. Schematic drawing of the sheep model which allows for bilateral simultaneous cement pressurization and collection of blood via the external iliac veins

⊡ Fig. 15.7. Intraoperative view of the retroperitoneal situs. On the left the ballooned iliac vein after proximal ligation is shown, on the right the catheter is placed and secured

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Part V · Perioperative Management, Complications and Prevention

⊡ Fig. 15.8. Animal model setup during operation. On top cement apparatus with bilateral simultaneous pressurisation is shown. Via the retroperitoneal iliac vein catheter the draining blood could be collected during cementing to allow determination of the fatty contents

a

Influence of Pulsatile Lavage

15

Using the sheep model described above, we studied the effectiveness of both pulsatile and syringe lavage of equal volume with regard to their cleansing capabilities as measured by fat and bone-marrow intravasation. After randomisation, one side was lavaged with 250 ml irrigation using a bladder syringe, the contralateral femur with the identical volume but using a pulsatile lavage. Despite equal volume manual lavage produced significantly higher fat and bone marrow intravasation (p