530884
research-article2014
FAIXXX10.1177/1071100714530884Foot & Ankle InternationalHickey
2012 International Federation of Foot & Ankle Societies (IFFAS) Award for Excellence
The Effect of Lower Limb Cast Immobilization on Calf Muscle Pump Function: A Simple Strategy of Exercises Can Maintain Flow
Foot & Ankle International® 1–5 © The Author(s) 2014 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/1071100714530884 fai.sagepub.com
Ben A. Hickey, BM, MRCS, MSc1, Amy Morgan, MBBCh, MRCS1, Neil Pugh, BSc, MSc, PhD, FInstP, CPhys1, and Anthony Perera, MBChB, MRCS, MFSEM, PG, Dip (Med Law), FRCS (Orth)1
Abstract Background: We have investigated the role of the calf muscle pump in casted patients. An audit of venous thromboembolism (VTE) in casted patients showed that the thrombosis occurred in the casted leg; this has not been previously assessed. We postulated that local factors play a major role, and we set out to assess the calf muscle pump in casted patients and to determine whether this can be optimized despite below-knee cast immobilization. Methods: We measured the flow in the popliteal vein using a validated method of Doppler ultrasound measurement of peak velocity with and without a below-knee plaster cast. Results: We demonstrated that a simple strategy of toe and ankle exercises can maintain venous return despite belowknee cast immobilization. Conclusion: This is the first study to examine the effect of the calf muscle pump in the presence of a plaster cast. Major muscle groups such as the flexor hallucis longus and gastrocsoleus extend beyond the field of control of the cast and can still be recruited. Clinical Relevance: We recommend that all patients treated with a below-knee cast be given a program of exercises that can be comfortably performed with the cast; this could provide a useful, inexpensive, and safe thromboprophylaxis strategy acting at the site of greatest risk and targeting a major cause of VTE. Keywords: calf pump, cast, immobilization, mechanical thromboprophylaxis Lower limb cast immobilization is associated with venous thromboembolism (VTE). A 2008 Cochrane review of 6 randomized controlled trials (RCTs) on the use of chemical prophylaxis found that the nontreatment group had a VTE incidence of 4.3% to 40%.12 Although the association between lower limb cast immobilization and VTE is well documented, the causal relationship between cast and VTE has not been fully explained.2,7 Interpretation of the link between casting and VTE is complex due to the variety of injuries sustained, cast types, and individual patient risk factors for VTE. Even in the absence of lower limb cast immobilization, minor leg injuries such as ankle sprains significantly increase the risk of symptomatic DVT.13 VTE prophylaxis is highly topical, and there is great debate on the efficacy and risks of chemical prophylaxis. Review of national society guidelines (eg, American Orthopaedic Foot and Ankle Society, British Orthopaedic Foot and Ankle Society) shows that there is no consensus.11 The debate on recommending widespread prophylaxis hinges on the fact that the incidence of VTE in casted patients may be low while the
risks of chemical prophylaxis, such as hematoma and heparininduced thrombocytopenia, are concerning. Chemical prophylaxis is a rather blunt instrument with a general effect rather than a local one. It is clear from Virchow’s triad of thrombosis, that endothelial dysfunction and venous stasis are components of thrombogenesis localized to the site of injury.14 It is clear that endothelial dysfunction cannot be controlled or modulated, but mechanical prophylaxis has been demonstrated to have an effect in controlling venous stasis in hip and knee arthroplasty. It has been felt that stasis is the major issue with cast-induced risk and that the cast prevents the use of mechanical treatment. Even though several studies on VTE in trauma patients have been conducted, the site of the thrombosis has not 1
University Hospital of Wales, Cardiff, Wales, UK
Corresponding Author: Ben A. Hickey, BM, MRCS, MSc, 10 Trafalgar Road, Penylan, Heath Park, Cardiff, Wales, CF14 4XW, UK. Email: [email protected]
Downloaded from fai.sagepub.com at GEORGIAN COURT UNIV on March 26, 2015
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been described in relation to the side of immobilization. The aim of this study was to establish the role of local factors in VTE after cast immobilization and to assess the role of the calf muscle pump in a casted limb.
Methods Site of Immobilization and Site of VTE A consecutive cohort of 721 patients who had lower limb cast treatment at the University Hospital of Wales for any reason were included. Patients under the age of 18 years and duplicates were excluded. Patient identifiers were crossreferenced with the thromboembolism service database to identify those who sustained symptomatic VTE within 6 months of cast treatment. Routine thromboprophylaxis was not used during the study period.
Role of the Calf Muscle Pump in a Casted Limb The calf muscle pump was measured and assessed using Doppler ultrasound measurement of velocity in the popliteal vein. This technique has been validated and used recently by Izumi et al6 and Griffin et al4 to determine the effects of calf compression and electrical stimulation on calf pump function. The aim of the study was to measure popliteal vein velocities with and without below-knee cast and to assess the effect of muscle contraction on this flow. Twenty healthy adult volunteers between the ages of 21 and 58 years of age (mean 31 years) were enrolled in this prospective study with institutional review board and local research and ethics committee approval. Eleven were female. All participants signed a consent form prior to participation. Participants with medical history of peripheral vascular disease, diabetes, varicose veins, VTE, or previous foot and ankle surgery were excluded because these factors could have an adverse effect on calf pump function. A standardized protocol was followed. For each participant, baseline popliteal vein velocity was measured in the right leg using Doppler ultrasound (cm/s) with the participant in the seated position. The participant was then shown a toe or ankle movement and was asked to perform the movement to his or her best effort, during which peak systolic velocity was measured at the popliteal vein. After each movement, the toe and ankle were returned to the neutral position for at least 1 minute to allow the baseline velocity to return to normal before the next movement was performed. Popliteal vein velocity was measured at baseline and during 4 movements, including toe dorsiflexion, toe plantar flexion, ankle dorsiflexion, and ankle plantar flexion. All measurements were performed by the senior consultant medical physicist (N.P.) with responsibility for performing Doppler ultrasound in our university hospital. Once all measurements were recorded for each movement, a standardized below-knee, 3-layer, fiberglass
polymer cast (BSN Delta-Lite, Germany) was applied over wool and stockinette by the same orthopaedic surgeon. Popliteal vein velocity measurements at baseline and during movement were then repeated for each of the 4 movements with the cast in situ. Although ankle movements of dorsiflexion and ankle plantar flexion were not possible with the cast in situ, participants could still perform isometric contraction of muscle groups. Group means were calculated for each movement before and after cast application to allow comparison between groups. Statistical Analysis. A sample size calculation determined that 20 participants were required to detect a statistically significant change in pre-post cast peak systolic velocity at 80% power. Statistical analysis was performed using the group mean baseline and peak systolic velocity before and after cast application using the paired t test at the 5% alpha level. Two-sided P values of less than .05 were considered statistically significant. All statistical analysis was performed using SPSS for Windows (SPSS, Chicago, IL).
Results Site of Immobilization and Site of VTE The overall incidence of symptomatic VTE within 6 months following cast treatment was 3.1% (n = 22). Eighteen of these were deep venous thromboses (DVTs), and 4 were pulmonary emboli. The majority of DVTs occurred in the below-knee veins, with only 1 case involving the aboveknee veins (incidence 0.1%). All symptomatic VTE events occurred in the limb that had been casted.
Role of the Calf Muscle Pump in a Casted Limb Baseline Velocities. We collected 240 baseline measurements of resting popliteal velocity. The baseline is calculated as a mean because of the physiological baseline variability that is shown in the Doppler image in Figure 1. The mean resting popliteal vein velocity was 10.42 cm/s (range, 4.2-32.1 cm/s). The standard deviation was 6.48 cm/s, which reflects the physiological baseline variability that exists. The spreads for each participant’s 12 measures are shown in Figure 2. There was no difference in baseline velocity when a cast was applied and the leg was at rest. Muscle Contracture Without Cast. All movements tested resulted in a statistically significant increase in peak systolic velocity compared with baseline measurement (P = .0001) without a cast (Table 1). Active toe dorsiflexion increased the velocity in the popliteal vein from baseline to a mean precast peak of 53.6 cm/s (range, 12.8-152.8 cm/s). Active toe plantar flexion resulted in an increase in velocity from baseline to a mean precast peak of 49.7 cm/s (range,
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Hickey Table 2. Comparison of Mean Peak Popliteal Vein Velocities Without and With a Below-Knee Cast.
Exercise Seated toe dorsiflexion Seated toe plantar flexion Seated ankle dorsiflexion Seated ankle plantar flexion
Precast Mean Peak Systolic Velocity, cm/s
Mean Peak Systolic Velocity, cm/s
P Value
53.6 (12.8-152.8)
59.1 (10.5-184.1)
.572
49.7 (15.5-127.7)
57.3 (20.9-108.3)
.299
88.2 (23.2-234.2)
.045a
115.4 (31.5-189)
86.6 (39.9-158.9) 112.9 (34.1-265.5)
.23
a
Statistically significant result.
15.5-127.7 cm/s). Ankle plantar flexion increased velocity from baseline to a mean precast peak of 86.6 cm/s (range, 39.9-158.9 cm/s). Ankle dorsiflexion increased velocity from baseline to a mean precast peak of 115.4 cm/s (range, 31.5-189 cm/s).
Figure 1. Measurement of mean peak popliteal vein velocity (cm/s) on Doppler ultrasound.
Muscle Contracture With a Below-Knee Cast In Situ. Active toe dorsiflexion increased the velocity in the popliteal vein from baseline to a mean postcast peak of 59.1 cm/s (range, 10.5-184.1 cm/s) (pre- to postcast peak mean difference P = .572). Active toe plantar flexion resulted in an increase in velocity from baseline to a mean postcast peak of 57.3 cm/s (range, 20.9-108.3 cm/s) (pre- to postcast peak mean difference P = .299). Ankle plantar flexion increased velocity from baseline to a mean postcast peak of 112.9 cm/s (range, 34.1-265.5 cm/s) (pre- to postcast mean difference P = .23). Ankle dorsiflexion increased velocity from baseline to a mean postcast peak of 88.2 cm/s (range, 23.2-234.2 cm/s) (pre- to postcast mean difference P = .045). Although the postcast peak velocity was reduced compared with precast peak for ankle dorsiflexion, the postcast mean peak velocity still increased more than 10 times from baseline levels. Results of pre- and postcast mean peak differences are shown in Table 2.
Figure 2. Box-and-whisker plot of baseline popliteal vein velocity (cm/s).
Table 1. Effect of Muscle Contraction on Popliteal Vein velocity in the Noncasted Leg.
Exercise Seated toe dorsiflexion Seated toe plantar flexion Seated ankle dorsiflexion Seated ankle plantar flexion a
Mean Peak Mean Resting Systolic Velocity Baseline Venous Achieved With Velocity, cm/s Movement, cm/s
P Value a
10.42 (4.2-32.1) 59.1 (10.5-184.1) .0001
10.42 (4.2-32.1) 57.3 (20.9-108.3) .0001a 10.42 (4.2-32.1) 88.2 (23.2-234.2) .0001a 10.42 (4.2-32.1) 112.9 (34.1-265.5) .0001a
Statistically significant result.
Discussion The audit we conducted of symptomatic DVT in orthopaedic patients in a below-knee cast showed that the thrombosis occurs in the casted limb. We believe that this powerfully demonstrates the importance of local factors such as endothelial dysfunction and venous stasis in causation. The numbers we have analyzed are small, and therefore more studies are needed to explore this link. However, given the very significant difference between the injured/casted limb and the noninjured/noncasted limb, it is likely that hypercoagulability is of lower importance in this particular group of
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Foot & Ankle International
patients than local factors; otherwise, there would have been a more even spread. We believe this highlights the importance of maintaining the calf muscle pump, because endothelial damage cannot be influenced at this time. This is the first study into the effects of a below-knee cast on calf muscle pump function. We have shown that even with a below-knee cast in situ, toe and ankle dorsiflexion and plantar flexion movements significantly increase peak systolic velocity measured at the popliteal vein to between 57.3 cm/s and 112.9 cm/s, which is 6 to 10 times mean baseline levels. These findings are similar to those reported by Izumi et al,6 who found that ankle movements in the uncasted limb resulted in popliteal velocities of 75 cm/s (range, 40-152 cm/s). Comparing precast and postcast peak velocities, we found that the cast did not significantly reduce velocities created by active toe movements or ankle plantar flexion. Although peak velocity resulting from ankle dorsiflexion was reduced by the presence of a below-knee cast compared with peak velocity in the uncasted leg (P = .045), active ankle movement with cast in situ still resulted in a statistically significant increase in peak velocity from 10.3 cm/s at baseline to 88.2 cm/s during movement (P = .0001). This was 75% of the maximum achievable without the cast. These findings are clinically relevant for several reasons. Until now an assumption has been made that lower limb cast immobilization resulted in loss of the calf pump and that this venous stasis could not be influenced. However, our results show that although movement of the foot and ankle are reduced, active movements still stimulate calf pump function. We were unable to reliably measure popliteal velocities during knee movement due to technical difficulties. However, it is likely that knee flexion and extension will also affect popliteal velocity and venous blood flow as the gastrocnemius origin is above the knee joint. In the setting of hip arthroplasty, mechanical thromboprophylaxis has been shown to be effective in reducing the incidence of DVT.1,10 It is therefore possible that our findings may translate to reduced incidences of VTE in patients with lower limb cast immobilization. Localized measures of mechanical thromboprophylaxis, as we have shown, may help reduce the incidence of localized complication of VTE in these patients. We have developed a program of gentle toe and knee movements and isometric ankle muscle contracture that have all been shown to improve calf pump function. Of course, adequate pain control is important to enable these movements to occur. It is good practice to encourage patients to maintain knee and toe movements when they are in a cast. Our results demonstrate that these movements are important in maintaining physiological popliteal vein flow, which may be significant in reducing the risk of VTE. In much the same way as airline passengers are now taking control of managing
their flight risk, patients should be advised to perform these movements to reduce venous stasis. This requires that patients be given sufficient information during consultation, including written information, regarding the nature of their VTE risk and how this can be managed. This may be an effective safe and inexpensive way of reducing VTE risk. It is important that patients’ adherence be regularly checked when they are seen by the surgeon, the plaster technicians, or physiotherapists in order to improve adherence to this routine of exercises. Although there is evidence that chemical thromboprophylaxis reduces the incidence of VTE in patients treated with lower limb cast immobilization, 6 small RCTs totaling 1536 patients found that 9.8% (down from 17.1%) of patients still experienced a DVT despite administration of low-molecular-weight heparin (LMWH).3,8,12 If our findings are confirmed in clinical studies, they may be useful in improving the success rate in high-risk patients who are given chemical prophylaxis. However, it is possible that our recommendations may be most useful in patients who are not felt to require LMWH because they are low risk but who are nonetheless still at some risk. In trauma patients treated with cast, Achilles tendon injury has been highlighted as being associated with a particularly high risk of venous thrombo-embolism, with rates of up to 34% reported.5,9,12 This increase in risk may be associated with the fact that there is a significant loss of the calf pump due to the rupture or the equinus position. In this group, maximization of the pump may not be possible. Also it is likely that weight bearing results in some increase in flow, but this was not measured in our study because this will vary with the type of injury/surgery and the resulting amount of pain. We acknowledge several limitations to our study. First, we performed measurements on healthy participants and excluded participants with peripheral vascular disease, diabetes, varicose veins, DVT, or previous foot and ankle surgery. Second, participants were asked to perform movements to their best efforts. This is likely to have resulted in a bestcase result, which may not represent clinical practice. However, the increases between baseline and peak popliteal velocity reached extreme statistical significance (P < .0001) in all cases, and therefore we expect that these movements would also result in significant increases in patients who may have impaired calf pump function due to comorbidity. The movements we recommend can occur naturally in patients with below-knee casts as they mobilize during the course of their day, and the movements do not need to be dramatic to achieve good flow. Therefore we think that focusing on these movements regularly throughout the day will not have any detrimental effect on fracture alignment, but this will need to be investigated. We have approval from our local research and ethical committee and are in the process of performing a further study to investigate these questions.
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Hickey
Conclusion This is the first study to examine the effect of a lower limb cast on calf pump function. Despite cast immobilization, toe and ankle flexion and extension movements significantly increased peak systolic velocity measured at the popliteal vein. We recommend that all patients treated with below-knee cast immobilization be advised to perform regular knee, toe, and ankle exercises because this reduces venous stasis and may reduce risk of DVT. We believe that this should be offered routinely and that high-risk patients should continue to be offered LMWH until further evidence is available. Declaration of Conflicting Interests The author declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding The author received no financial support for the research, authorship, and/or publication of this article.
References 1. Asano H, Matsubara M, Suzuki K, Morita S, Shinomiya K. Prevention of pulmonary embolism by a foot sole pump. J Bone Joint Surg Br. 2001;83(8):1130-1132. 2. Bergqvist D, Lowe G. Venous thromboembolism in patients undergoing laparoscopic and arthroscopic surgery and in leg casts. Arch Intern Med. 2002;162:2173-2176. 3. Ettema HB, Kollen BJ, Verheyen CC, Büller HR. Prevention of venous thromboembolism in patients with immobilization of the lower extremities: a meta-analysis of randomized controlled trials. J Thromb Haemost. 2008;6(7):1093-1098. 4. Griffin M, Nicolaides AN, Bond D, Geroulakos G, Kalodiki E. The efficacy of a new stimulation technology to increase
venous flow and prevent venous stasis. Eur J Vasc Endovasc Surg. 2010;40(6):766-771. 5. Healy B, Beasley R, Weatherall M. Venous thromboembolism following prolonged cast immobilisation for injury to the tendo Achillis. J Bone Joint Surg Br. 2010;92(5):646-650. 6. Izumi M, Ikeuchi M, Mitani T, Taniguchi S, Tani T. Prevention of venous stasis in the lower limb by transcutaneous electrical nerve stimulation. Eur J Vasc Endovasc Surg. 2010;39(5):642-645. 7. Kujath P, Spannagel U, Habscheid W. Incidence and prophylaxis of deep venous thrombosis in outpatients with injury of the lower limb. Haemostasis. 1993;23(suppl 1):20-36. 8. Nokes TJ, Keenan J. Thromboprophylaxis in patients with lower limb immobilization—review of current status. Br J Haematol. 2009;146(4):361-368. 9. Patil S, Gandhi J, Curzon I, Hui A CW. Incidence of deep-vein thrombosis in patients with fractures of the ankle treated in a plaster cast. J Bone Joint Surg Br. 2007;89(10):1340-1343. 10. Pitto RP, Hamer H, Heiss-Dunlop W, Kuehle J. Mechanical prophylaxis of deep-vein thrombosis after total hip replacement a randomised clinical trial. J Bone Joint Surg Br. 2004;86(5):639-642. 11. Struijk-Mulder MC, Etterna HB, Verheyen CC, Buller HR. Comparing consensus guidelines on thromboprophylaxis in orthopaedic surgery. J Thromb Haemost. 2010;8(4):678-683. 12. Testroote M, Stigter W, de Visser DC, Janzing H. Low molecular weight heparin for prevention of venous thromboembolism in patients with lower-leg immobilization. Cochrane Database Syst Rev. 2008;(4):CD006681. 13. Van Stralen KJ, Rosendaal FR, Doggen CJ. Minor injuries as a risk factor for venous thrombosis. Arch Intern Med. 2008;168(1):21-26. 14. Virchow RLK. Thrombose und Embolie. Gefässentzündung und septische Infektion. Gesammelte Abhandlungen zur wissenschaftlichen Medicin. Frankfurt am Main, Germany: Von Meidinger & Sohn; 1856. Translation in Matzdorff AC, Bell WR. Thrombosis and Embolie (1846-1856). Canton, MA: Science History Publications; 1998.
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research-article2014
FAIXXX10.1177/1071100714530884Foot & Ankle InternationalHickey
2012 International Federation of Foot & Ankle Societies (IFFAS) Award for Excellence
The Effect of Lower Limb Cast Immobilization on Calf Muscle Pump Function: A Simple Strategy of Exercises Can Maintain Flow
Foot & Ankle International® 1–5 © The Author(s) 2014 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/1071100714530884 fai.sagepub.com
Ben A. Hickey, BM, MRCS, MSc1, Amy Morgan, MBBCh, MRCS1, Neil Pugh, BSc, MSc, PhD, FInstP, CPhys1, and Anthony Perera, MBChB, MRCS, MFSEM, PG, Dip (Med Law), FRCS (Orth)1
Abstract Background: We have investigated the role of the calf muscle pump in casted patients. An audit of venous thromboembolism (VTE) in casted patients showed that the thrombosis occurred in the casted leg; this has not been previously assessed. We postulated that local factors play a major role, and we set out to assess the calf muscle pump in casted patients and to determine whether this can be optimized despite below-knee cast immobilization. Methods: We measured the flow in the popliteal vein using a validated method of Doppler ultrasound measurement of peak velocity with and without a below-knee plaster cast. Results: We demonstrated that a simple strategy of toe and ankle exercises can maintain venous return despite belowknee cast immobilization. Conclusion: This is the first study to examine the effect of the calf muscle pump in the presence of a plaster cast. Major muscle groups such as the flexor hallucis longus and gastrocsoleus extend beyond the field of control of the cast and can still be recruited. Clinical Relevance: We recommend that all patients treated with a below-knee cast be given a program of exercises that can be comfortably performed with the cast; this could provide a useful, inexpensive, and safe thromboprophylaxis strategy acting at the site of greatest risk and targeting a major cause of VTE. Keywords: calf pump, cast, immobilization, mechanical thromboprophylaxis Lower limb cast immobilization is associated with venous thromboembolism (VTE). A 2008 Cochrane review of 6 randomized controlled trials (RCTs) on the use of chemical prophylaxis found that the nontreatment group had a VTE incidence of 4.3% to 40%.12 Although the association between lower limb cast immobilization and VTE is well documented, the causal relationship between cast and VTE has not been fully explained.2,7 Interpretation of the link between casting and VTE is complex due to the variety of injuries sustained, cast types, and individual patient risk factors for VTE. Even in the absence of lower limb cast immobilization, minor leg injuries such as ankle sprains significantly increase the risk of symptomatic DVT.13 VTE prophylaxis is highly topical, and there is great debate on the efficacy and risks of chemical prophylaxis. Review of national society guidelines (eg, American Orthopaedic Foot and Ankle Society, British Orthopaedic Foot and Ankle Society) shows that there is no consensus.11 The debate on recommending widespread prophylaxis hinges on the fact that the incidence of VTE in casted patients may be low while the
risks of chemical prophylaxis, such as hematoma and heparininduced thrombocytopenia, are concerning. Chemical prophylaxis is a rather blunt instrument with a general effect rather than a local one. It is clear from Virchow’s triad of thrombosis, that endothelial dysfunction and venous stasis are components of thrombogenesis localized to the site of injury.14 It is clear that endothelial dysfunction cannot be controlled or modulated, but mechanical prophylaxis has been demonstrated to have an effect in controlling venous stasis in hip and knee arthroplasty. It has been felt that stasis is the major issue with cast-induced risk and that the cast prevents the use of mechanical treatment. Even though several studies on VTE in trauma patients have been conducted, the site of the thrombosis has not 1
University Hospital of Wales, Cardiff, Wales, UK
Corresponding Author: Ben A. Hickey, BM, MRCS, MSc, 10 Trafalgar Road, Penylan, Heath Park, Cardiff, Wales, CF14 4XW, UK. Email: [email protected]
Downloaded from fai.sagepub.com at GEORGIAN COURT UNIV on March 26, 2015
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Foot & Ankle International
been described in relation to the side of immobilization. The aim of this study was to establish the role of local factors in VTE after cast immobilization and to assess the role of the calf muscle pump in a casted limb.
Methods Site of Immobilization and Site of VTE A consecutive cohort of 721 patients who had lower limb cast treatment at the University Hospital of Wales for any reason were included. Patients under the age of 18 years and duplicates were excluded. Patient identifiers were crossreferenced with the thromboembolism service database to identify those who sustained symptomatic VTE within 6 months of cast treatment. Routine thromboprophylaxis was not used during the study period.
Role of the Calf Muscle Pump in a Casted Limb The calf muscle pump was measured and assessed using Doppler ultrasound measurement of velocity in the popliteal vein. This technique has been validated and used recently by Izumi et al6 and Griffin et al4 to determine the effects of calf compression and electrical stimulation on calf pump function. The aim of the study was to measure popliteal vein velocities with and without below-knee cast and to assess the effect of muscle contraction on this flow. Twenty healthy adult volunteers between the ages of 21 and 58 years of age (mean 31 years) were enrolled in this prospective study with institutional review board and local research and ethics committee approval. Eleven were female. All participants signed a consent form prior to participation. Participants with medical history of peripheral vascular disease, diabetes, varicose veins, VTE, or previous foot and ankle surgery were excluded because these factors could have an adverse effect on calf pump function. A standardized protocol was followed. For each participant, baseline popliteal vein velocity was measured in the right leg using Doppler ultrasound (cm/s) with the participant in the seated position. The participant was then shown a toe or ankle movement and was asked to perform the movement to his or her best effort, during which peak systolic velocity was measured at the popliteal vein. After each movement, the toe and ankle were returned to the neutral position for at least 1 minute to allow the baseline velocity to return to normal before the next movement was performed. Popliteal vein velocity was measured at baseline and during 4 movements, including toe dorsiflexion, toe plantar flexion, ankle dorsiflexion, and ankle plantar flexion. All measurements were performed by the senior consultant medical physicist (N.P.) with responsibility for performing Doppler ultrasound in our university hospital. Once all measurements were recorded for each movement, a standardized below-knee, 3-layer, fiberglass
polymer cast (BSN Delta-Lite, Germany) was applied over wool and stockinette by the same orthopaedic surgeon. Popliteal vein velocity measurements at baseline and during movement were then repeated for each of the 4 movements with the cast in situ. Although ankle movements of dorsiflexion and ankle plantar flexion were not possible with the cast in situ, participants could still perform isometric contraction of muscle groups. Group means were calculated for each movement before and after cast application to allow comparison between groups. Statistical Analysis. A sample size calculation determined that 20 participants were required to detect a statistically significant change in pre-post cast peak systolic velocity at 80% power. Statistical analysis was performed using the group mean baseline and peak systolic velocity before and after cast application using the paired t test at the 5% alpha level. Two-sided P values of less than .05 were considered statistically significant. All statistical analysis was performed using SPSS for Windows (SPSS, Chicago, IL).
Results Site of Immobilization and Site of VTE The overall incidence of symptomatic VTE within 6 months following cast treatment was 3.1% (n = 22). Eighteen of these were deep venous thromboses (DVTs), and 4 were pulmonary emboli. The majority of DVTs occurred in the below-knee veins, with only 1 case involving the aboveknee veins (incidence 0.1%). All symptomatic VTE events occurred in the limb that had been casted.
Role of the Calf Muscle Pump in a Casted Limb Baseline Velocities. We collected 240 baseline measurements of resting popliteal velocity. The baseline is calculated as a mean because of the physiological baseline variability that is shown in the Doppler image in Figure 1. The mean resting popliteal vein velocity was 10.42 cm/s (range, 4.2-32.1 cm/s). The standard deviation was 6.48 cm/s, which reflects the physiological baseline variability that exists. The spreads for each participant’s 12 measures are shown in Figure 2. There was no difference in baseline velocity when a cast was applied and the leg was at rest. Muscle Contracture Without Cast. All movements tested resulted in a statistically significant increase in peak systolic velocity compared with baseline measurement (P = .0001) without a cast (Table 1). Active toe dorsiflexion increased the velocity in the popliteal vein from baseline to a mean precast peak of 53.6 cm/s (range, 12.8-152.8 cm/s). Active toe plantar flexion resulted in an increase in velocity from baseline to a mean precast peak of 49.7 cm/s (range,
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Hickey Table 2. Comparison of Mean Peak Popliteal Vein Velocities Without and With a Below-Knee Cast.
Exercise Seated toe dorsiflexion Seated toe plantar flexion Seated ankle dorsiflexion Seated ankle plantar flexion
Precast Mean Peak Systolic Velocity, cm/s
Mean Peak Systolic Velocity, cm/s
P Value
53.6 (12.8-152.8)
59.1 (10.5-184.1)
.572
49.7 (15.5-127.7)
57.3 (20.9-108.3)
.299
88.2 (23.2-234.2)
.045a
115.4 (31.5-189)
86.6 (39.9-158.9) 112.9 (34.1-265.5)
.23
a
Statistically significant result.
15.5-127.7 cm/s). Ankle plantar flexion increased velocity from baseline to a mean precast peak of 86.6 cm/s (range, 39.9-158.9 cm/s). Ankle dorsiflexion increased velocity from baseline to a mean precast peak of 115.4 cm/s (range, 31.5-189 cm/s).
Figure 1. Measurement of mean peak popliteal vein velocity (cm/s) on Doppler ultrasound.
Muscle Contracture With a Below-Knee Cast In Situ. Active toe dorsiflexion increased the velocity in the popliteal vein from baseline to a mean postcast peak of 59.1 cm/s (range, 10.5-184.1 cm/s) (pre- to postcast peak mean difference P = .572). Active toe plantar flexion resulted in an increase in velocity from baseline to a mean postcast peak of 57.3 cm/s (range, 20.9-108.3 cm/s) (pre- to postcast peak mean difference P = .299). Ankle plantar flexion increased velocity from baseline to a mean postcast peak of 112.9 cm/s (range, 34.1-265.5 cm/s) (pre- to postcast mean difference P = .23). Ankle dorsiflexion increased velocity from baseline to a mean postcast peak of 88.2 cm/s (range, 23.2-234.2 cm/s) (pre- to postcast mean difference P = .045). Although the postcast peak velocity was reduced compared with precast peak for ankle dorsiflexion, the postcast mean peak velocity still increased more than 10 times from baseline levels. Results of pre- and postcast mean peak differences are shown in Table 2.
Figure 2. Box-and-whisker plot of baseline popliteal vein velocity (cm/s).
Table 1. Effect of Muscle Contraction on Popliteal Vein velocity in the Noncasted Leg.
Exercise Seated toe dorsiflexion Seated toe plantar flexion Seated ankle dorsiflexion Seated ankle plantar flexion a
Mean Peak Mean Resting Systolic Velocity Baseline Venous Achieved With Velocity, cm/s Movement, cm/s
P Value a
10.42 (4.2-32.1) 59.1 (10.5-184.1) .0001
10.42 (4.2-32.1) 57.3 (20.9-108.3) .0001a 10.42 (4.2-32.1) 88.2 (23.2-234.2) .0001a 10.42 (4.2-32.1) 112.9 (34.1-265.5) .0001a
Statistically significant result.
Discussion The audit we conducted of symptomatic DVT in orthopaedic patients in a below-knee cast showed that the thrombosis occurs in the casted limb. We believe that this powerfully demonstrates the importance of local factors such as endothelial dysfunction and venous stasis in causation. The numbers we have analyzed are small, and therefore more studies are needed to explore this link. However, given the very significant difference between the injured/casted limb and the noninjured/noncasted limb, it is likely that hypercoagulability is of lower importance in this particular group of
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Foot & Ankle International
patients than local factors; otherwise, there would have been a more even spread. We believe this highlights the importance of maintaining the calf muscle pump, because endothelial damage cannot be influenced at this time. This is the first study into the effects of a below-knee cast on calf muscle pump function. We have shown that even with a below-knee cast in situ, toe and ankle dorsiflexion and plantar flexion movements significantly increase peak systolic velocity measured at the popliteal vein to between 57.3 cm/s and 112.9 cm/s, which is 6 to 10 times mean baseline levels. These findings are similar to those reported by Izumi et al,6 who found that ankle movements in the uncasted limb resulted in popliteal velocities of 75 cm/s (range, 40-152 cm/s). Comparing precast and postcast peak velocities, we found that the cast did not significantly reduce velocities created by active toe movements or ankle plantar flexion. Although peak velocity resulting from ankle dorsiflexion was reduced by the presence of a below-knee cast compared with peak velocity in the uncasted leg (P = .045), active ankle movement with cast in situ still resulted in a statistically significant increase in peak velocity from 10.3 cm/s at baseline to 88.2 cm/s during movement (P = .0001). This was 75% of the maximum achievable without the cast. These findings are clinically relevant for several reasons. Until now an assumption has been made that lower limb cast immobilization resulted in loss of the calf pump and that this venous stasis could not be influenced. However, our results show that although movement of the foot and ankle are reduced, active movements still stimulate calf pump function. We were unable to reliably measure popliteal velocities during knee movement due to technical difficulties. However, it is likely that knee flexion and extension will also affect popliteal velocity and venous blood flow as the gastrocnemius origin is above the knee joint. In the setting of hip arthroplasty, mechanical thromboprophylaxis has been shown to be effective in reducing the incidence of DVT.1,10 It is therefore possible that our findings may translate to reduced incidences of VTE in patients with lower limb cast immobilization. Localized measures of mechanical thromboprophylaxis, as we have shown, may help reduce the incidence of localized complication of VTE in these patients. We have developed a program of gentle toe and knee movements and isometric ankle muscle contracture that have all been shown to improve calf pump function. Of course, adequate pain control is important to enable these movements to occur. It is good practice to encourage patients to maintain knee and toe movements when they are in a cast. Our results demonstrate that these movements are important in maintaining physiological popliteal vein flow, which may be significant in reducing the risk of VTE. In much the same way as airline passengers are now taking control of managing
their flight risk, patients should be advised to perform these movements to reduce venous stasis. This requires that patients be given sufficient information during consultation, including written information, regarding the nature of their VTE risk and how this can be managed. This may be an effective safe and inexpensive way of reducing VTE risk. It is important that patients’ adherence be regularly checked when they are seen by the surgeon, the plaster technicians, or physiotherapists in order to improve adherence to this routine of exercises. Although there is evidence that chemical thromboprophylaxis reduces the incidence of VTE in patients treated with lower limb cast immobilization, 6 small RCTs totaling 1536 patients found that 9.8% (down from 17.1%) of patients still experienced a DVT despite administration of low-molecular-weight heparin (LMWH).3,8,12 If our findings are confirmed in clinical studies, they may be useful in improving the success rate in high-risk patients who are given chemical prophylaxis. However, it is possible that our recommendations may be most useful in patients who are not felt to require LMWH because they are low risk but who are nonetheless still at some risk. In trauma patients treated with cast, Achilles tendon injury has been highlighted as being associated with a particularly high risk of venous thrombo-embolism, with rates of up to 34% reported.5,9,12 This increase in risk may be associated with the fact that there is a significant loss of the calf pump due to the rupture or the equinus position. In this group, maximization of the pump may not be possible. Also it is likely that weight bearing results in some increase in flow, but this was not measured in our study because this will vary with the type of injury/surgery and the resulting amount of pain. We acknowledge several limitations to our study. First, we performed measurements on healthy participants and excluded participants with peripheral vascular disease, diabetes, varicose veins, DVT, or previous foot and ankle surgery. Second, participants were asked to perform movements to their best efforts. This is likely to have resulted in a bestcase result, which may not represent clinical practice. However, the increases between baseline and peak popliteal velocity reached extreme statistical significance (P < .0001) in all cases, and therefore we expect that these movements would also result in significant increases in patients who may have impaired calf pump function due to comorbidity. The movements we recommend can occur naturally in patients with below-knee casts as they mobilize during the course of their day, and the movements do not need to be dramatic to achieve good flow. Therefore we think that focusing on these movements regularly throughout the day will not have any detrimental effect on fracture alignment, but this will need to be investigated. We have approval from our local research and ethical committee and are in the process of performing a further study to investigate these questions.
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Hickey
Conclusion This is the first study to examine the effect of a lower limb cast on calf pump function. Despite cast immobilization, toe and ankle flexion and extension movements significantly increased peak systolic velocity measured at the popliteal vein. We recommend that all patients treated with below-knee cast immobilization be advised to perform regular knee, toe, and ankle exercises because this reduces venous stasis and may reduce risk of DVT. We believe that this should be offered routinely and that high-risk patients should continue to be offered LMWH until further evidence is available. Declaration of Conflicting Interests The author declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding The author received no financial support for the research, authorship, and/or publication of this article.
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venous flow and prevent venous stasis. Eur J Vasc Endovasc Surg. 2010;40(6):766-771. 5. Healy B, Beasley R, Weatherall M. Venous thromboembolism following prolonged cast immobilisation for injury to the tendo Achillis. J Bone Joint Surg Br. 2010;92(5):646-650. 6. Izumi M, Ikeuchi M, Mitani T, Taniguchi S, Tani T. Prevention of venous stasis in the lower limb by transcutaneous electrical nerve stimulation. Eur J Vasc Endovasc Surg. 2010;39(5):642-645. 7. Kujath P, Spannagel U, Habscheid W. Incidence and prophylaxis of deep venous thrombosis in outpatients with injury of the lower limb. Haemostasis. 1993;23(suppl 1):20-36. 8. Nokes TJ, Keenan J. Thromboprophylaxis in patients with lower limb immobilization—review of current status. Br J Haematol. 2009;146(4):361-368. 9. Patil S, Gandhi J, Curzon I, Hui A CW. Incidence of deep-vein thrombosis in patients with fractures of the ankle treated in a plaster cast. J Bone Joint Surg Br. 2007;89(10):1340-1343. 10. Pitto RP, Hamer H, Heiss-Dunlop W, Kuehle J. Mechanical prophylaxis of deep-vein thrombosis after total hip replacement a randomised clinical trial. J Bone Joint Surg Br. 2004;86(5):639-642. 11. Struijk-Mulder MC, Etterna HB, Verheyen CC, Buller HR. Comparing consensus guidelines on thromboprophylaxis in orthopaedic surgery. J Thromb Haemost. 2010;8(4):678-683. 12. Testroote M, Stigter W, de Visser DC, Janzing H. Low molecular weight heparin for prevention of venous thromboembolism in patients with lower-leg immobilization. Cochrane Database Syst Rev. 2008;(4):CD006681. 13. Van Stralen KJ, Rosendaal FR, Doggen CJ. Minor injuries as a risk factor for venous thrombosis. Arch Intern Med. 2008;168(1):21-26. 14. Virchow RLK. Thrombose und Embolie. Gefässentzündung und septische Infektion. Gesammelte Abhandlungen zur wissenschaftlichen Medicin. Frankfurt am Main, Germany: Von Meidinger & Sohn; 1856. Translation in Matzdorff AC, Bell WR. Thrombosis and Embolie (1846-1856). Canton, MA: Science History Publications; 1998.
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