Skip to main content
Online Exclusives

Current Insights And Recommendations For Tourniquet Use In Foot And Ankle Surgery – Part 2: Potential Complications

Due to a lack of concise, standardized guidelines for implementation in foot and ankle surgery, these authors provide a literature review and extrapolate recommendations from existing data existing on safe lower extremity tourniquet use. This article is part of a three-part series covering indications, complications and recommendations for use.

When examining the litany of documented adverse events associated with tourniquet use, there are three easily-identified, broad categories of tourniquet-related complications: muscle injury; nerve injury; and coagulopathy. All of these complications fundamentally relate to ischemia and compression resulting from tourniquet use. While one can instinctively think of nerve and muscle damage as related to direct pressure (or compression), all three categories are more likely secondary to a combination of both ischemic and compressive factors.

What Is The Relationship Between Muscle Injury And Tourniquet Use?

Muscle Injury. This can manifest as decreased contractile strength; reperfusion injury; pain or post-tourniquet syndrome. Skeletal muscle injury in relation to tourniquet use is reasonably well-documented and is influenced both by the compression and ischemia created from a tourniquet. The skeletal muscles distal to the tourniquet experience these effects at a molecular level, primarily through prolonged inadequate blood flow (i.e. ischemia) and subsequent restoration of circulation (i.e. reperfusion injury).

When creating an ischemic environment in skeletal muscle via application of a tourniquet, the response at the cellular level includes decreased protein synthesis, increased degradation of protein and an up-regulation of cell stress pathways (including increased glycerol), creating an environment for reperfusion injury.1-3 The rate of skeletal muscle metabolic recovery with reperfusion depends on the duration of ischemia;1-2 this recovery rate lengthens significantly after three hours of ischemia secondary to adenosine triphosphate (ATP) depletion in an anaerobic metabolic environment.4-8

Aside from reperfusion injury at a cellular level, one can also observe muscular injury changes at the histologic level. Following one to three hours at a 350mmHg (400mmHg for human reference) tourniquet setting, early signs of muscle damage in human, canine and rabbit studies included inflammatory reactions, intra-fiber and extracellular edema, mild focal and regional necrosis, and granular degeneration.6,7,9-11 The combined effect of muscle ischemia with micro-traumatic changes from tourniquet use results in the coined phenomena “post-tourniquet syndrome,” characterized by stiffness, pallor, weakness and subjective numbness of the affected extremity (without objective anesthesia).12

Along with ischemic injury to skeletal tissues, compression injuries via tourniquet application can result in muscular deficits post-operatively.4,13-16

In a rabbit model, quadriceps musculature compressed at 350 mmHg for two hours demonstrated markedly decreased function at two days postop (21 percent of normal) with restoration to only 83 percent of normal at three weeks.6,17 Longer periods of post-operative monitoring in total knee arthroplasty (TKA) trials (up to three months), which demonstrate quadriceps muscular deficits with tourniquet use at the three-month mark in comparison to the control group (no tourniquet utilized).18

When considering the use of a tourniquet during surgery, the complications on a physiologic level may seem remote, however, these changes could potentially result in functional abnormalities that interfere with patient rehabilitation and overall outcomes. Currently, increased interest in tourniquet-induced muscle injury and its implication on post-operative outcomes may shed additional light on proposed tourniquet standards.18,19

What You Should Know About Nerve Injury And Surgical Tourniquets

Nerve Injury. Though seemingly rare, the reported risk of neurological complications (sensory neuropathy, pain, paralysis) stemming from tourniquet use is documented to range between 0.1 and 7.7 percent, primarily been documented in studies utilizing thigh tourniquets.20-25 Along with incidence, the severity of nerve injuries related to tourniquet usage also varies. Reports range anywhere from a mild transient functional loss to permanent irreversible damage.24 One might question the exact relationship between tourniquet use and nerve function based on this variance.

Generally well-studied via multimodal examination techniques, including histologic evaluation, nerve conduction velocity (NCV) studies and electromyography (EMG), the two primary postulated etiologies that we observed for tourniquet-induced nerve injury are ischemia and direct mechanical effects (i.e. pressure, shearing forces, etc.).

Compression to a nerve can result in axonal degeneration, as well as have a direct effect to the Nodes of Ranvier (via paranodal myelin invagination), thereby impacting the quality of nerve function.26,27 In their 1972 study, Ochoa and colleagues demonstrated and explained the functional impact of tourniquet use as it relates to nerve injury; with severe nerve injuries resulting in Wallerian degeneration, creating a loss of nerve excitability distal to the lesion origin (recovery may take many months), intermediate nerve injuries resulting in a local conduction block with preservation of distal excitability (recovery may take several weeks) and mild nerve injuries producing a physiological block (immediate recovery occurring with pressure release).26

Though utilizing much higher tourniquet pressures than currently acceptable, historical studies helped demonstrate that nerve injury and dysfunction is most prominent at the outer edges of the tourniquet cuff where shear stress is maximal, sparing the central cuff portion, and sparing the nerves distal to the cuff from direct injury.26 As with the natural history of nerve injuries, dependent on the severity, partial or incomplete nerve lesions are generally likely to undergo spontaneous resolution within six months.12

Though nerve injury correlated to tourniquet use variables (duration, pressure, population, etc.) in human subjects is not abundatnt in literature, some studies do exist. In 1979, one clinical study aimed to distinguish the relationship between EMG abnormalities, the duration of tourniquet inflation and patient clinical recovery time as it relates to thigh tourniquet use during orthopedic procedures.28 This study demonstrated that compression duration resulted in distinct differences in EMG abnormalities, with short tourniquet time (less than 15 minutes) revealing 22 percent of subjects with EMG abnormalities and longer tourniquet time (greater than 60 minutes) resulting in 85 percent of subjects with EMG abnormalities. In total, 62.5 percent of patients in the study had documented changes on EMG postop; with an average duration of 51 days (ranging from 27 days to five months) prior to resolution.28 The authors hypothesized this delayed recovery to result from a slowly-resolving axonal compression syndrome caused by prolonged inflation of the pneumatic tourniquet. This study supports the inverse relationship between duration of tourniquet use and nerve function; with greater duration of tourniquet use resulting EMG changes both in the proximal thigh muscles (quadriceps) and extending to posterior lower leg muscles (gastrocnemius). The authors also demonstrate a direct relationship between duration of use and time to clinical recovery (i.e. increased tourniquet inflation time is related to increased time to clinical recovery).28

Instead of looking at the specific changes in neurological function and characterizing the severity of nerve injury, some studies aim to quantify the overall probability of nerve injury with tourniquet use and identify any risk factors.20,26,29 As previously mentioned, the incidence of nerve injury ranges anywhere from 0.1 to 7.7 percent with the majority of literature derived from thigh tourniquet use.20-23,25

A 2018 retrospective review of close to 40,000 total knee arthroplasties, identified risk factors for nerve injury with tourniquet use and found a total incidence of 0.16 percent.25 One risk factor described in this review and others is the relationship demonstrated between increased peroneal nerve palsies (i.e. foot drop) and patients with lumbar pathologies (history of lumbar stenosis, lumbar spine surgery, etc.).25,30,31 This review also identified an increased incidence of nerve injury in the female gender, hypothesized to be secondary to reduced soft tissue (muscle/fat), thought to protect the nerve from direct injury via compression.25

From a 2006 retrospective review of neurologic complications during orthopedic procedures, authors noted that nerve palsies documented included peroneal and tibial nerves, 89 percent of the peroneal nerve palsies resolved, 100 percent of the tibial nerve palsies recovered, reperfusion intervals only modestly decreased the probability of nerve injury and, in general, the probability of neurologic dysfunction increased with tourniquet time (incidence of palsies increased when tourniquet time is greater than 150 minutes).20 Other studies echo the observance of mononeuropathy incidence being greater in sciatic (approximately 91 percent, tibial and peroneal) distributions, followed by femoral distribution (approximately nine percent of all tourniquet-related mononeuropathies) but fail to find a direct relationship between tourniquet time and nerve injury probability.20 Though tourniquet time and specific nerve-related injury could be ‘debatable,’ the use of a tourniquet for two or less hours is the standard of care until randomized control trials establish a more optimal tourniquet time.

What About CRPS?

When discussing nerve injuries and tourniquet usage, it is prudent to mention complex regional pain syndrome type I (CRPS-I; also referred to as reflex sympathetic dystrophy) and how, if at all, it relates to tourniquet usage. Some propose that CRPS-I may be secondary to an ischemia-reperfusion injury in which there is alteration on a microcirculatory level leading to persistent inflammation and symptoms resembling CRPS-I.32 Others researching this topic suggest a physiologic alteration of oxygen consumption that occurs with subsequent reperfusion after tourniquet deflation, leading to increased formation of toxic oxygen radicals and predisposing an individual to the development of CRPS.33

This theory has led to certain recommendations of perioperative prophylactic measures targeted to reduce the radicals and/or scavengers, thus hypothetically decreasing the chance of CRPS recurrence or progression of the condition.33 In 2009, Besse and colleagues attempted to elucidate the relationship between tourniquet use and CRPS development by evaluating for factors associated with CRPS occurrence after foot and ankle surgery. In this study, they demonstrated a 10-fold increased risk and statistically significant correlation for patients with prior history of CRPS and development of the condition after surgery.34

Though an association in literature between CRPS diagnosis and a history of CRPS exists34, the relationship between development of CRPS and tourniquet usage remains unclear. However, with the information at hand, surgeons planning to operate with use of a tourniquet on patients with a history of CRPS should consider implementation of preventative modalities and measures to decrease risk of CRPS recurrence until there is further clarification of the association between tourniquets and CRPS incidence.

Summarizing The Key Findings Regarding Tourniquets And Nerve Injury

In general, the findings from our literature review on tourniquet-induced nerve injuries are as follows:

• Nerve injury incidence ranges from 0.1 to 7.7 percent;20-23, 25

• Mechanical pressure directly under the cuff is a greater factor in nerve injury than distal ischemia created by the tourniquet;12, 26, 35 

• Nerve injury is most marked at the proximal and distal edges of a compression tourniquet, where shear stress forces are maximal;23,26

• Most commonly involved mononeuropathies are (in descending order): peroneal nerve > tibial nerve > femoral nerve (no obturator mononeuropathies were identified in reviews); and20,25

• Risk factors for nerve injuries include female gender, preoperative history of lumbar disease or lumbar surgery, anesthesia duration greater than two hours, prior history of CRPS.25,34

What Impact Might Tourniquet Use Have On Coagulopathies?

Deep Vein Thrombosis (DVT)/ Pulmonary Embolism (PE). Application of a pneumatic tourniquet creates potential for changes in coagulability and fibrinolysis; however, the act of a surgical procedure alone may also cause a hypercoagulable state independent of tourniquet use.12 For instance, pain created either by the surgery or the tourniquet application provokes the release of catecholamines, which in turn promotes platelet aggregation, altogether leading to a hypercoagulable state.36

Research indicates a grossly under-reported incidence of DVTs postoperatively in foot and ankle surgery37,38 and no statistically significant correlation between DVT formation or pulmonary embolic events and tourniquet use.39 Therefore, it is difficult to determine the exact rate of DVT/PE in lower extremity procedures with tourniquet use, and moreover how that complication rate impacts current practice (as DVT is regarded by some as a low-risk complication and standardized prophylaxis is not currently routinely implemented).

In a 2018 study, Sullivan and colleagues attempted to determine the probability of DVT in lower extremity midfoot and hindfoot procedures via ultrasound at the standard two- and six-week postoperative follow up.37 Of 114 procedures, the ubiquity of DVT was 25.4 percent, with a majority (68.9 percent) of the diagnoses occurring at the two-week mark and the remainder diagnosed at the six- week postoperative visit. All DVTs found were distal to the popliteal vein.37 Within the study population, only six percent of DVTs were clinically detectable. Factors that increased risk of early DVT findings were age (greater than or equal to 62 years) and tourniquet time (greater than or equal to 68 minutes). However, there were no statistically significant factors between late DVT findings and age or tourniquet duration.37

Though multiple studies focused on the development of venous thromboembolic events found an increased hypercoagulable state in relation to lower extremity tourniquet use, a consistent, statistically significant correlation has yet to be determined.12,37,39-41

Dr. Wilson is a third-year Podiatric Medicine and Surgery resident at St. Mary’s Medical Center in San Francisco, Calif.

Dr. Oloff is the Podiatric Medicine and Surgery Residency Program Director at St. Mary’s Medical Center in San Francisco, Calif. He is an attending physician at the Palo Alto Medical Foundation in Burlingame, Calif.

Editor’s Note: For part 1 of this three-part series, “Current Insights And Recommendations For Tourniquet Use In Foot And Ankle Surgery – Part 1: Indications And Precautions,” visit https://tinyurl.com/4wcfbhzw .

Online Exclusives
By Amy G. Wilson, DPM and Lawrence M. Oloff, DPM, FACFAS
References

1. Leurcharusmee P, Sawaddiruk P, Punjasawadwong Y, Chattipakorn N, Chattipakorn SC. The possible pathophysiological outcomes and mechanisms of tourniquet-induced ischemia-reperfusion injury during total knee arthroplasty. Oxid Med Cell Longev. 2018;2018:8087598. doi: 10.1155/2018/8087598.

2. Rasmussen LE, Holm HA, Kristensen PW, Kjaersgaard-Andersen P. Tourniquet time in total knee arthroplasty. Knee. 2018;25(2):306-313.

3. Muyskens JB, Hocker AD, Turnbull DW, et al. Transcriptional profiling and muscle cross-section analysis reveal signs of ischemia reperfusion injury following total knee arthroplasty with tourniquet. Physiol Rep. 2016;4(1):e12671.

4. Patterson S, Klenerman L, Biswas M, Rhodes A. The effect of pneumatic tourniquets on skeletal muscle physiology. Acta Orthop Scand. 1981;52(2):171-175.

5. Sapega AA, Heppenstall B, Chance B, Park YS, Sokolow D. Optimizing tourniquet application and release times in extremity surgery. J Bone Joint Surg Am. 1985;67:303-314.

6. Pedowitz RA, Gershuni DH, Schmidt AH, Fridén J, Rydevik BL, Hargens AR. Muscle injury induced beneath and distal to a pneumatic tourniquet: A quantitative animal study of effects of tourniquet pressure and duration. J Hand Surg Am. 1991;16(4):610-621.

7. Pedowitz RA, Nordborg C, Rosengvist AL, Rvdevik BL. Nerve function and structure beneath and distal to a pneumatic tourniquet applied to rabbit hindlimbs. Scand J Plast Reconstr Surg Hand Surg. 1991;25(2):109-120.

8. Pedowitz AR, Gershuni DH, Fridén J, Garfin SR, Rydevik BL, Hargens AR. Effects of reperfusion intervals on skeletal muscle injury beneath and distal to a pneumatic tourniquet. J Hand Surg Am.1992;17(2): 245-255.

9. Klenerman L, Lewis JD. Incompressible vessels. Lancet. 1976;1(7963):811-812.

10. Heppenstall RB, Balderston R, Goodwin C. Pathophysiologic effects distal to a tourniquet in the dog. J Trauma. 1979;19(4):234-238.

11. Appell HJ, Gloser S, Duarte JA, Zellner A, Soares JM. Skeletal muscle damage during tourniquet-induced ischaemia. The initial step towards atrophy after orthopaedic surgery? Eur J Appl Physiol Occup Physiol. 1993;67(4):342–347.

12. Kam PC, Kavanagh R, Yoong FF. The arterial tourniquet: pathophysiological consequences and anaesthetic implications. Anaesthesia. 2001;56(6):534-545.

13. Krebs DE. Isokinetic, electrophysiologic, and clinical function relationships following tourniquet-aided knee arthrotomy. Phys Ther. 1989;69(10):803–815.

14. Jacobson MD, Pedowitz RA, Oyama BK, Tryon B, Gershuni DH. Muscle functional deficits after tourniquet ischemia. Am J Sports Med. 1994;22(3):372-377.

15. Mizner RL, Petterson SC, Stevens JE, Vandenborne K, Snyder-Mackler L. Early quadriceps strength loss after total knee arthroplasty. The contributions of muscle atrophy and failure of voluntary muscle activation. J Bone Joint Surg Am. 2005;87(5):1047–1053.

16. Meier W, Mizner RL, Marcus RL, Dibble LE, Peters C, Lastayo PC. Total knee arthroplasty: muscle impairments, functional limitations, and recommended rehabilitation approaches. J Orthop Sports Phys Ther. 2008;38(5):246–256.

17. Mohler LR, Pedowitz RA, Lopez MA, Gershuni DH. Effects of tourniquet compression on neuromuscular function. Clin Orthop Relat Res. 1999;359:213-220.

18. Dennis DA, Kittelson AJ, Yang CC, Miner TM, Kim RH, Stevens-Lapsley JE. Does tourniquet use in tka affect recovery of lower extremity strength and function? A randomized trial. Clin Orthop Relat Res. 2016;474(1):69-77.

19. Page RS, Williams S, Selvaratnam A, et al. Protocol for a single-centre, parallel-arm, double-blind randomised trial evaluating the effects of tourniquet use in total knee arthroplasty on intra-operative and post-operative outcomes. BMC Musculoskelet Disord. 2018;19(1):435.

20. Horlocker TT, Hebl JR, Gali B, et al. Anesthetic, patient, and surgical risk factors for neurologic complications after prolonged total tourniquet time during total knee arthroplasty. Anesth Analg. 2006;102(3):950-955.

21. Odinsson A, Finsen V. Tourniquet use and its complications in Norway. J Bone Joint Surg (Br). 2006;88(8):1090-1092.

22. Jacob AK, Mantilla CB, Sviggum HP, Schroeder DR, Pagnano MW, Hebl JR. Perioperative nerve injury after total knee arthroplasty: regional anesthesia risk during a 20-year cohort study. Anesthesiology. 2011;114(2):311–317.

23. Estebe JP, Davies JM, Richebe P. The pneumatic tourniquet: mechanical, ischaemia-reperfusion and systemic effects. Eur J Anaesthesiol. 2011;28(6):404-411.

24. Olivecrona C, Blomfeldt R, Ponzer S, Stanford BR, Nilsson BY. Tourniquet cuff pressure and nerve injury in knee arthroplasty in a bloodless field: a neurophysiological study. Acta Orthop. 2013;84(2):159-164.

25. Shetty T, Nguyen JT, Sasaki M, et al. Risk factors for acute nerve injury after total knee arthroplasty. Muscle Nerve. 2018;57(6):946-950.

26. Ochoa J, Fowler TJ, Gilliatt RW. Anatomical changes in peripheral nerves compressed by a pneumatic tourniquet. J Anat. 1972;113:433–455.

27. Hodgson AJ. A proposed etiology for tourniquet-induced neuropathies. J Biomech Eng. 1994;116(2):224-227.

28. Saunders KC, Louis DL, Weingarden SI, Waylonis GW. Effect of tourniquet time on postoperative quadriceps function. Clin Orthop Relat Res. 1979;143:194-199.

29. Fitzgibbons PG, Digiovanni C, Hares S, Akelman E. Safe tourniquet use: a review of the evidence. J Am Acad Orthop Surg. 2012;20(5):310-319.

30. Park JH, Restrepo C, Norton R, Mandel S, Sharkey PF, Parvizi J. Common peroneal nerve palsy following total knee arthroplasty prognostic factors and course recovery. J Arthroplasty. 2013;28:1538–1542.

31. Ward JP, Yang LJ-S, Urquhart AG. surgical decompression improves symptoms of late peroneal nerve dysfunction after TKA. Orthopedics. 2013;36:515–519.

32. Coderre TJ, Bennett GJ. A hypothesis for the cause of complex regional pain syndrome - type I (reflex sympathetic dystrophy): pain due to deep- tissue microvascular pathology. Pain Med. 2010;11(8):1224–1238.

33. Veldman PH, Goris RJ. Surgery on extremities with reflex sympathetic dystrophy. Unfallchirurg. 1995;98(1):45-48.

34. Besse JL, Gaydene S, Galand-Desme S, Lerat JL, Moyen B. Effect of vitamin C on prevention of complex regional pain syndrome type I in foot and ankle surgery. J Foot Ankle Surg. 2009;15:179–182.

35. Denny-Brown D, Brenner C. Paralysis of nerve induced by direct pressure and by tourniquet. Arch Neurol Psychiatry. 1944;51(1):1-26.

36. Kohro S, Yamakage M, Arakawa J, Kotaki M, Omote T, Namiki A. Surgical/tourniquet pain accelerates blood coagulability but not fibrinolysis. Br J Anaesth. 1998;80(4):460-463.

37. Sullivan M, Dominiq-Eusebio I, Haigh K, Paulo-Panti J, Omari A, Hang J. Prevalence of deep vein thrombosis in low-risk patients after elective foot and ankle surgery. Foot Ankle Int. 2019;40(3):330-335.

38. Solis G, Saxby T. Incidence of DVT following surgery of the foot and ankle. Foot Ankle Int. 2002;23(5):411-414.

39. Jarrett PM, Ritchie IK, Albadran L, Glen SK, Bridges AB, Ely M. Do thigh tourniquets contribute to the formation of intra-operative venous emboli? Acta Orthop Belg. 2004;70(3):253-259.

40. Liem TK, Huynh TM, Moseley SE, et al. Symptomatic perioperative venous thromboembolism is a frequent complication in patients with a history of deep vein thrombosis. J Vasc Surg. 2010;52(3):651-657.

41. Hirota K, Hashimoto H, Kabara S, et al. The relationship between pneumatic tourniquet time and the amount of pulmonary emboli in patients undergoing knee arthroscopic surgeries. Anesth Analg. 2001;93(3):776-780.

 

 

 

Back to Top