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Review Article

Safe Tourniquet Use: A Review of the Evidence

Fitzgibbons, Peter G. MD; DiGiovanni, Christopher MD; Hares, Sayed MD; Akelman, Edward MD

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Journal of the American Academy of Orthopaedic Surgeons: May 2012 - Volume 20 - Issue 5 - p 310-319
doi: 10.5435/JAAOS-20-05-310
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For hundreds of years, surgeons have used tourniquets to afford a bloodless surgical field in extremity surgery. The tourniquet may be used to minimize blood loss and improve visualization within the surgical field.

The decision to use a tourniquet is based on many factors, including the technical demands of the procedure, the location and duration of the procedure, and the anticipated blood loss. Efforts to minimize or ameliorate blood loss using pharmacologic or other methods (eg, tranexamic acid, hypotensive anesthesia, intraoperative blood salvage) may affect this decision. In every case, the benefits of tourniquet use must be weighed against the risks.

The deleterious effects of prolonged tourniquet use are well established. Published and anecdotal recommendations abound regarding appropriate pressure, design, duration of inflation, and number of acceptable reinflations for any given patient in a single surgical setting. Increased emphasis on quality and cost control in healthcare institutions has led to the development of protocols for acceptable practice standards, including protocols for tourniquet use.

In the institution of the senior authors (C.D. and E.A.), an effort to establish a policy for tourniquet use involved a detailed review of the literature. Published protocols advocate a range of practices, and the strength of the evidence is variable1-3 (Table 1). These standards have medical, financial, and legal implications; as such, they must be grounded in a solid understanding of medical facts.

Table 1
Table 1:
Published Recommendations on Tourniquet Use

Animal and human studies of tourniquet use are summarized in Table 2 and Table 3, respectively. These studies present information on the acceptable limits of tourniquet duration, pressure, and design. Other important factors include skin protection under the tourniquet, blood loss, and techniques for attenuating metabolic changes.

Table 2
Table 2:
Findings of Animal Model Tourniquet Studies
Table 2
Table 2:
Table 3
Table 3:
Findings of Clinical Tourniquet Studiesa
Table 3
Table 3:

Complications of Tourniquet Use

Tourniquet-related pathogenesis is related to ischemia and compression. The metabolic effects are related to the sequelae of ischemic tissue, whereas nerve and muscle damage are more likely a function of direct compression beneath the tourniquet itself. Controversy exists regarding the influence of tourniquet design on compressive damage to the soft tissues. Tourniquet width is of particular interest.

Muscle Injury

Skeletal muscle injury is reasonably well documented. Studies have measured tourniquet-induced changes in technetium-99m pyrophosphate (99mTc PYP) uptake in muscle, contractile function, and histology. In a rabbit model, 99mTc PYP uptake was found to be elevated following use of a thigh tourniquet for 2 hours at 200 or 350 mm Hg of pressure and for 4 hours at pressure as low as 125 mm Hg.48 Uptake was greatest at the site of compression in the thigh, which is indicative of particular vulnerability to compression.

Tourniquet use impairs muscle contractile function, with compressed muscle experiencing greater dysfunction than the more distal ischemic muscle.12 In a rabbit model, quadriceps musculature compressed at 350 mm Hg of pressure for 2 hours demonstrated markedly decreased function at 2 days postoperatively (21% of normal).49 However, the muscle demonstrated restoration to 83% of normal at 3 weeks. Lower leg muscles experienced a milder decrement initially than did the quadriceps, with variable recovery to near normal levels.

Multiple studies have documented tourniquet-induced muscle injury at a histologic level.11 In a canine study, early signs of muscle damage, including granular degeneration, inflammatory reaction, and edema, were found following 1 to 2 hours of compression at 350 mm Hg.6 In a rabbit model, notable focal and regional necrosis was noted in the thigh 2 days after a 4-hour tourniquet time at 350 mm Hg of pressure.48 Cellular infiltration and milder necrosis were noted in the leg. Marked but less severe changes were seen with tourniquet pressure measuring 350 mm Hg for a duration of 2 to 3 hours.

Nerve Injury

Nerve injury caused by tourniquet use has been documented on histologic examination, electromyography (EMG), and nerve conduction velocity (NCV) studies. Compared with skeletal muscle, nerve tissue seems to be less vulnerable to acute injury, although the effects of injury appear to be longer-lasting in nerve tissue following mild to moderate insult.

In one histologic study, rat sciatic nerve structure was evaluated with electron microscopy 14 days after application of a tourniquet at 300 mm Hg of pressure for periods of 30 minutes to 3 hours.8 Damage ranged from no change to mild change at 30 minutes to complete myelin dissolution and Schwann cell hypertrophy at 3 hours. Myelin sheath rupture appeared after 2 hours; this finding has been confirmed in other studies. 10 Similar findings have been noted in light microscopy studies, with mild changes at 2 hours progressing to significant edema with prolonged times at tourniquet pressure of 350 mm Hg.50 As with skeletal muscle studies, damage was worse in compressed tissue than in ischemic tissue.

Nerve injury has been measured on EMG and NCV studies, as well.9 One clinical study documented changes on EMG in 62.5% of orthopaedic patients postoperatively.51 EMG abnormality lasted an average of 51 days (patients were examined monthly), and prolonged tourniquet time contributed to the incidence and severity of abnormalities. NCV studies in rabbits have shown significant changes with compression lasting 2 and 4 hours at tourniquet pressure of 350 mm Hg, although notable changes are mild or absent in distal nerves.26,27 Clinically, the incidence of peroneal and tibial nerve palsy rises with tourniquet times >150 minutes. 31

Metabolic Dysfunction

Studies measuring metabolic parameters have attempted to address the mechanisms underlying tourniquetinduced injury of muscle and nerve tissue. Lactic acid, pH, glucose, and reactive oxygen metabolites such as hypoxanthine and xanthine are acutely affected by tourniquet use.52-55

Most studies have reported a rapid return to normal local acid-base balance following tourniquet release. For example, pH has been found to normalize within 20 minutes following pressure of 300 mm Hg for 3 hours in a canine model16 and within 40 minutes following pressure of 300 mm Hg for 4 hours in monkeys.7 In humans, measurements in the right atrium have demonstrated minor changes in pH after tourniquet release, and metabolic indicators have been found to normalize within 120 minutes of tourniquet cessation.7 In dogs, adenosine triphosphate levels do not fall at tourniquet durations of <3 hours. Although the adenosine triphosphate buffer phosphocreatinine drops markedly, it is usually reconstituted within minutes.14

Coagulopathy and Deep Vein Thrombosis

Several clinical studies have demonstrated increased fibrinolytic activity following tourniquet use, but no clinically significant changes have been documented.56-58 Multiple studies have investigated the role of the tourniquet in the production of pulmonary emboli and the resulting clinically significant cardiopulmonary symptoms. Pulmonary emboli have been recorded by transesophageal echocardiogram during knee arthroscopies and arthroplasties performed with and without tourniquets. 37,57,59 In one study, the incidence ranged from 6% to 79% depending on the procedure performed, with a nonstatistically significant increased incidence of emboli in the patients on whom a tourniquet was used.37 None of the studies found clinically relevant cases of pulmonary embolus. Another study found a decreased rate of deep vein thrombosis following tourniquet use, which was presumed to be the result of increased fibrinolytic activity. 30

Clinical Recovery and Pain

More recent investigations have focused on the impact of tourniquet use on clinical recovery and pain. The parameters for gross injury to extremities and frank necrosis of tissue have been fairly well defined, but these newer clinical studies attempt to define the incidence of more subtle injury that is reversible in the long term but may have a measurable impact on recovery.

Several studies have compared surgery with and without tourniquet use.28,29,38,41 Two such studies evaluated patients undergoing anterior cruciate ligament reconstruction. With similar tourniquet durations and inflation pressures, patients on whom a tourniquet was used had increased quadriceps atrophy and measurable EMG changes28 as well as decreased strength29 compared with the nontourniquet group at 4- to 12-week follow-up. No differences were found between patients at 1-year follow-up in either study. Similarly, Kirkley et al38 found no significant differences in clinical parameters after knee arthroscopy. One level I study that compared open reduction and internal fixation of the ankle with and without a tourniquet found greater pain, swelling, and complications up to 6 weeks postoperatively in the tourniquet group.40

Recommendations for Tourniquet Use

Recommendations for safe tourniquet use are listed in Table 4. No one protocol is appropriate for all situations and patients. The three factors that must be considered in every case are duration of tourniquet use, inflation pressure, and tourniquet design.

Table 4
Table 4:
Recommendations for Safe Tourniquet Use


One difficulty in applying the results of experimental studies in clinical practice is that durations studied tend to increase in increments of ≥1 hour. Although this makes it more feasible to conduct studies, it likely contributes to the establishment of 2 hours as a common upper limit. A threshold of 2.5 hours may have clinical relevance, but this threshold is nonexistent in basic science research. In general, animal studies suggest that at 2 hours of tourniquet inflation, the histologic, electrophysiologic, and functional impact of the tourniquet, while measurable, remains reversible.6,7,9,10,12-14,16,24,25,27 Most changes following tourniquet times of 3 hours also were temporary, depending on the measurements and duration of the study.6,7,11,13,23

Few clinical studies use tourniquet times >2 hours. In one such study, Horlocker et al31 evaluated prolonged tourniquet times in persons undergoing revision total knee arthroplasty (average, 145 min). The rate of postoperative tibial and/or peroneal nerve palsy was 7.7%. Long-term consequences were few, with complete recovery in 100% of tibial palsies and 89% of peroneal palsies. For procedures involving a tourniquet time of ≥180 minutes, a deflation interval of ≥30 minutes was associated with fewer neurologic complications (22% incidence) than were those without a deflation interval (42% incidence) or with an interval <30 minutes (39% incidence).

High-quality clinical studies (levels I and II) with tourniquet times of ≤2 hours indicate that although electrophysiologic changes and muscle atrophy are detectable at short-term follow-up, functional differences are rare, and long-term outcomes are equivalent between standard tourniquet groups and groups with low or no tourniquet time.28,29,38-41,46,47 The customary 2-hour tourniquet time limit seems to be derived largely from animal studies that begin to show changes at 2 to 3 hours and from clinical studies that demonstrate few negative consequences within that time limit. In the absence of a compelling clinical need for consistent tourniquet times >2 hours, a controlled clinical study of prolonged tourniquet times is likely unnecessary. No data contradict the practice of maintaining tourniquet inflation for >2 hours in the rare clinical situations in which it is necessary.

Reperfusion intervals have been studied in animals and humans. Protocols differ substantially, but most studies support the use of a reperfusion interval and find that longer intervals result in diminution of tissue damage.14,31

Inflation Pressure

Many animal and human studies employ inflation pressures higher than those typically used in clinical practice. Those human clinical studies cited in Table 3 that employed fixed inflation pressures reported an average thigh tourniquet pressure of 338 mm Hg.28-31,33,34,36-41,44-46 In a large study of tourniquet use and its complications, the average pressure was 300 mm Hg.37 Animal data clearly demonstrate that higher inflation pressures impart greater insult on compressed nerve and muscle than do lower pressures.10,13,50 Most of these changes have been shown by using tourniquet pressures up to 1,000 mm Hg, so it is difficult to extrapolate from the literature the significance of a difference in 25 or 50 mm Hg at lower pressures. Few clinical studies show significant or frequent pathology within the ranges studied; thus, pressures employed clinically (ie, ≤300 mm Hg) seem to be well within a safe zone of use.

Several techniques have been described for determining limb occlusion pressure (LOP). Because this measurement accounts for the specific tourniquet configuration and limb girth, it would seem to be a more accurate representation of arterial occlusion than systolic blood pressure. Techniques for measuring LOP involve the use of a commercial device, monitoring of the obliteration of distal pulses with a Doppler stethoscope during cuff inflation, or use of a formula based on limb circumference. 60,61 One report indicates that measurement and use of LOP plus a safety margin may allow for a tourniquet inflation pressure that is lower than the standard fixed inflation pressure.60 Both methods typically involve a pressure margin above the LOP or systolic blood pressure that should allow for intraoperative variation in blood pressure. No studies have demonstrated a difference in clinical outcomes attributable to the use of LOP in determining tourniquet pressure.

Recommendations for tourniquet pressure setting commonly use lower values for the upper extremity than for the lower extremity. No clinical studies exist indicating that either extremity is more prone to injury than the other. One study measuring the pressure at which capillary bleeding occurs found lower values for the upper extremity than for the lower extremity.62 A tourniquet pressure of 200 mm Hg in the upper extremity and 250 mm Hg in the lower extremity was found to be adequate to produce a bloodless field in normotensive persons of average build. This difference is presumably a function of limb girth, with occlusion occurring at a lower pressure in the upper limb.

Tourniquet Design

The development of new tourniquets has spurred debate regarding the safety and efficacy of different types of tourniquets. These debates largely revolve around the effect of the width of the tourniquet on both the pressure setting required to achieve a bloodless field and the pathogenesis of soft-tissue injury.

In a baboon model, Ochoa et al10 demonstrated nerve damage directly beneath the cuff and suggested that the damage is caused by the gradient of pressure at the edge of the cuff. The width of the tourniquet itself was not studied. However, the implication that use of a narrower cuff might result in less nerve damage has been used in part to justify the recent development of a narrow nonpneumatic silicone ring tourniquet.63,64

A recent study found median nerve conduction to be more severely affected with the use of a 14-cm tourniquet than with a 7-cm tourniquet following 15 minutes of inflation.32 With both sizes of tourniquet, conduction normalized by 30 minutes after deflation. Other studies have suggested that a wider cuff is safer because it allows for the occlusion of blood flow at a lower pressure.65,66 No studies have demonstrated clinical benefit in terms of neurologic changes or functional outcomes with the use of a particular tourniquet design.


Clinical situations involving tourniquet use require at least three decisions: the type (ie, shape) of tourniquet, inflation pressure, and continuous duration of occlusive pressure. These questions are often addressed separately in recommendations. However, studies have shown that although each has its own effect on target outcomes, these factors are additive and the exact relationship between them is unclear.9 For example, the clinical difference between 120 and 140 minutes of tourniquet time is not clear, and the additional impact of 25 or 50 mm Hg more or less inflation pressure on that time difference is unknown.

The available clinical and basic scientific data on tourniquet use do not indicate a significant risk of complications within the confines of typical use during orthopaedic surgery, and no single standard exists for tourniquet use in all settings. In general, for procedures involving <2 hours of tourniquet time, standard practices should suffice in terms of inflation pressure and tourniquet design. Preoperative identification of procedures that are likely to involve prolonged tourniquet times (ie, >2 hours) allows the surgeon, anesthesiologist, and operating room staff ample time to agree on and institute measures that may ameliorate known risks that are difficult to clearly define. In such situations, recommendations include the use of wide, shaped cuffs, the preoperative measurement of LOP by either Doppler stethoscope or commercial device, and the use of a reperfusion interval at 2 hours for procedures lasting >2.5 hours.


Evidence-based Medicine: Levels of evidence are described in the table of contents. In this article, references 28, 34, 38, 40, 41, 46, 57, 58, and 66 are level I studies. References 7, 29, 32, 33, 39, 42, 43, 47, 51-56, 59-62, 64, and 65 are level II studies. References 44 and 45 are level III studies. References 30, 31, and 35-37 are level IV studies. Reference 63 is level V expert opinion.

References printed in bold type are those published within the past 5 years.

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