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Review article

The pneumatic tourniquet: mechanical, ischaemia–reperfusion and systemic effects

Estebe, Jean-Pierre; Davies, Joanna M; Richebe, Philippe

Author Information
European Journal of Anaesthesiology: June 2011 - Volume 28 - Issue 6 - p 404-411
doi: 10.1097/EJA.0b013e328346d5a9



The first recorded use of a tourniquet was by a Roman surgeon in the second century AD. In 1817, a French surgeon, Jean-Louis Petit, described his device for haemostasis, which he named the ‘tourniquet’. The pneumatic tourniquet was introduced by Harvey Cushing in 1904 as an adjunct for surgery on the extremities. It is widely used to achieve relatively bloodless surgery, improve the identification of vital structures and expedite surgical procedures. Tourniquets are also used in combat and civilian emergency settings.

Patient safety has been improved and complications reduced by the development of wide, contoured and electronically controlled pneumatic cuffs. Despite this, tissue injury by compression under the pneumatic tourniquet cuff, and ischaemia–reperfusion injuries still occur. The combination of these different mechanical, ischaemia–reperfusion and systemic effects could explain the prolonged hospitalisation time and delayed return to work observed in tourniquet versus non-tourniquet groups.1–3

We have previously reviewed the effects of tourniquet use in orthopaedic surgery.4,5 Based on human and experimental studies published since 2000, this review describes the impact of mechanical, ischaemia–reperfusion and systemic effects of the pneumatic tourniquet, new techniques to minimise these effects and some of the proposed treatments for tourniquet-induced injury. We searched the MEDLINE database for studies using the term ‘pneumatic tourniquet’. All full-text randomised and non-randomised, controlled trials, case reports, letters, and guidelines were included.

Mechanical effects

Mechanical effects are those caused by direct compression of structures underneath the inflated tourniquet cuff. Use of correctly fitted and placed tourniquet cuffs with inflation pressures kept to a minimum reduces the potentially damaging impact of this compression.

Limb exsanguination

Limb exsanguination before tourniquet inflation is usually accomplished by mechanical means such as an Esmarch bandage, Rhys-Davies exsanguinator or crepe bandage. Aggressive exsanguination with any device increases the risk of disseminating tumour cells or infection and dislodgement of deep venous thromboses (DVTs) resulting in potentially fatal pulmonary emboli.6 Exsanguination of the limb by elevation alone is a slightly less effective, but is a safe and easy procedure. It permits better visualisation of superficial vessels compared with complete exsanguination, allowing better haemostasis.7 To achieve maximum exsanguination, it is recommended to elevate the arm at 90° for 5 min and elevate the leg at 45° for 5 min, without arterial compression, while the limb is surgically prepared and draped. If the pneumatic tourniquet is effective in occluding the extraosseous blood supply, some intraosseous blood supply is retained, which can make it difficult to obtain a completely bloodless field.8

Pressure under tourniquet

Skin, muscles, nerves and vessels may be damaged by the mechanical pressure of the tourniquet, as a result of sagittal forces causing compression, and axial forces causing stretching, due to the uneven distribution of pressure under the cuff (see Fig. 1).

Fig. 1
Fig. 1

Instead of using an arbitrary pressure (100–150 and 50–75 mmHg above systolic pressure for the lower and upper limbs, respectively),9 the minimal arterial occlusion pressure (AOP) should be determined before tourniquet application in order to minimise tissue injury.10 The AOP depends on the size of the tourniquet used.11 Graham's formula states:

AOP = [(systolic pressure−diastolic pressure) (limb circumference)/3(cuff width)] + diastolic pressure.12

The tourniquet pressure is then set at AOP and 50–75 mmHg. Using this formula, the tourniquet pressure can be decreased by 20–40% in adults11 and by more than 50% in children,13 compared with the arbitrary pressures often used. The tourniquet pressure must be adjusted during surgery relative to blood pressure. Recently, a new device has been introduced that synchronises the non-invasive blood pressure with the tourniquet pressure.14

If the AOP is not determined (as above), the tourniquet pressure used should be set at 75–100 mmHg above systolic arterial pressure.15 A pressure that occludes venous but not arterial blood flow can induce venous congestion, which is easily recognised during surgery. Calcified, non-compressible arteries may also cause tourniquet failure. The mass of tissue affected by the tourniquet is greater in the leg than in the arm. The tourniquet is usually applied at the most proximal part of the extremity, but placing it as distally as surgery allows (forearm, wrist, calf and forefoot) minimises the mass of tissue affected. A tourniquet at the calf must be positioned 3–4 cm below the fibular head (mid calf) to avoid injury to the common peroneal nerve.

The shape of the tourniquet is critical. A contoured rather than a straight tourniquet should be used for conical shaped limbs to minimise excessive pressure on one edge of the cuff, particularly in obese or very muscular patients (see Fig. 1). A wide or contoured cuff achieves haemostasis at lower inflation pressures than a narrow cuff and is painless when pressure is limited to the lowest effective level.16,17 Despite a possible risk of increased nerve injury, the widest curved cuff appropriate to the size of the extremity must be chosen (that is, wider than half the limb's diameter: >5 cm for the upper and >9 cm for the lower limb); the cuff should overlap by at least 7 cm but no more than 15 cm and must be connected to an integrated cuff inflation system.11,17–19

Tissue injury


Wrinkle-free padding beneath the tourniquet is essential for reducing skin damage due to shearing stresses.20 To avoid chemical burns beneath the tourniquet, it must be separated from the operative field with a self-adhesive plastic drape before skin preparation.21,22 The tourniquet cuff should not be rotated to a new position after it has been inflated, as shearing forces may damage underlying tissues.


It has been clearly demonstrated in both animal and human studies that compression injury due to the tourniquet results in a more significant loss of muscle functional strength, contractile speed and fatigability than tourniquet-induced ischaemia.10,23 Clinically relevant conclusions are difficult to draw from animal studies because small animals have a different muscle fibre composition and vulnerability than humans.24


Temporary nerve injuries may be underdiagnosed because of limb weakness postoperatively, as well as rapid recovery of the nerve. Reports of temporary or persistent nerve palsies and functional sequelae are uncommon in the literature, but nerve injuries do occur, especially at higher pneumatic tourniquet cuff pressures and after prolonged tourniquet inflation.25,26 According to the literature, the risk of nerve injury varies between 0.1 and 7.7%.26–28 Tourniquet-induced neurological injuries caused by shearing forces secondary to compression are more common than those resulting from ischaemia.29,30 In most cases of nerve injury, the damage occurs to the section of nerve directly under and near the edges of the cuff, and is associated with myelin disturbance and displacement of the nodes of Ranvier.31 A recent volunteer study showed that directly compressing a nerve causes focal ischaemia, inducing a localised axonal depolarisation, followed by hyperpolarisation upon release of compression.32 Hyperkalemia also reduces the transaxonal potassium currents. A short duration (4–13 min) of compression is sufficient to impair the transmission of stimuli and cutaneous afferents.33 Electromyography abnormalities have been noted during and after tourniquet use and may persist for up to 6 months afterwards.34

Tourniquet pain can be explained by ischaemia and compression, but it is increased with hyperalgesia phenomena (for example, when a traumatic injury is a primary stimulating factor).35 Thus, in addition to localised mechanisms, sensitisation of the central nervous system may also play a part in the tourniquet pain process. Evidence of expansion of the spinal receptive field of nociceptor neurons in response to tourniquet pain has been seen in animal studies.36 The pain tolerance in volunteer studies is approximately 20–30 min.16,37 In the absence of regional or general anaesthesia, topical application of a eutectic mixture of lidocaine–prilocaine (EMLA) cream (Astra Zeneca, London, UK) is as effective as circumferential subcutaneous anaesthesia in the reduction of tourniquet pain.38,39 Morphine added to a lidocaine epidural solution during regional anaesthesia significantly delays the onset of tourniquet pain.40


Tourniquet use may damage intravascular endothelium. Arterial complications after total knee arthroplasty are rare, but the consequences can be disastrous (vascular reconstruction or amputation), particularly in the presence of peripheral arterial disease or ipsilateral peripheral arterial reconstruction.41 Careful monitoring of the vascular status of the limb is required in the early postoperative period to detect any vascular compromise.

Ischaemia and reperfusion effects

Duration of ischaemia

The ‘safe’ duration of tourniquet-induced ischaemia remains controversial.41 The maximum recommended period of tourniquet-induced ischaemia is 1 h.4,5,42 However, it has also been demonstrated that 3 h of continuous ischaemia will not produce irreversible damage in healthy muscle, although it will result in widespread sublethal injury to cells.43 After 1 h, it is common practice to deflate the tourniquet intermittently in an attempt to minimise the ischaemic damage.4 Reperfusion periods can be initiated within 45–60 min of ischaemia and must be at least 10 min to be beneficial. Reperfusion initiated after 2 h of ischaemia tends to exacerbate muscle injury.5 Beyond 60–90 min of ischaemia, the pathophysiological processes and inflammatory cascade are greater than the biological mechanisms of protection and brief periods of reperfusion are associated with a worsening of the injury rather than decreasing it.

Effects of reperfusion

Tourniquet release is associated with an immediate 10% increase in limb girth due to refilling of the vessels and hyperaemia. This causes an increase in intracompartmental pressure in the reperfused limb. Over the first postoperative day, the initial limb girth can increase by 50%.44 Swelling can remain significant for 6 weeks postoperatively.44 Releasing the tourniquet prior to haemostasis and closure reduces inflation time, allowing for a period of reperfusion and swelling before bandage or cast application. This may reduce complications associated with an increase in intracompartmental pressure compared with applying the dressing before tourniquet release. Deflation should be quick to prevent capillary bleeding. Just after the deflation, anaesthetic drugs sequestered in the exsanguinated limb are released and may be detected in some patients or when the bispectral index is used.45,46 This may be important in elderly or debilitated patients.47

Ischaemia–reperfusion results in a complex cascade of responses that can lead to muscle degeneration and loss of function. Despite the frequent use of tourniquets during limb surgery, it remains difficult to identify manifestations of ischaemia–reperfusion in humans, but effects have been seen in animal models.48 Signs of primary injury (vasodilatation and erythema) have been observed immediately after 1 h of tourniquet use. Secondary injury presents as a progression of cell injury despite reperfusion, which can end in a ‘no-reflow phenomenon’, when blood flow does not return to all areas after a long period of ischaemia. Leucocytes play a significant role in this phenomenon with adhesion in postcapillary venules, microvascular barrier disruption and oedema formation.48

Described in 1951, the ‘post-tourniquet syndrome’ combines weakness, stiffness, oedema, dysaesthesia and pain. These symptoms may be wrongly attributed to surgical trauma or to lack of patient motivation.4

Wound infection

The risk factors for infectious complications of arthroscopy include prolonged tourniquet inflation time.49 The systemic inflammatory response to tourniquet use may be explained by profound and sustained endothelial dysfunction and neutrophil activation.42 Wound hypoxia during lower limb orthopaedic surgery is also greater with tourniquet use than without.50,51 This may be relevant to wound healing and infection. Tourniquets (and exsanguinators) can also be a source of infection.52,53 Parenteral prophylactic antibiotics must be administered 10–20 min before tourniquet inflation and isolation of the operative site from the systemic circulation. After inflation of the tourniquet, antibiotics may not reach the exsanguinated limb. If the tourniquet has been inflated, regional intravenous injection of an antibiotic is a good alternative.54 However, antibiotic administration 10 min before the tourniquet release seems to be as effective as before inflation.55


Skeletal muscle may be severely affected, even during relatively short periods of tourniquet use.48,56 Functional muscle loss seems to be worse if there is haemorrhage before tourniquet application.57 After anterior cruciate ligament reconstruction, the amount of vastus muscle amyotrophy after tourniquet use is significantly greater than that without tourniquet use.58,59 Cases of rhabdomyolysis with acute renal failure and compartment syndrome have been reported after tourniquet duration of more than 4 h but also with shorter inflation times (45–120 min).60,61 Interestingly, loss of strength,40 or electromyographic abnormalities,62 can also be observed in the contralateral limb, suggesting a sensitisation of the central nervous system.

The mechanism of muscle damage due to ischaemia and subsequent reperfusion is well understood. Complement activation, mast cell degranulation, neutrophil adhesion and infiltration, and microvascular dysfunction all play a role. During ischaemia, a cascade of ATP depletion, acidosis and ion imbalance occurs. The production of cytokines, reactive oxygen species and rapid calcium influx into the cells, which occurs progressively during reperfusion,63 is more damaging and causes mitochondrial dysfunction that leads to cellular apoptosis and necrosis.64 This does not seem to affect the contralateral side.65

Muscle injury seems to be greater in older patients, probably due to a greater susceptibility of aged skeletal muscle to ischaemia–reperfusion injury and to local attenuation of insulin-like growth factor-1 gene expression, which reduces regenerative mechanisms.66


Limb dysfunction during ischaemia and reperfusion may be largely the result of axonal or neuromuscular junction injury, or both.48 After tourniquet deflation, a warming sensation, quickly turning into an aching sensation of burning, is associated with limb reperfusion.16,37 During reperfusion, the hyperaemic flow response in nerves is more prolonged than that in muscle.26,28 The factors that incite the ischaemic nerves to spontaneously discharge and cause paraesthesias upon reperfusion are not known.

Postoperative pain control is important for optimal functional recovery from surgery.44,67 Pain scores are often similar or lower in orthopaedic patients without tourniquet use.44,68 In order to reduce pain following arthroscopy, intra-articular injection of local anaesthetics must be performed either 10 min before tourniquet deflation, to allow fixation of local anaesthetics before the washout period, or 30 min after deflation.69,70


The risk of DVT is significantly increased with a tourniquet time of more than 60 min.60 Following knee arthroscopy, the incidence of DVT diagnosed using contrast venography is approximately 18% 1 week after surgery.71 The formation of a DVT begins during tourniquet inflation and continues after deflation due to an increase in circulating markers of thrombosis (plasma D-dimer, tissue plasminogen activator, angiotensin-converting enzyme, antithrombin-III and protein C).72–74 Inflammation and haemostasis are linked by common activation pathways and feedback regulation. Tourniquet use exaggerates these responses, which peak on pneumatic tourniquet deflation and remain elevated on postoperative days 1 and 2.75–77

Systemic effects

In randomised studies, tourniquet use during knee replacement surgery does not reduce total blood loss.78,79 A meta-analysis of such surgery confirms that there is an initial increase in blood loss in groups without tourniquet use, but no difference in total blood loss or transfusion in comparison with patients in whom a tourniquet was used.1 An increase in local fibrinolysis postoperatively after tourniquet deflation, secondary to release of fibrinolytic factors from the surgical site, may explain the increased risk of bleeding into the joint or drains.80–83 The benefit of surgical haemostasis after tourniquet deflation is still under debate due to the risk of increased blood loss, but prospective studies support this.84,85

Cardiovascular effects

Tourniquet application has significant effects on the cardiovascular system. The mean arterial pressure increases progressively after inflation secondary to pain.86 Regional anaesthesia is better than general anaesthesia for moderating the cardiovascular response to tourniquet pain.86 Preoperative intravenous injection of a small dose of ketamine,87,88 dexmedetomidine,89 magnesium sulphate,90 oral dextromethorphan91 or clonidine92 can reduce the increase in systolic arterial pressure associated with inflation, reflecting an analgesic effect.

A brief period of hypotension upon deflation, secondary to metabolic and lactic acidosis and hyperkalaemia, can cause myocardial depression and even cardiac arrest in elderly or debilitated patients after prolonged lower limb surgery.93 Hypovolaemia may be observed after tourniquet deflation, due in part to haemorrhage at the surgical site but mostly to a combination of reactive vasodilatation and increased microvascular permeability in the reperfused limb during the first hour.

Pulmonary effects

Fatal or near-fatal pulmonary embolism was first reported after use of the Esmarch bandage and tourniquet inflation in orthopaedic surgery and was subsequently reported after tourniquet deflation.94–96 A significant correlation was noted between the occurrence of emboli and the duration of tourniquet application.78 Emboli occur during pneumatic tourniquet inflation and femur reaming in 27% of patients and in all patients after tourniquet deflation.82,88 Pulmonary embolism during orthopaedic surgery can result from fat embolism due to invasion of the medullary cavity.96,97 Air and cement emboli have also been reported after tourniquet release.98 The occurrence of emboli in patients undergoing invasive surgery (for example, knee replacement surgery) may be more frequent compared with non-invasive surgery (such as diagnostic arthroscopy).99 Even in the absence of a patent foramen ovale, cerebral microemboli frequently occur (60%) upon tourniquet release (probably through the opening of recruitable pulmonary vessels).100,101

Acute lung injury can be observed after limb reperfusion, with increased microvascular permeability, sequestration of neutrophils, and generation of oxygen-free radicals.77 Powerful neutrophil activation causes oxidative stress and has been used in an animal model to develop ‘tourniquet shock’ by applying two tourniquets simultaneously to both lower limbs of an animal.5

Neurological effects

Tourniquet deflation may be accompanied by a dangerous increase in intracranial pressure due to a simultaneous increase in carbon dioxide and a decrease in the systemic blood pressure upon release of the tourniquet. This could lead to a severe reduction in cerebral perfusion pressure with potentially disastrous consequences in patients with brain injuries.102 When propofol or sevoflurane (but not isoflurane) is used to maintain anaesthesia, hyperventilation after tourniquet deflation to minimise hypercapnia can prevent an increase in cerebral perfusion pressure.103

Treatment of ischaemia–reperfusion injury

New treatments have been proposed to help prevent or reduce the effects of ischaemia–reperfusion. Ischaemic preconditioning, defined as a brief period of ischaemia followed by tissue reperfusion (three or four cycles of 5 min of ischaemia with a cuff placed around the ipsilateral or contralateral arm or leg, followed by a 5 min of reperfusion) immediately before the clinical use of the tourniquet can be used to decrease the systemic effects of ischaemia–reperfusion after tourniquet use on upper or lower limbs, including attenuation of pulmonary dysfunction.104–107 Nitric oxide synthase and heme oxygenase have been implicated in this process.108,109 Ischaemic preconditioning of limbs also has anti-inflammatory effects on remote organs.110,111

Experimentally, ischaemic postconditioning, with intermittent repetitive interruptions to reperfusion after a prolonged period of ischaemia, has been found to be comparable with ischaemic preconditioning with regard to neuroprotective effects on spinal cord ischaemia.112 Interestingly, preconditioning and postconditioning can be applied on the contralateral limb with a significant effect on vascular endothelium dysfunction (vasoconstriction and thrombosis).110 These effects can be partially explained by humoral factors or neurologic pathways.

Prostaglandin analogues do not seem to reduce muscle injury.113 Antioxidants have a cytoprotective effect that could be attributed to inhibition of neutrophil adherence activation and scavenging of superoxide radicals.114,115 In humans, inhaled nitric oxide before, during and after the tourniquet application reduces inflammation in lower limb extremities.116,117 Heme oxygenase, which catalyses the breakdown of heme to iron, biliverdin IXa, and carbon monoxide may also be beneficial (carbon monoxide has a very similar action to nitric oxide).108 Administration of an endothelial xanthine oxidase inhibitor (allopurinol) or a radical scavenger such as vitamin E can decrease oxidative stress and oedema in postischaemic skeletal muscle.5 Another free radical scavenger (edaravone) given during early reperfusion seems to be effective in reducing nerve injury due to oxidative stress.118 To reduce microvascular reperfusion injury following tourniquet ischaemia in striated muscle, buflomedil or flurbiprofen can also be used.119

Local hypothermia using cold gel packs reduces metabolic demand by reducing ischaemic and anoxic degeneration, but, although it could be effective during ischaemia, it may aggravate injury after reperfusion.92,120

Phosphodiesterase-3 inhibitors can be used as inodilators (positive inotropes and arteriovenous dilators) to reduce DVT. A peri-operative infusion of milrinone can significantly attenuate platelet activation and monocyte tissue factor expression during knee replacement surgery without increasing peri-operative blood loss.121 Regional limb heparinisation is not effective in reducing the embolic phenomena after pneumatic tourniquet release.96 It is difficult to recommend the use of a particular technique to reduce ischaemia–reperfusion injury as none are in routine clinical use at this time. Preconditioning and postconditioning are easy to apply and can be performed when the tourniquet time is predicted to be more than (or is more than) 2–3 h.


The variable quality of the articles reviewed makes it difficult to establish an overview of the existing evidence on pneumatic tourniquet use, but the basic science confirms that there are transient changes attributable to its use. In practice, the tourniquet is a useful tool for good visualisation for extremity surgery, but it carries a risk of adverse effects. If the main indication is obtaining a good surgical visualisation (for example, in microsurgery), it should not be based just on haemostasis; a step-by-step haemostasis and pharmacological vasoconstriction may be used easily to obtain a bloodless field. Several relative contraindications to the use of a tourniquet have been described in the literature, including severe atherosclerotic disease, severe crush injuries, diabetes mellitus, sickle-cell disease and severe brain injury.5 Proven or suspected DVT, presence of calcified vessels, rheumatoid arthritis and other collagen-vascular diseases associated with vasculitis, as well as localised tumours, are also relative contraindications.4

To minimise adverse effects, the tourniquet must be used within the framework of strict procedures and protocols, with well adapted and regularly checked equipment. The location of the tourniquet must be as distal as is surgically possible. The AOP must be measured, and the tourniquet inflated to an AOP and 50–75 mmHg (or 75–100 mmHg greater than the SBP). The duration of tourniquet use should, ideally, be less than 1 h. Reperfusion periods can be initiated after 45–60 min of ischaemia for longer tourniquet times. To keep the duration of ischaemia as short as possible, tourniquet deflation prior to haemostasis and closure is preferable. After deflation, monitoring of the vascular and neurological status of the limb must be performed regularly and a temporary bandage or split plaster cast should be used for the first 2 days to allow for swelling and evaluation.


No financial support or sponsorship is declared. The authors declare no conflicts of interest.


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bleeding; ischaemia–reperfusion; pneumatic tourniquet; pressure; thromboembolism

© 2011 European Society of Anaesthesiology