Complications of tourniquet use

                     Complications of tourniquet use

                                        DR KS DHILLON

Introduction

Pneumatic tourniquet was first introduced in 1904 by Harvey Cushing. Pneumatic tourniquets are widely used in orthopaedic surgery for upper and lower limb surgery as well as for Bier block anesthesia. There are five basic components of pneumatic tourniquets which include:
• An inflatable cuff
• A compressed gas source
• A pressure display
• A pressure regulator
• Connection tubing.
There should at least be 3 inches overlap of the tourniquet cuff but the overlap should not exceed 6 inches [1]. Excessive overlap can cause an increase in pressure leading to injury to the underlying skin. Too little overlap can compromise effective tourniquet inflation resulting in  unexpected release or inadequate constriction. It is recommended that the width of the cuff should be wider than half of the limb’s diameter. Wider cuffs reduce the risk of injury to underlying soft tissues [1]. Wider cuffs occlude blood flow at a lower pressure [1]. Tourniquets are usually positioned on the limb at the point of the maximum circumference such as the upper thigh and upper arm. Despite the fact that tourniquets have been used for many years, the optimal inflation pressure has not been established by any study. Most surgical texts recommend a cuff pressure of between 200-300 mmHg for adults. For the upper limb the recommended inflation pressure is obtained by adding 50-75 mm Hg to the systolic blood pressure and for the lower limb by adding 100-150 mm Hg to the systolic blood pressure [2]. Typically orthopaedic surgeons use inflation pressure of 250 mm Hg for upper arm and 300 mm Hg for the thigh. Use of lowest effective inflation pressure is recommended to minimize risk of tourniquet related nerve injury.

No strict guidelines exist for duration of tourniquet inflation. Generally the safe time limit is between 1 to 3 hours. The situation should be reassessed at 2 hours and if the anticipated duration is more then 2.5 hours then a 10-min deflation interval is recommended. In pediatric patients, inflation time should not exceed 75 min for lower extremities [3].

Pathophysiological effects of tourniquet use

When a tourniquet is inflated there is interruption of blood supply which leads to tissue hypoxia, hyperkalemia and acidosis [4]. Tissue ischemia leads to functional changes in the cell and cell membrane. The transport across the membranes is affected with sodium entering the cell and potassium leaving the cell.  Adenosine triphosphatase is activated, adenosine triphosphate (ATP) is used up and mitochondria are stimulated as increased lactate produces acidosis [5]. The calcium regulation is affected and nuclear function and protein synthesis become depressed. The cell begins to swell, and further membrane changes follow with altered hormonal effects and mitochondrial uncoupling. Finally, leakage of  lysosomes occurs with intracellular and mitochondria disruption and the cell becomes destroyed [5].

According to experimental data the severity of tourniquet ischemia is time, tissue and species dependant [6]. Human trials have demonstrated time-dependent hypoxia and acidosis in the venous blood taken from distal to the cuff [7,8]. Venous pH falls to 7 at 2 hours with resultant muscle fatigue, structural changes and muscle damage. If the ischemia time exceeds 1.5 hours the serum creatine phosphokinase (CPK) concentration is elevated [9,10]. Metabolic recovery of muscle is impaired if intracellular adenosine triphosphate (ATP) is depleted after three hours of ischemia [11].

Deflation of the tourniquet leads to reperfusion which allows replenishment of energy supplies as well as elimination of toxic metabolites. At this stage, pulmonary embolization is most likely to occur  [12,13,14]. Echocardiography during surgery has shown that embolization of echogenic material is common following deflation of the tourniquet. The   composition and clinical relevance of these emboli however is uncertain [14]. Peak embolization usually occurs about fifty seconds after deflation of the tourniquet [15]. This may be inversely proportional to the duration of tourniquet time [12].

Although the risk for postoperative deep venous thrombosis in orthopedic extremity surgery is significant, the tourniquet does not appear to be an independent risk factor [16,17,18,19,20].
Tourniquet use, however, adds a significant risk to the release of large venous emboli in patients undergoing intramedullary instrumentation, cementing or insertion of a prosthesis in the lower limb [21].

Avoidance of tourniquets in high-risk cases may be useful to prevent unnecessary embolization [21].
Inflation of the tourniquet can cause hypercoagulability and fibrinolysis. Tissue trauma causes release of catecholamines, which leads to platelet aggregation and a hypercoagulable state [22,23]. Tourniquet deflation on the other hand is associated with thrombolytic activity. Tissue anoxia leads to activation of the antithrombin III and protein C pathways which can lead to post tourniquet bleeding [24,25].

Tourniquet related complications

Tourniquets can cause complications that range from minor and self-limiting to severe and sometimes even fatal. The complications can be local or systemic. The local effects are due to compression and systemic effects are usually related to inflation and deflation of the tourniquet and the resulting ischemia and reperfusion phases.

Local complications

Skin injury

Skin injuries are uncommon. Excessive tourniquet time and poorly placed tourniquets can lead to cutaneous abrasions, blisters and even pressure necrosis [26]. Alcohol-based skin preparations can cause chemical burns beneath the tourniquet [27,28]. Friction burns can result if the tourniquet is unpadded, or if the tourniquet telescopes away from its padding during the surgery [29]. The risk of skin injury is higher in children, the obese, the elderly, and patients with peripheral vascular disease [30].

Vascular injury

The incidence of vascular injury is low with use of the tourniquet. The incidence of direct vascular injury with tourniquet use in patients undergoing knee arthroplasty is between 0.03% to 0.14% [32]. It is usually seen in patients with peripheral vascular disease who are having lower limb surgery [33,34]. The vascular injury is most likely due to fracture of an atheromatous plaque or by thrombosis of a severely atheromatous blood vessels [35]. Tourniquet use is a relative contraindication in patients with peripheral arterial disease [36]. Such at-risk patients should be identified preoperatively. In up to 44% of the patients acute arterial injury may not be detected on the day of the surgery [37]. Hence it is important to carry out neurovascular examination at intervals following surgery. Arteriography and aggressive revascularization are critical to achieving salvage of the limb. Outcomes of treatment following correction of direct injury are excellent, but for thrombotic injury, the results are not so good even if corrected early [38].

Nerve injury

Nerve injuries from tourniquet use can range from paresthesias to paralysis. The estimated incidence of upper limb nerve injury is about 1:6200 and for lower limb nerve injury is about 1:3700. The overall incidence of permanent nerve injury with tourniquet use is 0.032% [39].
Mechanical pressure rather then distal ischemia appears to be the main cause of the nerve injury [40].

Compression of the nerve leads to microvascular congestion and oedema, which leads to inadequate tissue perfusion and degeneration of the axons [41]. High tourniquet pressures and faulty pressure gauges have been implicated in several reports [42]. Excessive continuous compression times increase the risk of neuropathy and delayed recovery of function [43]. Axonal injury leads to muscle weakness, loss of sensation and neuropathic pain. Nerve regeneration following injury occurs at about 3-4 mm per day [44].

The most commonly injured upper limb nerve is the radial nerve followed by ulna and median nerves. In the lower limbs the most commonly injured nerve is the common peroneal nerve.

Muscle injury

Tissue ischemia occurs beneath the cuff as well as distal to the cuff when tourniquet is inflated. Functional and microscopic changes occur in the tissues which are directly proportional to the duration and the pressure applied. Reversal of these changes is significantly prolonged after three hours of ischemia [45,46]. Two hours after tourniquet inflation at pressures of 200 mmHg to 350 mmHg ischaemic necrosis sets in below the cuff. Histological changes distal to the cuff are seen after four hours [47]. The muscle ischemia, oedema, and microvascular congestion leads to the post-tourniquet syndrome which is characterized by stiffness, paresis, pallor, and paraesthesia [48,49]. Unusually high pressures and prolonged tourniquet time leads to rhabdomyolysis [50,51].
Compartment syndrome is an uncommon complication of tourniquet use, and it results from a combination of anoxic edema, reperfusion hyperemia and hematoma formation [52,53,54].

Systematic complications

Cardiovascular effects

Cardiovascular changes occur during exsanguination of the limb and inflation of the tourniquet and on deflation of the tourniquet. With exsanguination of the limb, there is an increase in blood volume and systemic vascular resistance which leads to a transient increase in central venous pressure. Exsanguination of both lower limbs can add about 700-800 ml to the circulation which is about 15% of the blood volume [55]. This leads to an augmentation of the central venous pressure. Heart rate, systolic and diastolic pressures also increase after 30-60 min of tourniquet inflation due to ischemia and tourniquet pain. The syndrome of tachycardia and hypertension which occurs is referred to as ‘tourniquet pain’, and it is believed to be driven by a cutaneous neural feedback mechanism [56]. For about 30 mins it is well-tolerated without analgesia [57] but for longer periods sedation is required [58].

This transient rise in central venous pressure and systolic blood pressure occurs in two-thirds of patients having tourniquets applied under general anesthesia, but only in about 2.7% of patients undergoing spinal anesthesia [59].

The effects of these hemodynamic changes are minimal in healthy patients, but patients who have poor cardiac function may not be able to tolerate these changes. These changes will usually persist until tourniquet deflation and the response to analgesic drugs and increasing the depth of anesthesia is generally poor. Some of the interventions to reduce cardiovascular stress include, ketamine, dexmedetomidine, magnesium sulfate, clonidine, and remifentanil infusion [30].

Tourniquet deflation is a critical stage. During deflation sudden drop in central venous pressure and mean arterial pressures can occur. Cardiac arrests have also been reported following cuff deflation [30]. The reasons for these hemodynamic changes are a combination of a shift in blood volume back into the limb and the shift of metabolites from the ischemic limb into the systemic circulation. These hemodynamic changes are more pronounced with the simultaneous use of tourniquets on both lower limbs. Tourniquet release is associated with a rise in the pCO2. The pCO2 rise increases the blood flow to the middle cerebral artery by about 50% which usually lasts less than ten minutes [60,61]. This may lead to secondary brain injury in patients who have increased intracranial pressure [62,63].
Cerebral blood flow velocity changes can be prevented by maintaining normocapnia after tourniquet deflation [64].

Metabolic effects

Inflation and deflation of tourniquet results in several metabolic changes. The Arterial pH, PaCO2, PaO2, lactic acid, and potassium levels change significantly after release of the tourniquet and the degree of change is dictated largely by the duration of ischemia time. These changes are usually well tolerated by the fit patients. However, in the elderly patients, and in those undergoing mechanical ventilation who are usually unable to compensate for the metabolic load, as well as in patients with poor cardiorespiratory reserve, these changes may become clinically significant [65,66,67].

Potassium leakage leads to hyperkalemia in the early reperfusion stage [68] and this hyperkalemia has been implicated in sudden mortality [69]. This risk can be mitigated ensuring that agents to reduce acidosis and hyperkalemia are available. There should also be a high index of suspicion for such problems.

Metabolic changes are usually fully reversed within 30 min of tourniquet deflation. The metabolic changes are more pronounced with bilateral tourniquet use.

Temperature changes

The core body temperature gradually increases with tourniquet inflation, and decreases when the tourniquet is released [70]. The reason for an increase in temperature is because the available surface area for heat loss decreases after tourniquet application resulting in less heat transfer from the central to the peripheral compartment. Deflation on the other hand leads to a transient fall in core temperature due to the redistribution of body heat and hypothermic blood from the ischemic limb. Maintenance of core body temperature during surgery reduces this decline in temperature [71,72]. High surface area to volume ratio (body habitus) in children causes
a greater increase in core temperature, and hence children should not be actively warmed during surgery [73,74].

Reperfusion syndrome

Deflation of tourniquet re-establishes the circulation to the limb which allows for restoration of energy and removal of toxic metabolites. Paradoxically, however, reperfusion can induce an extension of ischaemic damage [75] and it can lead to several complications which are known as the ‘Reperfusion Syndrome’. The reperfusion can lethally injure cells that had sublethal ischemic damage. This is mediated in part by oxygen free radicals. Research in a feline model showed that three hours of ischemia followed by one hour of reperfusion was worse than four hours of ischemia [76]. Research also shows that gradual return of circulation to ischemic tissues results in less tissue injury [77].

In the pathogenesis of reperfusion syndrome, one of the key components is upregulation of surface adhesion molecules on the vascular endothelium  [78] and their subsequent interaction with the activated neutrophils [79,80].  Further damage to injured tissue occurs with transendothelial migration of neutrophils, with the release of reactive oxygen species and cytokines [81]. The reperfusion syndrome has two main components, the local component which causes an exacerbation of the regional ischaemic damage, and the systemic component which can cause secondary organ failure remote from the site of ischemia.

The systemic sequelae can result in increased pulmonary microvascular permeability which can lead to ARDS and both renal and cardiac injuries can occur which can lead to other severe and often fatal complications [82,83].

Hematological effects

Tourniquet inflation during surgery creates a hypercoagulable state. This is due to increased platelet aggregation as well as stimulation of coagulation factors. Stimulation of coagulation factors is caused by tissue damage and catecholamines release in response to pain from surgery as well as pain from tourniquet application [84,85,86].

There is a short period of increased fibrinolytic activity after deflation of the tourniquet. This is due to the release of tissue plasminogen activator, activating the anti-thrombin III and thrombomodulin- protein C anticoagulant system. This results in increased post tourniquet bleeding. The increase in fibrinolysis is maximal at 15 min after tourniquet deflation and returns to preoperative levels within 30 min of tourniquet deflation [87,88].

Zahavi et al. [89] reported that ischemia from tourniquet use increases levels of plasma beta-thromboglobulin and plasma thromboxane-B2 and this increases the risk of thrombosis in patients undergoing knee replacement. Katsumata et al. [90] reported that during knee replacement, the use of a tourniquet can promote the local release of neutrophil elastase from the neutrophils which together with reactive-oxygen derivatives, can contribute to the development of venous thrombosis and pulmonary embolism.

Respiratory effects

Respiratory changes are rare with the use of a tourniquet and they are mainly seen during the deflation of the tourniquet. On deflation of tourniquet, there is a transient increase in end-tidal carbon dioxide (EtCO2) tension because of efflux of hypercapnic venous blood and metabolites into the systemic circulation from the limb [91,92]. The increase in EtCO2 is related to the duration of ischemia in the limb. EtCO2 increase is greater with the lower limb tourniquet and is greater in men as compared to women. The EtCO2 peaks at 1–3 min after deflation of tourniquet and returns to baseline at about 10–13 min in a spontaneously breathing patient. It will, however, take longer in mechanically ventilated patients unless the minute volume is increased [92,93,94].

Cerebral circulatory effects

Cerebral circulatory changes are due to the increase in EtCO2 after tourniquet deflation. Increased EtCO2 increases the cerebral blood flow in 2 min but it, however, returns to baseline within 10 min. Patients with reduced intracranial compliance are at higher risk for complications related to the increase in cerebral blood flow. Hence all attempts to maintain normocapnia must be made to prevent this increase in cerebral blood flow during deflation [92,95,96].

Besir and Tugcugil [97] reported an increase in intracranial pressure in the early period after tourniquet deflation (after 5 min). The increase was related to the tourniquet time and not to the tourniquet pressure.

Contraindications

There are no absolute contraindications to the use of a tourniquet. Several relative contraindications to tourniquet use have been described in the literature [98].

These include:
• Severe atherosclerotic disease
• Severe crush injuries
• Head injury
• Peripheral neuropathy
• Severe infection in the limb
• Localized tumors
• Arteriovenous (AV) fistula
• DVT in the limb
• Rheumatoid arthritis, and other collagen vascular
          diseases with vasculitis
• Calcified vessels
• Poor skin condition of the limb
• Sickle cell disease.

Conclusion

Tourniquets are useful for upper and lower limb surgery. Tourniquets reduce blood loss and provide a bloodless field during surgery. They are also widely used for Bier block anesthesia. Proper padding under the cuff is important to prevent soft tissue injury. Safe limits of cuff pressure and safe duration of the cuff inflation must be carefully observed.

Improper use of tourniquets can result in serious local and systemic complications including mortality. The use of tourniquets should be avoided in patients with severe atherosclerotic disease, severe crush injuries, head injury, peripheral neuropathy, severe infection in the limb, localized tumors, arteriovenous (AV) fistula, DVT in the limb, rheumatoid arthritis, and other collagen vascular diseases with vasculitis, calcified vessels, poor skin condition of the limb and in patients with Sickle cell disease. There is a need for careful patient monitoring and care after deflation of the tourniquet and a careful search for postoperatively neurological deficit.

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