Tourniquets are widely used in extremity surgery to provide a bloodless field and minimize blood loss. Injury to tissues may occur due to the direct mechanical effects of the tourniquet, and the tourniquet may affect the skin, muscle tissue, and peripheral nerves under the tourniquet. Direct injury to vascular structures may occur, and prosthetic grafts are particularly susceptible. Systemic effects of tourniquets occur at inflation and deflation and depend on the duration of ischemia and the size of the involved limb. Hypertension during tourniquet inflation may occur as a result of increased systemic vascular resistance, autotransfusion, or pain. At deflation, hypotension, hypercapnia, and metabolic acidosis may occur. Symptoms suggestive of nerve injury following tourniquet use should prompt further evaluation up to electrodiagnostic studies; the prognosis for recovery from most nerve injuries is good. Efforts to prevent tourniquet complications should focus on careful patient selection as well as the use of the lowest possible pressure and shortest duration (less than 2 hours) of ischemia.
Keywordsextremity, peripheral nerve injury, tourniquet
A 75-year-old woman is undergoing a revision of a left total knee arthroplasty under spinal anesthesia and intravenous sedation. She is morbidly obese, on chronic opioids for pain relief, and an insulin-dependent diabetic. A continuous adductor canal catheter is placed for postoperative pain control before the placement of a single-shot spinal anesthetic. A conventional rectangular thigh tourniquet is placed for surgical hemostasis. After limb exsanguination, the cuff pressure is set at 300 mm Hg. Surgery proceeds uneventfully, with a total tourniquet time of 2 hours. The spinal anesthetic resolves, and the adductor canal catheter is removed on postoperative day 2. Subsequently, she complains of numbness and weakness in her left leg.
Tourniquets are commonly used during surgery of the upper and lower extremities to minimize intraoperative blood loss. Tourniquet use has a very long history and a low (but not zero) incidence of complications. These may take many forms, ranging from localized and relatively minor skin tears to neurologic dysfunction ( Box 55.1 ). Direct compression of neural, vascular, and muscular structures, as well as ischemia and reperfusion, contribute to the pathophysiology of tourniquet complications. Postoperative neurologic dysfunction after tourniquet use is a well-documented but infrequent phenomenon, and permanent defects are rare. Systemic effects may occur, which may reflect the direct effect of limb compression (e.g., pulmonary embolism) or systemic inflammation as a result of ischemia of underlying tissues.
Reduced antibiotic penetration
Right-sided heart failure
Deep venous thrombosis
Arterial tourniquets are widely used in upper and lower extremity surgery and in intravenous regional anesthesia. This practice continues because it is widely accepted that the benefit from minimizing surgical blood loss and creating a bloodless operative field exceeds the risk of tourniquet-related complications. It is important for anesthesiologists to be aware of the potential for tourniquet-related tissue injury, systemic effects of tourniquet inflation and deflation, and the possibly catastrophic events that could occur at these times.
It should be recognized that surgeons and anesthesiologists share any medicolegal liability for tourniquet-related complications. Documentation should include the location of the tourniquet, the use of padding and draping, and inflation pressure and duration. Tourniquet pressure relative to systemic blood pressure values, prolonged inflation, and total vascular occlusion times must be communicated to the surgical team and documented on the anesthesia record.
Pressure-related injuries to skin, muscles, nerves, and blood vessels depend on the pressure of tourniquet inflation and its duration. Injuries occur as a result of direct pressure, but axial stretching and shearing forces may also occur, especially at the edges of the tourniquet. The absence of arterial blood flow distal to the tourniquet causes ischemia, which leads to progressive acidosis, hypoxemia, and hypercarbia. The associated release of inflammatory mediators increases capillary permeability and causes tissue edema, which worsens ischemic injury, especially after reperfusion. Ultrastructural cellular changes are detectable after 30 minutes of ischemia but are reversible with ischemia lasting 2 hours or less. High-energy intracellular phosphate depletion occurs more gradually. However, injury to the Na + ,K + -ATPase–dependent ion exchange pump causes extracellular potassium leak and intracellular edema. The sarcoplasmic reticulum loses glycogen, the mitochondria swell, and myelin degeneration occurs. Cellular necrosis ensues if ischemia is not corrected.
A list of tissue sites affected by local tourniquet pressure follows.
Trauma to the skin can be caused by pressure necrosis due to inadequate padding between the skin and tourniquet or friction burns due to movement of a poorly applied tourniquet. Obese patients with redundant upper extremity skin folds are at increased risk for skin injury. Skin preparation solutions may soak into the padding under the tourniquet, resulting in full-thickness chemical burns.
Myocytes are very sensitive to compression and ischemia. Injury is more severe with lengthy tourniquet inflation or high pressure. Usually, injury is greatest beneath the tourniquet. Associated ischemia, edema, and microvascular congestion cause the post-tourniquet syndrome. This includes stiffness, pallor, and weakness (not paralysis), with subjective extremity numbness. Rhabdomyolysis may occur if the tourniquet is inflated for a prolonged period of time under high pressure. Compartment syndrome may occur after tourniquet deflation as a result of edema and reperfusion hyperemia.
Mechanical pressure compresses nerves directly beneath the tourniquet cuff, and shear forces at the proximal and distal edges of the cuff also cause nerve injury ranging from paresthesia to complete paralysis. Distal ischemia plays a lesser role. The contribution of tourniquet time to the development of nerve injury is unclear, and paralysis has been reported with as little as 30 minutes of tourniquet inflation. Lower extremity nerve injury usually involves the sciatic nerve. The upper extremity appears to be more commonly associated with tourniquet related nerve injury than the lower extremity, with radial nerve injury more frequently observed than either ulnar or median nerve injury. When tourniquet-related nerve injury occurs in the lower extremity, the sciatic nerve is the most likely to be affected.
Localized nerve injuries tend to be neuropraxic injuries, with structural damage limited to the myelin sheath surrounding individual axons, without injury to the axon itself. Neuropraxic injuries tend to be self-limiting, with an excellent prognosis for complete recovery within a period of several days to weeks. In contrast, axonotmetic injuries involve damage to the axon itself, resulting in loss of signaling function once electrical excitability is lost and depolarization can no longer occur. These injuries take longer to recover as the axon must regenerate along the connective tissue highway, and some injuries may not completely recover. Rarely, a permanent nerve deficit occurs ( Table 55.1 ).
|Neuropraxia||Myelin sheath damaged|
|Axon remains intact|
|Axonotmesis||Myelin sheath and axon damaged|
|Requires regeneration of nerve tissue|
|Recovery may be incomplete|
|Neurotmesis||Complete destruction of nerve|
|Requires surgical repair|
Arteries and veins, especially prosthetic grafts (e.g., arteriovenous fistulas, arterial bypass grafts), are susceptible to traumatic injury from mechanical compression. Although direct arterial injury is rare (0.03% to 0.14% incidence), fractured atherosclerotic plaque may cause localized thrombosis or embolize distally to cause ischemia. Although deep venous thrombosis (DVT) is a known and common complication of lower limb surgery, tourniquets bear no relation to deep venous stasis and thrombus formation. Rather, systemic hypercoagulability is due to catecholamine release and platelet aggregation caused by tourniquet-related or surgical pain. In contrast, active bleeding after tourniquet release may be aggravated by ischemia-caused tissue plasminogen activator release and fibrinolysis.
Systemic effects occur with tourniquet inflation and deflation. The intensity and duration of these derangements are directly proportional to the length of tourniquet inflation time and the size and number of tourniquet-isolated limbs. The following effects are observed.
Limb exsanguination and rapid tourniquet inflation shunt blood into the central circulation (autotransfusion) and increase systemic vascular resistance. As much as 800 mL of blood is autotransfused with the simultaneous inflation of bilateral thigh tourniquets. This causes a transient increase in central venous pressure and systolic blood pressure, which gradually returns to baseline. In patients with compromised left ventricular function, congestive heart failure due to circulatory overload and cardiac arrest has been reported.
Tourniquet-induced hypertension is common. Patients develop an increase in heart rate and systolic and diastolic blood pressures within 30 to 60 minutes of inflation, which persists until tourniquet deflation. This increase in mean arterial pressure has been attributed to (1) an acute increase in systemic vascular resistance with removal of a vascular bed; (2) limb exsanguination before tourniquet cuff inflation, which causes acute central blood volume expansion; and (3) pain associated with tourniquet compression and limb ischemia. The incidence of this constellation of vital signs is related to the type of anesthesia, and ranges from 2.5% of patients under brachial plexus anesthesia to 67% of patients under general anesthesia. A cutaneous mechanism is thought to be responsible, as demonstrated by the attenuation of tourniquet discomfort by topical eutectic mixture of local anesthetic agents (EMLA). A sympathetically mediated pathway may be unlikely given the lack of effectiveness of stellate ganglion block in reducing upper arm tourniquet discomfort in a limited size volunteer study. The leading hypothesis for the mechanism of tourniquet pain is the loss of inhibition of unmyelinated, slow-conducting C fibers. These fibers are usually inhibited by fast, myelinated A-delta fibers, which are blocked at the tourniquet site after approximately 30 minutes of tourniquet inflation and mechanical compression.
Tourniquet deflation results in reduced blood pressure and central venous pressure secondary to a shift of blood volume back into the extremity and postischemic reactive vasodilation. Also, with reperfusion, metabolites released from ischemic areas into the systemic circulation have the potential to cause myocardial depression and further reduce blood pressure. Hypotension is usually self-limited (≤15 minutes).
End-tidal carbon dioxide (ETCO 2 ) increases after tourniquet release owing to the efflux of hypercapnic venous blood from the ischemic limb into the systemic circulation. The peak ETCO 2 increase occurs within the first minute after deflation, and it returns to baseline approximately 10 to 13 minutes later. Spontaneously breathing patients compensate by increasing their respiratory rate. However, those with controlled ventilation require a transient increase in minute ventilation by 50% for about 5 minutes to maintain normocapnia. Hyperventilation can prevent the associated increase in cerebral blood volume and intracranial pressure that might otherwise be detrimental to a patient with intracranial hypertension.
Elevated serum lactate and reduced pH are observed for approximately 30 minutes after reperfusion of the isolated extremity. The degree of change is proportional to the duration of tourniquet inflation.
Blood Oxygen Saturation
Arterial oxygen saturation usually remains normal. However, as large volumes of deoxygenated blood are returned to the central circulation after tourniquet release, mixed venous oxygen saturation is transiently decreased.
Impaired Antibiotic Penetration
Intravenously administered antibiotics may not penetrate to the operative site if the tourniquet is inflated before or while the antibiotics are still being administered. An interval of 5 minutes between antibiotic administration and tourniquet inflation is probably adequate to allow antibiotic penetration.
Core Body Temperature
Most patients remain normothermic during tourniquet use. Tourniquet inflation above arterial pressure transiently increases core body temperature, and tourniquet deflation transiently decreases it. The decline in core body temperature due to the return of hypothermic venous blood from the previously occluded limb into the systemic circulation is usually 0.7°C or less.
Deep Venous Thrombosis, Pulmonary or Systemic Thromboembolism
These potentially devastating complications may occur with lower limb trauma and surgery, but rarely intraoperatively. Although studies with transesophageal echocardiography have shown up to a 70% incidence of right atrial embolization following tourniquet release, most emboli are small and are unlikely to cause major morbidity. However, this risk is increased in patients with hypercoagulable states and thrombus due to trauma or prolonged immobilization. In this setting, it is believed that thrombus becomes dislodged during limb exsanguination or with tourniquet inflation. Catastrophic events such as DVT or pulmonary or systemic thromboembolism are more likely to occur postoperatively during rehabilitation. Use of enoxaparin for DVT prophylaxis has dramatically reduced the incidence of fatal pulmonary embolism. However, given that pulmonary and cerebral emboli have been reported during both inflation and deflation of tourniquets, anesthesiologists should be especially vigilant during these times. Attention should be focused on the patient’s neurologic status and any sudden, unexpected changes in arterial oxygen saturation and ETCO 2 . Significant pulmonary emboli result in an acute reduction in ETCO 2 , with tachycardia and hypotension, followed by hypoxemia and myocardial ischemia. Right ventricular dysfunction may also be observed (also see Chapter 65 , Chapter 142 ).
Given the increased use of regional blocks for lower extremity surgery, which significantly reduces postoperative pain scores and permits earlier ambulation, how does one differentiate a nerve injury related to use of a tourniquet from one related to regional anesthesia?
Posttourniquet syndrome is the most common problem associated with tourniquet use. Mild weakness, diffuse subjective numbness, swelling, stiffness, and slight pallor of the affected limb usually develop several hours after tourniquet deflation. Furthermore, ischemic injury to muscle is distinguished from nerve injury by normal nerve conduction studies and the presence of elevated creatine kinase (MM) enzymes and myoglobinuria.
If the tourniquet has produced a compressive nerve injury, it may be difficult to distinguish this injury from one related to regional block, particularly when the tourniquet or the edge of the tourniquet overlaps the site of the peripheral nerve block. Tourniquet-related nerve injury can range from paresthesia to complete paralysis of the affected limb. Fortunately, localized tourniquet-related nerve injury is often neuropraxic, in which case the prognosis for full recovery is good, although axonometic injuries can also occur. In these cases, the prognosis for recovery depends on the extent of axonal damage and whether or not the neural connective tissue architecture remains intact (see Table 55.1 ).
Brief neurologic assessment of the affected extremity should follow surgery and be compared with the preoperative examination. Evidence of severe motor and sensory deficits requires neurologic consultation and electrodiagnostic studies to determine the site and severity of the injury, as well as the prognosis for recovery. With regional anesthesia, there may be a delay in the diagnosis of nerve injury, especially if indwelling catheters are used for postoperative analgesia.
Acute compartment syndrome has been observed immediately after surgery or after a delay of several hours. Reactive hyperemia occurring after tourniquet deflation may result in swelling of the limb by as much as 10%, potentially exacerbating this complication, especially if tight dressings or casts are used. The limb is typically swollen, muscles are stiff, and pain is more severe than the physical findings would suggest. This diagnosis is confirmed when compartment pressure monitoring indicates elevated pressure. Neurologic dysfunction is also a common sequela.
Postoperative complex regional pain syndrome type I or II may present weeks or months after surgery. Burning pain and autonomic dysfunction develop, followed by dystrophic changes in the extremity.
Skin injuries are usually evident on tourniquet cuff removal. Ecchymoses, persistent erythema, bullae formation, or skin burns may be present.
Vascular insufficiency due to arterial injury should be suspected when cuff deflation does not result in reperfusion of all or part of the extremity.
The potential for a postoperative nerve injury (PNI) may influence the choice of anesthesia technique for anesthesiologists working in a higher-risk malpractice environment, when faced with treating patients at elevated risk for tourniquet-induced PNI. Factors that may increase the risk of complications with tourniquet use are listed in Box 55.2 .