When To Use Tourniquets
Tourniquets have a checkered history and hyperbolic claims continue to muddy the water. Past and current combat experience in the SW Asian theaters has drawn renewed attention to them because injuries to limbs have been a major source of life-threatening bleeding. There, they are being used successfully to control obvious and potentially serious bleeding. In the later case, they are applied before a proper assessment is possible e.g., multiple casualties, continued live fire. The tourniquets used are relatively cheap and can be lifesaving if used properly. As with anything in medicine, nothing works 100% of the time.
Clinical and laboratory studies have shown that the minimum effective pressure cannot be reliably predicted using a standard pressure or a simple formula based on the factors listed above. For each individual limb, cuff, and cuff application there is a unique cuff pressure required to occlude arterial flow in the limb, known as the Limb Occlusion Pressure (LOP). These studies have demonstrated that the best way to optimize cuff pressure is to apply the cuff and, after induction of anesthesia and prior to cuff inflation, measure the LOP with the applied cuff. Cuff pressure is then set to the LOP plus a predetermined safety margin which allows for changing conditions during the procedure.
There is no clearcut rule as to how long a tourniquet may be inflated safely, although various investigators have addressed effects of ischemia on muscle and nerve to define a relatively "safe" period of tourniquet hemostasis. In practice, safe tourniquet inflation time depends greatly on the patient's anatomy, age, physical status, and the vascular supply to the extremity. Unless instructed otherwise, report to the surgeon when 60 minutes of tourniquet time has elapsed. There is general agreement that for reasonably healthy adults, 90 minutes should not be exceeded without releasing the tourniquet for a short time.
Tourniquets should be at least 1½ inches wide, and pulled very tight, to properly shut off blood flow. Medical supply companies make tourniquets that do the job best.
One study found detectable levels of anesthetic agent in the general circulation even while the tourniquet was properly inflated. The authors suggested that the hemodynamics in the skeleton allowed endosteal (intraosseous, medullary) venous outflow from the extremity, using the bone as a tourniquet bypass while the tourniquet still effectively blocked extraosseous arterial inflow and venous return. Thus, venous blood from the extremity slowly entered the general circulation through this intraosseous skeletal bypass.
Important: This content reflects information from various individuals and organizations and may offer alternative or opposing points of view. It should not be used for medical advice, diagnosis or treatment. As always, you should consult with your healthcare provider about your specific health needs.
Systemic effects Several systemic effects occur with inflation and deflation of a limb tourniquet. Cardiovascular effects After limb exsanguination and tourniquet inflation, there is an increase in systemic vascular resistance and an effective increase in circulating blood volume. This leads to an increase in central venous pressure and in most instances an accompanying increase in systolic arterial pressure, both of which are usually transient. Application of bilateral thigh tourniquets can increase the effective circulating blood volume by up to 15% (∼750 ml in an adult). Such large increases in circulating blood volume may cause large and sustained increases in central venous pressure and circulatory overload. Cardiac failure and cardiac arrest have been reported after the application of bilateral thigh tourniquets. Following the initial transient increase in arterial pressure, it is common to see a second, gradual increase in arterial pressure. This is thought to accompany the development of tourniquet pain and develops a variable period of time after inflation. The rise in arterial pressure can be attenuated by the addition of ketamine (0.25 mg kg−1),2 this may also help with tourniquet pain.3 On tourniquet deflation, post-ischaemic reactive hyperaemia is seen; this causes a transient increase in the volume of blood in the limb compared with baseline levels. Simultaneously, metabolites from the ischaemic limb are released into the systemic circulation. In combination with the redistribution of blood flow, this often causes a decrease in both central venous and systolic pressures, which is temporary but can be dramatic. Respiratory effects Deflation of the tourniquet is followed almost immediately by an increase in end-tidal carbon dioxide concentration (F e′co2) which usually peaks within 1 min. The increase in F e′co2 occurs for two reasons: mixed venous P co 2 increases (after release of hypercapnic blood from the ischaemic area distal to the tourniquet into the systemic circulation) and also cardiac output increases after tourniquet deflation (in response to the decrease in arterial pressure described above). The peak increase in end-tidal CO2 concentration is greater with deflation of lower limb tourniquets (0.7–2.4 kPa) than with upper limb tourniquets (0.1–1.6 kPa).4 The duration of the increase in F e′co2 depends on the ventilatory characteristics of the patient. In spontaneously breathing patients, minute ventilation increases rapidly and so F e′co2 returns to baseline values within 3–5 min. In patients undergoing controlled ventilation, the F e′co2 will typically remain raised for >6 min unless minute ventilation is deliberately increased. Central nervous system effects The increase in Paco2 which accompanies deflation of the tourniquet causes an increase in cerebral blood flow. Measurements of middle cerebral artery blood flow velocity show an increase of up to 50%. In patients with head injuries, the increase in cerebral blood flow can cause an increase in intracranial pressure and worsen the degree of secondary brain injury. Hyperventilation after tourniquet deflation can prevent deleterious increases in intracranial pressure by maintaining normocapnia. Haematological effects The haematological effects of tourniquets are complicated. Tourniquet inflation during surgery is associated with a global hypercoagulable state. This is attributable to increased platelet aggregation caused by catecholamines released in response to pain from surgery and the tourniquet itself. However, there is no difference in the incidence of deep vein thrombosis in surgery on lower limbs performed with and without a tourniquet. After deflation of the tourniquet, there is a brief period of increased fibrinolytic activity. This increase is maximal at 15 min and returns to preoperative levels within 30 min of tourniquet release, but may nevertheless cause increased bleeding. The increase in fibrinolysis is caused by release of tissue plasminogen activator, which is thought to be produced by the vasa vasorum in the affected limb in response to the acidosis and hypoxaemia associated with tourniquet application. Temperature effects Inflation of arterial tourniquets is associated with a gradual increase in core body temperature caused by reduced heat transfer to and heat loss from the ischaemic limb. The magnitude of this increase is small, ∼0.5°C after 2 h of inflation. Tourniquet deflation causes a transient decrease in core temperature, primarily caused by redistribution of body heat. In addition, it is associated with the return to the systemic circulation, of a small amount of hypothermic blood from the ischaemic limb. Metabolic effects Deflation of the tourniquet after 1–2 h of ischaemia is associated with small increases in plasma concentrations of potassium and lactate. Peak increases of 0.3 and 2 mmol litre−1, respectively, occur 3 min after deflation.5 Lactate and carbon dioxide returning to the systemic circulation from the ischaemic limb cause a reduction in arterial pH. Reperfusion of the ischaemic limb and the other haemodynamic changes associated with tourniquet deflation can cause brief increases in oxygen consumption and carbon dioxide production. The magnitude of these changes correlates with the duration of ischaemia. All of these changes are fully reversed within 30 min of tourniquet deflation.
Clinical and laboratory studies have shown that the minimum effective pressure cannot be reliably predicted using a standard pressure or a simple formula based on the factors listed above. For each individual limb, cuff, and cuff application there is a unique cuff pressure required to occlude arterial flow in the limb, known as the Limb Occlusion Pressure (LOP). These studies have demonstrated that the best way to optimize cuff pressure is to apply the cuff and, after induction of anesthesia and prior to cuff inflation, measure the LOP with the applied cuff. Cuff pressure is then set to the LOP plus a predetermined safety margin which allows for changing conditions during the procedure.
There is no clearcut rule as to how long a tourniquet may be inflated safely, although various investigators have addressed effects of ischemia on muscle and nerve to define a relatively "safe" period of tourniquet hemostasis. In practice, safe tourniquet inflation time depends greatly on the patient's anatomy, age, physical status, and the vascular supply to the extremity. Unless instructed otherwise, report to the surgeon when 60 minutes of tourniquet time has elapsed. There is general agreement that for reasonably healthy adults, 90 minutes should not be exceeded without releasing the tourniquet for a short time.
Tourniquets should be at least 1½ inches wide, and pulled very tight, to properly shut off blood flow. Medical supply companies make tourniquets that do the job best.
One study found detectable levels of anesthetic agent in the general circulation even while the tourniquet was properly inflated. The authors suggested that the hemodynamics in the skeleton allowed endosteal (intraosseous, medullary) venous outflow from the extremity, using the bone as a tourniquet bypass while the tourniquet still effectively blocked extraosseous arterial inflow and venous return. Thus, venous blood from the extremity slowly entered the general circulation through this intraosseous skeletal bypass.
Important: This content reflects information from various individuals and organizations and may offer alternative or opposing points of view. It should not be used for medical advice, diagnosis or treatment. As always, you should consult with your healthcare provider about your specific health needs.
Systemic effects Several systemic effects occur with inflation and deflation of a limb tourniquet. Cardiovascular effects After limb exsanguination and tourniquet inflation, there is an increase in systemic vascular resistance and an effective increase in circulating blood volume. This leads to an increase in central venous pressure and in most instances an accompanying increase in systolic arterial pressure, both of which are usually transient. Application of bilateral thigh tourniquets can increase the effective circulating blood volume by up to 15% (∼750 ml in an adult). Such large increases in circulating blood volume may cause large and sustained increases in central venous pressure and circulatory overload. Cardiac failure and cardiac arrest have been reported after the application of bilateral thigh tourniquets. Following the initial transient increase in arterial pressure, it is common to see a second, gradual increase in arterial pressure. This is thought to accompany the development of tourniquet pain and develops a variable period of time after inflation. The rise in arterial pressure can be attenuated by the addition of ketamine (0.25 mg kg−1),2 this may also help with tourniquet pain.3 On tourniquet deflation, post-ischaemic reactive hyperaemia is seen; this causes a transient increase in the volume of blood in the limb compared with baseline levels. Simultaneously, metabolites from the ischaemic limb are released into the systemic circulation. In combination with the redistribution of blood flow, this often causes a decrease in both central venous and systolic pressures, which is temporary but can be dramatic. Respiratory effects Deflation of the tourniquet is followed almost immediately by an increase in end-tidal carbon dioxide concentration (F e′co2) which usually peaks within 1 min. The increase in F e′co2 occurs for two reasons: mixed venous P co 2 increases (after release of hypercapnic blood from the ischaemic area distal to the tourniquet into the systemic circulation) and also cardiac output increases after tourniquet deflation (in response to the decrease in arterial pressure described above). The peak increase in end-tidal CO2 concentration is greater with deflation of lower limb tourniquets (0.7–2.4 kPa) than with upper limb tourniquets (0.1–1.6 kPa).4 The duration of the increase in F e′co2 depends on the ventilatory characteristics of the patient. In spontaneously breathing patients, minute ventilation increases rapidly and so F e′co2 returns to baseline values within 3–5 min. In patients undergoing controlled ventilation, the F e′co2 will typically remain raised for >6 min unless minute ventilation is deliberately increased. Central nervous system effects The increase in Paco2 which accompanies deflation of the tourniquet causes an increase in cerebral blood flow. Measurements of middle cerebral artery blood flow velocity show an increase of up to 50%. In patients with head injuries, the increase in cerebral blood flow can cause an increase in intracranial pressure and worsen the degree of secondary brain injury. Hyperventilation after tourniquet deflation can prevent deleterious increases in intracranial pressure by maintaining normocapnia. Haematological effects The haematological effects of tourniquets are complicated. Tourniquet inflation during surgery is associated with a global hypercoagulable state. This is attributable to increased platelet aggregation caused by catecholamines released in response to pain from surgery and the tourniquet itself. However, there is no difference in the incidence of deep vein thrombosis in surgery on lower limbs performed with and without a tourniquet. After deflation of the tourniquet, there is a brief period of increased fibrinolytic activity. This increase is maximal at 15 min and returns to preoperative levels within 30 min of tourniquet release, but may nevertheless cause increased bleeding. The increase in fibrinolysis is caused by release of tissue plasminogen activator, which is thought to be produced by the vasa vasorum in the affected limb in response to the acidosis and hypoxaemia associated with tourniquet application. Temperature effects Inflation of arterial tourniquets is associated with a gradual increase in core body temperature caused by reduced heat transfer to and heat loss from the ischaemic limb. The magnitude of this increase is small, ∼0.5°C after 2 h of inflation. Tourniquet deflation causes a transient decrease in core temperature, primarily caused by redistribution of body heat. In addition, it is associated with the return to the systemic circulation, of a small amount of hypothermic blood from the ischaemic limb. Metabolic effects Deflation of the tourniquet after 1–2 h of ischaemia is associated with small increases in plasma concentrations of potassium and lactate. Peak increases of 0.3 and 2 mmol litre−1, respectively, occur 3 min after deflation.5 Lactate and carbon dioxide returning to the systemic circulation from the ischaemic limb cause a reduction in arterial pH. Reperfusion of the ischaemic limb and the other haemodynamic changes associated with tourniquet deflation can cause brief increases in oxygen consumption and carbon dioxide production. The magnitude of these changes correlates with the duration of ischaemia. All of these changes are fully reversed within 30 min of tourniquet deflation.