Arterial tourniquets

Metadata

Author: Deloughry, J. L., & Griffiths, R.
Full Title: Arterial tourniquets
Category: #articles

Highlights

ATP and creatine phosphate are exhausted after 2 and 3 h, respectively. Lactate concentration increases with the switch to anaerobic metabolism and, with the increasing PCO2, contributes to the development of an intracellular acidosis. Changes to the histological appearances of muscle ﬁbres occur after tourniquet inﬂation. Marked changes in mitochondrial morphology ischaemia. Muscle are visible after 1 h of underlying the tourniquet subjected to both ischaemia and compression is prone to developing changes such as local ﬁbre necrosis after inﬂation times as short as 2 h. (Page 1)
is a device which is used to A tourniquet control the ﬂow of blood to and/or from an extremity. (Page 1)
The word tourniquet itself derives from the French verb tourner (to turn) and was ﬁrst used by the eighteenth-century French surgeon Louis Petit describing the screw-like device he strapped to the thighs of patients undergoing leg amputations, to reduce blood loss. (Page 1)
The arterial tourniquet is usually a pneumatic device consisting of an inﬂatable cuff connected to a compressed gas supply. The measurable and high pressures that such tourniquets can generate allow controlled arterial compression and distal circulatory stasis. (Page 1)
release, Microvascular injury occurs in muscle after ischaemia of greater than (cid:2)2 h duration. After tourniquet increased vascular permeability results in interstitial and intracellular oedema which frequently leads to the ‘posttourniquet syndrome’, in which the patient has a swollen, pale, stiff limb with weakness but no paralysis. This post-tourniquet syndrome typically lasts 1– 6 weeks. (Page 1)
A physiological conduction block develops between 15 and 45 min after inﬂation of a cuff around the arm to a supra-systolic pressure. The conduction block affects both motor and sensory modalities and is reversible after deﬂation of the cuff. The rate of development of this conduction block is the same with cuff pressures of 150 and 300 mm Hg which suggests that ischaemia rather than direct compression is the cause. (Page 1)
Local effects are the result of tissue ischaemia distal to the inﬂated tourniquet and a combination of ischaemia and compression of the tissues beneath it. (Page 1)
Following inﬂation of the tourniquet, there is a progressive decrease in PO2 and an increase in PCO2 within muscle cells. Energy stores steadily decline with time and intracellular stores of (Page 1)
Direct mechanical compression of nerves is responsible for a second, longer lasting nerve conduction block called ‘tourniquet paralysis’. Higher cuff pressures (e.g. 1000 mm Hg maintained for .1 h) can cause morphological changes within the larger myelinated nerves which is most marked at the sites where the pressure gradient between compressed and uncompressed nerve is greatest: at the proximal and distal edges of the tourniquet. The pressure gradient results in displacement of the nodes of Ranvier, stretching and degeneration of ... paranodal myelin and impaired nerve conduction lasting up to 6 months. (Page 1)
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. (Page 2)
inﬂation, After limb exsanguination and tourniquet 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. (Page 2)
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 there is a brief period of increased ﬁbrinolytic the tourniquet, 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. (Page 2)
Application of bilateral thigh tourniquets can increase the effective circulating blood volume by up to 15% ((cid:2)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 it is common to see a second, gradual increase in arterial pressure. This is thought to accompany the development of tourtime after niquet pain and develops a variable period of inﬂation. The rise in arterial pressure can be attenuated by the addition of ketamine (0.25 mg kg21),2 this may also help with tourniquet pain. increase in arterial pressure, transient (Page 2)
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. (Page 2)
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 (Page 2)
Tourniquet deﬂation causes a transient decrease in core temperature, primarily caused by redistribution of body heat. (Page 2)
Deﬂation of the tourniquet is followed almost immediately by an increase in end-tidal carbon dioxide concentration (FE0 CO2) which usually peaks within 1 min. The increase in FE0 CO2 occurs for two reasons: mixed venous PCO2 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 limb tourniquets (0.1– 1.6 kPa).4 The duration of upper the increase in FE0 CO2 depends on the ventilatory characteristics of the patient. In spontaneously breathing patients, minute ventilation increases rapidly and so FE0 CO2 returns to baseline values within 3– 5 min. In patients undergoing controlled ventilation, the FE0 CO2 will typically remain raised for .6 min unless minute ventilation is deliberately increased. (Page 2)
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 litre21, 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. (Page 2)
Acute vascular insufﬁciency is thought to occur when mechanical pressure from the tourniquet damages atheromatous vessels, causing plaque rupture. (Page 3)
Out of 63 484 operations performed under a tourniquet, only 26 complications that might have been caused by the tourniquet were reported (an incidence 0.04%). (Page 3)
.6 Lower limb tourniquets were more likely to produce neurological complications than upper limb tourniquets. The nerves most commonly affected are the sciatic nerve in the lower limb and the radial nerve in the upper limb. (Page 3)
Inﬂation of a tourniquet is followed by the development of a dull, aching pain. Such pain can accompany otherwise adequate regional anaesthesia and can be severe enough to necessitate conversion to general anaesthesia. (Page 3)
It is thought that tourniquet pain is predominantly mediated by unmyelinated, slowly conducting C-ﬁbres which, as stated earlier, are less affected by the compressive effects of tourniquet inﬂation than larger ﬁbres. One theory suggests that tourniquet pain arises from selective transmission by cutaneous C-ﬁbres; these ﬁbres are continuously stimulated by skin compression from the tourniquet, and their post-synaptic effect at the dorsal horn is no longer inhibited by input from larger nerve ﬁbres whose transmission has been blocked. This theory is supported by the ﬁnding that during i.v. regional anaesthesia, tourniquet analgesia is prolonged by application of EMLA cream beneath the tourniquet (Page 3)
Large diameter nerve ﬁbres are more susceptible to pressure, so there is a relative sparing of sensation compared with motor function. The role of mechanical pressure in nerve injury probably explains why the Esmarch bandage (which can generate pressures .1000 mm Hg) is associated with a higher incidence of nerve injury. The effects of nerve compression at the site of tourniquet application may make injury at a more distal site (caused by ischaemia or surgical trauma) more likely due to the neural ‘double crush’. (Page 3)
tourniquet pain can complicate spinal or epidural anaesthesia, despite apparently adequate anaesthesia of the sensory dermatome underlying the tourniquet. One explanation of this is offered by the in vitro ﬁnding that smaller unmyelinated C-ﬁbres are more resistant to local anaesthetic-induced conduction block than larger, myelinated A-ﬁbres.10 After intrathecal administration of an adequate dose of local anaesthetic, conduction in both A- and C-ﬁbres is blocked. However, as the concentration of local anaesthetic in the cerebrospinal ﬂuid decreases, C-ﬁbres start to conduct impulses before the A-ﬁbres, resulting in a dull tourniquet pain in the presence of an anaesthetic which, assessed by pinprick, appears adequate. (Page 3)
Very rarely the post-ischaemic swelling and oedema, in combination with reperfusion hyperaemia, may lead to the development of a compartment syndrome. Rhabdomyolysis directly related to the tourniquet use has been reported, but is extremely rare. (Page 3)
there is no completely satisfactory solution. Various techniques have been used, including increasing the density of central neuraxial block by using adjuncts to bupivacaine such as epinephrine, morphine, and clonidine. (Page 3)
some success has also been reported with the administration of preoperative gabapentin and the use of low-dose (0.1 mg kg21) i.v. ketamine. (Page 4)
A gradual increase in arterial pressure is frequently observed a variable time after tourniquet inﬂation. The exact mechanism of this tourniquet-induced hypertension is not known, but it has been suggested that it represents activation of the sympathetic nervous system in response to the development of tourniquet pain. (Page 4)
Most recommendations in the literature suggest a period of 1.5 –2 h in a healthy adult, which corresponds to the point at which muscle ATP stores are depleted. Although ischaemia has typically been associated with muscular rather than neurological injury, there is an approximate three-fold increase in the risk of neurological complications for each 30 min increase in tourniquet time.7 (Page 4)
It is generally considered that the tourniquet should be left deﬂated for 10–15 min before re-inﬂation and this seems to correspond to restoration of muscle ATP levels. It is important to re-exsanguinate the limb before inﬂating the cuff again after reperfusion. (Page 4)
The Association of peri-operative Registered Nurses (AORN) in the USA recommends inﬂating tourniquets to pressures based on the limb occlusion pressure (LOP).12 This value is determined by gradually increasing the pressure in the tourniquet while assessing distal blood ﬂow with a Doppler probe held over a distal artery. The LOP is the pressure in the cuff at which the arterial pulse disappears. The LOP is usually higher than systolic pressure because the pressure from the tourniquet which is transmitted to deep underlying soft tissues is frequently less than that in the tourniquet itself. The percentage of transmitted tourniquet pressure varies inversely with limb circumference (hence the practice of using higher pressures on the thigh than on the upper arm). (Page 4)

Arterial tourniquets

Metadata

Author: Deloughry, J. L., & Griffiths, R.
Full Title: Arterial tourniquets
Category: #articles

Highlights

ATP and creatine phosphate are exhausted after 2 and 3 h, respectively. Lactate concentration increases with the switch to anaerobic metabolism and, with the increasing PCO2, contributes to the development of an intracellular acidosis. Changes to the histological appearances of muscle ﬁbres occur after tourniquet inﬂation. Marked changes in mitochondrial morphology ischaemia. Muscle are visible after 1 h of underlying the tourniquet subjected to both ischaemia and compression is prone to developing changes such as local ﬁbre necrosis after inﬂation times as short as 2 h. (Page 1)
is a device which is used to A tourniquet control the ﬂow of blood to and/or from an extremity. (Page 1)
The word tourniquet itself derives from the French verb tourner (to turn) and was ﬁrst used by the eighteenth-century French surgeon Louis Petit describing the screw-like device he strapped to the thighs of patients undergoing leg amputations, to reduce blood loss. (Page 1)
The arterial tourniquet is usually a pneumatic device consisting of an inﬂatable cuff connected to a compressed gas supply. The measurable and high pressures that such tourniquets can generate allow controlled arterial compression and distal circulatory stasis. (Page 1)
release, Microvascular injury occurs in muscle after ischaemia of greater than (cid:2)2 h duration. After tourniquet increased vascular permeability results in interstitial and intracellular oedema which frequently leads to the ‘posttourniquet syndrome’, in which the patient has a swollen, pale, stiff limb with weakness but no paralysis. This post-tourniquet syndrome typically lasts 1– 6 weeks. (Page 1)
A physiological conduction block develops between 15 and 45 min after inﬂation of a cuff around the arm to a supra-systolic pressure. The conduction block affects both motor and sensory modalities and is reversible after deﬂation of the cuff. The rate of development of this conduction block is the same with cuff pressures of 150 and 300 mm Hg which suggests that ischaemia rather than direct compression is the cause. (Page 1)
Local effects are the result of tissue ischaemia distal to the inﬂated tourniquet and a combination of ischaemia and compression of the tissues beneath it. (Page 1)
Following inﬂation of the tourniquet, there is a progressive decrease in PO2 and an increase in PCO2 within muscle cells. Energy stores steadily decline with time and intracellular stores of (Page 1)
Direct mechanical compression of nerves is responsible for a second, longer lasting nerve conduction block called ‘tourniquet paralysis’. Higher cuff pressures (e.g. 1000 mm Hg maintained for .1 h) can cause morphological changes within the larger myelinated nerves which is most marked at the sites where the pressure gradient between compressed and uncompressed nerve is greatest: at the proximal and distal edges of the tourniquet. The pressure gradient results in displacement of the nodes of Ranvier, stretching and degeneration of ... paranodal myelin and impaired nerve conduction lasting up to 6 months. (Page 1)
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. (Page 2)
inﬂation, After limb exsanguination and tourniquet 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. (Page 2)
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 there is a brief period of increased ﬁbrinolytic the tourniquet, 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. (Page 2)
Application of bilateral thigh tourniquets can increase the effective circulating blood volume by up to 15% ((cid:2)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 it is common to see a second, gradual increase in arterial pressure. This is thought to accompany the development of tourtime after niquet pain and develops a variable period of inﬂation. The rise in arterial pressure can be attenuated by the addition of ketamine (0.25 mg kg21),2 this may also help with tourniquet pain. increase in arterial pressure, transient (Page 2)
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. (Page 2)
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 (Page 2)
Tourniquet deﬂation causes a transient decrease in core temperature, primarily caused by redistribution of body heat. (Page 2)
Deﬂation of the tourniquet is followed almost immediately by an increase in end-tidal carbon dioxide concentration (FE0 CO2) which usually peaks within 1 min. The increase in FE0 CO2 occurs for two reasons: mixed venous PCO2 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 limb tourniquets (0.1– 1.6 kPa).4 The duration of upper the increase in FE0 CO2 depends on the ventilatory characteristics of the patient. In spontaneously breathing patients, minute ventilation increases rapidly and so FE0 CO2 returns to baseline values within 3– 5 min. In patients undergoing controlled ventilation, the FE0 CO2 will typically remain raised for .6 min unless minute ventilation is deliberately increased. (Page 2)
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 litre21, 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. (Page 2)
Acute vascular insufﬁciency is thought to occur when mechanical pressure from the tourniquet damages atheromatous vessels, causing plaque rupture. (Page 3)
Out of 63 484 operations performed under a tourniquet, only 26 complications that might have been caused by the tourniquet were reported (an incidence 0.04%). (Page 3)
.6 Lower limb tourniquets were more likely to produce neurological complications than upper limb tourniquets. The nerves most commonly affected are the sciatic nerve in the lower limb and the radial nerve in the upper limb. (Page 3)
Inﬂation of a tourniquet is followed by the development of a dull, aching pain. Such pain can accompany otherwise adequate regional anaesthesia and can be severe enough to necessitate conversion to general anaesthesia. (Page 3)
It is thought that tourniquet pain is predominantly mediated by unmyelinated, slowly conducting C-ﬁbres which, as stated earlier, are less affected by the compressive effects of tourniquet inﬂation than larger ﬁbres. One theory suggests that tourniquet pain arises from selective transmission by cutaneous C-ﬁbres; these ﬁbres are continuously stimulated by skin compression from the tourniquet, and their post-synaptic effect at the dorsal horn is no longer inhibited by input from larger nerve ﬁbres whose transmission has been blocked. This theory is supported by the ﬁnding that during i.v. regional anaesthesia, tourniquet analgesia is prolonged by application of EMLA cream beneath the tourniquet (Page 3)
Large diameter nerve ﬁbres are more susceptible to pressure, so there is a relative sparing of sensation compared with motor function. The role of mechanical pressure in nerve injury probably explains why the Esmarch bandage (which can generate pressures .1000 mm Hg) is associated with a higher incidence of nerve injury. The effects of nerve compression at the site of tourniquet application may make injury at a more distal site (caused by ischaemia or surgical trauma) more likely due to the neural ‘double crush’. (Page 3)
tourniquet pain can complicate spinal or epidural anaesthesia, despite apparently adequate anaesthesia of the sensory dermatome underlying the tourniquet. One explanation of this is offered by the in vitro ﬁnding that smaller unmyelinated C-ﬁbres are more resistant to local anaesthetic-induced conduction block than larger, myelinated A-ﬁbres.10 After intrathecal administration of an adequate dose of local anaesthetic, conduction in both A- and C-ﬁbres is blocked. However, as the concentration of local anaesthetic in the cerebrospinal ﬂuid decreases, C-ﬁbres start to conduct impulses before the A-ﬁbres, resulting in a dull tourniquet pain in the presence of an anaesthetic which, assessed by pinprick, appears adequate. (Page 3)
Very rarely the post-ischaemic swelling and oedema, in combination with reperfusion hyperaemia, may lead to the development of a compartment syndrome. Rhabdomyolysis directly related to the tourniquet use has been reported, but is extremely rare. (Page 3)
there is no completely satisfactory solution. Various techniques have been used, including increasing the density of central neuraxial block by using adjuncts to bupivacaine such as epinephrine, morphine, and clonidine. (Page 3)
some success has also been reported with the administration of preoperative gabapentin and the use of low-dose (0.1 mg kg21) i.v. ketamine. (Page 4)
A gradual increase in arterial pressure is frequently observed a variable time after tourniquet inﬂation. The exact mechanism of this tourniquet-induced hypertension is not known, but it has been suggested that it represents activation of the sympathetic nervous system in response to the development of tourniquet pain. (Page 4)
Most recommendations in the literature suggest a period of 1.5 –2 h in a healthy adult, which corresponds to the point at which muscle ATP stores are depleted. Although ischaemia has typically been associated with muscular rather than neurological injury, there is an approximate three-fold increase in the risk of neurological complications for each 30 min increase in tourniquet time.7 (Page 4)
It is generally considered that the tourniquet should be left deﬂated for 10–15 min before re-inﬂation and this seems to correspond to restoration of muscle ATP levels. It is important to re-exsanguinate the limb before inﬂating the cuff again after reperfusion. (Page 4)
The Association of peri-operative Registered Nurses (AORN) in the USA recommends inﬂating tourniquets to pressures based on the limb occlusion pressure (LOP).12 This value is determined by gradually increasing the pressure in the tourniquet while assessing distal blood ﬂow with a Doppler probe held over a distal artery. The LOP is the pressure in the cuff at which the arterial pulse disappears. The LOP is usually higher than systolic pressure because the pressure from the tourniquet which is transmitted to deep underlying soft tissues is frequently less than that in the tourniquet itself. The percentage of transmitted tourniquet pressure varies inversely with limb circumference (hence the practice of using higher pressures on the thigh than on the upper arm). (Page 4)