Definition of Tourniquet: a constricting or compressing device used to control venous and arterial circulation to an extremity for a particular duration.
Tourniquets are commonly used during limb surgeries (particularly in plastic and orthopaedic surgery) to limit blood loss and optimise surgical conditions. The application of a tourniquet results in physiological changes which, although mostly tolerated in healthy individuals, may not be well-tolerated by those with poor cardiac function or other associated comorbidities. Below is a list of these changes as well as clinical practice points which must be considered by anaesthetists when an arterial tourniquet is applied.
TOURNIQUET SPECIFICATIONS
- Cuff width >50% of the limb’s diameter. Wider cuffs decrease injury risk to underlying tissue by dispersing pressure over a larger surface area.
- Recommended cuff pressure for adults is 200-300mmHg, however, optimal cuff pressure is yet to be established. A lower cuff pressure minimises injury to tissue. Limb occlusion pressure (LOP) may be used as a guide:
- LOP <130mmHg = Add 40mmHg
- LOP 131-190mmHg = Add 60mmHg
- LOP >190mmHg = Add 80mmHg
- Keep inflation time minimal. If duration is >2.5 hours, deflate cuff for 10 minutes at this point. Thereafter, deflate cuff for 10 minutes every hour.
- Apply to limb at point of maximum circumference.
LOCALISED COMPLICATIONS
NERVE INJURY
- Can range from paraesthesia to paralysis.
- Caused predominately by compression, but ischaemia also contributes.
- Compression causes intraneural microvascular abnormalities in segment of nerve adjacent to cuff. Resulting oedema causes compromised tissue nutrition and axonal degeneration.
- Maximal at proximal and distal edges of cuff where shear stress is greatest.
- More common in upper limbs than lower limbs.
- Most common upper limb nerve injury is the radial nerve, followed by the ulnar and median nerves.
- Most common lower limb nerve injury is the common peroneal nerve.
MUSCLE INJURY
- Caused by ischaemia and mechanical deformation of tissue. Greatest at sites distal to the tourniquet.
- Minimised by use of lower inflation pressures.
VASCULAR INJURY
- Direct vascular injury is uncommon and mostly occurs in children, obese, elderly, and patients with peripheral vascular disease.
SKIN INJURY
- Tourniquet inflation may result in pressure necrosis or friction burns.
- Chemical burns may occur when skin preparation solution seeps beneath the tourniquet and is held against the skin under pressure.
SYSTEMIC COMPLICATIONS
CARDIOVASCULAR
- Increased CVP – due to increases in blood volume (up to 15%, from fluid shifts) and systemic vascular resistance from limb exsanguination and tourniquet inflation.
- Increased HR, Systolic BP and Diastolic BP – after 30-60 minutes of tourniquet inflation; related to tourniquet pain and ischaemia.
- Responds poorly to analgesia or increasing anaesthetic depth.
- Interventions which may reduce cardiovascular stress include ketamine, dexmedetomidine, magnesium sulphate, clonidine, and remifentanil infusion.
- Hypotension following cuff deflation – drop in CVP and MAP due to shift of blood volume back into limb and release of ischaemic mediators into systemic circulation.
- Treat with IV fluids and vasopressors.
RESPIRATORY
- Increased ETCO2 following cuff deflation – outflow of hypercapnic venous blood and metabolites into the systemic circulation.
- Related to duration of ischaemia and is greater with larger limbs/muscles.
- Peaks at 1-3 minutes following deflation.
- Treat by increasing minute ventilation.
CEREBRAL
- Increased cerebral blood flow following cuff deflation – secondary to increased ETCO2 following cuff deflation.
- Patients with increased ICP at risk of adverse effects.
- Prevented adverse outcomes by maintaining normocapnia (increasing minute ventilation).
HAEMATOLOGICAL
- Hypercoagulable state – tourniquet inflation and surgical pain, which increases platelet aggregation and coagulation factors.
- Transient increase in fibrinolytic activity on cuff deflation – release of tPA causes activation of antithrombin III and thrombomodulin-protein C anticoagulant system, contributing to post-tourniquet bleeding.
- Maximal at 15 minutes and returns to baseline within 30 minutes of tourniquet release.
- Risk of precipitating sickle cell crisis due to circulatory stasis, acidosis, and hypoxaemia.
METABOLIC
- Production of ischaemic mediators including CO2, lactate and K+ may result in the following changes following tourniquet release:
- Increased serum K+ by approximately 0.2mmol/L (peaks at 3 mins)
- Increased serum lactate by ~ 2mmol/L (remains elevated for 30 mins)
- Decrease in pH due to CO2 and lactate (maximal decrease at 4 mins)
- Increased oxygen consumption and CO2 production following tourniquet release.
- Treat by increasing FiO2 and minute ventilation.
- Above changes are dependent on duration of tourniquet inflation.
TEMPERATURE
- Increasing core body temperature following tourniquet application – reduced surface area for heat loss causing less heat transfer from the central to the peripheral compartment.
- Fall in core body temperature following cuff deflation – redistribution of body heat and hypothermic blood from the ischaemic limb.
PHARMACOLOGICAL
- Altered volume of distribution of medication – tourniquet inflation isolates limb from the remainder of the body.
- Give prophylactic antibiotics 5-10 minutes prior to cuff inflation to allow tissue penetration.
PAIN
- Typically, resistant to systemic analgesia and deepening of anaesthesia.
- Pain manifests as tachycardia and hypertension under general anaesthesia and occurs 30-60 minutes after cuff inflation.
- Proposed mechanisms of tourniquet pain:
- Pain transmitted by C-fibres, which are normally inhibited by A-delta fibres. After approximately 30 minutes, A-delta fibres are blocked by mechanical compression, while C-fibres remain functioning.
- Release of prostaglandins from injured cells, which increases pain perception by sensitising and exciting pain receptors.
- Limb ischaemia results in central sensitisation via NMDA receptor activation due to repeated nociceptive afferent input from affected limb.
SUMMARY / CLINICAL PRACTICE POINTS
- Pre tourniquet inflation:
-
- Check tourniquet specifications (width, length, presumed inflation pressure) and limb pressure.
- Know your patients past medical history. Check for cardiac, haematological, or intracranial pathology, as well as any prior nerve or muscle issues.
- Check surgical tourniquet inflation time with surgeon. Plan for short deflation if longer than 2 to 2.5 hours.
- Check patients’ K+ level and kidney function.
- Administer IV antibiotics 5-10 minutes prior to tourniquet inflation.
- Tourniquet inflation:
-
- Record duration of tourniquet inflation. Deflate cuff at appropriate intervals (10 minutes of deflation after the first 2.5 hours and then 10 minutes every 1 hour).
- Use lowest tourniquet pressures possible to reduce blood loss and optimise surgical conditions.
- Pain – manifests as tachycardia and hypertension after 30-60 minutes; resistant to standard treatments. Interventions which may assist in reducing associated cardiovascular stress include ketamine, dexmedetomidine, magnesium sulphate, clonidine, and remifentanil infusion. However, treatment is ultimately through tourniquet deflation.
- Ensure warming devices are on and functioning in anticipation for decrease in temperature following cuff deflation.
- Tourniquet deflation:
-
- Increased ETCO2 – increase minute ventilation to maintain normocapnia, (particularly if increased ICP is a concern)
- Hypotension – be prepared to administer IV fluids and vasopressors as required. Often unwell patients are given a fluid load prior and vasopressor infusion. Increased to maintain a higher MAP prior to deflation.
- Hypoxaemia – monitor saturations, as cuff deflation increases oxygen consumption. Increased FiO2 is rarely needed.
- Increased K+ – monitor ECG. If patient at risk of complications associated with metabolic effects of tourniquet (end stage renal failure, preop higher K+), assess with a VBG.
- Decreased temperature – ensure use of warming devices as required.
References
- Kumar K, Railton C, Tawfic Q. Tourniquet application during anesthesia:“What we need to know?”. Journal of Anaesthesiology, Clinical Pharmacology. 2016 Oct;32(4):424.
- Kam PC, Kavanaugh R, Yoong FF. The arterial tourniquet: pathophysiological consequences and anaesthetic implications. Anaesthesia. 2001 Jun;56(6):534-45.
