Basic skills

Uses and precautions of

tourniquets

A modern pneumatic tourniquet

Fastening strap
Velcro fastening
surface

Peter C A Kam

Velcro
surface

Abstract

Rubberized
surface of
tourniquet

This contribution reviews the use of tourniquets and discusses local

(skin, nerve, muscle, vascular) injuries associated with their use. It also
discusses the systemic (cardiovascular, respiratory, cerebral circulatory,
haematological, metabolic, temperature) effects of tourniquet use.

Dual cuff
valve

Keywords arterial tourniquets; general surgery; local injuries; systemic

effects

Pressure
monitor

Modern pneumatic tourniquets consist of a cuff wrapped around

the limb and then inflated, a compressed gas source, and a mechanism with a pressure gauge to maintain the desired cuff pressure (Figure 1).
Arterial tourniquets reduce blood loss and provide better
operative conditions during extremity surgery. Tourniquets are
also used to prevent systemic toxicity of drugs that are given in
high doses into the isolated limb, such as during intravenous
regional anaesthesia, intravenous regional sympathectomy in the
management of complex regional pain syndromes, and isolated
limb perfusion with cytotoxic drugs (e.g. melphalan) in the treatment of localized cancers (e.g. melanoma and soft tissue sarcoma) in the extremities. There is no place for arterial tourniquet
as a first aid measure for severe haemorrhage that can instead
be controlled effectively by elevating the limb and applying wellpadded pressure bandages over the wound.
The risks and benefits of a tourniquet must be assessed before
use because the risks increase in patients with comorbidities
(peripheral vascular disease, old age), with high tourniquet pressure and prolonged duration of tourniquet application.

Figure 1

Nerve injuries associated with tourniquets range from paraesthesia to complete paralysis. In the UK, the incidence of paralysis associated with the pneumatic tourniquet per year is 1 per
11,000 population in the upper limb, and 1 per 250,000 population in the lower limb. The peripheral nerve most frequently
injured is the radial nerve, followed by the ulnar, median and
sciatic nerves. The use of an esmarch bandage tourniquet to
exsanguinate the limb is not recommended because it generates pressures >1000 mmHg (133.3 kPa), resulting in a higher
incidence of nerve injury. Maximal exsanguination can be
achieved by elevation of the arm (90) and leg (45) for five
minutes.
Direct pressure beneath the cuff and shearing pressures at the
edge of the cuff are the major causes of nerve injury. Axonal
degeneration results from intraneural microvascular abnormal
ities and oedema formation and can lead to neuropraxia (axonal
dysfunction). Axial compression causing damage at the nodes
of Ranvier may occur. Prolonged neurological deficits are due to
axonal disruption.

Local injuries
Localized complications result from compression to underlying
skin, nerve, muscle and blood vessels beneath the cuff or tissue
ischaemia distal to the tourniquet.
Skin injury: erythema of the skin is common, but of little consequence. Bullous lesions after prolonged tourniquet inflation
(and friction burns caused by movement of poorly applied tourniquets) may occur.

Muscle injury: the tourniquet causes tissue ischaemia beneath

and distal to the cuff, resulting in metabolic (depletion of adeno
sine triphosphate), cellular and microvascular changes. Muscle
injury is greatest beneath the tourniquet because of combined
ischaemia and mechanical deformation, and may persist after
tourniquet deflation. Toxic oxygen radicals and other oxidant
molecules (e.g. hydrogen peroxide) are produced in the ischaemic tissues. Following tourniquet release after 24 hours of
ischaemia, increased microvascular permeability in muscle and
nerve leads to interstitial and intracellular oedema that may take

Peter C A Kam FRCA FANZA FCARCSI FHKCA(Hon) is Nuffield Professor of

Anaesthetics, University of Sydney, Australia. Conflicts of interest: none
declared.
Q1

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Basic skills

Respiratory effects: tourniquet deflation is associated with a

transient increase in end-tidal carbon dioxide tension (ETCO2) by
0.132.4 kPa that peaks within one minute and returns to baseline values within 1013 minutes. The transient hypercapnoea,
greater with lower limb tourniquets (0.662.4 kPa) compared to
upper limb tourniquets (0.131.6 kPa), is due to the efflux of
hypercapnoeic venous blood from the ischaemic limb into the
systemic circulation. It can be prevented by increasing the minute alveolar ventilation by 50% for five minutes after tourniquet
deflation in artificially ventilated patients.

up to a month to resolve. The combined effect of muscle ischaemia, oedema and microvascular congestion commonly leads
to post-tourniquet syndrome, characterized by stiffness, pallor,
weakness without paralysis and subjective numbness of the
extremity. This post-anoxic oedema, together with reperfusion
hyperaemia and haematoma formation, can result in a compartment syndrome.
Vascular injury: mechanical pressure from a tourniquet in
surgery of the lower limb can cause arterial injury in patients
with peripheral vascular disease via fracture of an atheromatous
plaque. The lack of blood flow due to the tourniquet may cause
thrombosis in atherosclerotic vessels. Tourniquets are contraindicated in patients with absent distal pulses, poor capillary return,
a calcified femoro-popliteal system or who have had previous
vascular surgery on the involved limb.

Cerebral circulatory changes: multi-trauma patients with severe

head injuries can suffer marked intracranial pressure increases
when lower limb tourniquets are released. The rapid increase in
ETCO2 following deflation of the tourniquet is associated with a
50% increase in the velocity of blood flow in the middle cerebral
artery. This peaks at about 24 minutes and returns to normal
within 810 minutes. The resultant increased cerebral blood volume can contribute to secondary brain injury. Normocapnoea
maintained by hyperventilation following tourniquet deflation
can prevent the increase in intracranial pressure.

Tourniquet pressure and usage time

The concept of minimum effective pressure is important for preventing pressure-related skin, muscle and nerve injuries. The
elderly, trauma patients, and those with peripheral vascular disease are more susceptible to muscle injury. For longer surgical
procedures, the tourniquet should be deflated every two hours
to allow ten minutes of reperfusion of the muscles beneath and
distal to the cuff.
Nerve injuries associated with a pneumatic tourniquet are
usually caused by excessive inflation pressures due to faulty
aneroid pressure gauges. An inflation pressure of 200 mmHg
for the upper limb, and 250350 mmHg for the lower limb is
recommended in healthy patients. Tourniquet inflation to a pressure 50150 mmHg above systolic pressure has been also suggested. In children, lower tourniquet pressures (175 30 mmHg
for the upper limb, 210 10 mmHg for the lower limb) are
recommended. Significantly lower arterial occlusion pressure
(184 mmHg for the upper limb, 208 mmHg for the lower limb)
can be achieved with a curved and wider (12 cm) tourniquet cuff
compared with standard straight tourniquet cuff.

Haematological effects: pain caused by the tourniquet and

surgery provoke the release of catecholamines, which promote
platelet aggregation and may initially result in systemic hypercoagulability. However, limb tissue ischaemia following tourniquet inflation promotes tissue plasminogen activator release,
activating the antithrombin III and thrombomodulin-protein-C
anticoagulant systems in the occluded limb and causing systemic
thrombolysis when the tourniquet is deflated. Tourniquet deflation can be associated with post-tourniquet bleeding caused by a
brief (30 minutes) increase in thrombolytic activity in peripheral
blood.
Reports of fatal pulmonary emboli associated with lower limb
exsanguination, tourniquet inflation and deflation suggest that
tourniquets are contraindicated in patients at high risk of deep
vein thrombosis (e.g. previous history of venous thrombosis, prolonged immobilization, pelvic and lower limb fractures). Echogenic small (miliary) and large venous emboli can be detected by
transoesophageal echocardiography following tourniquet deflation during total knee arthroplasty. Potentially fatal pulmonary
embolisms have occurred after intramedullary guide insertion,
femoral reaming and cementing of long-stemmed femoral prostheses. There is about a five-fold increased risk of large venous
embolism associated with the use of a tourniquet in patients
undergoing total knee arthroplasty. Low doses of heparin given
intraoperatively (e.g. 1000 U before tourniquet inflation in knee
arthroplasty) may prevent fatal pulmonary embolism during and
after total joint arthroplasties.

Systemic effects of tourniquet use

Systemic effects are related to the inflation or deflation of the
tourniquet.
Cardiovascular effects: haemodynamic changes associated
with tourniquet inflation or deflation are not well tolerated by
patients with poor cardiac reserve. Following limb exsanguination and tourniquet inflation, the circulating blood volume and
systemic vascular resistance increases. Exsanguination of both
lower limbs increases the circulating blood volume by about
15% (about 800 ml in an adult), and circulatory overload and
cardiac arrest have been reported. After tourniquet inflation for
3060 minutes, patients may develop an increase in heart rate,
systolic and diastolic pressures that persists until tourniquet
deflation (a phenomenon termed tourniquet pain that is resistant to analgesics and increased anaesthetic depth).
Following deflation of the tourniquet, central venous pressure
and blood pressure decrease to below baseline values transiently
for 15 minutes. This is caused by a shift of blood back into the
limb where ischaemic reactive hyperaemia causes vasodilation
in the limb.

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Metabolic changes: after 12 hours of ischaemia, arterial

serum potassium and lactate concentrations increase by 0.28
0.32 mmol/l and by 2.13 mmol/l respectively for about 30 minutes after deflation. Lactic acid released from the ischaemic
limb and the increase in arterial partial pressure of CO2 causes
a transient (1030 minutes) decrease in arterial pH. Oxygen
consumption and carbon dioxide production are increased
by 55% and 80% respectively, two minutes after tourniquet
release and return to pre-release values within eight minutes.
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2007 Elsevier Ltd. All rights reserved.

Basic skills

These changes are dependent on the duration of tourniquet

inflation.

in core temperature by 12 C results from the redistribution of

body heat and the return of hypothermic venous blood from the
tourniquet limb into the systemic circulation.

Temperature changes: a rise in the temperature of the body

core occurs during the inflation of arterial tourniquets because of
reduced metabolic heat transfer from the central compartment to
the peripheral compartment, and also from decreased heat loss
from distal skin. After tourniquet deflation, a transient decrease

SURGERY 26:2

Antibiotic administration
Prophylactic antibiotics for surgery should be given intra
venously at least five minutes before tourniquet inflation to
ensure adequate penetration of tissues.

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2007 Elsevier Ltd. All rights reserved.