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Complications of

Orthopaedic Surgery
By: D. Ramkeesoon
Ojectives

• Tourniquet Application and Complications

• Reperfusion Injury

• Bone Cement Implantation Syndrome


Tourniquet Application
and its Complications
Tourniquet use
• Tourniquets are devices which are used to control
the flow of blood to and/or from an extremity.

• The arterial tourniquet is usually a pneumatic


device consisting of an inflatable cuff connected to
a compressed gas supply.

• The most common use for such tourniquets is in


surgical procedures on the extremities,where a
bloodless surgical field is required.
Site Application

• The upper arm and thigh have sufficient muscle


bulk to distribute the cuff pressure evenly and are
the recommended sites.

• The cuff should be positioned at the point of


maximum circumference of the limb.
Cuff Width and Length

• For the upper arm: width of 20% greater than the


circumference of the upper arm

• For the thigh: width of 40% greater than the


circumference of the thigh

• Cuff length should exceed the circumference of


the extremity by 7-15cm.
Cuff Inflation Pressure
• Based on the unseated patient’s blood pressure
measured on the ward pre-op.

• Upper limb: Systolic BP + 50mmHg

• Lower limb: Twice systolic BP

• However the Association of peri-operative


Registered Nurses recommends inflating
tourniquets to pressures based on the limb
occlusion pressure (LOP).
Tourniquet Duration

• All tourniquets should be kept inflated for the


minimum length of time possible.

• Most recommendations suggest a period of 1.5-2


hours in a healthy adult which usually
corresponds to the point at which muscle ATP
stores are depleted.
Physiological Effects of
Tourniquet Application
• Local Effects:

• Muscle: progressive decrease in PO2 and increase in PCO2


following inflation. Lactate concentrations increases with the
switch to anaerobic metabolism leading to intracellular
acidosis.

Muscle underlying the tourniquet is subjected to


both ischemia and compression which leads to local fibre
necrosis

Microvascular injury occurs in muscle after ischemia of


greater than 2 hours duration.
Physiological Effects of
Tourniquet Application
• Local Effects:

• Nerve: a physiological conduction block develops


between 15-45 mins after inflation. The conduction
block affects both motor and sensory functions and
is reversible after deflation.

Direct mechanical compression of nerves is


responsible for a second, longer lasting nerve
conduction block called ‘tourniquet paralysis’.
Physiological Effects of
Tourniquet Application
• Systemic Effects:

• Cardiovascular: after limb exsanguination and


tourniquet inflation, there is an increase in SVR
and an effective increase in circulating blood
volume. This leads to an increase in CVP and an
increase in systolic arterial pressure, both of
which are transient.
• Respiratory: Deflation of the tourniquet is followed
almost immediately by an increase in end tidal
CO2, which usually peaks within 1 min.

• CNS: the increase in PaCO2 which accompanies


deflation causes an increase in cerebral blood
flow.
• Temperature: inflation of arterial tourniquets are
associated with a gradual increase in core body
temperature caused by reduced heat transfer to
and heat loss from the ischaemic limb.

• Metabolic: deflation of the tourniquet after 1-2


hours of ischaemia is associated with small
increases in plasma concentration of K+ and
lactate.
Complications

• Nerve Injury: neurological injuries after tourniquet


use are probably the most common complication.
The nerves most commonly affected are the
sciatic nerve in the lower limb and the radial in
the upper limb.

• Muscle Injury: post tourniquet syndrome results in


a stiff swollen weak limb.
• Skin Injury: chemical burns are the most common
form of skin injury. Friction burns can also occur
as a result of poorly applied tourniquets.

• Intraoperative bleeding: common causes include


incomplete exsanguination of the limb and a
poorly fitting or under pressurised cuff.
Tourniquet Pain
• Inflation of a tourniquet is followed by the development of
a dull aching pain.

• It is thought that tourniquet pain is mediated by


unmyelinated slowly conducting C-fibres which are less
affected by the compressive effect than the larger fibres.

• Various techniques have been employed to improve


tourniquet pain which include increasing the density of
central neuraxial block by using adjuncts, administation of
gabapentin pre-op or use of small doses of Ketamine
(0.25mg/kg) before tourniquet inflation.
Reperfusion injury
Reperfusion Injury
• Definition:
• Reperfusion injury or reperfusion insult, sometimes called
ischemia-reperfusion injury (IRI) or reoxygenation injury, is the
tissue damage caused when blood supply returns to tissue (re- +
perfusion) after a period of ischemia or lack of oxygen (anoxia or
hypoxia).

• The absence of oxygen and nutrients from blood during the


ischemic period creates a condition in which the restoration of
circulation results in inflammation and oxidative damage through
the induction of oxidative stress rather than (or along with)
restoration of normal function.
Mechanism
Treatment

• Therapeutic Hypothermia or TTM

• Hydrogen Sulphide

• Cyclosporin
Bone Cement
Implantation Syndrome
(BCIS)
Composition of bone cement:
• Poly(methyl methacrylate) (PMMA) (90%)
Powder polymer: pre-polymerized PMMA
Initiator: dibenzoylperoxide
Liquid monomer (MMA)
Activator: N,N-dimethyl-p-toluidine

• Antibiotics Gentamicin, tobramycin, clindamycin

• Radiographic contrast material (10%) Zirconium dioxide or


Bone Cement Implantation
Syndrome

• Definition:

• BCIS has no agreed definition; it is characterized by a number of clinical


features that may include hypoxia, hypotension, cardiac arrhythmias,
increased pulmonary vascular resistance (PVR) and cardiac arrest.

• Usually occurs around the time of cementation, prosthesis insertion, reduction


of the joint or, occasionally, limb tourniquet deflation in a patient undergoing
cemented bone surgery.
Classification of BCIS

Grade 1: moderate hypoxia (SpO2 ,94%) or a decrease in sy

Grade 2: severe hypoxia (SpO2 ,88%) or hypotension (decre

Grade 3: cardiovascular collapse requiring cardiopulmonary


Clinical Features of BCIS

• BCIS has a wide spectrum of clinical features that range from


tran- sient desaturation and hypotension to cardiac arrhythmias
and cardiac arrest at the time of cement deployment.

• Clinical reports and studies all demonstrate the presence of right


ventricular failure secondary to increased pulmonary artery
pressure (PAP) as the underlying cause of systemic hypotension
and sudden cardiac arrest.

• The cause of the acute increase in pulmonary vascular re-


sistance (PVR) remains uncertain. It may be due to deposition of
cement or fat emboli or may be a result of systemic absorption of
the volatile monomer.
• Regardless of the cause, the thin-walled and
compliant right ventricle rapidly dilates and shifts
of the interven-tricular septum to the left thereby
reducing the volume of the left ventricular cavity.

• This occurs because the total volume of the heart


cannot expand within such a rapid time frame, as
it is con- strained by the pericardium.

• These changes cause an immediate decrease in


left ventricular compliance, reduced ventricular
filling, and cardiac output (CO).
Risk factors for the development of BCIS:

• Patient factors:
1. ASA III – IV
2. Pre-existing pulmonary hypertension
3. Significant cardiac disease
4. Osteoporosis

• Surgical factors:
1. Pathological fracture
2. Intertrochanteric fracture
3. Long-stem arthroplasty
Aetiology and
Pathophysiology of BCIS
• While the aetiology and pathophysiology of BCIS is
poorly under- stood, several models have been
proposed

A. Monomer-Mediated Model

B. Embolus- Mediated Model which proposes 2


aetiologies:

1. Mechanical Effects

2. Mediator Effects
Management of BCIS
• Studies have shown that BCIS is a reversible, time-limited phenomenon.

• The PAPs can normalize within 24 h and non-diseased hearts can recover within
minutes to hours. This means that aggressive resuscitation and supportive treatment
is essential to reduce the morbidity and mortality of this potentially life-threatening
situation.

• When BCIS is suspected, resuscitation should be based on general principles.

1. The inspired oxygen concentration should be increased to 100%.

2. The management of cardiovascular collapse should be in line with the treatment of


right ventricular failure,4 including i.v. fluid therapy, the use of pulmonary
vasodilators for reducing PAP, and the use of inotropes (dobutamine and milrinone)
to maintain right ventricular contractility.

3. If simple measures fail, intraoperative CO monitoring should be used, After


operation, the patient should be managed in an intensive care unit setting.
Prevention of BCIS

s to mitigate risk of bone cement implantation syndrome advised by the National Patient S
References
• Khanna, G. “Bone Cement and Implications in
Anaesethesia.”
Https://Watermark.silverchair.com, 23 Feb. 2012,
academic.oup.com/bjaed/article-
pdf/12/4/213/770329.

• Wikipedia, Free Encyclopedia. “Reperfusion


Injury.” www.wikipedia.com, 12 Aug. 2017,
en.wikipedia.org/wiki/Reperfusion_Injury.
Thank You.

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