• soft tissue infection, most often wound infection (Chapter 12) with surgical site and traumatic wound infection being a significant risk
• bone infection (osteomyelitis) and joint infection (infective arthritis) (Chapter 13)
• urinary tract infection and
• respiratory tract infection.

Healthcare-associated infection is the main cause of infection in orthopaedic and trauma patients, acquired by transfer from one person or surface to another. The way by which an infection can spread involves five links in the ‘chain of infection (HPA 2013).’ Understanding how the links are made is important in understanding the ways in which the chain can be broken and infection prevented:

1. A causative organism – a pathogenic organism is present which is capable of causing infection.
2. A reservoir of infection – a place (human or environmental) which provides ideal conditions for the causative organism to multiply including a supply of nutrients.
3. A portal of exit – allows the organism to leave the reservoir, e.g. in body fluids, on the skin (particularly the hands), in various body fluids such as respiratory droplets.
4. A mode of transmission – a method through which the organism is spread to another person and acquired by them. The most common methods of transfer are through body fluids, on the hands of patients and healthcare workers and ingestion along with airborne transmission of organisms during surgery.
5. A susceptible patient – who is vulnerable to infection because their immune response is compromised. This risk is greater in hopitalised patients, those who are injured and/or undergo surgery, those of greater or of very young age or with concurrent medical conditions that cause a reduction in the immune response and those who are malnourished.

The prevention of orthopaedic infections is particularly important because of the potentially devastating consequences of transfer of infection to bone and resultant osteomyelitis which is difficult to eradicate and results in long term pain and distress. The avoidance of osteomyelitis is a central aim of infection control in the orthopaedic and trauma setting. A major concern is the ability of remote infections such as urinary tract infections and surgical site infections to transfer to sites of orthopaedic implants as a result of ‘seeding’ of bacteria to implant sites.

The prevention and control of infection

Prevention and control of infection measures have been standardised as a result of a large body of amassed evidence which demonstrates the most effective approaches (See Box 9.1. for an example of evidence-based guidelines). These include the following (Pratt et al., 2007):

• Environmental hygiene through rigorous cleaning processes
• Hand hygiene: many healthcare-associated infections are transferred from one person to the other on the hands of healthcare staff
• The use of personal protective equipment to provide a barrier between the healthcare provider and a source of infection
• The safe use and disposal of sharps: high risk of blood borne infection from accidental inoculation with contaminated sharps
• Preventing infections associated with the use of short-term indwelling urethral catheters, which provide a major portal for infection
• Preventing infections associated with central venous catheters – with a significant danger of blood-borne infection.

Box 9.1 Evidence digest

Shock

Shock is a complex life-threatening state resulting in a significant reduction in systemic tissue perfusion and subsequent reduced oxygen (O₂) delivery to the tissues. Early recognition and management are vital in increasing the patient’s chance of survival. This physiological syndrome creates cellular dysfunction with an imbalance between O₂ delivery and O₂ consumption. Oxygen deprivation leads to cellular hypoxia and derangement of critical cellular processes which can progress to organ failure and death (Kleinpell 2007). The circulatory system no longer sustains essential functions such as the provision of nutrients and O₂ to cells and removal of waste. Without intervention, the result is sequential cell death, end-organ damage, multi-system organ failure and death.

Garretson and Malberti (2007) describe four distinct stages of shock which are initially reversible but then rapidly become irreversible:

• Stage 1 Initial stage of shock This is reversible, but easily overlooked due to an absence of clinical signs to indicate impending shock. There is a reduction in cardiac output with a change from aerobic to anaerobic metabolism, which can lead to lactic acidosis (due to the inadequate clearance of lactic acid from the blood).
• Stage 2 Compensatory stage of shock There is an attempt to regain homeostasis and improve the perfusion of tissues. The sympathetic nervous system produces catecholamine which dilates the bronchi and constricts peripheral blood vessels. Water conservation is initiated by the release of aldosterone by the adrenal/renal system.
• Stage 3 Progressive stage of shock The body has lost the compensatory mechanism that sustains the perfusion of tissues, resulting in metabolic and repository acidosis along with electrolyte imbalance. There is a visible deterioration.
• Stage 4 – Refractory stage of shock This presents with irreversible cellular and organ damage. The condition becomes unresponsive to treatment and death is imminent (Hand 2001).

Hypovolaemic shock (HS)

Hand (2001) defines hypovolaemic shock as:

(a life threatening condition due to failure of the body to provide the tissues with sufficient oxygen and nutrients to meet cellular needs.) (p 45)

There is excessive fluid loss, (e.g. the blood loss from bleeding). Prevention requires ensuring adequate cardiac output and circulation volume. With a blood loss of 750 ml the body may enter the compensated stage and changes to vital signs will occur (Bench 2004). A 40% fluid loss threatens life.

The patient will present with:

• anxiety, restlessness and altered mental state due to decreased cerebral perfusion and subsequent hypoxia
• hypotension due to decreased circulatory volume
• rapid, weak, thready pulse and tachycardia due to decreased blood flow
• cool, clammy skin due to vasoconstriction
• mottled skin, especially in the fingers and toes due to insufficient perfusion
• rapid, deep respirations due to sympathetic nervous system stimulation and acidosis
• hypothermia resulting from decreased perfusion and evaporation of sweat
• thirst and dry mouth, due to reduced fluid and urinary output
• fatigue due to inadequate oxygenation
• systolic blood pressure <90 mm Hg or 40 mm Hg below baseline.

Management includes accurate patient assessment and fluid balance with fluid/blood replacement. Bleeding must be controlled to restore blood volume with infusions of hypertonic crystalloid solutions and/or blood products (Docherty 2002). Blood replacement with packed red cells is administered if there is blood loss to prevent hypoxia. Accurate fluid assessment and documentation are essential with accurate measurement and documentation of intake and output. Treatment can include vasopressors to stimulate contraction of the muscular tissues of the heart, capillaries and arteries. Physical assessment should not depend totally on the ‘monitoring equipment’ but ‘looking’ at the patient holistically – observing for the signs of shock. Supplementary oxygen may be prescribed to counteract the respiratory effects of shock.

Cardiogenic shock

Cardiogenic shock is associated with a decline in cardiac output and tissue hypoxia, despite adequate fluid volume. A damaged left ventricle is unable to pump effectively and cardiac output is reduced to less than 2.2 L/min (normal being 4–8 L/min) (Bench 2004). McLuckie (2003) reports the older female patient to be at a higher risk of developing this type of shock, as well as those with a history of MI and diabetes. It can be a complication of either acute myocardial infarction (MI) and other cardiac conditions, often resulting in death.

The clinical presentation is similar to hypovolaemic shock but the patient can deteriorate more quickly. There may be:

• Raised central venous pressure (CVP), chest pain, anxiety and feelings of doom and demise (Hand 2001). Pain relief and reducing anxiety will help reduce the patient’s cardiac workload.
• Absent pulse with tachyarrhythmia.
• There may be evidence of distended jugular veins due to increased jugular venous pressure.

The main goal is to re-establish circulation to the myocardium, minimise heart muscle damage and improve the heart’s effectiveness as a pump (Garretson and Malberti 2007). Evaluation of arterial blood gases (ABG) and cardiac monitoring are essential. Intervention includes oxygen therapy to reduce the workload of the heart by reducing tissue demands for blood flow. The myocardium can be reperfused by thrombolysis (e.g. injection of streptokinase). Early intervention is pivotal as the effect is reduced within hours of onset and development of shock. Mechanical vascularisation such as percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG) (Man and Nolan 2006) is advocated for those patients less than 75 years (Sleeper et al., 2005). The administration of cardiac drugs to increase the heart’s pumping action is also used as a treatment option e.g. inotropics (e.g. Dopamine) and vasopressors (nitroglycerin).

Septic shock

Septic shock is a serious condition that occurs when an overwhelming infection leads to low blood pressure and low blood flow. The brain, heart, kidneys and liver may not work properly or fail. Sources of infection include septicaemia, osteomyelitis in bone, endocarditis and pericarditis of the heart, cellulitis and wound infections and urinary tract infections. The mortality rate is estimated to be around 40–50% (Oppert et al., 2005). Early recognition may be difficult and the practitioner’s role central in recognising condition changes and seeking medical attention.

A classic sign of septic shock is absolute and relative hypovolaemia (Garretson and Malberti 2007):

• absolute – result of vomiting, sweating or oedema
• relative – result of vasodilatation and peripheral blood pooling.

Presentation includes hypotension, altered coagulation, inflammation, impaired circulation at a cellular level, anaerobic metabolism, changes in mental status and multiorgan failure. There may also be alteration in coagulation due to the inflammatory response.

Fluid resuscitation is central in management, but fluid type remains under debate (Vincent and Gerlach 2004). Other treatment options include vasopressor therapy and continuous and accurate blood pressure (BP) monitoring using an arterial catheter. Blood transfusion may be necessary when central venous oxygen saturation is less than 70% and haematocrit less than 30%. Alternatively, if greater than 30% the inotrope Dobutamine may be used alongside supplemental O₂ therapy. It is necessary to identify and control/remove the source of infection and to administer antibiotics when a diagnosis has been confirmed, with drug type dependent on pathogen. However, controversy remains over the actual time frame. A broad spectrum antibiotic should be administered within three hours of entering an accident and emergency department (Garretson and Malberti 2007). Corticosteroid therapy may be used for the anti-inflammatory effect but high doses have not been shown to more effective (Oppert et al., 2005).

A Surviving Sepsis Campaign (SCC) now common practice within UK hospitals was a 2002 initiative of the European Society of Intensive Care Medicine, the International Sepsis Forum, and the Society of Critical Care Medicine. The ‘bundles’ approach is intended to simplify the complex processes of the care of patients with severe sepsis. This set of care interventions are derived from a collection of evidence-based practice guidelines. When implemented in their entirety they are likely to have an enhanced effect when compared to implementing each individual guideline The SSC aims to reduce mortality from sepsis via a multi-point strategy, primarily by:

• building awareness of sepsis
• improving diagnosis
• increasing the use of appropriate treatment
• educating healthcare professionals
• improving post-ICU care
• developing guidelines of care
• facilitating data collection for the purposes of audit and feedback.

For further information visit the http://www.survivingsepsis.org website.

Venous thromboembolism

Venous thromboembolism (VTE) is a condition in which a blood clot (thrombus) forms in a vein. Blood flow through the affected vein can be limited by the clot, and may cause swelling and pain. Venous thrombosis occurs most commonly in the deep veins of the leg or pelvis; this is known as a deep vein thrombosis (DVT). An embolism occurs if all or a part of the clot breaks off from the site where it forms and travels through the venous system. If the clot lodges in the lung, a potentially serious and sometimes fatal condition, pulmonary embolism (PE) occurs. Venous thrombosis can occur in any part of the venous system. However, DVT and PE are the commonest manifestations of venous thrombosis. The term VTE embraces both the acute conditions of DVT and PE and also the chronic conditions which may arise after acute VTE, such as post-thrombotic syndrome and pulmonary hypertension; both problems being associated with significant ill-health and disability.

Orthopaedic patients are often predisposed to be at significant risk of developing a VTE due to the nature of their disease and condition. The most significant risk factors are outlined in the UK by the National Institute for Health and Clinical Excellence (NICE 2010):

• active cancer or cancer treatment
• age over 60 years
• critical care admission
• dehydration
• known thrombophilias
• obesity (body mass index [BMI] over 30 kg/m²)
• one or more significant medical comorbidities (for example: heart disease; metabolic, endocrine or respiratory pathologies; acute infectious diseases; inflammatory conditions)
• personal history or first-degree relative with a history of VTE
• use of hormone replacement therapy
• use of oestrogen-containing contraceptive therapy
• varicose veins with phlebitis.

These risk factors are reflected globally and lead to 25 000 patient deaths per year in UK hospitals alone; the largest proportion of these deaths being in the orthopaedic patient (NICE 2010). There are three factors responsible for the development of VTE:

• venous stasis
• vein injury
• blood chemistry changes.

These factors were first described by Rudolph Virchow and are commonly referred to as ‘Virchow’s Triad’. It is now generally accepted that it is usually a combination of these factors that causes a thrombus to form, rather than one factor in isolation. The inherent impaired physical mobility and activity intolerance that affects orthopaedic patients gives rise to circulatory stasis. If they also have existing conditions of, or have experienced trauma, to the circulatory system and in addition have alterations in blood coagulation then they are in real danger of developing a VTE (Davis 2004a).

Although there have been numerous trials, there remains uncertainty about how to prevent VTE (NICE 2010, Davis 2004a). The true incidence of DVT and PE is very hard to calculate. More patients have less invasive surgery and emphasis is placed on early mobilisation and early discharge from hospital. Prophylaxis (both mechanical and pharmacological) is widely used, but practice varies and implementation is patchy. There is a strong sense that DVT and PE are less of a problem than they used to be in surgical patients but this may be hidden from the clinicians by early discharge rather than being truly reduced; 80% of DVT are subclinical and the average DVT occurs on the 7th postoperative day, often after the patient has left hospital (NICE 2010).

Risk assessment

The majority of hospitalised orthopaedic patients would be considered at risk of developing a VTE and should receive appropriate prophylactic interventions. Those in the community or following discharge are also at risk. Assessment is based on some, but not all, of the predisposing factors referred to previously. See NICE (2010) guidance on VTE in the hospitalised patient for a current example of a risk assessment tool for the UK. All surgical patients are recommended to be assessed.

Methods of prevention

Due to the characteristic uncertainty of the evidence currently available, prevention is contentious, but recommendations do exist that identify those preventative methods most likely to be successful. Guidance often relates to specific fields such as orthopaedics and even specific forms of surgery such as hip fracture and hip and knee replacement.

Pharmacological

These include (Autar 2009a):

• fondaparinux
• heparins
• vitamin K antagonists
• aspirin
• dabigatran
• rivaroxaban.

Mechanical

• anti-embolism or graduated compression stockings (Autar 2009b)
• intermittent pneumatic compression devices (Davis and O’Neill 2002)
• foot impulse devices (Davis and O’Neill 2002).

Care

• early mobilisation and leg exercises
• hydration (but through the oral route not intravenous).

Current guidelines recommend the use of these interventions in combination. They also increasingly highlight the patient’s view such as the difficulty and discomfort associated with graduated compression stockings (NICE 2010). All prophylactic interventions carry risk as well as benefit and these must be balanced in any care decisions for individual patients. The risk of bleeding is an example with pharmacological interventions for VTE.

The linking of evidence through an EBP approach to orthopaedic nursing practice is well illustrated by the issue of VTE. Research, such as in areas of early mobilisation and hydration is often lacking or the research is so poor quality that it cannot be relied upon to direct practice decisions. Even when evidence is strong it has to be applied consistently and with knowledge and understanding. Davis (2004b) discusses ways in which the problems of translation and utilisation can be overcome with respect to VTE.

Fat embolism syndrome (FES)

The term ‘fat embolism’ (FE) denotes the presence of fat globules in the peripheral circulation and lung parenchyma most commonly following fracture of long bones, pelvis or other major trauma. ‘Fat embolism syndrome’ is a severe manifestation of FE where the patient presents with a triad of dyspnoea, petechiae (rash) and mental confusion. It is usually asymptomatic, but a few patients will develop signs and symptoms of multiorgan dysfunction, particularly involving the triad of lungs, brain and skin. A variety of theories to explain FES are reported within the literature. Jain et al. (2008) report three:

• Mechanical theory suggests a mechanical obstruction in the pulmonary capillaries resulting from fat emboli within the marrow or adipose tissue. Some fat particles then pass into the systemic circulation via cardiac or pulmonary routes to embolise in the renal, cerebral, skin or retinal capillaries.
• Toxic theory proposes that free fatty acids (FFA), released at the time of trauma or during breakdown of fat in the lung, directly affect the pneumocytes, resulting in an inflammatory response and acute respiratory distress syndrome. The FFA may originate from lipid stores mobilised by circulating catecholamines.
• Obstructive theory proposes that a chemical event at the trauma site releases mediators that affect the solubility of circulating lipids, resulting in coalescence and subsequent embolisation. Normally chylomicrons may coalesce into fat globules large enough to occlude pulmonary capillaries.

Risk factors include young age, closed and multiple fractures, conservative intervention for long bone fractures along with intramedullary nailing and nailing or reaming of medullary cavities. The clinical features of FES often develop 24–72 hours after trauma when fat droplets acting as emboli become impacted in the pulmonary microvasculature and other microvascular beds such as in the brain (Shaikh 2009). Long bone fractures should be reduced as soon as possible after injury and any reaming of the bone conducted with great care in an effort to prevent further emboli.

Reports of mortality and morbidity vary:

• A mortality rate of 5–15% is reported by Shaikh (2009) and Jain et al. (2008). It is also reported that, even with severe respiratory failure associated with FE, it seldom leads to death (Shaikh, 2009).
• Coma, ARDS, pneumonia and congestive heart failure are poor prognostic signs.
• Shaikh (2009) reports that patients with increased age and multiple co-morbidities and/or decreased physiologic reserves have worse outcomes.

Fat embolism occurs rarely in paediatric trauma patients. A ‘lethal case report’ discusses a case of FES in a nine-year-old boy after a direct blunt trauma and a pelvic fracture. On the second day post-trauma, the child showed signs of bowel perforation and septic shock which led to an acute aggravation of the pulmonary symptoms of FES, cardiac arrest and death – illustrating the potentially disastrous sequelae. The response to the case was to advocate prevention by early fracture stabilisation (Teeuwen et al., 2009).

Diagnosis

Shaikh (2009) proposes that a high level of suspicion is needed to diagnose FES. A combination of clinical criteria and MRI of the brain will enable early and accurate diagnosis. The condition is commonly diagnosed on the basis of the clinical features and by excluding other causes. Gurd and Wilson’s diagnostic criteria are shown in Box 9.3 where identification of FES requires the presence of at least one major criterion and at least four minor criteria.

Box 9.3 Signs of Fat Embolism Syndrome (Gurd and Wilson 1974. Reproduced with permission from The British Editorial Society of Bone & Joint Surgery.)