• 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.)

Interventions

Non-drug: High flow rate oxygen is given to maintain arterial tension within the normal range. Mechanical ventilation may be required, necessitating transfer to the intensive care unit. Restriction of fluids/use of diuretics can minimise fluid accumulation in the lungs as long as circulation is sustained. Maintenance of intravascular volume with ‘IV’ fluids or blood is vital as shock can exacerbate lung injury caused by FES.

Drugs: Heparin, steroids, alcohols and dextran have been reported to be ineffective by Enneking (1995). More recently Al-Khuwaitir et al. (2002) report a high dose of corticosteroids are effective in preventing FES. The use of steroids is a controversial issue (see Box 9.5 for exploration of the evidence).

Box 9.5 Evidence digest. Reproduced with permission from Canadian Medical Association

Acute compartment syndrome

Compartment syndrome (ACS) is a clinical condition that occurs when there is an increase in pressure and/or a decrease in the size of a muscle compartment resulting in reduced capillary blood flow and leading to cell death. If the pressure is not relieved within hours, irreversible damage to the tissues and nerves may result in contractures, paralysis, loss of sensation and amputation (Judge 2007). The most common site is the anterior compartment of the lower leg. Any compartment can be affected, although the majority of cases present with a tibial fracture. The condition can be difficult to diagnose in all patients but especially in children, with delays in diagnosis leading to disastrous outcomes (Bae et al., 2001).

The patient can present with ACS as a result of:

• trauma – fracture, haematoma, vascular damage, electrical injuries
• oedema-related – frostbite, burns
• coagulopathies – genetic, iatrogenic, acquired
• other – external compression.

In acute compartment syndrome, limb compression leads to local pressure with local tamponade (blockage). This results in capillary necrosis and oedema with increased compartment pressure and muscle ischaemia. This then leads to compartment tamponade, nerve injury and muscle infarction.

Symptoms can vary, but the patient will most often present with parasthesia, tingling and numbness as pressure increases within the compartment of the limb which will feel tense and warm on palpation. The skin will feel tight and appear shiny. Pain will usually appear ‘out of proportion to the injury’ even at rest and can be elicited or worsened by passive stretching of the involved compartment. The pain may be throbbing, increases with elevation of the extremity and is unrelieved by opioids.

Late signs may include a pale limb, greyish or whitish in tone with a prolonged capillary refill time. In the latter stages the skin will feel cool on palpation with paralysis another late sign. The patient may also not respond to direct neural stimulation due to damage to the myoneural junction and a weak pulse or pulselessness to the effected limb. These late signs demonstrate that neurovascular and muscle damage have already occurred and the priority for the practitioner is to recognise the condition from the early signs so that permanent damage can be prevented.

Bandages and dressing should be removed if ACS is suspected and the limb should not be elevated even though this is a common principle of care for the orthopaedic/trauma patient with swelling and pain.

Measurement of the compartment (C) pressure is helpful but not standard practice in all clinical units. The normal resting pressure within a closed compartment varies with Edwards (2004) reporting 0–8 mm Hg and Nye (1996) 0–10 mm Hg. The pressure of a compartment can be established percutaneously using a wick/slit catheter or wick catheter attached to a pressure transducer. The Stryker intra-compartmental monitor system is commonly used in conjunction with an 18 gauge needle to determine C pressure. McQueen (1996) suggested that there is inadequate tissue perfusion when tissue pressure rises within compartment to within 30 mm Hg of the patient’s diastolic B/P >30 mm Hg.

Neurovascular assessment

All patients who have a musculoskeletal injury, undergone orthopaedic surgery or cast immobilisation of a limb are at risk of developing neurovascular compromise which can lead to compartment syndrome. Peripheral neurovascular assessment involves the systematic assessment of the neurological and vascular integrity of a limb, with the aim of recognising any neurovascular deficit promptly (Judge 2007). Tissue damage deteriorates with time, therefore prompt identification and intervention is necessary. There does not however appear to be a consensus on best practice and frequency in completing and documenting neurovascular assessment with a view to reducing patient risk and promoting early identification of neurovascular compromise.

In keeping with the most common symptoms of ACS, Dykes (1993) recommends a 5-P approach to neurovascular assessment with a focus on:

• pain
• pulses
• pallor
• parasthesia
• paralysis.

Judge (2007) more recently recommends that neurovascular observations should include the assessment of pain, paralysis (movement), paraesthesia (sensation), presence of pulses and/or capillary refill and swelling. Pain is central to all neurovascular assessment as the most common, earliest and important presenting symptom of compartment syndrome. Empirical, review and discussion literature all suggests pain as the only true warning symptom of acute compartment syndrome. Grottkau et al.’s (2005) retrospective study of 133 cases of compartment syndrome reported that 90% of patients complained of pain. A multidimensional approach should be applied encompassing the use of a valid (ability to measure) and reliable (consistency) pain assessment tool (Clarke 2003). Shields and Clarke (2011) also recommend the use of a dedicated chart to record pain intensity and type, alongside warmth, sensation, colour, capillary refill time and the movement of the affected and unaffected limb as an important method of collecting and comparing data from baseline onwards.

A central aspect of care of the patient with suspected ACS is to treat any suspicion as a medical emergency requiring immediate medical attention. It is essential that the practitioner informs a senior member of medical staff immediately so that intervention can be instigated.

Surgical intervention

Fasciotomy is the management option of choice for ACS; the fascia is divided along the length of the compartment to release pressure. The pressure at which fasciotomy is performed is based on the clinical picture/rising pressure. Following the procedure the wound is usually left open for approximately five days until the soft tissues have recovered and swelling has begun to subside. Muscle and skin grafting may be required.

Urinary tract infection (UTI)

The urinary tract is the most common source of healthcare-associated infection. Because of stasis in the urinary system during anaesthesia, surgery and post-operative recovery the risk is high in all surgical patients and in those with restricted mobility. In the orthopaedic and trauma patient, such stasis may be prolonged.

The urinary tract is usually sterile above the distal 1 cm of the urethra although the perineum is colonised with resident bacteria from the skin and bowel which can gain entry through the urethral meatus. Emptying the bladder usually removes any potential pathogens (Weston 2008), but if the urethra is opened by a urethral catheter, a method of transmission for invading organisms to enter the bladder is provided. This risk of infection is, therefore, significantly increased by bladder catheterisation, so this should be avoided in orthopaedic patients because of the link between bacteriuria and implant site infection (Heaney 2011). It has been shown that the longer the catheter is in situ, the greater the likelihood of UTI (Stephan et al., 2008). If there are unavoidable reasons for catheterisation (e.g. urinary retention) it is essential that a closed drainage system is maintained with meticulous regard for hygiene and asepsis during insertion of the catheter and subsequent care and that the catheter is removed as soon as possible. Other risk factors for UTI include dehydration and this is one of many reasons for ensuring that adequate oral or intravenous fluids are administered.

The prevention of UTI involves early mobilisation and ensuring that the patient has good fluid balance in order to reduce urinary stasis and ensure that urine does not become concentrated. Older people sometimes voluntarily restrict fluid intake as do those with any degree of urinary incontinence or difficulty in getting to the toilet and it is important to discuss the implications of this with the patient. There is some limited evidence that drinking cranberry juice prevents UTI, but the amount that is required and the timing is uncertain (Jepson and Craig 2009). It is possible that the right amount of any oral fluid is useful and the presence of a moderate amount of vitamin C in cranberry and other fruit juice is also beneficial in supporting the immune system as a whole. Ensuring a good standard of perineal/penile hygiene, especially in the immobile patient, is also important as is early mobilisation and a return to normal toileting habits as soon as possible. Research also suggests that the existence of a UTI pre-operatively can predispose the patient to surgical site infection (SSI) following orthopaedic surgery even if there are no symptoms (Ollivere et al., 2008). This confirms the possibility of UTI as a remote source for SSI and possible implant infection and highlights the need for preoperative screening for UTI by urinalysis (identifying protein and blood).

Identifying and treating UTI as early as possible is essential in order to prevent any likely transmission to remote sites and to the ureters and kidneys. The main symptoms which might alert the practitioner to the presence of UTI are:

• a need to urinate frequently – often passing small amounts
• pain on passing urine
• lower abdominal/pubic pain.

The first two are less likely to be evident in the patient with an indwelling urinary catheter and other symptoms might include pyrexia, general feeling of being unwell and mild to severe confusional state/delirium. The presence of blood or protein on urinalysis is also indicative of infection. If UTI is suspected a mid-stream sample of urine should be taken for culture and sensitivity.

Treatment of UTI involves treatment with an appropriate course of antibiotics along with adequate pain relief and good oral or ‘IV’ hydration.

Urinary retention

A significant reason for urinary catheterisation in the orthopaedic patient is urinary retention which is frequently reported following orthopaedic surgery. It is defined as an inability to pass urine even though the patient has a full bladder. This can result in a great deal of pain and distress for the patient and can lead to bladder distention and urinary tract infection. Retention can also lead to UTI, adverse autonomic responses such as vomiting, hypotension and cardiac dysrhythmia and permanent damage to the bladder with resultant future urinary problems (Baldini et al., 2009). Early recognition of the problem is, therefore, essential and should be included as an aim for all postoperative care. There is no evidence that routine catheterisation intraoperatively as a method of prevention is beneficial and the risk of haematogenous spread of infection to the surgical site is too great for this to be advised.

The main symptom of urinary retention is pain and discomfort in the lower part of the abdomen in a patient who is unable to pass urine in spite of good fluid balance. This can, however, be masked post-operatively by the effects of general and regional anaesthesia, nerve blockade and analgesia. Bladder catheterisation can also be used as a method of assessing bladder volume and diagnosing retention through measurement of residual volume of urine. This, however, carries with it the risk of infection associated with perurethral catheterisation. The literature suggests that the use of nurse-led ultrasound to assess bladder volume is a relatively simple and appropriate way for the practitioner to monitor bladder volume and identify retention whilst avoiding unnecessary catheterisation (Edmond 2009).

Once retention has been identified, the treatment usually involves bladder catheterisation. It is recommended that this is done as an in-out catheterisation rather than with an indwelling catheter and that antibiotic prophylaxis is essential (Baldini et al., 2009). It may be necessary for the bladder volume to be monitored for up to 48 hours postoperatively, but most problems tend to resolve once the patient begins to mobilise and is able to visit the toilet to void.

Respiratory tract infection

Pneumonia (lower respiratory tract infection) is a potentially fatal hospital-acquired infection in orthopaedic and trauma patients. It is the most common cause of hospital deaths for patients following hip fracture. Mucosal surfaces in the respiratory tract contain large numbers of resident flora which combat pathogenic attack. The upper respiratory tract is lined with ciliated epithelium which, along with the cough reflex, helps to expel bacteria (Weston 2008) and other particles. It is when these mechanisms are suppressed that the patient is prone to respiratory tract infection. Inhaled pathogens are able to combat these mechanisms and reach the lungs. Patients who have undergone surgery or suffered trauma are at risk. The risk is also increased by advanced age, concurrent medical conditions, general anaesthesia, depleted nutrition and immobility.

Measures for prevention of respiratory tract infection in the orthopaedic patient include:

• avoidance of elective surgery in patients with pre-existing respiratory infections (usually viral) through preoperative screening
• post-operative pain relief to facilitate coughing and deep breathing
• early post-operative mobilisation
• since chest infection is often hospital-acquired, universal infection control precautions are an essential aspect of prevention.

Observation of the at-risk patient for symptoms of pneumonia is essential in enabling early management. Symptoms may be insidious or develop quite suddenly and include:

• shortness of breath/rapid and/or shallow breathing
• a cough which may or may not be productive initially
• sputum which may be yellow, green, brown or blood stained – a specimen should be obtained for culture
• chest pain
• pyrexia
• tachycardia
• acute confusion
• general malaise and fatigue
• loss of appetite.

A diagnosis of pneumonia is made based on the above symptoms along with chest auscultation (abnormal lung sounds can be hard) and chest X-ray (demonstrating lung consolidation). There will also be a raised white cell count. A positive sputum culture will help to identify the causative organism and direct treatment.

Management of pneumonia should be commenced immediately due to the potentially life-threatening nature of the infection. This should include the following considerations:

• Antibiotic therapy according to the nature and sensitivity of the pathogen causing the pneumonia. The timeliness and appropriateness of this is central to the recovery of the patient along with other supporting measures but may be complex if a resistant strain of bacteria is the causative organism.
• Constant monitoring of vital signs of the patient with a view to detecting and acting upon any further deterioration.
• Maintenance of hydration using intravenous infusion of fluids if necessary.
• Optimum nutrition – using nutritional supplementation, nasogastric or enteral feeding as necessary.
• The patient should be cared for sitting up or in the semi-recumbent position, providing their orthopaedic condition allows.
• Deep breathing exercises and chest physiotherapy.

Constipation

Constipation is a very common and significant complication which can either be acute or chronic. In the orthopaedic and trauma patient it is often caused by a decrease in bowel action due to a combination of factors that lead to hard, dry stools that are difficult and/or painful to pass. The problem is defined by the patient and may include what they feel to be ‘unsatisfactory’ or incomplete defecation. Constipation is known to be more common in women, possibly due to hormonal factors. Although it is thought there is a link between the incidence of constipation and increasing age, this is most likely because of the greater incidence of other precipitating factors in older people. Some other common causes of constipation in the orthopaedic and trauma patient include:

• Dehydration – leading to desiccated stools.
• Reduced mobility – resulting in weakness in the accessory muscles which help bowel evacuation.
• Reduced or changed dietary intake – resulting in a diet which is depleted or lacking in fibre.
• Pharmacological agents – one of the main side effects of many drugs is constipation: in the orthopaedic and trauma patient both opioid and non-opioid analgesic agents are implicated, but other drugs such as antidepressants can also contribute to because of the slowing effect on peristaltic action (Richmond and Wright 2004).

Hospitalised patients and those reliant on others for toileting needs often resist the urge to pass bowel movements because of embarrassment or pain associated with the required activity – particularly if they require a bed pan (Cohen 2009). Because of embarrassment patients may not be willing to inform a health professional of the problem. These are issues which it is essential the practitioner is sensitive to.

Impaction, where faeces become trapped in the lower part of the large bowel, is very distressing for the patient. The most serious consequence of untreated constipation and impaction is bowel obstruction by a volvulus which becomes a surgical emergency and can be fatal. It is essential that this is avoided through careful assessment and prevention.

The most important aspect of the prevention and management of constipation is the early and continuous assessment of bowel activity. Because nearly all orthopaedic and trauma patients have at least one risk factor for constipation and because of the reluctance of patients to discuss difficulties with the nurse it is essential that a proactive daily assessment of bowel activity is made. Box 9.6 discusses evidence related to the development of a constipation risk assessment scale. ‘Normal’ bowel habits vary from one person to another and the practitioner must take this into account when assessing bowel function – considering the patients’ normal frequency of opening their bowels. If constipation lasts more than a few weeks and/or is associated with other symptoms such as abdominal mass/pain or blood in the stools, then a medical referral is made to rule out other more serious causes of constipation.

Proactive prevention of constipation is an important aspect of the care of the orthopaedic and trauma patient. It is important that this is incorporated into the standard care of all patients at risk of constipation and is not left until constipation has begun to occur. Prevention involves management of the causes and risk factors for constipation. This generally includes helping to provide conditions for toileting routines which are as near to normal for the patient as possible with due consideration of privacy and position:

• Monitor – daily assessment and recording of bowel activity.
• Diet – ensuring the diet contains or is supplemented with foodstuffs high in dietary fibre.
• Hydration – ensuring that the patient takes plenty of oral fluids.
• Exercise – within the limits and abilities of the patient; when unable to walk there may be benefit from abdominal exercise such as pelvic tilt (JBI 2008).

It is important that any tendency to constipation is managed as soon as possible after symptoms occur. The management of constipation generally involves the use of pharmacological laxatives. There are several different types of laxative which work in different ways:

• Bulking agents – contain fibrous material which absorb water in the bowel and make stools softer.
• Peristaltic stimulants – useful where peristaltic action is reduced.
• Osmotic laxatives – encourage the absorption of fluid into the stools.
• Stool softeners – lubricate and moisten stools.

When constipation is opiate-induced it is advisable to begin treatment with a combination of an osmotic laxative and a peristaltic stimulant. If this treatment fails to resolve constipation or faecal impact is suspected, treatment with suppositories or enemas along with peristaltic stimulants may be required.

Box 9.6 Evidence digest. Reproduced with permission from John Wiley & Sons

Recommended further reading

1. Dellinger, R.P., Levy, M.M., Rhodes, A. et al. (2013) Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2012. Critical Care Medicine, 41(2), 580–637.
2. Hilton, A.K., Pellegrino, V.A. and Scheinkestel, C.D. (2008) Avoiding common problems associated with intravenous fluid therapy. The Medical Journal of Australia, 189, 509–513.
3. National Institute for Health and Clinical Excellence (NICE) (2010) Venous thromboembolism: Reducing the Risk. CG92 Available at: http://guidance.nice.org.uk/CG92/NICEGuidance/pdf/English (accessed 30 March 2014).
4. Royal College of Nursing (RCN) (2013) Right Blood, Right Patient, Right Time: RCN Guidance for Improving Transfusion Practice. London: RCN. Available at: http://www.rcn.org.uk/__data/assets/pdf_file/0009/78615/002306.pdf (accessed 30 March 2014).

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