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National Collaborating Centre for Women's and Children's Health (UK). Surgical Site Infection: Prevention and Treatment of Surgical Site Infection. London: RCOG Press; 2008 Oct. (NICE Clinical Guidelines, No. 74.)

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Surgical Site Infection: Prevention and Treatment of Surgical Site Infection.

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1.1. Surgical site infection

Infections that occur in the wound created by an invasive surgical procedure are generally referred to as surgical site infections (SSIs). SSIs are one of the most important causes of healthcare-associated infections (HCAIs). A prevalence survey undertaken in 2006 suggested that approximately 8% of patients in hospital in the UK have an HCAI. SSIs accounted for 14% of these infections and nearly 5% of patients who had undergone a surgical procedure were found to have developed an SSI.1 However, prevalence studies tend to underestimate SSI because many of these infections occur after the patient has been discharged from hospital.

SSIs are associated with considerable morbidity and it has been reported that over one-third of postoperative deaths are related, at least in part, to SSI.2 However, it is important to recognise that SSIs can range from a relatively trivial wound discharge with no other complications to a life-threatening condition. Other clinical outcomes of SSIs include poor scars that are cosmetically unacceptable, such as those that are spreading, hypertrophic or keloid, persistent pain and itching, restriction of movement, particularly when over joints, and a significant impact on emotional wellbeing.3

SSI can double the length of time a patient stays in hospital and thereby increase the costs of health care. Additional costs attributable to SSI of between £814 and £6626 have been reported depending on the type of surgery and the severity of the infection.4,5 The main additional costs are related to re-operation, extra nursing care and interventions, and drug treatment costs. The indirect costs, due to loss of productivity, patient dissatisfaction and litigation, and reduced quality of life, have been studied less extensively.

The wound healing process

The ‘normal’ wound healing process has been identified as involving three overlapping major phases:

  • inflammation, with cascades of processes that can be further subdivided into early (first 24 hours) and late phases (normally up to 72 hours)
  • regeneration
  • maturation.

The wound healing process is a complex one that involves many interacting cells, cytokines and growth factors, carbohydrates and proteins, all of which cascade into and act within the wound margins and across the wound bed at different rates and at different speeds.

The key cells that are involved in this process have been identified as:

Early inflammation (the first 24 hours) begins with haemostasis through vasoconstriction, thrombin formation and platelet aggregation. Platelets release cytokines and other factors that directly influence leucocyte and monocyte activity. Late inflammation (24–72 hours) involves the release of vasodilators and other agents that increase the permeability of the local capillary bed allowing serum and white cells to be released into the area surrounding the wound, through complex interactions of adhesion molecules, and other systems, in margination and diapedesis. The function of this phase of wound healing is to ensure that the wound bed is free of bacteria and other contaminants and to create the optimum environment for the production of granulation tissue and for epithelialisation.

Regeneration follows over the next few days to weeks and this phase of the wound healing process is characterised by an increase in fibroblast mitogenic activity and endothelial cell mitotic activity, with epithelial cell migration and the synthesis of collagen and metalloproteinases. This is a very dynamic balance of synthesis and breakdown of effete tissues and cells.

Maturation, which is also known as the remodelling phase, is the final phase of wound healing and can take up to 2 years to complete. Granulation tissue gradually matures into scar tissue, which over time pales (as the neovascularisation required for healing by scar tissue redresses), shrinks and thins. This repair process is governed by fibroblasts and proteases that normally maintain a balance between deposition and degradation of tissue. Over time, immature collagen fibrils are replaced by mature collagen fibres, improving the tensile strength of the scar tissue, but only to 80% of that of normal skin.6

Pathogenesis of surgical site infection

The development of an SSI depends on contamination of the wound site at the end of a surgical procedure and specifically relates to the pathogenicity and inoculum of microorganisms present, balanced against the host’s immune response.

The microorganisms that cause SSIs are usually derived from the patient (endogenous infection), being present on their skin or from an opened viscus. Exogenous infection occurs when microorganisms from instruments or the theatre environment contaminate the site at operation, when microorganisms from the environment contaminate a traumatic wound, or when microorganisms gain access to the wound after surgery, before the skin has sealed. Rarely, microorganisms from a distant source of infection, principally through haematogenous spread, can cause an SSI by attaching to a prosthesis or other implant left in an operative site. Practices to prevent SSI are therefore aimed at minimising the number of microorganisms introduced into the operative site, for example by:

  • removing microorganisms that normally colonise the skin
  • preventing the multiplication of microorganisms at the operative site, for example by using prophylactic antimicrobial therapy
  • enhancing the patient’s defences against infection, for example by minimising tissue damage and maintaining normothermia
  • preventing access of microorganisms into the incision postoperatively by use of a wound dressings.

Staphylococcus aureus is the microorganism most commonly cultured from SSIs. When a viscus, such as the large bowel, is opened, tissues are likely to be contaminated by a whole range of organisms. For example, after colorectal surgery enterobacteriaceae and anaerobes are encountered and may act in synergy to cause SSI.

In prosthetic surgery, the presence of the foreign body (for example, a vascular graft after arterial bypass surgery or a prosthetic joint in orthopaedic surgery) reduces the number of pathogenic organisms required to cause an SSI. In this environment, normally non-pathogenic organisms such as Staphylococcus epidermidis (coagulase-negative staphylococcus) may also cause an SSI. Operations on sites that are normally sterile (‘clean’) thus have relatively low rates of SSI (generally less than 2%), whereas after operations in ‘contaminated’ or ‘dirty’ sites, rates may exceed 10%.7

Management of surgical site infection

Most SSIs respond to the removal of sutures with drainage of pus if present and, occasionally, there is a need for debridement and open wound care. Many complications of postoperative wounds do not represent infection but exudation of tissue fluid or an early failure to heal, which is common in patients with a high body mass index (BMI). Incomplete sealing of the wound edges can often be managed by using a delayed primary or secondary suture or closure with adhesive tape, but in larger open wounds the granulation tissue must be healthy with a low bioburden of colonising or contaminating organisms if healing is to occur. It is likely that over 15% of postoperative wounds are treated with antibiotics, possibly inappropriately, something which can contribute to the problem of antibiotic resistance.

The appropriate treatment of established SSIs requires careful monitoring and communication between the multidisciplinary postoperative team (surgeons, intensivists, microbiologists, nurses) and the primary care team. If patients are to be returned home early then any SSI needs to be recognised and treated appropriately. Release of pus, debridement and parenteral antibiotics, if indicated, usually requires a return to secondary care. Extensive wound breakdown may need specialist wound management to reduce bacterial burden in the open wound. Wound bed preparation may be required to encourage healing by secondary intention or facilitate secondary suture.

1.2. Aim of the guideline

Clinical guidelines have been defined as ‘systematically developed statements which assist clinicians and patients in making decisions about appropriate treatment for specific conditions’. This clinical guideline concerns the prevention and treatment of SSI.

It has been developed with the aim of providing guidance on the patient’s journey throughout the preoperative, intraoperative and postoperative phases of surgery.

1.3. Areas outside of the remit of the guideline

This guideline does not address:

  • prophylaxis and management of antibiotic-resistant bacteria
  • management of the operating theatre environment and environmental factors
  • anaesthetic factors relating to SSI.

1.4. For whom is the guideline intended?

This guideline is of relevance to those who work in or use the NHS in England, Wales and Northern Ireland, in particular:

  • all healthcare professionals who are involved in the care of surgical patients, including GPs, surgeons, nursing and tissue viability staff and pharmacists
  • those responsible for commissioning and planning healthcare services, including primary care trust commissioners, and public health, trust and care home managers
  • surgical patients, their families and other caregivers.

A version of this guideline for patients, carers and the public, entitled ‘Understanding NICE guidance: Surgical site infection’, is available from the NICE website ( or from NICE publications on 0845 003 7783 (quote reference number N1702).

1.5. Who has developed the guideline?

The guideline was developed by a multi-professional and lay working group (the Guideline Development Group or GDG) convened by the National Collaborating Centre for Women’s and Children’s Health (NCC-WCH). Membership included:

  • two surgeons
  • a tissue viability nurse
  • two microbiologists
  • a theatre nurse
  • a surveillance coordinator
  • an infection control specialist
  • two patient/carer representatives.

Staff from the NCC-WCH provided methodological support for the guideline development process, undertook systematic searches, retrieval and appraisal of the evidence and health economics modelling and, together with the GDG Chair, wrote successive drafts of the guideline.

During the development of the guideline, the GDG identified a need for expert advice from an anaesthetist and additional clinical representation from a surgeon and a theatre nurse. Expert advisers were appointed by the GDG to advise on each of these issues, although they were not involved in the final decisions regarding formulation of recommendations.

All GDG members’ interests were recorded on declaration forms provided by NICE. The form covered consultancies, fee-paid work, shareholdings, fellowships and support from the healthcare industry.

Organisations with interests in SSI were encouraged to register as stakeholders for the guideline, and registered stakeholders were consulted throughout the guideline development process. The process of stakeholder registration was managed by NICE.

1.6. Other relevant documents

This guideline is intended to complement other existing and proposed works of relevance, including related NICE guidance:

  • This guideline updates NICE Technology Appraisal 24: ‘Guidance on the use of debriding agents and specialist wound care clinics for difficult to heal surgical wounds’.
  • The effects of maintenance of normothermia are addressed in the ‘Inadvertent perioperative hypothermia’ guideline (NICE clinical guideline 65), available from

1.7. Guideline methodology

This guideline was commissioned by NICE and developed in accordance with the guideline development process outlined in the NICE Technical Manual.

1.7.1. Literature search strategy

Initial scoping searches were executed to identify relevant guidelines (local, national and international) produced by other development groups. The reference lists in these guidelines were checked against subsequent searches to identify missing evidence.

Relevant published evidence to inform the guideline development process and answer the clinical questions was identified by systematic search strategies. The clinical questions are presented in Appendix B. Additionally, stakeholder organisations were invited to submit evidence for consideration by the GDG provided it was relevant to the topics included in the scope and of equivalent or better quality than evidence identified by the search strategies.

Systematic searches to answer the clinical questions formulated and agreed by the GDG were executed using the following databases via the ‘Ovid’ platform: Medline (1950 onwards), Embase (1980 onwards) and the Cumulative Index to Nursing and Allied Health Literature (CINAHL; 1982 onwards). The most recent search conducted for the three Cochrane databases (Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews, and the Database of Abstracts of Reviews of Effects) was undertaken in quarter 1, 2008. Searches to identify economic studies were undertaken using the above databases and the NHS Economic Evaluation Database (NHS EED).

Search strategies combined relevant controlled vocabulary and natural language in an effort to balance sensitivity and specificity. Unless advised by the GDG, searches were not date specific. Language restrictions were applied to searches, and publications in languages other than English were not appraised. Both generic and specially developed methodological search filters were used appropriately.

There was no systematic attempt to search grey literature (conferences, abstracts, theses and unpublished trials). Hand searching of journals not indexed on the databases was not undertaken.

Searches were conducted during a 7 month period between September 2007 and April 2008. Evidence published after this date has not been included in the guideline. September 2007 should thus be considered the starting point for searching for new evidence for future updates to this guideline.

Further details of the search strategies, including the methodological filters employed, are available on the accompanying CD-ROM.

1.7.2. Synthesis of clinical effectiveness evidence

Evidence relating to clinical effectiveness was reviewed using established guides and classified using the established hierarchical system presented in Table 1.1. This system reflects the susceptibility to bias that is inherent in particular study designs.

Table 1.1. Levels of evidence for intervention studies.

Table 1.1

Levels of evidence for intervention studies.

The type of clinical question dictates the highest level of evidence that may be sought. In assessing the quality of the evidence, each study was assigned a quality rating coded as ‘++’, ‘+’ or ‘−’. For issues of therapy or treatment, the highest possible evidence level (EL) is a well-conducted systematic review or meta-analysis of randomised controlled trials (RCTs; EL = 1++) or an individual RCT (EL = 1+). Studies of poor quality were rated as ‘−’. Usually, studies rated as ‘−’ should not be used as a basis for making a recommendation, but they can be used to inform recommendations. For issues of prognosis, the highest possible level of evidence is a cohort study (EL = 2). A level of evidence was assigned to each study appraised during the development of the guideline.

For each clinical question, the highest available level of evidence was selected. Where appropriate, for example if a systematic review, meta-analysis or RCT existed in relation to a question, studies of a weaker design were not considered. Where systematic reviews, meta-analyses and RCTs did not exist, other appropriate experimental or observational studies were sought.

Clinical evidence for individual studies was extracted into evidence tables (provided on the accompanying CD-ROM) and a brief description of each study was included in the guideline text. The body of evidence identified for each clinical question was synthesised qualitatively in clinical evidence statements that accurately reflected the evidence. Quantitative synthesis (meta-analysis) was performed for this guideline where sufficient numbers of similar studies were identified to merit such analysis.

1.7.3. Health economics

The aims of the economic input to the guideline were to inform the GDG of potential economic issues relating to the prevention and treatment of SSI and its complications, and to ensure that recommendations represented cost-effective use of healthcare resources.

The GDG prioritised a number of clinical questions where it was thought that economic considerations would be particularly important in formulating recommendations. A systematic search for published economic evidence was undertaken for these questions. For economic evaluations, no standard system of grading the quality of evidence exists and included papers were assessed using a quality assessment checklist based on good practice in decision-analytic modelling.8 Reviews of the very limited relevant published economic literature are presented alongside the clinical reviews or as part of appendices detailing original economic analyses (see below).

Health economic considerations were aided by original economic analysis undertaken as part of the development of the guideline where robust clinical effectiveness data were available and UK cost data could be obtained. For this guideline, the areas prioritised for economic analysis were:

The results of each economic analysis are summarised briefly in the guideline text with full cost-effectiveness models presented in Appendices D–G.

1.7.4. Forming and grading recommendations

For each clinical question, recommendations for clinical care were derived using, and linked explicitly to, the evidence that supported them. In the first instance, informal consensus methods were used by the GDG to agree clinical and cost-effectiveness evidence statements. Statements summarising the GDG’s interpretation of the evidence and any extrapolation from the evidence used to form recommendations were also prepared. In areas where no substantial clinical research evidence was identified, the GDG considered other evidence-based guidelines and consensus statements or used their collective experience to identify good practice. The health economics justification in areas of the guideline where the use of NHS resources (interventions) was considered was based on GDG consensus in relation to the likely cost-effectiveness implications of the recommendations. The GDG also identified areas where evidence to answer their clinical questions was lacking and used this information to formulate recommendations for future research.

Towards the end of the guideline development process, formal consensus methods were used to consider all the clinical care recommendations and research recommendations that had been drafted previously. The GDG identified ten key priorities for implementation (key recommendations), which were those recommendations expected to have the biggest impact on care and outcomes for adults and children undergoing surgical incisions through the skin.

The GDG also identified five key priorities for research, which were the most important research recommendations.

1.7.5. External review

This guideline has been developed in accordance with the NICE guideline development process. This has included giving registered stakeholder organisations the opportunity to comment on the scope of the guideline at the initial stage of development and on the evidence and recommendations at the concluding stage.

1.8. Schedule for updating the guideline

Clinical guidelines commissioned by NICE are published with a review date 4 years from date of publication. Reviewing may begin earlier than 4 years if significant evidence that affects guideline recommendations is identified sooner. The updated guideline will be available within 2 years of the start of the review process.

Copyright © 2008, National Collaborating Centre for Women’s and Children’s Health.

No part of this publication may be reproduced, stored or transmitted in any form or by any means, without the prior written permission of the publisher or, in the case of reprographic reproduction, in accordance with the terms of licences issued by the Copyright Licensing Agency in the UK []. Enquiries concerning reproduction outside the terms stated here should be sent to the publisher at the UK address printed on this page.

The use of registered names, trademarks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant laws and regulations and therefore for general use.

Bookshelf ID: NBK53735


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