Cierre primario versus cierre tardío para el tratamiento de las heridas traumáticas no provocadas por mordeduras en el transcurso de 24 horas después de la lesión
Resumen
Antecedentes
Las heridas traumáticas agudas son uno de los motivos más frecuentes de visitas al servicio de urgencias. Tradicionalmente, el cierre primario se ha reservado para las heridas traumáticas que se presentan en el transcurso de seis horas después de la lesión y que el cirujano de atención considera "limpias", mientras que para las otras heridas se utiliza el cierre primario tardío como una forma de controlar la infección de la herida. El cierre primario tiene el beneficio potencial de la cicatrización rápida de la herida, pero la amenaza potencial de aumentar la infección de la misma. Actualmente, no existen pruebas para guiar la toma de decisiones clínicas sobre el momento adecuado para el cierre de las heridas traumáticas.
Objetivos
Determinar el efecto sobre el tiempo hasta la cicatrización del cierre primario versus el cierre tardío para el tratamiento de las heridas traumáticas no provocadas por mordeduras que se presentan en el transcurso de 24 horas después de la lesión. Investigar los efectos adversos del cierre primario en comparación con el cierre tardío para el tratamiento de las heridas traumáticas no provocadas por mordeduras que se presentan en el transcurso de 24 horas después de la lesión.
Métodos de búsqueda
En mayo 2013, para esta primera actualización, se hicieron búsquedas en el registro especializado del Grupo Cochrane de Heridas (Cochrane Wounds Group); Registro Cochrane Central de Ensayos Controlados (Cochrane Central Register of Controlled Trials), (CENTRAL) (The Cochrane Library); Ovid MEDLINE; Ovid MEDLINE (In‐Process & Other Non‐Indexed Citations); Ovid EMBASE; y en EBSCO CINAHL. No hubo restricciones con respecto al idioma, la fecha de publicación ni el ámbito de estudio.
Criterios de selección
Ensayos controlados aleatorios que compararon el cierre primario con el cierre tardío de las heridas traumáticas no provocadas por mordeduras.
Obtención y análisis de los datos
Dos autores de la revisión evaluaron de forma independiente los resultados de las búsquedas contra los criterios de inclusión. Ningún estudio cumplió los criterios de inclusión para esta revisión.
Resultados principales
Debido a que ningún estudio cumplió los criterios de inclusión, no fue posible realizar un metanálisis ni una descripción narrativa de los mismos.
Conclusiones de los autores
Actualmente, no existen pruebas sistemáticas para guiar la toma de decisiones clínicas con respecto al momento adecuado para el cierre de las heridas traumáticas. Se necesitan estudios de investigación sólidos para investigar el efecto del cierre primario en comparación con el cierre tardío para el tratamiento de las heridas traumáticas no provocadas por mordeduras que se presentan en el transcurso de 24 horas después de la lesión.
PICO
Resumen en términos sencillos
Cierre inmediato o cierre tardío para el tratamiento de las heridas traumáticas en las primeras 24 horas después de la lesión
Las heridas traumáticas agudas, por ejemplo, desgarros, cortes y rasguños, son el motivo más frecuente de las visitas al servicio de urgencias. El cierre primario (unir los bordes de la herida con sutura, cinta adhesiva, grapas o pegamento) se utiliza generalmente en las heridas que se tratan rápidamente (en el transcurso de las seis horas después de la lesión) y que están limpias de residuos. Las heridas se pueden contaminar debido a la suciedad y los residuos, y en estos casos, no pueden cerrarse hasta más tarde, lo que significa un cierre tardío. Si ocurre lo anterior, la herida se limpia, después de los dos o tres días se verifica si permanece limpia, y luego se cierra. Lo anterior reduce las probabilidades de infección. El cierre primario tiene el efecto beneficioso potencial de la cicatrización rápida de la herida, pero puede aumentar las probabilidades de infección de la misma.
Se intentó determinar los efectos sobre la cicatrización y cualquier efecto adverso del cierre inmediato en comparación con el cierre tardío. Se buscaron ensayos controlados aleatorios en la bibliografía médica, pero no se encontraron estudios que respondieran a la pregunta. Actualmente, no existen pruebas para indicar el mejor momento para el cierre de las heridas traumáticas agudas para promover la mejor cicatrización.
Authors' conclusions
Background
Description of the condition
Acute traumatic wounds are said to be one of the most common reasons for people to present to the emergency department (Hollander 1999; Silbert 1981). More than 11 million patients with traumatic wounds are seen annually in emergency departments throughout the USA (Hollander 1995). Traumatic wounds (wounds resulting from injury), range from minor lacerations to those with extensive tissue damage. The extent of tissue damage is dependent upon the nature of the object causing the injury as well as the mechanism of injury. The Centers for Disease Control and Prevention has classified wounds of any origin into four categories: clean, clean/contaminated, contaminated and dirty/infected (Garner 1985). Traumatic wounds fall into the last two categories. Open, fresh traumatic wounds are categorised as contaminated, while old traumatic wounds that have retained devitalised (dead) tissue and those that involve existing clinical infection or perforated viscera (internal organs) are categorised as dirty/infected. In contrast, those categorised as clean are uninfected operative wounds in which no inflammation is encountered and the respiratory, alimentary, genital or urinary tract are not entered (Garner 1985). What this classification does not say, however, is what time span constitutes 'fresh' or 'old' traumatic wounds. Traumatic wounds do not always occur in isolation but can be associated with organ damage other than soft tissues (skin, subcutaneous tissue, muscle and their associated neurovascular supply). The management of traumatic wounds involving other structures (for instance bone, viscera) is governed by the nature of the organ involved and not merely by the timing of the injury in relation to presentation (Hohmann 2007; Rippon 1999; Robert 2006; Scherping 2007). Whilst traumatic wounds can result from many types of injury (for example, crush injury, blast injury, animal bites) we will not consider studies of traumatic wounds caused by animal bites as this is the subject of another Cochrane Review (in preparation).
Description of the intervention
In the management of traumatic wounds, basic principles of wound care need to be followed to obtain stable, long‐term coverage, ultimately restoring form and function (Lee 2009). There has not been a significant change in these principles over the years (Hollander 1999). Wound care generally involves cleaning the wound and then re‐approximating the wound edges until natural healing occurs (Hollander 1999). Judgement and surgical skill are necessary in deciding whether a wound is best allowed to heal by first intention (where the wound edges are approximated), secondary intention (where the wound is left open initially and closure is effected with granulation tissue which forms from the base and both sides of the wound towards the surface of the wound), or third intention (where the wound is initially left open and observed until there is no clinical evidence of inflammation or contamination then the wound edges are approximated). Healing by third intention is also referred to as delayed primary closure (Dorland 2003; Kumar 2005; Lorenz 2008). For traumatic wounds healing by first intention, primary closure has traditionally been reserved for traumatic wounds presenting within six hours of injury and considered 'clean' by the attending surgeon, with the rest undergoing delayed primary closure as a means of controlling wound infection. The wound undergoing delayed closure is first debrided (foreign material and devitalised or contaminated tissue is removed), then dressed and inspected on a daily basis for 48 to 72 hours after which it is closed, provided there is no further devitalised tissues or inflammation (McLatchie 2002).
How the intervention might work
The wound repair or healing process can be thought of as having overlapping phases that include inflammation, proliferation and remodelling. The wound is re‐epithelialised during the proliferation phase before the scar matures in the remodelling phase (Lorenz 2008). Considering that remodelling can continue for two years, completion of re‐epithelialisation has been one of the factors examined to assess the progress of wound healing in the short term. This progress has most recently been accurately measured by high resolution ultrasound scanning in B‐mode (Dyson 2003; Lorenz 2008; Rippon 1999). Theoretically, epithelialisation of the wound when the edges are approximated occurs within 24 to 48 hours (Lorenz 2008). It would therefore be expected that the wound that is closed primarily would epithelialise and progress through the remaining processes of wound healing earlier than the wound whose closure is delayed by 48 hours or more.
Why it is important to do this review
In the clinical setting there are several factors that may not only slow down or stop the healing process, but may also result in unsightly and dysfunctional scars, and very rarely mortality. These include infection, poor nutrition, deficient oxygen and blood supply, chemotherapy, radiation and some disease states such as diabetes mellitus (Lorenz 2008). Infection is of particular importance in traumatic wounds. Traumatic wounds are classified by the Centers for Disease Control and Prevention as either contaminated or dirty/infected (Garner 1985), with a predicted relative probability that a wound will become infected of 10% to 17%, and over 27% respectively (Garner 1985). This suggests a potential harm if undertaking primary closure of traumatic wounds after surgical debridement, even in the absence of clinical infection (Garner 1985). The objective assessment of clinical infection is still a challenge, however, given the unavailability of a validated assessment tool (Garner 1985; Hollander 1995)
On the other hand, a threshold number of bacteria in the wound appears to be necessary to overcome host resistance and cause clinical infection. Bacterial contamination of wounds results in clinical infection and delayed wound healing if more than 105 organisms per gram of tissue are present in the wound (Lorenz 2008). Experience in microsurgical reconstruction suggests that microbial contamination of wounds could be held within tolerable limits for longer periods (up to 72 hours) through a correctly performed surgical debridement (Godina 1986). In addition, several reports (Faisham 2001; Harley 2002; Weitz‐Marshall 2002) suggest infections of traumatic wounds are not caused by the initial contamination, but instead the organisms are acquired secondarily from the hospital.
Given that surgical debridement has the potential to reduce wound infection, primary closure following debridement of traumatic wounds without clinical infection therefore has the potential benefit of rapid wound healing. Currently, however, there is no systematic evidence to guide clinical decision‐making on the best timing for closure of traumatic wounds.
Objectives
To determine the effect of primary closure compared with delayed closure for non bite traumatic wounds presenting within 24 hours post injury on time to healing.
To explore the adverse effects of primary closure compared with delayed closure for non bite traumatic wounds presenting within 24 hours post injury.
Methods
Criteria for considering studies for this review
Types of studies
Randomised controlled trials (RCTs) comparing primary closure with delayed closure of non bite traumatic wounds. We excluded cluster‐randomised trials and studies with cross‐over designs because these are not appropriate for answering this particular question.
Types of participants
Inclusion criteria
People of any age presenting with non bite traumatic wounds in any setting within 24 hours of injury.
Exclusion criteria
We excluded wounds with clinical infection at presentation and wounds involving more than just the soft tissues (skin, subcutaneous tissue, muscle and their neurovascular bundles). We excluded studies of traumatic wounds caused by animal bites as this is the subject of another Cochrane Review (in preparation).
Types of interventions
Primary closure compared with delayed closure.
Primary closure is defined as the approximation of the wound edges immediately following debridement (the removal of foreign material and devitalised or contaminated tissue) or cleaning, whichever is appropriate. This is regardless of what is used to approximate the wound edges. Delayed closure is defined as the approximation of the wound edges at least 48 hours following debridement or cleaning, whichever is appropriate.
Types of outcome measures
Primary outcomes
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Objective measures of wound healing, such as time to healing (where healing is defined as complete re‐epithelialisation as measured by high resolution ultrasound scan, or as defined by trial authors); proportion of wounds healed within a specified time period.
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Wound infection defined clinically as purulent discharge or erythema associated with pus (or as defined by trial authors).
Secondary outcomes
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Number of surgical procedures.
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Cosmetic outcome, using one or more validated cosmetic scores, such as the Cosmetic Visual Analogue Score (CVAS) or the Wound Evaluation Score (WES).
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Death.
Search methods for identification of studies
For the search methods used in the original review see Appendix 1
Electronic searches
In May 2013, for this first update, we searched the following electronic databases to identify reports of relevant randomised clinical trials:
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Cochrane Wounds Group Specialised Register (searched 22 May 2013)
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The Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library 2013, Issue 4)
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Ovid MEDLINE (2011 to May Week 2 2013)
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Ovid MEDLINE (In‐Process & Other Non‐Indexed Citations May 21, 2013)
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Ovid EMBASE (2011 to 2013 Week 20);
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EBSCO CINAHL (2011 to 17 May 2013).
We searched the Cochrane Central Register of Controlled Trials (CENTRAL) using the following MeSH headings and keywords:
#1 MeSH descriptor Wounds, Penetrating explode all trees
#2 MeSH descriptor Lacerations explode all trees
#3 MeSH descriptor Fractures, Open explode all trees
#4 (laceration* or gunshot or (gun NEXT shot) or "stab" or stabbing or stabbed):ti,ab,kw
#5 ((traumatic NEXT wound*) or (acute NEXT wound*)):ti,ab,kw
#6 ((mechanical NEXT trauma) or polytrauma):ti,ab,kw
#7 (blast or crush or avulsion) NEXT injur*:ti,ab,kw
#8 (#1 OR #2 OR #3 OR #4 OR #5 OR #6 OR #7)
#9 MeSH descriptor Wound Healing explode all trees
#10 wound NEXT closure*:ti,ab,kw
#11 wound NEXT repair*:ti,ab,kw
#12 (primary NEXT (closure* or repair*)):ti,ab,kw
#13 (secondary NEXT (closure* or repair*)):ti,ab,kw
#14 (delay* NEXT (closure* or repair*)):ti,ab,kw
#15 (#9 OR #10 OR #11 OR #12 OR #13 OR #14)
#16 (#8 AND #15)
The search strategies for Ovid MEDLINE, Ovid EMBASE and EBSCO CINAHL can be found in Appendix 2; Appendix 3 and Appendix 4 respectively. We combined the Ovid MEDLINE search with the Cochrane Highly Sensitive Search Strategy for identifying randomised trials in MEDLINE: sensitivity‐ and precision‐maximising version (2008 revision) (Lefebvre 2011). We combined the EMBASE and CINAHL searches with the trial filters developed by the Scottish Intercollegiate Guidelines Network (SIGN 2010). There were no restrictions on the basis of date or language of publication.
Searching other resources
We searched the bibliographies of all retrieved and relevant publications identified by the above strategies for further studies.
Data collection and analysis
Selection of studies
Two review authors (ME, GB) independently assessed for inclusion all the citations identified as a result of the searches. Two review authors read the titles and abstracts to decide which should be included in the review. There were no disagreements over which studies to include. We retrieved those citations which appeared to be eligible for inclusion in full and the two review authors further assessed them independently. The review authors themselves were not blinded as they were aware of the authors' names, publication details, institutions and results. We added those papers which did not meet the inclusion criteria to the Characteristics of excluded studies with the reason for their exclusion noted.
Data extraction and management
Data extraction was to be performed independently by two review authors, using an agreed form (see Appendix 5). We planned to resolve discrepancies through discussion or, if necessary, consulting a third person from the Wounds Group editorial base. Data were to be double‐entered into Review Manager software (RevMan 5) (RevMan 2008) and checked for accuracy by one of the review authors (Dr Grace Banda). When information regarding any of the above were unclear, we planned to attempt to contact the authors of the original trial reports to provide further details.
Assessment of risk of bias in included studies
Two review authors were going to independently assess risk of bias for each study using the criteria outlined in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2009). This tool identifies six distinct areas including sequence generation, allocation concealment, blinding of participants and outcome assessors, incomplete outcome data, selective outcome reporting and other potential threats to validity (see Appendix 6). Any disagreement would be resolved by discussion or by involving a third assessor.
We would make explicit judgements about whether studies are at high risk of bias, according to the criteria given in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2009). With reference to all six domains we would assess the likely magnitude and direction of the bias and whether we considered it likely to impact on the findings. We would explore the impact of the level of bias through undertaking sensitivity analyses (seeSensitivity analysis).
Measures of treatment effect
Dichotomous data
For dichotomous data, we would have presented results as summary risk ratio (RR) with 95% confidence intervals (CI).
Continuous data
For continuous data, we would have used the difference in means (MD) (with 95% CI) if outcomes were measured in the same way between trials. We we would have used the standardised mean difference (SMD) to combine trials that measured the same outcome, but used different methods.
Time‐to‐event data
Time to complete wound healing is time‐to‐event data and the most appropriate way of summarising time‐to‐event data would be to use methods of survival analysis and express the intervention effect as a hazard ratio. It is not appropriate to analyse time‐to‐event data using methods for continuous outcomes (e.g. using mean times‐to‐event) as the relevant times are only known for the subset of participants who have had the event. Censored participants must be excluded, which almost certainly will introduce bias.
Unit of analysis issues
We did not include cluster‐randomised trials and studies with cross‐over designs because these are not appropriate designs for this research question.
Dealing with missing data
We intended to note levels of attrition for included studies. We intended to explore the impact of including studies with high levels of missing data (15% or greater of the participants) in the overall assessment of treatment effect by using sensitivity analysis. We would consider studies to be at high risk of bias if they had inadequate randomisation and allocation concealment procedures and had unclear or inadequate blinding of outcome assessment.
We planned to carry out analyses for all dichotomous outcomes, as far as possible, on an intention‐to‐treat basis, i.e. we would attempt to include all participants randomised to each group in the analyses. The denominator for each outcome in each trial would be the number randomised minus any participants whose outcomes are known to be missing.
Assessment of heterogeneity
We planned to use the I² statistic to measure heterogeneity among the trials in each analysis. This examines the percentage of total variation across studies due to heterogeneity rather than to chance. If we identified substantial heterogeneity (I² statistic greater than 60%) and pooling was appropriate we would have used a random‐effects model to pool data.
Data synthesis
We intended to carry out statistical analysis using the Review Manager software (RevMan). We would have used fixed‐effect inverse variance meta‐analysis for combining data where trials examined the same intervention, and the trials’ populations and methods are judged sufficiently similar. Where there is clinical or methodological heterogeneity between studies sufficient to suggest that treatment effects may differ between trials we would have considered using a random‐effects meta‐analysis or not combining data.
Subgroup analysis and investigation of heterogeneity
We planned to carry out the following subgroup analyses if there were sufficient data:
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acute traumatic wounds presenting within a specified time period (up to six hours, between six and up to 24 hours);
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acute traumatic wounds with concurrent treatments such as debridement or antibiotics in comparison with wounds treated without additional intervention.
Sensitivity analysis
We had planned to use a fixed‐effect meta‐analysis for combining study data if the trials had been judged to be sufficiently similar. In the event of important heterogeneity (for example, I² greater than 60%), we would have considered using a random‐effects model or not combining the data. We would have considered studies with inadequate randomisation and allocation concealment procedures and those with unclear or inadequate blinding of outcome assessment to be at high risk of bias. For studies at high risk of bias, we had planned a sensitivity analysis omitting them.
Results
Description of studies
See Characteristics of excluded studies.
Results of the search
The original search retrieved 380 citations. We excluded most of these articles on the basis of the primary topic focus being other than assessment of acute traumatic wounds presenting within 24 hours post injury. We excluded a further seven articles that had ambiguous titles after retrieving their abstracts. We obtained full‐text papers for five studies for further assessment. None of these studies met the inclusion criteria of our review for varied reasons which are noted in the Characteristics of excluded studies.
For this update, the search retrieved 50 citations, none of which considered acute traumatic wounds within 24 hours of injury and none were retrieved in full.
Included studies
No studies met the inclusion criteria for the review.
Excluded studies
In the original search, we excluded studies from the review for the following reasons:
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the outcome of interest was anal incontinence (Nordenstam 2008);
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not a RCT, wounds involved bones (De Long 1999);
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looked at colon repair (Kamwendo 2002);
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looked at dog bite lacerations (Maimaris 1988); and
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not a RCT (van de Baar 2010).
Risk of bias in included studies
Since no studies met the inclusion criteria, it was not possible to undertake a risk of bias assessment.
Effects of interventions
Since no studies met the inclusion criteria, neither a meta‐analysis nor a narrative description of studies was possible.
Discussion
The question of the best timing of closure of acute traumatic wounds is very important and the answer to it is long overdue. The need for evidence‐based clinical guidance in this regard cannot be overemphasised considering how common the condition in question is (Hollander 1995; Hollander 1999; Silbert 1981). The finding of no studies for possible inclusion in this review is therefore very surprising.
The understanding of the mechanism of wound healing has given us an insight into the potential benefits of primary closure on the duration of wound healing (Lorenz 2008). It would therefore be expected that researchers would begin to look at the safety of extending the time post injury for allowing primary closure. So far this has only been done retrospectively in form of case studies, with conflicting results. In one study of 300 hand and forearm lacerations, Morgan et al found that lacerations closed within four hours had a lower infection rate than lacerations closed more than four hours after injury (7% versus 21%, respectively) (Morgan 1980). On the other hand, Baker and Lanuti (Baker 1990) did not find a difference in infection rate for lacerations closed less than or more than six hours from the time of injury in 2834 paediatric patients. In another study of 204 lacerations, Berk et al found that facial lacerations healed well regardless of the time to closure. In contrast, trunk and extremity lacerations had lower rates of healing if they were closed more than 19 hours after the time of injury (63% to 75%) than if they were closed earlier (75% to 91%) (Berk 1988). A more recent prospective cohort study done in the Netherlands showed that there was no significant relationship between wound age and the presence of infection after suturing. The only parameters that significantly predicted wound infection were location of the wound at the lower extremity compared to head as reference and age of the patient in the fourth quartile compared to the first quartile (van de Baar 2010).
Robust evidence of harm or benefit can only be obtained from high‐quality randomised clinical trials. A randomised controlled trial has been done comparing primary closure versus delayed closure for traumatic wounds involving viscera (colon) whose management is more complex than that of traumatic wounds (Velmahos 2002). It should therefore be practically feasible to carry out a randomised clinical trial of adequate quality to answer this question. Researchers should now focus on designing good quality randomised clinical trials to provide the basis for the timing of wound closure in patients presenting with acute traumatic wounds within 24 hours of injury.
