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Is the use of specific time cut-off or "golden period" for primary closure of acute traumatic wounds evidence based? A systematic review.

ABSTRACT: The time cut-off for primary closure of acute wounds is not clearly defined in the literature or in the surgical textbooks. It is even unclear whether the wound age increases wound infection rate. The scarcity of scientific evidence may explain the diverse wound management practices. To give guidance for further research in the field, this systematic review assessed recent evidence on the impact of wound age on the infection rate and on the selection of wound closure method. Using predefined criteria, we systematically searched Cochrane Central Register of Controlled Trials/CENTRAL, Cochrane Database of Systematic Reviews, MEDLINE, Scopus, Web of Science Core Collection, Current Contents, SciELO Citation Index, KCI-Korean Journal Database, Russian Science Citation Index, BIOSIS Citation Index, Data Citation Index, LILACS/Latin American and Caribbean Health Sciences Literature, and African Index Medicus; as well as online trial registries: ClinicalTrials.gov, WHO International Clinical Trials Registry Platform/WHO ICTRP, and CenterWatch. Nine studies met the selection criteria and were included in the review. This review could not establish the time frame for primary closure of wounds. The time intervals mentioned in many surgical textbooks were supported by only a few low-quality studies. More important factors to be considered when delaying primary closure of acute wounds were the history of diabetes, wound location, wound length, and the presence of a foreign body.

SUBMITTER: Jaman J

PROVIDER: S-EPMC8771236 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:We evaluate patients with shock and traumatic brain injury who were previously enrolled in an out-of-hospital clinical trial to test the association between out-of-hospital time and outcome.This was a secondary analysis of patients with shock and traumatic brain injury who were aged 15 years or older and enrolled in a Resuscitation Outcomes Consortium out-of-hospital clinical trial by 81 emergency medical services agencies transporting to 46 Level I and II trauma centers in 11 sites (May 2006 through May 2009). Inclusion criteria were systolic blood pressure less than or equal to 70 mm Hg or systolic blood pressure 71 to 90 mm Hg with pulse rate greater than or equal to 108 beats/min (shock cohort) and Glasgow Coma Scale score less than or equal to 8 (traumatic brain injury cohort); patients meeting both criteria were placed in the shock cohort. Primary outcomes were 28-day mortality (shock cohort) and 6-month Glasgow Outcome Scale-Extended score less than or equal to 4 (traumatic brain injury cohort).There were 778 patients in the shock cohort (26% 28-day mortality) and 1,239 patients in the traumatic brain injury cohort (53% 6-month Glasgow Outcome Scale-Extended score ?4). Out-of-hospital time greater than 60 minutes was not associated with worse outcomes after accounting for important confounders in the shock cohort (adjusted odds ratio [aOR] 1.42; 95% confidence interval [CI] 0.77 to 2.62) or traumatic brain injury cohort (aOR 0.77; 95% CI 0.51 to 1.15). However, shock patients requiring early critical hospital resources and arriving after 60 minutes had higher 28-day mortality (aOR 2.37; 95% CI 1.05 to 5.37); this finding was not observed among a similar traumatic brain injury subgroup.Among out-of-hospital trauma patients meeting physiologic criteria for shock and traumatic brain injury, there was no association between time and outcome. However, the subgroup of shock patients requiring early critical resources and arriving after 60 minutes had higher mortality.

Project description:BACKGROUND:Thalamic dysfunction has been implicated in overall chronic neurological dysfunction after traumatic brain injury (TBI), however little is known about the underlying histopathology. In experimental diffuse TBI (dTBI), we hypothesize that persisting histopathological changes in the ventral posteromedial (VPM) nucleus of the thalamus is indicative of progressive circuit reorganization. Since circuit reorganization in the VPM impacts the whisker sensory system, the histopathology could explain the development of hypersensitivity to whisker stimulation by 28days post-injury; similar to light and sound hypersensitivity in human TBI survivors. METHODS:Adult, male Sprague-Dawley rats underwent craniotomy and midline fluid percussion injury (FPI) (moderate severity; 1.8-2.0atm) or sham surgery. At 1d, 7d, and 28days post-FPI (d FPI) separate experiments confirmed the cytoarchitecture (Giemsa stain) and evaluated neuropathology (silver stain), activated astrocytes (GFAP), neuron morphology (Golgi stain) and microglial morphology (Iba-1) in the VPM. RESULTS:Cytoarchitecture was unchanged throughout the time course, similar to previously published data; however, neuropathology and astrocyte activation were significantly increased at 7d and 28d and activated microglia were present at all time points. Neuron morphology was dynamic over the time course with decreased dendritic complexity (fewer branch points; decreased length of processes) at 7d FPI and return to sham values by 28d FPI. CONCLUSIONS:These data indicate that dTBI results in persisting thalamic histopathology out to a chronic time point. While these changes can be indicative of either adaptive (recovery) or maladaptive (neurological dysfunction) circuit reorganization, they also provide a potential mechanism by which maladaptive circuit reorganization could contribute to the development of chronic neurological dysfunction. Understanding the processes that mediate circuit reorganization is critical to the development of future therapies for TBI patients.

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Is the use of specific time cut-off or "golden period" for primary closure of acute traumatic wounds evidence based? A systematic review.

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