ReviewDer Orthopade2005
[Traumatic brain injury: impact on timing and modality of fracture care].
Review in Der Orthopade, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Early versus late intramedullary nailing for traumatic femur fracture management: meta-analysis.Journal of orthopaedic surgery and research · 2018Pooled it
- Timing of fracture fixation for femur and pelvis fractures in patients with severe traumatic brain injury - an analysis of the TraumaRegister DGUEuropean journal of trauma and emergency surgery : official publication of the European Trauma Society · 2026Article
- The impact of arterial hypertension on polytrauma and traumatic brain injury.Deutsches Arzteblatt international · 2012Article
- ATLS(R) and damage control in spine trauma.World journal of emergency surgery : WJES · 2009Article
- Polytrauma--pathophysiology and management principles.Langenbeck's archives of surgery · 2008Review
- [The relevance of the inflammatory response in the injured brain].Der Orthopade · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) represents the major "killing factor" after trauma in young individuals. Those patients who survive the initial injury are highly susceptible to secondary insults to the injured brain which are mainly caused by hypotension and/or hypoxia in the early resuscitative period. Furthermore, a potent inflammatory cascade is initiated within the injured brain which leads to the development of brain edema and delayed neuronal cell death. This profound endogenous neuroinflammatory response after TBI, which is phylogenetically aimed at repairing lesioned tissue and defending the brain from invading pathogens, is in large part responsible for the extent of secondary brain damage and adverse outcome. Thus, the optimal management of the multiply injured patient, based on a thorough understanding of the pathophysiological alterations after TBI, should avoid an iatrogenic "second hit" which may be devastating to the injured brain. The standard approach of "early total care" for isolated fractures should be strictly avoided in brain-injured patients in favor of an "orthopedic damage control" concept with temporary external fixation of long bone fractures and priority given to early transfer to intensive care. The present review provides an up-to-date overview on the neuroinflammatory pathophysiology of brain injury and its implications for an optimized concept of fracture care in TBI patients.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.