The Injury Mechanism of Traumatic Amputation.
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ABSTRACT:
SUBMITTER: Rankin IA
PROVIDER: S-EPMC8082077 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:We report a case of a near-complete amputation of the forefoot of a 20-year-old man as a result of a motorboat propeller injury sustained in a saltwater river. He was treated with open reduction, percutaneous pinning, extensor tendon repair, and an extended course of antibiotic prophylaxis. We review the literature regarding motorboat propeller injuries to the foot and ankle.
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Project description:IntroductionTakotsubo or stress cardiomyopathy is a syndrome of transient left ventricular systolic dysfunction seen in the absence of obstructive coronary artery disease.Case reportWe describe a case of stress cardiomyopathy diagnosed in the emergency department (ED) using point-of-care ultrasound associated with traumatic hand amputation. The patient suffered a near-complete amputation of the right hand while using a circular saw, subsequently complicated by brief cardiac arrest with rapid return of spontaneous circulation. Point-of-care ultrasonography in the ED revealed the classic findings of takotsubo cardiomyopathy, including apical ballooning of the left ventricle and hyperkinesis of the basal walls with a severely reduced ejection fraction. After formalization of the amputation and cardiovascular evaluation, the patient was discharged from the hospital in stable condition 10 days later.ConclusionEmergency physicians should be aware of the possibility of stress cardiomyopathy as a cause for acute decompensation, even in isolated extremity trauma.
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Project description:Protein citrullination is a calcium-driven post-translational modification proposed to play a causative role in the neurodegenerative disorders of Alzheimer's disease, multiple sclerosis (MS), and prion disease. Citrullination can result in the formation of antigenic epitopes that underlie pathogenic autoimmune responses. This phenomenon, which is best understood in rheumatoid arthritis, may play a role in the chronic dysfunction following traumatic brain injury (TBI). Despite substantial evidence of aberrations in calcium signaling following TBI, there is little understanding of how TBI alters citrullination in the brain. The present investigation addressed this gap by examining the effects of TBI on the distribution of protein citrullination and on the specific cell types involved. Immunofluorescence revealed that controlled cortical impact in rats profoundly up--regulated protein citrullination in the cerebral cortex, external capsule, and hippocampus. This response was exclusively seen in astrocytes; no such effects were observed on the status of protein citrullination in neurons, oligodendrocytes or microglia. Further, proteomic analyses demonstrated that the effects of TBI on citrullination were confined to a relatively small subset of neural proteins. Proteins most notably affected were those also reported to be citrullinated in other disorders, including prion disease and MS. In vivo findings were extended in an in vitro model of simulated TBI employing normal human astrocytes. Pharmacologically induced calcium excitotoxicity was shown to activate the citrullination and breakdown of glial fibrillary acidic protein, producing a novel candidate TBI biomarker and potential target for autoimmune recognition. In summary, these findings demonstrate that the effects of TBI on protein citrullination are selective with respect to brain region, cell type, and proteins modified, and may contribute to a role for autoimmune dysfunction in chronic pathology following TBI.
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Project description:BackgroundPatients who undergo lower extremity amputation secondary to the complications of diabetes or peripheral artery disease have poor long-term survival. Providing patients and surgeons with individual-patient, rather than population, survival estimates provides them with important information to make individualized treatment decisions.MethodsPatients with peripheral artery disease and/or diabetes undergoing their first unilateral transmetatarsal, transtibial or transfemoral amputation were identified in the Veterans Affairs Surgical Quality Improvement Program (VASQIP) database. Stepdown logistic regression was used to develop a 1-year mortality risk prediction model from a list of 33 candidate predictors using data from three of five Department of Veterans Affairs national geographical regions. External geographical validation was performed using data from the remaining two regions. Calibration and discrimination were assessed in the development and validation samples.ResultsThe development sample included 5028 patients and the validation sample 2140. The final mortality prediction model (AMPREDICT-Mortality) included amputation level, age, BMI, race, functional status, congestive heart failure, dialysis, blood urea nitrogen level, and white blood cell and platelet counts. The model fit in the validation sample was good. The area under the receiver operating characteristic (ROC) curve for the validation sample was 0·76 and Cox calibration regression indicated excellent calibration (slope 0·96, 95 per cent c.i. 0·85 to 1·06; intercept 0·02, 95 per cent c.i. -0·12 to 0·17). Given the external validation characteristics, the development and validation samples were combined, giving a total sample of 7168.ConclusionThe AMPREDICT-Mortality prediction model is a validated parsimonious model that can be used to inform the 1-year mortality risk following non-traumatic lower extremity amputation of patients with peripheral artery disease or diabetes.
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Project description:Traumatic finger/thumb amputations are some of the most prevalent traumatic injuries affecting Americans each year. Rates of replantation after traumatic finger/thumb amputation, however, have been declining steadily across U.S. hospitals, which may make these procedures less accessible to minorities and vulnerable populations. The specific aim of this study was to examine racial variation in finger replantation after traumatic finger/thumb amputation.Using a two-level hierarchical model, the authors retrospectively compared replantation rates for African American patients with those of whites, adjusting for patient and hospital characteristics. Patients younger than 65 years with traumatic finger/thumb amputation injuries who sought care at a U.S. trauma center between 2007 and 2012 were included in the study sample.The authors analyzed 13,129 patients younger than 65 years with traumatic finger/thumb amputation. Replantation rates declined over time from 19 percent to 14 percent (p = 0.004). Adjusting for patient and hospital characteristics, African Americans (OR, 0.81; 95 percent CI, 0.66 to 0.99; p = 0.049) were less likely to undergo replantation procedures than whites, and uninsured patients (OR, 0.73; 95 percent CI, 0.62 to 0.84; p < 0.0001) were less likely than those who were privately insured.Despite advancements in microsurgical techniques and the increasing use of reconstructive surgery in other fields, finger/thumb replantation rates are declining in the United States and vulnerable populations are less likely to undergo replantation after amputation injuries. Regionalization of care for these injuries may not only provide a higher quality care but also reduce variations in treatment.Risk, III.
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Project description:A successful case of crossover replantation of the left foot to the stump of the right leg was described. The lower extremities were amputated at different levels. On the left side, there was a complete amputation in the distal part of the lower leg with comminuted fracture of the distal tibia. On the right side, there was a complete amputation in the hindfoot with comminuted fracture of both the talus and calcaneus. Since anatomical replantation was impossible, we performed crossover replantation of the left foot to the right lower leg. At the latest follow-up examination, forty-six months after the accident, the patient walked independently with a prosthesis on the stump of the left leg. Crossover replantation should be considered in bilateral amputations for the salvage of at least one extremity.
| S-EPMC8851088 | biostudies-literature
Project description:A substantial number of individuals have long-lasting adverse effects from a traumatic brain injury (TBI). Depression is one of these long-term complications that influences many aspects of life. Depression can limit the ability to return to work, and even worsen cognitive function and contribute to dementia. The mechanistic cause for the increased depression risk associated with a TBI remains to be defined. As TBI results in chronic neuroinflammation, and priming of glia to a secondary challenge, the inflammatory theory of depression provides a promising framework for investigating the cause of depression following a TBI. Increases in cytokines similar to those seen in depression in the general population are also increased following a TBI. Biomarker levels of cytokines peak within hours-to-days after the injury, yet pro-inflammatory cytokines may still be elevated above physiological levels months-to-years following TBI, which is the time frame in which post-TBI depression can persist. As tumor necrosis factor ? and interleukin 1 can signal directly at the neuronal synapse, pathophysiological levels of these cytokines can detrimentally alter neuronal synaptic physiology. The purpose of this review is to outline the current evidence for the inflammatory hypothesis of depression specifically as it relates to depression following a TBI. Moreover, we will illustrate the potential synaptic mechanisms by which tumor necrosis factor ? and interleukin 1 could contribute to depression. The association of inflammation with the development of depression is compelling; however, in the context of post-TBI depression, the role of inflammation is understudied. This review attempts to highlight the need to understand and treat the psychological complications of a TBI, potentially by neuroimmune modulation, as the neuropsychiatric disabilities can have a great impact on the rehabilitation from the injury, and overall quality of life.
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Project description:Open fractures are characterized by disruption of the skin and soft tissue, which allows for microbial contamination and colonization. Preventing infection-related complications of open fractures and other acute wounds remains an evolving challenge due to an incomplete understanding of how microbial colonization and contamination influence healing and outcomes. Culture-independent molecular methods are now widely used to study human-associated microbial communities without introducing culture biases. Using such approaches, the objectives of this study were to (1) define the long-term temporal microbial community dynamics of open fracture wounds and (2) examine microbial community dynamics with respect to clinical and demographic factors. Fifty-two subjects with traumatic open fracture wounds (32 blunt and 20 penetrating injuries) were enrolled prospectively and sampled longitudinally from presentation to the emergency department (ED) and at each subsequent inpatient or outpatient encounter. Specimens were collected from both the wound center and adjacent skin. Culture-independent sequencing of the 16S ribosomal RNA gene was employed to identify and characterize microbiota. Upon presentation to the ED and time points immediately following, sample collection site (wound or adjacent skin) was the most defining feature discriminating microbial profiles. Microbial composition of adjacent skin and wound center converged over time. Mechanism of injury most strongly defined the microbiota after initial convergence. Further analysis controlling for race, gender, and age revealed that mechanism of injury remained a significant discriminating feature throughout the continuum of care. We conclude that the microbial communities associated with open fracture wounds are dynamic in nature until eventual convergence with the adjacent skin community during healing, with mechanism of injury as an important feature affecting both diversity and composition of the microbiota. A more complete understanding of the factors influencing microbial contamination and/or colonization in open fractures is a critical foundation for identifying markers indicative of outcome and deciphering their respective contributions to healing and/or complication.
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Project description:Recently, age-related timing dissociation between the superficial and deep venous systems has been observed; this was particularly pronounced in patients with normal pressure hydrocephalus, suggesting a common mechanism of ventriculomegaly. Establishing the relationship between venous drainage and ventricular enlargement would be clinically relevant and could provide insight into the mechanisms underlying brain ageing. To investigate a possible link between venous drainage and ventriculomegaly in both normal ageing and pathological conditions, we compared 225 healthy subjects (137 males and 88 females) and 71 traumatic brain injury patients of varying ages (53 males and 18 females) using MRI-based volumetry and a novel perfusion-timing analysis. Volumetry, focusing on the CSF space, revealed that the sulcal space and ventricular size presented different lifespan profiles with age; the latter presented a quadratic, rather than linear, pattern of increase. The venous timing shift slightly preceded this change, supporting a role for venous drainage in ventriculomegaly. In traumatic brain injury, a small but significant disease effect, similar to idiopathic normal pressure hydrocephalus, was found in venous timing, but it tended to decrease with age at injury, suggesting an overlapping mechanism with normal ageing. Structural bias due to, or a direct causative role of ventriculomegaly was unlikely to play a dominant role, because of the low correlation between venous timing and ventricular size after adjustment for age in both patients and controls. Since post-traumatic hydrocephalus can be asymptomatic and occasionally overlooked, the observation suggested a link between venous drainage and CSF accumulation. Thus, hydrocephalus, involving venous insufficiency, may be a part of normal ageing, can be detected non-invasively, and is potentially treatable. Further investigation into the clinical application of this new marker of venous function is therefore warranted.
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Project description:BACKGROUND:?-Adrenergic agents suppress inflammation and may play an important role in posttraumatic infections. Mechanisms may include inhibition of MAP kinase signaling. We sought to determine whether MKP-1 contributed to catecholamine suppression of innate immunity and also wanted to know whether early catecholamine treatment after traumatic injury increases the risk of later nosocomial infection. METHODS:We performed experiments using THP-1 cells and peripheral blood mononuclear cells from healthy individuals. We exposed cells to epinephrine and/or LPS and measured inflammatory gene transcription and MAP kinase activation. We inhibited MKP-1 activity to determine its role in catecholamine-induced immune suppression. Finally, we studied injured subjects to determine whether early catecholamine treatment was associated with nosocomial infection. RESULTS:Epinephrine increases MKP-1 transcripts and protein and decreases LPS-induced p38 and JNK phosphorylation and TNF-? gene transcription. RNAi inhibition of MKP-1 at least partially restores LPS-induced TNF-? gene expression (p = 0.024). In the clinical cohort, subjects treated with ?-adrenergic agents had an increased risk of ventilator-associated pneumonia (aOR = 1.9; 95% CI = 1.3-2.6) and bacteremia (aOR = 1.5; 95% CI = 1.1-2.3). CONCLUSIONS:MKP-1 may have a role in catecholamine-induced suppression of innate immunity, and exogenous catecholamines might contribute to nosocomial infection risk.
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