Geriatric trauma

Adams, Sasha D.; Holcomb, John B.

doi:10.1097/mcc.0000000000000246

Cited by 60 publications

(79 citation statements)

References 39 publications

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“…Impaired adaptive and homeostatic mechanisms are associated to a diminished physiological reserve[4] and, therefore, an impaired response to a physical insult[4,9]. In addition, comorbidities are commonly associated with an increased use of medical treatments that can also affect the response to injury[1,3,4]. …”

Section: Physiological Considerations and Effect Of Medicationsmentioning

confidence: 99%

“…In addition, they are receiving chronic medications that can affect hear rate and blood pressure[1,3,4], blunting the response to injury in hemodynamically compromised patients[1]. …”

Section: Physiological Considerations and Effect Of Medicationsmentioning

confidence: 99%

“…In the following years, it is expected that people over 65 years will represent up to one-fifth of the world population[1,3] and almost 39% of trauma admissions by 2050[4]. This will constitute a major problem worldwide, but especially in developed countries with higher life expectancy.…”

Section: Introductionmentioning

confidence: 99%

“…Although the number of articles dealing with this topic showed a 6-fold increase in the last 25 years[3], the optimal management of these patients remains to be determined. A specific ad-hoc Geriatric Trauma Committee was constituted by the American Association for the Surgery of Trauma[2].…”

Section: Introductionmentioning

confidence: 99%

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Severe trauma in the geriatric population

Llompart‐Pou¹,

Pérez-Bárcena²,

Chico‐Fernández³

et al. 2017

WJCCM

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Geriatric trauma constitutes an increasingly recognized problem. Aging results in a progressive decline in cellular function which leads to a loose of their capacity to respond to injury. Some medications commonly used in this population can mask or blunt the response to injury. Falls constitute the most common cause of trauma and the leading cause of trauma-related deaths in this population. Falls are complicated by the widespread use of antiplatelets and anticoagulants, especially in patients with brain injury. Under-triage is common in this population. Evaluation of frailty could be helpful to solve this issue. Appropriate triaging and early aggressive management with correction of coagulopathy can improve outcome. Limitation of care and palliative measures must be considered in cases with a clear likelihood of poor prognosis.

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Section: Physiological Considerations and Effect Of Medicationsmentioning

confidence: 99%

“…In addition, they are receiving chronic medications that can affect hear rate and blood pressure[1,3,4], blunting the response to injury in hemodynamically compromised patients[1]. …”

Section: Physiological Considerations and Effect Of Medicationsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Severe trauma in the geriatric population

Llompart‐Pou¹,

Pérez-Bárcena²,

Chico‐Fernández³

et al. 2017

WJCCM

View full text Add to dashboard Cite

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“…Advanced age is also a significant factor contributing to impaired recovery after TBI (Coronado et al, 2005; Czosnyka et al, 2005; Hukkelhoven et al, 2003) including increased risk for developing AD/dementia. This is particularly important in the context of growing aged populations of civilians and Veterans (Ortman et al, 2014), greater numbers of geriatric patients with chronic survival after head trauma (Adams and Holcomb, 2015), and increasing burden of elderly TBI patients on the health care system (Thompson et al, 2006). Recently, there is an indication of reduced inpatient mortality after TBI (Maxwell et al, 2015).…”

Section: Effect Of Aging On Aβ-induced Risk For Developing Ad Aftementioning

confidence: 99%

Disordered APP metabolism and neurovasculature in trauma and aging: Combined risks for chronic neurodegenerative disorders

Ikonomović

Abrahamson

2017

Ageing Research Reviews

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Traumatic brain injury (TBI), advanced age, and cerebral vascular disease are factors conferring increased risk for late onset Alzheimer’s disease (AD). These conditions are also related pathologically through multiple interacting mechanisms. The hallmark pathology of AD consists of pathological aggregates of amyloid-β (Aβ) peptides and tau proteins. These molecules are also involved in neuropathology of several other chronic neurodegenerative diseases, and are under intense investigation in the aftermath of TBI as potential contributors to the risk for developing AD and chronic traumatic encephalopathy (CTE). The pathology of TBI is complex and dependent on injury severity, age-at-injury, and length of time between injury and neuropathological evaluation. In addition, the mechanisms influencing pathology and recovery after TBI likely involve genetic/epigenetic factors as well as additional disorders or comorbid states related to age and central and peripheral vascular health. In this regard, dysfunction of the aging neurovascular system could be an important link between TBI and chronic neurodegenerative diseases, either as a precipitating event or related to accumulation of AD-like pathology which is amplified in the context of aging. Thus with advanced age and vascular dysfunction, TBI can trigger self-propagating cycles of neuronal injury, pathological protein aggregation, and synaptic loss resulting in chronic neurodegenerative disease. In this review we discuss evidence supporting TBI and aging as dual, interacting risk factors for AD, and the role of Aβ and cerebral vascular dysfunction in this relationship. Evidence is discussed that Aβ is involved in cyto- and synapto-toxicity after severe TBI, and that its chronic effects are potentiated by aging and impaired cerebral vascular function. From a therapeutic perspective, we emphasize that in the fields of TBI- and aging-related neurodegeneration protective strategies should include preservation of neurovascular function.

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