Prevalence and risk factors for post-traumatic stress, anxiety, and depression in sepsis survivors after ICU discharge

Calsavara, Allan Jefferson Cruz; Costa, Priscila A.; Nobre, Vandack; Teixeira, Antônio Lúcio

doi:10.1590/1516-4446-2020-0986

Cited by 24 publications

(27 citation statements)

References 42 publications

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“…It has been reported that more than 19 million septic patients each year ( Prescott and Angus, 2018 ). As one of the major manifestations of SAE, long-term mental health issues affect as many as 58% of surviving septic patients ( Prescott and Angus, 2018 ; Calsavara et al, 2021 ), leading to poor quality of life and a heavy economic burden. However, the concrete mechanism of long-lasting mental disorders in septic patients is not clear.…”

Section: Discussionmentioning

confidence: 99%

Neuronal MD2 induces long-term mental impairments in septic mice by facilitating necroptosis and apoptosis

Fan

et al. 2022

Front. Pharmacol.

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Sepsis-associated encephalopathy (SAE) is a complication of sepsis with high morbidity rates. Long-lasting mental health issues in patients with SAE result in a substantial decrease in quality of life. However, its underlying mechanism is unclear, and effective treatments are not available. In the current study, we explored the role of apoptosis and necroptosis related to mental dysfunction in sepsis. In a mouse model of sepsis constructed by cecal ligation and puncture (CLP), altered behavior was detected by the open field, elevated-plus maze and forced swimming tests on the fourteenth day. Moreover, apoptosis- and necroptosis-associated proteins and morphological changes were examined in the hippocampus of septic mice. Long-lasting depression-like behaviors were detected in the CLP mice, as well as significant increases in neuronal apoptosis and necroptosis. Importantly, we found that apoptosis and necroptosis were related according to Ramsay’s rule in the brains of the septic mice. Inhibiting myeloid differentiation factor 2 (MD2), the crosstalk mediator of apoptosis and necroptosis, in neurons effectively reduced neuronal loss and alleviated depression-like behaviors in the septic mice. These results suggest that neuronal death in the hippocampus contributes to the mental impairments in SAE and that inhibiting neuronal MD2 is a new strategy for treating mental health issues in sepsis by inhibiting necroptosis and apoptosis.

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Section: Discussionmentioning

confidence: 99%

Neuronal MD2 induces long-term mental impairments in septic mice by facilitating necroptosis and apoptosis

Fan

et al. 2022

Front. Pharmacol.

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“…It has been reported that more than 19 million individuals develop sepsis each year [16]. As one of the major manifestations of SAE, long-term mental dysfunction affects 29 % of surviving septic patients [16,17], which leads to poor quality of life and a heavy economic burden. However, the concrete mechanism of long-lasting mental impairments in septic patients is not clear.…”

Section: Discussionmentioning

confidence: 99%

Neuronal MD2 Induces Long-term Mental Impairments in Septic Mice by Facilitating Necroptosis and Apoptosis

Fan¹,

et al. 2021

Preprint

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Sepsis-associated encephalopathy (SAE) is a complication of sepsis that has high morbidity rates. Long-lasting depression is a major mental health disorder in patients with SAE that results in a substantial decrease in quality of life and economic burden. However, the underlying mechanism of SAE is unclear, and effective treatments are not available. In the current study, we explored the role of apoptosis and necroptosis related to depression in sepsis. In a mouse model of cecal ligation and puncture (CLP), we detected mental impairments by the open field test, elevated-plus maze and forced swimming test on the fourteenth day. Moreover, apoptosis- and necroptosis-associated proteins and morphological changes were examined in the hippocampus of the septic mice. These mice showed depression-like behaviors at 14 days after CLP, with substantial increases in neuronal apoptosis and necroptosis. Importantly, we found that apoptosis and necroptosis were related according to Ramsay’s rule in the brains of the septic mice. Inhibiting the function of MD2, the crosstalk mediator of apoptosis and necroptosis, in neurons effectively reduced neuronal loss and alleviated depression-like behaviors in the septic mice. These results suggest that neuronal death in the hippocampus contributes to the mental impairments in SAE and that inhibiting neuronal MD2 is a new strategy for treatment of mental health issues in sepsis by inhibiting necroptosis and apoptosis.

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“…Individuals with a preexisting psychiatric history are at greater risk for developing any combination of these distressing outcomes while in the ICU 75,76 . Recent studies also suggest that psychological symptoms may continue to be elevated after ICU stays 71,77‐80 …”

Section: Literature Review/methodsmentioning

confidence: 99%

“…Moreover, diagnostic criteria for each of these disorders include symptoms pertaining to cognition (eg, difficulty concentrating) 13 . These symptoms and disorders often present comorbidly in ICU survivors (eg, PICS) 78,87 and further underscore the complex and multifactorial etiology of ICU‐related cognitive impairment 88 …”

Section: Literature Review/methodsmentioning

confidence: 99%

“…Clinical interview and observation provide pertinent information regarding patients' functional status, yet providers are likely to underestimate the frequency or degree of cognitive impairment experienced by ICU survivors 12,105 . In a systematic review, prevalence of cognitive impairments was shown to be higher when objective measures were used following ICU discharge 4,78 . Systematic use of assessment tools can help providers identify and intervene on cognitive impairment early.…”

Section: Literature Review/methodsmentioning

confidence: 99%

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Intensive care‐related cognitive impairment: A biopsychosocial overview

Tingey

Dasher

Bunnell

et al. 2022

PM&R

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Advancements in critical care medicine have improved survival rates for patients experiencing critical illness in intensive care units (ICUs). Although mortality has declined, more than half of ICU survivors experience functional impairments that persist beyond discharge. Of particular concern is ICU‐related cognitive impairment, which can extend across the care continuum, ranging from acute and transient presentations in the ICU (eg, delirium) to long‐term impairments years after discharge. ICU‐related cognitive impairment has received increased attention in the literature, particularly as it relates to ICU survivors who have received and survived critical care in the context of the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) pandemic and are now experiencing postacute sequelae of SARS‐CoV‐2 infection. The medical complexity and heterogeneity of ICU survivors, coupled with the multifactorial etiology of ICU‐related cognitive impairments, lead to challenges in how to optimize care for ICU survivors at various stages of recovery. This review aims to provide an overview of cognitive outcomes associated with critical illness by integrating recent literature focused on etiology, assessment, and interventions in the context of ICU‐related cognitive impairments. The narrative review employs a biopsychosocial framework to comprehensively evaluate the multifactorial nature of ICU‐related cognitive outcomes. Authors also highlight that multidisciplinary teams composed of key rehabilitation providers are likely best suited for optimizing recovery trajectories of ICU survivors.

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Prevalence and risk factors for post-traumatic stress, anxiety, and depression in sepsis survivors after ICU discharge

Cited by 24 publications

References 42 publications

Neuronal MD2 induces long-term mental impairments in septic mice by facilitating necroptosis and apoptosis

Neuronal MD2 induces long-term mental impairments in septic mice by facilitating necroptosis and apoptosis

Neuronal MD2 Induces Long-term Mental Impairments in Septic Mice by Facilitating Necroptosis and Apoptosis

Intensive care‐related cognitive impairment: A biopsychosocial overview

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