“…When patients required readmission to the ICU after discharge, only data from the first admission were analyzed. We used the Third International Consensus Definition (Sepsis-3) ( 18 ) and the Society for Cardiovascular Angiography and Interventions ( 19 ) shock stages C, D, and E to define both septic shock and cardiogenic shock, respectively. For the purposes of this study, we define shock to include both of the aforementioned definitions of septic shock and cardiogenic shock; no patients in our study suffered from hypovolemic or obstructive shock.…”
OBJECTIVES:
The pathophysiology of delirium is complex and incompletely understood. Inflammation is hypothesized to be integral to its development due to effects on blood brain barrier integrity, facilitation of leukocyte extravasation into brain parenchyma, and propagation of neuroinflammation. Septic shock is the prototypical condition associated with ICU delirium; however, the relative contribution of resultant hypotension and systemic inflammation to the development of delirium is unknown.
DESIGN:
This was a prospective exploratory study.
SETTING:
A multidisciplinary ICU at an academic medical center in Phoenix, AZ.
PATIENTS:
Critically ill patients older than or equal to 18 years old admitted to the ICU.
INTERVENTIONS:
None.
MEASUREMENTS AND MAIN RESULTS:
Screening for delirium was performed using the Confusion Assessment Method for the ICU tool. The levels of C-C motif ligand 2 (CCL2), C-C motif ligand 3, C-X-C motif chemokine ligand 1, C-X-C motif chemokine ligand 10, and interleukin-8 were measured in serum samples obtained within 12 hours of ICU admission. Univariate and multivariate analyses were performed to assess the association of delirium with patient data pertaining to hospital course, laboratory values, vital signs, medication administration, and levels of the aforementioned chemokines. Forty-one of 119 patients (34.5%) in the study cohort developed ICU delirium. Each chemokine studied was associated with delirium on univariate analyses; however, CCL2 was the only chemokine found to be independently associated with the development of delirium on multivariable analysis. The association of increased CCL2 levels with delirium remained robust in various models controlling for age, presence of shock, Sequential Organ Failure Assessment score, Acute Physiology and Chronic Health Evaluation IV score, mean arterial pressure at presentation, lowest mean arterial pressure, and total opioid, midazolam, propofol, and dexmedetomidine exposure.
CONCLUSIONS:
The demonstrated relationship between CCL2 and delirium suggests this chemokine may play a role in the development of delirium and warrants further investigation.
“…When patients required readmission to the ICU after discharge, only data from the first admission were analyzed. We used the Third International Consensus Definition (Sepsis-3) ( 18 ) and the Society for Cardiovascular Angiography and Interventions ( 19 ) shock stages C, D, and E to define both septic shock and cardiogenic shock, respectively. For the purposes of this study, we define shock to include both of the aforementioned definitions of septic shock and cardiogenic shock; no patients in our study suffered from hypovolemic or obstructive shock.…”
OBJECTIVES:
The pathophysiology of delirium is complex and incompletely understood. Inflammation is hypothesized to be integral to its development due to effects on blood brain barrier integrity, facilitation of leukocyte extravasation into brain parenchyma, and propagation of neuroinflammation. Septic shock is the prototypical condition associated with ICU delirium; however, the relative contribution of resultant hypotension and systemic inflammation to the development of delirium is unknown.
DESIGN:
This was a prospective exploratory study.
SETTING:
A multidisciplinary ICU at an academic medical center in Phoenix, AZ.
PATIENTS:
Critically ill patients older than or equal to 18 years old admitted to the ICU.
INTERVENTIONS:
None.
MEASUREMENTS AND MAIN RESULTS:
Screening for delirium was performed using the Confusion Assessment Method for the ICU tool. The levels of C-C motif ligand 2 (CCL2), C-C motif ligand 3, C-X-C motif chemokine ligand 1, C-X-C motif chemokine ligand 10, and interleukin-8 were measured in serum samples obtained within 12 hours of ICU admission. Univariate and multivariate analyses were performed to assess the association of delirium with patient data pertaining to hospital course, laboratory values, vital signs, medication administration, and levels of the aforementioned chemokines. Forty-one of 119 patients (34.5%) in the study cohort developed ICU delirium. Each chemokine studied was associated with delirium on univariate analyses; however, CCL2 was the only chemokine found to be independently associated with the development of delirium on multivariable analysis. The association of increased CCL2 levels with delirium remained robust in various models controlling for age, presence of shock, Sequential Organ Failure Assessment score, Acute Physiology and Chronic Health Evaluation IV score, mean arterial pressure at presentation, lowest mean arterial pressure, and total opioid, midazolam, propofol, and dexmedetomidine exposure.
CONCLUSIONS:
The demonstrated relationship between CCL2 and delirium suggests this chemokine may play a role in the development of delirium and warrants further investigation.
“…2 The latter statement, which still holds true today, underscores the critical importance of ongoing work such as the SCAI SHOCK Clinical Expert Consensus Update. 3 On the path to modern CS care, several notable historic milestones provide context for points specifically highlighted in the current consensus document. In 1942, Drs Stead and Ebert detailed 2 distinct phenotypes of a "shock syndrome produced by failure of the heart" using clinical, radiographic, and laboratory data.…”
mentioning
confidence: 99%
“…9 As the number of CS registries and RCTs grew, so too did variability in reported survival, ascribable in part to unquantified differences in baseline severity of illness, i.e., the proportion of patients who were already in extremis at the time of study entry. 1,3 Twenty years later and 107 years after the first credible description of CS, the 2019 SCAI clinical expert consensus statement on the classification of CS codified CS diagnosis and risk stratification, quickly gaining multisociety endorsement as well as wide recognition by clinicians. 10 In this inaugural issue of the Journal of the Society for Cardiovascular Angiography and Interventions (JSCAI), Naidu SS, on behalf of the SCAI SHOCK Writing Group, presents the revised SCAI SHOCK Stages Classification Clinical Expert Consensus Update.…”
mentioning
confidence: 99%
“…Table 3 of the revised schema offers much-needed guidance for improving the precision of CS staging, vis-a-vis numerical cutoff values, categories broken down by typical clinical features, and therapy-based criteria to judge transitions between stages. 3 Despite this, it should be recognized that many aspects of CS staging still entail some degree of subjectivity and thus may result in variable staging, even within a given center. Similarly, timing and implementation of therapies that follow staging, such as mechanical circulatory support (MCS), are highly variable and will impact how the recovery/deterioration pathways outlined in Figure 5 are applied within a given system of care.…”
mentioning
confidence: 99%
“…Similarly, timing and implementation of therapies that follow staging, such as mechanical circulatory support (MCS), are highly variable and will impact how the recovery/deterioration pathways outlined in Figure 5 are applied within a given system of care. 3 Greater visual clarity is given to the SCAI SHOCK pyramid figure (Figure 4), now depicted in gradations of color to reflect increasing severity within each stage. The inherent heterogeneity of cardiac arrest (CA) is acknowledged, and accordingly, the "A" modifier is now designated only for patients with CA with suspected anoxic brain injury.…”
A novel haemodynamic metric—CPO ratio—measure the capacity of native heart recovery after PVAD in cardiogenic shock and may outperform absolute CPO value and other parameters!
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