Diagnosis of adrenal failure in critically ill patients

Moraes, Rafael Barberena; Czepielewski, Mauro Antônio; Friedman, Gilberto; Borba, Evandro Lucas de

doi:10.1590/s0004-27302011000500001

Cited by 15 publications

(17 citation statements)

References 37 publications

(42 reference statements)

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“…Because ACTH-cortisol responses did not predict outcome independently of disease severity, a low cortisol response to ACTH may be a marker rather than a mediator of severe disease and associated mortality. (2,28) This result suggests that abnormal cortisol levels lack attributable mortality but may be a sign of severe disease. Although the overall disease severity and mortality were similar in our study and that of Annane et al., (26) our findings are in contrast to the results of that study and those of other reports, which demonstrated that increased cortisol values contributed to mortality prediction independently of disease severity.…”

Section: Discussionmentioning

confidence: 94%

“…(1,2) Blunted adrenal corticosteroid production during critical illness, particularly septic shock, has been termed relative adrenal insufficiency (RAI) or critical illness-related corticosteroid insufficiency (CIRCI). During CIRCI, cortisol serum levels are considered insufficient for the degree of stress (even when supranormal), as manifested by a poor response to additional stimuli.…”

Section: Introductionmentioning

confidence: 99%

“…(4-15) However, it is unknown whether ACTH-cortisol responses in severe sepsis and septic shock are caused by or contribute to critical illness and, thus, have a marker or mediator role in regard to mortality. (2) …”

Section: Introductionmentioning

confidence: 99%

“…(2,16,17) Baseline cortisol levels alone could also be used to help identify CIRCI; however, no trials could identify a baseline cortisol cutoff point that could be used to diagnose CIRCI or guide therapy. (2,18,19) In the course of severe disease, low levels of cortisol-binding proteins and hypoalbuminemia may lower total cortisol levels and responses to ACTH independently of free cortisol levels and in the absence of CIRCI. (20-22) However, the measurement of free cortisol (biologically active) in serum or saliva is not widely available and requires further studies in critical care patients.…”

Section: Introductionmentioning

confidence: 99%

“…(20-22) However, the measurement of free cortisol (biologically active) in serum or saliva is not widely available and requires further studies in critical care patients. (2,13) Instead, the cortisol/albumin ratio has been used to estimate free cortisol because albumin binds cortisol, although to a lesser extent than cortisol-binding globulin (CBG). Both albumin and CBG levels may decrease to the same extent in critical illness.…”

Section: Introductionmentioning

confidence: 99%

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Insuficiência adrenal relativa como preditora de gravidade de doença e mortalidade do choque séptico

Dalegrave¹,

Silva²,

Becker³

et al. 2012

Rev. bras. ter. intensiva

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ObjectiveTo evaluate if cortisol responses to 250 µg of intravenously administered adrenocorticotropic hormone are related to disease severity and, hence, mortality. MethodsThis is a retrospective study in a medical-surgical intensive care unit of a university hospital. We studied 69 consecutive patients with septic shock over a 1-yr period; these patients underwent a short 250-µg adrenocorticotropic hormone test because they exhibited >6 hours of progressive hemodynamic instability requiring repeated fluid challenges and vasopressor treatment to maintain blood pressure. The test was performed by intravenously injecting 250 µg of synthetic adrenocorticotropic hormone and measuring cortisol immediately before injection, 30 minutes post-injection and 60 minutes post-injection. ResultsThe mean APACHE II score was 22±7. The intensive care unit mortality rate at day 28 was 55%. Median baseline cortisol levels (19 [11-27] µg/dL versus 24 [18-34] µg/dL, p=0.047) and median baseline cortisol/albumin ratios (7.6 [4.6-12.3] versus 13.9 [8.8-18.5]; p=0.01) were lower in survivors than in non-survivors. Responders and non-responders had similar baseline clinical data and outcomes. The variables that were significantly correlated with outcome based on the area under the ROC curves (AUC) were APACHE II (AUC=0.67 [0.535 to 0.781]), baseline cortisol (µg/dl) (AUC=0.662 [0.536 to 0.773], peak cortisol (µg/dl) (AUC=0.642 [0.515 to 0.755]) and baseline cortisol/albumin (AUC=0.75 [0.621 to 0.849]). ConclusionsIncreased basal cortisol is associated with mortality and disease severity. Cortisol responses upon adrenocorticotropic hormone stimulation were not related to outcome. The cortisol/albumin ratio does not predict unfavorable outcomes better than total cortisol levels or help to improve the accuracy of the adrenocorticotropic hormone test.

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Section: Discussionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Insuficiência adrenal relativa como preditora de gravidade de doença e mortalidade do choque séptico

Dalegrave¹,

Silva²,

Becker³

et al. 2012

Rev. bras. ter. intensiva

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Acute Inflammation and Metabolism

et al. 2018

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Inflammation is an adaptive process to the noxious stimuli that the human body is constantly exposed to. From the local inflammatory response to a full-blown systemic inflammation, a wide complex sequence of events occurs. Persistent immunosuppression and catabolism may ensue, until multiple organ failure finally sets in. And since clinically useful and specific biomarkers are lacking, diagnosis may come late. A thorough understanding of these events (how they begin, how they evolve, and how to modulate them) is imperative, but as yet poorly studied. This review aims to consolidate current knowledge of these events so that the management of these patients is not only evidence-based, but also built on an understanding of the inner workings of the human body in health and in disease.

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Endocrine changes after pediatric traumatic brain injury

Rose

Auble

2011

Pituitary

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Traumatic brain injury (TBI) is a very common occurrence in childhood, and can lead to devastating long term consequences. Recent research has focused on the potential endocrine consequences of TBI in adults. The research in children is less robust. This paper reviews current literature regarding TBI and possible hypothalamic and pituitary deficiencies in childhood. Acute endocrine changes are commonly found after TBI in pediatric patients, which can include changes in hypothalamic-pituitary-adrenal axis and antidiuretic hormone production and release. In the long term, both temporary and permanent alterations in pituitary function have been found. About 30% of children have hypopituitarism up to 5 years after injury. Growth hormone deficiency and disturbances in puberty are the most common, but children can also experience ACTH deficiency, diabetes insipidus, central hypothyroidism, and elevated prolactin. Every hormonal axis can be affected after TBI in children, although growth hormone deficiency and alterations in puberty are the most common. Because transient and permanent hypopituitarism is common after TBI, survivors should be screened serially for possible endocrine disturbances. These children should undergo routine surveillance at least 1 year after injury to ensure early detection of deficiencies in hormonal production in order to permit normal growth and development.

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Diagnosis of adrenal failure in critically ill patients

Cited by 15 publications

References 37 publications

Insuficiência adrenal relativa como preditora de gravidade de doença e mortalidade do choque séptico

Insuficiência adrenal relativa como preditora de gravidade de doença e mortalidade do choque séptico

Acute Inflammation and Metabolism

Endocrine changes after pediatric traumatic brain injury

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