Adrenocortical function during septic shock

Bouachour, G.; Tirot, P.; Gouëllo, J. P.; Mathieu, Éric; Vincent, J.-F.; Alquier, P

doi:10.1007/bf02425155

Cited by 158 publications

(107 citation statements)

References 34 publications

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“…Cytokine release and metabolic derangements in critical illness can also impair cortisol inactivation (19,39) and clearance from the circulation (35). Consistent with other reports (15,54), early peak cortisol and ACTH levels did not correlate with survival in the present study, suggesting that the acute phase of the HPA axis response to septic shock is not very sensitive to disease severity or eventual outcome. However, time to recovery of the HPA axis toward an unstressed state did reflect severity.…”

Section: Discussionsupporting

confidence: 87%

“…Serial evaluations were critical to understanding the evolution of HPA axis dysfunction over the course of severe sepsis. In patients with septic shock, Bouachour et al (15) similarly found that cortisol levels were elevated acutely in survivors and nonsurvivors alike and that nonsurvivors maintained persistently elevated levels over time. In canines with parvoviral diarrhea, Schoeman et al (54) found, similar to our model of experimental pneumonia, that on admission, survivors and nonsurvivors had similarly elevated cortisol levels, but by 24 h, cortisol was significantly higher among animals that eventually died from the infection.…”

Section: Discussionmentioning

confidence: 99%

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Hypothalamic-pituitary-adrenal axis in lethal canine Staphylococcus aureus pneumonia

Cortés‐Puch

Hicks

Sun

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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The clinical significance and even existence of critical illness-related corticosteroid insufficiency is controversial. Here, hypothalamic-pituitary-adrenal (HPA) function was characterized in severe canine Staphylococcus aureus pneumonia. Animals received antibiotics and titrated life-supportive measures. Treatment with dexamethasone, a glucocorticoid, but not desoxycorticosterone, a mineralocorticoid, improves outcome in this model. Total and free cortisol, adrenocorticotropic hormone (ACTH). and aldosterone levels, as well as responses to exogenous ACTH were measured serially. At 10 h after the onset of infection, the acute HPA axis stress response, as measured by cortisol levels, exceeded that seen with high-dose ACTH stimulation but was not predictive of outcome. In contrast to cortisol, aldosterone was largely autonomous from HPA axis control, elevated longer, and more closely associated with survival in early septic shock. Importantly, dexamethasone suppressed cortisol and ACTH levels and restored ACTH responsiveness in survivors. Differing strikingly, nonsurvivors, sepsis-induced hypercortisolemia, and high ACTH levels as well as ACTH hyporesponsiveness were not influenced by dexamethasone. During septic shock, only serial measurements and provocative testing over a well-defined timeline were able to demonstrate a strong relationship between HPA axis function and prognosis. HPA axis unresponsiveness and high aldosterone levels identify a septic shock subpopulation with poor outcomes that may have the greatest potential to benefit from new therapies. septic shock; sepsis; corticosteroids; adrenal insufficiency; cortisol; adrenocorticotropic hormone; aldosterone "RELATIVE ADRENAL DEFICIENCY" in critically ill patients with otherwise normal hypothalamic-pituitary-adrenal (HPA) function was recently renamed "critical illness-related corticosteroid insufficiency" (CIRCI) (33). However, there are no widely accepted criteria for the diagnosis and treatment of this hypothetical condition (40,41,57,58). No test of HPA function reliably predicts outcome, and the relative importance of endogenous glucocorticoid (cortisol) vs. mineralocorticoid (aldosterone) activity to survival is not known. Importantly, patient selection for corticosteroid therapy in sepsis has varied in clinical practice and across randomized trials, in which benefit has not been reproducible (4,40,41,57).To date, HPA testing in patients with septic shock has focused primarily on criteria for inadequate cortisol production using both random cortisol levels and adrenocorticotropic hormone (ACTH)-stimulated adrenal responsiveness. However, both low and high cortisol levels have been associated with worst outcomes (5, 23, 39, 52). Total cortisol increases of less than 9 g/dl in response to high-dose ACTH (250 g) (5) or a random total cortisol below an arbitrary cutoff (e.g., Ͻ10 to Ͻ25 g/dl) (6,20,23,(33)(34)(35) have been proposed to define CIRCI (33). However, neither high-nor low-dose (1 g) ACTH stimulation testing has been shown to identify sept...

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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Hypothalamic-pituitary-adrenal axis in lethal canine Staphylococcus aureus pneumonia

Cortés‐Puch

Hicks

Sun

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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“…The incidence of adrenal insufficiency increases with the severity of the illness, and the reported incidence averages 25-40% in septic shock patients. [251][252][253] Adrenal insufficiency during septic shock develops in many patients and resolves when the patient recovers. These observations suggest that mediators released during septic shock impair function of the HPA axis.…”

Section: Hpa (Dys)function In Human Sepsismentioning

confidence: 99%

Review: Endotoxin and the hypothalamo-pituitary-adrenal (HPA) axis

Beishuizen

Thijs

2003

Journal of Endotoxin Research

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Endotoxin is considered to be a systemic (immunological) stressor eliciting a prolonged activation of the hypothalamo-pituitary-adrenal (HPA) axis. The HPA-axis response after an endotoxin challenge is mainly due to released cytokines (IL-1, IL-6 and TNF-a) from stimulated peripheral immune cells, which in turn stimulate different levels of the HPA axis. Controversy exists regarding the main locus of action of endotoxin on glucocorticoid secretion, since the effect of endotoxin on this neuro-endocrine axis has been observed in intact animals and after ablation of the hypothalamus; however, a lack of LPS effect has been described at both pituitary and adrenocortical levels. The resulting increase in adrenal glucocorticoids has well-documented inhibitory effects on the inflammatory process and on inflammatory cytokine release. Therefore, immune activation of the adrenal gland by endotoxin is thought to occur by cytokine stimulation of corticosteroidreleasing hormone (CRH) production in the median eminence of the hypothalamus, which, in turn stimulates the secretion of ACTH from the pituitary. Acute administration of endotoxin stimulates ACTH and cortisol secretion and the release of CRH and vasopressin (AVP) in the hypophysial portal blood. During repeated endotoxemia, tolerance of both immune and HPA function develops, with a crucial role for glucocorticoids in the modulation of the HPA axis. A single exposure to a high dose of LPS can induce a long-lasting state of tolerance to a second exposure of LPS, affecting the response of plasma TNF-a and HPA hormones. Although there are gender differences in the HPA response to endotoxin and IL-1, these responses are enhanced by castration and attenuated by androgen and estrogen replacement. Estrogens attenuate the endotoxin-induced stimulation of IL-6, TNF-a and IL-1ra release and subsequent activation in postmenopausal women. There appears to be a temporal and functional relation between the HPA-axis response to endotoxin and nitric oxide formation in the neuro-endocrine hypothalamus, suggesting a stimulatory role for nitric oxide in modulating the HPA response to immune challenges. demonstrate higher plasma levels of IL-1 and TNF-a. Elevation of plasma glucocorticoids results in suppression of cytokines such as IL-1, IL-6, and TNF-a and in up-regulation of other cytokines, such as IL-4 and IL-10, and cytokine receptors. Thus, by regulation of cytokine production and action, the HPA axis contributes to modulation of the response to inflammation/infection. In addition, the role of HPA activation has been suggested to be a negative feedback system provided by the immunosuppressive activity of glucocorticoids, limiting inflammatory responses and preventing the immune system from over-reacting and causing tissue damage or autoimmunity.As early as 1957, Wexler et al. suggested that LPS could induce ACTH release since they found a depletion of ascorbic acid and cholesterol in the adrenal glands. 10 Moreover, LPS was not able to cause these changes in hypophysectomized rats. ...

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“…15 In serious cases, as stated above, an increase in serum cortisol levels is to be expected, particularly when there is sepsis and septic shock. 13,22 Specifically with these patients this response is not only due to physical stress, but also to the liberation of cytokines into the plasma, by immune cells, during the inflammatory process. 15 The three main cytokines involved are tumor necrosis factor a, interleukin-1 and interleukin-6, contribute significantly to stimulate the hypothalamus-pituitary-adrenal axis, both synergistically and independently.…”

Section: The Hypothalamus Pituitary Adrenal Axis and Cortisol Secretionmentioning

confidence: 99%

“…The incidence of adrenal insufficiency reported in literature for patients in septic shock, suffers from a strong influence from the criteria adopted to define the diagnosis oscillating from 17% to 54%. 12,14,16,18,19,22 With respect of adults work proliferates on adrenal insufficiency in severe cases, particularly sepsis patients. Work by Annane et al 12 performed at an intensive care unit in France merits prominence as does work by Marik and Zaloga 26 carried out in Washington.…”

Section: Criteria Used To Define Adrenal Insufficiencymentioning

confidence: 99%

Insuficiência adrenal na criança com choque séptico

Casartelli¹,

García²,

Piva³

et al. 2003

J. Pediatr. (Rio J.)

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Objective: To review the criteria for diagnosing and treating adrenal insufficiency in patients with septic shock. Sources of data:Articles published in Brazilian and foreign journals selected through these publications' websites and Medline, as well as references cited in key articles Summary of the findings:The literature reports a range betwen 17 and 54 % for the finding of adrenal insufficiency in patients with septic shock. There is no consensus for diagnosing adrenal insufficiency in patients suffering from critical diseases, particularly in patients with septic shock. The presence of volumerefractory and catecholamine-resistant septic shock suggests this condition, while basal cortisol under 25 µg/dl is a diagnostic criterion indicating adrenal insufficiency. The adrenal stimulation test is a useful resource for identifying patients with relative adrenal insufficiency. Our testing option for adrenal stimulation in children is the use of corticotropin in low doses (0.5 µg/1,73 m²). An increase of less than 9 µg/dl in the value of postcorticotropin-stimulated cortisol suggests the presence of occult (relative) adrenal insufficiency. In patients with septic shock presenting adrenal insufficiency, either suspected or confirmed, the administration of hydrocortisone in shock or stress doses can be vital for a favorable clinical outcome. Conclusions:The existing data, although controversial, already provides a basis to determine when to begin hormone replacement therapy, the serum level of cortisol accepted as adequate, and the choice of corticotropin doses for performing the adrenal stimulation test and diagnosing occult or relative adrenal insufficiency in patients with septic shock. J Pediatr (Rio J) 2003;79(Suppl 2):S169-S76: Sepsis, septic shock, adrenal cortex, adrenal gland hypofunction, glucocorticoids, adrenal cortex function tests.

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Adrenocortical function during septic shock

Cited by 158 publications

References 34 publications

Hypothalamic-pituitary-adrenal axis in lethal canine Staphylococcus aureus pneumonia

Hypothalamic-pituitary-adrenal axis in lethal canine Staphylococcus aureus pneumonia

Review: Endotoxin and the hypothalamo-pituitary-adrenal (HPA) axis

Insuficiência adrenal na criança com choque séptico

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