Adrenal Insufficiency in the Surgical Intensive Care Unit Patient

Barquist, Erik; Kirton, Orlando C.

doi:10.1097/00005373-199701000-00006

Cited by 128 publications

(73 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In contrast, other authors have reported significantly higher rates of insufficient adrenal response in critical illness (12) especially in those with a prolonged stay in ICU, and in those over 55 years of age (13)(14)(15). In view of such conflicting published data, we performed a prospective study to investigate the immediate impact of major surgery on the tests used to diagnose adrenal insufficiency.…”

Section: Introductionmentioning

confidence: 92%

Assessing adrenal status in patients before and immediately after coronary artery bypass graft surgery

Debono¹,

Sheppard²,

Irving³

et al. 2011

European Journal of Endocrinology

View full text Add to dashboard Cite

Objective: Patients with cortisol deficiency poorly tolerate any systemic inflammatory response syndrome (SIRS), and may die if not treated with sufficient exogenous glucocorticoids. Controversy surrounds what constitutes a 'normal' adrenal response in critical illness. This study uses conventional tests for adrenal insufficiency to investigate cortisol status in patients undergoing elective coronary artery bypass surgery, a condition frequently associated with SIRS. Design: A prospective, observational study. Methods: Thirty patients with impaired left ventricular function (ejection fraction O23% !50%) underwent basal ACTH measurement, and a short cosyntropin test (250 mg, i.v.) 1 week preoperatively, and at C4 h following induction of general anaesthesia. Preoperatively, a 30 min cortisol level post cosyntropin O550 nmol/l was taken as a normal response. Results: Prior to surgery, all patients had a normal response to cosyntropin. Postoperatively, eight patients (26.7%) did not achieve stimulated cortisol levels O550 nmol/l and the mean peak cortisol postoperatively was lower (1048 vs 730 nmol/l; P!0.001). There was a significant rise in ACTH after surgery (21 vs 184 ng/l; PZ0.007) and reduction in D-cortisol post cosyntropin (579 vs 229 nmol/l; P!0.001). There was no change in basal cortisol pre-and post-operatively (447 vs 501; PZ0.4). All patients underwent routine, uneventful postoperative recovery. Conclusion: Up to one quarter of patients with a normal cortisol status preoperatively demonstrated a raised ACTH and deficient cortisol response postoperatively. Despite these responses, all patients had uneventful outcomes. These data reinforce the need for caution when interpreting results of endocrine testing following major surgery or in the intensive care environment, and that prognostic value of these results may be of limited use.

show abstract

Section: Introductionmentioning

confidence: 92%

Assessing adrenal status in patients before and immediately after coronary artery bypass graft surgery

Debono¹,

Sheppard²,

Irving³

et al. 2011

European Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…This constellation of effects suggests a shift of pregnenolone metabolism away from both mineralocorticoid and adrenal androgen pathways toward the glucocorticoid pathway, orchestrated by an unknown peripheral driving force. Ultimately, the latter mechanism may also fail, as indicated by a 20-fold higher incidence of adrenal insuf®ciency in critically ill patients over the age of 50 years and being treated on the intensive care unit for more than 14 days (89). The fact that this type of relative adrenal failure coincides with adverse outcomes suggests that high levels of glucocorticoids remain essential for hemodynamic stability.…”

Section: Pituitary±adrenal Axismentioning

confidence: 99%

Novel insights into the neuroendocrinology of critical illness

Berghe

2000

European Journal of Endocrinology

226

104

View full text Add to dashboard Cite

An unexplained hallmark of prolonged critical illness is the fact that food does not prevent or reverse protein wasting, while fat is paradoxically accrued. This`wasting syndrome' often persists after the underlying disease has been resolved and thus perpetuates intensive care dependency. Although the crucial role of an intact hypothalamus±pituitary axis for homeostasis during stress is well recognized, the differences between the neuroendocrine changes observed in acute and prolonged critical illness were only recently described. Novel insights in this area are reviewed here.The initial endocrine stress response consists primarily of a peripheral inactivation of anabolic pathways while pituitary activity is essentially ampli®ed or maintained. These responses presumably provide the metabolic substrates and host defense required for survival and to delay anabolism, and thus should be considered as adaptive and bene®cial. Persistence of this acute stress response throughout the course of critical illness was hitherto assumed. This assumption has now been invalidated, since a uniformly reduced pulsatile secretion of ACTH, TSH, LH, prolactin (PRL) and GH has been observed in protracted critical illness, causing diminished stimulation of several target organs. Impaired pulsatile secretion of anterior pituitary hormones in the chronic phase of critical illness seems to have a hypothalamic rather than a pituitary origin, as administration of relevant releasing factors evoked immediate and pronounced pituitary hormone release. A reduced availability of TRH, one of the endogenous ligands of the GH-releasing peptide (GHRP) receptor (such as the recently discovered ghrelin) and, in very long-stay critically ill men, also of GHRH, appear to be involved. This hypothesis was further explored by investigating the effects of continuous i.v. infusion of GHRH, GHRP, TRH and their combinations for several days. Pulsatile secretion of GH, TSH and PRL was re-ampli®ed by relevant combinations of releasing factors which also substantially increased circulating levels of IGF-I, GH-dependent binding proteins, thyroxine and tri-iodothyronine (T3) while avoiding a rise in reverse T3. Active feedback-inhibition loops prevented overstimulation of target organs and metabolic improvement was noted with the combined infusion of GHRP and TRH. Whether this novel endocrine strategy will also enhance clinical recovery from critical illness remains to be explored.

show abstract

“…88 Such risk of adrenal atrophy in prolonged ICU stay-patients also helps to explain the reported 20-fold higher incidence of symptomatic adrenal insufficiency in critically ill patients being treated in the intensive care unit for more than 14 days. 89 It remains to be investigated whether CRH or ACTH could offer a potential to prevent or treat adrenal failure in the prolonged phase of critical illness 90 .…”

Section: The Pituitary-adrenocortical Axis In the Acute Phase Of Critmentioning

confidence: 99%

On the Neuroendocrinopathy of Critical Illness. Perspectives for Feeding and Novel Treatments

Berghe

2016

Am J Respir Crit Care Med

View full text Add to dashboard Cite

Adrenal Insufficiency in the Surgical Intensive Care Unit Patient

Abstract: Screening of critically ill patients for adrenal insufficiency, particularly those with prolonged ICU stay and age greater than 55 years, is warranted.

Cited by 128 publications

References 11 publications

Assessing adrenal status in patients before and immediately after coronary artery bypass graft surgery

Assessing adrenal status in patients before and immediately after coronary artery bypass graft surgery

Novel insights into the neuroendocrinology of critical illness

On the Neuroendocrinopathy of Critical Illness. Perspectives for Feeding and Novel Treatments

Contact Info

Product

Resources

About