Acute and Prolonged Critical Illness as Different Neuroendocrine Paradigms 1

Langouche

2019

Endocrine Connections

Self Cite

Critical illness is hallmarked by major changes in all hypothalamic–pituitary–peripheral hormonal axes. Extensive animal and human studies have identified a biphasic pattern in circulating pituitary and peripheral hormone levels throughout critical illness by analogy with the fasting state. In the acute phase of critical illness, following a deleterious event, rapid neuroendocrine changes try to direct the human body toward a catabolic state to ensure provision of elementary energy sources, whereas costly anabolic processes are postponed. Thanks to new technologies and improvements in critical care, the majority of patients survive the acute insult and recover within a week. However, an important part of patients admitted to the ICU fail to recover sufficiently, and a prolonged phase of critical illness sets in. This prolonged phase of critical illness is characterized by a uniform suppression of the hypothalamic–pituitary–peripheral hormonal axes. Whereas the alterations in hormonal levels during the first hours and days after the onset of critical illness are evolutionary selected and are likely beneficial for survival, endocrine changes in prolonged critically ill patients could be harmful and may hamper recovery. Most studies investigating the substitution of peripheral hormones or strategies to overcome resistance to anabolic stimuli failed to show benefit for morbidity and mortality. Research on treatment with selected and combined hypothalamic hormones has shown promising results. Well-controlled RCTs to corroborate these findings are needed.

Section: The Five Main Neuroendocrine Axesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Anterior pituitary function in critical illness

Langouche

2019

Endocrine Connections

Self Cite

“…After OHCA and subsequent successful cardiopulmonary resuscitation, a condition called postcardiac arrest syndrome develops, and in the intensive care unit, SIH is encountered [15,16]. The degree of metabolic disturbance is a combination of two factors: the extent of ischemic injury and the quality of postresuscitation care [1].…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of early glucose regulation disturbance after out-of-hospital cardiopulmonary resuscitation: An explorative prospective study

et al. 2019

BackgroundHyperglycemia is common and associated with increased mortality after out-of-hospital cardiac arrest (OHCA) and return of spontaneous circulation (ROSC). Mechanisms behind ultra-acute hyperglycemia are not well known. We performed an explorative study to describe the changes in glucose metabolism mediators during the prehospital postresuscitation phase.MethodsWe included patients who were successfully resuscitated from out-of-hospital cardiac arrest in two physician-staffed units. Insulin, glucagon, and glucagon-like peptide 1 (GLP-1) were measured in prehospital and hospital admission samples. Additionally, interleukin-6 (IL-6), cortisol, and HbA1c were measured at hospital admission.ResultsThirty patients participated in the study. Of those, 28 cases (71% without diabetes) had sufficient data for analysis. The median time interval between prehospital samples and hospital admission samples was 96 minutes (IQR 85–119). At the time of ROSC, the patients were hyperglycemic (11.2 mmol/l, IQR 8.8–15.7), with insulin and glucagon concentrations varying considerably, although mostly corresponding to fasting levels (10.1 mU/l, IQR 4.2–25.2 and 141 ng/l, IQR 105–240, respectively). GLP-1 increased 2- to 8-fold with elevation of IL-6. The median glucose change from prehospital to hospital admission was -2.2 mmol/l (IQR -3.6 to -0.2). No significant correlations between the change in plasma glucose levels and the changes in insulin (r = 0.30, p = 0.13), glucagon (r = 0.29, p = 0.17), or GLP-1 levels (r = 0.32, p = 0.15) or with IL-6 (r = (-0.07), p = 0.75), cortisol (r = 0.13, p = 0.52) or HbA1c levels (r = 0.34, p = 0.08) were observed. However, in patients who did not receive exogenous epinephrine during resuscitation, changes in blood glucose correlated with changes in insulin (r = 0.59, p = 0.04) and glucagon (r = 0.65, p = 0.05) levels, demonstrating that lowering glucose values was associated with a simultaneous lowering of insulin and glucagon levels.ConclusionsHyperglycemia is common immediately after OHCA and cardiopulmonary resuscitation. No clear hormonal mechanisms were observed to be linked to changes in glucose levels during the postresuscitation phase in the whole cohort. However, in patients without exogenous epinephrine treatment, the correlations between glycemic and hormonal changes were more obvious. These results call for future studies examining the mechanisms of postresuscitation hyperglycemia and the metabolic effects of the global ischemic insult and medical treatment.

“…It is not clear whether, in the setting of critical illness, these changes are beneficial and promote recovery and are therefore adaptive, or if they are rather a direct result or cause of the illness and associated organ failures and are therefore maladaptive [1][2][3][4]. Other neuroendocrine changes involving other hypothalamic-pituitary axes can also occur in the setting of critical illness.…”

Section: Introductionmentioning

confidence: 99%

Nonthyroidal illness syndrome in children

Marks

2009

Endocr

Neuroendocrine changes in the hypothalamic-pituitary-thyroid axis during critical illness result in nonthyroidal illness syndrome (NTIS) characterized by abnormal thyrotropin (TSH) and thyroid hormone levels. Studies looking at the natural history of neuroendocrine changes during critical illness have revealed the presence of NTIS. NTIS has been described in a variety of patient settings. Many studies have tried to uncover the pathophysiology behind NTIS and several theories are proposed. Whether NTIS requires treatment or intervention is still controversial and the results of the treatment studies are arguably mixed. Whether implicitly stated or not, the underlying purpose of all the natural history, pathophysiology, or treatment studies is to determine whether NTIS is adaptive or maladaptive. Some studies have illustrated a correlation between illness severity and the degree of NTIS but a cause and effect relationship is still elusive. The human studies can be divided between those with either adult or pediatric subjects, with much less data available in the latter. This review examines the available literature on NTIS with an emphasis on the pediatric literature.