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Pediatric ICU management
Published in David E. Wesson, Bindi Naik-Mathuria, Pediatric Trauma, 2017
Jason O. Robertson, Adam M. Vogel
During periods of significant stress, cortisol levels are increased through activation of the hypothalamic–pituitary–adrenal (HPA) axis in order to maintain homeostasis. Cortisol increases the availability of energy substrates; maintains cardiovascular tone, endothelial integrity, and distribution of fluids within the vascular compartments; potentiates vasoconstriction; and counteracts the inflammatory cascade modulating immune responses [28]. Despite the fact that many critically ill patients have elevated plasma cortisol concentrations, these levels often reflect production that is inadequate to meet the body’s increased demand. This “functional” or “relative” adrenal insufficiency is termed critical illness-related corticosteroid insufficiency (CIRCI) and may result from a decrease in adrenal steroid production, tissue resistance to glucocorticoids, or structural damage to the adrenal gland, hypothalamus, or pituitary gland from either hemorrhage or infarction. Secondary adrenal insufficiency may also occur following long-term therapy with exogenous glucocorticoids. While reported prevalence varies by population, rates as high as 60%–90% have been seen in patients with septic shock, and a large multicenter, prospective study of critically ill children (comprising trauma, sepsis, and surgery) identified an incidence of adrenal insufficiency of 30% [28, 29]. When there is no structural damage to the HPA axis, CIRCI is reversible in most patients. In the pediatric population, there is some disagreement on diagnostic criteria, although delay in diagnosis and treatment may be fatal.
Insights into the possible impact of COVID-19 on the endocrine system
Published in Archives of Physiology and Biochemistry, 2023
Adel Abdel-Moneim, Ahmed Hosni
Importantly, lymphopenia, seen in about 50% of previous coronavirus patients, was associated with elevated serum cortisol levels (Panesar et al.2004). Therefore, the absence of lymphopenia in patients with COVID-19 may be used as a hypocortisolism marker and a low threshold should be maintained for starting glucocorticoid therapy in case of shock or ARDS (Pal 2020). Furthermore, the administration of glucocorticoids has been used extensively in the management of most severely ill COVID-19 patients. In addition, because glucocorticoids have anti-inflammatory, immune-suppressive, and antiproliferative properties, their use must be justified in critical illness-related corticosteroid insufficiency. On the other hand, long-term glucocorticoid administration can induce Cushing syndrome signs or dysfunction of the HPA axis (Ferraù et al.2020).
The role of steroids in severe CAP
Published in Hospital Practice, 2020
David Nora, Wagner Nedel, Thiago Lisboa, Jorge Salluh, Pedro Póvoa
The first data on the use of corticosteroids in pneumonia is from 1940. Perla et al. [45] described shorter recovery times and no circulatory collapse in 17 pneumonia patients treated with adrenal cortical extracts but without antibiotic therapy. The concept of critical illness-related corticosteroid insufficiency [46] (CIRCI) has boosted the emergence of several clinical trials on steroids as adjuncts in CAP treatment. Significant effects were found in patients treated with steroids: improvement in PaO2/FiO2 ratio [47], faster resolution of fever [48], faster radiological improvement [48,49], shorter time to nonspecific clinical stability, shorter length of stay (LOS) [49–51] and lower plasmatic [52,53] and bronchoalveolar lavage (BAL) fluid levels of inflammatory mediators [54,55]. In patients with CAP and shock, both hydrocortisone alone [52] or in combination with fludrocortisone, as studied by Annane et al. [56]. improved hemodynamic parameters and shortened the time under vasopressor therapy.
Pharmacological management of sepsis in adults with a focus on the current gold standard treatments and promising adjunctive strategies: evidence from the last five years
Published in Expert Opinion on Pharmacotherapy, 2019
Evdoxia Kyriazopoulou, Evangelos J. Giamarellos-Bourboulis
Critically ill patients undergo endocrine changes affecting the pituitary axis. Cortisol is overproduced under stress and during sepsis its biological breakdown is excessively diminished due to reduction in the activity of the appropriate kidney and liver reductases. Both mechanisms lead to high levels of cortisol disproportionately to the ACTH levels, a phenomenon called ‘ACTH-cortisol dissociation’. Despite the high cortisol levels, a resistance to its action is described in sepsis referred to as ‘relative adrenal insufficiency’ [50]. The Society of Critical Care Medicine and the European Society of Intensive Care Medicine have published one guideline position paper in 2008 and another 2017 on this syndrome that they describe as critical illness-related corticosteroid insufficiency (CIRCI). This is mainly characterized by hypotension refractory to fluid resuscitation and it is clinically manifested by confusion, delirium, or coma whereas putative laboratory findings are hypoglycemia, hyponatremia, hyperkalemia, metabolic acidosis and hypereosinophilia [50]. Although there is no pathognomonic diagnostic test, random plasma cortisol is usually below 10 μg/dl and delta cortisol lower than 9 μg/dL 60 min after cosyntropin administration. This background led to the concept that early replacement of failing adrenal production with low-dose of hydrocortisone may reverse CRCI and improve patient outcomes.