cosyntropin and Shock

The cosyntropin stimulation study (CSS) measures the patient's ability to adequately mount a cortisol response. Clinically, CSS results may not be used to guide hydrocortisone use. The objective of this study was to examine how the CSS results are associated with clinical parameters, mortality/disease severity, and use of glucocorticoids in pediatric patients with catecholamine- and fluid-resistant shock.. This was a retrospective cohort study of patients who had a CSS during 2009-2014 in the intensive care unit at a children's hospital. Data collected included clinical variables, mortality, biochemical studies, and glucocorticoid use. PRISM III scores were used to determine the association between CSS results and disease severity. Adequate response to cosyntropin was defined as peak cortisol of 18 µg/dL or higher.. Of the 76 patients that underwent CSS, 68 (89%) had an adequate response to cosyntropin. There was a positive correlation between peak cortisol and PRISM III score (r = 0.45, r2 = 0.2). Glucocorticoid was administered in 52/76 (68%) despite several patients with normal CSS results.. Sicker patients were more likely to have an adequate response to CSS. Clinically, glucocorticoid supplementation was not based on CSS results. Further prospective studies are needed to elucidate if CSS is a valuable clinical tool.

Topics: Adolescent; Adult; Catecholamines; Child; Child, Preschool; Cosyntropin; Drug Resistance; Female; Glucocorticoids; Humans; Hydrocortisone; Infant; Infant, Newborn; Intensive Care Units; Male; Retrospective Studies; Severity of Illness Index; Shock

Topics: Adrenal Insufficiency; Aged, 80 and over; Cosyntropin; Female; Hormones; Humans; Hydrocortisone; Shock

Graded caval occlusion in conscious rabbits caused a biphasic cardiovascular response. Phase I was characterized by a fall in systemic vascular conductance so that arterial pressure was maintained. When cardiac output had fallen to 64 +/- 3% of its baseline level, phase II supervened. During phase II, conductance rose abruptly and arterial pressure fell to a life-threatening level (< 40 mm Hg). Intravenous (i.v.) or central (fourth ventricular) administration of the adrenocorticotrophin (ACTH) fragment ACTH-(1-24) prevented the occurrence of phase II. The central dose of ACTH-(1-24) needed to block the occurrence of phase II was approximately 39 times less than the i.v. dose. Central administration of the delta 1-opioid receptor agonist [D-Pen2,D-Pen5]enkephalin (DPDPE) reversed this effect of both central and i.v. ACTH-(1-24). I.v. ACTH-(1-24) also lowered arterial pressure while raising cardiac output and vascular conductance. These effects were insensitive to propranolol and hyoscine methyl bromide, and were not mimicked by cortisol or adrenaline. It is concluded that ACTH-(1-24) has an acute, adrenal-independent, peripheral vasodilator effect as well as a central, anti-shock, effect.

Topics: Animals; Cosyntropin; Enkephalin, D-Penicillamine (2,5)-; Enkephalins; Epinephrine; Hemodynamics; Hydrocortisone; Nitroprusside; Propranolol; Rabbits; Scopolamine; Shock

No clear criteria exist to rule out hypoadrenal shock by cosyntropin (alpha 1-24-corticotropin, a synthetic subunit of adrenocorticotropic hormone) testing in persons who have critical nonadrenal illness. Four patients in the surgical intensive care unit with critical multisystem disease and refractory high cardiac output, low vascular resistance shock had significantly diminished or terminated vasopressor requirements after institution of hydrocortisone sodium succinate infusion in doses simulating physiologic stress response (100 to 300 mg of hydrocortisone per day). In each case, cosyntropin testing revealed serum cortisol levels higher than those usually associated with hypoadrenal shock. Positive response was defined as maintenance of blood pressure with a decrease to less than 25% of baseline pressor requirements within 48 hours of treatment. We hypothesize a syndrome of functional hypoadrenalism in patients with multisystem critical illness and refractory shock responsive to glucocorticoid administration in doses simulating physiologic stress response despite cosyntropin stimulation test results that would rule out hypoadrenalism in a normal person.

Topics: Adrenal Cortex Function Tests; Adrenal Insufficiency; Cosyntropin; Critical Illness; Humans; Hydrocortisone; Male; Middle Aged; Shock

Topics: Animals; Blood Volume; Cosyntropin; Female; Male; Portal Vein; Rats; Rats, Inbred Strains; Regional Blood Flow; Shock; Vena Cava, Inferior

Topics: Animals; Brain; Cosyntropin; Heart; Myocardium; Rats; Receptors, Adrenergic; Shock; Spleen

Topics: Aged; Cosyntropin; Female; Humans; Male; Shock

In an experimental model of hypovolemic shock in rats, produced by withdrawing about 50% of the estimated total blood volume, and causing 100% deaths within 30 min, ACTH-(1-24) dose-dependently improved arterial and pulse pressure and increased survival rate. The intracerebroventricular (i.c.v.) route of administration was more effective than the intravenous (i.v.) route: at the dose of 24 micrograms/kg, 45% and 91% of rats were still surviving 2 hr after i.v. and i.c.v. treatment, respectively. At higher doses of ACTH-(1-24), the survival rate rose to 100% regardless of the route of administration, but arterial pressure increased more after i.c.v. than after i.v. injection. These data suggest that the CNS plays an important role in the anti-shock effect of ACTH.

Topics: Adrenocorticotropic Hormone; Animals; Blood Pressure; Cosyntropin; Female; Injections, Intravenous; Injections, Intraventricular; Pulse; Rats; Rats, Inbred Strains; Shock

Topics: Adrenal Glands; Adrenalectomy; Adrenocorticotropic Hormone; Animals; Blood Pressure; Cosyntropin; Female; Rats; Rats, Inbred Strains; Shock; Shock, Hemorrhagic; Time Factors

ACTH-(1-24), intravenously injected at the dose of 160 micrograms/kg to rats bled to the point of otherwise irreversible hypovolemic shock, causes a prompt and sustained increase in blood pressure and pulse amplitude, all treated rats surviving at the end of the experiment (2 hr). Bilateral vagotomy, as well as atropine sulphate (2 mg/kg i.p. immediately before bleeding), almost completely abolishes the anti-shock activity of ACTH. These data indicate that a central cholinergic pathway and vagal afferent (but not efferent) fibers play an important role in the anti-shock effect of ACTH.

Topics: Adrenocorticotropic Hormone; Animals; Atropine; Blood Pressure; Cosyntropin; Female; Pulse; Rats; Rats, Inbred Strains; Shock; Vagotomy