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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of a 65-year-old lady who presented with acute confusion and profound hyponatraemia (plasma sodium of 97 mmol/L). Five years earlier she had developed sepsis and was found to have hyponatraemia, thought to be due to syndrome of inappropriate antidiuretic hormone secretion. The patient was lost to follow-up. The patient was covered with steroids and investigations confirmed primary adrenal failure with flat response of cortisol to adrenocorticotropic hormone (ACTH) stimulation and very high level of ACTH. Adrenal auto-antibodies were negative and a computed tomography of the adrenals showed bilateral adrenal calcifications, suggestive of previous haemorrhage or infarction. Bilateral adrenal calcification due to haemorrhage/infarction usually does not present with severe hyponatraemia; however, adrenal insufficiency should be excluded in all cases of severe hyponatraemia. In suspected cases, patients should be treated with steroids, even when symptoms or signs are absent, while results of investigations are awaited.
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PMID:An unusual case of profound hyponatraemia and bilateral adrenal calcifications. 1979 4

A central feature of the endocrine pathophysiology of septic shock is thought to be the existence of adrenal dysfunction. Based on changes in glucocorticoid secretion and responsiveness, protein binding, and activity. These changes have been described by the terms "Relative Adrenal Insufficiency" (RAI), or "Critical Illness Related Corticosteroid Insufficiency" (CIRCI), and form part of the rationale for trials of glucocorticoid treatment in septic shock. Diagnostic criteria for these conditions have been based on plasma cortisol profiles and have proven notoriously difficult to establish. The uncertainty in this area arises from the inability of current tests to clearly identify who is truly glucocorticoid "deficient" at a cellular level, and hence who requires supplemental glucocorticoid administration. Emerging data suggest that there may be abnormalities in the tissue activity of glucocorticoids in patients with severe sepsis and plasma profiles may not be reliable indicators of tissue glucocorticoid activity, We put forward an alternative point of view, that is the spectrum of adrenocortical dysfunction in sepsis - plasma and tissue, can be grouped under the umbrella of a "sick euadrenal syndrome" rather than an adrenocortical insufficiency.
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PMID:Adrenocortical (dys)function in septic shock - a sick euadrenal state. 2192 73

Cardiovascular failure in sepsis involves a combination of hypovolemia, decreased vascular tone, myocardial depression and microcirculatory alterations. Fluids represent the first line therapeutic intervention, with controversy regarding the type of fluid. Recent data indicate that albumin is safe and might even be beneficial in specific subgroups. Starches may be an alternative, although concerns exist on potential detrimental effects on renal function of old generation starches. Trials testing new generation starches are ongoing. When fluids fail to correct hypotension, vasopressor agents are used. Various adrenergic agents increase blood pressure, especially dopamine, noradrenaline and adrenaline, by stimulating alpha-adrenergic receptors. They also variably stimulate beta-adrenergic receptors, increasing cardiac contractility, heart rate, and splanchnic perfusion, but with increased risk of arrhythmias, immunomodulation and increased metabolism. Furthermore, dopamine stimulates dopaminergic receptors, resulting in doubtful effects on splanchnic and renal perfusion, but also in endocrine alterations. Do these pharmacologic differences among the various alpha-adrenergic agents translate into clinical differences? Several randomized trials tested the effects of these agents on outcome. Epinephrine produces more undesired effects than norepinephrine, but no clear cut differences on outcome were observed in underpowered trials. Norepinephrine should be preferred over dopamine, as suggested in one large trial and confirmed in a meta-analysis. Vasopressin may be considered as an alternative or in addition to adrenergic agents. In one large trial, no significant difference in outcome was observed, and the exact role of vasopressin still needs clarification. Finally, various inotropic agents can counteract septic myocardial depression. So far, no study supports their routine use, but these may be justified on an individual basis.
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PMID:Clinical management of the cardiovascular failure in sepsis. 2350

There is limited information on the long-term natural history of adrenal function in adrenal hemorrhage following sepsis. The 19-year history of a patient is described who suffered adrenal hemorrhage during pneumococcal sepsis. Adrenal reserve using Cosyntropin testing with the 250 mcg dose was evaluated at seven time points during this interval, and a close observation of the patient enabled clinical correlation with adrenal status. The cosyntropin testing showed a 60 minute cortisol level post-hemorrhage of: 303.4 nmol/L (11.0 mcg/dL), one month; 656.6 nmol/L (23.8 mcg/dL), 1 year 10 months; and 714.5 nmol/L (25.9 mcg/dL), 19 years. Over the years the patient experienced hypoadrenal symptoms requiring both hydrocortisone and fludrocortisone until her adrenal function consistently demonstrated a 60 minute cortisol level of ~ 717.3 nmol/L (26 mcg/dL). Adrenal calcifications were visualized by ultrasound imaging and ultimately resolved. In conclusion, the patient's hypothalamic-pituitary-adrenal system appeared to have ultimately restored normal basal adrenal function 19 years after the initial hemorrhage, and the dynamic cosyntropin data indicate that normal adrenal function should not be assumed with a 60 minute cortisol level of 496.6 - 551.8 nmol/L (18 - 20 mcg/dL). Finally, mineralocorticoid as well as glucocorticoid may be important for improved mental acuity in primary hypoadrenalism.
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PMID:A 19-YEAR STORY OF ADRENAL HEMORRHAGE, ADRENAL INSUFFICIENCY, AND ADRENAL RECOVERY: DYNAMIC COSYNTROPIN RESULTS WITH TREATMENT CONSIDERATIONS. 3114 34


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