сепсис

[terro]

Есть ли у кого нибудь ссылки на источники где толково обосновывается применение гормонов при сепсисе вне септического шоко?
Ваше мнение о необходимости применения высоких доз стероидов( 10мг/кг по пред.) при сепсисе без шока.

[Dr.Vad]

Isr Med Assoc J 2003 Jan;5(1):51-5
Corticosteroids in sepsis: a new concept for an old drug.
Klaitman V, Almog Y.
Medical Intensive Care Unit, Soroka Medical Center, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheva, Israel.
Sepsis is an inflammatory syndrome caused by infection. Consequently, anti-inflammatory therapy in sepsis has been a subject of extensive research, and corticosteroids have long been used to treat severe infections. However, studies conducted in the 1980s failed to demonstrate any beneficial effects of high dose, short-term steroid therapy in sepsis and this therapy was therefore abandoned in the last decade. Recently, a new concept has emerged with more promising results--low dose, long-term hydrocortisone therapy- and this approach is now being evaluated in the treatment of septic shock. It is supported by the observation that many sepsis patients have relative adrenal insufficiency. Moreover, the anti-inflammatory effects of steroids and their ability to improve reactivity to catecholamines further contribute to their effects in sepsis. Large randomized clinical trials will be required to determine the exact role of corticosteroids in septic shock.

Corticosteroid administration for critically ill patients
Bartelink AK, van Deuren M, Hermus AR, Gemke RJ, Thijs LG.
In critically ill patients, the hypothalamic-pituitary-adrenal axis is usually activated, resulting in elevated plasma cortisol levels. This enables the human organism to cope with sepsis, trauma and other forms of stress. During critical illness, total adrenal insufficiency rarely occurs. On the other hand, septic shock can be accompanied by a relative deficit of cortisol. Causes of this relative adrenal insufficiency are a dysfunction of the hypothalamic-pituitary-adrenal axis and/or cortisol resistance. There are no strict biochemical criteria available to diagnose relative adrenal insufficiency; clinical observation is the decisive factor. In randomised trials with patients in septic shock, a more rapid haemodynamic recovery was obtained with physiological doses of hydrocortisone than with a placebo. The observed haemodynamic response following hydrocortisone administration supports the concept of relative adrenal insufficiency.

Ned Tijdschr Geneeskd 2001 Sep 8;145(36):1749-51
[Relative adrenocortical insufficiency with sepsis, diagnosed and treated with hydrocortisone supplementation]
Kingma MF, van der Werf TS, Tulleken JE, Zijlstra JG, Ligtenberg JJ.
An 82-year-old woman was admitted to the ICU with septic shock and multiple organ failure. Despite the lack of a persistent septic focus she continued to be dependent on large doses of norepinephrine whilst receiving adequate antimicrobial therapy. After a trial treatment with hydrocortisone the norepinephrine infusion could be withdrawn within a few days and she made a full recovery. In the case of seriously ill patients the diagnosis 'relative adrenocortical insufficiency' is predominantly made on the basis of the clinical picture. The remarkable clinical response to the administration of hydrocortisone (400 mg in the first 24 h) confirmed the diagnosis. The dosage of vasopressors can be reduced remarkably quickly. The stimulatory test for adrenocorticotropin hormone (ACTH) has no added value as reference values for critically ill patients are not available and because the results do not predict the response to the treatment.

Crit Care Med 2001 Feb;29(2):310-6 The hypothalamic-pituitary-adrenal axis of patients with severe sepsis: altered response to corticotropin-releasing hormone.
Schroeder S, Wichers M, Klingmuller D, Hofer M, Lehmann LE, von Spiegel T, Hering R, Putensen C, Hoeft A, Stuber F.
Klinik und Poliklinik fur Anasthesiologie und Spezielle Intensivmedizin, Rheinische Friedrich-Wilhelms-Universitat Bonn, Bonn, Germany.
OBJECTIVE: To investigate the functional integrity of the hypothalamic-pituitary-adrenal (HPA) axis in patients with severe sepsis by stimulating with corticotropin-releasing hormone (CRH). DESIGN: Prospective observational study in consecutive intensive care unit patients with severe sepsis. SETTING: Surgical intensive care unit and outpatient department of endocrinology in a university hospital. PATIENTS: The study included 20 patients with the diagnosis of severe sepsis; six critically ill, nonseptic patients after major surgery; ten patients with primary adrenal insufficiency; ten patients with anterior pituitary insufficiency; and ten individuals without clinical signs of HPA axis disturbance. INTERVENTIONS: CRH tests were performed with an intravenous bolus injection of 100 microg of human CRH. MEASUREMENTS AND MAIN RESULTS: We studied the functional integrity of the HPA axis in patients with severe sepsis by performing the CRH test. In addition, during the period of severe sepsis, we repeatedly measured basal plasma concentrations of adrenocorticotropin hormone (ACTH) and cortisol. The mean basal plasma cortisol concentration was decreased significantly in nonsurvivors with severe sepsis (288.8 +/- 29.1 [sem] nmol/L) compared with survivors (468.1+/- 18.6 nmol/L; p <.01). By calculating the ACTH/cortisol indices, we found no evidence for adrenal insufficiency in patients with severe sepsis. The mean ACTH/cortisol indices of nonsurvivors with severe sepsis (0.02 +/- 0.008) and survivors (0.01 +/- 0.002) were significantly lower compared with the index of patients with primary adrenal insufficiency (6.8 +/- 1.0; p <.001). In contrast, in nonsurvivors with severe sepsis, the plasma cortisol response to CRH stimulation was impaired compared with survivors: The mean basal cortisol concentration within the CRH test was 269.4 +/- 39.8 nmol/L in nonsurvivors compared with 470.8 +/- 48.4 nmol/L in survivors and increased to a peak value of 421.6 +/- 72.6 nmol/L in nonsurvivors and 680.7 +/- 43.8 nmol/L in survivors (p <.02). However, the change in plasma cortisol, expressed as mean +/- sem and calculated by subtracting the basal cortisol from the peak cortisol after CRH stimulation, was not significantly different in survivors with severe sepsis (243.5 +/- 36.1, range 111.0-524.0 nmol/L, n = 15) compared with nonsurvivors (161.0 +/- 38.9, range 42.0-245.0 nmol/L, n = 5; p >.05). CONCLUSIONS: We found lower basal plasma cortisol concentrations in nonsurvivors compared with survivors of severe sepsis. In addition, the plasma cortisol response to a single CRH stimulation was impaired in nonsurvivors compared with survivors. Reduced responses to CRH stimulation may reflect a state of endocrinologic organ dysfunction in severe sepsis.

[Dr.Vad]

Relative eosinophilla and functional adrenal insufficiency in critically ill patients

Albertus Beishuizen, Istv&aacute;n Vermes, , Bonno S Hylkema and Clemens Haanen

Departments of Clinical Chemistry and Internal Medicine, Medical Spectrum Twente, Hospital Group, PO Box 50000, 7500 KA, Enschede, Netherlands


The number of circulating eosinophils was noted to be a marker for adrenocortical function by Thorn 50 years ago,[1] but then relegated to oblivion. Present day electronic cell counters provide accurate data on eosinophil counts, which suggests a practical method to estimate the biological effect of glucocorticoids. The concept of occult or relative adrenal insufficiency in critically ill patients has replaced the notion of complete adrenal insufficiency. [2] However, at present no strict biochemical criteria for relative adrenal insufficiency are available.
We studied in critically ill patients the sensitivity of eosinophil counting with respect to the adrenal function and compared these data with the conventional high-dose (250 g) Synacthen stimulation test (SST), in addition with the more sensitive low dose (1 g) SST.[3]
We prospectively studied, during a 12-month period, all 612 patients admitted to the medical-surgical intensive care unit (ICU) by daily measuring the percentage of eosinophils with electronic cell counting. In patients with eosinophil counts higher than 3% and present in ICU longer than 24 hours SSTs were done and their clinical data were collected.
A relative eosinophilia of at least 3% was noticed in 7% (40 of 570 assessable) of patients. The low-dose SST was abnormal in 10 of 40 (25%) patients with relative eosinophilia; the high-dose SST showed abnormal results in only 2 of them (5%). Clinical suspicion for relative adrenal insufficiency was high in 8 of 10 cases with at least 3% circulating eosinophils. Treatment with hydrocortisone resulted in haemodynamic improvement in seven of these eight patients.
Although strict diagnostic criteria for inadequate adrenocortical reserve during stressful conditions are still not established, we found the low-dose SST more sensitive in detecting relative adrenal insufficiency in comparison with the standard-dose SST. We also observed that an increase in circulating eosinophils in critically ill patients is associated with clinical signs of relative adrenal insufficiency. We conclude that relative eosinophilia, detected by electronic cell counting, in patients under stressful conditions, should be considered as a warning sign for insufficient adrenocortical function. Raised eosinophil counts suggest relative adrenal insufficiency in critically ill patients.