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Intensive care medicine · Sep 1996
Comparative Study Clinical Trial Controlled Clinical TrialA comparison of the adrenocortical response during septic shock and after complete recovery.
- J Briegel, G Schelling, M Haller, W Mraz, H Forst, and K Peter.
- Institut für Anaesthesiologie, Ludwig-Maximilians-Universität München, Klinikum Grosshadern, Germany. josef.briegel@ana.med.uni-muenchen.de
- Intensive Care Med. 1996 Sep 1;22(9):894-9.
ObjectiveTo compare the adrenocortical response to corticotropin during septic shock and after complete recovery.DesignProspective clinical study.SettingMultidisciplinary intensive care unit in a university hospital.Patients20 consecutive patients surviving septic shock. All patients met the American College of Chest Physicians/Society of Critical Care Medicine criteria for septic shock. In addition, the presence of high-output circulatory failure with a cardiac index > 41/min per m2 was a criterion for enrollment in the study. Complete recovery from septic shock was defined as discontinuation of any supportive therapies. Severity of illness during septic shock and after recovery was graded using the Acute Physiology and Chronic Health Evaluation (APACHE) II scoring system.InterventionsIn each patient, two short corticotropin stimulation tests were done during septic shock and after recovery.Measurements And ResultsBasal cortisol levels recorded during septic shock and after recovery did not differ (medians: 18.8 vs 18.9 micrograms/dl). However, the response to corticotropin was significantly attenuated during septic shock when compared with the response after recovery (medians: 7.7 vs 14.7 micrograms/dl; p = 0.02). After recovery, patients' stress response was less, as indicated by a reduction in APACHE II scores (medians: 21 vs 5 points; p < 0.01).ConclusionsAdrenocortical response to corticotropin is attenuated in patients with septic shock and high-output circulatory failure compared to the response in the much less stressful condition after recovery. The attenuated adrenocortical responsiveness may be explained by effects of circulating mediators from the systemic inflammatory response.
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