Abstract
ObjectiveVasopressin (AVP) secretion during an osmotic challenge is frequently altered in the immediate post-acute phase of septic shock. We sought to determine if this response is still altered in patients recovering from septic shock.DesignProspective interventional studySettingIntensive care unit (ICU) at Raymond Poincaré and Etampes Hospitals.PatientsNormonatremic patients at least 5 days post discontinuation of catecholamines given for a septic shock.InterventionOsmotic challenge involved infusing 500 mL of hypertonic saline solution (with cumulative amount of sodium not exceeding 24 g) over 120 minutes.Measurements and main resultsPlasma AVP levels were measured 15 minutes before the infusion and then every 30 minutes for two hours. Non-responders were defined as those with a slope of the relation between AVP and plasma sodium levels less than < 0.5 ng/mEq. Among the 30 included patients, 18 (60%) were non-responders. Blood pressure and plasma sodium and brain natriuretic peptide levels were similar in both responders and non-responders during the course of the test. Critical illness severity, hemodynamic alteration, electrolyte disturbances, treatment and outcome did not differ between the two groups. Responders had more severe gas exchange abnormality. Thirst perception was significantly diminished in non-responders. The osmotic challenge was repeated in 4 non-responders several months after discharge and the abnormal response persisted.ConclusionMore than half of patients recovering from septic shock have an alteration of osmoregulation characterised by a dramatic decrease in vasopressin secretion and thirst perception during osmotic challenge. The mechanisms of this alteration but also of the relationship between haematosis and normal response remain to be elucidated.
Highlights
It has been proposed that relative arginine-vasopressin (AVP) deficiency contributes to hypotension in septic shock [1], which is a life threatening complication of infection with a mortality rate ranging from 35 to 70% [2]
We opted for two separate cohorts as we considered that serial osmotic tests could not be achieved because of the high mortality rate between post-acute and recovery phases, the discharge of patients recovering rapidly from septic shock and the occurrence of a contraindication to hyperosmolar loading
From January 2010 to June 2011, all adults patients who were admitted with septic shock to either of the two participating general intensive care units (ICU) and who survived at least five days after the discontinuation of vasopressor therapy were included
Summary
It has been proposed that relative arginine-vasopressin (AVP) deficiency contributes to hypotension in septic shock [1], which is a life threatening complication of infection with a mortality rate ranging from 35 to 70% [2]. Plasma AVP levels have been shown to decrease during septic shock and after 36 hours to be, inappropriately within the normal range despite hypotension in about a third of septic shock patients [4]. One mechanism for this could be an alteration of the osmoregulation of AVP release. We designed a project to determine, in two separate cohorts, whether AVP secretion during an osmotic challenge is altered in the post-acute phase (i.e. 3 days from onset) and after recovery from septic shock, respectively. We opted for two separate cohorts as we considered that serial osmotic tests could not be achieved because of the high mortality rate between post-acute and recovery phases, the discharge of patients recovering rapidly from septic shock and the occurrence of a contraindication to hyperosmolar loading
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