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Vasodilatory shock in severe acute pancreatitis without sepsis: Is there any place for hydrocortisone treatment?
Author(s) -
Eklund A.,
Leppäniemi A.,
Kemppainen E.,
Pettilä V.
Publication year - 2005
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.2004.00585.x
Subject(s) - medicine , norepinephrine , acute pancreatitis , shock (circulatory) , septic shock , pancreatitis , sepsis , catecholamine , hydrocortisone , anesthesia , hemodynamics , dopamine
Background: Hydrocortisone (HC) has been reported to rapidly improve hemodynamics and reduce the time to vasopressor cessation in septic shock, but none has focused on this effect in acute pancreatitis. We therefore performed a study to assess the effects of hydrocortisone on catecholamine‐dependent shock among patients with severe acute pancreatitis. Methods: A retrospective, case‐controlled study among 10 patients with severe acute pancreatitis and HC treatment for catecholamine‐dependent shock was performed. The control group comprised 11 conventionally treated patients with the same severity of pancreatitis and circulatory shock according to the norepinephrine support required. In focus were the first 48 h from the start of HC administration in the HC group and from the reference point in the control group, respectively. The reference point for the control group was the time point at which doses of norepinephrine exceeded 0.3 µg kg −1 min −1 . Results: Patients in the HC group were weaned off norepinephrine in a significantly shorter time (61 h in HC group vs. 141 h, P = 0.016). The HC group received significantly less norepinephrine (area under curve of norepinephrine dose, P = 0.041). The reduction in norepinephrine dose was comparable at 24 h, being −0.051 (−0.208–0.022) µg kg −1 min −1 in the HC group vs. −0.026 (−0.150–0.030) µg kg −1 min −1 in the controls ( P = 0.307), and at 48 h with respective figures of −0.206 (−0.317 to −0.102) µg kg −1 min −1 and −0.103 (−0.178–0.029) µg kg −1 min −1 ( P = 0.072), from the start of HC administration. Conclusion: According to our data it seems reasonable to formulate a hypothesis that low doses of HC shorten the time to vasopressor cessation and rapidly reduce the need for norepinephrine support in patients with shock associated with severe acute pancreatitis without sepsis.