TIMING OF LOW DOSE VASOPRESSIN IN SEPTIC SHOCK

Col Vikas Srivastava

Abstract


INTRODUCTION
Sepsis, severe sepsis and septic shock are a common occurrence in the
intensive care units (ICU) worldwide and despite significant
improvements in intensive care, carry high mortality in critically ill
patients. [1] One of the major concerns in treatment strategies in
patients with septic shock is the development of progressive
cardiovascular failure due to hypo responsiveness to catecholamines
and excessive vasodilation. Norepinephrine (NE) is recommended to
be used as the rst choice vasopressor [2] Dopamine and Dobutamine
are recommended to be used along with Norepinephrine for select
patients. However a lot of patients become resistant to catecholamines
even when used in high doses. In these patients Vasopressin is added to
NE with intent of either raising blood pressure or decreasing NE
dosage. Studies show that in most patients of septic shock, vasopressin
concentrations are elevated initially but within 24-48 hours the levels
decrease to normal range.[3] However in routine clinical practice we
see that there is a denite improvement in clinical parameters within the
rst few hours of initiating vasopressin infusion and often there is a
dilemma when vasopressin should be discontinued and let the routine
catecholamines act now the sensitivity to catecholamines is restored
with vasopressin. There is also a concern in many primary physicians
that vasopressin may further contribute to decrease in urine output. We
therefore thought of comparing the effects of vasopressin on the
hemodynamic parameters at 8 hours and 24 hours of initiating
vasopressin infusion. The aim of this study was to see the effects of low
dose vasopressin on hemodynamic and oxygen utilization parameters
in septic shock patients resistant to catecholamines, at 8 hours and 24
hours of initiation of infusion.


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References


Vincent JL. EPIC II: sepsis around the world. Minerva Anestesiol 2008;74:293-6.

Dellinger RP, Levy MM, Rhodes A et al. Surviving sepsis guidelines 2012. International Guidelines for Management of Severe Sepsis and Septic Shock: 2012. Crit Care Med 2013; 41(2): 580-637.

Singer M, Deutschman CS, Seymour CW et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016;315(8):801-810.

Landry DW, Levin HR, Gallant EM, et al. Vasopressin deficiency contributes to the vasodilation of septic shock. Circulation 1997; 95: 1122-5.

Sharshar T, Blanchard A, Paillard M, et al: Circulating vasopressin levels in septic shock. Crit Care Med 2003; 31:1752–1758.

Landry DW, Levin HR, Gallant EM, et al. Vasopressin pressor hypersensitivity in vasodilatory septic shock. Crit Care Med 1997; 25: 1279-82.

Malay MB, Ashton RC, Jr, Landry DW, Townsend RN: Low-dose vasopressin in the treatment of vasodilatory septic shock. J Trauma 1999, 47:699-703.

Luckner G, Dunser MW, Jochberger S, Mayr VD, Wenzel V, Ulmer H, Schmid S, Knotzer H, Pajk W, Hasibeder W, Mayr AG, Friesenecker B: Arginine vasopressin in 316 patients with advanced vasodilatory shock. Crit Care Med 2005, 33:2659-2666.

Dunser MW, Mayr AJ, Ulmer H, Ritsch N, Knotzer H, Pajk W, Luckner G, Mutz NJ, Hasibeder WR: The effects of vasopressin on systemic hemodynamics in catecholamine-resistant septic and postcardiotomy shock: a retrospective analysis. Anesth Analg 2001; 93:7-13.

Patel BM, Chittock DR, Russell JA, Walley KR: Beneficial effects of short-term vasopressin infusion during severe septic shock. Anesthesiology 2002, 96:576-582.

Russell JA, Walley KR, Singer J, Gordon AC, Hebert PC, Cooper DJ et al. Vasopressin versus norepinephrine infusion in patients with septic shock. N Engl J Med 2008;358:877- 87.


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