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Terlipressin in the treatment of catecholamine resistant septic shock


Vasopressin plasma levels are low in advanced septic shock and treatment with low dose vasopressin can reverse catecholamine resistance [1]. Terlipressin, a vasopressin analogue with long half life time, was found to exert less gastrointestinal and myocardial side effects in patients with acute variceal hemorrhage compared with vasopressin. Little is known about effects and side effects of terlipressin administration in patients with septic shock.


Retrospective study of 14 patients with acute liver failure and septic shock treated with terlipressin for norepinephrine resistant shock. Seven patients were monitored with gastric tonometry during terlipressin therapy. Hemodynamic and metabolic parameters as well as liver function tests were measured sequentially over a 72 hour period and compared to base line levels with ANOVA for repeated measurements.


One to 3 mg of terlipressin were administered in divided doses over 24 hours. There was an increase in blood pressure (MAP) accompanied by a significant decrease in norepinephrine (NE) requirements over time. Nine patients were weaned off catecholamine support. Cardiac index, stroke volume (SVI) and metabolic parameters as well as liver function tests remained unchanged. The mucosal-arterial Pco2 gap increased significantly over time indicating impaired gastric mucosal perfusion. There was no improvement in the severity of organ failure (SOFA) during terlipressin treatment (Table).



Terlipressin can reverse vasopressor resistant septic shock. The increase in mucosal-arterial Pco2 gradient during terlipressin treatment raises concerns of significant gastrointestinal side effects associated with this novel therapy.


  1. Landry DW, Levin HR, Gallant EM, et al.: Vasopressin deficiency contributes to the vasodilation of septic shock. Circulation 1997, 95: 1122-1125.

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Auzinger, G., O'Callaghan, P., Harry, R. et al. Terlipressin in the treatment of catecholamine resistant septic shock. Crit Care 6 (Suppl 1), P131 (2002).

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