Terlipressin for norepinephrine-resistant septic shock

doi:10.1016/S0140-6736(02)08225-9

The Lancet

Volume 359, Issue 9313, 6 April 2002, Pages 1209-1210

https://doi.org/10.1016/S0140-6736(02)08225-9 Get rights and content

Summary

Norepinephrine-resistant hypotension when associated with septic shock has a high rate of mortality, which might possibly be reduced by infusion of low-dose vasopressin. However, rebound hypotension often arises after treatment is stopped, and the drug usually has to be administered for several days. We report use of terlipressin, a long-acting vasopressin analogue, in eight patients with septic shock who did not respond to corticosteroids and methylene blue. A significant rise in blood pressure that lasted for at least 5 h was seen in all patients after a single bolus, allowing reduction or cessation of norepinephrine administration in seven patients. We were able to discharge four patients from intensive care subsequently. Terlipressin seems to be an effective rescue therapy, which is able to restore blood pressure in patients with catecholamine-resistant septic shock, without obvious complication.

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There are more references available in the full text version of this article.

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We reviewed the different studies using the terms “refractory septic shock” and/or “catecholamine resistance” and/or “high dose norepinephrine” so as to highlight the heterogeneity of the definitions used by authors addressing such concepts.
A systematic review was conducted assessing the papers reporting data on refractory septic shock. We used keywords as exact phrases and subject headings according to database syntax.
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Marked inconsistencies were identified in the usage of the terms for refractory septic shock. There is a pressing need to determine consensus definitions so as to establish a common language in the medical literature and to harmonize future studies.
Studies on vascular response to full superantigens and superantigen derived peptides: Possible production of novel superantigen variants with less vasodilation effect for tolerable cancer immunotherapy
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Superantigens (SAgs) are a class of antigens that cause non-specific activation of T-cells resulting in polyclonal T cell activation and massive cytokine release and causing symptoms similar to sepsis, e.g. hypotension and subsequent hyporeactivity. We investigated the direct effect of SAgs on vascular tone using two recombinant SAgs, SEA and SPEA. The roles of Nitric Oxide (NO) and potentially hyperpolarization, which is dependent on the K⁺ channel activation, were also explored. The data show that SEA and SPEA have direct vasodilatory effects that were in part NO-dependent, but completely dependent on activation of K⁺ channels. Our work also identified the functional regions of one of the superantigens, SPEA, that are involved in causing the vasodilation and possible hypotension. A series of 20 overlapping peptides, spanning the entire sequence of SPEA, were designed and synthesized. The vascular response of each peptide was measured, and the active peptides were identified. Our results implicate the regions, (61–100), (101–140) and (181–220) which cause the vasodilation and possible hypotension effects of SPEA. The data also shows that the peptide 181–220 exert the highest vasodilation effect. This work therefore, demonstrates the direct effect of SAgs on vascular tone and identify the active region causing this vasodilation. We propose that these three peptides could be effective novel antihypertensive drugs. We also overexpressed, in E.coli, four superantigens from codon optimized genes.
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During early treatment of haemorrhagic shock, cerebral perfusion pressure can be restored by small-volume resuscitation with vasopressors. Whether this therapy is improved with additional fluid remains unknown. We assessed the value of terlipressin and lactated Ringer's solution (LR) on early recovery of microcirculation, tissue oxygenation, and mitochondrial and electrophysiological function in the rat cerebral cortex.
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Research LettersTerlipressin for norepinephrine-resistant septic shock

Summary

Vasopressin deficiency contributes to the vasodilatation of septic shock

Circulation

Low-dose vasopressin in the treatment of vasodilatory septic shock

J Trauma

Research Letters
Terlipressin for norepinephrine-resistant septic shock