Comparison of Vasopressin and Other Pressors in Septic Shock

Shock, Septic Clinical Trial

Official title:

Comparative Prospective Study of Vasopressin and Catecholamine in Septic Shock

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT00269685
• Other study ID #: 00-33-R2
• Status: Completed
• Phase: Phase 2/Phase 3
• First received: December 22, 2005
• Last updated: May 26, 2006
• Start date: July 2000

Study information

• Verified date: August 2005
• Source: Université de Sherbrooke
• Contact: n/a
• Is FDA regulated: No
• Health authority: Canada: Health Canada
• Study type: Interventional

Clinical Trial Summary

The purpose of this study is to compare the classical tactics in the treatment of septic shock (dopamine, noradrenalin and dobutamine) to the use of vasopressin as first choice pressor.

Vasopressin seems to be an interesting alternative in the treatment of septic shock. To this date, available studies have showed that it could correct hyperkinetic syndrome and vasoplegia in septic shocks without noticeable side effect. It as been demonstrated that vasopressin improves renal function, as no effect on digestive organs and as no metabolic effect.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 20
• Accepts healthy volunteers: No
• Gender: Both
• Age group: 18 Years and older

Eligibility

Inclusion Criteria:

• Legally major patient presenting a septic shock.

The time window between beginning of symptoms and onset of treatment is established at 12 hours.

The patient must be intubated and mechanically ventilated.

Patient presenting a mean arterial blood pressure of less than 60 mm Hg after adequate fluid resuscitation (at least 1 L of colloid or crystalloid) and 10 ug/Kg/min of dopamine.

Patient presenting a cardiac index of at least 3 L/min/m2

Exclusion Criteria:

• Shock other than septic

• cardiac hypokinesia

• a pre-existing organic renal failure that needs hemodyalisis

• oesophagal or gastric phatology that would lead to a naso-gastric tube contraindication

Study Design

Allocation: Randomized, Endpoint Classification: Safety Study, Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Treatment

Related Conditions & MeSH terms

• Shock
• Shock, Septic

Intervention

Drug:
• vasopressin

Locations

Country	Name	City	State
n/a

Sponsors (1)

Lead Sponsor	Collaborator
Université de Sherbrooke

References & Publications (6)

American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med. 1992 Jun;20(6):864-74. Review. — View Citation

Landry DW, Levin HR, Gallant EM, Ashton RC Jr, Seo S, D'Alessandro D, Oz MC, Oliver JA. Vasopressin deficiency contributes to the vasodilation of septic shock. Circulation. 1997 Mar 4;95(5):1122-5. — View Citation

Luk J, Ajaelo I, Wong V, Wong J, Chang D, Chou L, Reid IA. Role of V1 receptors in the action of vasopressin on the baroreflex control of heart rate. Am J Physiol. 1993 Sep;265(3 Pt 2):R524-9. — View Citation

Malay MB, Ashton RC Jr, Landry DW, Townsend RN. Low-dose vasopressin in the treatment of vasodilatory septic shock. J Trauma. 1999 Oct;47(4):699-703; discussion 703-5. — View Citation

Reid IA. Role of vasopressin deficiency in the vasodilation of septic shock. Circulation. 1997 Mar 4;95(5):1108-10. Review. — View Citation

Rozenfeld V, Cheng JW. The role of vasopressin in the treatment of vasodilation in shock states. Ann Pharmacother. 2000 Feb;34(2):250-4. Review. — View Citation

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	To compare the efficiency of vasopressine to the standard and usual treatment of septic shock on the reverse of the hemodynamic criterion of septic shock
Secondary	To compare these two categories of treatment on:
Secondary	tonometric parameters
Secondary	renal function
Secondary	in term of tolerance: metabolic effects (increase in lactate and glycaemia), cardiac effects (tachycardia being defined as a heart rate increase of 15%), increase of cardiac enzymes (troponine, CK, CK-MB), and cutanuous vasoconstriction.