Shock, Vasopressin Causing Adverse Effects in Therapeutic Use, Vasopressin Deficiency, Vasopressor Adverse Reaction
Conditions
Keywords
Vasopressin, Shock
Brief summary
Arginine-vasopressin (AVP) is a non-catecholaminergic hormone produced in the hypothalamus and released into the circulation via the neurohypophysis. It has different actions depending on the receptors through which it acts: V1 (vasoconstriction, platelet aggregation, efferent arteriole constriction of the renal glomerulus, glycogenolysis); V2 (water reabsorption, release of von Willebrand factor and factor VIII); V3 (increased cortisol and insulin). Septic shock is the most common cause of vasoplegic shock and its management includes control of the focus, early antibiotic therapy, volume resuscitation, vasopressor therapy, support of various organ dysfunctions, as well as monitoring and follow-up. The Surviving Sepsis Campaign (a global initiative to improve sepsis management) recommends noradrenaline as the first line of vasopressor therapy and early addition of AVP as a second line rather than further up-titration of noradrenaline when signs of hypoperfusion persist, through its action primarily on V1. The rationale for its use in septic shock would be: * endogenous vasopressin deficiency present in septic shock; * as a catecholamine-sparing strategy, reducing the side effects of catecholamines; * its potential nephroprotective effect; * its use should be early. The uncertainties surrounding the use of AVP in septic shock and other types of shock are many, hence the need for this registry.
Detailed description
The main objective is to characterise the routine clinical practice of vasopressin use in the context of shock in a multicentre observational study. By collecting clinical, analytical and echocardiographic data in a uniform manner, describing the time sequence of vasopressin and/or noradrenaline use; how long vasopressin is used; and which vasoconstrictor is more frequently withdrawn earlier: vasopressin or noradrenaline. The secondary objectives are: * to assess what motivated the decision to initiate AVP: type of shock, perfusion parameters, noradrenaline dose; * to define the impact of initiating AVP on noradrenaline dose (whether the dose can be reduced or not), on cardiac function (whether echocardiographic data improve or worsen) and on perfusion data (whether laboratory and clinical data such as lactate, capillary refill time, mottling score or diuresis improve or worsen); * estimate what is the dose range of AVP used and what is the maximum dose used in routine clinical practice; * observe when AVP is stopped, how (abruptly or progressively); * describe the incidence of side effects of AVP, whether it is related to the dose of AVP and the comorbidities of the patients; * assess medium/long-term outcomes: 28- and 90-day mortality, ICU and hospital stay, days of vasopressor support, days of mechanical ventilation, days of renal replacement.
Interventions
DRUGVasopressin
Patients treated with vasopressin
Sponsors
Hospital Universitario 12 de Octubre
Study design
Observational model
OTHER
Time perspective
PROSPECTIVE
Eligibility
Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
No
Inclusion criteria
* Any patient over 18 years of age who is in shock and requires the administration of vasoconstrictors, to whom vasopressin is administered in the operating theatre and/or critical care unit, according to best clinical practice.
Exclusion criteria
* Non-consent by patient/legal representatives
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Characterise the clinical practice of vasopressin use in the context of shock in a multicentre observational study. | 90 days | Describing the time sequence of vasopressin and/or noradrenaline use (what is initiated first) during shock |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| Define the impact of starting AVP on noradrenaline dose | Up to 7 days | Define the impact of starting AVP on noradrenaline dose (microgram/kg/minute) |
| Define the impact of starting AVP on lactate level | Up to 7 days | Define the impact of starting AVP on lactate level (mmol/L) |
| Observe when AVP is discontinued and how | Up to 7 days | Describe number of participants what AVP is discontinued first and how (abruptly or progressively) |
| Estimate the range of doses of AVP used | Up to 7 days | Estimate the range of doses of AVP used and the maximum dose used in routine clinical practice. |
| Incidence of side effects | Up to 7 days | Describe the incidence of side effects, whether it is related to AVP dose and patients' comorbidities. |
| Assess what prompted the decision to initiate AVP | Up to 7 days | Assess what prompted the decision to initiate AVP: type of shock (vasoplegic, hypovolemic,...), perfusion parameters (as lactate) or noradrenaline dose (microgram/kg/minute) |
| 90-day all-cause mortality | 90 days | Death on or before study day 90 |
| Incidence of new renal replacement therapy | From onset of shock until hospital discharge, an average of 2 weeks | New receipt of renal replacement therapy after onset of shock |
| Vasopressor-free days to day 28 | 28 days | Number of days between day 28 and the end of the last period of vasopressor therapy prior to day 28 |
| Intensive care unit-free days to day 28 | 28 days | Number of days between day 28 and the end of the last period of intensive care unit admission prior to day 28. |
| Hospital-free days to day 28 | 28 days | Number of days between day 28 and the end of the last period of hospital admission prior to day 28 |
| 28-day all-cause mortality | 28 days | Death on or before study day 28 |
Countries
Spain
Contacts
Primary ContactRaquel García Álvarez, MD
Outcome results
None listed