Ventilator-induced Lung Injury Vortex in Patients With SARS-CoV-2

ARDS Clinical Trial

— VILIVORTEX  

Official title:

Ventilator-induced Lung Injury Vortex in Patients With SARS-CoV-2

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT04174313
• Other study ID #: Nestor Pistillo
• Status: Completed
• Start date: March 10, 2020
• Est. completion date: June 9, 2021

Study information

• Verified date: August 2021
• Source: Hospital El Cruce
• Contact: n/a
• Is FDA regulated: No
• Study type: Observational

Clinical Trial Summary

The concept of Ventilator-induced Lung Injury Vortex (VILI vortex) has recently been proposed as a progressive lung injury mechanism in which the alveolar stress/strain increases as the ventilable lung "shrinks" (1). This positive feedback inexorably leads to the acceleration of lung damage, with potentially irreversible results. Little is known about the clinical aspects of this condition. Understanding its behavior could contribute to changing its potential devastating impact.

The objective of this study is to evaluate the incidence of VILI vortex in patients with acute respiratory syndrome (ARDS) secondary to COVID-19, to establish a connection between this phenomenon and mortality, and to identify the factors that have an impact on its development.

Description:

Mechanical ventilation is an essential tool for the treatment of patients with acute respiratory distress syndrome (ARDS). However, as with other strategies, it is not free of complications. Inadequate ventilation may have a negative impact on pulmonary and systemic hemodynamics, and it could both cause structural damage to pulmonary parenchyma and activate inflammation (2). This process is known as ventilator-induced lung injury (VILI) and may promote the development of multiple organ failure and, eventually, death.

VILI results from the interaction between the mechanical load applied to the ventilable lung and its capacity to tolerate it. Factors such as tidal volume (Vt), driving pressure (ΔP), inspiratory flow rate (VI), respiratory rate (RR), excessive inspiratory effort, high levels of FiO2 and, in some cases, PEEP, have been involved in damage mechanism. In that sense, the concept of mechanical power (MP) tries to encompass most of these factors within a measurable unit (3). Furthermore, the decrease in ventilable lung volume (baby lung concept), the heterogeneous lung compromise in ARDS), and the presence of cofactors that have a negative impact on the lung (fluid overload, presence of sepsis or shock) could increase its susceptibility to damage (4-5).

Due to the fact that the mechanical conditions of the lung change dynamically with the progression of the disease, the ventilatory strategy needs constant adjustments in order to maintain a balance between the load and the size of the ventilable lung (concept of ergonomic ventilation). In fact, a protective ventilatory strategy of low tidal volume (Vt: 6 ml/kg/PBW) and limited plateau pressure (PPlat <30 cmH2O) may cause damage if the functional residual capacity (FRC) decreases significantly, thus making a lower number of alveoli (including capillaries) withstand a higher mechanical load per unit.

The concept of VILI vortex has recently been proposed as a progressive lung injury mechanism in which the alveolar stress/strain increases as the ventilable lung "shrinks". This positive feedback inexorably leads to the acceleration of lung damage, with potentially irreversible results (1). Little is known about the clinical aspects of this condition. Understanding its behavior could contribute to changing its potential devastating impact.

The objective of this study is to evaluate the incidence of VILI vortex in patients with ARDS secondary to COVID-19, to establish a connection between this phenomenon and mortality, and to identify the factors that have an impact on its development.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 65
• Est. completion date: June 9, 2021
• Est. primary completion date: March 11, 2021
• Accepts healthy volunteers: No
• Gender: All
• Age group: 18 Years to 75 Years

Eligibility

Inclusion Criteria: ARDS

-

Exclusion Criteria:

Patients with do-not-resuscitate (DNR) orders and pregnant women. Cardiac arrest before ICU admission. Extra corporeal membrane oxygenation (ECMO) requirement within the first 24 h of ICU admission and chronic obstructive pulmonary disease with gold class 3 or 4, or home oxygen therapy

Related Conditions & MeSH terms

• ARDS
• Lung Injury
• Mechanical Ventilation Complication
• Ventilator-Induced Lung Injury
• Wounds and Injuries

Intervention

Diagnostic Test:
• CT scan
Mechanical variables and PaO2/FiO2 were registered daily for 14 days or until initiating assisted ventilation. These data were obtained in passive mechanical conditions. Ventilator-induced lung injury vortex was defined as a progressive increase in driving pressure (?P) as Vt remained constant or even decreased. Refractory hypoxemia was defined as PaO2/FiO2 <100 despite the optimization of mechanical ventilation and prone positioning.

Locations

Country	Name	City	State
Argentina	Nestor Pistillo	Avellaneda	Buenos Aires

Sponsors (1)

Lead Sponsor	Collaborator
Hospital El Cruce

Country where clinical trial is conducted

Argentina, 

References & Publications (5)

Beitler JR, Malhotra A, Thompson BT. Ventilator-induced Lung Injury. Clin Chest Med. 2016 Dec;37(4):633-646. doi: 10.1016/j.ccm.2016.07.004. Epub 2016 Oct 14. Review. — View Citation

Gattinoni L, Pesenti A. The concept of "baby lung". Intensive Care Med. 2005 Jun;31(6):776-84. Epub 2005 Apr 6. — View Citation

Gattinoni L, Tonetti T, Quintel M. Regional physiology of ARDS. Crit Care. 2017 Dec 28;21(Suppl 3):312. doi: 10.1186/s13054-017-1905-9. Review. — View Citation

Marini JJ, Gattinoni L. Time Course of Evolving Ventilator-Induced Lung Injury: The "Shrinking Baby Lung". Crit Care Med. 2020 Aug;48(8):1203-1209. doi: 10.1097/CCM.0000000000004416. — View Citation

Vasques F, Duscio E, Cipulli F, Romitti F, Quintel M, Gattinoni L. Determinants and Prevention of Ventilator-Induced Lung Injury. Crit Care Clin. 2018 Jul;34(3):343-356. doi: 10.1016/j.ccc.2018.03.004. Review. — View Citation

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Number of Participants Who Survived and Died	The number of patients who died and survived was compared between patients with SARS-CoV-2 who progressed with VILI VORTEX and without VILI VORTEX)	90 days
Primary	Number of Patients With and Without Refractory Hypoxemia	The number of patients that evolved with refractory hypoxemia was compared between the patients with SARS-CoV-2 that evolved with VILI VORTEX and without VILI VORTEX) Refractory hypoxemia was defined as PaO2/FiO2 <100 despite the optimization of mechanical ventilation and prone positioning.	90 days
Primary	Number of Patients With Complications	The following variables and complications were also observed during the period of analysis: incidence of pneumonia associated with mechanical ventilation, need for noradrenaline over 0.1 ?/kg/min for more than 24 h, positive blood cultures, accumulated fluid balance, dialysis treatment, clinical and/or echocardiographic evidence of heart failure, lactate =2 mmol/L in at least two consecutive samples, presence of persistent fever (=38º at least once a day for three consecutive days), and the highest value of ferritin, D-dimer, C-reactive protein, troponin I and LDH obtained during the first 14 days of invasive mechanical ventilation.; VILI vortex patients had positive blood cultures, moderate to severe shock, persistent fever and fluid balance was considerably more positive.	90 days