An observational study in Acute on Chronic Liver Failure, sponsored by Institute of Liver and Biliary Sciences, India. Not yet recruiting at 1 site in India. Open to participants aged 18 Years to 70 Years. Per ClinicalTrials.gov, last updated 2023-11-03.
Sponsored by Institute of Liver and Biliary Sciences, India · Observational
Shock is a clinical state of tissue hypoxia. This hypoxia may be brought about by either decreased perfusion or the inability of the cell to extract oxygen in the presence of adequate perfusion. This causes cellular dysfunction. The most encountered form of shock seen in cirrhotics is septic shock. Septic shock has underlying cellular and metabolic abnormalities in addition to circulatory dysfunction. The circulatory dysfunction in sepsis is in the form of severe vasodilatation with high cardiac index. Cirrhosis is a state of hyperdynamic circulation. The mortality of septic shock in these group of patients is still higher. Sepsis-3 definition of septic shock describes it as a dysregulated immune response to an infection, leading to systemic inflammation, vasodilation, and organ impairment (3). Practically, to define septic shock it requires the lactate to be more than 2 mmol/L and there should be requirement of vasopressors after adequate fluid resuscitation.
Increased lactate levels can indicate tissue hypoxia, excessively rapid aerobic glycolysis, or reduced clearance. As lactate is a normal product of glucose and pyruvate metabolism, any increase in glucose metabolism and / or decrease in pyruvate metabolism will increase lactate generation. This was observed even in the presence of adequate tissue oxygenation. In sepsis, the inflammatory response appears to be associated with an increase in glycolysis and impaired pyruvate dehydrogenase activity. Thus, cytoplasmic pyruvate increases with greater lactate formation. The glycolytic enzyme complex lactate dehydrogenase (LDH) regenerates nicotinamide adenine dinucleotide (NAD) when pyruvate is reduced to lactate via a redox-coupled process in anaerobic glycolysis (Embden-Meyerhof pathway). Since lactate is overproduced and underutilised in tissue hypoxia due to poor mitochondrial oxidation, lactate has traditionally been used as a diagnostic marker for tissue hypoxia. However, up to 70% of the body's lactate elimination occurs in the liver
Aim and Objective -
Secondary objectives:
Methodology:
Study population: Patients of ACLF with septic shock who get admitted to our ICU with a diagnosis of septic shock in the age group 18 - 70 years.
Study design: Prospective observational study Study period: 3 months
Study Location: Department of Hepatology, ILBS, New Delhi
Definitions Sepsis will be defined as a SOFA score more than 2 (or increase in SOFA score >2) in a patient with a suspected infection
Septic shock will be defined as Subset of patients with sepsis with hypotension (MAP \<65) unresponsive to fluid boluses AND with lactate >2mmol/L despite adequate fluid resuscitation
Reversal of Shock will be defined as maintenance of MAP > 65mmHg after discontinuation of all vasopressors for 6 hours.
Lactic Acidosis
Hyperlactatemia
We have taken a sample size of 100 arbitrarily
445 studies on the registry are indexed under Liver Failure; 69 are open to participants now.
This study's planned enrollment of 100 is below the median of 129 across 146 observational studies indexed under Liver Failure.
Browse Liver Failure studies →Institute of Liver and Biliary Sciences, India is the lead sponsor of 296 studies on the registry; 84 are open to participants now.
Counted across the registry records on this site, refreshed daily.
Patients of ACLF with septic shock who get admitted to our ICU with a diagnosis of septic shock in the age group 18 - 70 years.
Exclusion Criteria:
No intervention
Number of participants survived at day 7
Time frame: 7 days
lactate clearance and delta lactate will be measured --> lactate clearance = (Initial lactate - current lactate) Initial lactate * 100, Delta lactate = Initial lactate - current lactate
Time frame: 0 hours
lactate clearance and delta lactate will be measured --> lactate clearance = (Initial lactate - current lactate) Initial lactate * 100, Delta lactate = Initial lactate - current lactate
Time frame: 6 hours
lactate clearance and delta lactate will be measured --> lactate clearance = (Initial lactate - current lactate) Initial lactate * 100, Delta lactate = Initial lactate - current lactate
Time frame: 12 hours
lactate clearance and delta lactate will be measured --> lactate clearance = (Initial lactate - current lactate) Initial lactate * 100, Delta lactate = Initial lactate - current lactate
Time frame: 24 hours
lactate clearance and delta lactate will be measured --> lactate clearance = (Initial lactate - current lactate) Initial lactate * 100, Delta lactate = Initial lactate - current lactate
Time frame: 48 hours
lactate clearance and delta lactate will be measured --> lactate clearance = (Initial lactate - current lactate) Initial lactate * 100, Delta lactate = Initial lactate - current lactate
Time frame: 72 hours
Impact of delta arterial lactate at 6 hours on length of hospital stay (measured in days).
Time frame: 28 days
Impact of delta arterial lactate at 6 hours on need of invasive ventillation (Yes/no)
Time frame: 7 days
Impact of delta arterial lactate at 6 hours on number of days of invasive ventillation (Measured in days)
Time frame: 7 days
Impact of lactate clearance at 6 hours on length of hospital stay (measured in days).
Time frame: 28 days
impact of lactate clearance at 6 hrs on need of invasive ventillation (Yes/no),
Time frame: 7 days
impact of lactate clearance at 6 hrs on number of days of invasive ventillation (Measured in days)
Time frame: 7 days
Length of hospital stay (measured in days).
Time frame: 28 days
Need of ventilation
Time frame: 28 days
Days of ventilation
Time frame: 28 days
impact of oxygenation measured by PF ratio at 0H on delta lactate at 6 hours
Time frame: 6 hours
Correlation between presence or absence of metabolic acidosis with delta lactate at 6 hours
Time frame: 6 hours
Number of patients with effect of anion gap at 0H if metabolic acidosis is present on the delta lactate at 6 hours
Time frame: 6 hours
Number of patients with effect of ejection fraction / cardiac outout on delta arterial lactate at 6 hours
Time frame: 6 hours
To study the impact of presence or absence of multi drug resistant organism (in culture or PCR anallysis) on delta lactate at 6 hours
Time frame: 7 days
The effect of need of renal replacement therapy (till day 7) on delta lactate at 6 hours
Time frame: 7 days
The effect of number of days of continuous renal replacement therapy (till day7) on delta lactate at 6 hours
Time frame: 7 days
The amount of fluid resuscitated and its effect on delta lactate at 6 hours
Time frame: 7 days
Number of patients with number of patients with Noradrenaline requirement and effect on delta lactate at 6 hours
Time frame: 7 days
To study the effect of lactate kinetics on 28 day mortality and to study the other factors affecting 28 day mortality
Time frame: 28 days
Coerrelation between presence or absence of respiratory acidosis on the delta lactate at 6 hours
Time frame: 6 hours
Plan to share: Undecided
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Institute of Liver and Biliary Sciences, India