Sepsis, Management & Advances in Metabolomics

Abstract

Though there have been developments in clinical care and management, early and accurate diagnosis and risk stratification are still bottlenecks in septic shock patients. Since septic shock is multifactorial with patient-specific underlying co-morbid conditions, early assessment of sepsis becomes challenging due to variable symptoms and clinical manifestations. Moreover, the treatment strategies are traditionally based on their progression and corresponding clinical symptoms, not personalized. The complex pathophysiology assures that a single biomarker cannot identify, stratify, and describe patients affected by septic shock. Traditional biomarkers like CRP, PCT, and cytokines are not sensitive and specific enough to be used entirely for a patient's diagnosis and prognosis. Thus, the need of the hour is a sensitive and specific biomarker after comprehensive analysis that may facilitate an early diagnosis, prognosis, and drug development. Integration of clinical data with metabolomics would provide means to understand the patient's condition, stratify patients better, and predict the clinical outcome.

Keywords: biomarker; critical care; metabolomics; sepsis; septic shock.

Figure 1

Schematic representation of sepsis and septic shock. (A) A localized infection caused by microbes, (B) the microbes enter the system, (C) leaking of the blood vessels, (D) immune response by the body causing uncontrolled hyperinflammation, (E) which starts affecting various organs causing multi-organ failure.

Figure 2

Schematic representation of pathways obliterated in septic shock. Highlighted in red are metabolites altered in septic shock. Briefly, sepsis induces acute kidney injury (AKI) in the kidney, leading to hypoxia in the lungs and liver. This is followed by COPD (Chronic obstructive pulmonary disease) and ARDS (acute respiratory distress syndrome) in the lungs, cardiovascular failure, and acute liver injury.

Figure 3

Schematic representation of metabolic changes in response to immune response.