Maternal Sepsis
Sanjeewa Padumadasa, Malik Goonewardene in Obstetric Emergencies, 2021
Sepsis occurs when the body’s response to infection causes injury to its own tissues and organs. As a result of the stimulus presented by toxins of the infecting agent, the body’s defence cells release large amounts of pro-inflammatory cytokines, which activate the endothelial tissue. This results in the production of various inflammatory mediators and causes a wide range of systemic changes across the body. Furthermore, this leads to an imbalance between oxygen supply and consumption, which is followed by generalised tissue hypoperfusion, cell hypoxia, anaerobic metabolism, hyperlactataemia and acidaemia that culminate in multiple organ dysfunction. The excessive inflammatory response that occurs with sepsis includes extravasation of albumin and fluid; the result is intravascular hypovolaemia. This is compounded by the decreased systemic vascular resistance which occurs as a result of cytokines. These factors, along with microvascular occlusion due to thrombi resulting from disseminated intravascular coagulation, contribute to tissue hypoxia. Cardiac oedema and lowered myocardial compliance lead to decreased diastolic filling and less stroke volume. Together with reduced oncotic pressure, these predispose to the development of pulmonary oedema, especially with aggressive fluid resuscitation. Fever during the first trimester has been discovered to be associated with a heightened incidence of neural tube defects, oral clefts and congenital heart disease. Antipyretic therapy with paracetamol is beneficial.
Role of Bacteria in Blood Infections
K. Balamurugan, U. Prithika in Pocket Guide to Bacterial Infections, 2019
Sepsis is a severe clinical complication by host inflammatory response triggered against any infection. Sepsis is an irregulated host immune response that leads to organ dysfunction (Singer et al., 2016). It is one of the most common causes of hospitalization, and untreated sepsis cases are potentially fatal. Anyone can have sepsis, but it is prevalent in individuals who are older or immunocompromised. Some of the common causes of sepsis are pneumonia, kidney infection, and bacteremia. It ranges from mild sepsis to septic shock syndrome. Untreated sepsis leads to septic shock syndrome, which results in difficulty in breathing and decrease in platelet counts, urine output, and blood pressure. In addition, septic shock causes blood clots that cause organ failure and ultimately leads to death.
Cutaneous manifestations of sepsis
Biju Vasudevan, Rajesh Verma in Dermatological Emergencies, 2019
Sepsis is defined as systemic inflammatory response syndrome (SIRS) secondary to a documented infection. The host response to infection leading to sepsis is a continuum that ranges from sepsis to severe sepsis to septic shock and multiple organ dysfunction syndrome (MODS) [1]. The symptoms of sepsis are often nonspecific and include fever with chills, confusion, anxiety, breathlessness, nausea, vomiting, malaise, and fatigue. But these symptoms are not universal or pathognomonic. Even though fever is a common symptom, some cases may have hypothermia in the presence of tachycardia and tachypnea. Like the other clinical features of sepsis, cutaneous manifestations are also not pathognomonic, but the presence of them may be extremely useful for the clinician to arrive at a diagnosis as well as to assess the severity of the condition.
Consensus analysis via weighted gene co-expression network analysis (WGCNA) reveals genes participating in early phase of acute respiratory distress syndrome (ARDS) induced by sepsis
Published in Bioengineered, 2021
Qing Fang, Qilai Wang, Zhiming Zhou, An Xie
ABSTRACT The understanding of mechanism during conversion from sepsis to sepsis-related ARDS remains limited. In this study, we collected gene expression matrix from the Gene Expression Omnibus (GEO) database and constructed networks using weighted gene co-expression network analysis (WGCNA) to identify the consensus and opposite modules between sepsis and sepsis-induced ARDS and obtained 27 consensus modules associated with sepsis and sepsis-related ARDS, including one model (160 genes) with opposite correlation and 1 sepsis-ARDS specific model with 34 genes. Differentially expressed genes analysis, functional enrichment and protein-protein interactions analyses of candidate genes were performed; 15 of these genes showed different expressions in sepsis-induced ARDS patients, compared with sepsis patients; genes were enriched in processes associated with ribosome, tissue mechanics and extracellular matrix. Feature selection analysis revealed that three genes, TLCD4, PRSS30P, and ZNF493, showed moderate performance in identifying sepsis-induced ARDS from sepsis. Ribosome-related genes indicate crucial roles in the development of sepsis-induced ARDS.
Sepsis, severe sepsis and septic shock: changes in incidence, pathogens and outcomes
Published in Expert Review of Anti-infective Therapy, 2012
Sepsis has been around since the dawn of time, having been described for more than 2000 years, although clinical definitions are recent. The consensus sepsis definitions have permitted worldwide epidemiological studies of sepsis to be conducted. We now recognize the common nature of sepsis and the consistency of its disease – particularly severe sepsis and septic shock. The incidence of sepsis, severe sepsis and septic shock continues to increase, and although Gram-positive bacterial pathogens remain the most common cause of sepsis, fungal organisms are increasing rapidly. We have made progress over the past half-century in identifying and treating patients with sepsis, and decreasing fatality rates reflect this progress. However, owing to the increasing incidence of sepsis, the number of people who die each year continues to increase. The mortality with sepsis, particularly related to treating organ dysfunction, remains a priority to clinicians worldwide and is deserving of greater public health attention.
The Role of the Liver in Sepsis
Published in International Reviews of Immunology, 2014
Despite the progress made in the clinical management of sepsis, sepsis morbidity and mortality rates remain high. The inflammatory pathogenesis and organ injury leading to death from sepsis are not fully understood for vital organs, especially the liver. Only recently has the role of the liver in sepsis begun to be revealed. Pre-existing liver dysfunction is a risk factor for the progression of infection to sepsis. Liver dysfunction after sepsis is an independent risk factor for multiple organ dysfunction and sepsis-induced death. The liver works as a lymphoid organ in response to sepsis. Acting as a double-edged sword in sepsis, the liver-mediated immune response is responsible for clearing bacteria and toxins but also causes inflammation, immunosuppression, and organ damage. Attenuating liver injury and restoring liver function lowers morbidity and mortality rates in patients with sepsis. This review summarizes the central role of liver in the host immune response to sepsis and in clinical outcomes.