Current Views on the Diagnosis of Sepsis in Newborns
Sepsis morbidity is increasing and according to various data ranges from 28 to 50 %. Sepsis occupies second-third place among the causes of neonatal death. The outcome of treatment directly depends on the time of diagnosis and the start of treatment. Early diagnosis of sepsis allows the use of timely and rational intensive care, antibacterial one in particular. Clinical criteria for sepsis diagnosis include presence of a focus of infection in combination with two or three signs of systemic inflammatory response; severe sepsis is characterized by identified source of infection in conjunction with multiple organ failure. Physiological characteristics of newborns involve a tendency to generalized reactions in response to the impact of damaging factors, including infection. Therefore, clinical stages of sepsis in newborns develop rapidly, and it is difficult to distinguish them in time; neonatal sepsis almost always presents with multiple organ failure. Neonatal sepsis may be caused by more than 40 kinds of opportunistic and pathogenic microorganisms. One should also not underestimate the role of viruses in the development and pathogenesis of sepsis. Newborns are most often found to have cytomegalovirus, respiratory syncytial virus and herpes. In addition to the analysis of clinical presentation, bacteriological and biochemical monitoring of the newborn, as well as the study of blood coagulation system indices for early diagnosis of sepsis in neonates, it is advisable to study hormone procalcitonin (PCT) rate. Increased plasma concentrations of PCT in generalized infection allow to use it as a marker of septic complications. Nitric oxide is considered to play a key role in the pathogenesis of septic shock, although most of its mechanisms of action are poorly understood in sepsis. A noticeable excitement among clinicians was caused by determination of pro-inflammatory mediators that contribute to the development of sepsis and systemic inflammatory response syndrome, as well as determination of their deyotropic effects. Tumor necrosis factor and interleukin-1 became first of these endogenous mediators requiring determination. The list became more prominent at the account of other cytokines, neutrophilic leukocyte degranulation products, platelets and clotting factors formed on their surface, additional fragments, thrombocyte-activating factors and derivatives of arachidonic acid. The list also includes a new class of mediators, namely chemokines (that trigger strong effect activation and chemotaxis of leukocytes). This approach is distinguished by a sufficiently high reliability, but, unfortunately, is relatively expensive for most clinics. Other factors are undoubtedly still waiting to be discovered.
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