**5. Pathophysiology**

6 Neonatal Bacterial Infection

staphylococcus.

neonates to die at home.

**Figure 4.** K. Nemsadze, Neonatology, 2010 [1]

sepsis

**4. Etiology and epidemiology** 

**Etiological Structure of Sepsis in Developed Countries** 

**Figure 3.** J. Garcia-Prats et al.,SeminPediatrInfect Dis, 2000;11:4 [6]

**Etiological Structure of Sepsis in Tbilisi Children's Central Hospital** 

Consequently, the main causative agents of neonatal sepsis are bacteria such as

Klebsiella, acinetobacter and staphylococcus aureus can be the cause of early as well as late

Late sepsis is usually a nosocomial disease although is some cases it may be connected with vertical infection. Pseudomonas, salmonella and serratia can often cause late sepsis. Many factors impact the etiological structure, including the quality of life, cultural traditions, practice of antibiotic therapy and the possibility of distorted results caused by many In the presence of sepsis, the response of infection released anti-inflammatory mediators can't localize anti-inflammatory process. Generalized infection is formed as sepsis. The cause of sepsis (SIRS) is multi-factorial: Activation of anti-inflammatory mediators; complement ischemia of tissues; cytopathology; changes in apoptosis rate. Cellular damage with discharge of anti-inflammators (IL1, IL6 TNF- Tumor Necrosis Factor) and antiinflammatory mediators increase the probability of developing multi-organ failure. The cardiovascular system, pulmonary system, gastro-intestinal tract, kidneys and neurological system are most frequently damaged. Given mediators stimulate production of various proteins called as reagents of acute phase. Any kinds of inflammation stimulus, including infection, trauma and ischemia causes marginal extravasations and activation of granulocytes and monocytes with the simultaneous release of anti-inflammatory cytokines including interleukins IL1, IL6 TNF (Tumor Necrosis Factor) [7]

### **Sepsis is caused by Systemic Inflammatory Response (SIR)**

It is widely known that sepsis educes as a result of Systemic Inflammatory Response (SIR). In the process of opsonization and macrophage phagocytosis pathogens cause the formation of various anti-inflammatory mediators (cytokines) which damage vessel endothelium the result of which is the release of tissue factors. The coagulation system is activated and fibrinolysis inhibitor activity is increased. [8,9]

### **Anti-inflammatory Mediators are Reagents of the Acute Phase**

After the patient is stabilized, normalization and a secondary increase in the levels of CBC indicate the sepsis complication (*subdural empyema and bacterial meningitis* [10]. *S*epsis may change the metabolism of neonates. The change in metabolism may be described in two phases

*Ebb Phase Flow Phase*

#### **EBB Phase**

The initial EBB phase lasts 1-3 days. In this phase the neonate is at the stage of compensation while metabolism is slowed.

#### **EBB Phase Consists of Some Clinical Symptoms:**


#### **Flow Phase**

Flow Phase follows the initial Ebb Phase. In this phase the organism goes into a hyperactive state, which is particularly conditioned by a hyper inflammatory reaction. In many cases flow phase leads to patient mortality.
