**3. Pathophysiology fluid overload in sepsis and ARDS**

In ARDS patients, some theories suggest that fluid overload can aggravate the patient's condition. Widespread injury of both lung and systemic endothelium with a resultant increase in permeability and expression of adhesion molecule is characteristic of ARDS/ALI [13]. Injury to the microvascular endothelium of the lung was first known almost 30 years ago [14, 15]. A variety of circulating markers of endothelial cell injury and activation have been studied in patients with ARDS/ALI. Endothelin-1, a vasoconstrictor and proinflammatory peptide is released by endothelial cell as a result of injury, is increased in the plasma of patients with ARDS/ALI as is von Willebrand factor (VWF) antigen, another marker of endothelial cell activation and injury [13, 16]. Higher levels of plasma VWF were independently associated with mortality by multivariate analysis in two independent studies. Although injury to the lung microvascular endothelial is the underlying cause of increased permeability pulmonary edema in ARDS/ALI, endothelial injury and activation may also lead to obstruction or destruction of the lung microvascular bed in ARDS/ALI case [15]. The degree of obstruction and destruction of the lung microvascular bed is an important determinant of outcome and can be estimated by the pulmonary dead space fraction [1, 15].

(albumin) and artificial (gelatin, dextran, and hydroxyethyl starch (HES)) [7]. In contrast to the crystalloid fluid distributed among compartments, the colloidal fluid will remain in the

Measuring and Managing Fluid Overload in Pediatric Intensive Care Unit

http://dx.doi.org/10.5772/intechopen.79293

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Gelatins, a polypeptide derived from collagen bovine, have the same extravascular extension as albumin but are associated with the risk of renal damage. HES is a high-molecular weight synthetic polymer and is associated with high incidence of renal failure and coagulation dis-

A study comparing the effects of crystalloid with HES found that the use of HES could reduce the amount of fluid intake (30% less than crystalloid), increasing CVP faster, decreasing the

The resuscitation phase aims to restore intravascular volume, increase blood pressure, increase urine output, restore peripheral perfusion and increase consciousness level [17]. Aggressive fluid administration in this phase is associated with fluid overload [21]. The amount of fluid required in this phase also varies and depends on the individual patient [23]. Fluid management without adequate monitoring can increase the risk of volume overload [21]. Management using a vasopressor need not be delayed and aims to restore and maintain

Predicting fluid delivery can reduce the risk of over-giving and unnecessary fluid [24]. Monitoring cardiac output and evaluation of vena cava diameter with ultrasound is one of the mechanisms used to monitor the amount of incoming fluid [25]. This method still has limitations due to the varied reference values that are used to assess the clinical patient, as each individual differs in the amount of fluid that enters depending on body weight, renal ability, and type of illness being suffered [26]. Some of these hemodynamic variables cannot be adequately calculated in patients with inadequate ventilation and receive low tidal volume. In the case of unstable hemodynamics, relative hypovolemia may occur due to the

Calculating central venous saturation and CVP does not show high sensitivity and specificity to predict fluid response [21]. It is estimated that more than 50% of patients are admitted to the ICU because of sepsis and do not respond adequately to this volume test [28]. Signs of tissue hypoperfusion such as lactate and central venous saturation are generally used to evaluate the appropriate time to stop fluid resuscitation [29]. A retrospective study of 405 septic patients receiving therapy based on the central venous saturation target and mean arterial pressure (MAP) protocols indicated a high risk of FO and mortality [30]. However, regular evaluation of venous saturation to evaluate resuscitation responses is more commonly used

In patients with critical illness and treated in the ICU, FO should be avoided [23]. Treatment of fluid administration depends on each individual in the resuscitation phase. As described

incidence of shock but increasing chances for RRT and increasing mortality [22].

renal perfusion, optimize diuresis, and prevent fluid accumulation [10].

administration of sedative drugs or infectious processes [27].

and is associated with fluid overload [31].

**4.3. Maintenance volume**

vascular cavity for more than 16 h [8].

**4.2. Volume resuscitation**

ease [8].

Fluid management in sepsis patients is necessary to increase the perfusion of vital organs in order to restore the patient's hemodynamics. However, there has been no research suggesting the amount of fluid dosage in sepsis patients. Based on early goal directed therapy (EGDT) for the treatment of severe sepsis and septic shock, targeted fluid therapy used central venous pressure (CVP) [7, 17]. However, the target cvp is 8–12 mmHg to ensure intravascular volume. However, the EGDT guidelines do not limit the extent to which these fluids should be administered to patients. Even some recent studies suggest that fluid administration according to the EGDT concept has been abandoned because it is more likely to make hypervolemia and increase mortality rates in the first 48, 72, and 96 h post-EGDT [17]. This increase in mortality rates is more likely to be caused by FO, as FO may aggravate capillary leakage and contribute to or worsen edema in patients' lung with sepsis and septic shock. FO can also create intraabdominal hypertension, leading to organ hypoperfusion that will eventually fall on organ failure [18].
