**2. Pathophysiology and measuring fluid overload**

In general, the vascular endothelial allows free exchange of water, electrolyte, glucose, and nutrients components into and out of the tissue independently because of their permeability to the components. This transcapillary component exchange capability is affected by factors such as hydrostatic pressure, endothelial tone, and oncotic pressure. The fluid passing through the intact endothelial barrier and going to the extravascular generally will be reabsorbed by the lymphatic system to reduce edema. However, damage of endothelial barrier caused by the inflammatory process and edema will be easier to occur. The endothelial barrier is commonly known as glycocalyx, a network-rich carbohydrate and protein bond that regulates the process of exchanging fluid to extravascular (**Figure 1**) [8].

in mortality. Patients who received RRT increased by 25% in critically ill patients. One of the risk factors is an increase in FO% levels between 10 and 20% [1, 11]. Similarly, in patients with ARDS, it is known that fluid retention increases mortality. Fluid overload with edema and extravasation manifestations into the third cavity is associated with failure of several systems such as the cardiovascular system, central nervous system, hepatic system, and digestive systems that stimulate malabsorption of nutrients and malnutrition in children. Fluid management for each critical illness in children is not the same depending on the clinical condition of the patient, but patients with high levels of FO% more frequently can cause failure of several

Measuring and Managing Fluid Overload in Pediatric Intensive Care Unit

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

5

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

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

organs [1–3, 12].

**Figure 1.** Schematic representation of glycocalyx [8].

Beside its own endothelial tissue structure, intravascular volume stability is also regulated by baroreceptors located in the carotid, atrial, and afferent renal arterioles. The renin-angiotensin-aldosterone system (RAAS) will be readily activated resulting in natriuretic peptide secretion in the event of intravascular volume changes [10]. Activation of the RAAS system and the secretion of natriuretic peptides make water and sodium retained by the kidneys to maintain intravascular volume. Imbalance between intravascular and extravascular fluid or component like natrium will facilitate intravascular fluid to the interstitial so that edema, ascites, pleural effusion may occur. Some studies use FO percentage (FO%) as a tool to estimate the amount of fluid retention [9, 10].

$$\text{FO} \,\%= \left[ \left( \text{fluid admittance} \,\text{-} \,\text{fluid eliminated} / \text{body weight when first arrived} \right) \times 100 \,\text{ (1)} \right]$$

The fluids are measured in liters while the body weight measured in kilogram. FO% ≥ 10% is associated with high morbidity rates, such as worsening oxygenation levels, longer mechanic ventilator usage time, increased risk of renal replacement therapy (RRT), even to an increase Measuring and Managing Fluid Overload in Pediatric Intensive Care Unit http://dx.doi.org/10.5772/intechopen.79293 5

**Figure 1.** Schematic representation of glycocalyx [8].

increased risk of morbidity, mortality, additional time of mechanical ventilation, additional

In patients who already have critically ill also shown that fluid overload shows a negative effect. Flori et al. [2] conducted post-hoc study about the association positive fluid balance with worse clinical outcomes in children with ALI. This study showed the increment of 10 mL/kg/day fluid balance was associated with increasing mortality. Moreover, the increments were also associated with fewer ventilator-free days. Flori also suggested that fluid overload itself may be a risk factor for mortality regardless of initial presenting severity of illness [2]. In another study involving 778 patients with septic shock post resuscitation also found that fluid overload increased up to twice the mortality rate [5]. Vincent et al. [7] in their research on sepsis patients found that each addition of a positive fluid balance after 72 h was associated with an increased odds ratio of mortality by 10%. Sutawan et al. [6] study also found that fluid overload was associated with mortality (OR 11.5; 95% CI: 3.7–35.6; p < 0.001)

In general, the vascular endothelial allows free exchange of water, electrolyte, glucose, and nutrients components into and out of the tissue independently because of their permeability to the components. This transcapillary component exchange capability is affected by factors such as hydrostatic pressure, endothelial tone, and oncotic pressure. The fluid passing through the intact endothelial barrier and going to the extravascular generally will be reabsorbed by the lymphatic system to reduce edema. However, damage of endothelial barrier caused by the inflammatory process and edema will be easier to occur. The endothelial barrier is commonly known as glycocalyx, a network-rich carbohydrate and protein bond that

Beside its own endothelial tissue structure, intravascular volume stability is also regulated by baroreceptors located in the carotid, atrial, and afferent renal arterioles. The renin-angiotensin-aldosterone system (RAAS) will be readily activated resulting in natriuretic peptide secretion in the event of intravascular volume changes [10]. Activation of the RAAS system and the secretion of natriuretic peptides make water and sodium retained by the kidneys to maintain intravascular volume. Imbalance between intravascular and extravascular fluid or component like natrium will facilitate intravascular fluid to the interstitial so that edema, ascites, pleural effusion may occur. Some studies use FO percentage (FO%) as a tool to estimate the amount

FO % = [(fluid administrated − fluid eliminated/body weight when first arrived] × 100 (1)

The fluids are measured in liters while the body weight measured in kilogram. FO% ≥ 10% is associated with high morbidity rates, such as worsening oxygenation levels, longer mechanic ventilator usage time, increased risk of renal replacement therapy (RRT), even to an increase

hospitalization time, and increased need for renal replacement therapy (RRT) [5, 6].

with a range of 12.9 ± 7.9% on 120 subjects.

4 Current Topics in Intensive Care Medicine

of fluid retention [9, 10].

**2. Pathophysiology and measuring fluid overload**

regulates the process of exchanging fluid to extravascular (**Figure 1**) [8].

in mortality. Patients who received RRT increased by 25% in critically ill patients. One of the risk factors is an increase in FO% levels between 10 and 20% [1, 11]. Similarly, in patients with ARDS, it is known that fluid retention increases mortality. Fluid overload with edema and extravasation manifestations into the third cavity is associated with failure of several systems such as the cardiovascular system, central nervous system, hepatic system, and digestive systems that stimulate malabsorption of nutrients and malnutrition in children. Fluid management for each critical illness in children is not the same depending on the clinical condition of the patient, but patients with high levels of FO% more frequently can cause failure of several organs [1–3, 12].
