**4.2. Volume resuscitation**

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

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

There is no ideal fluid used for resuscitation of shock patients. At least the fluid used has a similar chemical composition to the plasma and can eliminate shock signals without adding fluid extravasation to the interstitial cavity. Currently, the fluid used is colloidal fluid and

Crystalloids are more recommended as first-line therapy to restore hemodynamics in patients with shock [20]. Crystalloids are made up of ions with various tonicities and can be freely distributed. The saline liquor is more isotonic to the plasma but has a higher concentration of chloride and is more at risk of hyperchloremic metabolic acidosis and increases the risk of kidney failure [18]. The fluid such as the ringger is more hypotonic than the extracellular fluid and is also associated with hyperchloremia but has a pH that is more similar to plasma

Colloid is a fluid containing macromolecules with the usefulness of increasing the oncotic pressure and maintaining the amount of fluid that already exists in the vascular and even absorb fluid in extracellular to intracellular [5, 8]. Colloids are classified according to natural

can be estimated by the pulmonary dead space fraction [1, 15].

on organ failure [18].

6 Current Topics in Intensive Care Medicine

crystalloid fluid [19].

pH [19–21].

**4. Managing fluid overload**

**4.1. Composition of resuscitation fluids**

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

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 administration of sedative drugs or infectious processes [27].

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 and is associated with fluid overload [31].
