**4.4. How to monitor fluid overload in our patients?**

Conventional indicators, such as MAP, pulse, weight, peripheral edema, are not reliably used in patients with critical illness. MAP and pulse rate are highly fluctuative due to drug use. Indicators of fluid volume such as end-diastolic volume and intrathoracic volume may be useful but still require further study for clinical validation. Cardiac index monitoring and ejection fractions can be used to diagnose FO. In patients with mechanical ventilation, the absence of variation in pulse pressure may indicate the presence of FO [10].

A study of 49 patients using Doppler crosslinks could predict better diuresis using the index compared with changes in pulse pressure and increased MAP after fluid administration. This suggests that renal hemodynamic enhancement is essential for the occurrence of urinary output and reduces FO [34].

In sepsis patient with hypotension, the renal autoregulation mechanism is damaged by microcirculation changes. In this phase, vasopressor administration is often used to keep renal perfusion adequate, and a diuretic process still exists. Research in adults who analyzed the use of noradrenaline to keep MAP between 65 and 75 mmHg showed increased renal perfusion, with increased urine output, and less likely to require RRT. Furthermore, noradrenaline administration in patients with septic shock becomes an option for optimizing renal perfusion. The target of MAP in patients with septic shock differs depending on the history of blood pressure in patients, and patients with a normal history of takanan do not show significant gains for achieving MAP targets [35].

The use of loop diuretics such as furosemide to prevent fluid retention was said effective for inducing diuresis in children and adults. Low doses of diuretics (furosemide = 0.2 mg/kg/dose) may prevent the acute episode from hypovolemia. Continuous administration of furosemide infusions (0.1–0.3 mg/kgbb/day) may also be performed, and both can maintain drug concentrations in the renal tubules and prevent compensatory mechanisms of sodium reabsorption. A decrease in blood volume is also avoided to avoid hemodynamic deterioration. The use of long diuretics can cause resistance and known to use combination of loop diuretic and thiazide are also said to be effective [23].

The use of sedation drugs may cause vasiness and increase hemodynamic instability and thus increases the risk of excessive fluid administration. Provision of sedation also makes the patient should bed rest and is a risk factor for microvascular dysfunction and eventually fluid fertilization returns. This of course increases the time of ventilator use and increases the length of stay in the ICU and the hospital [36].
