When you have too much sodium in your body, your body starts retaining water to balance it out. Unfortunately, this water retention can cause new problems throughout your body. Mild hypervolemia or water retention can be perfectly normal from time to time—caused by eating a lot of salty foods or by hormonal changes.
These conditions may include:. Further testing for kidney function can help your doctor decide which steps to take next.
Treatment for hypervolemia will usually focus on ridding the body of excess fluid. This may require taking diuretic medication to increase urine production. Your doctor will also focus on treating the underlying cause of the hypervolemia. This may mean addressing kidney, liver or heart issues. One of the goals of dialysis is to help remove as much excess fluid as possible to get you close to your dry weight. Here are some tips for managing fluid:.
Healthy kidneys pull extra fluid out of your body and send it away in your urine. If you have kidney failure at stage 5 chronic kidney For people with chronic kidney disease CKD , a lower sodium Understanding Hypervolemia and Fluid Overload.
What are the signs and symptoms of hypervolemia? It's also a good idea to know your test results and keep a list of the medicines you take. Author: Healthwise Staff. Care instructions adapted under license by your healthcare professional. If you have questions about a medical condition or this instruction, always ask your healthcare professional. Healthwise, Incorporated disclaims any warranty or liability for your use of this information.
Healthwise, Healthwise for every health decision, and the Healthwise logo are trademarks of Healthwise, Incorporated. It looks like your browser does not have JavaScript enabled. Please turn on JavaScript and try again. Important Phone Numbers. Topic Contents What is fluid overload? What are the symptoms? How is it treated? Where can you learn more? The administration of crystalloids solutions that are recommend for the initial management of patients with or at risk of AKI, and also in patients with sepsis expands the extracellular compartment, but over time since critically ill patients have a increased capillary leak intravenous solutions will leave the circulation and distribute in the extracellular volume leading to edema and to fluid overload.
These results in impaired oxygen and metabolite diffusion, distorted tissue architecture, obstruction of capillary blood flow and lymphatic drainage, and disturbed cell to cell interactions that may then contribute to progressive organ dysfunction Table 1. These effects are prominent in encapsulated organs liver and kidneys [ 11 — 13 ]. Fluid overload is not only a consequence of fluid therapy but also occurs during severe sepsis secondary to the release of complement factors, cytokines and prostaglandin products and altered organ microcirculation [ 14 ].
In this context, edema is attributed to a combination of increased capillary permeability to proteins and increased net trans-capillary hydrostatic pressure through reduced pre-capillary vasoconstriction [ 15 ].
Several observational studies have demonstrated a correlation between fluid overload and mortality in critically ill patients with acute respiratory distress syndrome, acute lung injury, sepsis, and AKI.
Bouchard et al. After adjusting for severity of illness, AKI patients with fluid overload had increased 30 day and 60 day mortality. Among survivors, AKI patients who required renal replacement therapy had a significantly lower level of fluid accumulation at initiation of dialysis and at dialysis cessation than non-survivors. Renal recovery was significantly lower in patients with fluid overload [ 1 ]. In children, a multicenter prospective study found that the percentage of fluid accumulation at initiation of CRRT was significantly lower in the survivors Lungs are one of the organs in which adverse effects of fluid overload are most evident, which can lead to acute pulmonary edema or acute respiratory distress syndrome [ 16 ].
Several studies have provided evidence associating positive fluid balances with poorer respiratory outcomes. In one of these studies, septic shock patients with acute lung injury who received conservative fluid management after initial fluid resuscitation had lower in-hospital mortality [ 17 ].
In another study, Wiedemann et al. Patients randomized to the conservative fluid strategy had lower cumulative fluid balance, improved oxygenation index and lung injury score, increased number of ventilator-free days, and reduction in the length of ICU stay. It is worth to mention that the conservative fluid management strategy did not increase the incidence or prevalence of shock during the study or the need for renal replacement therapies [ 5 ].
Fluid overload recognition and assessment in critically ill patients requires an accurate documentation of intakes and outputs; however, there is a wide variation in how this information is recorded, reviewed and utilized. Mehta RL and Bouchard J proposed some useful definitions to help us to standardize the approach and facilitated comparisons [ 10 ]:. Daily fluid balance : daily difference in all intakes and all outputs, which frequently does not include insensible losses.
Cumulative fluid balance : sum of each day fluid balance over a period of time. Fluid overload : usually implies a degree of pulmonary edema or peripheral edema.
Fluid accumulation : positive fluid balance, with or without linked fluid overload. Percentage of fluid overload adjusted for body weight : cumulative fluid balance that is expressed as a percent. Fluid overload percentage can be calculated using the following formula [ 19 ]:. Accurate volume status evaluation is essential for appropriate therapy as inadequate assessment of volume status can result in not providing necessary treatment or in the administration of unneeded therapy, both associated with increased mortality.
We will describe some of these methods. The usefulness of medical history, symptoms, and signs along with routine diagnostic studies chest radiograph, electrocardiogram, and serum B-type natriuretic peptide BNP that differentiate heart failure from other causes of dyspnea in the emergency department were evaluated in a meta-analysis.
Importantly, signs like pulmonary rales, lower extremity edema, and jugular venous distention have significant limits for assessing fluid overload. There are some studies that have correlated these sings during physical examination and invasive measures e. Butman et al. Using hepato-jugular reflux and Valsalva maneuvers, Marantz et al.
On the other hand, in a prospective study, physical signs of fluid overload were compared with hemodynamic measurements in 50 patients with known chronic heart failure. Chest x-ray has been one of the most used tests to evaluate for hypervolemia. Radiographic sings of volume overload include dilated upper lobe vessels, cardiomegaly, interstitial edema, enlarged pulmonary artery, pleural effusion, alveolar edema, prominent superior vena cava, and Kerley lines.
Additionally, these radiographic sings can be minimal in patients with late-stage heart failure [ 24 ]. The X-ray technique and the clinical status of patient impact radiographic performance for detecting volume overload. Portably chest X-ray, reduce the sensitivity of findings of volume overload [ 26 ], and pleural effusions can be missed if the film is performed supine.
Conversely, the frequency of volume overload findings in the chest X-ray increased with the severity of fluid overload such as severe heart failure [ 28 ]. High levels of BNP can be found with volume overload; however, some conditions like myocardial infraction and pulmonary embolism can cause elevated levels of BNP. Other conditions that have to be taken into account when evaluating BNP levels are obesity, associated with lower BNP levels and renal failure, associated with high BNP levels.
Patients with heart failure who have elevated base-line levels of BNP. The greatest utility of BNP levels is in the absence of elevation, since low BNP levels have a high negative predictive value for excluding heart failure diagnosis.
On the other hand, high BNP levels can be non-specific for volume overload [ 26 ]. It is a noninvasive, inexpensive and highly versatile test that transforms electrical properties of tissues into clinical information [ 29 ].
Bioimpedance vector analysis BIVA measures whole body fluid volume and is based on patterns of the resistance-reactance graph, relating body impedance to body hydration [ 29 ]. Clinical information on hydration is obtained through patterns of vector distribution with respect to the healthy population of the same race, sex, class of body mass index, and age. Changes in tissue hydration status below ml are detected and ranked. BIVA was examined as an indicator of fluid status compared to central venous pressure CVP in critically ill patients [ 30 ].
In this study patients were classified in three groups according to their CVP value: low 0 to 3 mmHg ; medium 4 to 12 mmHg ; and high 13 to 20 mmHg. The combined evaluation of peripheral tissue hydration BIVA and central filling pressure CVP could provide a useful clinical assessment instrument in the planning of fluid therapy in critically ill patients, particularly in those with low CVP [ 31 ].
Sonographic artifacts known as B-lines that suggest thickened interstitial or fluid-filled alveoli can be detected using thoracic ultrasound Fig. PCWP and fluid accumulation in lungs have been correlated with the presence of B-lines "comet-tail images" in patients with congestive heart failure [ 32 ]. Agricola et al. Lung comet tail image. In the presence of extravascular lung water the reflection of the ultrasound beam on the sub-pleural interlobular septa thickened by edema creates comet-tail reverberation artifacts.
The ultrasound appearance is of a vertical, discrete, hyperechogenic image that arises from the pleural line and extends to the bottom of the screen moving synchronously with the respiration white arrows.
The measurement of the inferior vena cava IVC diameter can also be use to assess volume status. Normal diameter of IVC is 1. In an observational study on blood donors, Lyon et al. Significant differences were found between the IVCd e before and after blood donation and between IVCd i before and after donation 5. In patients treated for hypovolemia, Zengin et al. The IVCd was measured ultrasonographically by M-mode in the subxiphoid area and the RVd was measured in the third and fourth intercostals spaces before and after fluid resuscitation.
As compare with healthy volunteers average diameters in hypovolemic patients of the IVC during inspiration and expiration, and right ventricule diameter were significantly lower. After fluid resuscitation, there was a significant increase in mean IVC diameters during inspiration and expiration as well as in the right ventricule diameter [ 35 ].
Bedside inferior vena cava diameter and right ventricule diameter evaluation could be a practical noninvasive instrument for fluid status estimation and for evaluating the response to fluid therapy in critically ill patients.
Diuretics, especially loop diuretics, remain a valid therapeutic alternative for relieving symptoms and improving pathophysiological states of fluid overload such as congestive heart failure and in patients with AKI. At this time, there is no evidence that favors ultrafiltration over diuretic use in volume overload patients with or without AKI in terms of less progression of AKI, improved clinical outcomes or reduce incidence of AKI [ 36 ]. Despite that more patients developed AKI during diuretic treatment, numerous studies have demonstrated that more aggressive use of loop diuretics to achieve greater volume removal is associated with improved outcomes Table 2 [ 37 — 40 ].
What should be the goal of urine output when using diuretics to manage fluid overload? Diuretics could be either administered by bolus or using a continuous infusion. There has been controversy about which of these strategies is better; some authors advocate that diuretic infusion is superior to boluses since urinary output could be maintain easily [ 41 ]. In one study diuretic infusion was associated with greater diuresis and this was achieved with a lesser dose [ 42 ]; infusion was also associated with fewer adverse events such as worsening AKI, hypokalemia, and ototoxicity.
Since common electrolyte disturbances could be encountered during diuretic therapy, it is important to monitor electrolytes levels and also to assess acid-based status.
In order to avoid hypokalemia, administration of oral potassium it is easy. Measuring urinary potassium concentration and calculating the daily losses of potassium, which require replacement is a strategy that can be used to estimate daily potassium requirements.
Another strategy is the use of potassium-sparing diuretics like spironolactone. Hypomagnesemia is frequently found during diuretic therapy, magnesium replacement can be achieved either intravenously or orally, typically with 20—30 mmoL per day. Finally in some patients, chloride losses exceed sodium losses and hypochloremic metabolic alkalosis develops; this is usually corrected with the administration of potassium chloride and magnesium chloride.
A recent comprehensive review have shown that torsemide and bumetanide have more favorable pharmacokinetic profiles than furosemide, and in the case of torsemide it could be more efficacious than furosemide in patients with heart failure decreased mortality, decrease hospitalizations, and improved New York Heart Association functional classification.
In AKI patients, as compared with torsemide the use of furosemide was associated with a significant improvement in urine output. Moreover, two trials comparing bumetanide with furosemide showed conflicting results [ 44 ]. Finally, in patients with AKI the response to furosemide may be reduced due to multiple mechanisms including a reduced tubular secretion of furosemide and blunted response of Na-K-2Cl co-transporters at the loop of Henle [ 45 ].
This reduced response to furosemide in AKI patients often requires the use of higher doses that may increase the risk of ototoxicity, especially as the clearance of furosemide is severely reduced in AKI. High doses of furosemide may also result in myocardial dysfunction secondary to furosemide induced vasoconstriction [ 46 ]. Accurate management of fluid balance becomes obligatory with the ultimate goal of improving pulmonary gas exchange and organ perfusion while maintaining stable hemodynamic parameters.
The optimal renal replacement therapy for patients with AKI and fluid overload has not been defined yet and there is still an ongoing debate. Some large observational studies have suggested that CRRT is an independent predictor of renal recovery among survivors [ 48 — 50 ]. In the absence of definite data to support the use of particular type of renal replacement therapy, one should consider CRRT and IHD as complementary therapies.
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