When taking care of a patient with hyperkalemia, which principle is priority

Background

Fluid overload is frequently found in critically ill patients with acute kidney injury [AKI]. Increasing fluid overload should not merely be considered an expected consequence of fluid resuscitation or severe AKI, it should be seen as a probably mediator of adverse outcomes. In critically ill patients, recent studies have highlighted the role of fluid overload on adverse outcomes [1]. Observational studies in pediatric patients who required continuous renal replacement therapy [CRRT] have shown an association between fluid overload and mortality [2–4]. Restrictive fluid management strategies are beneficial during acute respiratory distress syndrome and following major surgery since they reduce the duration of mechanical ventilation and the rate of cardiopulmonary complications [5, 6]. In concert with these data, the control and optimization of fluid balance is a key element of critically ill patients management, since inadequate fluid removal is associated with peripheral edema and pulmonary edema, which can retard weaning from mechanical ventilation, or compromise wound healing. We will focus on the evaluation and management of fluid overload in the intensive care unit [ICU].

Discussion

The role of fluid therapy in the development of fluid overload

In critically ill patients, adequate fluid resuscitation is essential to the restoration of cardiac output, systemic blood pressure and renal perfusion in patients with cardiogenic or septic shock [7, 8]. Prompt and adequate treatment with intravenous solutions can also prevent or limit subsequent AKI [9]. Achieving an appropriate level of volume management requires knowledge of the underlying pathophysiology, evaluation of volume status, selection of appropriate solution for volume repletion, and maintenance and modulation of the tissue perfusion [10].

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].

Table 1 Consequences of fluid overload in organ systems

Full size table

Fluid overload and outcomes

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., have shown that patients with fluid overload defined as an increase in body weight of over 10 % had significantly more respiratory failure, need of mechanical ventilation, and more sepsis. 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 [14.2 % ±15.9 % vs. 25.4 % ±32.9 %, P = 0.03] [3].

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. randomized 1000 patients to either a conservative or to a liberal strategy of fluid management. 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]. Finally, in the Vasopressin in Septic Shock Trial [VASST] study authors found that higher positive fluid balance correlated significantly with increased mortality with the highest mortality rate observed in those with central venous pressure >12 mmHg [18].

Fluid overload recognition and assessment

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]:

1. 1.

   Daily fluid balance: daily difference in all intakes and all outputs, which frequently does not include insensible losses.

2. 2.

   Cumulative fluid balance: sum of each day fluid balance over a period of time.

3. 3.

   Fluid overload: usually implies a degree of pulmonary edema or peripheral edema.

4. 4.

   Fluid accumulation: positive fluid balance, with or without linked fluid overload.

5. 5.

   Percentage of fluid overload adjusted for body weight: cumulative fluid balance that is expressed as a percent. A cutoff of ≥10 % has been associated with increased mortality. Fluid overload percentage can be calculated using the following formula [19]:

$$ \%\ \mathbf{Fluid}\ \mathbf{overload}=\left[\left[\mathrm{total}\ \mathrm{fluid}\ \mathrm{in}-\mathrm{total}\ \mathrm{fluid}\ \mathrm{out}\right]/\mathrm{admission}\ \mathrm{body}\ \mathrm{weight}\times 100\right] $$

Fluid status assessment

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. There are several methods to evaluate fluid status; however, most of the tests currently used are fairly inaccurate. We will describe some of these methods.

• History and physical examination:

  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. Many features increased the probability of heart failure, with the best feature for each category being the presence of past history of heart failure [positive LR = 5.8; 95 % CI, 4.1–8.0]; paroxysmal nocturnal dyspnea [positive LR = 2.6; 95 % CI, 1.5–4.5]; third heart sound gallop [positive LR = 11; 95 % CI, 4.9–25.0]; chest radiograph showing pulmonary venous congestion [positive LR = 12.0; 95 % CI, 6.8–21.0]; and electrocardiogram showing atrial fibrillation [positive LR = 3.8; 95 % CI, 1.7–8.8]. A low serum BNP proved to be the most useful test [serum BNP