Keywords

FormalPara IFA Commentary

There is a relationship between fluid resuscitation, fluid accumulation and secondary intrabdominal hypertension (IAH). Evidence supports this relationship in patients with sepsis, acute pancreatitis, severe burn injury, emergency surgery and severe trauma. Among the fluids, crystalloids are more likely to contribute to a cumulative positive balance and IAH, compared to colloids and hypertonic solutions. IAP should be measured during fluid resuscitation using a bladder catheter with an infusion of no more than 25 mL 0.9% saline. Overzealous fluid administration can lead to secondary IAH and venous congestion and may affect any organ of the body. The effect of IAH on the gut includes intestinal edema, mesenteric vein compression, decreased perfusion, bacterial translocation and disruption of the gut microbiome. The development of IAH is usually associated with worse patient outcomes. Fluid stewardship is recommended for the use of IV fluids during different phases based on the ROSE model. The IAH can be managed with medical management. De-resuscitation with active fluid removal may require diuretics or ultrafiltration in a few cases. However, the timing of renal replacement therapy during resuscitation is currently unclear. Surgical decompression or escharotomy may be required in case of (primary) abdominal compartment syndrome.

FormalPara Learning Objectives

After reading this chapter, you will:

  1. 1.

    Understand the pathophysiology of intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS).

  2. 2.

    Understanding the terminology, primary and secondary IAH, ACS, and discussing global increased permeability syndrome (GIPS) and capillary leak.

  3. 3.

    Recognize fluid resuscitation as one of the major risk factors leading to increased intra-abdominal pressure (IAP) and secondary IAH and ACS.

  4. 4.

    Comprehend that as venous return is already impeded in IAH the combination of positive pressure ventilation and PEEP may lead to dramatic effects on cardiovascular and kidney function.

  5. 5.

    Learn that fluids should initially be titrated based on volumetric preload indicators and functional hemodynamic parameters and they should be tapered when IAP increases.

  6. 6.

    Understand that during the deresuscitation phase, in selected patients there may be a potential place for hypertonic solutions (like hypertonic lactated saline or albumin 20%) together with a combination treatment of diuretics or ultrafiltration via renal replacement therapy.

  7. 7.

    Learn that patients treated with an open abdomen may lose substantial amounts of fluids and nitrogen (hypercatabolic) which needs to be substituted with isotonic replacement fluids and nutritional support.

FormalPara Case Vignette

A 42-year-old male with a body mass index of 23 kg/m2 and no relevant past medical history was admitted to the surgical intensive care unit (ICU) after a pneumonectomy, pericardectomy and partial thoracic wall resection for invasive pulmonary cancer. After admission to the ICU, the patient remained in refractory shock. A surgical revision was performed on the first postoperative day (POD 1) where diffuse oozing was found but no significant bleeding. Over the next 5 postoperative days, the patient developed a significant capillary leak syndrome with intravascular underfilling and extravascular (interstitial) fluid accumulation. There was increased pulse pressure variation (PPV) above 20%, a positive passive leg raising test, fluid responsive hypotension (after a bolus of 4 mL/kg intravenous fluid), need for inotropes (dobutamine) and vasopressors (norepinephrine at a dose of 0.4 μg/kg/min), and worsening renal function.

Questions

  • Q1. What fluids should be administered?

  • Intravenous fluids were given liberally (mainly balanced crystalloids but in the operating room 2 L of saline was given over 30 min) and the cumulative fluid balance reached on POD 7 was in excess of 10 L. During the first postoperative week, intra-abdominal pressure (IAP) increased daily from 14 mmHg until it reached 29 mmHg on POD 8, confirming the diagnosis of secondary abdominal compartment syndrome (, i.e., IAP >20 mmHg with new or deteriorating organ dysfunction, caused by pathology outside the abdominal cavity).

  • Q2. How do you interpret the increased PPV in the setting of ACS?

  • The clinical condition of the patient deteriorated further with impaired oxygenation despite lung protective ventilation and a continuous infusion of neuromuscular blockade (cisatracurium). Nitric oxide ventilation was attempted (because of pulmonary hypertension on transesophageal echocardiography) with only partial success and the patient progressed to anuria. At this time, a decompressive laparotomy (DL) was performed at the bedside in the ICU, which revealed no intra-abdominal abnormalities. Immediately after opening the peritoneum, a dramatic improvement in ventilation parameters and oxygenation was observed, and diuresis resumed.

  • Q3. Were all medical management options used before DL?

  • A Bogota bag was used for temporary abdominal closure, followed by placement of a vacuum-assisted closure (VAC) dressing 2 days later. Each day, around 4 L of fluid were drained via the VAC system.

  • Q4. Do you have any concerns regarding the interstitial (third) space fluid losses?

  • Despite the initial improvement after decompressive laparotomy, renal function deteriorated again and continuous venovenous hemofiltration (CVVH) with ultrafiltration was started at POD 13. The vasopressor dose remained at a low level (0.05 μg/kg/min norepinephrine), and ventilator support could be kept at low levels throughout the remainder of the patient’s clinical course.

  • Q5. Is there a role for hypertonic solutions and diuretics in this patient?

Introduction

Intra-abdominal hypertension (IAH) occurs in 25% of critically ill patients on admission and it is an independent risk factor for morbidity and mortality. About one patient in two will develop IAH at some point within the first week of ICU stay while 5% will develop full-blown abdominal compartment syndrome (ACS) as will be discussed further. Different risk factors for IAH have been identified and studied and fluid resuscitation is one of them. This paper will look at the relationship between overzealous fluid administration and the development of secondary IAH and ACS. Chap. 25 will discuss fluid accumulation syndrome and deresuscitation.

This chapter will focus on adult patients, and more information on fluid therapy in children can be found in Chap. 20. Some other chapters will discuss fluids in specific populations: sepsis (Chap. 14), heart failure (Chap. 15), trauma (Chap. 16), neurocritical care (Chap. 17), perioperative setting (Chap. 18), burns (Chap. 19), liver failure (Chap. 21), and COVID-19 (Chap. 26).

Definitions

Intra-abdominal Pressure

The IAP is the steady-state pressure concealed within the abdominal cavity [1]. The IAP can be directly measured via the intraperitoneal cavity either via a Verres needle connected to a pressure transducer during laparoscopy, during chronic ambulatory peritoneal dialysis or in the case of paracentesis for tense ascites. However, the gold standard for intermittent IAP estimation is via the bladder with a maximal instillation of 20–25 mL (1 mL/kg in children up to 10 kg) of sterile saline through a urinary catheter. The transducer should be zeroed at the level where the midaxillary line crosses the iliac crest and IAP should be expressed in mmHg (conversion factor from mmHg to cmH2O is 1.36). IAP should be measured at end-expiration in the supine position whilst abdominal muscle contractions are absent. Normal IAP is approximately 5–7 mmHg in adults, and around 10 mmHg in critically ill patients, but depends on body weight and level of obesity [2]. After abdominal surgery, IAP is usually around 12–14 mmHg.

Intra-abdominal Hypertension and Abdominal Compartment Syndrome

According to the Abdominal Compartment Society (WSACS, www.wsacs.org), intra-abdominal hypertension (IAH) is defined as a sustained increase in IAP equal to or greater than 12 mmHg [1]. IAH can be further classified into primary, secondary or tertiary IAH [1]. Primary IAH originates from injury or disease within the abdominopelvic cavity (e.g., a ruptured abdominal aortic aneurysm, bowel perforation and spleen rupture), whereas secondary IAH results from conditions that have an extra-abdominal origin (e.g., sepsis, major burns or other conditions requiring massive fluid resuscitation) [3]. Tertiary IAH refers to the more chronic condition of an open and frozen abdomen after initial treatment for either primary or secondary IAH. IAH is graded as follows: grade I between 12 and 15 mmHg, grade II between 15 and 20 mmHg, grade III between 20 and 25 mmHg, and grade IV are IAP values above 25 mmHg. Abdominal compartment syndrome (ACS) is defined as a sustained increase in IAP above 20 mmHg that is associated with new organ dysfunction/failure. The abdominal perfusion pressure (APP), ideally a value higher than 60 mmHg, is calculated by subtracting the IAP from the mean arterial pressure (MAP).

Hemodynamic Effects and Impact on End-Organ Function

The presence of IAH leads to elevation of the diaphragm, which increases intrathoracic pressure and compromises cardiac function by decreasing preload and cardiac output and increasing afterload [4]. Moreover, the rise in intrathoracic pressure also affects pulmonary function [5] and may lead to intracranial hypertension due to functional obstruction of cerebral venous outflow [6]. The development of renal dysfunction due to increased IAP is attributed to compression of the renal veins and arteries, decreased renal arterial blood flow, venous congestion and reduced cardiac output. The gut seems to be particularly vulnerable to increases in IAP. Besides a reduction in arterial perfusion of intra-abdominal organs, IAH leads to a compression of mesenteric veins causing venous hypertension, intestinal edema and ileus (Fig. 22.1).

Fig. 22.1
A cyclic chart for the pathophysiological cycle of fluid overload flows as follows. 1, fluid resuscitation. 2, intestinal edema. 3, visceral swelling. 4, I A H and A C S. 5, mesenteric vein and V C I compression. 6, reduced venous return, congestion. 7, reduced C O and M O F.

The vicious pathophysiological cycle of fluid overload leads to intra-abdominal hypertension and abdominal compartment syndrome with subsequent kidney dysfunction. ACS abdominal compartment syndrome, CO cardiac output, IAH intra-abdominal hypertension, MOF multiple organ failure, VCI vena cava inferior

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The pathophysiological impact of elevated IAP on the various organ systems mimics a state similar to sepsis. To restore hemodynamic stability, fluid resuscitation is often the first choice. However, administering large amounts of fluids may result in secondary IAH and ACS. The increased IAP stimulates anti-diuretic hormone (ADH), further promoting fluid retention [7] as well as renin-angiotensin-aldosterone release [8]. Besides the main impact on cardiorespiratory function, IAH affects all organ functions within and outside the abdominal cavity [9].

Globally Increased Permeability Syndrome

As a result of the pathological changes associated with injury, capillary permeability increases, causing a loss of colloid oncotic pressure and net extravasation of fluid to the interstitial and intracellular spaces [10]. Isotonic, hypotonic and small molecular weight (colloid) solutions (including albumin) have been shown to leak across the capillary bed causing edema. These fluid shifts are magnified by conventional fluid resuscitation protocols and may lead to visceral edema. In the lungs, fluid extravasation and increased permeability of the pulmonary capillaries can lead to pulmonary edema and increased extravascular lung water. In the GI tract, splanchnic edema can increase IAP and cause a decrease in tissue oxygenation, increased gut susceptibility to infection, impaired wound healing and ileus. Therefore administering intravenous fluids potentially induces a vicious cycle, where interstitial edema induces organ dysfunction that contributes to fluid accumulation (Fig. 22.1). Peripheral and generalized edema is not only of cosmetic concern, as believed by some, but it is harmful to the patient as a whole and can cause organ edema and deterioration in organ function. Some patients will not progress to the “flow” phase spontaneously and will remain in a persistent state of global increased permeability syndrome and ongoing fluid accumulation. The global increased permeability syndrome can hence be defined as fluid overload in combination with new-onset organ failure. This is referred to as “the third hit of shock” [11]. The percentage of fluid accumulation is calculated by dividing the cumulative fluid balance in litres by the patient’s baseline body weight and multiplying it by 100. Fluid overload is defined at any stage of illness as greater than 10% fluid accumulation and is associated with worse outcomes [12]. Studies demonstrate an association between fluid overload, illustrated by the increase in the cumulative fluid balance and worse outcomes in critically ill patients with septic shock.

Fluids and IAH

Why Do We Like Fluids in IAH?

Fluids are a double-edged sword, especially in patients with IAH. The importance of increasing circulating blood volume in patients with IAH and ACS has been known for decades, and the implementation of guidelines and protocols for fluid management in sepsis has saved countless lives. However, is this really always the case? Burn resuscitation is a well-known example, where mortality was significantly decreased using aggressive crystalloid resuscitation. In recent years the pendulum has swung back toward a more cautious approach to fluid resuscitation as the deleterious effects of fluid accumulation became apparent. In fact, most burn resuscitation guidelines are still based on the Parkland formula published in the 1960s and guided by crude static markers such as arterial pressure, central venous pressure or urine output. In another example, septic shock is managed with fluid resuscitation at a dose of 30 mL/kg that can be started within the first hour. This is the first and foremost therapeutic action recommended in the Surviving Sepsis Campaign Guidelines [13]. The problem is not in the fluid per se but in the dose, timing and protocols that guide our treatment. Understanding of the pathophysiology has improved and more sophisticated and reliable devices for monitoring have recently been developed, challenging previous concepts of fluid resuscitation and responsiveness.

Recently, the phenomenon of ‘fluid creep’ has also been described in critically ill patients [14]. In their study of 14,654 patients during their cumulative ICU stay of 103,098 days, Van Regenmortel et al. found that maintenance and replacement fluids accounted for 24.7% of the mean daily total fluid volume, far exceeding resuscitation fluids (6.5%) and were the most important sources of sodium and chloride overload. Fluid creep represented 32.6% of the mean daily total fluid volume. Therefore, in septic patients, non-resuscitation fluids had a larger absolute impact on cumulative fluid balance than resuscitation fluids. Recently, more attention is being paid to the different phases of IV fluid management (and the ROSE concept). However, we must pay attention that the pendulum is not swinging back toward more restrictive fluid management and the use of early vasopressors [15,16,17]. The final results of the ongoing RADAR-2 and CLASSIC trials will shed more light on this topic [16, 18].

Understanding the Linkage Between Over Fluids and IAH?

The dangers of under-resuscitation in terms of the amount or timing of fluid administration are clear, but the adverse effects of over-resuscitation, especially using crystalloids, are only recently being recognized. There is increasing evidence that IAH may be the missing link between over-resuscitation, multi-organ failure and death [19, 20]. Risk factors for the development of IAH and definitions related to IAH and ACS as published by the World Society for the abdominal compartment syndrome are listed in Table 22.1 [3].

Table 22.1 Risk factors for intra-abdominal hypertension
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Secondary ACS has been described in trauma, burns and sepsis. The multi-centre studies on the prevalence and incidence of IAH in mixed ICU patients also showed that a positive net fluid balance as well as a positive cumulative fluid balance were predictors for poor outcomes, whereas non-survivors had a positive cumulative fluid balance [21, 22]. Similar results have also been found by Alsous where at least 1 day of negative fluid balance (≤−500 mL) achieved by the third day of treatment was a good independent predictor of survival in patients with septic shock [23]. However, one must be aware of potential confounders (pre-resuscitation status, ongoing (abdominal) sepsis, comorbidities, etc.) as this was a retrospective observational study. In light of this increasing body of evidence regarding the association between massive fluid resuscitation, intra-abdominal hypertension, organ dysfunction and mortality, it seems wise to at least incorporate IAP as a parameter in all future studies regarding fluid management and to question current clinical practice guidelines, not in terms of whether to administer intravenous fluids at all, but in terms of the parameters we use to guide our treatment.

Do Patients with IAH Have a More Positive Fluid Balance?

A recent systematic review combining pooled data was available from 1517 patients obtained from an individual patient meta-analysis and seven cohort or case-controlled studies [12]. The pooled results revealed that the 597 patients with IAH (incidence being 39.4%) had a more positive fluid balance than those without IAH (7777.9 ± 3803 mL versus 4389.3 ± 1996.4 mL) (Fig. 22.2). The cumulative fluid balance after 1 week of ICU stay was on average 3388.6 ± 2324.2 mL more positive. The Forest plot is shown in Fig. 22.3.

Fig. 22.2
A column chart titled cumulative fluid balance after 1-week plots the following values. (No I A H, 4389.3) and (I A H, 7777.9).

Bar graph showing mean cumulative fluid balance after 1 week of intensive care unit (ICU) stay. Light grey bars showing data in patients without intra-abdominal hypertension, IAH (left) vs those with IAH (right). (Adapted from Malbrain et al. with permission [12])

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Fig. 22.3
A table lists columns for study or subgroup, mean and S D of no I A H, mean and S D of I A H, total, weight, and mean difference with a graph for the mean difference. The graph records all the plots in favors negative F B.

Forest plot looking at cumulative fluid balance after 1 week of ICU stay in patients with and without intra-abdominal hypertension (IAH). (Updated and adapted from Malbrain et al. [12])

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An extensive review of the literature (between 1999 and 2020) identified 32 prospective studies investigating the relationship between intravenous fluids and IAH. We will briefly discuss the data obtained from the literature review in relation to different patient populations.

Relation Between Fluids and IAH in Severe Burn Patients

O′ Mara et al. compared crystalloid and colloid resuscitation regimens in patients with massive burns [24]. Patients in the crystalloid group received more fluids per kilogram body weight, both in the first 24 h and during the whole course of resuscitation. This led to a significantly higher increase in IAP. Ruiz-Castilla et al., studied 25 severely burned adult patients and found that the prevalence of IAH was higher in patients with >20% TBSA burned. Also, the patients with IAH received significantly more crystalloids in the first 24 h after admission [25]. Similarly, Oda and co-workers found that in shock associated with burn, fluid resuscitation with low-volume hypertonic lactated saline can reduce the risk of secondary ACS compared to resuscitation with Ringers’ lactate solution [26]. In another study by Oda et al., a significant correlation between IAP and resuscitation volume was found, and most patients with ACS received more than 300 mL/kg/24 h [27]. Kuntscher found that the CVP is more influenced by IAP than by the actual intravascular volume status of the patient, however, there was a poor correlation between IAP and total blood volume [28]. Mbiine et al., also found a higher incidence of IAH among burn patients who were fluid overloaded, albeit not significant [29]. In the work of Wise et al., a group of 56 adult burn patients were examined and patients who developed ACS had higher cumulative fluid balances [30] (Table 22.2).

Table 22.2 Summary of studies in burn patients examining the relation between fluid resuscitation and IAH
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Relation Between Fluids and IAH in Severe Acute Pancreatitis

Zhao et al. studied 120 patients with severe acute pancreatitis (SAP) receiving three different resuscitation solutions [31]. Incidence of IAH and ACS were significantly lower in subgroups with lower fluid resuscitation volume. Similarly, Mao et al. found in a group of 76 patients with SAP that the incidence of ACS was significantly lower in patients with lower initial fluid resuscitation [32]. In the study of Du et al. involving 41 patients with SAP, colloid resuscitation correlated with less IAH, while the total amount of IV fluid did not differ significantly between colloid and crystalloid groups [33]. This has pointed to the possibility that not only the amount but also the type of fluid used is important in the prevention of IAH. Ke and co-workers studied 56 patients with SAP and found that the fluid balance during the first day of ICU admission was an independent predictor for the development of IAH [34] (Table 22.3).

Table 22.3 Summary of studies in severe acute pancreatitis examining the relation between fluid resuscitation and IAH
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Relation Between Fluids and IAH in Trauma Patients

Balogh et al., found that trauma patients who developed ACS, either primary or secondary, had more fluids infused than patients without ACS [35]. Similarly, Mahmood et al. showed in a group of 117 trauma patients that those with higher IAP received significantly more blood transfusions as well as more crystalloids during the first 2 h of hospitalization [36]. In the recent study by Vatankhah et al. patients with blunt abdominal trauma who developed ACS received significantly more intravenous fluids, both crystalloids and blood products, in the first 24 h of their hospital stay [37]. Raeburn et al. studied 77 trauma patients requiring post-injury damage control laparotomy and were divided into two groups according to the development of ACS [38]. The patients with ACS received more intravenous fluids, however, this difference did not reach significance, which was contrary to the previously published work in the field (Table 22.4).

Table 22.4 Summary of studies in trauma patients examining the relation between fluid resuscitation and IAH
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Relation Between Fluids and IAH in Mixed ICU Patients

The incidence of IAH and ACS in a group of 40 medical ICU patients with a positive fluid balance of more than 5 L/24 h was high, with 85% developing IAH and 25% developing ACS [39]. Cordemans et al. had similar findings where the average positive cumulative fluid balance after 1 week was higher in critically ill patients developing IAH [40]. Moreover, increased mean IAP was determined as an independent risk factor for not achieving conservative late fluid management (defined as even-to-negative fluid balance on at least two consecutive days during the first week of ICU stay). Dalfino et al. studied a group of 69 patients undergoing elective cardiac surgery [41]. Twenty-two patients (31.8%) developed IAH. In this subgroup, baseline values of IAP, although normal, were significantly higher. The duration of surgery was also longer and fluid balance was higher. In the subsequent analysis, the positive fluid balance comprised one of three independent predictors for developing IAH, with baseline IAP and central venous pressure. Similarly, Muturi et al. in their work involving 113 surgical ICU patients, found that large volume intravenous fluid administration over 24 h and a positive fluid balance were significantly associated with the development of IAH [42]. Moreover, among IAH patients, those who subsequently developed ACS had a higher fluid balance and received more intravenous fluids in 24 h. In the recent work of Kotlińska-Hasiec et al. [43], patients undergoing hip or knee replacement were divided into liberal or restrictive fluid therapy subgroups. A rise in IAP after surgery was seen in both subgroups, but it was significantly greater in the liberal subgroup. Furthermore, a strong correlation between IAP and extra-cellular water content was noticed in the liberal subgroup, which is in keeping with the theory of fluid extravasation being one of the important mechanisms in the development of IAH. Šerpytis and Ivaškevičius studied 77 patients after abdominal surgery and found a significant positive correlation between the daily changes in IAP and the daily changes in fluid balance during all three postoperative days, i.e. IAP increased with a positive fluid balance and decreased with a negative one [44]. Biancofiore and co-workers studied 108 patients after orthotopic liver transplantation. They found that patients with IAH (31%) received a significantly higher amount of IV fluids than those with a normal IAP [45].

Acute renal failure developed in 17 recipients (16%), 11 (65%) of whom had IAH (p < 0.01), with a mean IAP of 27.9 ± 9.9 mmHg vs 18.6 ± 5.2 mmHg in those without acute renal failure (p < 0.001). Intraoperative transfusions of more than 15 units packed RBC, respiratory failure and IAH (p < 0.01) were independent risk factors for renal failure.

Iyer et al. also found that patients who developed IAH received significantly more intravenous fluids in the first 24 h of admission (4.24 L vs 2.75 L in non-IAH patients, p < 0.001), and their fluid balance was significantly more positive after 24 h (2.47 L vs 1.23 L, p < 0.001) [46]. Dalfino and co-authors recruited a group of 123 patients admitted to a general ICU [47]. The primary end-point of the study was the relationship between intra-abdominal hypertension (IAH) and acute renal failure. IAH was detected in 30.1% of patients. This study showed that the cumulative fluid intake in the first 72 h after admission was higher in IAH patients, although this difference was not significant. On the contrary, cumulative fluid balance in the first 72 h was significantly higher in IAH patients (3.76 L vs 0.68 L, p < 0.001). Consequently, a positive fluid balance was found to be an independent risk factor of IAH (p = 0.002). Vidal et al. observed that patients with IAH had consistently higher daily and cumulative fluid balances [48]. Malbrain et al. showed that among six etiological factors and ten predisposing conditions possibly correlated with IAH, only two were significantly associated, namely fluid resuscitation (OR 3.3; 95% CI 1.2–9.2) and polytransfusion (transfusion of >6 units of packed red blood cells in the 24 h before the study entry) [21].

In a multi-centre, prospective epidemiologic study, patients with IAH had significantly higher rates of massive fluid resuscitation (>3.5 L of colloids or crystalloids in the 24 h before the study) [49]. Fluid resuscitation was one of four independent predictors of IAH (OR, 1.88; 95%CI 1.04–3.42; p = 0.04), including independent of admission type (medical or surgical). The occurrence of IAH during the ICU stay was also an independent predictor of mortality (relative risk of 1.85; 95%CI1.12–3.06; p = 0.01). Patients with IAH on admission had significantly higher SOFA scores during their stay than patients without IAH. Blaser et al. investigated independent risk factors for IAH in a group of 563 mechanically ventilated ICU patients [50]. Patients with IAH received significantly more large volume fluid resuscitation (>5 L/24 h). However, fluid resuscitation was not considered an independent risk factor. In a more recent study by the same group, the prevalence, risk factors and outcomes of intra-abdominal hypertension in a mixed multicentre ICU population of 491 patients were investigated [51]. Nearly half of all patients (n = 240; 48.9%) developed IAH during the observation period, and nearly half (46.3%) had primary IAH. One of the independent risk factors for the development of IAH was a positive daily fluid balance (OR 1.1638, p = 0.001). Dabrowski et al. found a strong correlation between IAP and total body water, extracellular water content and volume excess in critically ill patients and between IAP and extracellular water content in surgical patients [52].

Finally, a meta-analysis combining individual patient databases of different studies including 1669 patients showed that the only independent predictors for IAH were SOFA score and fluid balance on the day of admission [53] (Table 22.5).

Table 22.5 Summary of studies examining the relation between fluid resuscitation and IAH
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Does IAP Improve with Interventions Acting on Reducing Fluid Balance?

Thirteen studies investigated the effects of fluid removal (use of furosemide or renal replacement therapy with net ultrafiltration) on IAP (Fig. 22.4). These were case studies or small series [24, 40, 44, 54,55,56,57,58,59,60,61,62]. A total fluid removal of 4876.3 ± 4178.5 mL resulted in a drop in IAP from 19.3 ± 9.1 to 11.5 ± 3.9 mmHg (Fig. 22.5). A dose-related effect was observed: the more negative the net fluid balance or fluid removal the greater the decrease in IAP (Fig. 22.6). Although difficult if not impossible to prove, many of these studies were done in patients who were over-resuscitated. The impact of diuretics or fluid removal may be variable when applied as a general strategy. The use of diuretics is preferred but this should be done in a targeted approach, where one looks at the different contributors to IAH, and acts accordingly. The different medical management strategies are summarized in Fig. 22.7.

Fig. 22.4
A table lists columns for study or subgroup, mean and S D of treatment, mean and S D of control, total, weight, and mean difference with a graph for the mean difference. The graph records all the plots in favors treatment.

Forest plot looking at the effect of fluid removal on intra-abdominal pressure. (Updated and adapted from Malbrain et al. [12])

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Fig. 22.5
A column chart with error handles plot I A P for before and after. The plotted values are (before, 19.3 + or minus 9.2) and (after, 11.5 + or minus 3.9).

Boxplot showing the effect of fluid removal (after) on intra-abdominal pressure (IAP, mmHg). Solid line indicates median IAP with interquartile range. (Adapted from Malbrain et al. with permission [12])

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Fig. 22.6
A line and dot plot of delta I A P versus delta fluid balance with an upward-sloping line and the following highest and lowest values. (Negative 4, 500) and (negative 16, negative 10800). Here, y = 380.88 x minus 970.08 and R square = 0.5121.

Pearson correlation graph showing the change in intra-abdominal pressure (ΔIAP) in relation to the amount of fluid removed (ΔFluid Balance). (Adapted from Malbrain et al. with permission [12])

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Fig. 22.7
A medical management algorithm flowchart is as follows. Beginning medical management to reduce I A P. Measuring I A P periodically and titrate therapy to maintain I A P. Evacuation of intraluminal contents, space-occupying lesions, improving abdominal wall compliance, and optimizing fluid administration and systemic regional perfusion.

WSACS 2013 intra-abdominal hypertension/abdominal compartment syndrome medical management algorithm. (Figure reproduced and adapted with permission from Kirkpatrick et al. according to the Open Access CC BY Licence 4.0 [1])

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Recommendations for Fluid Management in Secondary IAH

Note: This section presents some recommendations and suggestions for prevention and treatment of fluid accumulation in patients with or at risk for IAH, based on personal experience of the co-authors. It does not aim to provide an exhaustive, graded and concise overview of the literature as current evidence is mostly limited to observational, retrospective or small clinical studies and more randomized trials are needed to better establish a personalized approach to fluid management in IAH.

Question 1. Is There Evidence to Prefer Albumin (Any Tonicity) or Hypertonic Solutions to Crystalloids During General Management?

Several studies evaluated the use of albumin as a resuscitation fluid. Except for patients with traumatic brain injury, current evidence suggests that albumin is well tolerated as a resuscitation fluid. However, there is no evidence suggesting that albumin offers outcome benefits over crystalloid solutions. A retrospective study in 114 patients showed that the use of PAL (PEEP set at level of IAP followed by albumin 20% followed by furosemide) treatment was able to keep cumulative fluid balance ‘in check’ with a significant drop in IAP and EVLWI and a rise in P/F ratio [63]. This also resulted in faster weaning and improved survival when compared to a matched control group.

  • We recommend against the use of high-dose (20–25%) albumin as resuscitation fluid in early phase of IAH patients.

  • We recommend against the use of low-dose (4%) albumin as resuscitation fluid in IAH patients with low blood pressure.

  • We recommend using hypertonic albumin 20% only in selected patients, in the late phase of septic shock and during deresuscitation of patients with secondary IAH.

  • We suggest against the use of hypertonic saline solutions as resuscitation fluids in IAH patients with low blood pressure.

Question 2. Is There Evidence to Prefer Colloids to Crystalloids During General Management?

In a randomized controlled trial involving 41 patients with SAP, hydroxyethyl starch resuscitation resulted in a decrease in IAP, and reduced need for mechanical ventilation compared to cases where Ringer’s lactate was used. HES resuscitation led to a decrease in the IAP and reduced the use of mechanical ventilation, achieving a negative fluid balance before such a balance was achieved by a Ringer’s lactate solution [33]. However, from randomized controlled trials there is no evidence that resuscitation with colloids reduces the risk of death, compared to resuscitation with crystalloids, in patients with trauma, burns or following surgery [64].

  • We suggest against the use of synthetic colloids as resuscitation fluids in IAH patients with low blood pressure.

  • We recommend against the use of starch solutions in patients with sepsis-associated secondary IAH and low blood pressure.

  • We suggest using crystalloids as first-line resuscitation fluids in IAH patients with low blood pressure.

  • We recommend against the use of glucose-containing hypotonic solutions and other hypotonic solutions (osmolality <260 mosm/L) as resuscitation fluids in general and IAH patients.

Question 3. Is There Evidence to Prefer Using Buffered Crystalloids During General Management?

Wu et al. conducted a randomized controlled trial in 40 patients with SAP comparing resuscitation with 0.9% saline to Ringer’s lactate solution and found that patients who were resuscitated with Ringer’s lactate solution had reduced systemic inflammation compared with those who received saline. There was, however, no difference in outcome between study groups [65]. A recent meta-analysis from 2018 confirmed the anti-inflammatory effects of Ringer’s lactate and showed that it tended to have lower mortality rates compared to 0.9% saline [66].

A RCT involving 60 patients with acute pancreatitis, but without systemic inflammatory response syndrome or organ failure, received either aggressive vs. standard resuscitation with Ringer’s lactate solution. There was a greater rate of clinical improvement with aggressive hydration vs. standard practice [67].

According to the Working Group IAP/APA Acute Pancreatitis Guidelines Ringer’s lactate is the recommended fluid for initial resuscitation in acute pancreatitis [68].

Balanced solutions have been shown to be superior to unbalanced solutions for fluid replacement [69]. Ringer’s acetate seems to be the most appropriate choice for large replacements [70].

The recently conducted pragmatic SMART study confirmed the superiority of buffered (so-called balanced) solutions over (ab)normal saline (NaCl 0.9%) [71]. Among 15,802 critically ill adults, the use of balanced crystalloids for intravenous fluid administration resulted in a lower rate of the composite outcome of death from any cause, new renal-replacement therapy, or persistent renal dysfunction than the use of saline.

  • We recommend using buffered (or balanced) crystalloids as first-line resuscitation fluids in IAH patients with low blood pressure.

Question 4. Is There Evidence Regarding the Best Maintenance Solution in IAH?

In a large retrospective study, Van Regenmortel found that maintenance fluid accounted for volume, sodium and chloride overload exceeding resuscitation fluids. This burden can be avoided by adopting a hypotonic (and balanced) maintenance strategy [14]. Similar results were found when comparing glucose 5% plus Na154 (0.9% saline) vs Na54 as maintenance solution in patients undergoing thoracic surgery [72].

  • We recommend the use of crystalloids as preferred maintenance fluids in IAH patients.

  • We recommend against the use of colloids, glucose- and salt- containing isotonic solutions, or albumin as maintenance fluids in IAH patients.

  • We recommend the use of hypotonic and balanced crystalloids as preferred maintenance fluids in IAH patients.

  • We suggest monitoring electrolytes (Na+, Cl−) and osmolality as a safety endpoint for fluid therapy in IAH patients.

Question 5. Is There Evidence to Prefer Hypertonic Solutions for the Management of Acute Rise in IAP?

Several animal studies proved that hypertonic saline (HTS) resuscitation improves hemodynamics [73,74,75,76]. HTS treatment allows smaller fluid volume resuscitation in the burn shock period and reduces the risk of low abdominal perfusion and secondary ACS [26]. The American Burn Association evaluated the efficacy of HTS in burn patients, but currently has not found clear evidence in favour of, or against them. Additional studies are required to define the correct dosage and timing [77].

  • We recommend against the use of mannitol solution for reducing increased IAP.

  • We recommend the use of hypertonic saline solution for reducing increased IAP in selected patients.

  • We suggest using a predefined trigger for starting osmotherapy to treat elevated IAP.

  • We suggest using a combination of clinical, laboratory and worsening organ function variables (defined as a SOFA score equal to or greater than 3) in combination with IAP >20 mmHg for starting osmotherapy to treat elevated IAP.

  • We suggest using an IAP threshold >25 mmHg, independent of other variables, as a trigger for starting osmotherapy to reduce IAP.

  • We recommend against the use of an IAP threshold below 15 mmHg independent of other variables as a trigger for starting osmotherapy to reduce IAP.

  • We suggest monitoring measured serum osmolarity and electrolytes to limit the side effects of osmotherapy.

  • We suggest monitoring IAP response to hyperosmolar fluids to limit the side effects of osmotherapy.

Question 6. Is There Evidence for the Best Management in Case of ACS and Intestinal Ischemia?

  • We recommend assessing the efficacy of fluid infusion in ACS patients with suspicion of intestinal ischemia using a multimodal approach that includes arterial blood pressure, cardiac output and reversal of IAP-related hypoperfusion as the main endpoints.

  • We suggest that an increase in the plasma disappearance rate of indocyanine green, and improvements in renal resistive index should be used as secondary endpoints when assessing the efficacy of fluids for the reversal of intestinal ischemia in ACS patients.

Question 7. Is There Evidence Regarding Impact of Fluid Load on IAH?

Two RCTs in 76 and 115 patients with SAP show that rapid, uncontrolled fluid resuscitation (10–15 mL/kg/h or until a haematocrit <35% within 48 h) significantly worsened the rates of infections, abdominal compartment syndrome, the need for mechanical ventilation and even mortality. Hematocrit should be maintained between 30% and 40% in the acute response stage [32].

  • We suggest monitoring the effects of any fluids administered on IAP, arterial blood pressure and fluid balance as secondary variables to limit the side effects.

  • We suggest that clinicians consider targeting normovolaemia during fluid replacement in IAH patients.

  • We recommend the use of a multimodal approach, guided by the integration of more than a single hemodynamic variable, to optimize fluid therapy in IAH patients.

  • We recommend considering using IAP, arterial blood pressure and fluid balance as the main endpoints to optimize fluid therapy in IAH patients.

  • We suggest integrating other variables (such as cardiac output, functional haemodynamics, S(c)vO2, blood lactate, base deficit, urinary output, extravascular lung water, bio-electrical impedance analysis, capillary leak index, pulmonary vascular permeability index) to optimize fluid therapy in IAH patients.

  • We recommend against the use of central venous pressure alone (as CVP may be erroneously increased) as an (safety) endpoint for guiding fluid therapy in IAH patients.

  • We suggest the use of restrictive fluid strategies (aiming for an overall neutral to negative fluid balance within the first week) in IAH patients.

  • We suggest using body weight, daily and cumulative fluid balance as a safety endpoint for fluid therapy in IAH patients.

  • We suggest monitoring measured osmolarity, total protein levels, haematocrit levels and colloid oncotic pressure as a safety endpoint for fluid therapy in IAH patients.

Question 8. Is There Evidence Regarding Resuscitation with Fresh Frozen Plasma?

Wang et al. conducted a RCT in 132 patients with SAP concerning the effect of fluid resuscitation with fresh frozen plasma. FFP shortens the duration of positive fluid balance, decreases the amount of positive fluid balance within 72 h, reduces the duration of mechanical ventilation and admissions to the ICU and improves PaO2/FiO2 and mortality in SAP [78].

  • We recommend against the use of fresh frozen plasma as resuscitation fluid in IAH patients.

Question 9. Is There Evidence Regarding Adjunctive Use of High-Dose Vitamin C?

In the 1990s, Matsuda et al. were able to reduce fluid requirements and edema formation during burn resuscitation in dogs and guinea pigs by using high-dose ascorbic acid therapy [79, 80].

A few years later they reproduced the beneficial effects of high-dose ascorbic acid in humans in a prospective, randomized study [81].

During the first 24 h, resuscitation fluid volume requirements were significantly reduced. Ascorbic acid has an apparent (osmotic) diuretic effect that may lead to hypovolemia. The decreased insensible fluid losses may also lead to a reduced inflammatory response and earlier mobilization of fluid.

  • We recommend against the use of adjunctive high-dose ascorbic acid in the treatment of IAH patients.

Case Vignette

Questions and Answers

Going back to the clinical vignette the patient was in profound septic shock and capillary leak with intravascular underfilling and extravascular fluid overload.

  • Q1. What fluids should be administered?

  • A1. Fluids should be administered, however, a combination of balanced crystalloids (e.g. PlasmaLyte) with hypertonic solutions (like albumin 20%) guided by plasma albumin levels, osmolality and serum colloid oncotic pressure. The combination of vasopressors should allow fluids to be limited. Source control must be checked and adequate. It must be noted that traditional filling pressures like CVP may be erroneously increased and volumetric preload parameters may better reflect the true filling status in IAH.

  • The patient was fluid responsive as shown by the high PPV and the positive passive leg raising test.

  • Q2. How do you interpret the increased PPV in the setting of ACS?

  • A2. The clinician must be aware that IAP can falsely increase PPV and SVV, for instance when IAP goes up from 10 to 20 mmHg this may result in an increase of PPV from 12% to 24%. Therefore, our traditional thresholds identifying fluid responsiveness must be adapted when IAP is increased.

  • The clinical condition of the patient deteriorated further and a decompressive laparotomy was performed at the bedside in the ICU, which revealed no intra-abdominal abnormalities.

  • Q3. Were all medical management options used before DL?

  • A3. Before DL is chosen all medical management options must be tried and evaluated. In this case, it would have been an option (in view of the positive cumulative fluid balance) to mobilize the excess fluids with albumin 20% in combination with diuretics or CVVH and aggressive ultrafiltration. Only when all medical options fail should surgery be undertaken.

  • Each day, around 4 L of fluid were drained via the VAC system.

  • Q4. Do you have any concerns regarding the interstitial (third) space fluid losses?

  • A4. Third space fluid losses can be substantial in patients with open abdomen and TAC with VAC. These fluid and nitrogen losses need to be taken into account and replaced when indicated.

  • Despite the initial improvement after decompressive laparotomy renal function deteriorated again and continuous venovenous hemofiltration (CVVH) with ultrafiltration was started.

  • Q5. Is there a role for hypertonic solutions and diuretics in this patient?

  • A5. As stated above hypertonic solutions can be an option in selected cases, and can be used at the later deresuscitation phase in combination with diuretics or CVVH and UF.

Conclusion

Intravenous fluid administration plays an important role in the development of secondary IAH and ACS. Multiple pathophysiological mechanisms have been described. Fluid resuscitation in IAH is a double-edged sword, that can improve cardiac output initially, but overzealous ongoing fluid administration can further increase IAP, leading to fluid accumulation, and organ dysfunction including AKI. Daily and cumulative fluid balance has been identified as an independent risk factor in several clinical studies and can contribute to the development of IAH, and a vicious cycle leading to venous congestion, gut oedema with diminished gut contractility and organ failure. Evidence identifying the best resuscitation targets and management strategies regarding type, timing and amountof fluids in patients with IAH is scarce and further research is required.

Take Home Messages

  • There is a clear relationship between amount and dose of (crystalloid) fluid resuscitation, fluid accumulation and secondary IAH.

  • Development of IAH is more likely in the setting of sepsis (capillary leak), severe burn injury, severe acute pancreatitis, emergency surgery and trauma and the presence of the deadly triad (coagulopathy, acidosis, hypothermia).

  • Fluid resuscitation in IAH may preserve cardiac output, however, it does not prevent organ damage (vicious cycle and double-edged sword).

  • Fluid resuscitation leads also to venous congestion (or venous hypertension), which in turn results in gut edema and diminished gut contractility.

  • Fluid removal with diuretics or CVVH may restore cumulative fluid balance and lower IAP.

  • Medical management comes first and surgical decompression can be used as a last resort, also in secondary ACS.

  • Elevated vascular permeability due to a stress-related inflammatory response associated with positive fluid balance leads to extravascular fluid accumulation, which is likely to result in gastrointestinal tract edema and increased IAP.

  • Development of ACS in burns is associated with the total burned surface area TBSA (>20%) and the total amount of administered fluid volume (>300 mL/kg)

  • In cases of SAP, the less fluids patients receive after the initial resuscitation, the lower the risk of developing secondary IAH and/or ACS.

  • Crystalloids are associated with more positive fluid balance and a greater likelihood of developing IAH compared to colloids or hypertonic solutions.