Fluid resuscitation

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Fluid resuscitation: when less becomes more…

Inneke E De laet (1) Jan J De Waele (2) Manu LNG Malbrain (1)

(1) ZNA Stuivenberg Hospital, Antwerp, Belgium (2) Ghent University Hospital, Ghent, Belgium

Corresponding Author:

Manu LNG Malbrain ICU Director ZNA Stuivenberg Lange Beeldekensstraat 267 2060 Antwerpen Belgium Tel: +32 3 217 7399 Fax: + 32 3 217 7574 e-mail: [email protected]

Introduction Fluid resuscitation has been a cornerstone of critical care medicine for as long as critical care medicine has existed. It has been on intensivists’ mind in times when heart rate and blood pressure were the only available monitoring tools and has stayed with us after every new technological revolution from the pulmonary artery catheter (PAC) to the non-invasive cardiac output monitoring tools we use today. But no catheter will improve outcome on its own: the advantage can only be found in the way we use it, and in the protocol behind that drives the variables. Over the years, our fluid management has not changed as much as the technology used to guide it. Although there are enough recent data to indicate that current fluid management strategies may increase morbidity and mortality (1, 2) as well as prevent it, these data have been slow to seep through into guidelines and protocols, possibly harming patients. This book chapter will focus on recent scientific data regarding risks of current fluid management and offer some clues for future research.

Why do we like fluids? The importance of increasing circulating blood volume in hypovolemic shock, such as in trauma patients, has been apparent for decades and undoubtedly, the implementation of guidelines and protocols for fluid management in trauma (such as the Advanced Trauma Life Support protocol put forward by the American College of Surgeons) has saved countless lives. After the success obtained in hypovolemic shock, aggressive fluid resuscitation has been studied in distributive shock as well. Burn resuscitation is a well known example, where mortality was significantly decreased using aggressive crystalloid resuscitation . In fact, most burn resuscitation guidelines in the 21st century are still based on the Parkland formula published in de 1960’s . In septic shock as well, fluid resuscitation is the first and foremost therapeutic action recommended in the Surviving Sepsis Campaign Guidelines (3).

Traditionally, fluid resuscitation protocols are aimed at correction of “basic” physiologic parameters such as blood pressure, central venous pressure (CVP) and urine output. The advantages of this approach are multiple and easy to understand: these parameters are readily available at the beside and do not require expensive and operator dependent equipment, leading to broader applicability worldwide. Although many aspects of intensive care medicine have undergone extensive changes in the last 20 years, insights in pathophysiology have evolved dramatically and more sophisticated and reliable devices for monitoring and therapy are developed every day, the concept of fluid resuscitation as an ubiquitous positive influence on patient outcome has scarcely been challenged. Over time, the only significant evolution regarding the use fluid resuscitation as such has been the gradual increase in emphasis on the importance of time. Both in trauma and burns, delayed fluid resuscitation has been associated with increased mortality and ATLS guidelines as well as burn resuscitation guidelines have stressed the importance of prompt administration of fluids for a long time. The importance of time in sepsis was highlighted more recently in the landmark paper by Rivers et al. (4) and current sepsis guidelines have embraced this concept completely (3).

Which fluids do we like? The ultimate goal of treatment in shock is to restore the balance between oxygen demand and oxygen delivery, which means to optimize cardiac output and effective circulating volume. Therefore, the goal of fluid resuscitation is to restore circulating blood volume, which may mean substitution of external losses, supplying volume to a dilated vascular system, or supplementing internal losses due to third spacing or capillary leak. This has traditionally been accomplished using isotonic crystalloid solutions which contain mainly NaCl. Since the Na+ ion is an extracellular ion, crystalloid solutions will be evenly distributed throughout the extracellular body water compartment after IV administration. This means that

IV administration of 1000mL of NaCl 0.9% solution leads to approximately 200 to 300mL of intravascular compartment expansion and in order to achieve a 1000mL increase in cicrulating volume, 3000 to 5000mL of isotonic crystalloid solution have to be administered. In the search for fluids that would selectively expand the intravascular compartment, colloids, both synthetic and natural, were evaluated. According to Starling’s equation (Fig 1) they should tip the balance in favor of fluid movement from the interstitial to the intravascular compartment and thus plasma volume expansion. However, several studies could not show a survival benefit in favor of colloid resuscitation using either albumin or synthetic colloid solutions in several clinical situations. Furthermore, colloids are more expensive, albumin and gelatins were manufactured as derivatives from human and animal tissue and therefore carried a small risk for disease transmission and synthetic colloids were associated with adverse effects such as anaphylaxis, renal failure and coagulation defects. These findings resulted in the incorporation of crystalloid solutions in guidelines as the gold standard for fluid resuscitation, especially in North American literature and guidelines . The implementation of structured aggressive fluid resuscitation in a multitude of ICU patient populations has undoubtedly decreased mortality, but it has also lead to administration of enormous amounts of crystalloid solution in the first 24 hours after major trauma, burns or septic shock. In several studies, mean administration of more than 30 liters of crystalloids over 24 hours has been reported! In situations associated with capillary leak this approach leads to development of massive tissue edema and the iatrogenic complications that ensue may lead to multiple organ failure and death. Reports of mortality secondary to massive fluid resuscitation after trauma or shock are appearing increasingly over the last 10 years.

Do we like fluids too much?

The dangers of under-resuscitation in terms of 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 intraabdominal hypertension (IAH) may be the missing link between overresuscitation, multiple organ failure and death (5). 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 1 and Table 2 (6). Intra-abdominal pressure (IAP) and abdominal compartment syndrome (ACS) have been concepts well known to trauma surgeons for years (7-9) and as early as 1999, they were the first to report similar clinical findings in patients who received massive fluid resuscitation after extra-abdominal injury (10). The mechanism through which massive fluid resuscitation causes IAH is probably related to capillary leak and edema, both of the abdominal wall (leading to decreased abdominal wall compliance) and of the bowel wall (leading to increased abdominal volume). Both these mechanisms have been implicated in the development of IAH (Fig 2). In a retrospective series by Maxwell et al, the incidence of abdominal decompression among non-abdominal trauma victims was found to be 0.5% (10). The mean amount of fluids administered was 19 ± 5 liters of crystalloid and 29 ± 10 units of packed red blood cells, the mortality was 67% and non-survivors were decompressed approximately 20 hours later than survivors. The authors suggested that the incidence of secondary ACS may be higher than previously thought in non-abdominal trauma victims and that early decompression may improve outcome since some improvement in organ function after decompression was seen. They recommended IAP monitoring in patients receiving high amounts of fluid resuscitation. A landmark paper by Balogh et al confirmed these findings (1). In his series, 11 (9%) of 128 standardized shock resuscitation patients developed secondary ACS. All presented in severe shock (systolic blood pressure 85 ± 5 mm Hg, base deficit 8.6 ± 1.6 mEq/L), with severe injuries (injury severity score 28 ± 3) and

required aggressive shock resuscitation (26 ± 2 units of blood, 38 ± 3 L crystalloid within 24 hours). All cases of secondary ACS were recognized and decompressed within 24 hours of hospital admission. After decompression, the bladder pressure and the systemic vascular resistance decreased, while the mean arterial pressure, cardiac index, and static lung compliance increased. The mortality rate was 54%. Those who died failed to respond to decompression with increased cardiac index and a sustained decrease in IAP. In analogy to trauma, secondary ACS has since been described also in burns and sepsis. The multiple 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 outcome, nonsurvivors had a positive cumulative fluid balance of about 6 liters versus 1 liter in survivors (11, 12). Similar results have also been found by Alsous: at least 1 day of negative fluid balance (< or = -500 mL) achieved by the third day of treatment was a good independent predictor of survival in patients with septic shock. (13). Very recently, Daugherty et al conducted a prospective cohort study among 468 medical ICU patients (14). Forty patients (8,5%) had a net positive fluid balance of more than 5L after 24 hours (after all risk factors for primary ACS served as exclusion criteria). The incidence of IAH in this group was a staggering 85% and 25% developed secondary ACS. The study was not powered to detect differences in mortality and outcome parameters were not statistically different between patients with or without IAH and ACS. Nevertheless, there was a trend towards higher mortality in the IAH groups and mortality figures reached 80% in the ACS group. Although epidemiologic research regarding this subject is virtually nonexisting, the increase in reported series seems to indicate increasing incidence of this highly lethal complication. 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 put into question current clinical practice guidelines, not in terms of whether to administer fluids at all, but in terms of the parameters we use to guide our treatment.

So how should we use our fluids? To administer or not to administer fluids, that is not the question, but the nature and the quantity of our fluid resuscitation still need to be addressed. As a result of the increasing problems with massive fluid resuscitation, many researchers have gone back to the concept of small volume resuscitation. This concept, to achieve the same physiologic goals as in ‘classical’ crystalloid resuscitation using smaller volumes, implies the use of hypertonic or hyperosmotic solutions. In American literature there is a lot of attention for hypertonic saline in several indications (15, 16). European literature and clinical practice, having never abandoned colloid administration completely, focus mainly on new synthetic colloids such as 130kD hydroxyethyl starch (HES). Attempts to combine both strategies have lead to several studies using mixed hypertonic saline and colloid infusions e.g. hyperHES, a solution consisting of NaCl 7.2% in HES with mixed results. Although good results have been obtained with small volume resuscitation in most of these studies, many of them unfortunately make no mention of IAP or incidence of IAH and ACS at all. In the area of burn resuscitation there are some exceptions: Oda et al did report a reduced risk for abdominal compartment syndrome (17) (as well as lower fluid requirements during the first 24 hours and lower peak inspiratory pressures after 24 hours) when using hypertonic lactated saline for burn resuscitation and O Mara et al reported lower fluid requirements and lower IAP using colloids (18).

Another major issue in guiding fluid therapy is the lack of reliable resuscitation targets in patients with IAH or ACS. From a theoretical point of view, fluid administration is warranted as long as it promotes cardiac output and thus oxygen delivery. Therefore, the parameter we are most interested in is fluid responsiveness. Since this phenomenon is hard to measure or calculate it is traditionally substituted with cardiac preload which is, essentially, a volumetric parameter (although many definitions are used). Since cardiac volumes are also hard to measure, preload is usually estimated using cardiac filling pressures (central venous pressure (CVP) and pulmonary artery occlusion pressure (PAOP)). However, in IAH, the increased IAP is partially transmitted to the thorax in a variable manner dependent mostly on compliance of the abdominal and thoracic wall. The transmission index is estimated to be around 50% (19, 20). This mechanism leads to an increase in all intrathoracically measured pressures including CVP and PAOP which in this situation, although measured correctly, are no longer a reliable measure for cardiac preload. In situations of IAH, ‘volumetric indices’ such as global end-diastolic volume (GEDV), right ventricular end-diastolic volume (RVEDV) or left ventricular end-diastolic area (LVEDA) have been shown to be more reliable estimates for cardiac preload, but even they do not necessarily represent fluid responsiveness. Several non invasive cardiac output monitoring tools also provide measurements of systolic pressure variations (SPV), stroke volume variation (SVV) and pulse pressure variation (PPV) which have been shown to correlate well with fluid responsiveness (21). However, Duperret et al showed that SPV, SVV and PPV are increased in euvolemic pigs with IAH, which may compromise their use in clinical practice (22). They found that the systolic pressure (SPV) and pulse pressure variations (PPV), and inferior vena cava flow fluctuations were dependent on IAP values which caused changes in pleural pressure swings, and this dependency was more marked during hypovolaemia. A group of investigators from Brazil found that SPV is modified by haemorrhage but it is also influenced

by pneumoperitoneum or thus IAH. In contrast, PPV was modified by haemorrhage but not by pneumoperitoneum (23). These findings would suggest that PPV should be used preferentially instead of SPV to detect hypovolaemia and guide fluid therapy during laparoscopic surgery. However IAP was only increased to 10 mmHg, a very low value since most laparoscopic insufflators are limited to 14 mmHg and intra-abdominal hypertension (IAH) has been defined as an IAP above 12 mmHg (24). Both studies suggest that (some) dynamic indices are not exclusively related to volaemia in the presence of increased IAP. The results of Duperret also suggest a dose-related effect since pressure variations were more pronounced during abdominal banding gradually increasing IAP with 5 mmHg steps up to 30 mmHg. Systolic pressure variations were 6.1 ± 3.1%, 8.5 ± 3.6% and 16.0 ± 5.0% at 0, 10, and 30 mmHg IAP respectively in normovolaemic animals (mean ± SD; p< 0.01 for IAP effect). They were 12.7 ± 4.6%, 13.4 ± 6.7%, and 23.4 ± 6.3% in hypovolaemic animals (p< 0.01 vs normovolaemic group). However, both authors did not assess the isolated effect of hypovolemia (without the increased IAP) on SPV and PPV in their model which might have created some bias whilst interpreting the results, especially related to the time-course of their animal experiments. With regard to preload, Duperret looked at left ventricular enddiastolic pressure and LVEDA and found that the increase in the IAP induced a progressive increase in intrathoracic pressure, as indicated by the increased pleural pressure swings, and therefore a relative hypovolaemia owing to a redistribution of blood volume. Although this factor is likely to play a role at the highest values of IAP as a decrease in LVEDA was observed, a moderate value of IAP was, on the contrary, associated with an increase in thoracic blood volume as previously shown (22). Duperret observed an increase in the LVEDA and in the transmural left-ventricular enddiastolic pressure. Since the authors did not subject the animals to a fluid challenge they were unable to ascertain whether SPV, SVV and PPV still

represented fluid responsiveness although the pigs were euvolemic prior to the IAH. After all, IAH in itself may induce hypovolemia and lead to increased SVV and PPV. The studies by Bliacheriene and Duperret show the importance of the interactions between different compartments namely the thoracic and abdominal compartment (25). Recently, simultaneous changes in IAP and central venous pressure (CVP) tracings were studied in 24 patients during spontaneous breathing (26). A first group included 18 patients without active expiration and the second group included 6 patients with active expiration. The best CVP was defined as the end-expiratory CVP during relaxed breathing. To correct for the effect of expiratory muscle activity (uncorrected CVP), a corrected CVP was calculated by subtracting the changes in IAP (Δ IAP) from the end-expiratory CVP during active expiration. The bias compared to the best CVP was lower for corrected CVP (2.3±2 mmHg) than for uncorrected CVP (12.5±4.7 mmHg). The most important clinical findings from this study were that first, in the presence of active expiration a reasonable estimate of transmural CVP can be obtained by subtracting the expiratory increase in IAP from the end-expiratory CVP and second, this approach may lessen the likelihood that fluid therapy would be withheld from hypovolemic patients . In a recent study by Valenza and colleagues, not only the transmural CVP, but also volumetric measurements of preload, were unaffected by IAH or increased PEEP (27). This confirms the superiority of “volumetric” indices of resuscitation adequacy, like GEDV over “barometric” intracardiac filling pressure measurements, such as end-expiratory CVP or PAOP (19, 28).

The clinical relevance of these recent observations is obvious: First, these studies stress the importance of linking the different compartments whilst interpreting compartmental (intravascular) pressures. Second, It advocates the routine use of IAP monitoring in daily

clinical practice whilst observing the dynamic changes in IAP and intracardiac filling pressures during respiration. As a rule of thumb a rough estimate of transmural CVP can be obtained by subtracting half the IAP from the end-expiratory obtained CVP value since average abdomino-thoracic transmission is around 50% (25). Third, the abdominal compliance can be estimated by looking at the changes in IAP during respiration. Fourth, the Surviving Sepsis Campaign Guidelines advocate the use of "barometric" indices of preload as CVP and PAOP but we know that these are erroneously increased in case of IAH and ACS. Therefore future resuscitation strategies would preferably be guided by "volumetric" preload indices and the assessment of fluid responsiveness with functional hemodynamics (SVV or PPV) or at least include IAP monitoring with adjustment of barometric target parameters according to IAP. The complexity of the issue should not delay the introduction of IAP monitoring in fluid resuscitation guidelines any longer.

This concerns all critical care physicians who choose to use end-expiratory intracardiac filling pressures to guide the resuscitation of their patients. Using uncorrected barometric preload indices places the patient at risk for under- or overresuscitation with resultant organ dysfunction, failure, and increased mortality.

Several authors suggest that, in analogy to cerebral perfusion pressure in the brain, abdominal perfusion pressure (APP, mean arterial pressure – intra-abdominal pressure) might be a better resuscitation target than MAP (29, 30).

If my patient develops secondary ACS, how do I get the fluids out? Decompressive laparotomy (DL) is still the only available definitive treatment for established ACS. In a systematic review De Waele et al demonstrated that DL has a proven beneficial effect on organ function, but mortality after DL remains high (around 50%) (31). Delay of treatment has been proposed as a possible explanation for this high mortality. Therefore, any patient with full blown (primary) ACS should be decompressed immediately, whatever the cause of the IAH. However, in the earlier stages of IAH without or with mild organ dysfunction, other strategies may prove to be beneficial (32). Intra-abdominal hypertension in general is most frequently caused by either an increased intra-abdominal volume or decreased abdominal wall compliance (Fig. 2) and both these mechanisms are being implicated in the case of secondary ACS. Massive fluid resuscitation can lead to large amounts of free fluid being accumulated in the abdominal cavity and development of edema, both in de bowel wall (leading to increased volume) and the abdominal wall (leading to decreased compliance). The increased intra-thoracic and intraabdominal pressures cause disturbances in the thoraco-abdominal lymphatic flow which further promotes the formation of edema and free intraperitoneal fluid, leading to a negative spiral. Therapeutic measures are aimed at decreasing abdominal volume or increasing abdominal wall compliance. Intra-abdominal volume can be reduced by actively searching for and draining free intraperitoneal fluid. In order to avoid further fluid overload, fluid administration should be restricted and small volume resuscitation should be used (with hypertonic and/or hyperoncotic solutions), as described above. Decreased abdominal wall compliance due to edema is another important target for treatment. The aim of treatment is to decrease the amount of extracellular extravascular or interstitial water without compromising intravascular effective circulating volume. Theoretically this can be achieved by expanding

the intravascular compartment using hyperoncotic solutions (such as albumin 5% or 20%) to increase fluid flow from the interstitial space to the intravascular compartment, followed by diuretics to clear the excess fluid from the intravascular space. Some positive results have been reported by the combination of albumin and furosemide. However, this approach can only be used when renal function is sufficient to respond to diuretic administration. Since the kidney is the organ most easily affected by IAH (probably due to its unique anatomical position and blood supply) even at levels far lower than the IAP of 20mmHg that defines ACS, the combination of albumin and diuretics is often of little use. However, in patients with renal dysfunction, renal replacement therapy (RRT) with aggressive ultrafiltration can provide even better control of excess fluids. Continuous renal replacement therapy (CRRT) especially provides a minute-to-minute control so that fluid extraction is only limited by the patient’s hemodynamic tolerance. Kula et al described excellent fluid control, as well as a beneficial effect on IAP and respiratory function using CVVH with ultrafiltration (33). An additional benefit of RRT might lie in the removal of cytokines from the bloodstream, as was described by Jiang et al. in patients with acute pancreatitis, where CRRT lead to a decrease both in IAP and plasma interleukin-6 levels (34). In our institution we proposed the term PAL therapy, an acronym that stands for PEEPalbumine 20%-lasix (furosemide). The philosophy behind is that high PEEP levels (equal to IAP) force the alveolar fluids into the interstitium, the albumin will then attract the interstitial fluid towards the intravascular space while the lasix will finally remove the excess fluids out of the patient. In anuric patients PAL becomes PAU where the U stands for aggressive ultrafiltration with CVVH. Other non-surgical options for treatment of IAH, unrelated to fluid management, such as the administration of neuromuscular blockers (35) or drainage of intra-abdominal collections (36) are listed in Table 3.

If all these non-surgical interventions fail and the patient progresses to overt ACS, decompressive laparotomy (DL) should be considered immediately, even when no intraabdominal pathology can be found. The invariably high mortality described in literature for secondary ACS, may be partly due to a reluctance in surgeons and critical care physicians to resort to surgery in these patients. In the previously mentioned series by Daugherty et al, 10 patients with secondary ACS after massive fluid resuscitation were described (14). None of the 10 patients with ACS (appropriately defined as IAP>20mmHg and new or progressive organ dysfunction) were surgically decompressed. The authors state that these patients were not deemed to be surgical candidates due to moribund state or a downward trend in IAP following diuretics, fluid restriction or dialysis. One patient arrested immediately prior to planned decompression and could not be resuscitated. Although these patients were apparently adequately treated with non-surgical methods aimed at the cause of the ACS i.e. the fluid overload, one is left to wonder if prompt DL could have improved the outcome in those patients who did not improve with non-surgical measures.

Conclusion Although fast and adequate fluid resuscitation remains a cornerstone of ER and ICU treatment in many conditions, this strategy carries the risk of fluid overload. Fluid overresuscitation has been shown to cause morbidity and mortality and intra-abdominal hypertension may be the missing link between fluid overload and unfavourable outcome. Therefore, IAP should be monitored in all patients receiving massive amounts of fluid resuscitation and hemodynamic targets should be adapted according to IAP values. In situations with massive fluid requirements, small volume resuscitation may be considered. In case of IAH, non-surgical strategies to decrease fluid overload and decrease IAP have proved

to be successful in some cases. If overt ACS develops, prompt decompressive laparotomy should be considered, whatever the cause of the ACS.

Figure 1. The Starling equation Capillaries act rather like a leaky hosepipe; although the bulk of the fluid continues along the pipe, the pressure forces come out of the walls. Hydrostatic (blood) pressure is not the only force acting to cause fluid movement in and out of the capillaries. The plasma proteins that cannot cross the capillary walls exert an osmotic pressure to draw water back into the capillaries which outweighs the hydrostatic pressure at the venous end of the capillaries. The net pressure at the arteriolar site is + 8 mmHg and forces fluids into the interstitium, the net pressure at the venular site is -7 mmHg and drives fluids back into the capillaries. Each day about 20 L is lost while 16L is regained.

Force INTO interstitium INTO capillaries

Pressure

Pc πi πc Pi Net pressure

Arteriole 30 mmHg 6 mmHg - 28 mmHg - 0 mmHg + 8 mmHg INTO interstitium

Jv = Kf([Pc − Pi] − σ[πc − πi]) Jv is the net fluid movement between compartments The other factors are: 1. Capillary hydrostatic pressure ( Pc ) 2. Interstitial hydrostatic pressure ( Pi ) 3. Capillary oncotic pressure ( πc ) 4. Interstitial oncotic pressure ( πi ) 5. Filtration coefficient ( Kf ) 6. Reflection coefficient ( σ )

Venule 15 mmHg 6 mmHg - 28 mmHg - 0 mmHg -7 mmHg INTO capillaries

Figure 2. Relationship between intra-abdominal volume, abdominal wall compliance and intra-abdominal pressure

Diaphragm action

Cab =

IAV Cab = 0

Abdominal contraction

Rib cage action IAP

Intra-abdominal volume (IAV) versus intra-abdominal pressure (IAP). The direction of the movement associated with the sole action of the rib cage inspiratory muscles, abdominal expiratory muscles and the diaphragm are shown. The direction of the latter depends on abdominal compliance (Cab) but is constrained within the sector shown.

Table 1. Risk factors for the development of IAH according to the World Society of the Abdominal Compartment Syndrome Related to diminished abdominal wall compliance − Mechanical ventilation, especially fighting with the ventilator and the use of accessory muscles − Use of positive end expiratory pressure (PEEP) or the presence of auto-PEEP − Basal pleuroneumonia − High body mass index − Pneumoperitoneum − Abdominal (vascular) surgery, especially with tight abdominal closures − Pneumatic anti-shock garments − Prone and other body positioning − Abdominal wall bleeding or rectus sheath hematomas − Correction of large hernias, gastroschisis or omphalocoele − Burns with abdominal eschars Related to increased intra-abdominal contents − Gastroparesis / gastric distention / Ileus / Colonic pseudo-obstruction − Abdominal tumour − Retroperitoneal/ abdominal wall hematoma − Enteral feeding

Related to abdominal collections of fluid, air or blood − Liver dysfunction with ascites − Abdominal infection (pancreatitis, peritonitis, abscess,…) − Haemoperitoneum

− Pneumoperitoneum

Related to capillary leak and fluid resuscitation − Acidosis* (pH below 7.2) − Hypothermia* (core temperature below 33°C) − Coagulopathy* (platelet count below 50000/mm3 OR an activated partial thromboplastin time (APTT) more than 2 times normal OR a prothrombin time (PTT) below 50% OR an international standardised ratio (INR) more than 1.5) − Polytransfusion / trauma (> 10 units of packed red cells / 24 hours) − Sepsis (as defined by the American – European Consensus Conference definitions) − Severe sepsis or bacteraemia − Septic shock − Massive fluid resuscitation (> 5 liters of colloid or > 10 litres of crystalloid / 24 hours with capillary leak and positive fluid balance) − Major burns

Table 2. Definitions regarding IAH and ACS as published by the World Society of the Abdominal Compartment syndrome

Definition 1

IAP is the steady-state pressure concealed within the abdominal cavity.

Definition 2

APP = MAP – IAP

Definition 3

FG = GFP – PTP = MAP – 2 * IAP

Definition 4

IAP should be expressed in mmHg and measured at end-expiration in the complete supine position after ensuring that abdominal muscle contractions are absent and with the transducer zeroed at the level of the mid-axillary line.

Definition 5

The reference standard for intermittent IAP measurement is via the bladder with a maximal instillation volume of 25 mL of sterile saline.

Definition 6

Normal IAP is approximately 5-7 mmHg in critically ill adults.

Definition 7

IAH is defined by a sustained or repeated pathologic elevation of IAP > 12 mmHg.

Definition 8

Definition 9

IAH is graded as follows: •

Grade I: IAP 12-15 mmHg

•

Grade II: IAP 16-20 mmHg

•

Grade III: IAP 21-25 mmHg

•

Grade IV: IAP > 25 mmHg

ACS is defined as a sustained IAP > 20 mmHg (with or without an APP < 60 mmHg) that is associated with new organ dysfunction / failure.

Definition 10

Primary ACS is a condition associated with injury or disease in the abdomino-pelvic region that frequently requires early surgical or

interventional radiological intervention. Definition 11

Secondary ACS refers to conditions that do not originate from the abdomino-pelvic region.

Definition 12

Recurrent ACS refers to the condition in which ACS redevelops following previous surgical or medical treatment of primary or secondary ACS.

Table legend: ACS – abdominal compartment syndrome, APP – abdominal perfusion pressure, FG – filtration gradient, GFP – glomerular filtration pressure, IAH – intra-abdominal hypertension, IAP – intra-abdominal pressure, MAP – mean arterial pressure, PTP – proximal tubular pressure

Table 3. Non-surgical treatment strategies in IAH 1. Improvement of abdominal wall compliance – Sedation – Pain relief (not fentanyl!) – Neuromuscular blockade – Body positioning – Negative fluid balance – Skin pressure decreasing interfaces – Weight loss – Percutaneous abdominal wall component separation 2. Evacuation of intraluminal contents – Gastric tube and suctioning – Gastroprokinetics (erythromycin, cisapride, metoclopramide) – Rectal tube and enemas – Colonoprokinetics (neostygmine, prostygmine bolus or infusion) – Endoscopic decompression of large bowel – Colostomy – Ileostomy 3. Evacuation of peri-intestinal and abdominal fluids – Ascites evacuation in cirrhosis – CT- or US-guided aspiration of abscess – CT- or US-guided aspiration of hematoma – Percutaneous drainage of (blood) collections – Ascites evacuation in cirrhosis 4. Correction of capillary leak and positive fluid balance – Albumin in combination with diuretics (furosemide) – Correction of capillary leak (antibiotics, source control,…) – Colloids instead of cristalloids – Dobutamine (not dopamine!) – Dialysis or CVVH with ultrafiltration – Ascorbinic acid in burn patients 5. Specific therapeutic interventions – Continuous negative abdominal pressure (CNAP) – Negative external abdominal pressure (NEXAP) – Targeted abdominal perfusion pressure (APP) – (experimental: Octreotide and melatonin in ACS)

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