There was positive agreement among HCPs worldwide over 2013 WSACS recommendations and draft statements on the pathophysiology, definition, measurement of IAP, and management of IAH and ACS. The new candidate statements for which agreement was less broad included: (1) A normal IAP of 10 mmHg in critically ill patients, (2) The accuracy of the clinical assessment and estimation of the IAP, (3) The use of the intragastric route as an alternative to the intravesical route for IAP measurement, and (4) Patient positioning for measurement of the IAP. The results of this survey and the comments will inform the development of future WSACS consensus guidelines.

The abdominal cavity can be assumed to be an enclosed space surrounded by rigid bones (lower ribs, costal arch, spine and pelvis) and a partially stretchable abdominal wall [15]. For the measurement of IAP, the abdominal cavity and its contents can be considered relatively noncompressible and fluid in character, to which Pascal’s law can be applied. Pascal’s law states that pressure change at any point of an enclosed incompressible fluid compartment is equally transmitted to every other point and to the walls of the compartment. Hence, pressure measured at one point is representative of pressure throughout the abdominal cavity, and the IAP can be estimated at various locations, including the bladder (most commonly), stomach, rectum, uterus or inferior vena cava [7, 16, 17]. This oversimplification was challenged by a few respondents, who argued that tissues of different densities, such as gas and solid (abdominal viscera, stools, etc.), are common contents of the abdomen. Some respondents even reported that the IAP is a steady-state pressure within the abdominal cavity and pointed to physiological variations during respiration or positive pressure ventilation, along with routine changes in the abdominal contents and hydration status.

Abdominal wall compliance (Cab) is a surrogate for abdominal wall expansion and is determined mainly by the abdominal wall muscles and, to a lesser extent, diaphragm elasticity. The Cab is measured by the ratio of the change in intraabdominal volume (∆IAV) to the change in IAP at the end of expiration (∆IAPee) at a given time point. For example, if for a 1000 mL increase in IAV, IAPee would increase from 10 to 15 mmHg, the Cab would then be equal to 1000/(15–10), or thus 200 ml/mmHg. As ∆IAV is usually unknown, tidal volume (VT) excursions in mL can be used instead, and ∆IAP can be simplified and further calculated by the difference between IAP end-inspiration (IAPei) and IAPee [18,19,20]. The relationship between the IAV and IAP (pressure-volume curve) of Cab is curvilinear, with an initial phase being linear [21]. On the other hand, at higher grades of IAH, minor changes in the IAV produce an exponential increase in the IAP, and vice versa. The initial position on the pressure-volume curve is important for determining the actual Cab [22, 23]. Abdominal pressure variation (APV) is a noninvasive surrogate of Cab and is calculated as a percentage of the ∆IAP to the mean IAP. There is an inverse relationship between APV and Cab. The respiratory abdominal variation test (RAVT) measures Cab in patients on invasive mechanical ventilation via the following equation: tidal volume change (∆VT)/∆IAPei. An incremental ∆VT (e.g., from 4 over 6 to 8 ml/kg) will only increase IAPei [18, 24]. In spontaneously breathing patients, APV produced by gradual changes in the HOB can be used for Cab measurement (positional abdominal variation test) [18, 25]. The emergence of continuous IAP monitoring techniques will provide further insights into heart–lung-abdominal interactions. Overall, comments received from respondents for these equations highlight the need for further clarification and evidence regarding the clinical utility, validation and measurement methodology of abdominal compliance.

There are four major compartments in the body: the head, thorax, abdomen, and extremities. The pathological rise in pressure in one compartment may lead to organ dysfunction in other compartments because of intercompartmental and organ-organ crosstalk interactions, which is referred to as poly-compartment syndrome (PCS) [26]. The comments about the presence of additional compartments, such as the retroperitoneum, pelvis, and omentum highlight the complexity and diversity of anatomical compartments that warrant consideration beyond the four major compartments initially proposed.

The percentage pressure transmission from the thorax to the abdomen is called the thoracoabdominal index, and from the abdomen to the thorax, the abdominothoracic index of transmission, which is, on average, approximately 50% [27,28,29]. Rapid-onset multiorgan dysfunction may result from PCS and is associated with high morbidity and mortality [30]. The abdominal perfusion pressure (APP) is calculated as the difference between the MAP and the IAP and is a marker of visceral perfusion and a better predictor of outcomes in critically ill patients than the IAP alone [31, 32]. There is some evidence for the superiority of APP- over MAP-targeted resuscitation in patients with sepsis to prevent a decline in the glomerular filtration rate (GFR) [33, 34]. However, the respondents expressed uncertainty and a lack of evidence for the target of 60 mmHg for the APP and suggested a more individualized approach.

Acute kidney injury (AKI) is a consistent manifestation of IAH/ACS [34,35,36]. IAH reduces renal perfusion pressure (RPP) and the filtration gradient (FG). In normal individuals, FG is calculated as the difference between the glomerulus filtration pressure (GFP) and proximal tubular pressure (PTP). However, in the presence of IAH, the GFP is dependent on the difference between the mean arterial pressure (MAP) and the IAP, and the PTP is approximated as the IAP. Thus, the equation of FG can be amended as the difference between MAP and two times the IAP, illustrating the greater impact of IAP on FG [2, 15]. Other proposed formulas for RPP include MAP–IAP–central venous pressure (CVP), and in mechanically ventilated patients, MAP–IAP–CVP–Pmean (where Pmean is the mean alveolar pressure) [37]. IAH may cause or exacerbate AKI, and new-onset oliguria/anuria may increase the risk of ACS in patients with IAH [34]. Future guidelines should include the dynamics and respiratory variations of IAP measurements and address the importance of Cab, organ-organ interactions (PCS), the role of perfusion pressures (APP, RPP) and venous congestion [38]. Few respondents expressed concern and suggested further research and evidence to support the validity and usefulness of the formula in clinical practice, considering the complexity of equations.

Some studies have shown a lower accuracy and sensitivity of the clinical estimation of the IAP than of the quantitative measurement of the IAP [39, 40]. However, in this survey, nearly one-third of the respondents agreed with the statement that the clinical estimation of IAP is accurate. The respondents commented that clinical assessment may provide useful information in some instances, but direct measurement of the IAP remains the gold standard for accuracy. HCPs with less than ten years of clinical experience, nonintensivists and physicians other than those from internal medicine and surgery were in favor of the clinical estimation of IAP. Similar findings were reported in other cross-sectional surveys on knowledge and awareness of IAH and ACS [4, 5, 41]. In our opinion, clinical examination not only underestimates the IAP but also, more importantly, delays the timely management of IAH and ACS [39]. Our results emphasize the need for continuous education, advocacy and awareness about IAH/ACS among HCPs.

IAP measurement through the intravesical route using an instillation volume of 20-25 ml of sterile saline is widely used and is currently considered a reference standard [3]. Despite the agreement, the respondents expressed divergent opinions on the optimal volume of saline. The intragastric route using a 50-75 ml instillation volume has been suggested as a valid alternative for IAP measurement [42,43,44]. However, the statement failed to reach the desired agreement because the respondents emphasized the need for further validation, clear guidelines, and evidence supporting its use. Bladder or intragastric routes are traditionally the preferred techniques for continuously monitoring IAP [43]. The WSACS guidelines recommend intermittent IAP measurement every 4-6 h in those with suspected or confirmed IAH or ACS. Recently, newer techniques of continuous IAP measurement have been tested with conflicting results [45, 46]. However, some recent results from in vitro, animal, and first-in-human validation with TraumaGuard and Serenno devices seem promising [47, 48]. Despite the use of different methods for the continuous measurement of the IAP, the gold standard has yet to be identified [16, 17]. Continuous intra-abdominal pressure (CIAP) monitoring, which offers numerous benefits that enhance care and outcomes, is essential for managing critically ill patients in the twenty-first century. CIAP allows real-time trend monitoring of the IAP, enabling clinicians to observe dynamic changes and prompt timely interventions to prevent complications. It captures the effects of body position changes on the IAP, aiding patient management. The CIAP assesses treatment effectiveness by showing continuous pressure changes and facilitates the calculation of continuous abdominal perfusion pressure (CAPP), ensuring adequate organ perfusion. It helps calculate the area under the curve (AUC) or the time above a certain IAP threshold (TAT), reflecting the cumulative pressure time burden of elevated pressures and the severity of hypertension. The CIAP also helps identify patients at risk of complications. It provides insights into PCS by monitoring interactions between different body compartments, such as the abdomen, thorax, and brain. The abdominal-thoracic index (ATI) and thoracoabdominal index (TAI) can be monitored to understand intercompartmental pressure transmission, aiding in optimizing mechanical ventilation settings [12]. The IAP should be measured in the supine position at end-expiration, with the transducer zeroed at the midaxillary level [1]. HOB elevation can significantly increase the IAP [16, 49, 50]. Nevertheless, the IAP can be measured in an elevated HOB or prone position, but a consistent body position should be maintained during serial measurements [51]. Many respondents questioned the relevance and implications of measuring the IAP in different positions and suggested standardization of the measurement of IAP, especially, practicality concerns while measuring in prone positioning.

Previous WSACS guidelines recommended that abdominal contractions be absent during IAP measurement [2, 3]. This translates to IAP measurements being more reliable in a completely sedated and mechanically ventilated patient. However, it is a misconception that patients must be fully asleep or under neuromuscular blockers to obtain a correct IAP value or that the IAP is untrustworthy in awake patients or those receiving noninvasive mechanical ventilation [52]. In this survey, a greater proportion of intensivists and those who participated in previous WSACS research or guidelines agreed with the statement that IAP measurements are trustworthy in awake and spontaneously breathing patients. There are a few reservations about its accuracy and interpretability, necessitating careful consideration and further validation.

The baseline IAP varies across individuals, and previous guidelines recommended a baseline IAP of 5-7 mmHg in critically ill adults [3]. Non-intensivists and physicians (internal medicine and surgery) favored a 5-10 mmHg baseline IAP for healthy adults. Researchers have not clearly determined whether healthy adults are obese or pregnant and have suggested a broader range for physiological IAP. Some researchers have proposed modifications to a range of 0-5 mmHg in healthy adults and emphasized the impact of factors such as body mass index (BMI) on IAP.

Considering the impact of disease severity and position and the impact of interventions such as mechanical ventilation on critically ill patients, a higher threshold for normal IAP (~ 10 mmHg) may be more reasonable. However, an agreement regarding the statement could not be reached. There are queries about the evidence supporting this assertion and concerns about defining a single value as "normal" for critically ill patients, given the variability in disease and patient characteristics. A few respondents proposed a range of 7-12 mmHg. However, the baseline IAP varies widely, and higher baseline IAP values of 12-14 mmHg have been reported in morbidly obese, obstetric, and liver cirrhosis patients with ascites [52,53,54].

In critically ill patients, IAH is defined as sustained or recurrent elevation of the IAP equal to or above 12 mmHg [1, 55]. Some respondents suggested defining “sustained” and “repeated” and increasing the threshold to more than 15 mmHg because of factors such as high BMI. Similarly, rather than a specific IAP, respondents suggested focusing on organ dysfunction (not necessarily using SOFA or quick SOFA score) to define ACS. In awake, non-critically ill patients without risk factors for IAH, abdominal muscle activity may transiently increase the IAP to as high as 20 mmHg [49]. Some laboratory data support sustained exposure for 90 min to even slightly elevated IAP, which may increase intestinal permeability and mucosal damage in rats [56, 57]. However, there is a lack of human data to support the fact that transient IAP increases to produce any discernible organ dysfunction. Hence, the diagnosis of IAH/ACS requires a sustained increase in IAP in three or more measurements over 1-2 h apart for ACS and 4-6 h apart for IAH. The respondents suggested the use of a clinical context rather than an arbitrary duration and more frequent or continuous measurements of IAP in ACS patients to determine the frequency of measurement. The correlation between the impact of IAH and severity grade is controversial, and even lower grades may be associated with a negative impact on tissue perfusion and patient outcomes such as length of stay or duration of mechanical ventilation [58]. Thus, the diagnosis of ACS is not dependent solely on the absolute value of the IAP but also on new-onset organ dysfunction/failure [53]. The factors that need to be considered for diagnosis include the technique and context of IAP measurement, baseline IAP, rapid progression, and duration of IAH [7].

IAH is characterized by a continuum from asymptomatic elevation of the IAP to life-threatening organ dysfunction/failure known as ACS, which requires immediate intervention. Depending on the absolute value of the IAP, IAH can be graded as Grade I (IAP 12-15 mmHg), Grade II (IAP 16-20 mmHg), Grade III (IAP 21-25 mmHg), or Grade IV (IAP > 25 mmHg) [1, 7]. Few respondents suggested two grades using only a cutoff of 20 mmHg to simplify and reduce unnecessary complexity.

IAH can be classified on the basis of etiology, acuity of onset, and risk factors. Patients with IAH can be broadly divided into medical, surgical, trauma and burn patients [59, 60]. Although, ACS is nowadays an uncommon diagnosis in critically ill adults (incidence rate of 0.17%), the associated morbidity and mortality is significantly higher compared to patients without ACS. Gastrointestinal and cardiovascular are common etiologies for ACS [61]. IAH (or ACS) can be defined as primary or secondary, respectively, on the basis of whether the origin of the inciting condition or disease is within the abdominopelvic region. Primary IAH caused by abdominal trauma, peritonitis, surgery, intrabdominal masses, or ascites frequently requires radiological or surgical intervention for its management [59]. Whereas, secondary IAH is caused by the systemic causes in the absence of primary intraperitoneal injury or intervention. Recurrent IAH (or ACS) is characterized by a resurgence after the treatment of primary or secondary IAH/ACS and has a worse patient prognosis [62, 63]. Compared with the absolute IAP, the classification based on the acuity of onset as hyperacute, acute, subacute, or chronic is of greater prognostic significance [64]. However, few respondents expressed ambiguity in the current classification, especially in overlapping conditions, retroperitoneum pathology, and definitions of radiological intervention.

Future definitions should establish what is meant by “consecutive” measurements and “sustained” increased IAP, and this should probably not differ between IAH and ACS to avoid confusion, especially in light of new continuous IAP monitoring techniques, as discussed previously. These new monitoring tools also allow us to calculate other derived parameters, such as the area under the curve or the time above a certain threshold. Analogous to increased intracranial pressure, the pressure-time burden is likely more strongly correlated with adverse outcomes than a single increased IAP value [65, 66]. Few respondents argued against localized IAH, as it did not manifest a systemic elevation and suggested revising it to "organ-specific IAH". Future guidelines must better define and classify the different distinct types of IAH and ACS.

The optimal management of patients with IAH/ACS should consider the duration and etiology of IAH/ACS, the presence of an intra-abdominal pathology and/or the development of local compartment syndrome. The respondents asked for clarification on “local” compartment syndrome and proposed other considerations, such as assessing the trajectory or the consequences of the condition and response to previous therapies for IAH/ACS. The duration of IAH (or thus the pressure time burden) rather than the development of IAH was found to be an independent predictor of 60-day mortality in surgical patients [67]. In another prospective study of critically ill surgical patients, a longer duration of IAH was associated with greater serum lactate and organ dysfunction, longer intensive care unit (ICU) and hospital lengths of stay, longer durations of vasopressor and ventilator requirements and even higher 30-day mortality [68]. The etiology of IAH/ACS is another crucial element considered in the classification of IAH/ACS. The etiology of IAH helps determine the type and urgency of treatment. A transient increase in the IAP after elective abdominal hernia repair may be managed conservatively [