The polycompartment syndrome: a concise state-of-the-art review

Manu L.N.G. Malbrain1, Derek J. Roberts2, Michael Sugrue3, Bart L. De Keulenaer4, Rao Ivatury5, Paolo Pelosi6, Frederik Verbrugge7, 8, Robert Wise9, Wilfried Mullens7, 10

1Intensive Care Unit, ZiekenhuisNetwerk, Antwerp, Belgium

2Departments of Surgery and Community Health Sciences, University of Calgary and the Foothills Medical Centre, Calgary, Alberta, Canada

3Letterkenny Hospital and the Donegal Clinical Research Academy, Donegal, Ireland, and University College Hospital, Galway, Ireland

4Intensive Care Unit, Fremantle Hospital, Western Australia, Australia and School of Surgery, University of Western Australia, Crawley, Western Australia, Australia 

5Professor emeritus, former Chair, Division of Trauma, Critical Care and Emergency Surgery, VCU Medical Centre, Richmond, VA, USA

6Department of Surgical Sciences and Integrated Diagnostics, University of Genoa, Genoa, Italy

7Department of Cardiology, Ziekenhuis Oost-Limburg, Genk, Belgium

8Doctoral School for Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium

9Department of Critical Care, Edendale Hospital, Perioperative Research Group, University of Kwazulu Natal, South Africa

10Biomedical Research Institute, Hasselt University, School of Life Sciences, Diepenbeek, Belgium


A compartment syndrome is defined as an increase in the compartmental pressure to such an extent that the viability of the tissues and organs within the compartment are threatened. The term describes a syndrome and not a disease, and as such there are many diseases and underlying pathophysiological processes that may lead to such a scenario.

The aim of this review is to give a state-of-the-art overview on the current knowledge on different compartment syndromes and how they may interact. Suggested definitions are included. There are four major compartments in the human body: the head, chest, abdomen, and the extremities. Initially, the term multicompartment syndrome was suggested when more than one compartment was affected. But this led to confusion as the term multi- or multiple compartment syndromes is mostly used in relation to multiple limb trauma leading to compartment syndrome requiring fasciotomy. Only recently was the term ‘polycompartment syndrome’ coined to describe a condition where two or more anatomical compartments have elevated pressures. When more than one compartment is affected, an exponential detrimental effect on end-organ function to both immediate and distant organs can occur. Within each compartment, the disease leading towards a compartment syndrome can be primary or secondary. The compliance of each compartment is the key to determining the transmission of a given compartmental pressure from one compartment to another. The intra-abdominal pressure helps to explain the severe pathophysiological condition occurring in patients with cardiorenal, hepatopulmonary and hepatorenal syndromes. Initial treatment of a compartment syndrome should be focused on the primary compartment and is based on three principles: lowering of compartmental pressure, supporting organ perfusion, and optimisation and prevention of specific adverse events. Clinicians need to be aware of the existence of the polycompartment syndrome and the interactions of increased compartmental pressures between compartments.

Key words: abdominal pressure, intracranial pressure, intrathoracic pressure, abdominal compartment, renal compartment, extremity compartment, thorax compartment, compartment syndrome, polycompartment, compliance

Anestezjologia Intensywna Terapia 2014, tom XLVI, nr 5, 449466

A compartment syndrome is defined as an increased pressure in a closed anatomic space, which threatens the viability of enclosed and surrounding tissue [1]. Within the body there exist four major compartments, namely the head, chest, abdomen, and extremities. Within each of these compartments individual organs may be affected by compartment syndromes. Table 1 summarises the different compartments and related pathophysiologic and clinical implications of compartment syndromes in these locations.

Table 1A. The four compartments: pathophysiology and monitoring















Primary physiologic parameter

Intracranial pressure (ICP)

Orbital compartment pressure (OCP)

Intra-ocular pressure (IOP)

Intra thoracic pressure (ITP)

Filling pressure (CVP, PAOP)

Intra-abdominal pressure (IAP)

Perihepatic pressure, upper IAP (UIAP)

Peritubular pressure (PTP), renal venous pressure (RVP)

Pelvic compartment pressure, lower IAP (LIAP)

Extremity compartment pressures (ECP)

Secondary parameter

Cerebral perfusion pressure (CPP) = MAP ICP, compliance

Orbital perfusion pressure (OPP) = MAP OCP

Ocular perfusion pressure (OPP) = MAP IOP

Peak, plateau and mean airway pressure, lung and chest wall compliance

Coronary perfusion pressure (CoPP) = DBP PAOP = DBP ITP

Abdominal perfusion pressure (APP) = MAP IAP

Liver perfusion pressure = MAP UIAP

Renal perfusion pressure (RPP) = MAP - RVP

Pelvic perfusion pressure = MAP LIAP

Peripheral arterial perfusion pressure, tissue perfusion pressure (TPP) = capillary pressure ECP

CP measure­ment

Fluid filled ventriculostomy, airfilled balloon-tipped catheter, parenchymal solid state microchip transducer

Orbital tissue tension manometry (not possible in clinical practice)

Ocular tissue tension manometry

Oesophageal pressure measurement via a balloon-tipped catheter; surrogate parameters:

Palv (Ppeak, Pplat, Pmean)

via deep venous or Swan-Ganz catheter

Via bladder (FoleyManometer, AbViser valve)

Via stomach (Spiegelberg, Pulsion Medical Systems)

Estimation of UIAP via stomach (Spiegelberg, Pulsion Medical Systems)

Estimation of PTP and RVP via bladder (Foley­Manometer, AbViser valve)

Estimation of LIAP via bladder (Foley­Manometer, AbViser valve)

via a needle connected to a fluid-filled pressure transducer system


Intracranial hypertension (ICH): ICP > 15 mm Hg

Intra-orbital hypertension: OCP > 20 mm Hg

Intra-ocular hypertension: IOP > 17 mm Hg

ITP > 15 mm Hg

CVP > 20 mm Hg

PAOP > 25 mm Hg

Intra-abdominal hypertension (IAH): IAP 12 mm Hg

Perihepatic hypertension: UIAP > 12 mm Hg

Renal hyper­tension: PTP or RVP > 12 mm Hg

Pelvic hypertension: LIAP > 12 mm Hg

Extremity hypertension: ECP > 15 mm Hg

Intracranial compartment syndrome (ICS) cerebral herniation: ICP > 25mm Hg

Orbital compartment syndrome (OCS): OCP > 30 mm Hg

Ocular compartment syndrome (OCS): IOP > 30 mm Hg

Thoracic compartment syndrome (TCS): ITP > 25 mm Hg

Cardiac compartment syndrome (CCS) cardiac tamponade

Abdominal compartment syndrome (ACS): IAP > 20 mm Hg

Liver compartment syndrome (LCS): UIAP > 20 mm Hg

Kidney compartment syndrome (KCS): PTP or RVP > 20 mm Hg

Pelvic compartment syndrome (PCS): LIAP > 20 mm Hg

Extremity compartment syndrome (ECS): ECP > 30 mm Hg


Primary (tumour, sub- or epidural haematoma,…) Secondary (auto-PEEP, hypoxia or hypercarbia, hyper-tension, ventilation, seizures, ,…)

Postoperatively (oedema, mass lesion,…)

Intrinsic (tumour) Extrinsic (traumatic retrobulbar haemorrhage) Combination (fluid resuscitation, burn injury)

Intrinsic (glaucoma) Extrinsic (posttraumatic glaucoma)

Combination (fluid resuscitation, burn injury)

Post cardiac surgery,

spontaneous mediastinal or pleural haemorrhage, tumour, COPD with dynamic hyperinflation, tension pneumothorax

Trauma, tumour, spontaneous bleeding, fluid resuscitation

Primary IAH: associated with injury or disease in the abdomino-pelvic region

Secondary IAH: does not originate from the abdomino-pelvic region

Recurrent IAH: chronic state of IAH

Primary: associated with injury or disease in the liver

Secondary: mostly related to massive fluid overload

Primary: associated with injury or disease in the kidney

Secondary: mostly related to massive fluid overload

Primary: associated with injury or disease in the pelvis

Secondary: mostly related to massive fluid overload

Crush injury

Trauma with fractures

Bleeding disorders


Table 1B. The four compartments: implications and management















Potential implica­tion

Brain death

Blindness, eye muscle paralysis


Cardiopulmonary collapse

Cardiac collapse, electromechanical dissociation

Multiple organ dysfunction

Liver failure

Kidney failure

Kidney failure (retroperitoneal haematoma)

Extremity loss

Thera­peu­tic inter­ven­tion

Lower ICP: CSF drainage

Lower orbital compartment pressure (OCP)

Lower IOP

Lower ITP

Evacuate pericardiac effusion

Lower IAP: ascites drainage, medical management

Lower UIAP: ascites drainage, medical management

Lower PTP or RVP: ascites drainage, medical management

Lower LIAP: ascites drainage, medical management

Lower ECP: optimize fluid management

Increase CPP: vasopressors, fluids

Increase orbital PP

Increase OPP

Escharotomy, chest tube

Pericardiac tube,

Increase APP: vasopressors, fluids, escharotomy

Increase liver PP: vasopressors, fluids

Increase kidney PP: vasopressors, fluids

Increase pelvic PP: vasopressors, fluids

 Increase TPP

Rescue therapy 

Open compartment

Open compartment

Open compart­ment

Open compartment

Open compartment

Open compartment

Open compartment

Open compartment

Open compartment

Open compartment

Decompressive craniectomy

Orbital decompression

Ocular decom­pression

Decompressive sternotomy

Decompressive pericardiectomy, pericardiotomy

Decompressive laparotomy

Decompressive laparotomy, hepatic decapsulation

Decompressive laparotomy, renal decapsulation

Decompressive laparotomy, gluteal fasciotomy

Decompressive fasciotomy


Adaptation of ventilatory support essential, recognition life saving, and avoidance of vegetative state (postanoxic encephalopathy)

Recognition of syndrome can be eye saving

Recognition of syndrome can be eye saving

Recognition of syndrome can be life saving; Adaptation of ventilatory support essential

Recognition of syndrome can be life saving

Prevention of bacterial translocation and MODS can be life saving

Prevention of bacterial translocation and MODS can be liver and life saving

Recognition of syndrome can be kidney saving

Recognition of syndrome can be kidney saving

Recognition can be limb saving

Effect on (up­stream)

IOP, cardio-respiratory function (SVR, PVR)

Eye, eye muscles

Lung (Palv), ICP, IAP, CVP, PAOP

Lung, ICP

All other compartments (Lung, ICP, ITP, CVP, PAOP,…), limbs

All other compartments (Lung, ICP, ITP, CVP, PAOP,…), HARS, HAPS

All other compartments (Lung, ICP, ITP, CVP, PAOP,…), CARS

All other compartments (Lung, ICP, ITP, CVP, PAOP,…)

Kidney (rhabdo­myolysis), lungs, heart

Affected by (down­stream)

intracardiac pressures (CVP, PAOP), ITP, PEEP and IAP



IAP (abdomino-thoracic transmission 50% on average), mechanical ventilation (PEEP)

ITP, IAP (abdomino-thoracic transmission 50% on average), mechanical ventilation (PEEP)

ITP, mechanical ventilation (PEEP)

ITP, mechanical ventilation (PEEP)

ITP, mechanical ventilation (PEEP)

ITP, mechanical ventilation (PEEP)

IAP (diminished venous return)

APP abdominal perfusion pressure; CARS cardio-abdominal renal syndrome; CP compartment pressure; CPP cerebral perfusion pressure; CSF cerebrospinal fluid; CVP central venous pressure; ECP extremity compartment pressure; HAPS hepato-abdominal pulmonary syndrome; HARS hepato-abdominal renal syndrome; IAP intra-abdominal pressure; ICP intracranial pressure; IOP intra-ocular pressure; ITP intrathoracic pressure; LIAP lower intra-abdominal pressure; MODS multiple organ dysfunction syndrome; OCP orbital compartment pressure; OPP orbital or ocular perfusion pressure; PAOP pulmonary artery occlusion pressure; PEEP positive end-expiratory pressure; PTP —peritubular pressure; RVP renal venous pressure; TPP tissue perfusion pressure; UIAP upper intra-abdominal pressure

As a result of differing anatomy and physiology within each location, compartment syndromes may manifest in a multitude of ways, some of which remain relatively poorly understood. The abdominal compartment has unique effects because it is geographically situated ‘up-stream’ from the extremities and ‘down-stream’ from the chest. Therefore, it may influence the physiology and pathophysiology of each of these other compartments.

A therapeutic conflict is a situation where each of the possible therapeutic decisions carries some potential harm. The presence of a compartment syndrome often plays a role when we are dealing with these dilemmas. In high-risk critically ill patients, the decision about fluid administration in particular should be done within this context. Therapeutic conflicts pose the greatest challenge for protocolised cardiovascular management in anaesthetised and critically ill patients, where our decisions can make a significant difference to outcome [2, 3].

Scalea et al. first introduced the term ‘multiple compartment syndrome’ in a study of 102 patients with increased intra-abdominal (IAP), intrathoracic (ITP), and intracranial pressure (ICP) after severe traumatic brain injury [4]. They suggested that different compartments within the body are not isolated and independent entities, but instead should be considered closely interconnected. The term multi- or multiple compartment syndrome is now mostly used in relation to multiple limb trauma leading to compartment syndrome, thus necessitating fasciotomy. However, the term polycompartment syndrome (PCS) was only recently coined in order to avoid confusion [5]. Organ-organ interactions and resulting polycompartment syndromes may occur more frequently than clinicians report.

The purpose of this state-of-the-art review was to provide a critical overview of current literature examining the pathophysiology, clinical presentation/epidemiology, and management of the polycompartment syndrome, beginning with an illustrative case [6−8].

Illustrative case: polycompartment syndrome with secondary limb compartment syndrome and primary head and abdomen compartment syndromes

A 23-year-old man was involved in a high-speed car crash. He was hypotensive at the scene and during the 40 minute transport to hospital. After an Emergency Department assessment, he underwent an exploratory laparotomy, which included a splenectomy, and peri-hepatic packing. His abdomen was left open with a Bogota bag. ICP monitoring was conducted as a result of a severe traumatic brain injury (TBI) and a massive blood transfusion was given during the first 24 hours of the intensive care unit (ICU) management.

After 24 hours in the ICU, primary abdominal fascial closure was performed. He subsequently developed Grade IV (IAP above 25 mm Hg) intra-abdominal hypertension (IAH) with a sustained IAP of 28 mm Hg, consistent with a primary abdominal compartment syndrome (ACS) [9]. Both lower limbs, which had not sustained primary injury, were noted to be swollen and tense on palpation, and the anterior and posterior extremity compartment pressures were 42 and 38 mm Hg respectively, indicating secondary limb compartment syndrome. At this time the IAP was 38 mm Hg. In response to these findings, abdominal decompression was performed, together with complete bilateral lower limb fasciotomies. During limb surgery, ischaemic and necrotic muscle was found in the lateral compartment, and an extensive debridement was undertaken. While abdominal decompression initially reduced both IAP and ICP, ICP subsequently rose and remained high until the patient’s eventual recovery four weeks later. The increased ICP resulted from a combination of primary (related to TBI) and secondary (related to ACS) insults, while the extremity compartment syndrome developed secondary to ACS.

This case also nicely demonstrates that open abdomen treatment does not always prevent the re-occurence of an abdominal compartment syndrome.


Although an increased compartment pressure will increase venous resistance and decrease perfusion pressure in the implicated compartment, it may also affect other compartments (Fig. 1).


Figure 1. Interactions between the four main body compartments (head, chest, abdomen and extremities). Arrows indicate interactions between different compartments. The head contains the intracranial, intra-orbital and intra-ocular compartments. The chest contains the thorax, lungs and heart, each of which can develop a compartment syndrome. The abdomen contains the abdominal, hepatic, renal, and pelvic compartments. Solid lines show direct effects by transmission of mechanical pressure forces. Dotted lines show indirect distant effects between compartments (see text for explanation, adapted from [7]). ACS abdominal compartment syndrome; CCS cardiac compartment syndrome; ECS extremity compartment syndrome; HCS hepatic compartment syndrome; ICS intracranial compartment syndrome; RCS renal compartment syndrome; OCS orbital compartment syndrome; PCS pelvic compartment syndrome; TCS thoracic compartment syndrome

The resulting impact on organ function and viability can be devastating. What follows is a discussion on the four major compartments and the different syndromes that can occur. The cause of a compartment syndrome may be primary (e.g. tumours and trauma), but most often it will be a secondary insult. This typically occurs after massive fluid resuscitation in the setting of trauma and the well-described lethal triad (coagulopathy, hypothermia, acidosis), or during sepsis with poor source control and ongoing capillary leak as suggested previously [10−13].


Intracranial compartment syndrome

The intracranial contents are confined within a rigid bony cage. According to the Monroe-Kellie doctrine, any increase in volume within the intracranial compartment (e.g. an expanding traumatic intracranial haematoma) leads to a reciprocal decrease in the volume of cerebrospinal fluid and intracranial venous blood volume [14]. When compensation mechanisms are exhausted, an increase in ICP with a corresponding decrease in cerebral perfusion pressure (CPP), defined as mean arterial pressure (MAP) minus ICP, may result [14].


Treatment options for intracranial hypertension (ICH) either focus on lowering ICP (by evacuation of cerebrospinal fluid or a variety of other techniques aimed at decreasing brain tissue oedema) or raising CPP (by maintaining an adequate MAP with fluids or vasopressors) [15, 16]. However, fluid therapy used to support CPP may exacerbate visceral oedema, promote ascites, and increase IAP, which in turn may increase intrathoracic (ITP), internal jugular venous, and intracranial pressures (possibly through decreased intracranial venous drainage via the jugular veins) [16]. Therefore, in patients with severe TBI, treatment decisions that may result in a vicious cycle, increasing pressures in various compartments, should be carefully considered [4].

However, despite these theoretical concerns, the effects of IAP and ITP on ICP have not been extensively studied to date, and remain a challenging area for fundamental and clinical investigators [17−24]. Remarkably, patients with polycompartment syndrome receive significantly more fluids during the first week of ICU stay and predictably their ICU/hospital admission is prolonged [4]. While there was also a trend towards higher mortality in these patients (42% vs 31%), statistical significance was not reached. PCS should be considered in multiple injured patients with increased ICP who do not respond to conventional therapy [4].

Orbital compartment syndrome

Acute orbital compartment syndrome (OCS) is a rare complication of increased pressure within the orbit. An increased intra-orbital pressure may cause decreased orbital perfusion pressure by a mechanism similar to that occurring with CPP. Because intra-orbital pressure cannot be measured directly, intraocular pressure (IOP) can be used as a surrogate, indirect estimation (as pressures within the orbit are directly transmitted to the eye). Ocular/orbital perfusion pressure (OPP) can be calculated as follows:


Orbital compartment syndrome presents with typical signs and symptoms (eye pain, reduced ocular motility, diplopia and pro-optosis) resulting in progressive visual deficits and is mostly seen in relation to retrobulbar haematomas or trauma [25]. Recognition and prompt treatment is of paramount importance to prevent permanent blindness. A study in burn patients reported that increased IOP corresponded with fluid administration volume given during the first 24 hours of hospitalisation and with the presence of peri-ocular burns [26]. Other conditions associated with orbital compartment syndrome include infection, inflammation, spinal surgery, vascular problems with ophthalmic artery or retinal vein occlusion, optic nerve sheath compression, traumatic asphyxia syndrome and bleeding diathesis or disseminated intravascular coagulopathy as seen in sepsis [25]. Orbital compartment syndrome has even been described after orbital extravasation of X-ray contrast material [25]. Intra-orbital compartment syndrome needs to be differentiated from intra-ocular compartment syndrome as seen with (secondary) glaucoma, especially in trauma patients [27].

Ocular compartment syndrome

The eye is situated in the orbital compartment and any pressure increase within this compartment, even if the eye itself is not affected, will result in an increased intra-ocular pressure as discussed above. However, primary intra-ocular compartment syndrome can also occur in relation to increased IOP without intra-orbital compartment syndrome, as seen with primary (e.g. narrow angle glaucoma, tumours) or secondary (e.g. post-traumatic) glaucoma. Intra-ocular hypertension is defined as IOP > 17 mm Hg while ocular compartment syndrome occurs at IOP above 2530 mm Hg.


Thoracic compartment syndrome

Thoracic compartment syndrome results as an accumulation of air, fluid or blood in the chest and has traditionally been described in trauma. It has also been described in patients undergoing cardiac surgery, where in the setting of substantial myocardial oedema, mediastinal haematomata, noncardiogenic pulmonary oedema, or acute ventricular dilatation, sternal closure may precipitate cardiac tamponade leading to haemodynamic instability or even collapse [28, 29]. Although it has been described in the setting of thoracic trauma damage control procedures, thoracic compartment syndrome is rare in patients with thoracic trauma due to the limited survival when injuries are significant enough to result in massive intrathoracic tissue oedema after resuscitation. Tension pneumothorax or haemopneumothorax (with increased ITP) occurs most often in patients with polytrauma or following an iatrogenic injury related to insertion of a central venous catheter, diagnostic or therapeutic procedure. However, traumatic cardiac tamponade can be seen as a primary thoracic compartment syndrome (see below). In the ICU, increased ITP is most commonly related to sepsis, capillary leak, aggressive fluid resuscitation, positive pressure ventilation with high PEEP (positive end-expiratory pressure) or dynamic hyperinflation, pneumothorax, COPD with auto-PEEP, diminished chest wall compliance (e.g. morbid obesity or circumferential chest burns), lung fibrosis and ARDS [30]. Rising ITP, reflected as an increase in mean or peak inspiratory pressures during thoracic wall closure, may serve as an early warning that a patient is at risk for thoracic compartment syndrome [6]. Increased ITP (normally < 57 mm Hg) can be measured by a balloon-tipped catheter positioned in the lower third of the oesophagus and will affect the lungs, heart and brain by limiting venous return (Fig. 1)[31]. Since increased ITP, like raised IAP, is most commonly related to excessive fluid resuscitation, both frequently coexist [32, 33]. Important issues to consider include:

  1. 1. PEEP should be set to counteract ITP and IAP while at the same time avoiding over-inflation of already well-ventilated regions of lung [34, 35]. The fact that PEEP is expressed in cm H2O (with a conversion factor of 1.36 to mm Hg) takes into account the average abdomino-thoracic index of transmission of around 50% [31, 34]

Best PEEP (cmH2O) = IAP (mm Hg)

  1. 2. During lung protective ventilation, plateau pressures should be limited to transmural or transpulmonary plateau pressures (Pplattm) below 30 to 35 cm H2O, otherwise end-tidal CO2 will increase [36].

Pplattm = Pplat ITP = Pplat IAP/2 < 35 cm H2O

  1. 3. Increased ITP and IAP decrease lymphatic drainage and facilitate lung oedema as discussed elsewhere in this article [37, 38]. Therefore, monitoring of extravascular lung water index (EVLWI) may be beneficial in guiding de-resuscitation [39, 40].
  2. 4. IAP increases with inspiration (IAPei) and decreases with exhalation (IAPee) during spontaneous respiration and mechanical ventilation. Therefore, ΔIAP and the abdominal pressure variation (APV), expressed as a percentage, may indirectly predict abdominal wall compliance (Fig. 2) [5, 41].


Figure 2. Respiratory variations of intra-abdominal pressure (IAP) are an indirect estimation of abdominal wall compliance. A raw data tracing of continuous IAP monitoring recorded with balloon-tipped nasogastric probe connected to CiMON monitor (Pulsion Medical Systems, Munich, Germany) obtained in a mechanically ventilated patient showing breath-to-breath variations in IAP (∆IAP). Ventilator settings were: inspiratory positive airway pressure (IPAP) = 25 cm H2O and positive end-expiratory pressure (PEEP) = 10 cm H2O. The tracing shows the respiratory variations in IAP as well as the arterial pulse pressure variations (because of the vicinity of the heart to the nasogastric probe) at a heart rate (HR) of 120 beats per minute, highlighted by the circle. Mean IAP was 18.5 mm Hg with IAP = 17 mm Hg at end expiration (IAPee) and IAP = 20 mm Hg at end inspiration (IAPei), resulting in a ∆IAP (defined as IAPei − IAPee) = 3 mm Hg. The abdominal pressure variation (APV) can be calculated as ∆IAP divided by mean IAP (i.e. 3/18.5 = 16.2 %). Higher APV values for a given ventilator setting correspond to lower abdominal wall compliance. The thoraco-abdominal index (TAI) of transmission can then be calculated as ∆IAP divided by (Pplateau minus PEEP) or thus 3/15 = 20%



Cardiac compartment syndrome

Within the thorax, cardiac tamponade may be considered as a specific compartment syndrome. By definition, cardiac tamponade occurs as a result of an accumulation of fluid or air in the pericardium, usually as a result of trauma, haemorrhage, infection, or tumour [42]. The result is impaired filling of the ventricles and decreased cardiac output (CO). Strikingly, as little as 250 mL of fluid can cause acute cardiac tamponade, whereas under chronic conditions much greater amounts of fluid can accumulate as the cardiovascular system compensates with the slower, gradual accrual [43].

A similar condition arises when either ITP directly (in the case of thoracic compartment syndrome), or IAP indirectly (in the case of abdominal compartment syndrome) compresses the cardiac chambers. The latter is due to an upward movement of the diaphragm. In the case of increased ITP or IAP, coronary perfusion pressure (CoPP) is lowered:


with DBP = diastolic blood pressure and PAOP = pulmonary artery occlusion pressure.

Increased ITP also results in a more difficult preload assessment because of falsely increased invasively measured filling pressures [30, 44]. When the ITP or IAP rises above values of 10−12 mm Hg, CO drops due to an increased afterload (systemic vascular resistance), a decreased preload (diminished venous return, and falsely increased barometric filling pressures), and left ventricular compliance (due to the tamponade effect of increased ITP) [31, 45−48], as discussed below. This often manifests with tachycardia, a decreased MAP, and pulsus paradoxus (or an increased pulse pressure variation). Cardiovascular dysfunction and failure (low CO, high SVR) are common in conditions of increased ITP or IAP [49, 50]. All these can result in right ventricular dysfunction with secondary tricuspid valve regurgitation. Right ventricular function is predominantly load-dependent and successful response to intensive medical therapy predicts good outcome in heart failure patients [44, 51]. Eventually, the increased right-sided pressure and heart failure result in hepatic congestion, leading to hepatic fibrosis and cirrhosis. In addition to the more direct effects of cardiac tamponade, further distant effects on other organs may manifest (Fig.  1). Important issues to consider include:

  1. 1. Invasively measured haemodynamics (through a pulmonary artery catheter [PAC]) are difficult to interpret in conditions of increased ITP or IAP. This is because pressure-based or ‘barometric’ estimates of intravascular volume expressed as PAOP and central venous pressure (CVP) are increased. The importance of this is reflected in a patient’s volume status being misinterpreted, potentially resulting in the institution of inappropriate and potentially detrimental therapy [5, 52].
  2. 2. Transmural (tm) filling pressures, involving the end-expiration value (ee) and ITP, may better reflect true preload status [34, 36]:



  1. 3. The index of transmission (IT) of alveolar pressures onto the vasculature allows for the calculation of CVPtm and can be estimated as suggested by Teboul et al. [53]. The IT is higher in patients with good respiratory compliance (such as those with emphysema) and low in those with poor compliance (ARDS, lung fibrosis):

IT = (CVPei CVPee)/(Pplat PEEP)


  1. 4. A quick estimate of transmural filling pressures can also be obtained by subtracting half of the IAP from the end-expiratory filling pressure, as the average abdomino-thoracic index of transmission is 50% (illustrated in Fig. 3) [54]:

CVPtm = CVPee IAP/2



Figure 3. Calculation of abdomino-thoracic index (ATI) of transmission at the bedside. Simultaneous ECG, CVP and IAP tracing before (pre) and during (post) abdominal compression with a Velcro belt used to prevent incisional hernia. The abdomino-thoracic index of transmission can be calculated as follows: The change in endexpiratory CVP: ∆CVPee = CVPee/post CVPee/pre = 22 15 = 7 mm Hg The change in endexpiratory IAP: ∆IAPee = IAPee/post IAPee/pre = 23 12 = 11 mm Hg The abdomino-thoracic index of transmission = ∆CVPee/∆IAPee = 7/11 = 63%

  1. 5. ‘Volumetric’ preload estimates such as right ventricular end diastolic volume index (RVEDVi), or global end diastolic volume index (GEDVi), are useful alternatives to pressure-based measurements in conditions of increased ITP [48, 55−58]. Correction of the GEDVi in relation to the global ejection fraction (GEF) can be used to fine-tune the true preload status in this setting [59].
  2. 6. The haemodynamic effects of IAH are aggravated by hypovolemia and the application of PEEP [60-64], whereas hypervolemia has only a temporary protective effect since it can aggravate tissue oedema, thus triggering a vicious cycle [23].
  3. 7. Increased IAP leads to an increase in the ITP, and provides an explanation for the pulse pressure variation and stroke volume variation increase (with PPV preferred over SVV) [65]. Our traditional threshold for fluid responsiveness therefore needs to be adapted in patients with IAH [66]. Fluid responsiveness in IAH is defined as a PPV above 20% rather than the usual 12% threshold. Systolic pressure variation should not be used in the setting of increased IAP or ITP because the increase seen in IAH and ACS only reflects a ΔUp phenomenon [67, 68].
  4. 8. Increased IAP can lead to a false negative passive leg raising test since venous return from the legs and splanchnic pool may be impeded, causing a smaller endogenous fluid challenge [69, 70]


Limb, or extremity, compartment syndrome is a condition in which the pressure in a closed muscle compartment increases to a level that reduces capillary blood perfusion below the level necessary for tissue viability [6]. Permanent loss of function and muscle contraction may occur. Extremity compartment syndrome can be measured by a needle connected to a fluid-filled pressure transducer system. Normal compartment pressure (CP) values should be < 20 mm Hg [6]. This technique can be used to guide the need for surgical intervention.

Tissue perfusion pressure = Arteriolar (capillary) pressure extremity CP

Extremity compartment syndrome is more common in obese patients where it mostly results from fractures following trauma (especially of the tibia), tight plaster casts, muscle contusions, bleeding disorders, burns (with eschars), venous obstruction, and arterial occlusion with post-ischaemic swelling [6]. Extremity compartment syndrome will result in muscle compression and rhabdomyolysis, which may cause hypovolemia, acute kidney injury (AKI), coagulopathy, acute lung injury (ALI), and shock [6]. Therefore, extremity compartment syndrome can also contribute to distant effects on other organs (Fig. 1). In the case of established extremity compartment syndrome, the only definitive treatment is decompressive fasciotomy, and muscle debridement in a case of necrosis [6, 71]. Initially, fluid resuscitation can be used to counteract the deleterious effects of extremity compartment syndrome on distant organ function. However, this may eventually also lead to a vicious cycle with increased tissue oedema and a further rise in compartmental pressures.

Apart from its influence on other distant organs, extremity compartment pressures may be influenced by increased IAP. ACS or pelvic compartment syndrome both diminish venous return from the extremities, promoting further limb swelling. Monitoring of high-risk patients should be undertaken. Wall et al. defined categories of high-risk patients warranting invasive monitoring [72]:

  • Males aged > 35 years with fractures of the tibia and/or the radius/ulna
  • High-energy injuries (open fractures and/or severe soft tissue injuries)
  • Soft tissue injuries in males aged > 35 years with a bleeding disorder or receiving anticoagulants
  • Crush injuries
  • Prolonged limb compression (i.e. following drug overdose)
  • High-risk patients should be assessed for extremity compartment syndrome at least every 4 h for a minimum of 24 h after the precipitating injury


Hepatic compartment syndrome

As a result of the liver being an encapsulated organ, local haematoma formation caused by trauma or bleeding diathesis (oral anticoagulants, liver cirrhosis) may compromise tissue perfusion by causing hepatic compartment syndrome [73, 74]. Local hepatic compartment syndrome, or increased upper abdominal compartment pressures, has been described following major liver surgery (trauma, tumour resection, liver transplantation) [75−78]. Furthermore, the liver appears to be particularly susceptible to injury in the presence of elevated surrounding pressures, especially in a case of IAH or ACS [79]. The causes are probably multifactorial and related to altered haemodynamics, damage to the microcirculation, and the presence of interstitial oedema. Animal and human studies have shown impairment of hepatic cell function and liver perfusion, even with only a moderately elevated IAP of 10 mm Hg [79, 80]. Plasma disappearance rate for indocyaninegreen may be a useful parameter, as it correlates not only with liver function and perfusion but also with IAP [81−83]. Increased IAP leads to decreased hepatic arterial flow, decreased venous portal flow, and an increase in portal-systemic collateral circulation, causing decreased lactate clearance, altered glucose metabolism, and altered mitochondrial function [76, 80].

Renal compartment syndrome

The association between IAH and renal impairment has been known for more than 150 years [84]. However, the exact pathophysiological interplay between IAP and acute kidney injury has only been studied intensively in recent years [77, 85, 86]. Elevated IAP significantly decreases renal blood flow and causes renal venous hypertension through pressure transduction, leading to renal dysfunction and failure [87, 88]. Oliguria develops at IAP >15 mm Hg and values > 25 mm Hg are associated with anuria, even in the presence of normovolemia [89, 90]. As expected, in the setting of hypovolemia or sepsis, renal function is more easily compromised [89, 90]. Renal perfusion pressure (RPP) and renal filtration gradient (FG) have been proposed as key factors in the development of IAP-induced renal failure:


Where RVP = renal vein pressure


Where GFP = glomerular filtration pressure and PTP = proximal tubular pressure

The above equations are, however, probably too simplistic since they don’t take into account the autoregulatory effect of the afferent arterioles in the kidney. Autoregulation will keep renal blood flow (RBF) relatively constant, with a MAP between 75 and 200 mm Hg. In addition, these equations do not take into account a varying degree of vasoconstriction that may be present in the kidneys, depending on the underlying pathology leading to ACS. Nevertheless, in conditions of increased IAP, the RVP may be substituted by IAP, and the above equations become:


FG = MAP – 2 × IAP

As stated before, these equations have limitations related to their inability to account for vasoconstriction and autoregulation [91]. However, theoretically the changes in IAP may have a greater impact on renal function and urine production than changes in the MAP. Therefore, it should not be surprising that decreased renal function, as evidenced by the development of oliguria, is one of the first signs of IAH. The kidneys may be considered the ‘canary in the coalmine’ for IAH [86]. An increasing number of observational studies have identified that IAH (IAP 12 mm Hg) is independently associated with renal impairment and increased mortality [77, 85, 92, 93]. The exact pathophysiological mechanisms of this are not yet fully elucidated, but may be multifactorial and include reduced renal blood flow, reduced CO, increased SVR, and alterations in neurohumoral factors [86]. Within the capsule of the kidney itself, local haematoma formation (caused by trauma or bleeding diathesis) may have a further adverse effect on tissue perfusion, causing a local renal compartment syndrome [94−96].

Pelvic compartment syndrome

Three major compartments can be identified in the pelvic region, including the gluteus medius-minimus, gluteus maximus, and iliopsoas compartments. These are distinguished from the smaller compartment of the tensor fasciae latae muscle. Pelvic compartment syndrome is rare, and a clear history of trauma is often lacking [97−99]. It is often associated with drug and alcohol abuse, infections (necrotising fasciitis), and the use of anticoagulant therapy, especially low molecular weight heparin in the setting of diminished kidney function in the elderly [98, 100]. Increased pelvic compartment pressures may eventually increase IAP and affect kidney function due to bilateral ureteral obstruction, or by the same effects as described above in renal compartment syndrome. Measurement of upper and lower abdominal compartment pressures may provide helpful information [75]. Moreover, the presence of a massive intrapelvic haematoma, causing increased retroperitoneal pressure, can precipitate renal failure [101]. Decompressive fasciotomy of the gluteal compartment is probably the treatment of choice [6].

Abdominal compartment syndrome

Similarly to the head and the Monroe-Kellie doctrine, the abdomen can be considered as a closed box with partially rigid (spine, pelvis and costal arch) and partially flexible sides (abdominal wall and diaphragm) [1, 102]. Since the abdominal cavity can be considered as a relatively non-compressible and primarily fluid-containing compartment, behaving in accordance with Pascal’s law, the IAP measured at one point can be assumed to represent the IAP throughout the entire abdomen [103−105]. In normal conditions, IAP ranges from 0 to 5 mm Hg [106, 107]. However, certain physiological conditions such as morbid obesity, ovarian tumours, cirrhosis, or pregnancy, may be associated with chronic IAP elevations of 1015 mm Hg [1, 107−109].

The gold standard method for measuring IAP involves the use of a transurethral Foley catheter connected to a manometer (Holtech Medical, Charlottenlund, Denmark), or coupled to an AbViser valve (ConvaTec Medical, formerly Wolfe-Tory, UT, USA), or any other ‘home-made’ system that includes a pressure-measuring technique [103]. Continuous IAP measurement may be performed via a balloon-tipped catheter placed into the stomach (Spiegelberg, Hamburg, Germany or CiMON, Pulsion Medical Systems, Munich, Germany) [110−112]. Continuous IAP monitoring has the additional benefit of showing real-time interactions between the different compartments [5].

The term ACS was first used by Fietsam et al. in the late 1980s to describe the pathophysiologic alterations resulting from IAH secondary to aortic aneurysm surgery [113]. The World Society on the Abdominal Compartment Syndrome (WSACS www.wsacs.org) was founded in 2004 to serve as a peer-reviewed forum and educational resource for all clinicians with an interest in understanding IAH and abdominal compartment syndrome. The first consensus definitions were in 2006 and 2007 [1, 114], and these were updated in 2013 [9]. Table 2 summarises the latest consensus definitions, while the new 2013 consensus definitions (including polycompartment syndrome) are listed in Table 3.

Table 2. Consensus definitions. Definitions regarding intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) according to the 2006 and 2013 WSACS guidelines update (adapted from Malbrain et al. [1] and Kirkpatrick et al. [9])


2006 definitions


2013 definitions


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


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






FG = GFP PTP = MAP – 2 * IAP



IAP should be expressed in mm Hg 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


IAP should be expressed in mm Hg 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


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


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


Normal IAP is approximately 5−7 mm Hg in critically ill adults


IAP is approximately 5−7 mm Hg and around 10 mm Hg in critically ill adults


IAH is defined by a sustained or repeated pathologic elevation of IAP > 12 mm Hg


IAH is defined by a sustained or repeated pathologic elevation of IAP > 12 mm Hg


IAH is graded as follows:

Grade I: IAP 12−15 mm Hg

Grade II: IAP 16−20 mm Hg

Grade III: IAP 21−25 mm Hg

Grade IV: IAP > 25 mm Hg


IAH is graded as follows:

Grade I: IAP 12−15 mm Hg

Grade II: IAP 16−20 mm Hg

Grade III: IAP 21−25 mm Hg

Grade IV: IAP > 25 mm Hg


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


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


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


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


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


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


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


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

Table 3. New additional 2013 consensus definitions


New 2013 consensus definitions


A poly-compartment syndrome is a condition where two or more anatomical compartments have elevated compartmental pressures.


Abdominal compliance quantifies the ease of abdominal expansion, is determined by the elasticity of the abdominal wall and diaphragm, and is expressed as the change in intra-abdominal volume per change in intra-abdominal pressure in L (mm Hg)-1.


An open abdomen (OA) is any abdomen requiring a temporary abdominal closure due to the skin and fascia not being closed after laparotomy. The technique of temporary abdominal closure should be explicitly described.


The open abdomen is classified with the following grading system:

1 – No Fixation

1A: clean, no fixation

1B: contaminated, no fixation

1C: enteric leak, no fixation

2 – Developing Fixation

2A: clean, developing fixation

2B: contaminated, developing fixation

2C: enteroatmospheric/cutaneous fistula, developing fixation

3 and 4 – Frozen Abdomen

3: frozen abdomen, no fistula

4: frozen abdomen with enteroatmospheric/cutaneous fistula


Lateralisation of the abdominal wall refers to the phenomenon whereby the musculature and fascia of the abdominal wall, best seen by the rectus abdominis muscles and their enveloping fascia, move laterally away from the midline over time.

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; OA open abdomen; PTP proximal tubular pressure

According to these definitions, a polycompartment syndrome is a condition where two or more anatomical compartments have elevated compartmental pressures [9]. Table 4 lists some of the potential risk factors for the development of IAH [117, 118], including obesity (odds ratio (OR) 5.10; 95% confidence interval (CI), 1.92 to 13.58), sepsis (OR 2.38; 95% CI, 1.34 to 4.23), abdominal surgery (OR 1.93; 95% CI, 1.30 to 2.85), ileus (OR 2.05; 95% CI, 1.40 to 2.98), and large volume fluid resuscitation (OR 2.17; 95% CI, 1.30 to 3.63). All were identified as independent risk factors for IAH in a recent meta-analysis [118].

Table 4. Risk factors for the development of IAH and ACS

A. 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 pleuropneumonia
  • High body mass index#
  • Pneumoperitoneum
  • Abdominal surgery, especially with tight abdominal closures
  • Pneumatic anti-shock garments
  • Prone and other body positioning
  • Abdominal wall bleeding or rectus sheath haematomas
  • Correction of large hernias, gastroschisis or omphalocoele
  • Burns with abdominal eschars
  • Interstitial and abdominal wall oedema

B. Related to increased intra-luminal contents

  • Gastroparesis
  • Gastric distension
  • Ileus#
  • Volvulus
  • Colonic pseudo-obstruction (Ogilvie)
  • Intraluminal (colonic) abdominal tumour
  • Enteral feeding

C. Related to intra-abdominal collections of fluid, air, tissue or blood

  • Intra-abdominal or retroperitoneal tumour
  • Damage control laparotomy
  • Postoperative abdominal surgery#
  • Retroperitoneal haematoma
  • Liver dysfunction with ascites
  • Abdominal infection (pancreatitis, peritonitis, abscess,…)
  • Haemoperitoneum
  • Pneumoperitoneum
  • Laparoscopy with excessive inflation pressures
  • Major trauma (liver or spleen rupture)
  • Ruptured aortic aneurysm
  • Peritoneal dialysis

D. Related to capillary leak and fluid resuscitation

  • Acidosis* (pH below 7.2)
  • Hypothermia* (core temperature below 33°C)
  • Coagulopathy* (platelet count below 50,000/mm3 OR an activated partial thromboplastin time (APTT) more than two 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# (> 3 L of colloid or >10 L of crystalloid/24 hours with capillary leak and positive fluid balance)
  • Major burns

*The combination of acidosis, hypothermia and coagulopathy has been termed in the literature ‘the deadly triad’ [115, 116]#Indicates statistically significant risk factors according to a recent meta-analysis [116]

Analogous to the widely accepted and clinically utilised concept of CPP, abdominal perfusion pressure (APP) has been proposed as a more accurate predictor of visceral perfusion and a potential endpoint for resuscitation by considering both arterial inflow (MAP) and restrictions to venous outflow (IAP) [19, 49, 119, 120].


However, to date there have been no additional outcome benefits identified that would prompt the use of APP ahead of monitoring IAP [9]. More information on ACS with regard to IAP measurement, incidence, epidemiology, risk factors, pathophysiologic implications on end organ function, medical and surgical treatment are beyond the scope of the present review and are covered in other articles [9, 102, 103, 118, 121−122].


The clinical importance of the diverse aspects of polycompartment syndrome prompts a proposal of a new classification that stratifies the condition into two categories according to its underlying aetiology. Analogous to the classification of IAH or abdominal compartment syndrome, it is reasonable for polycompartment syndrome to be either primary or secondary, in view of the potential effect on organ function [124].

A primary compartment syndrome may be defined as a pathological rise of compartmental pressures with physical tissue or organ injury (i.e. intracranial haematoma or limb fracture).

In secondary compartment syndrome, there is no primary injury in the affected compartment and symptoms are solely based on pressure transmission from one compartment to another (i.e. abdominal compartment syndrome that develops following a tension pneumothorax) [124]. This was illustrated above in the case with polycompartment syndrome with secondary limb compartment syndrome and primary head and abdomen compartment syndromes.


1. Cardio-Abdominal-Renal Syndrome (CARS)

The abdominal compartment could potentially form a missing link in the pathophysiology of acute decompensated heart failure and cardio-renal syndrome [86, 91, 125−127]. Recently, our group reported that raised IAP was prevalent in patients with advanced heart failure and reduced left ventricular ejection fraction, and that this increase in IAP correlated with impaired renal function [128]. However, IAH and ACS, defined as 12 mm Hg and > 20 mm Hg respectively, are less frequent and frank ascites is rare [128]. Importantly, medical treatment resulting in a decrease in the IAP may improve renal function, and in cases of persistently high IAP, ultrafiltration has been proven beneficial [128, 129]. However, further studies are needed.

Notably, while organ dysfunction in the intensive care literature has only been described when IAP exceeds 12 mm Hg, patients with acute decompensated heart failure appear to develop worsening renal function at a lower IAP [128]. This might suggest that in this clinical setting renal reserve during increased IAP is limited. Furthermore, although the degree of renal dysfunction correlates with the degree of elevated IAP, there can be a wide range of IAPs in relation to serum creatinine levels at presentation [128]. While we can only speculate why this discrepancy exists, other mechanisms, including coexisting systemic congestion, pre-existing occult renal insufficiency, as well as drugs used during the treatment of acute decompensated heart failure, probably play a role.

Absolute increases in blood or interstitial volume may not occur in every episode of acute decompensated heart failure (AHDF). This was illustrated by Chaudhry et al. [130] who demonstrated that most heart failure patients gain only 1 kg of weight before admission for ADHF. This implies that vascular redistribution is another important mechanism for elevated cardiac filling pressures. The splanchnic vasculature normally contains about 25% of the total blood volume, a large part of which can quickly be recruited to the circulatory system through elastic recoil of the splanchnic veins and sympathetically-mediated venoconstriction [131, 132]. Because of the extensive orthosympathic innervations of abdominal capacitance veins, it is probable that more blood is distributed to the effective circulation in states of increased sympathetic nerve system activation, such as ADHF.

Consequently, we propose the term cardio-abdominal-renal syndrome or CARS, to emphasise the potentially important role of the abdominal compartment and splanchnic vasculature in the pathophysiology of ADHF and cardio-renal syndrome [91].

2. Hepato-Abdominal-Renal Syndrome (HARS)

Acute kidney injury is a severe complication in patients with decompensating liver cirrhosis, occurring in about 20% of patients, and is associated with poor outcomes [133]. Patients with cirrhosis are susceptible to developing renal failure because of the progressive vasodilatory state (secondary hyperaldosteronism) and reduced effective blood volume. Microcirculatory damage and shedding of the glycocalyx layer results in the movement of fluid across the physiological vascular barrier resulting in the accumulation of interstitial fluid, thus contributing to the formation of IAH and ACS. Hepatorenal syndrome is initiated by portal hypertension, and may be triggered by bacterial infections, nonbacterial systemic inflammatory reactions, excessive diuresis, gastrointestinal haemorrhage, diarrhoea, nephrotoxic agents and IAH [134]. The term HARS, hepato-abdominal-renal syndrome, succinctly describes this pathophysiological process, as increases in the IAP may be the missing link in the development of AKI in decompensated liver failure. In patients with portal hypertension and oesophageal varices, increases in IAP may have deleterious effects on variceal haemodynamics, markedly increasing the volume, pressure, and wall tension of the varices. Increases in IAP may furthermore contribute to the progressive dilatation that precedes the rupture of the varices resulting in new oesophageal bleeding [135]. In patients with portal hypertension and tense ascites, paracentesis may improve variceal wall stress [136] and kidney function if euvolaemia is maintained [137]. Orthotopic liver transplantation is the best current treatment and leads to a gradual recovery of renal function in the vast majority of patients.

3. Hepato-Abdominal-Pulmonary Syndrome (HAPS)

Liver-related causes of dyspnoea in chronic liver disease are common and can be related to pulmonary or extrapulmonary problems (e.g. cirrhotic myopathy and cardiomyopathy, muscle waisting) [138]. Pulmonary causes can be subdivided into parenchymal and extraparenchymal (e.g. pleural effusions or restrictive disease from tense ascites). Parenchymal causes can be either alveolar (e.g. aspiration pneumonia, basal atelectasis), interstitial (e.g. lymphocytic interstitial pneumonia, fibrosing alveolitis, COP, or noncardiogenic pulmonary oedema from fluid overload or hepato-abdominal-renal syndrome), or vascular (e.g. alveolar haemorrhage, hepatopulmonary syndrome or portopulmonary hypertension) [139].

Hepatopulmonary syndrome is defined as an arterial oxygenation defect induced by intrapulmonary vascular dilatations associated with hepatic disease, and its prevalence is estimated to be around 20% in patients awaiting orthotopic liver transplantation. The clinical triad consists of: 1) liver disease and/or portal hypertension; 2) the presence of intrapulmonary vascular dilatations; and 3) increased alveolar-arterial gradient resulting in orthodeoxia (arterial hypoxemia in the upright position) and platypnoea (improved oxygenation in supine position). Chronic liver disease with portal hypertension is often associated with (tense) ascites. Again it is proposed that IAP may play a key role in the development of dyspnoea in patients with chronic liver disease. The new term HAPS, or hepato-abdominal-pulmonary syndrome, describes this clinical problem. Indeed, increased IAP and portal hypertension in liver cirrhosis may lead to an elevation of nitric oxide levels and activation of the renin angiotensin aldosterone system [140]. The resulting vasodilation, water and sodium retention in combination with the hyperdynamic state will lead to expansion of systemic and central blood volumes and interstitial fluid accumulation, triggering a vicious cycle.


At present, in the setting of often limited evidence, we suggest that the management of patients with polycompartment syndrome should be based on three principles [141, 142]. Firstly, specific medical and surgical procedures are required to reduce compartment pressures (Table 5).

Table 5. Potential treatment options for compartment syndrome

1. Improvement of compartment wall compliance

  • Sedation and analgesia (not fentanyl)
  • Neuromuscular blockade
  • Body positioning
  • Negative fluid balance
  • Skin pressure decreasing interfaces
  • Weight loss
  • Percutaneous abdominal wall component separation
  • Subcutaneous linea alba fasciotomy (SLAF)
  • Escharotomies

2. Evacuation of intra-compartmental contents

  • Gastric tube and suctioning
  • CSF, ascites, pleural or pericardial drainage
  • Rectal tube and enemas
  • Chest tube and suctioning
  • Endoscopic decompression of large bowel
  • Colostomy or ileostomy
  • CT- or US-guided aspiration of abscess
  • CT- or US-guided aspiration of haematoma
  • Pericardiectomy

3. Correction of capillary leak and positive fluid balance

  • Albumin in combination with diuretics (furosemide)
  • Antibiotics and sepsis source control
  • Colloids (hypertonic albumin) instead of crystalloids
  • Dobutamine (not dopamine)
  • Dialysis or CVVH with ultrafiltration
  • Ascorbinic acid in burn patients

4. Specific therapeutic interventions

  • Targeted compartment perfusion pressure (PP > 55 mm Hg)
  • External negative compartment pressure

5. Rescue therapy

  • ICS: decompressive craniectomy
  • ACS: decompressive laparotomy
  • TCS: decompressive sternotomy
  • ECS: decompressive fasciotomy
  • PCS: decompressive gluteal fasciotomy
  • RCS: renal decapsulation
  • HCS: hepatic decapsulation
  • CCS: decompressive pericardiotomy
  • OCS: orbital decompression

These measures include improving compartment wall compliance, evacuation of intra-compartment contents, correction of capillary leak and positive fluid balance, and (surgical) rescue management. Secondly, general and organ supportive therapy (intensive care) of the critically ill patient should be tailored to individual needs. As suggested above, a major issue involves the iatrogenic injury caused by over-resuscitation with crystalloid fluids resulting in secondary compartment syndrome. Some studies have shown that the cautious administration of colloids not only seems to decrease the incidence of ACS in burn and trauma patients, but also the ACS associated complications and mortality, as well as the complications related to increased pressures in other compartments [10, 143−146]. The timing, speed, type and dose of fluid resuscitation will play a major role in future treatment and prevention of polycompartment syndrome. The motto is not to give too much fluid, but to give the right fluids judiciously. The results of the recent large randomised controlled trials showing harmful effects of hydroxyethyl starch fluids on kidney function may however complicate this clinical dilemma further [147]. Finally, optimisation and prevention of specific adverse events after surgical decompression resulting from ischaemia and reperfusion is warranted.


First defined in 2007, polycompartment syndrome is a constellation of physiological sequelae of increased compartmental pressures in multiple compartments of the body [4, 5]. While polycompartment syndrome is uncommon, its consequences can be significant. It may be beneficial to further classify into primary and secondary compartment syndromes (similar to ACS) and to recognise the different components of a polycompartment syndrome. Widespread use of (continuous) ICP and IAP monitoring, and in a subset of patients combining this with intermittent limb compartment pressure monitoring, will allow timely diagnosis of primary polycompartment syndrome. Given the existing guidelines on acute limb compartment syndrome, the World Society on the Abdominal Compartment Syndrome may need to consider guidelines for polycompartment syndromes in addition to abdominal compartment syndromes.

Within polycompartment syndrome, the abdomen plays a central role and the effect of IAH on different organ systems has been described, along with recommendations to monitor and compensate for these effects. Even chronic elevations of IAP seem to affect various organ systems in the body. The abdominal compartment does play a key role in the pathophysiology of acute decompensated heart failure, cardiorenal and hepatorenal syndromes. Therefore, in our opinion, the terms cardio-abdominal-renal syndrome or CARS and hepato-abdominal-renal syndrome or HARS seem to be more appropriate.

Different conditions precipitate the occurrence of polycompartment syndrome, including severe burns, massive fluid resuscitation, severe sepsis, and/or prolonged hypotension. The ultimate treatment goal of polycompartment syndrome is not only to decrease the compartment pressure (by improving compartment wall compliance), but also to improve organ function with the ultimate goal of decreasing mortality. Decompressive craniectomy, sternotomy, pericardiotomy, fasciotomy and laparotomy are the only treatment options that have been shown to reach these goals in the past. However, less invasive techniques and medical treatment strategies show promise in achieving compartment pressure reduction and organ function improvement. This is probably where the future lies.


Dr M.L.N.G. Malbrain is member of the medical advisory board of Pulsion Medical Systems and Holtech Medical and consults for Kinetic Concepts International and ConvaTec. The other authors have no possible conflicts of interest in relation to the contents of this review. Parts of this review have been previously published elsewhere in non peer-reviewed journals or as a book chapter [7, 8, 148−151].


  1. 1. Malbrain ML, Cheatham ML, Kirkpatrick A et al.: Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. I. Definitions. Intensive Care Med 2006; 32: 1722−1732.
  2. 2. Malbrain MLNG, Van Regenmortel N, Himpe D: Meeting report of the first international fluid academy day. Part 2: Results of the survey on the knowledge of hemodynamic monitoring and fluid responsiveness. Fluids 2012; 1: 15−26.
  3. 3. Kavanagh BP, Meyer LJ: Normalizing physiological variables in acute illness: five reasons for caution. Intensive Care Med 2005; 31: 1161−1167.
  4. 4. Scalea TM, Bochicchio GV, Habashi N et al.: Increased intra-abdominal, intrathoracic, and intracranial pressure after severe brain injury: multiple compartment syndrome. J Trauma 2007; 62: 647−656.
  5. 5. Malbrain ML, Wilmer A: The polycompartment syndrome: towards an understanding of the interactions between different compartments! Intensive Care Med 2007; 33: 1869−1872.
  6. 6. Balogh ZJ, Butcher NE: Compartment syndromes from head to toe. Crit Care Med 2010; 38 (Suppl): S445−451.
  7. 7. Malbrain MLNG, De laet I: A new concept: the polycompartment syndrome Part 1. Int J Intensive Care 2008, Autumn 2008: 19−24.
  8. 8. Malbrain MLNG, De laet I: A new concept: the polycompartment syndrome Part 2. Int J Intensive Care 2009, Spring 2009: 19−25.
  9. 9. Kirkpatrick AW, Roberts DJ, De Waele J et al: Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med 2013; 39: 1190−1206.
  10. 10. De laet IE, De Waele JJ, Malbrain MLNG: Fluid resuscitation and intra-abdominal hypertension. In: Vincent J-L (ed:) Yearbook of intensive care and emergency medicine. Springer-Verlag, Berlin 2008: 536−548.
  11. 11. Malbrain ML, De Laet I: AIDS is coming to your ICU: be prepared for acute bowel injury and acute intestinal distress syndrome. Intensive Care Med 2008; 34: 1565−1569.
  12. 12. Malbrain ML, De laet I: It’s all in the gut: introducing the concept of acute bowel injury and acute intestinal distress syndrome. Crit Care Med 2009; 37: 365−366.
  13. 13. Malbrain ML, Vidts W, Ravyts M, De Laet I, De Waele J: Acute intestinal distress syndrome: the importance of intra-abdominal pressure. Minerva Anestesiol 2008; 74: 657−673.
  14. 14. Andrews PJ, Citerio G: Intracranial pressure. Part one: historical overview and basic concepts. Intensive Care Med 2004; 30: 1730−1733.
  15. 15. Citerio G, Andrews PJ: Intracranial pressure. Part two: Clinical applications and technology. Intensive Care Med 2004; 30: 1882−1885.
  16. 16. De laet I, Citerio G, Malbrain ML: The influence of intraabdominal hypertension on the central nervous system: current insights and clinical recommendations, is it all in the head? Acta Clin Belg Suppl 2007; 62: 89−97.
  17. 17. Citerio G, Berra L: Central nervous system. In: Ivatury R, Cheatham M, Malbrain M, Sugrue M (ed:) Abdominal compartment syndrome. Landes Bioscience, Georgetown 2006: 144−156.
  18. 18. Citerio G, Vascotto E, Villa F, Celotti S, Pesenti A: Induced abdominal compartment syndrome increases intracranial pressure in neurotrauma patients: a prospective study. Crit Care Med 2001; 29: 1466−1471.
  19. 19. Deeren D, Dits H, Malbrain MLNG: Correlation between intra-abdominal and intracranial pressure in nontraumatic brain injury. Intensive Care Med 2005; 31: 1577−1581.
  20. 20. Bloomfield G, Saggi B, Blocher C, Sugerman H: Physiologic effects of externally applied continuous negative abdominal pressure for intra-abdominal hypertension. J Trauma 1999; 46: 1009−1014.
  21. 21. Bloomfield GL, Dalton JM, Sugerman HJ, Ridings PC, DeMaria EJ, Bullock R: Treatment of increasing intracranial pressure secondary to the acute abdominal compartment syndrome in a patient with combined abdominal and head trauma. J Trauma 1995; 39: 1168−1170.
  22. 22. Bloomfield GL, Ridings PC, Blocher CR, Marmarou A, Sugerman HJ: Effects of increased intra-abdominal pressure upon intracranial and cerebral perfusion pressure before and after volume expansion. J Trauma 1996; 40: 936−941.
  23. 23. Bloomfield GL, Ridings PC, Blocher CR, Marmarou A, Sugerman HJ: A proposed relationship between increased intra-abdominal, intrathoracic, and intracranial pressure. Crit Care Med 1997; 25: 496−503.
  24. 24. Saggi BH, Bloomfield GL, Sugerman HJ et al.: Treatment of intracranial hypertension using nonsurgical abdominal decompression. J Trauma 1999; 46: 646−651.
  25. 25. Lima V, Burt B, Leibovitch I, Prabhakaran V, Goldberg RA, Selva D: Orbital compartment syndrome: the ophthalmic surgical emergency. Surv Ophthalmol 2009; 54: 441−449.
  26. 26. Singh CN, Klein MB, Sullivan SR et al.: Orbital compartment syndrome in burn patients. Ophthal Plast Reconstr Surg 2008; 24: 102−106.
  27. 27. Bai HQ, Yao L, Wang DB, Jin R, Wang YX: Causes and treatments of traumatic secondary glaucoma. Eur J Ophthalmol 2009; 19: 201−206.
  28. 28. Kaplan LJ, Trooskin SZ, Santora TA: Thoracic compartment syndrome. J Trauma 1996; 40: 291−293.
  29. 29. Rizzo AG, Sample GA: Thoracic compartment syndrome secondary to a thoracic procedure: a case report. Chest 2003; 124: 1164−1168.
  30. 30. Cheatham ML, Malbrain ML: Cardiovascular implications of abdominal compartment syndrome. Acta Clin Belg Suppl 2007; 62: 98−112.
  31. 31. Wauters J, Claus P, Brosens N, McLaughlin M, Hermans G, Malbrain M, Wilmer A: Relationship between abdominal pressure, pulmonary compliance, and cardiac preload in a porcine model. Crit Care Res Pract 2012; 2012: 763181.
  32. 32. Talmor D, Sarge T, O’Donnell CR et al.: Esophageal and transpulmonary pressures in acute respiratory failure. Crit Care Med 2006; 34: 1389−1394.
  33. 33. Valenza F, Chevallard G, Porro GA, Gattinoni L: Static and dynamic components of esophageal and central venous pressure during intra-abdominal hypertension. Crit Care Med 2007; 35: 1575−1581.
  34. 34. Pelosi P, Quintel M, Malbrain ML: Effect of intra-abdominal pressure on respiratory mechanics. Acta Clin Belg Suppl 2007; 62: 78−88.
  35. 35. Regli A, Mahendran R, Fysh ET et al.: Matching positive end-expiratory pressure to intra-abdominal pressure improves oxygenation in a porcine sick lung model of intra-abdominal hypertension. Crit Care 2012; 16: R208.
  36. 36. Cortes-Puentes GA, Gard KE, Adams AB et al.: Value and limitations of transpulmonary pressure calculations during intra-abdominal hypertension. Crit Care Med 2013; 41: 1870−1877.
  37. 37. Malbrain M, Pelosi P: Open up and keep the lymphatics open: they are the hydraulics of the body! Crit Care Med 2006; 34: 2860−2862.
  38. 38. Malbrain ML, Pelosi P, De laet I, Lattuada M, Hedenstierna G: Lymphatic drainage between thorax and abdomen: please take good care of this well-performing machinery. Acta Clin Belg Suppl 2007; 62: 152−161.
  39. 39. Quintel M, Pelosi P, Caironi P et al: An increase of abdominal pressure increases pulmonary edema in oleic acid-induced lung injury. Am J Respir Crit Care Med 2004; 169: 534−541.
  40. 40. Cordemans C, De laet I, Van Regenmortel N et al.: Fluid management in critically ill patients: The role of extravascular lung water, abdominal hypertension, capillary leak and fluid balance. Ann Intensive Care 2012; 2 (Suppl 1): S1.
  41. 41. Sturini E, Saporito A, Sugrue M, Parr MJ, Bishop G, Braschi A: Respiratory variation of intra-abdominal pressure: indirect indicator of abdominal compliance? Intensive Care Med 2008; 34: 1632−1637.
  42. 42. Callaham M: Pericardiocentesis in traumatic and nontraumatic cardiac tamponade. Ann Emerg Med 1984; 13: 924−945.
  43. 43. Lee TH, Ouellet JF, Cook M, Schreiber MA, Kortbeek JB: Pericardiocentesis in trauma: a systematic review. J Trauma Acute Care Surg 2013; 75: 543−549.
  44. 44. Ameloot K, Gillebert C, Desie N, Malbrain ML: Hypoperfusion, shock states, and abdominal compartment syndrome (ACS). Surg Clin North Am 2012; 92: 207−220.
  45. 45. Kashtan J, Green JF, Parsons EQ, Holcroft JW: Hemodynamic effect of increased abdominal pressure. J Surg Res 1981; 30: 249−255.
  46. 46. Ridings PC, Bloomfield GL, Blocher CR, Sugerman HJ: Cardiopulmonary effects of raised intra-abdominal pressure before and after intravascular volume expansion. J Trauma 1995; 39: 1071−1075.
  47. 47. Richardson JD, Trinkle JK: Hemodynamic and respiratory alterations with increased intra-abdominal pressure. J Surg Res 1976; 20: 401−404.
  48. 48. Malbrain ML, Cheatham ML: Cardiovascular effects and optimal preload markers in intra-abdominal hypertension. In: Vincent J-L (ed:) Yearbook of intensive care and emergency medicine. Springer-Verlag, Berlin 2004: 519−543.
  49. 49. Cheatham M, Malbrain M: Abdominal perfusion pressure. In: Ivatury R, Cheatham M, Malbrain M, Sugrue M (ed:) Abdominal compartment syndrome. Landes Bioscience, Georgetown 2006: 69−81.
  50. 50. Cheatham M, Malbrain M: Cardiovascular implications of elevated intra-abdominal pressure. In: Ivatury R, Cheatham M, Malbrain M, Sugrue M (ed:) Abdominal compartment syndrome. Landes Bioscience, Georgetown 2006: 89−104.
  51. 51. Verhaert D, Mullens W, Borowski A et al.: Right ventricular response to intensive medical therapy in advanced decompensated heart failure. Circ Heart Fail 2010; 3: 340−346.
  52. 52. Qureshi AS, Shapiro RS, Leatherman JW: Use of bladder pressure to correct for the effect of expiratory muscle activity on central venous pressure. Intensive Care Med 2007; 33: 1907−1912.
  53. 53. Teboul JL, Pinsky MR, Mercat A et al.: Estimating cardiac filling pressure in mechanically ventilated patients with hyperinflation. Crit Care Med 2000; 28: 3631−3636.
  54. 54. Wauters J, Wilmer A, Valenza F: Abdomino-thoracic transmission during ACS: facts and figures. Acta Clin Belg Suppl 2007; 62: 200−205.
  55. 55. Cheatham ML, Block EF, Nelson LD, Safcsak K: Superior predictor of the hemodynamic response to fluid challenge in critically ill patients. Chest 1998; 114: 1226−1227.
  56. 56. Cheatham ML, Nelson LD, Chang MC, Safcsak K: Right ventricular end-diastolic volume index as a predictor of preload status in patients on positive end-expiratory pressure. Crit Care Med 1998; 26: 1801−1806.
  57. 57. Schachtrupp A, Graf J, Tons C, Hoer J, Fackeldey V, Schumpelick V: Intravascular volume depletion in a 24-hour porcine model of intra-abdominal hypertension. J Trauma 2003; 55: 734−740.
  58. 58. Michard F, Alaya S, Zarka V, Bahloul M, Richard C, Teboul JL: Global end-diastolic volume as an indicator of cardiac preload in patients with septic shock. Chest 2003; 124: 1900−1908.
  59. 59. Malbrain ML, De Potter TJ, Dits H, Reuter DA: Global and right ventricular end−diastolic volumes correlate better with preload after correction for ejection fraction. Acta Anaesthesiol Scand 2010; 54: 622−631.
  60. 60. Simon RJ, Friedlander MH, Ivatury RR, DiRaimo R, Machiedo GW: Hemorrhage lowers the threshold for intra-abdominal hypertension-induced pulmonary dysfunction. J Trauma 1997; 42: 398−403.
  61. 61. Burchard KW, Ciombor DM, McLeod MK, Slothman GJ, Gann DS: Positive end expiratory pressure with increased intra-abdominal pressure. Surg Gynecol Obstet 1985; 161: 313−318.
  62. 62. Pelosi P, Ravagnan I, Giurati G et al.: Positive end-expiratory pressure improves respiratory function in obese but not in normal subjects during anesthesia and paralysis. Anesthesiology 1999; 91: 1221−1231.
  63. 63. Sugrue M, D’Amours S: The problems with positive end expiratory pressure (PEEP) in association with abdominal compartment syndrome (ACS). J Trauma 2001; 51: 419−420.
  64. 64. Sussman AM, Boyd CR, Williams JS, DiBenedetto RJ: Effect of positive end-expiratory pressure on intra-abdominal pressure. South Med J 1991; 84: 697−700.
  65. 65. Malbrain ML, De Laet I: Functional haemodynamics during intra-abdominal hypertension: what to use and what not. Acta Anaesthesiol Scand 2008; 52: 576−577.
  66. 66. Malbrain ML, de Laet I: Functional hemodynamics and increased intra-abdominal pressure: same thresholds for different conditions ...? Crit Care Med 2009; 37: 781−783.
  67. 67. Duperret S, Lhuillier F, Piriou V et al.: Increased intra-abdominal pressure affects respiratory variations in arterial pressure in normovolaemic and hypovolaemic mechanically ventilated healthy pigs. Intensive Care Med 2007; 33: 163−171.
  68. 68. Bliacheriene F, Machado SB, Fonseca EB, Otsuke D, Auler JO, Jr., Michard F: Pulse pressure variation as a tool to detect hypovolaemia during pneumoperitoneum. Acta Anaesthesiol Scand 2007; 51: 1268−1272.
  69. 69. Mahjoub Y, Touzeau J, Airapetian N et al.: The passive leg-raising maneuver cannot accurately predict fluid responsiveness in patients with intra-abdominal hypertension. Crit Care Med 2010; 38: 1824−1829.
  70. 70. Malbrain ML, Reuter DA: Assessing fluid responsiveness with the passive leg raising maneuver in patients with increased intra-abdominal pressure: be aware that not all blood returns! Crit Care Med 2010; 38: 1912−1915.
  71. 71. Hoang C, Porter JM, Ursic CM: Compartment syndrome in multiple uninjured extremities: a case report. Am Surg 2002; 68: 127−129.
  72. 72. Wall CJ, Lynch J, Harris IA, Richardson MD, Brand C, Lowe AJ, Sugrue M: Clinical practice guidelines for the management of acute limb compartment syndrome following trauma. ANZ J Surg 2010; 80: 151−156.
  73. 73. Goldman R, Zilkoski M, Mullins R, Mayberry J, Deveney C, Trunkey D: Delayed celiotomy for the treatment of bile leak, compartment syndrome, and other hazards of nonoperative management of blunt liver injury. Am J Surg 2003; 185: 492−497.
  74. 74. Pearl LB, Trunkey DD: Compartment syndrome of the liver. J Trauma 1999; 47: 796−798.
  75. 75. Cresswell AB, Jassem W, Srinivasan P et al: The effect of body position on compartmental intra-abdominal pressure following liver transplantation. Ann Intensive Care 2012; 2 (Suppl 1): S12.
  76. 76. Cresswell AB, Wendon JA: Hepatic function and non-invasive hepatosplanchnic monitoring in patients with abdominal hypertension. Acta Clin Belg Suppl 2007; 62: 113−118.
  77. 77. Biancofiore G, Bindi ML, Romanelli AM et al.: Postoperative intra-abdominal pressure and renal function after liver transplantation. Arch Surg 2003; 138: 703−706.
  78. 78. Biancofiore G, Bindi ML, Romanelli AM et al.: Intra-abdominal pressure monitoring in liver transplant recipients: a prospective study. Intensive Care Med 2003; 29: 30−36.
  79. 79. Diebel LN, Wilson RF, Dulchavsky SA, Saxe J: Effect of increased intra-abdominal pressure on hepatic arterial, portal venous, and hepatic microcirculatory blood flow. J Trauma 1992; 33: 279−282.
  80. 80. Wendon J, Biancofiore G, Auzinger G: Intra-abdominal hypertension and the liver. In: Ivatury R, Cheatham M, Malbrain M, Sugrue M (ed:) Abdominal compartment syndrome. Landes Bioscience, Georgetown 2006: 138−143.
  81. 81. Michelet P, Roch A, Gainnier M, Sainty JM, Auffray JP, Papazian L: Influence of support on intra-abdominal pressure, hepatic kinetics of indocyanine green and extravascular lung water during prone positioning in patients with ARDS: a randomized crossover study. Crit Care 2005; 9: R251−257.
  82. 82. Hering R, Vorwerk R, Wrigge H et al.: Prone positioning, systemic hemodynamics, hepatic indocyanine green kinetics, and gastric intramucosal energy balance in patients with acute lung injury. Intensive Care Med 2002; 28: 53−58.
  83. 83. Malbrain ML, Viaene D, Kortgen A et al.: Relationship between intra-abdominal pressure and indocyanine green plasma disappearance rate: hepatic perfusion may be impaired in critically ill patients with intra-abdominal hypertension. Ann Intensive Care 2012, 2 (Suppl 1): S19.
  84. 84. Schein M: Abdominal compartment syndrome: historical background. In: Ivatury R, Cheatham M, Malbrain M, Sugrue M (ed:) Abdominal compartment syndrome. Landes Bioscience, Georgetown 2006: 1−7.
  85. 85. Sugrue M, Hallal A, D’Amours S: Intra-abdominal pressure hypertension and the kidney. In: Ivatury R, Cheatham M, Malbrain M, Sugrue M (ed:) Abdominal compartment syndrome. Landes Bioscience, Georgetown 2006: 119−128.
  86. 86. De laet I, Malbrain ML, Jadoul JL, Rogiers P, Sugrue M: Renal implications of increased intra-abdominal pressure: are the kidneys the canary for abdominal hypertension? Acta Clin Belg Suppl 2007; 62: 119−130.
  87. 87. Kirkpatrick AW, Colistro R, Laupland KB et al.: Renal arterial resistive index response to intraabdominal hypertension in a porcine model. Crit Care Med 2006; 35: 206−213.
  88. 88. Wauters J, Claus P, Brosens N, McLaughlin M, Malbrain M, Wilmer A: Pathophysiology of renal hemodynamics and renal cortical microcirculation in a porcine model of elevated intra-abdominal pressure. J Trauma 2009; 66: 713−719.
  89. 89. Bradley SE, Mudge GH, Blake WD, Alphonse P: The effect of increased intra-abdominal pressure on the renal excretion of water and electrolytes in normal human subjects and in patients with diabetes insipidus. Acta Clin Belg 1955; 10: 209−223.
  90. 90. Harman PK, Kron IL, McLachlan HD, Freedlender AE, Nolan SP: Elevated intra-abdominal pressure and renal function. Ann Surg 1982; 196: 594−597.
  91. 91. Verbrugge FH, Dupont M, Steels P, Grieten L, Malbrain M, Tang WH, Mullens W: Abdominal contributions to cardiorenal dysfunction in congestive heart failure. J Am Coll Cardiol 2013; 62: 485−495.
  92. 92. Sugrue M, Buist MD, Hourihan F, Deane S, Bauman A, Hillman K: Prospective study of intra-abdominal hypertension and renal function after laparotomy. Br J Surg 1995; 82: 235−238.
  93. 93. Sugrue M, Jones F, Deane SA, Bishop G, Bauman A, Hillman K: Intra-abdominal hypertension is an independent cause of postoperative renal impairment. Arch Surg 1999; 134: 1082−1085.
  94. 94. Stothert JC: Evaluation of decapsulation of the canine kidney on renal function following acute ischemia. J Surg Res 1979; 26: 560−564.
  95. 95. Gewertz BL, Krupski W, Wheeler HT, Brink BE, Fry WJ: Effect of renal decapsulation on cortical hemodynamics in the postischemic kidney. J Surg Res 1980; 28: 252−259.
  96. 96. Stone HL, Alexander WC: Abdominal blood flow changes during acceleration stress in anesthetized dogs. Aerosp Med 1968; 39: 115−119.
  97. 97. Bosch U, Tscherne H: The pelvic compartment syndrome. Arch Orthop Trauma Surg 1992; 111: 314−317.
  98. 98. Hessmann M, Rommens P: Bilateral ureteral obstruction and renal failure caused by massive retroperitoneal hematoma: is there a pelvic compartment syndrome analogous to abdominal compartment syndrome? J Orthop Trauma 1998; 12: 553−557.
  99. 99. Hessmann M, Rommens P: Does the intrapelvic compartment syndrome exist? Acta Chir Belg 1998; 98: 18−22.
  100. 100. Malbrain ML, De laet IE, Willems A, Van Regenmortel N, Schoonheydt K, Dits H: Localised abdominal compartment syndrome: bladder-over-gastric pressure ratio (B/G ratio) as a clue to diagnosis. Acta Clin Belg 2010; 65: 98−106.
  101. 101. Ertel W, Oberholzer A, Platz A, Stocker R, Trentz O: Incidence and clinical pattern of the abdominal compartment syndrome after ‘damage-control’ laparotomy in 311 patients with severe abdominal and/or pelvic trauma. Crit Care Med 2000; 28: 1747−1753.
  102. 102. Malbrain ML, De laet IE: Intra-abdominal hypertension: evolving concepts. Clin Chest Med 2009; 30: 45−70.
  103. 103. Malbrain ML: Different techniques to measure intra-abdominal pressure (IAP): time for a critical re-appraisal. Intensive Care Med 2004; 30: 357−371.
  104. 104. Malbrain M, Jones F: Intra-abdominal pressure measurement techniques. In: Ivatury R, Cheatham M, Malbrain M, Sugrue M (ed:) Abdominal compartment syndrome. Landes Bioscience, Georgetown 2006: 19−68.
  105. 105. Emerson H: Intra-abdominal pressures. Arch Intern Med 1911; 7: 754−784.
  106. 106. Sanchez NC, Tenofsky PL, Dort JM, Shen LY, Helmer SD, Smith RS: What is normal intra-abdominal pressure? Am Surg 2001; 67: 243−248.
  107. 107. De Keulenaer BL, De Waele JJ, Powell B, Malbrain ML: What is normal intra-abdominal pressure and how is it affected by positioning, body mass and positive end-expiratory pressure? Intensive Care Med 2009; 35: 969−976.
  108. 108. Sugerman H, Windsor A, Bessos M, Wolfe L: Intra-abdominal pressure, sagittal abdominal diameter and obesity comorbidity. J Intern Med 1997; 241: 71−79.
  109. 109. Sugerman HJ: Effects of increased intra-abdominal pressure in severe obesity. Surg Clin North Am 2001; 81: 1063−1075.
  110. 110. Wauters J, Spincemaille L, Dieudonne AS, Van Zwam K, Wilmer A, Malbrain ML: A Novel Method (CiMON) for Continuous Intra-abdominal Pressure Monitoring: Pilot Test in a Pig Model. Crit Care Res Pract 2012; 2012: 181563.
  111. 111. Malbrain ML, De Laet I, Viaene D, Schoonheydt K, Dits H: In vitro validation of a novel method for continuous intra-abdominal pressure monitoring. Intensive Care Med 2008; 34: 740−745.
  112. 112. De Potter TJ, Dits H, Malbrain ML: Intra- and interobserver variability during in vitro validation of two novel methods for intra-abdominal pressure monitoring. Intensive Care Med 2005; 31: 747−751.
  113. 113. Fietsam R, Jr., Villalba M, Glover JL, Clark K: Intra-abdominal compartment syndrome as a complication of ruptured abdominal aortic aneurysm repair. Am Surg 1989; 55: 396−402.
  114. 114. Malbrain ML, De laet I, Cheatham M: Consensus conference definitions and recommendations on intra-abdominal hypertension (IAH) and the abdominal compartment syndrome (ACS) the long road to the final publications, how did we get there? Acta Clin Belg Suppl 2007; 62: 44−59.
  115. 115. Burch JM, Moore EE, Moore FA, Franciose R: The abdominal compartment syndrome. Surg Clin North Am 1996; 76: 833−842.
  116. 116. Ivatury RR, Sugerman HJ, Peitzman AB: Abdominal compartment syndrome: recognition and management. Adv Surg 2001; 35: 251−269.
  117. 117. Malbrain ML, Chiumello D, Cesana BM et al: A systematic review and individual patient data meta-analysis on intraabdominal hypertension in critically ill patients: the wake-up project World Initiative on Abdominal Hypertension Epidemiology, a Unifying Project (WAKE-Up!). Minerva Anestesiol 2014; 80: 293−306.
  118. 118. Holodinsky JK, Roberts DJ, Ball CG et al: Risk factors for intra-abdominal hypertension and abdominal compartment syndrome among adult intensive care unit patients: a systematic review and meta-analysis. Crit Care 2013; 17: R249.
  119. 119. Cheatham ML, White MW, Sagraves SG, Johnson JL, Block EF: Abdominal perfusion pressure: a superior parameter in the assessment of intra-abdominal hypertension. J Trauma 2000; 49: 621−626.
  120. 120. Malbrain ML: Abdominal perfusion pressure as a prognostic marker in intra-abdominal hypertension. In: Vincent JL (ed:) Yearbook of Intensive Care and Emergency Medicine. Springer-Verlag, Berlin 2002: 792−814.
  121. 121. Reintam Blaser A, Parm P, Kitus R, Starkopf J: Risk factors for intra-abdominal hypertension in mechanically ventilated patients. Acta Anaesthesiol Scand 2011; 55: 607−614.
  122. 122. De Laet IE, Ravyts M, Vidts W, Valk J, De Waele JJ, Malbrain ML: Current insights in intra-abdominal hypertension and abdominal compartment syndrome: open the abdomen and keep it open! Langenbecks Arch Surg 2008; 393: 833−847.
  123. 123. Balogh Z, McKinley BA, Holcomb JB et al: Both primary and secondary abdominal compartment syndrome can be predicted early and are harbingers of multiple organ failure. J Trauma 2003; 54: 848−859.
  124. 124. Alder AC, Hunt JL, Thal ER: Abdominal compartment syndrome associated with tension pneumoperitoneum in an elderly trauma patient. J Trauma 2008; 64: 211−212.
  125. 125. Verbrugge FH, Mullens W, Malbrain MLNG: Worsening renal function during decompensated heart failure: the cardio-abdomino-renal syndrome (CARS). In: Vincent J-L (ed:) Yearbook of intensive care and emergency medicine. Springer-Verlag, Berlin 2012: 577−590.
  126. 126. Mohmand H, Goldfarb S: Renal dysfunction associated with intra-abdominal hypertension and the abdominal compartment syndrome. J Am Soc Nephrol 2011; 22: 615−621.
  127. 127. De Waele JJ, De Laet I, Kirkpatrick AW, Hoste E: Intra-abdominal hypertension and abdominal compartment syndrome. Am J Kidney Dis 2011; 57: 159−169.
  128. 128. Mullens W, Abrahams Z, Skouri HN et al.: Elevated intra-abdominal pressure in acute decompensated heart failure: a potential contributor to worsening renal function? J Am Coll Cardiol 2008; 51: 300−306.
  129. 129. Mullens W, Abrahams Z, Francis GS, Taylor DO, Starling RC, Tang WH: Prompt reduction in intra-abdominal pressure following large-volume mechanical fluid removal improves renal insufficiency in refractory decompensated heart failure. J Card Fail 2008;, 14: 508−514.
  130. 130. Chaudhry SI, Wang Y, Concato J, Gill TM, Krumholz HM: Patterns of weight change preceding hospitalization for heart failure. Circulation 2007; 116: 1549−1554.
  131. 131. Greenway CV: Role of splanchnic venous system in overall cardiovascular homeostasis. Fed Proc 1983; 42: 1678−1684.
  132. 132. Gelman S, Mushlin PS: Catecholamine-induced changes in the splanchnic circulation affecting systemic hemodynamics. Anesthesiology 2004; 100: 434−439.
  133. 133. Hartleb M, Gutkowski K: Kidneys in chronic liver diseases. World J Gastroenterol 2012; 18: 3035−3049.
  134. 134. Kramer L, Horl WH: Hepatorenal syndrome. Semin Nephrol 2002; 22: 290−301.
  135. 135. Escorsell A, Gines A, Llach J, Garcia-Pagan JC, Bordas JM, Bosch J, Rodes J: Increasing intra-abdominal pressure increases pressure, volume, and wall tension in esophageal varices. Hepatology 2002; 36: 936−940.
  136. 136. Kravetz D, Romero G, Argonz J et al.: Total volume paracentesis decreases variceal pressure, size, and variceal wall tension in cirrhotic patients. Hepatology 1997; 25: 59−62.
  137. 137. Umgelter A, Reindl W, Wagner KS et al.: Effects of plasma expansion with albumin and paracentesis on haemodynamics and kidney function in critically ill cirrhotic patients with tense ascites and hepatorenal syndrome: a prospective uncontrolled trial. Crit Care 2008; 12: R4.
  138. 138. Lambrecht GL, Malbrain ML, Coremans P, Verbist L, Verhaegen H: Orthodeoxia and platypnea in liver cirrhosis: effects of propranolol. Acta Clin Belg 1994; 49: 26−30.
  139. 139. Krowka MJ, Swanson KL, Frantz RP, McGoon MD, Wiesner RH: Portopulmonary hypertension: Results from a 10-year screening algorithm. Hepatology 2006; 44: 1502−1510.
  140. 140. Bloomfield GL, Blocher CR, Fakhry IF, Sica DA, Sugerman HJ: Elevated intra-abdominal pressure increases plasma renin activity and aldosterone levels. J Trauma 1997; 42: 997−1004.
  141. 141. Mayberry JC: Prevention of abdominal compartment syndrome. In: Ivatury R, Cheatham M, Malbrain M, Sugrue M (ed:) Abdominal compartment syndrome. Landes Bioscience, Georgetown 2006: 221−229.
  142. 142. Parr M, Olvera C: Medical management of abdominal compartment syndrome. In: Ivatury R, Cheatham M, Malbrain M, Sugrue M (ed:) Abdominal compartment syndrome. Landes Bioscience, Georgetown 2006: 230−237.
  143. 143. Cordemans C, De laet I, Van Regenmortel N et al.: Fluid management in critically ill patients: the role of extravascular lung water, abdominal hypertension, capillary leak, and fluid balance. Ann Intensive Care 2012; 2 (Suppl 1): S1.
  144. 144. Balogh Z, McKinley BA, Cocanour CS et al.: Supranormal trauma resuscitation causes more cases of abdominal compartment syndrome. Arch Surg 2003, 138(6): 637−642.
  145. 145. Cordemans C, De laet I, Van Regenmortel N et al.: Aiming for a negative fluid balance in patients with acute lung injury and increased intra-abdominal pressure: a pilot study looking at the effects of PAL-treatment. Ann Intensive Care 2012; 2 (Suppl 1): S15.
  146. 146. Malbrain MLNG, Cordemans C, Van Regenmortel N: Fluid overload is not only of cosmetic concern (Part II): Results from a meta-analysis and practical approach. ICU Management 2012; 12: 34−37.
  147. 147. Malbrain MLNG: The great fluid debate: faith and evidence. Intensive Care Monitor 2014; 21: 1.
  148. 148. Malbrain MLNG, De laet I: The polycompartment syndrome Part 1: Pathophysiology and pressure measurement of pelvic and abdominal compartment syndromes. ICU Management 2009; 9: 19−22.
  149. 149. Malbrain MLNG, De laet I: The polycompartment syndrome Part 2: From cardiac to thoracic the other compartment syndromes. ICU Management 2009; 9: 18−19.
  150. 150. Malbrain MLNG, De laet I, De Waele J: The polycompartment syndrome: what’s all the fuss about? In: Vincent J-L (ed:) Yearbook of intensive care and emergency medicine. Springer-Verlag, Berlin 2010: 465−484.
  151. 151. Malbrain MLNG: How to understand organ-organ interaction. ICU Management 2013; 13: 1014.

Adres do korespondencji:

Manu Malbrain, MD, PhD

Past President WSACS

ICU Director

Intensive Care Unit and High Care Burn Unit

ZiekenhuisNetwerk Antwerpen

ZNA Stuivenberg

Lange Beeldekensstraat 267

B-2060 Antwerp 6, Belgium

e-mail: manu.malbrain@skynet.be

Otrzymano: 24.09.2014 r.

Zaakceptowano: 7.11.2014 r.

Należy cytować wersję z:

Malbrain MNLG, Roberts DJ, Sugrue M et al.: The polycompartment syndrome: a concise state-of-the-art review, Anaesthesiol Intensive Ther 2014, vol. 46, no 5, 433450.

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