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Abdominal compartment syndrome (ACS) refers to multiorgan disfunction caused by increased intra-abdominal pressure (IAP) (16; 50; 70). There are few examples of compartment syndromes in medicine: increased intra-cranial pressure, subfascial edema or hemorrhage following crush injury to the extremities, glaucoma. All of them have one common feature: acute and sustained pressure raise in a relatively isolated space (compartment) disturbs circulation and leads to ischemia, disfunction and death of all organs and tissues enclosed within it. History Interest to IAP goes back to the second half of 19th century. Intra-abdominal hypertension (IAH) was first described more than 125 years ago by Marey (1868) and Burt (1870) after they had demonstrated the relationship between intra-abdominal pressure and respiratory function (20). However the interest to the problem wasn't systematic. In a series of random articles researchers have been describing hemodynamic, renal and respiratory effects of IAP (8; 20; 60; 81; 79; 83). Direct method of IAP measurement was introduced in 1931 (60). Development of laparascopic gynecology and surgery boosted extensive research on the effects of IAP. First, anesthesiologists and gynecologists in late 60-s and 70-s noticed acute rise in IAP to cause unstable hemodynamics (22; 38; 39). Publications of Richard and Krone switched the attention of surgeons towards the problem (22; 64). Careful animal and human studies of IAH and ACS has appeared through the last two decades. Etiology All factors causing IAH can lead to ACS. More frequently IAH develops after severe abdominal trauma, intra-abdominal or retroperitoneal hemorrhage, necrotizing pancreatitis, peritonitis, abdominal aortic surgery. It can also follow massive crystalloid infusions during resuscitation in patients with shock or burns. Thus, typical ACS scenario might be the following consequence of events: abdominal trauma and shock with abdominal organ ischemia, massive infusion therapy, reperfusion bowel and other organs edema and coagulopathy, intra-abdominal fluid accumulation and/or hemorrhage, IAH, ACS. Morbidity and mortality Despite numerous publications aimed at incidence, symptoms and management of ACS and IAH no exact data of ACS morbidity and mortality in critically ill patients exist to this time (43). IAH has been reported in 30% of patients after major abdominal surgery and trauma with ACS development in 5,5% of these patients (29). In medical ICUs IAH can develop in up to 24% of patients (50). Mortality rate for ACS is very high - 42-68% and 100% if it is left untreated. Pathophysiology Pressure raise in isolated cavity depends on elastic properties of its walls and volume of contents. The relationship between IAP and intra-abdominal volume is non-linear (fig 1). Abdominal wall compliance decreases with increasing intra-abdominal volume (hemorrhage, intra-abdominal organ edema, 3rd space fluid losses, etc), and IAP rises non-proportionally following equal volume increments (69). Barnes in his trials on dogs demonstrated that abdominal wall compliance decreased from 10,8 to 0,56 ml/mm Hg following IAP rise from 0 to 40 mm Hg (3). Abdominal wall compliance also depends on endo-abdominal fascia characteristics, abdominal muscles and fat. Abdominal muscles tension during pain and anxiety can also play role in decreased compliance (41). Pressure within the abdominal cavity is normally subatmospheric. Its increase (IAH) doesn't necessarily mean ACS. That is why the exact level of IAH which causes ACS remains a subject for discussion. The higher the IAP, from one side, and sicker the patient, from the other - the more the probability for ACS development (69). An opinion exists that ACS affects whole body from hair to toes (73). We'll emphasize its effects on major systems. Circulation IAH slows blood flow in the inferior vena cava decreasing venous return to the heart (3; 35; 61; 64; 66; 80). Besides, high IAP shifts the diaphragm upward and rises mean intrathoracic pressure (ITP) which acts on heart and vessels within the thoracic cavity (21; 44; 64). Raised ITP decreases pressure gradient across myocardium and impairs ventricular diastolic filling. Pulmonary capillary pressure also rises. Venous return to the left heart becomes even more compromised and stroke volume falls as well as cardiac output (CO) despite compensatory tachycardia (61). However, initially CO can remain unchanged or even rises due to blood shift from compressed abdominal venous bed. Temporary CO increase with the help of military anti-shock trousers (MAST) is classical example of this effect. Systemic vascular resistance (SVR) increases following IAH. SVR rise is attributed to direct vessels compression and, later on, fall of CO. Mean blood pressure (BP) increases, decreases or remains unchanged (3). It certainly drops in final stages of ACS. It is important to stress that any additional factor like hypovolemia or cardiac failure adds to deleterious effects of IAH. Pressure measurement in major vessels of the thoracic cavity or heart are not reliable in patients with ACS. They do not reflect neither the circulating blood volume nor cardiac performance (34; 73). Calculation of cardiac volumes and their indexes probably provides better information in ACS patients (15). Lymphatic flow through the thoracic duct falls proportionally to IAH and ceases when it reaches 30 sm H20. Respiratory system Increased IAP pushes the dome of the diaphragm up into the thoracic cavity. Mean ITP increases, functional residual capacity diminishes as well as other lung volumes. Alveoli in the dependent lung zones collapse causing atelectases (21; 59; 69; 21). The following ventilation/perfusion abnormalities increase pulmonary shunting. Diaphragm has to work with increasing efforts to sustain adequate minute ventilation. Oxygen cost of breathing rises dramatically. Hypoxemia and respiratory acidosis are early and common features of ACS. Respiratory failure develops rapidly and patient has to be put on mechanical ventilation (50). The symptoms of respiratory failure are often the first clinical signs of elevated IAP. They can be easily taken for acute lung injury (ALI) manifestation from other causes or agents. Renal system Relationship between renal impairment and IAP was first discribed in 1876 (83). IAH impairs renal circulation and glomerular filtration rate (8; 13). Oliguria probably starts when IAP rises over 10-15 mm Hg, anuria develops when it reaches 30 mm Hg (32; 74). Suggested mechanisms for renal failure (RF) include direct compression of renal parenchyma and vessels, elevated ADH levels, CO fall (61; 69). It must be mentioned that RF starts before CO and BP show to decrease. Time is needed for complete restoration of renal function after surgical intervention (50). Abdominal organs IAP of 15 mm Hg and higher impairs circulation in all abdominal and retroperitoneal organs except suprarenal glands (14; 26). Bowel perfusion diminishes non-proportionally to CO and develops earlier (9). Under IAH conditions intra-abdominal circulation starts to depend on the difference between systemic and intra-abdominal pressure. This difference has been called abdominal perfusion pressure (APP). APP is considered to play critical role in abdominal organ ischemia with bowel as the first target (17; 26). IAH causes mucus membrane acidosis and edema before other clinically obvious signs of ACS occur (9). IAH correlates well with gastric tonometry (40; 41). The latter has been suggested for estimating intra-abdominal perfusion in ACS patients (77). Lymphatic absorbtion of peritoneal fluid diminishes due to decreased lymphatic flow in the thoracic duct (50). CO fall and oliguria as well as massive infusion therapy intensify 3rd space fluid losses, bowel edema and finally exacerbate IAH, closing the vicious circle (fig 2) (41; 42; 45). Bacterial translocation (BT) from ischemic bowel to portal system and mesenterial lymphatic nodes - another consequence of ACS (27; 30). BT has been shown to develop within 1 hour after IAP reaches 25 mm Hg (23). Hepatic arterial blood flow diminishes when IAP>10 mm Hg but portal circulation is affected only when IAP reaches 20 mm Hg (25). The role of chronic IAP elevation in triggering varicose vein bleeding in cirrhotic and ascitic patients is still unknown (6). IAH worsens abdominal wall perfusion and prolongs postoperative wound healing (24). Central nervous system Neurologic complications of IAH have only recently become a subject for investigation (5). Acute IAH can elevate intra-cranial pressure. Impairment of venous flow and compression of epidural venous plexus are suggested mechanisms for this effect (6; 7). Cerebral perfusion pressure (CPP) decreases or remains unchanged depending on mean BP. IAH in patients with CNS injury is quite undesirable and must be corrected as soon as possible. It leads to brain ischemia even in mild and asymptomatic cases. Mortality in patients with moderate to severe combined CNS and abdominal trauma is twice as high compared with each of these traumas alone (6). IAH of 25 mm Hg decreases CPP of normal brain (6). Pneumoperitoneum during laparoscopy compromises ICP and should be used with caution in patients with CNS pathology. Some patients with morbid obesity and idiopathic intracranial hypertension experienced fall in cerebrospinal fluid pressure following weight loss after gastric bypass surgery. Their headache, systemic hypertension, vision and sleep apnea symptoms have also improved (1). Diagnostics and monitoring Clinical manifestations of ACS are nonspecific and misleading without high syndrome suspicion. High central venous or pulmonary artery wedge pressures, dyspnea and saturation drop, oliguria or decreased level of consciousness could be interpreted as multiorgan failure caused by sepsis, trauma, cardiac failure etc. For example, high CVP and oliguria suggest diuretic treatment rather than infusion therapy for a doctor not familiar with the syndrome. Suspicion is the key factor in ACS diagnostics. It is easy to confirm or exclude ACS if it is anticipated. However, physical examination per se doesn't give enough information about the level of IAP (43). The reliable data can be obtained only after IAP measurement. Normal values for IAP depend on body-mass index and are usually close to zero (49; 50; 51; 72). It has been suggested to consider abdomen as fluid compartment dependable on Pascal's law (8). According to the law pressure within fluid compartment is equally transmitted to every part of it. Therefore, IAP could be measured in various parts within abdominal cavity. These include the cavity itself, uterus, inferior vena cava, rectum, stomach or urinary bladder (76). The importance of IAP measurement has been considered by many (4). It can be measured both directly and indirectly. IAP measurement during laparoscopy is an example of direct methods. Measurements in inferior vena cava and abdominal organs refer to indirect methods. Gastric tonometry tube can be used for intragastric pressure measurement, anterior axillar line is taken for zero level (19; 78). There are few reports dealing with measuring IAP in the inferior vena cava (64). However, pressure measurement in urinary bladder has become most popular, simple, quick and inexpensive method for diagnostics and monitoring of elevated IAP (33; 36; 37; 46; 50; 84). Vesical wall acts as a passive conductor of IAP if intra-vesical volume is less than 100 ml. Foley catheter and manometer with transducer or simply drip and scale are needed for measurement (fig 3). Patient is in supine position. 70-100 ml of normal saline are infused into the bladder via aspiration port of Foley catheter with balloon inflated. Catheter is then clamped distally to the place of measurement and a drip or manometer system with two stop-cocks are attached to aspiration port by18G needle. Manometer is zeroed at upper level of symphisis pubis and data is displayed at bedside monitor. Intravesical pressure measurement can give false results in patients with bladder damage, tumor or pelvic hematoma. In such cases intragastric measurement seems to be a reasonable alternative. The derived APP is reported to be another appropriate treatment guide for ACS (17). Severity of IAH depends mainly on the level and acuteness of its raise. It also depends on patients' hemodynamics, breathing, renal and CNS function. Usually the syndrome develops within few hours (16; 69). We are not describing chronic IAP elevation as could be seen in liver cirrhosis or pregnancy when organism has enough time to adapt to intra-abdominal volume increase. ACS morbidity is directly proportional to IAP over 10 mm Hg. When IAP exceeds 35 mm Hg ACS develops in all patients and without surgical intervention leads to death in 100 per cent of cases. Four grades of IAH have been proposed (table 1). Although IAH of 10-15 mm Hg can cause physiologic changes, laparotomy is hardly recommended. A lot of patients develop IAH of 3-13 mm Hg after planned abdominal surgery without ACS signs (46). Second grade demands IAP monitoring, decompressive laparotomy could be considered. The latter is indicated for the majority with grade 3 IAH and for all patients with grade 4. Patients with IAP>35 mm Hg develop cardiac arrest within few hours. Treatment ACS is much easier to prevent than to treat. One should keep in mind the possibility of ACS development in high risk patient and measure IAP on regular basis. The only effective method of treatment which must be considered immediately after diagnosis is confirmed is surgical decompression of the abdominal cavity. Sometimes, when the symptoms are threatening decompression could be done even in ICU settings (2). Endoabdominal fascia is not sutured in postoperative period. Surgeons use temporary fascial closure with absorbable or non-absorbable meshes or other materials (Bogota bag) aiming to extend intra-abdominal compartment and lessen pressure within it (18; 69; 182). According to the questionnaire most of American trauma surgeons are acquainted with ACS manifestations and indications for abdominal decompression (56). Done in due course decompression immediately reverses adverse hemodynamic, respiratory and renal effects of IAH (54; 71). Complications which can follow the decompression include BP drop, asystole or pulmonary embolism (63). Acute decrease of BP usually is seen in hypovolemic patients and can be succesfully reversed with infusions. Asystole is associated with so-called post-decompression reperfusion syndrome and increased levels of curculating products of non-completed metabolism (e.g. adenosine). High susceptability for thrombus formation among ACS patients could be the cause of pulmonary embolism (73). Respiratory support (RS) Clinical manifestations of respiratory failure in ACS have much in common with those in acute lung injury (ALI). Patients with ACS need RS and early mechanical ventilation. IAP of 15 mm Hg and higher elevates peak and mean alveolar pressures during volume ventilation. RS modes are similar to those in ALI. Arterial blood oxygenation (PaO2) during mechanical ventilation in patients with ALI is directly proportional to inspiratory oxygen content (FiO2) and mean alveolar pressure (PAm). FiO2 > 0,6 and PAm > 32 cm H2O are associated with damage to lung parenchyma. RS guidelines in these patients recommend maximal attention to PAm. PAm should be preferably elevated by increasing positive end-expiratory pressure (PEEP) rather than tidal volume (TV). Moreover, the latter should be decreased to its possible minimum. The above mentioned tactics needs pressure-volume curve (compliance) plotting as a reasonable guide for setting PEEP and TV. It is difficult to construct the curve just for lungs at patients bedside. Thus total static pressure-volume curve of lungs and chest wall is that what usually is estimated in patient on respirator coupling different TVs and alveolar pressures. However it is chest wall compliance that primarily decreases in ACS and causes reduction of total compliance. If IAH is not suspected, let alone measured and monitored, search for acute respiratory distress syndrome (ARDS) causes can mislead from correct diagnosis thanks to the vast etiology of ARDS. Although there is a little difference in RS approach between two syndromes surgical decompression can improve situation in early ACS when the lung has not been damaged. If the correct diagnosis is delayed, agressive modes of respiratory support would inevitably lead to pulmonary baro- and biotrauma. In such case ALI (primary ARDS) can develop quickly and accompany ACS (secondary ARDS). There are few reports stressing the role of PEEP in these two syndromes. High PEEP recruits collapsed but otherwise healthy alveoli in dependent lung zones and improves compliance and gas exchange in ACS (secondary ARDS) patients but at a cost of even more rised IAP (31; 50). Mechanical ventilation in prone position also seems to be a reasonable option for ACS patients (57). In patients with primary ARDS high PEEP overdistends healthy lung zones and doesn't necessarily results in improved oxygenation (31). Intensivists know how challenging titration of PEEP could be in these patients. It should be noticed that PEEP used for RS in ACS aggravates IAH and further impairs bowel circulation (48). Everybody are aware of brain edema exacerbation caused by high PEEP levels in patients with CNS pathology. Filtration coefficient of bowel endothelium is 14000 times higher than that of brain. According to Srtarling's law for fluid flux around semipermeable membrane it's not difficult to imagine then how pressure rise in the inferior caval vein system shifts fluid into extravascular space. This effect is considered to be more pronounced in bowel than in brain tissue (45). Infusion therapy Infusion therapy is necessary for correcting hypovolemia, particularly prior to decompression. The severity of hypovolemia is very difficult to assess with common methods. 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