Abdominal Compartment Syndrome

Dr Michael Karakozov
Intensive Care Unit, Republican Hospital of Karelia
Petrozavodsk, Russia
tel 8142-764457 (W)
8142-744459 (H)
e-mail: karakozov@karelia.ru

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. Fast crystalloid infusion is recommended. If decompression is not undertaken massive infusions worsen bowel and other abdominal organs edema and close the vicious circle of ACS (12; 58).

Diuresis restores following decompression and doesn't react to conservative measures if surgery is delayed.

Recommendations

1. ACS deteriorates all vital functions. It strongly relates to mortality if unrecognized and untreated.
2. ACS morbidity (IAP > 12 mm Hg) in ICUs varies from 20% in medical to 30% in surgical patients. IAP after uncomplicated surgery can vary from 3 to 15 mm Hg. Patients who receive massive infusions (>10-12 l) in short time have increased risk for ACS development.
3. IAP should be measured repeatedly in critically care patients with suspected IAH.
4. Urgent surgical decompression is the only effective method of treatment ACS but the mortality remains high. Levels of IAH leading to ACS differ between patients but decompression is indicated for everyone when IAH equals 35 mm Hg.
5. Common hemodynamic parameters are affected by IAH and should not be used for estimation of cardiovascular and volemic status in ACS patient. Gastric tonometry correlates well with IAH and could be used for assessing its severity.
6. The best site for IAP measurement is urinary bladder. Anyway all other intra-abdominal sites can be considered.
7. Infusion therapy and mechanical ventilation are effective supportive measures but only in the beginning of ACS. Excessive infusion worsens bowel edema as well as high PEEP.
8. Complications which can be considered immediately after decompression include acute decrease of blood pressure, asystole and pulmonary embolism.

Bibliography

1. Amaral JF, Tsiaris W, Morgan T. Reversal of benign intracranial hypertension by surgically induced weight loss. Arch Surg 1987; 122:946-949

2. Barba CA. The intensive care unit as an operating room. Surg Clin North Am, 2000, Vol.80, N3

3. Barnes GE, Laine GA, Giam PY, Smith EE, Granger HJ. Cardiovascular responses to elevation of intra-abdominal hydrostatic pressure. Am J Physiol 1988; 248: R208-R213

4. 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 Mar;25(3):496-503

5. Bloomfield GL, Dalton JM, Sugerman HJ, Ridings PC et al. Treatment of increasing intracranial pressure secondary to the acute abdominal compartment syndrome in a patient with combined abdominal and head trauma. J Trauma 1995; 6:1168-1170

6. 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; 6:936-943

7. Bloomfield GL, Ridings PC, Blocher CR, Marmarou A, Sugerman GJ. A proposed relationship between increased intra-abdominal, intrathoracic, and intracranial pressure. Crit Care Med 1997; 25:496-503

8. Bradley SE, Bradley GP. The effect of intra-abdominal pressure on renal function in man. J Clin Invest 1947; 26:1010-1022

9. Bongard F, Pianim N, Dubecz, Klein SR. Adverse Consequences of increased intra-abdominal pressure on bowel tissue oxygen. J Trauma 1995; 3:519-525

10. Burch JM, Moore EE, Moore FA, Franciose R. The abdominal compartment syndrome. Surg Clin North Am, 1996; Vol 76, 4:833-842

11. Burchard KW, Ciombor DM, McLeod MK, Slotham GJ, Gann DS. Positive end-expiratory pressure with increased intra-abdominal pressure. Surg Gyn Obstet 1985; 161:313-318

12. Burrows R, Edington J, Robbs JV A wolf in wolf's clothing--the abdominal compartment syndrome. S Afr Med J 1995 Jan;85(1):46-8

13. Сaldwell CB, Ricotta JJ. Evaluation of intra-abdominal pressure and renal hemodynamics. Current Surgery, 1986; 11: 495-498

14.Сaldwell CB, Ricotta JJ. Changes in visceral blood flow with elevated intraadominal pressure. J Surg Research 1987; 43:14-20

15. Сheatham ML, Safcsak K, Block EFL, Nelson L. Preload assessment in patients with an open abdomen. J Trauma 1999; 1:16-22

16. Cheatham ML. Intra-abdominal hypertension and abdominal compartment syndrome. New Horiz 1999; 7:96-115

17. 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 Oct;49(4):621-6; discussion 626-7

18. Ciresi DL, Cali RF, Senagore AJ. Abdominal closure using nonabsorbable mesh after massive resuscitation prevents abdominal compartment syndrome and gastrointestinal fistula. American Surgeon 1999; 65:720-725

19. Collee GG, Lomax DM, Ferguson C, Hanson GC. Bedside measurement of intra-abdominal pressure (IAP) via an indwelling naso-gastric tube: clinical validation of the technique. Intensive Care Med 1993; 19:478-480

20. Coombs HC. The mechanism of regulation of intra-abdominal pressure. Am J Physiol. 1922; 61:159

21. Сullen DJ, Coyle JP, Teplick R, Long MC. Cardiovascular, pulmonary, and renal effects of massively increased intra-abdominal pressure in critically ill patients. Crit Care Med, 1989; 17:118-121

22. Diamant M, Benumof JL, Saidman LJ. Hemodynamics of increased intra-abdominal pressure: interaction with hypovolemia and halothane anesthesia. Anesthesiology 1978; 48: 23-27

23. Diebel LN, Dulchavsky SA, Brown WJ Splanchnic ischemia and bacterial translocation in the abdominal compartment syndrome. J Trauma 1997 Nov;43(5):852-5

24. Diebel L, Saxe J, Dulchavsky S. Effect of intra-abdominal pressure on abdominal wall blood flow. American Surgeon 1992; 58:573-576

25. Diebel LN, Wilson RF, Dulchavsky S, Saxe J. Effect of increased intra-abdominal pressure on hepatic arterial, portal venous, and hepatic microcirculatory blood flow. J Trauma 1992; 2:279-283

26. Diebel LN, Dulchavsky SA, Wilson RF. Effect of increased intra-abdominal pressure on mesenteric arterial and intestinal mucosal blood flow. J Trauma 1992; 1: 45-49

27. Diebel LN, Dulchavsky SA, Brown WJ. Splanchnic ischemia and bacterial translocation in the abdominal compartment syndrome. J Trauma 1997; 43:852-855

28. Emerson H. Intra-abdominal pressures. Arch Intern Med 1911; 7:754-784

29. Ertel W, Oberholzer A, Platz A, Stocker R, Trentz. 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

30. Gargiulo NJ, Simon RJ, Leon W, Machiedo GW. Hemorrhage exacerbates bacterial translocation at low levels of intra-abdominal pressure. Arch Surg 1998; 133:1351-1355

31. Gattinoni L, Pelosi P, Suter PM, Pedoto A, Vercesi P, Lissoni A. Acute respiratory distress syndrome caused by pulmonary and extrapulmonary disease. Different syndromes? Am J Respir Crit Care Med 1998; 158:3-11 (19)

32. Harman PK, Kron IL, McLachlan HD. Elevated intra-abdominal pressure and renal function. Ann Surg 1982; 196:594-597

33. Harrahill M. Intra-abdominal pressure monitoring. J Emerg Nurs 1998; 5:465-466

34. Hering R, Rudolph J, Spiegel TV, Hirner A, Hoeft A. Cardiac filling pressures are inadequate for estimating circulatory volume in states of elevated intra-abdominal pressure. Intensive Care Med 1998; 24(suppl): S409

35. Ho KW, Joynt GM, Tan P. A comparison of central venous pressure and common iliac venous pressure in critically ill mechanically ventilated patients. Crit Care Med 1998; 26:461-464

36. Iberti TJ, Kelly KM, Gentili DR, Hirsch S, Benjamin E. A simple technique to accurately determine intra-abdominal pressure. Crit Care Med, 1987; 15:1140-1142

37. Iberti TJ, Lieber CE, Benjamin E. Determination of intra-abdominal pressure using a transurethral bladder catheter: clinical validation of the technique. Anesthesiology 1989; 70: 47-50

38. Ivankovich AD, Albrecht RF, Zahed B, et al. Cardiovascular collapse during gynecological laparoscopy. Ill Med J 1974; 145:58-61

39. Ivankovich AD, Miletich DJ, Albrecht RF. Cardiovascular effects of intraperitoneal insufflation with carbon dioxide and nitrous oxide in the dog. Anesthesiology 1975; 42:281-287

40. Ivatury RR, Porter JM, Simon RJ, Islam S, John R, Stahl WM. Intra-abdominal hypertension after life-threatening penetrating abdominal trauma: Prophylaxys, incidence, and clinical relevance to gastric mucosal pH and abdominal compartment syndrome. J Trauma 1998; 44:1016-1023

41. Ivy ME, Atweh NA, Palmer J, Posenti PP, Pineau PA-CM, D'Aiuto M. Intra-abdominal hypertension and abdominal compartment syndrome in burn patients. J Trauma, 2000; 49: 387- 391

42. Ivy ME, Possenti PP, Kepros J, Atweh NA, et al. Abdominal compartment syndrome in patients with burns. J Burn Care Rehabil 1999; 20:351-353

43. Kirkpatrick AW, Brenneman FD, McLean RF, Rapanos T, Boulanger BR. Is clinical examination an accurate indicator of raised intra-abdominal pressure in critically injured patients? CJS, 2000, Vol. 43, 3:207-211

44. Kitano Y, Takata M, Sasaki N, Zhang Q, Yamamoto S, Miysaka K. Influence of increased abdominal pressure on steady-state cardiac performance. J Appl Physiol 1999; 86:1651-1656

45. Kopelman T., Harris C., Miller R., Arrillaga A. Abdominal compartment syndrome in patients with isolated extraperitoneal injuries. J Trauma. 2000; 49:744-749

46. Kron IL, Harman PK, Nolan SP. The measurement of intra-abdominal pressure as a criterion for abdominal re-exploration. Ann Surg 1984; 199:28-30

47. Lecours R. Intra-abdominal pressures. Ann Med Assoc J 1946; 55:450-459

48. Lozen Y. Intraabdomonal hypertension and abdominal compartment syndrome in trauma: pathophysiology and interventions. AACN Clinical issues 1999; 1:104-112

49. Malbrain MLNG, Wyffels E, Wilmer AP, Frans E, Daelemans R. Effects of raised intra-abdominal pressure (IAP) and subsequent abdominal decompression on cardiovascular and renal function in medical ICU patients. In Abstractbook of the 7th World Congress of Intensive Care Medicine. Ottawa, Canada, 1997:75

50. Malbrain MLNG. Abdominal pressure in the critically ill. Curr Opin Crit Care, 2000. 6:17-29

51. Malbrain MLNG. Relationship of body mass index (BMI), lactate and intra-abdominal pressure (IAP) to subsequent mortality in ICU patients. Crit Care 1999, 3(suppl 1):20

52. Malbrain MLNG. Bladder pressure or super syringe: correlation between intra-abdominal pressure and lower inflection point? Intensive Care Med 1999; 25(suppl 1): S110

53. Malbrain MLNG. The role of abdominal distension in the search for optimal PEEP in acute lung injury (ALI): PEEP-adjustment for raised intra-abdominal pressure (IAP) or calculation of Pflex? Crit Care Med 1999, 27(suppl): A157

54. Malbrain MLNG, Bakajika D. Effects of abdominal compression and decompression on cardiovascular and respiratory function. Intensive

55. Maxwell RA, Fabian TC, Croce MA, Davis KA Secondary abdominal compartment syndrome: an underappreciated manifestation of severe hemorrhagic shock. J Trauma 1999 Dec;47(6):995-9

56. Mayberry JC, Goldman RK, Mullins RJ, Brand DM, Crass RA, Trunkey DD. Surveyed opinion of American trauma surgeons on the prevention of the abdominal compartment syndrome. J Trauma 1999; 3:509-514

57. Mure M, Glenny RW, Domino KB, Hlastala MP. Pulmonary gas exchange improves in the prone position with abdominal distension. Am J Respir Crit Care Med 1998; 157:1785-1790 (28)

58. Mutoh T, Lamm WJE, Emdree LJ, Hildebrandt J. Volume infusion produces abdominal distension, lung compression, and chest wall stiffening in pigs. J Appl Physiol, 1992; 72:575-582

59. Obeid F, Saba A, Fath J, et al. Increases in intra-abdominal pressure affect pulmonary compliance. Arch Surg 130: 544-548, 1995

60. Overholt RH. Intraperitoneal pressure. Arch Surg 1931; 22:691-703

61. Pickhardt PJ, Shimony JS, Heiken JP, Buchman TG, Fisher AJ. The abdominal compartment syndrome: CT findings. AJR 1999; 173:575-579

62. Ranieri VM, Brienza N, Santostasi S, Puntillo F, Mascial et al. Impairment of lung and chest wall mechanics in patients with acute respiratory distress syndrome. Role of abdominal distension. Am J Respir Crit Care Med 1997; 156:1082-1091

63. Reeves ST, Pinosky ML, Byrne TK, Norcross ED Abdominal compartment syndrome. Can J Anaesth 1997 Mar;44(3):308-12

64. Richardson JD, Trinkle JK. Hemodynamic and respiratory alterations with increased intra-abdominal pressure. J Surg Res, 1976; 20:401-404

65. Robotham JL, Wise RA, Bromberger-Barnea B. Effects of changes in abdominal pressure on left ventricular performance and regional blood flow. Crit Care Med 1985; 10: 803-809

66. Rubinson RM, Vasco JS, Doppman JL, Morrow AG. Inferior caval obstruction fron increased intra-abdominal pressure. Arch Surg 1967; 94:766-770

67. Salkin D. Intraabdominal pressure and its regulation. Am Rev Tuberc 1934; 30:436-457

68. Savino JA, Cerabona T, Agarwal N, Byrne D. Manipulation of ascitic fluid pressure in cirrhotics to optimize hemodynamic and renal function. Ann Surg, 1988; Vol. 208, 4: 504-511

69. Schein M, Wittman DH, Aprahamian CC, Condon RE. The abdominal compartment syndrome: the physiological and clinical consequences of elevated intra-abdominal pressure. J Am Col Surg, 1995, 180:745-753

70. Shafik A, El-Sharkawy A, Sharaf WM. Direct measurement of intra-abdominal pressure in various conditions. Eur J Surg 1991; 163:883-887

71. Shelly MP, Robinson AA, Hesford JW, Park GR. Haemodynamic effects following surgical release of increased intra-abdominal pressure. Br J Anaesth, 1987; 59: 800-805

72. Sugerman H, Windsor A, et al. Intra-abdominal pressure, sagittal abdominal diameter and obesity co-morbidity. J Intern Med 1997, 241:71-79

73. Sugerman HJ, Bloomfield GL, Saggi BW. Multisystem organ failure secondary to increased intraabdominal pressure. Infection. 1999; 27:61-66

74. Sugrue M, Jones F, Deane SA, BishopG, Bauman A, Hillman K. Intra-abdominal hypertension is an independent cause of postoperative renal impairment. Arch Surg, 1999; 134:1082-1085

75. Sugrue M, Hilman KM. Intra-abdominal hypertension and intensive care. In Yearbook of intensive care and emergency medicine. Edited by Vincent JL, Berlin, Springer-Verlag 1998; 667-676

76. Sugrue M. Intra-abdominal pressure. Clin Int Care 1995; 6:76-79

77. Sugrue M, Jones F, Lee A, Buist M, Deane S, Bauman A, Hillman K. Intraabdominal pressure and gastric intramucosal pH: is there an association? World J Surg 1996; 20:988-991

78. Sugrue M, Buist MD, Lee A, Sanchez DJ, Hillman KM. Intra-abdominal measurement using a modified nasogastric tube: description and validation of a new technique. Intensive Care Med 1994; 20:588-590

79. Thorington JM, Schmidt CF. A study of urinary output and blood-pressure changes resulting in experimental ascites. Am J Med Sci 1923; 165: 880-886

80. Wachsberg RH, Sebastiano LL, Levine CD Narrowing of the upper abdominal inferior vena cava in patients with elevated intraabdominal pressure. Abdom Imaging 1998 Jan-Feb;23(1):99-102

81. Wagner GW. Studies on intra-abdominal pressure. Am J Med 1926; 171:697-707

82. Watson RA, Howdieshell TR Abdominal compartment syndrome. South Med J 1998 Apr;91(4):326-32

83. Wendt E. Uber den einfluss des intraabdominalen druckes auf die absonderungsgeschwindigkeit des harnes. Arch Physiologische Heikunde, 1876, 57: 525-527

84. Yol S, Kartal A, Tavli S, Tatkan Y. Is urinary bladder pressure a sensitive indicator of intra-abdominal pressure? Endoscopy 1998; 30:778-780

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