Intra-abdominal Hypertension in Medical Critically Ill Patients: A Narrative Review
Ortiz-Diaz, Enrique; Lan, Charlie K.
Pulmonary and Critical Care Medicine Section, Department of Medicine, Baylor College of Medicine, Baylor Clinic, Houston, Texas
Received 15 Oct 2013; first review completed 28 Oct 2013; accepted in final form 21 Nov 2013
Address reprint requests to Enrique Ortiz-Diaz, MD, Pulmonary and Critical Care Medicine Section, Department of Medicine, Baylor College of Medicine, Baylor Clinic, 11th floor, 6620 Main St, Suite 11D.33.6, Houston, TX 77030. E-mail: email@example.com.
No funding source was used for the creation of this article.
The authors have no conflicts of interests to declare.
ABSTRACT: Intra-abdominal hypertension/abdominal compartment syndrome (IAH/ACS) is a well-recognized entity among surgical subspecialties. Nevertheless, it has been proven to be present in the medical critically ill population. Prospective and retrospective observational studies have found medical patients with IAH/ACS to be associated with death in the intensive care unit and other poor outcomes. Frequently, it is underdiagnosed and undertreated in this patient group. Limitations encountered in these observational studies are their small population size and single-center design. In addition, most studies target consecutive intensive care unit admissions instead of limiting IAH/ACS screening to a predefined population confined by their risk factors (unspecified ascites, mechanical ventilation, positive fluid balance, etc.). Generally, medical patients with IAH/ACS are more severely ill compared with surgical patients. Furthermore, they are less likely to receive treatment targeted at lowering intra-abdominal pressure. Medical treatment of IAH/ACS has not been demonstrated to be specifically effective to avoid decompressive surgery. Identifying medical patients at risk of IAH represents an underresearched area for which training in measurement of abdominal pressure surrogates, awareness of its prevalence, and prevention and treatment of such condition could further improve outcomes in critically ill medical patients.
Intra-abdominal hypertension/abdominal compartment syndrome (IAH/ACS) contributes to multiorgan dysfunction syndrome (MODS), failure, and death in surgical critically ill patient populations (1–3). Intra-abdominal hypertension and ACS are conceptually defined by a spectrum of elevated pressures within this enclosed space. Its importance resides in the impairment of its organs’ viability (1). Intra-abdominal hypertension/ACS is categorized under the obstructive type of circulatory failure/shock (1). Despite critical illness, intraperitoneal pressures are no more than 5 to 7 mmHg (4–6). Although other routes exist with the purpose of measuring intra-abdominal pressure such as transgastric, intravascular (through the inferior vena cava), or percutaneous, intra-abdominal pressure’s criterion standard for measurement and diagnosis is intermittent or continuous bladder pressure measurement with urethral catheterization (7, 8). The World Society of Abdominal Compartment Syndrome has derived a consensus statement with definitions of IAH and ACS in 2006 and 2013 (9, 10). Intra-abdominal hypertension is defined as intra-abdominal pressure exceeding 12 mmHg. By consensus, ACS is defined as an intra-abdominal pressure exceeding 20 mmHg associated with new organ dysfunction. A clause within the definition includes that it may occur with or without an abdominal perfusion pressure (APP) (mean arterial pressure − intra-abdominal pressure) of less than 60 mmHg (9, 10). Categories within the definition include primary IAH/ACS in which there is a direct abdominal-pelvic injury and secondary IAH/ACS where there is not (10). Although it may represent an expected complication for complex abdominal-pelvic surgeries, medical critically ill patients have been found to be at risk to have and develop IAH/ACS (11–16).
After a brief summary of IAH/ACS’ history and pathophysiology, the main objective of the narrative review is to describe and summarize IAH/ACS incidence in nonsurgical patients. Furthermore, the association between IAH/ACS, mortality, and MODS in medical critically ill patient population is explored. In addition, IAH/ACS medical management and its prevention measures are briefly summarized. Finally, the current state of medical knowledge and awareness of IAH/ACS among medical intensivists will be described.
History and pathophysiology
Researched in animals and human subjects, IAH was first described in the latter half of the 19th century. It did not achieve practical clinical consideration until approximately a century later when pediatric, vascular, and trauma surgeons described that early abdominal fascial approximation could lead to multiorgan failure (17–22). Excluding trauma and other surgical factors, IAH’s pathophysiological mechanisms are based on three mechanisms shown in Table 1. Briefly, these mechanisms cause compression of the inferior vena cava causing decreased preload, thus reducing cardiac output (23–25). Afterload is further increased because of a parallel increase in aortic impedance and reflexively because of reduced stroke volume (26, 27). Contiguously, decreased extrathoracic compliance leads to variable increase in shunt fraction, dead space, and transalveolar pressures (28–30). Hypoperfusion leads to splanchnic-hepatic dysfunction/failure (31, 32), increased transmitted intracerebral pressure (7, 33), and particularly cessation of renal filtration gradient (34–36). Considering medical patients without causal abdominal pathology, patient characteristics predisposing toward IAH are high body mass index, invasive mechanical ventilation, positive fluid balance (>5 L), massive blood product transfusion, high Sequential Organ Failure Assessment (SOFA)/Acute Physiology and Chronic Health Evaluation II (APACHE II) scores, end-stage liver disease with ascites, and so on (11–16)
Epidemiologic studies in surgical intensive care unit (ICU) populations have estimated that IAH/ACS incidence is 4% to 81%, depending on whether IAH or ACS was used as end points (37, 38). When taking into account mixed surgical-medical populations, IAH incidence and prevalence vary between 32% and 56%, and 19% and 58% respectively (7, 33). In the same mixed ICU groups, ACS incidence was 2% to 10% (7, 33). Intra-abdominal hypertension/ACS has been demonstrated to be independently associated with worse patient-related outcomes (ICU and hospital mortality, higher SOFA scores including delta SOFA, increased ICU length of stay, mechanical ventilator days plus mechanical ventilator weaning failures) in the two largest multicentric prospective observational studies (7, 33). Recently, a systematic review was published with the objective of identifying IAH/ACS risk factors throughout an exhaustive literature search (39). Holodinsky and colleagues (39) reported obesity, sepsis, ileus, and fluid resuscitation as risk factors with IAH/ACS, although none reached statistical significance, and there was a considerable heterogeneity in the meta-analysis (I2 = 60.2%–82.7%) (39).
It is well known that patients with abdominal-pelvic surgeries/injuries and concurrent critical illness would be at risk of IAH/ACS. Nevertheless, several small observational single-center studies with medical ICU patients have shown the presence and development of IAH/ACS in the medical ICU (11–16) (Table 2). Kim and colleagues (11) published a small observational study in which 52% of their study population had a nonsurgical condition. Fifty-four percent of those had IAH. Reintam et al. (12) consecutively screened medical patients on invasive mechanical ventilation for IAH. Over a 2-year period, 95 patients (35% of the sample) had IAH/ACS. Intra-abdominal hypertension was found to be an independent predictor of mortality in this study (odds ratio [OR], 2.50; 95% confidence interval [CI], 1.08–5.78). Considering the IAH/ACS patient subset, 35% were diagnosed without a causal abdominal-pelvic pathology. Those who developed secondary IAH/ACS had a higher ICU mortality (51.4% vs. 30.0%; P = 0.032). Daugherty et al. (13) assessed the incidence of ACS in medical patients with secondary IAH/ACS on patients who received at least 5 L of positive fluid balance during the first 24 h in the ICU. They found that 85% of their study population had a bladder pressure of more than 12 mmHg. Within the IAH cohort, 20% had ACS. Despite their diagnosis, no patient received laparotomy because of an inappropriately high surgical risk. Santa-Teresa and colleagues (14) published data in which medical patients were consecutively screened for IAH/ACS risk factors (>2). Fifty-seven percent of the cohort had IAH/ACS on admission to ICU, and 100% developed it subsequently. Compared with the rest of the study population not at risk, those with IAH/ACS had a trend toward greater mortality, higher APACHE II and SOFA score, and higher length of ICU and hospital stay. Regueira and colleagues (15) prospectively studied septic shock patients in a medical-surgical ICU to determine the cumulative incidence of IAH. As a secondary objective, they sought to determine if IAH/ACS was associated with mortality and other parameters of organ dysfunction. Fifty percent of their sample was composed of medical patients. The incidence of IAH was 82.7% for the study population with 73.7% in the medical subgroup. Al-Dorzi et al. (16) published a study in cirrhotic ICU patients with severe sepsis. They included 62 patients with mean Child Pugh Score in the range 11 to 14 and high APACHE (mean, 30.1 [SD, 7.5]) and SOFA scores (mean, 14.9 [SD, 3.7]). Ninety-four percent of the patients had ascites. The observed mortality was 65.6% in the ICU. After adjusting with a multivariable regression model, IAH was associated with ICU mortality (OR, 12.20; 95% CI, 1.92–77.31) and the need for renal replacement therapy (OR, 6.78; 95% 1.29–35.70). Furthermore, authors performed receiver operating curves that showed similar discrimination for survivors and nonsurvivors using APP (0.74; P < 0.01) and IAH (0.71 P = 0.01) compared with APACHE II (0.71; P = 0.02). Lastly, Reintam and colleagues (12) performed a prospective observational study of 257 patients on mechanical ventilation to compare IAH/ACS incidence, time to onset, and outcomes (28-day, 90-day mortality, duration of mechanical ventilation, and ICU admission). Thirty-five patients had secondary IAH (13.6% of the sample). Secondary IAH occurred in patients with severe sepsis/septic shock (39%) and cardiopulmonary diseases (19%). Body mass index more than 30 kg/m2 was more often observed in patients with secondary IAH (44.1%) than in patients with primary IAH (25.9%) and in patients without IAH (18.1%). Patients with secondary IAH/ACS had higher SOFA scores, higher intra-abdominal pressures, and higher ICU mortality (P = 0.032) (12).
Prevention and surveillance
The World Society of Abdominal Compartment Syndrome uses the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system for its recommendation in the guidelines. Currently, a GRADE 1C recommendation is to perform surveillance for IAH as a regular practice in the ICU. For example, patients with aortic aneurysm repair, abdominal trauma, and severe burns (>40% body surface area) are established to have intra-abdominal pressure monitoring and APP of greater than 60 mmHg during resuscitation.
Identification and recruitment of medical patients by their IAH/ACS risk factors (Table 1) might be the first step to evaluate the effectiveness of therapy delivered to this group. In the same fashion, the US Critical Illness and Injury Trials Group has constructed a bedside model to identify patients at risk of ARDS to attempt to curb its morbidity and mortality by its prevention (40, 41).
Although having decompressive laparotomy has been the fastest and criterion standard treatment for IAH/ACS, medical critically ill patients are commonly considered to be poor surgical candidates (13). Moreover, decompressive laparotomy has a considerable risk for morbidity and mortality (9). In addition to its prevention and surveillance, multiple noninvasive recommendations organized into an algorithm by the World Society of Abdominal Compartment Syndrome (10) have been proposed (Table 3). The recommendations set was evaluated through the GRADE categories (42). Intra-abdominal hypertension/ACS medical (noninvasive treatments) received GRADE scores in the range of 1C to 2D (from observational studies, unsystematic clinical experience, seriously flawed randomized controlled trials) (42). The efficacy and safety of most of the recommendations are unknown because of lack of evidence. Lastly, a caveat in the recommendations acknowledged that IAH/ACS etiologies were heterogeneous (i.e., ascites, Ogilvie syndrome, increased interstitial edema of abdominal organs, etc.); thus, not every recommendation might be appropriate or effective for a clinician to choose and treat from the algorithm (10).
Is IAH/ACS a variable to be accounted in difficult-to-wean mechanically ventilated patients?
Difficult-to-wean/prolonged mechanical ventilation from invasive mechanical ventilation and extubation-failure patients are a group of critically ill patients who have been shown to be at higher risk for ICU and hospital mortality (43–46). Pathophysiological conditions associated with this clinical phenomenon are inability to meet muscle-loading demands to achieve minute ventilation (excessive secretions, weak-or-fatigued respiratory muscles, myocardial dysfunction, airway obstruction) and deficient neural ventilatory states to maintain a patent airway (46, 47). Yet, it remains unknown if IAH predisposes medical patients to liberation failure from mechanical ventilation by impairing diaphragmatic expansion, promoting atelectasis, ventilation-perfusion mismatch, and increasing the work of breathing in critically ill patients.
Current state of knowledge in the medical intensivist community
Despite its documented incidence and prevalence over the last 10 years, it is seldom assessed or even considered among internal medicine based intensivists. A syndrome presenting with hypotension, tachycardia, and narrow pulse pressure associated with clinical signs of peripheral hypoperfusion is a common but a nonspecific presentation of shock/circulatory failure to any critically ill patient. Intensivist surveys regarding their preferences in tools to monitor the general state of hemodynamics indicate a preference toward using blood pressure, urine output, central venous pressure, etc. (48, 49). Physical examination and measurement of abdominal girth are insensitive methods of diagnosis (50, 51). Intensivists rarely include abdominal pressure surrogates to assess for IAH/ACS. Kimball et al. (52) surveyed the academic Society of Critical Care Medicine members with different training backgrounds (surgical, anesthesia, medical, or pediatric) in the United States. Although their survey had a response rate of 35.7%, they found that 25% of medical intensivists had never managed IAH. Twenty-three percent of the same group was unaware of the bladder pressure–monitoring technique. This study concluded that there was great practice variability in surveillance, threshold pressure for diagnosis, and approach to treat IAH/ACS among multispecialist academic intensivist community (52). When considering other parts of the world where critical care is delivered, considerable unawareness, variability for suspicion, and approach to treatment are observed (53–55).
Prevention of IAH/ACS has to be accounted while a patient is resuscitated in the ICU. Quality improvement/initiative projects may target the education of the ICU staff about the implications and measurement of bladder pressure. Current IAH/ACS knowledge in medical patients is limited to small single-center studies with variable designs/end points and expert treatment algorithms and recommendations. Patients at risk should be prospectively recruited to assess incidence and other nonoperative therapeutic strategies (e.g., therapeutic paracentesis during periresuscitation/extubation period in the ICU, approach-to-treatment protocols to standardize current state of practice variability). Finally, it would be important to assess if managing IAH leads to a reduced rate of extubation failure.
Intra-abdominal hypertension/ACS is not an exclusive syndrome to abdominal-pelvic injuries or surgeries. Medical critically ill patients have been reported to be at risk through observational studies. Physicians who commonly work in medical ICUs do not consider measure or treat IAH in their patients. It is unknown if prevention through standard surveillance of intra-abdominal pressure would improve outcomes such as ICU mortality, duration of mechanical ventilation, and so on. Also, it is unknown if routine drainage of abdominal collections or ascites, gastric and/or colonic decompression, use of prokinetic agents, or even increased sedation and neuromuscular blockade are effective in improving patient-centered outcomes.
1. Ameloot K, Gillebert C, Desie N, Malbrain ML: Hypoperfusion, shock states, and abdominal compartment syndrome (ACS). Surg Clin North Am
92 (2): 207–220, 2012, vii.
2. Balogh Z, McKinley BA, Holcomb JB, Miller CC, Cocanour CS, Kozar RA, Valdivia A, Ware DN, Moore FA: Both primary and secondary abdominal compartment syndrome can be predicted early and are harbingers of multiple organ failure. J Trauma
54 (5): 848–859, 2003; discussion 859–861.
3. Raeburn CD, Moore EE, Biffl WL, Johnson JL, Meldrum DR, Offner PJ, Franciose RJ, Burch JM: The abdominal compartment syndrome is a morbid complication of postinjury damage control surgery. Am J Surg
182 (6): 542–546, 2001.
4. Sanchez NC, Tenofsky PL, Dort JM, Shen LY, Helmer SD, Smith RS: What is normal intra-abdominal pressure? Am Surg
67 (3): 243–248, 2001.
5. Chionh JJ, Wei BP, Martin JA, Opdam HI: Determining normal values for intra-abdominal pressure. ANZ J Surg
76 (12): 1106–1109, 2006.
6. Sugerman H, Windsor A, Bessos M, Wolfe L: Intra-abdominal pressure, sagittal abdominal diameter and obesity comorbidity. J Intern Med
241 (1): 71–79, 1997.
7. Malbrain ML: Different techniques to measure intra-abdominal pressure (IAP): time for a critical re-appraisal. Intensive Care Med
30 (3): 357–371, 2004.
8. De Waele JJ, De laet I, Malbrain ML: Rational intraabdominal pressure monitoring: how to do it? Acta Clin Belg Suppl
(1): 16–25, 2007.
9. De Waele JJ, Hoste EA, Malbrain ML: Decompressive laparotomy for abdominal compartment syndrome—a critical analysis. Crit Care
10 (2): R51, 2006.
10. Kirkpatrick AW, Roberts DJ, De Waele J, Jaeschke R, Malbrain ML, De Keulenaer B, Duchesne J, Bjorck M, Leppaniemi A, Ejike JC, 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. Am J Respir Crit Care Med
15 (187): 1294–1302, 2013.
11. Kim IB, Prowle J, Baldwin I, Bellomo R: Incidence, risk factors and outcome associations of intra-abdominal hypertension in critically ill patients. Anaesth Intensive Care
40 (1): 79–89, 2012.
12. Reintam A, Parm P, Kitus R, Kern H, Starkopf J: Primary and secondary intra-abdominal hypertension—different impact on ICU outcome. Intensive Care Med
34 (9): 1624–1631, 2008.
13. Daugherty EL, Hongyan L, Taichman D, Hansen-Flaschen J, Fuchs BD: Abdominal compartment syndrome is common in medical intensive care unit patients receiving large-volume resuscitation. J Intensive Care Med
22 (5): 294–299, 2007.
14. Santa-Teresa P, Munoz J, Montero I, Zurita M, Tomey M, Alvarez-Sala L, Garcia P: Incidence and prognosis of intra-abdominal hypertension in critically ill medical patients: a prospective epidemiological study. Ann Intensive Care
2 (Suppl 1): S3, 2012.
15. Regueira T, Bruhn A, Hasbun P, Aguirre M, Romero C, Llanos O, Castro R, Bugedo G, Hernandez G: Intra-abdominal hypertension: incidence and association with organ dysfunction during early septic shock. J Crit Care
23 (4): 461–467, 2008.
16. Al-Dorzi HM, Tamim HM, Rishu AH, Aljumah A, Arabi YM: Intra-abdominal pressure and abdominal perfusion pressure in cirrhotic patients with septic shock. Ann Intensive Care
2 (Suppl 1): S4, 2012.
17. Harman PK, Kron IL, McLachlan HD, Freedlender AE, Nolan SP: Elevated intra-abdominal pressure and renal function. Ann Surg
196 (5): 594–597, 1982.
18. Malbrain ML, Cheatham ML, Kirkpatrick A, Sugrue M, Parr M, De Waele J, Balogh Z, Leppaniemi A, Olvera C, Ivatury R, et al.: Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. I. Definitions. Intensive Care Med
32 (11): 1722–1732, 2006.
19. Hedenstierna G, Larsson A: Influence of abdominal pressure on respiratory and abdominal organ function. Curr Opin Crit Care
18 (1): 80–85, 2012.
20. Kashtan J, Green JF, Parsons EQ, Holcroft JW: Hemodynamic effect of increased abdominal pressure. J Surg Res
30 (3): 249–255, 1981.
21. Richards WO, Scovill W, Shin B, Reed W: Acute renal failure associated with increased intra-abdominal pressure. Ann Surg
197 (2): 183–187, 1983.
22. Kron IL, Harman PK, Nolan SP: The measurement of intra-abdominal pressure as a criterion for abdominal re-exploration. Ann Surg
199 (1): 28–30, 1984.
23. Caldwell CB, Ricotta JJ: Changes in visceral blood flow with elevated intraabdominal pressure. J Surg Res
43 (1): 14–20, 1987.
24. Richardson JD, Trinkle JK: Hemodynamic and respiratory alterations with increased intra-abdominal pressure. J Surg Res
20 (5): 401–404, 1976.
25. Lee SL, Anderson JT, Kraut EJ, Wisner DH, Wolfe BM: A simplified approach to the diagnosis of elevated intra-abdominal pressure. J Trauma
52 (6): 1169–1172, 2002.
26. Luca A, Cirera I, Garcia-Pagan JC, Feu F, Pizcueta P, Bosch J, Rodes J: Hemodynamic effects of acute changes in intra-abdominal pressure in patients with cirrhosis. Gastroenterology
104 (1): 222–227, 1993.
27. Ridings PC, Bloomfield GL, Blocher CR, Sugerman HJ: Cardiopulmonary effects of raised intra-abdominal pressure before and after intravascular volume expansion. J Trauma
39 (6): 1071–1075, 1995.
28. Williams M, Simms HH: Abdominal compartment syndrome: case reports and implications for management in critically ill patients. Am Surg
63 (6): 555–558, 1997.
29. Puri GD, Singh H: Ventilatory effects of laparoscopy under general anaesthesia. Br J Anaesth
68 (2): 211–213, 1992.
30. Kelman GR, Swapp GH, Smith I, Benzie RJ, Gordon NL: Caridac output and arterial blood-gas tension during laparoscopy. Br J Anaesth
44 (11): 1155–1162, 1972.
31. Eleftheriadis E, Kotzampassi K, Botsios D, Tzartinoglou E, Farmakis H, Dadoukis J: Splanchnic ischemia during laparoscopic cholecystectomy. Surg Endosc
10 (3): 324–326, 1996.
32. Knolmayer TJ, Bowyer MW, Egan JC, Asbun HJ: The effects of pneumoperitoneum on gastric blood flow and traditional hemodynamic measurements. Surg Endosc
12 (2): 115–118, 1998.
33. Deeren DH, Dits H, Malbrain ML: Correlation between intra-abdominal and intracranial pressure in nontraumatic brain injury. Intensive Care Med
31 (11): 1577–1581, 2005.
34. 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
134 (10): 1082–1085, 1999.
35. Doty JM, Saggi BH, Blocher CR, Fakhry I, Gehr T, Sica D, Sugerman HJ: Effects of increased renal parenchymal pressure on renal function. J Trauma
48 (5): 874–877, 2000.
36. Doty JM, Saggi BH, Sugerman HJ, Blocher CR, Pin R, Fakhry I, Gehr TW, Sica DA: Effect of increased renal venous pressure on renal function. J Trauma
47 (6): 1000–1003, 1999.
37. Smith C, Cheatham ML: Intra-abdominal hypertension and abdominal compartment syndrome in the medical patient. Am Surg
77 (Suppl 1): S67–S71, 2011.
38. Ivatury RR: Abdominal Compartment Syndrome
. Georgetown, TX: Landes Bioscience; 2006.
39. Holodinsky JK, Roberts DJ, Ball CG, Reintam Blaser A, Starkopf J, Zygun DA, Stelfox HT, Malbrain ML, Jaeschke RC, Kirkpatrick AW: Risk factors for intra-abdominal hypertension and abdominal compartment syndrome among adult intensive care unit patients: a systematic review and meta-analysis. Crit Care
17 (5): R249, 2013.
40. Trillo-Alvarez C, Cartin-Ceba R, Kor DJ, Kojicic M, Kashyap R, Thakur S, Thakur L, Herasevich V, Malinchoc M, Gajic O: Acute lung injury prediction score: derivation and validation in a population-based sample. Eur Respir J
37 (3): 604–609, 2011.
41. Gajic O, Dabbagh O, Park PK, Adesanya A, Chang SY, Hou P, Anderson H 3rd, Hoth JJ, Mikkelsen ME, Gentile NT, et al.: Early identification of patients at risk of acute lung injury: evaluation of lung injury prediction score in a multicenter cohort study. Am J Respir Crit Care Med
183 (4): 462–470, 2011.
42. Guyatt G, Oxman AD, Akl EA, Kunz R, Vist G, Brozek J, Norris S, Falck-Ytter Y, Glasziou P, DeBeer H, et al.: GRADE guidelines: 1. Introduction—GRADE evidence profiles and summary of findings tables. J Clin Epidemiol
64 (4): 383–394, 2011.
43. Frutos-Vivar F, Esteban A, Apezteguia C, Gonzalez M, Arabi Y, Restrepo MI, Gordo F, Santos C, Alhashemi JA, Perez F, et al.: Outcome of reintubated patients after scheduled extubation. J Crit Care
26 (5): 502–509, 2011.
44. Lone NI, Walsh TS: Prolonged mechanical ventilation in critically ill patients: epidemiology, outcomes and modelling the potential cost consequences of establishing a regional weaning unit. Crit Care
15 (2): R102, 2011.
45. MacIntyre NR, Epstein SK, Carson S, Scheinhorn D, Christopher K, Muldoon S, National Association for Medical Direction of Respiratory Care: Management of patients requiring prolonged mechanical ventilation: report of a NAMDRC consensus conference. Chest
128 (6): 3937–3954, 2005.
46. Thille AW, Richard JC, Brochard L: The decision to extubate in the intensive care unit. Am J Respir Crit Care Med
187 (12): 1294–1302, 2013.
47. Kulkarni AP, Agarwal V: Extubation failure in intensive care unit: predictors and management. Indian J Crit Care Med
12 (1): 1–9, 2008.
48. McIntyre LA, Hebert PC, Fergusson D, Cook DJ, Aziz A, Canadian Critical Care Trials Group: A survey of Canadian intensivists’ resuscitation practices in early septic shock. Crit Care
11 (4): R74, 2007.
49. Kastrup M, Markewitz A, Spies C, Carl M, Erb J, Grosse J, Schirmer U: Current practice of hemodynamic monitoring and vasopressor and inotropic therapy in post-operative cardiac surgery patients in Germany: results from a postal survey. Acta Anaesthesiol Scand
51 (3): 347–358, 2007.
50. Sugrue M, Bauman A, Jones F, Bishop G, Flabouris A, Parr M, Stewart A, Hillman K, Deane SA: Clinical examination is an inaccurate predictor of intraabdominal pressure. World J Surg
26 (12): 1428–1431, 2002.
51. 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? Can J Surg
43 (3): 207–211, 2000.
52. Kimball EJ, Rollins MD, Mone MC, Hansen HJ, Baraghoshi GK, Johnston C, Day ES, Jackson PR, Payne M, Barton RG: Survey of intensive care physicians on the recognition and management of intra-abdominal hypertension and abdominal compartment syndrome. Crit Care Med
34 (9): 2340–2348, 2006.
53. Silva JP, Teles F: Assessment of intensivists’ knowledge on abdominal compartment syndrome. Rev Bras Anestesiol
62 (4): 531–537, 2012.
54. Zhou JC, Zhao HC, Pan KH, Xu QP: Current recognition and management of intra-abdominal hypertension and abdominal compartment syndrome among tertiary Chinese intensive care physicians. J Zhejiang Univ Sci B
12 (2): 156–162, 2011.
55. Ravishankar N, Hunter J: Measurement of intra-abdominal pressure in intensive care units in the United Kingdom: a national postal questionnaire study. Br J Anaesth
94 (6): 763–766, 2005.
56. Reintam Blaser A, Parm P, Kitus R, Starkopf J: Risk factors for intra-abdominal hypertension in mechanically ventilated patients. Acta Anaesthesiol Scand
55 (5): 607–614, 2011.
57. Murcia-Saez IM, Sobrino-Hernandez ML, Garcia-Lopez F, Corcoles-Gonzalez V, Cortes-Monedero JL, Tendero-Egea A, Martinez-Garcia A, Salinas-Sanchez AS: Usefulness of intra-abdominal pressure in a predominantly medical intensive care unit. J Crit Care 25 (1): 175–e176, e171–e176, 2010.
58. Dalfino L, Tullo L, Donadio I, Malcangi V, Brienza N: Intra-abdominal hypertension and acute renal failure in critically ill patients. Intensive Care Med
34 (4): 707–713, 2008.
59. Vidal MG, Ruiz Weisser J, Gonzalez F, Toro MA, Loudet C, Balasini C, Canales H, Reina R, Estenssoro E: Incidence and clinical effects of intra-abdominal hypertension in critically ill patients. Crit Care Med
36 (6): 1823–1831, 2008.
60. Malbrain ML, Chiumello D, Pelosi P, Bihari D, Innes R, Ranieri VM, del Turco M, Wilmer A, Brienza N, Malcangi V, et al.: Incidence and prognosis of intraabdominal hypertension in a mixed population of critically ill patients: a multiple-center epidemiological study. Crit Care Med 33 (2): 315–322, 2005.
Intra-abdominal hypertension; abdominal compartment syndrome; primary abdominal compartment syndrome; secondary abdominal compartment syndrome; multiple organ dysfunction syndrome; medical intensivist; failure to wean from mechanical ventilation
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