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146
IAP cutoffs to dene IAH are lower in pediatric patients than in adults (10
instead of 20 mmHg). Different authors showed that organ failure is dramatically
improved by decompressive laparotomy (DL) with a lower baseline IAP.Beck
[12] in 2001 reported a 5-year retrospective study in which ten patients were
treated with DL.Interestingly they had ACS with an IAP as low as 16 mmHg.
The incidence of ACS was low (0.6%) reecting the conservative threshold for
intervention. Mortality was high (60%) and the authors suggested a too delayed
timing for DL.Pearson [17] in 2010 published a cohort of 26 emergent DLs in
the presence of ACS. ACS was dened as new-onset organ dysfunction in the
presence of an IAP > 12 mmHg. They had a 58% mortality and advocated for
earlier intervention as every patient dramatically improved after DL. More
recently Rollins [18] showed how DL performed with an IAP > 20 mmHg in
patients on extracorporeal membrane oxygenation (ECMO) yielded a 100% mor-
tality. A threshold of 10 mmHg has been chosen as a cutoff point for the deni-
tion of IAH.This cutoff takes into account the normal values of IAP in critically
ill kids (7 ± 3 mmHg) [16] and the evidence of an increase in mortality and ACS
with IAP as low as 12 mmHg.
Indications and contraindications to IAP measurements are similar to adults and
reported elsewhere.
12.5 Epidemiology andOutcome
Epidemiology of ACS and IAH in the pediatric population is unknown. The lack
of awareness of this syndrome in the pediatric intensivist community has been
already discussed [5, 6]. No national or society registry has been implemented
until now. Moreover custom-made denitions of IAH and ACS were quite com-
mon, especially when dening the number of organ failure or the IAP cutoff (e.g.,
20 instead of 10 [18]). All published case series are monocentric and show an
incidence of ACS between 0.6 and 9.9% with mortality as high as 100% for
ECMO patients (see Table 12.2). The only nationwide report is from Turkey,
where Horoz [19] performed a 1-day national inquiry in 11 PICUs. Four IAP
measurements were performed at 6 h intervals to all pediatric patients admitted in
that day. Patients had to be admitted for treatment and for a period longer than 24
h with no contraindication to IAP measurement. The total sample was 130 patients,
46% of which had IAH.The IAH group had higher lactate levels and higher inci-
dence of hypothermia and mechanical ventilation. Even though patients with IAH
had a similar hospital and PICU length of stay and mechanical ventilation days to
the non-IAH, they had a slightly higher mortality and higher rate of organ failure.
The study couldn’t rule out if the IAH was just a proxy of criticality or had any
causal effect in the development of organ failure and death. Surprisingly when
using a cutoff at 10 mmHg, almost half of the population is in the IAH group,
greatly affecting the test specicity.
D. Corbella et al.
147
12.6 Special, andCritical, Clinical Scenarios
12.6.1 Abdominal Wall Defects
Gastroschisis, omphalocele, and Cantrell syndrome are congenital defects of the
abdominal wall [20]. In 1948 Gross [4] proposed a staged closure of the abdomen,
and since then the concept of “abdominal domain” or better to “regain abdominal
Table 12.2 List of studies exploring incidence and mortality of IAP\ACS in pediatric patients,
according to their denitions
First author
(year)
Type of study Denition of ACS/IAH Incidence
Mortality in
patients with
ACS
Beck
(2001) [12]
Single center,
prospective
observational
IAP > 15 mmHg + two
between oliguria/anuria,
respiratory decompensation,
hypotension/shock,
metabolic acidosis
10 patients
out of 1762
(0.6%)
60%
Divarci
(2016) [36]
Single center,
prospective
observational
WASCS denition IAH 9%
ACS 4%
16%
Ejike
(2007) [37]
Single center,
prospective
observational
IAP > 12 + one new organ
dysfunction
14/294
(4.7%)
50%
Fontana
(2014) [25]
Single center,
retrospective, all
pediatric kidney
transplant
IAP > 20 + one new organ
dysfunction
9/420 (2.1%) None
reported
Gupte
(2010) [26]
Single center,
retrospective, all
pediatric intestinal
transplant
Not dened 4/49 50%
Horoz
(2015) [19]
Nationwide 1-day
survey on the day of
admission
WSACS denition IAH 60/130
(46.2%)
46.7%
(30-day
mortality)
Pearson
(2010) [17]
Single center,
retrospective,
patients undergoing
emergent laparotomy
IAP > 12 + onset of new
organ failure
26/264
(9.9%)
58%
Steinau
(2011) [38]
Single center,
retrospective
IAP > 12 + onset of new
organ failure
Unknown 6/28 (21.4%)
Thabet
(2016) [39]
Single center,
prospective
observational
WSACS denition IAH (22/175)
12.6%
ACS (7/175)
4%
6/7 (85.7%)
Neville
(2000) [40]
Single center,
retrospective
Abdominal distension and
respiratory and/or cardiac
failure
Unknown 35%
12 The Open Abdomen inInfants andChildren
148
domain” has been mainstream in neonatal surgery in order to avoid the detrimental
effect of ACS.Rizzo [21] proposed in 1996 the intraoperative vesical pressure to
guide wall closure. However, only recently, Schmidt [22] showed that the use of
intraoperative IAP via a bladder catheter could substantiate and standardize the
choice on how to close the abdominal wall. In their prospective study, a cutoff of
IAP > 20 mmHg was chosen for a staged closure. They had no difference between
the staged and primary closure groups in terms of frequency of complications, time
to begin oral feeding, and length of parenteral nutrition or hospital stay.
12.6.2 Congenital Diaphragmatic Hernia (CDH)
ACS develops in CDH patients when the organs herniated in the thorax are returned
into the abdomen in the presence of a mismatch between the volume of those organs
and the abdominal domain. Incidence of ACS and IAH are unknown in CDH
patients. Data from the Canadian network of pediatric surgeons [23] reported an
ACS incidence <1% and a delayed abdominal closure, based on clinical judgment,
of 10%. This study suggests an actual or perceived risk of ACS in at least 10% of
patients. A better and “justied” denition of an IAH to attempt a primary closure
should be object of study as the open abdomen treatment in these patients is related
with a prolonged hospitalization, morbidity, and ventilator days. Moreover the sud-
den development of ACS can have detrimental effect in an already unstable patient,
as the sudden increase in IAP can compromise cardiac output. The mismatch
between organs and domain may explain the observation of Dotta [24] that showed
a decrease in cerebral NIRS during CDH repair, with the lowest values registered
when the organs are placed in the abdominal cavity.
12.6.3 Solid Organ Transplantation
Solid organ transplantation with an adult graft is frequently complicated by some
degrees of ACS due to a mismatch between abdominal domain and adult graft. The
ideas at the basis of the use of a staged abdominal closure are to gain space by
allowing graft or bowel edema to reabsorb or to wait for the abdominal cavity to
stretch around the organs with a second-intention closure without compromising
graft perfusion. This has been described for every abdominal or retroperitoneal
organ. Fontana [25] reported nine cases of ACS out of 420 kidney transplants in his
25-year experience. All of them were pediatric patients who received an adult graft.
This brought his group to measure IAP during abdominal closure on a routine basis.
Intestinal or combined intestinal–liver transplantation with a mismatch between
recipient and donor is a well-known, although rare, cause of ACS. Gupte [26]
reports that since 2005 staged closure of the abdomen and pre-transplant abdominal
tissue expanders were applied routinely whenever a mismatch between donor and
D. Corbella et al.
149
recipient was found. This is the result of their previous experience of ACS with 50%
mortality. Sheth [27] reported similar results in the cohorts of patients from Necker.
Delayed primary closure of the abdomen in pediatric liver transplantation was con-
sidered an emergency therapy when important bowel edema, massive transfusion,
great donor graft mismatch, or bowel distension were detected [28]. Some centers
now report an incidence of delayed closure of 50%. This shows a passage from an
emergency treatment to a standard procedure when a risk of developing ACS is
foreseen [29].
12.6.4 Necrotizing Enterocolitis
Necrotizing enterocolitis(NEC) is characterized by extensive damage to the bowel
ranging from edema to necrosis and perforation. ACS is a well-known feature of the
NEC [30]. Anyway it not clear whether it has a causal role in the development of the
NEC or it just worsens the prognosis when the vicious circle of ischemia more pres-
sure more ischemia is started. Staged closure of the abdominal cavity was reported
as routinely performed by 25% of European pediatric surgeons [31] if a “tense clo-
sure” was suspected. In a study from Tanriverdi [32], an increase of IAP pressure
between serial measurements was dened as an early sign of NEC.Interestingly,
important abdominal impairment was detected for pressures as low as 10 mmHg
[30, 32], questioning the value of 20 mmHg that is currently felt as a safe threshold
for closing the abdomen in other neonatal diseases (i.e., wall defects [22]).
12.6.5 Pediatric Cardiac andECMO Patients
Children requiring surgery for congenital heart disease have a number of periopera-
tive risk factors for gut mucosal injury: young age, abnormal circulatory physiology
(duct-dependent circulation and single ventricle), suboptimal mucosal perfusion,
altered blood ow and hypothermia induced during cardiopulmonary bypass, and
surgical trauma. These factors may predispose to splanchnic hypoperfusion, disrup-
tion of the gut’s barrier function with development of endotoxemia, colonic disten-
sion, and IAH [33, 34].
Patients on ECMO are a peculiar challenge. An increased IAP reduces the return
to the venous cannula impairing perfusion, but an open abdomen treatment is bur-
dened by the risk of an unmanageable hemorrhage in anticoagulated patients. To
date three papers report the experience of ACS in pediatric patients on ECMO.Rollins
[18] in his cohort of seven patients that underwent laparotomy had no survival,
whereas Prodhan [35] had two survivors out of four patients treated with peritoneal
catheters. No formal IAP measurement was implemented. However, Rollins sug-
gests possibly better results had decompressive laparotomies been performed
earlier.
12 The Open Abdomen inInfants andChildren
150
References
1. Malbrain MLNG, Cheatham ML, Kirkpatrick A, Sugrue M, Parr M, De Waele J, etal. Results
from the international conference of experts on intra-abdominal hypertension and abdominal
compartment syndrome. I.Denitions. Intensive Care Med. 2006;32:1722–32.
2. Cheatham ML, Malbrain MLNG, Kirkpatrick A, Sugrue M, Parr M, De Waele J, etal. Results
from the international conference of experts on intra-abdominal hypertension and abdominal
compartment syndrome. II.Recommendations. Intensive Care Med. 2007;33:951–62.
3. Kirkpatrick AW, Roberts DJ, De Waele J, Jaeschke R, Malbrain MLNG, De Keulenaer B,
etal. Intra-abdominal hypertension and the abdominal compartment syndrome: updated con-
sensus denitions and clinical practice guidelines from the World Society of the Abdominal
Compartment Syndrome. Intensive Care Med. 2013;39:1190–206.
4. Gross RE. A new method for surgical treatment of large omphaloceles. Surgery.
1948;24:277–92.
5. Kimball EJ, Rollins MD, Mone MC, Hansen HJ, Baraghoshi GK, Johnston C, etal. Survey of
intensive care physicians on the recognition and management of intra-abdominal hypertension
and abdominal compartment syndrome. Crit Care Med. 2006;34:2340–8.
6. Kaussen T, Steinau G, Srinivasan PK, Otto J, Sasse M, Staudt F, etal. Recognition and man-
agement of abdominal compartment syndrome among German pediatric intensivists: results of
a national survey. Ann Intensive Care. 2012;2(Suppl 1):S8.
7. Balogh ZJ, Butcher NE. Compartment syndromes from head to toe. Crit Care Med.
2010;38:S445–51.
8. Malbrain MLNG, Roberts DJ, Sugrue M, De Keulenaer BL, Ivatury R, Pelosi P, etal. The
polycompartment syndrome: a concise state-of-the-art review. Anaesthesiol Intensive Ther.
2014;46:433–50.
9. Malbrain MLNG, Wilmer A.The polycompartment syndrome: towards an understanding of
the interactions between different compartments! Intensive Care Med. 2007;33:1869–72.
10. Scalea TM, Bochicchio GV, Habashi N, McCunn M, Shih D, McQuillan K, etal. Increased
intra-abdominal, intrathoracic, and intracranial pressure after severe brain injury: multiple
compartment syndrome. JTrauma. 2007;62:647–56. discussion 656.
11. Cheatham ML.Abdominal compartment syndrome: pathophysiology and denitions. Scand
JTrauma Resusc Emerg Med. 2009;17:10.
12. Beck R, Halberthal M, Zonis Z, Shoshani G, Hayari L, Bar-Joseph G.Abdominal compart-
ment syndrome in children. Pediatr Crit Care Med. 2001;2:51–6.
13. Sugrue M, Bauman A, Jones F, Bishop G, Flabouris A, Parr M, etal. Clinical examination is
an inaccurate predictor of intraabdominal pressure. World JSurg. 2002;26:1428–31.
14. Davis PJ, Koottayi S, Taylor A, Butt WW.Comparison of indirect methods of measuring intra-
abdominal pressure in children. Intensive Care Med. 2005;31:471–5.
Take-Home Message
• IAP should be performed routinely in every critically ill pediatric patient.
• An IAP > 10 mmHg should be considered an “ominous” sign and prompt
a more intensive monitoring of the patients even in those scenarios where
a different cutoff has been used before.
• DL should be considered early in the development of organ dysfunction
and not be used as the “last hope for hopeless cases.”
• When possible those cases should be reported in literature, and more
efforts should be poured in collecting data in prospective registry or trials.
D. Corbella et al.
151
15. De Waele J, Pletinckx P, Blot S, Hoste E.Saline volume in transvesical intra-abdominal pres-
sure measurement: enough is enough. Intensive Care Med. 2006;32:455–9.
16. Ejike JC, Bahjri K, Mathur M.What is the normal intra-abdominal pressure in critically ill
children and how should we measure it? Crit Care Med. 2008;36:2157–62.
17. Pearson EG, Rollins MD, Vogler SA, Mills MK, Lehman EL, Jacques E, etal. Decompressive
laparotomy for abdominal compartment syndrome in children: before it is too late. JPediatr
Surg. 2010;45:1324–9.
18. Rollins MD, Deamorim-Filho J, Scaife ER, Hubbard A, Barnhart DC.Decompressive lapa-
rotomy for abdominal compartment syndrome in children on ECMO: effect on support and
survival. JPediatr Surg. 2013;48:1509–13.
19. Horoz OO, Yildizdas D, Asilioglu N, Kendirli T, Erkek N, Anil AB, etal. The prevalance of
and factors associated with intra-abdominal hypertension on admission day in critically ill
pediatric patients: a multicenter study. JCrit Care. 2015;30:584–8.
20. Christison-Lagay ER, Kelleher CM, Langer JC.Neonatal abdominal wall defects. Semin Fetal
Neonatal Med. 2011;16:164–72.
21. Rizzo A, Davis PC, Hamm CR, Powell RW.Intraoperative vesical pressure measurements as a
guide in the closure of abdominal wall defects. Am Surg. 1996;62:192–6.
22. Santos Schmidt AF, Goncalves A, Bustorff-Silva JM, Oliveira-Filho AG, Miranda ML, Oliveira
ER, etal. Monitoring intravesical pressure during gastroschisis closure. Does it help to decide
between delayed primary or staged closure? JMater Fetal Neonatal Med. 2012;25:1438–41.
23. Maxwell D, Baird R, Puligandla P.Abdominal wall closure in neonates after congenital dia-
phragmatic hernia repair. JPediatr Surg. 2013;48:930–4.
24. Dotta A, Rechichi J, Campi F, Braguglia A, Palamides S, Capolupo I, etal. Effects of surgi-
cal repair of congenital diaphragmatic hernia on cerebral hemodynamics evaluated by near-
infrared spectroscopy. JPediatr Surg. 2005;40:1748–52.
25. Fontana I, Bertocchi M, Centanaro M, Varotti G, Santori G, Mondello R, etal. Abdominal
compartment syndrome: an underrated complication in pediatric kidney transplantation.
Transplant Proc. 2014;46:2251–3.
26. Gupte GL, Haghighi KS, Sharif K, Mayer DA, Beath SV, Kelly DA, etal. Surgical complica-
tions after intestinal transplantation in infants and children--UK experience. JPediatr Surg.
2010;45:1473–8.
27. Sheth J, Sharif K, Lloyd C, Gupte G, Kelly D, de Ville de Goyet J, etal. Staged abdominal
closure after small bowel or multivisceral transplantation. Pediatr Transplant. 2012;16:36–40.
28. Ong TH, Strong R, Zahari Z, Yamanaka J, Lynch S, Balderson G, etal. The management of
difcult abdominal closure after pediatric liver transplantation. JPediatr Surg. 1996;31:295–6.
29. Ziaziaris WA, Darani A, Holland AJA, Alexander A, Karpelowsky J, Shun A, etal. Delayed
primary closure and the incidence of surgical complications in pediatric liver transplant recipi-
ents. JPediatr Surg. 2015;50:2137–40.
30. Sukhotnik I, Riskin A, Bader D, Lieber M, Shamian B, Coran AG, etal. Possible importance
of increased intra-abdominal pressure for the development of necrotizing enterocolitis. Eur
JPediatr Surg. 2009;19:307–10.
31. Zani A, Eaton S, Puri P, Rintala R, Lukac M, Bagolan P, etal. International survey on the
management of necrotizing enterocolitis. Eur JPediatr Surg. 2015;25:27–33.
32. Tanriverdi S, Koroglu O, Uygur O, Celik A, Dulger F, Yalaz M, etal. Serial intravesical pres-
sure measurements can predict the presence and the severity of necrotizing enterocolitis. Eur
JPediatr Surg. 2013;23:243–8.
33. Floh AA, Slicker J, Schwartz SM.Nutrition and mesenteric issues in pediatric cardiac critical
care. Pediatr Crit Care Med. 2016;17:S243–9.
34. Pathan N, Burmester M, Adamovic T, Berk M, Ng KW, Betts H, etal. Intestinal injury and
endotoxemia in children undergoing surgery for congenital heart disease. Am J Respir Crit
Care Med. 2011;184:1261–9.
35. Prodhan P, Imamura M, Garcia X, Byrnes JW, Bhutta AT, Dyamenahalli U.Abdominal com-
partment syndrome in newborns and children supported on extracorporeal membrane oxygen-
ation. ASAIO J.2012;58:143–7.
12 The Open Abdomen inInfants andChildren
152
36. Divarci E, Karapinar B, Yalaz M, Ergun O, Celik A. Incidence and prognosis of intraab-
dominal hypertension and abdominal compartment syndrome in children. J Pediatr Surg.
2016;51:503–7.
37. Ejike JC, Humbert S, Bahjri K, Mathur M.Outcomes of children with abdominal compartment
syndrome. Acta Clin Belg. 2007;62(Suppl 1):141–8.
38. Steinau G, Kaussen T, Bolten B, Schachtrupp A, Neumann UP, Conze J, etal. Abdominal
compartment syndrome in childhood: diagnostics, therapy and survival rate. Pediatr Surg Int.
2011;27:399–405.
39. Thabet FC, Bougmiza IM, Chehab MS, Bafaqih HA, AlMohaimeed SA, Malbrain
MLNG.Incidence, risk factors, and prognosis of intra-abdominal hypertension in critically ill
children: a prospective epidemiological study. JIntensive Care Med. 2016;31:403–8.
40. Neville HL, Lally KP, Cox CS.Emergent abdominal decompression with patch abdomino-
plasty in the pediatric patient. JPediatr Surg. 2000;35:705–8.
D. Corbella et al.
153
© Springer International Publishing AG, part of Springer Nature 2018
F. Coccolini et al. (eds.), Open Abdomen, Hot Topics in Acute Care Surgery
and Trauma, https://doi.org/10.1007/978-3-319-48072-5_13
M.L. Cheatham, MD, FACS, FCCM (*) • K. Safcsak, RN, BSN
Orlando Regional Medical Center, Orlando, FL, USA
e-mail: michael.cheatham@orlandohealth.com
13
Intensive Care Unit Management
of the Adult Open Abdomen
Michael L. Cheatham and Karen Safcsak
13.1 Introduction
Elevated intra-abdominal pressure (IAP) is a common pathophysiologic finding
among critically ill patients [1]. Unfortunately, clinical recognition of this disease by
critical care physicians and nurses remains low [2, 3]. As a result, it is frequently
overlooked as a cause for patient deterioration until significant organ injury has
occurred, resulting in patient morbidity, increased resource utilization, and unneces-
sary mortality. The causative factors for pathologic increases in IAP are as diverse as
the patient populations that are at risk. Sepsis, traumatic injury, abdominal infection,
chronic kidney or liver dysfunction/failure, ileus, pancreatitis, and burns, among oth-
ers, have all been implicated in the development of intra-abdominal hypertension
(IAH) and abdominal compartment syndrome (ACS). Traditionally considered a dis-
ease of the surgical patient, IAH/ACS may well be more common among medical
patients where its development and presentation is typically more insidious [4].
Key Points
• Serial intra-abdominal pressure (IAP) measurements are essential in the
critically ill patient at risk for intra-abdominal hypertension (IAH) and/or
abdominal compartment syndrome (ACS).
• Multimodality medical management is effective at reducing elevated IAP
when implemented early.
• Prompt surgical decompression should be performed in patients whose
elevated IAP is refractory to nonoperative management strategies.
154
In this chapter, we will describe a comprehensive, evidence-based approach to
the management of the ICU patient at risk for elevated IAP. This strategy has been
developed over the past 20 years during the treatment of thousands of both medical
and surgical patients with IAH/ACS and has been demonstrated to significantly
reduce patient morbidity and mortality [5].
13.2 Pathophysiology
To understand the efficacy of the therapeutic tactics advocated in this strategy, an
understanding of the pathophysiologic implications of elevated IAP is essential. IAP
is determined by three factors: [1] abdominal organ volume, [2] presence of space-
occupying substances (such as blood, ascites/fluid, air, or tumor), and [3] abdominal
wall compliance. Therapies implemented to reduce the injurious effects of elevated
IAP must therefore confront one of these three factors. Normal adult IAP is less than
5 mmHg, but IAP in the post-laparotomy patient is typically 10–15 mmHg. In the
critically ill patient with septic shock, an IAP of 15–20 mmHg is common. Patients
with systemic hypoperfusion and organ dysfunction/failure commonly demonstrate
an IAP of 20–30 mmHg or greater. These pressures can have a catastrophic impact
upon organ perfusion and function leading to the significant morbidity and mortality
associated with both IAH and ACS. Although abdominal decompression signifi-
cantly improves survival in such patients, contrary to popular belief, IAP does not
become zero once a patient’s abdomen is open. IAH and ACS may both occur despite
the presence of an open abdomen and temporary abdominal closure.
IAP, however, is only part of the equation. As a result of patient variability, there
is no single-threshold IAP value that can be globally applied to the decision-making
of all patients. IAP alone lacks sufficient sensitivity and specificity at the clinically
appropriate thresholds of 10–25 mmHg to be useful as a resuscitation endpoint.
Abdominal perfusion pressure (APP), calculated as mean arterial pressure (MAP)
minus IAP, assesses not only the severity of IAP present, but also the adequacy of
the patient’s systemic and visceral perfusion. APP has been demonstrated to be
superior to both IAP and global resuscitation endpoints, such as arterial pH, base
deficit, and arterial lactate, in its ability to predict patient outcome [6]. It represents
an easily calculated parameter for guiding the resuscitation and management of the
patient with IAH/ACS, having been demonstrated to exceed the clinical prediction
of IAP alone in several clinical trials.
Clinical examination through abdominal palpation has a sensitivity of less than
50% for determining the presence of elevated IAP. Therefore, if IAH is suspected to
be present, IAP must be measured. Failure to identify IAH and/or ACS when pres-
ent is associated with reported mortality rates of up to 100%. When recognized and
appropriately treated, mortality can still reach 30–40% depending upon the etiology
of the disease process [5]. Serial determinations of IAP have been shown to reliably
detect the development of IAH and facilitate early treatment of ACS, with signifi-
cant reductions in patient morbidity and mortality. This is especially true in the
patient with an open abdomen where IAP and APP become essential resuscitative
M.L. Cheatham and K. Safcsak
155
parameters. Regrettably, studies demonstrate that many physicians and nurses do
not understand how to measure IAP or are reluctant to measure IAP in their patients
at risk [2, 3].
Elevated IAP causes significant impairment of cardiac, pulmonary, renal,
gastrointestinal, hepatic, central nervous system, and abdominal wall perfusion
and function, with each organ demonstrating its own unique vulnerability. This
differential response to IAP, coupled with the augmented susceptibility seen in
the presence of hypovolemia and comorbid disease, further complicates the
management of these complex patients. The detrimental effects of IAP on each
of these organ systems are described in Table 13.1. The possibility of IAH
Table 13.1 Pathophysiological implications of IAH/ACS
Organ system
Pathophysiological effects Clinical manifestations
Threshold
IAP
Cardiovascular Decreased preload/venous
return
Increased afterload
Compression of inferior
vena cava
Decreased cardiac output
Increased susceptibility to
hypovolemia
10 mmHg
Pulmonary Increased intrathoracic
pressure
Cephalad elevation of
diaphragm
Extrinsic compression of
pulmonary parenchyma
Alveolar atelectasis
Increased airway resistance
Hypoxemia
Hypercarbia
Elevated airway pressures
Increased intrapulmonary
shunt
Increased alveolar dead
space
15 mmHg
Renal Decreased renal blood flow
Renal vein compression
Renal parenchymal
compression
Oliguria
Anuria
Acute renal failure
15 mmHg
Gastrointestinal Decreased mesenteric blood
flow
Intestinal ischemia
Bacterial translocation/
sepsis
Increased susceptibility to
hypovolemia
Increased visceral edema/
capillary leak
Metabolic acidosis
10 mmHg
Hepatic Decreased hepatic vein
blood flow
Decreased portal vein blood
flow
Hepatic dysfunction/
failure
Metabolic acidosis
10 mmHg
Central nervous
system
Increased intrathoracic
pressure
Decreased cerebral venous
outflow
Increased intracranial
pressure
Decreased cerebral
perfusion pressure
15 mmHg
Abdominal wall Decreased abdominal wall
compliance
Decreased rectus sheath
blood flow
Fascial dehiscence 10 mmHg
IAP intra-abdominal pressure, IAH intra-abdominal hypertension, ACS abdominal compartment
syndrome
13 Intensive Care Unit Management of the Adult Open Abdomen