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The copyright of this thesis rests with the author and no quotation from it or information derived from it
may be published without proper acknowledgement.
A Study of Raised Intra-abdominal Pressure and the Abdominal CompartmentSyndrome in Liver Intensive Care
Cresswell, Ben
Awarding institution:King's College London
Download date: 01. Sep. 2020
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Title:A Study of Raised Intra-abdominal Pressure and the Abdominal CompartmentSyndrome in Liver Intensive Care
Author:Ben Cresswell
A Study of Raised Intra-abdominal Pressure and the Abdominal Compartment Syndrome in Liver
Intensive Care
Adrian B Cresswell MB ChB, FRCS
Submitted for degree of; MD(Res)
King’s College London
1
Acknowledgments
For my wife, Clodagh
With gratitude to my supervisors, Professor Julia Wendon and Mr Matthew Bowles
With acknowledgment of the assistance of the intensive care and surgical staff and patients at the Institute for Liver Studies at King’s College Hospital, London – especially Drs William Bernal,
Georg Auzinger and Pauline Kane
2
Contents
Page Number Abstract 6 Lists of Tables & Figures 8
Chapter
1 Introduction 12 1.1 What is Intra-abdominal Pressure 13 1.2 Historical Background 16 1.3 Definitions and Terminology 19 1.4 Epidemiology of IAH / ACS 25 1.5 Measurement of IAP 30 1.5.1 Techniques for Measurement of IAP 33 1.5.2 Screening Criteria 42 1.6 IAP and the Liver 45 1.7 IAP and the other Organ Systems 56 1.7.1 IAP and the Cardiovascular System 56 1.7.2 IAP and the Respiratory System 60 1.7.3 IAP and the Renal System 61 1.7.4 IAP and the Central Nervous System 62 1.8 Overview of Areas of Study 63 1.9 Considerations Regarding Study Design, 66
Data Collection and Analysis
2 Attitudes and Practice of Intra-abdominal Pressure 70 in the UK
2.1 Introduction – Previous Questionnaires and Surveys 71 2.2 Design of Questionnaire 80 2.3 Results 85 2.4 Discussion 95 2.5 Summary and Conclusions 98
3 Invitro & Invivo Evaluation of the Foley 99 Manometer Device for the Measurement of IAP
3.1 Introduction – Techniques available for the Measurement of 100 Intra-abdominal Pressure
3.2 Invitro Evaluation of the Foley Manometer 108 3.3 Comparison of Foley Manometer to Directly Transduced 115
Intra-peritoneal Pressure Recordings 3.4 Comparison of Foley Manometer to AbViser Device 122 3.5 Summary and Conclusions 126
3
4 Sources of Error in the Use of the 127 Foley Manometer
4.1 Introduction 128 4.2 Determining the Ideal Zero-Reference Point for the Measurement 130
of IAP 4.3 The Effect of Body Position on Measured IAP 141
4.4 The Effect of Priming Volume on Measured IAP 150 4.5 Vapour Lock 160 4.6 Discussion 161 4.7 Summary and Conclusions 165
5 An Observational Cohort Study of the Incidence 166
and Effects of Raised Intra-abdominal Pressure in the Liver Intensive Care Unit
5.1 Introduction and definitions 167 5.2 Methods 169 5.3 Results 174 5.3.1 Patient Demographics 174 5.3.2 Incidence of IAH & ACS 177 5.3.3 Association of Raised IAP with Length of Stay, Complications & Liver 178
Function 5.3.4 Factors Predicting Peak IAP 186 5.4 Discussion 191 5.5 Summary and Conclusions 197
6 Regional IAP Following Liver Transplantation 198 6.1 Introduction 199 6.2 Methods 202 6.3 Results 206 6.3.1 Compartmental Pressure Measurement & the effect of Body Position 210 6.3.2 Continuous Compartment Pressure Measurement 212 6.4 Discussion 215 6.5 Summary & Conclusion 221
7 Summary, Limitations and Conclusions 222
Bibliography 237
4
Appendix 250
1. i. IAP Questionnaire – Surgeons 252
ii. IAP Questionnaire – Anaesthetists 254
2. Peer-reviewed publications arising from thesis 256
i. Hepatic function and non-invasive hepatosplanchnic monitoring in patients with abdominal hypertension. Cresswell AB, Wendon JA. Acta Clin Belg. 2007;(1):113-8.
ii. The effect of different reference transducer positions on
intra-abdominal pressure measurement: a multicenter analysis. De Waele JJ, De Laet I, De Keulenaer B, Widder S, Kirkpatrick AW, Cresswell AB, Malbrain M, Bodnar Z, Mejia-Mantilla JH, Reis R, Parr M, Schulze R, Compano S, Cheatham M. Intensive Care Med. 2008 Jul;34(7):1299-303. 2008 Apr 4.
iii. The impact of body position on intra-abdominal pressure
measurement: a multicenter analysis. Cheatham ML, De Waele JJ, De Laet I, De Keulenaer B, Widder S, Kirkpatrick AW, Cresswell AB, Malbrain M, Bodnar Z, Mejia-Mantilla JH, Reis R, Parr M, Schulze R, Puig S; World Society of the Abdominal Compartment Syndrome (WSACS) Clinical Trials Working Group. Crit Care Med. 2009 Jul;37(7):2187-90.
iv. The effect of body position on compartmental intra-
abdominal pressure following liver transplantation. Cresswell AB, Jassem W, Srinivasan P, Prachalias AA, Sizer E, Burnal W, Auzinger G, Muiesan P, Rela M, Heaton ND, Bowles MJ, Wendon JA Annals of Intensive Care. 2012 5(2):S12
5
Abstract
Introduction
Interest in intra-abdominal pressure (IAP) measurement has increased significantly, with
evidence of its deleterious effects demonstrated on every organ. Despite the volume of
publications – several assumptions relating to the measurement of IAP remain unproven and
there is a paucity of data relating to patients in a specialised liver Intensive Therapy Unit (ITU).
Methods
This thesis encompasses a survey of the available literature and national attitudes / practice with
several clinical experiments;
Generic Questions
1. IAP measurement technique – validation of current gold-standard against alternatives
2. Identification of potential sources of error in measurement of IAP
3. Impact of body position and zero-reference point on IAP
Specialty Specific Questions
1. Incidence of raised IAP in specialised liver ITU and its link to complications / length of stay
2. Identification of early predictors of raised IAP
3. Study of regional abdominal compartmental variation in IAP
6
Results & Conclusions
• IAP is widely accepted by UK anaesthetists and surgeons, especially amongst those
more recently graduated. Knowledge and practice is variable however and requires
better education
• The Foley Catheter Manometer represents a reliable and valid tool for the measurement
of IAP, with excellent agreement to measurements obtained by other devices and directly
transduced intra-peritoneal pressure
• Body-position and bladder priming volumes both introduce significant clinical error in the
measurement of IAP
• Patients in liver ITU are at higher risk of developing elevated IAP than those in a general
ITU. Within this patient cohort, complications are associated with elevated IAP and IAP
is a better predictor of length of stay than other severity scores. A normal Day 1 IAP
reliably predicts that abdominal compartment syndrome will not occur during the
admission
• Significant variation in upper and lower IAP occurs following liver transplantation and this
regional variation can be manipulated by body positioning
7
List of Tables Chapter Table
Number Title Page
Number
1.1 WSACS Consensus Definitions 23 1.2 Summary of Studies Looking at the Incidence / Prevalence of IAH 28 1.3 The Richmond Agitation-Sedation Scale 67
1
1.4 WSACS Criteria for clinical equivalence of IAP measurement techniques
68
2.1 Summary of previous surveys of knowledge and practice relating to
IAP 72
2.2 Views regarding the existence of ACS reported by UK anaesthetists with or without an ITU practice
86
2.3 Views regarding the existence of ACS reported by UK general surgeons (further divided by sub-specialty interest)
87
2.4 Table summarising knowledge and practice relating to measurement of IAP
90
2.5 Table summarising practice relating to decompressive laparostomy 91 2.6 Comparison of intra-operative factors reported as making
laparostomy more likely 92
2.7 Comparison of post-operative factors making laparostomy more likely
93
2
2.8 Ranking of factors making laparostomy more likely, in order of importance, reported by surgeons and anaesthetists in the current study compared to the original research
94
3.1 Ideal characteristics for a system to measure IAP 100 3.2 Summary of the relative merits for various techniques used for the
measurement of IAP 106
3.3 Results of an in-vitro study of inter-observer variability in the use of the Holtech FoleyManometer
112
3.4 Results of comparison of IAP measurements made using the Holtech FoleyManometer and via direct transduction of pelvic intra-peritoneal pressure
119
3
3.5 Results of the comparison of IAP measured using the Holtech FoleyManometer and AbViser systems
124
4.1 Mean and standard deviation of distance (mm) between bony
landmarks and catheter balloon (bladder neck) 133
4.2 Comparison of IAP measured at symphysis pubis and iliac crest zero-reference points – local and multi-centre data presented
137
4.3 The effect of body position on measured IAP - local data and results of multi-centre study
145
4.4 Summary of the effects of bladder priming volume on the measured IAP expressed as bias over measurement obtained with a 25ml priming volume
152
4.5 Effect of different priming volumes on measured IAP over a standard minimum volume of 10mls
156
4
4.6 Comparison of observed bias in IAP measurement observed with various different devices
163
8
5.1 Measured end-points and definitions of summary measures
examined during epidemiological study of IAP in Liver ITU 171
5.2 Demographic details of patients recruited with a diagnosis of Acute Hepatic Dysfunction
174
5.3 Demographic details of patients recruited following HPB Surgery 175 5.4 Demographic details of patients recruited following Liver
Transplantation 175
5.5 Mean Peak IAP, Mean D1 IAP and Incidence of IAH & ACS for each of the study groups
177
5.6 Summary of length of stay observed amongst patients with normal (<12 mmHg) and elevated (> 12 mmHg) IAP
178
5.7 Variables included in the regression model to determine significant predictors of length of stay
179
5.8 Variables found to significantly contribute to a regression model to predict length of stay (all diagnoses)
179
5.9 Variables found to significantly contribute to a regression model to predict length of stay (HPB Surgery)
180
5.10 Variables found to significantly contribute to a regression model to predict length of stay (Liver Transplantation)
180
5.11 Relationship between the presence of IAH and the incidence of complications within the study groups
181
5.12 Summary of correlations between IAP and liver function – Pearson’s Product Moment Correlation Co-efficient
185
5.13 Volume of early fluid administration within the study groups 189
5
5.14 Regression analysis of the effect of early resuscitation volumes for predicting IAP
190
6.1 Comparison of compartmental IAP measured at supine and 30o
head of bed positions 206
6.2 Summary of compartmental pressure differences in subjects divided by whether the upper or lower compartment concealed the higher pressure
213
6
6.3 Summary of WSACS study of the effect of body position on IAP 218
9
List of Figures
Chapter Figure
Number Title Page
Number
1.1 Technique for measurement of IAP described by Kron 35 1.2 Technique for measurement of IAP described by Malbrain 36 1.3 AbViser device for the measurement of IAP 37 1.4 The Holtech FolyManometer System for the measurement of IAP 39 1.5 IAH / ACS Management Algorithm 44
1
1.6 Example of a Bland and Altman Plot of Agreement 68 2 2.1 A summary of volume of publications relating to IAP per year (1982
– 2006) 79
3.1 Set-up and use of the FoleyManometer system to measure IAP 108 3.2 Manufacturers instructions supplied with the Holtech
FoleyManometer 111
3.3 Experimental apparatus constructed to simulate measurement of IAP (visual screen to shield view of the cylinder from the subject omitted for clarity)
111
3.4 Measured simulated IAP using Foley Manometer (actual IAP = 18 mmHg). Bland and Altman absolute bias and limits of agreement marked by horizontal lines
113
3.5 Bland and Altman Plot to compare intra-vesical pressure (IBP) to lower intra-abdominal pressure (LIAP) at both 0o and 30o head of bed angles
120
3.6 Bland and Altman Plot to compare intra-vesical pressure (IBP) to intra-abdominal pressure (LIAP) at 0o (supine) head of bed angle
120
3.7 Bland and Altman Plot to compare intra-vesical pressure (IBP) to lower intra-abdominal pressure (LIAP) at 30o head of bed angle
121
3.8 The AbViser system to measure intra-vesical pressure 122
3
3.9 Bland and Altman Plot to compare IAP measured using the Holtech FoleyManometer and Abviser systems
124
4.1 Distance was measured from the centre of the catheter balloon to
the bony landmark (in the case of the iliac crest the catheter tip and landmark were identified on different slices)
132
4.2 Mean distance between bony landmarks and catheter balloon (bladder neck) overall and split by gender (Median, Inter-quartile Range and Range)
134
4.3 Bland and Altman Plots comparing symphysis pubis and iliac crest zero-reference points for the measurement of IAP from multi-centre data (left) and local study (right)
138
4.4 Bland and Altman Plot comparing IAP measured with a supine body position and a 15o head of bed angle (local data)
146
4.5 Bland and Altman Plot comparing IAP measured with a supine body position and a 30o head of bed angle (local data)
146
4.6 Bland and Altman Plot comparing IAP measurements made with bladder priming volumes of 10 & 50mls
157
4
4.7 Bland and Altman Plot comparing IAP measurements made with bladder priming volumes of 10 & 100mls
157
10
4.8 Bland and Altman Plot comparing IAP measurements made with bladder priming volumes of 10 & 200mls
158
4.9 Overall increase in median IAP observed with increasing bladder priming volumes
159
4.10 Individual increases in IAP observed with increasing bladder priming volumes
159
4.11 The problem of “vapour-lock” identified in the use of the Holtech FoleyManometer
160
5.1 There was a strong negative correlation between Peak IAP and Day
1 ICG Clearance 182
5.2 There was a strong negative correlation between Day 1 IAP and Day 1 ICG Clearance
183
5.3 There was a non-significant negative correlation between Peak IAP and Peak INR
184
5.4 There was a significant negative correlation between Day 1 IAP and Peak INR
185
5.5 Correlation between Day 1 and Peak IAP 186 5.6 No patient with a normal Day 1 IAP (green box) went on to develop
ACS during the period of their ITU admission 187
5.7 Day of diagnosis of IAH based on stage of admission 188
5
5.8 Day of ITU admission when Peak IAP reached 189
6.1 The experimental apparatus for measurement IAP by direct transduction of intra-peritoneal pressure at the liver and bladder and measurement of intra-vesical pressure using the Holtech FoleyManometer
203
6.2 Use of the Holtech FoleyManometer for the measurement of IAP 204 6.3 Bland and Altman Plot of agreement between intra-vesical pressure
(IBP) and lower intra-peritoneal pressure (LIAP) measurements made at all bed positions
207
6.4 Bland and Altman Plot of agreement between intra-vesical pressure (IBP) and lower intra-peritoneal pressure (LIAP) measurements with a supine body position – showing excellent agreement between the two
208
6.5 Bland and Altman Plot of agreement between intra-vesical pressure (IBP) and lower intra-peritoneal pressure (LIAP) measurements with a 30o head of bed angle – showing excellent agreement between the two
209
6.6 Bland and Altman Plot of agreement between intra-vesical pressure (IBP) and upper intra-peritoneal pressure (UIAP) measurements – showing poor agreement between the two
210
6
6.7 Bland and Altman Plot of agreement between lower (LIAP) and upper intra-peritoneal pressure (UIAP) measurements – showing poor agreement between the two
211
11
Chapter 1
Introduction
12
1 Introduction
1.1 What is Intra-abdominal Pressure?
The term intra-abdominal pressure (IAP) refers to the dynamic pressure generated within the
closed compartment of the abdomen and pelvis, and is a function of the interaction between the
pressure exerted by the abdominal contents and the mechanical properties of the abdominal wall
itself. The contents of the abdomen can be divided into those which are absolute, i.e. the
minimum volume occupied by the abdominal viscera and associated tissues and those which are
variable – by either gaseous distension or the accumulation of fluid in the form of visceral
oedema, ileus or ascites. It is alterations in these variable components, acting against the semi-
rigid constraints of the abdominal wall (the compliance of which may vary with pathology), which
leads to the problem of an acute rise in intra-abdominal pressure during a critical illness.
The concept of the anatomical compartment is well-established in terms of intracranial[1] and
muscle compartment monitoring[2]. Here, an increase in the volume of the compartment
contents results in a measurable increase in intra-compartmental pressure, which can lead to
damage to the organs of the compartment. The situation is relatively straightforward in these
cases because the compartment walls, bone in the case of the skull and rigid fascia in the case of
muscle compartments, represent a fixed and non-distensible vessel. An expansion within the
contents can lead to a reduction in blood flow and a direct pressure effect within the compartment
which is both clinically evident, in terms of reducing conscious level or limb pain and measurable
using intracranial or intra-fascial pressure transducers. The magnitude, and rate of pressure
change are important however and chronic conditions such as hydrocephalus[3], benign
intracranial hypertension[4] and chronic compartment syndrome of the limbs[5] are well described
13
and associated with less physiological upset. In this setting however it is normally easy to
differentiate between acute and chronic onset compartment syndromes.
The situation within the abdomen is similar in some respects but rather more complex.
The abdominal compartment is enclosed by both non-distensible (the bony pelvis, the posterior
wall and the intra-thoracic portion) and distensible (the lateral and anterior abdominal wall)
components, the contents of which are homogenous and contain fluid, gas and the abdominal
viscera (including the retroperitoneal structures). End organ function in this context is much more
difficult to define and elevated pressures can have variable effects on the cardiovascular,
respiratory, renal, G. I. and endocrine systems, along with transmitted pressure effects on the
respiratory and central nervous systems[6]. In this context the various organ systems, although
all demonstrably affected by raised intra-abdominal pressure, vary in their actual susceptibility
and defining critical levels for each system is difficult - especially so as damage may result from
direct pressure effects, indirect effects such as release of endotoxins or a combination of both[7].
Causes of raised intra-abdominal pressure are Catholic, and have been categorised as being
either primary (associated with injury or disease in the abdominopelvic region), secondary
(associated with conditions that do not originate from the abdomen such as sepsis, burns and
massive fluid resuscitation) and tertiary, or recurrent (ACS developing after treatment for primary
or secondary ACS)[8]. As such, individual causes are in no way confined to surgical or traumatic
injuries and diseases, so practically all critically ill patients remain at risk of developing this
condition.
In common with the other compartment syndromes a chronic form of the abdominal condition
exists and has been described in cases of morbid obesity[9] and ascites[10]
14
For these reasons, cause and effect have been difficult to separate[11], and defining threshold
values for abdominal pressure which impact on organ function has remained contentious for
several decades and only as recently as 2006 have standardised consensus definitions been
agreed[12]. Whilst there remains a lack of absolute consensus throughout the medical
community that raised intra-abdominal pressure represents a distinct clinical entity that requires
treatment, however there is a general acceptance that the phenomenon exists and that in some
patients, its treatment may be beneficial.
15
1.2 Historical Background.
Mention of intra-abdominal pressure has been noted as early as the middle of the 19th century.
The earliest references refer to the normal physiological changes in abdominal pressure related
to respiration and pregnancy but, according to the historical summary of a 1911 publication in the
Archives of Internal Medicine[13], a German named Wendt[14] in 1873, was the first to consider
the effects of raised abdominal pressure on organ function and noted a deterioration in urinary
output.
Emerson, went on to describe a series of elaborate physiological experiments involving the effect
of induced abdominal compartment syndrome on the organ systems of various mammals and
specifically considered effects on the cardiovascular and respiratory systems. The conclusion of
these experiments, namely that “excessive pressure artificially produced within the peritoneal
cavity, causes death from cardiac failure…” was one of the first to describe a clear link between
mortality and intra-abdominal pressure and has since been confirmed by numerous modern
studies[15-17].
Abdominal Compartment Syndrome as a surgical entity, was first noted by military surgeons, and
Gross in 1940, was reported as describing a “…continual battle, often somewhat brutal, while try
to pack intestinal loops into a cavity which was too small to receive them”. He went on to
associate this situation with respiratory failure, impaired venous return and intestinal
obstruction[18]. In the same year, a British Surgeon named Ogilvie, was the first to describe the
use of a laparostomy (leaving the abdomen open with a temporary dressing) following traumatic
wounds with subsequent skin grafting[19].
16
In the context of more elective surgery, Baggot, an Irish anaesthetist, in 1951 reported a high
mortality rate associated with cases of abdominal closure performed under great tension[20]. He
described both paediatric and adult cases but concluded that the underlying problem was an
excess of air trapped in the peritoneal cavity at the time of closure. He did, however, suggest that
the condition could be avoided by leaving the abdomen open.
The modern term of abdominal compartment syndrome, in the majority of recent review articles,
is most commonly attributed to Kron[6] and his colleagues in Charlottesville, Virginia in the 1980s.
In fact his paper, “The measurement of intra-abdominal pressure as a criterion for re-exploration”,
makes no mention of the term, although it is the first modern clinical paper to link oliguria in post-
operative patients with IAPs of >30 mmHg.
Abdominal compartment syndrome as a term, actually seems to have first been used by
Fietsam[21] who described a series of four cases of abdominal aortic aneurysm repair
complicated by an “intra-abdominal compartment syndrome”. All four cases had received
massive fluid resuscitation (more than 25 L of crystalloid) and the raised intra-abdominal pressure
was attributed to interstitial and retroperitoneal swelling with no evidence of active bleeding.
In 1984 Kron had described a series of 11 postoperative patients undergoing an acute elevation
of intra-abdominal pressure (above 30 mm Hg)[22]. This was the first modern description of the
measurement of intra-abdominal pressure via a transvesical route and built-on his previous
laboratory research showing that raised intra-abdominal pressure in dogs resulted in a significant
reduction in glomerular filtration rate[23].
In this clinical series an abdominal pressure of greater than 25 mmHg was considered criteria for
re-exploration of the abdomen. Seven patients underwent re-exploration for either haemostasis
or evacuation of blood clot and all displayed an improved diuresis postoperatively. Four patients
17
with an intra-abdominal pressure of greater than 25 mmHg who did not go undergo exploration
died.
This is a landmark paper, in that it described the first surgical intervention for abdominal
compartment syndrome showing an improved clinical outcome, and identified the correct
underlying mechanism for the improvement in respiratory function reported by Baggot in 1951 in
patients with open abdomens[20].
Since the 1990s more confirmation of the deleterious effects of raised intra-abdominal pressure
has appeared, both within the clinical setting and in various animal models. As interest and
acceptance of the concept grew, the number of studies considering the incidence, prevalence
and specific effects on organ function has also increased exponentially[24]. These, more recent
studies, will be discussed in context later in this chapter.
18
1.3 Definitions and Terminology
The study of raised intra-abdominal pressure has been hampered by many factors, some of
which will be expanded upon elsewhere in this thesis. One of the main problems has been a lack
of continuity in terminology between various reporters, and it was only within the last decade
(2004) that the initial consensus definitions were produced at the inaugural meeting of the World
Society of the Abdominal Compartment Syndrome (WSACS)[8]. The final versions of these
definitions were eventually agreed and published in 2006 [12]. It is these definitions that will be
used throughout the text of the thesis and a summary of the important terminology is provided in
the table below.
Normal intra-abdominal Pressure
Normal intra-abdominal pressure within healthy individuals is difficult to define with certainty, as
even indirect measurements of abdominal pressure are invasive to some degree. Only two
studies to consider the intra-abdominal pressure in normal, healthy humans appear to have been
performed[25, 26].
In the first, the investigators recruited 20 healthy subjects between the age of 18 and 30 years
(mean 22.7 years) with a BMI less than 30, and measured intra-abdominal pressure indirectly via
the urinary bladder. The mean pressure whilst supine and relaxed was 1.8 mm Hg (SD 2.2) and
this rose to 20 mm Hg on standing (highlighting the importance of posture on IAP measurement –
presumably due to a shift in the vertical weight of the abdominal organs on the bladder). The
investigators went on to study the effect of 13 physical manoeuvres on intra-abdominal pressure.
Interestingly, coughing and jumping lead to a far greater increase than performing abdominal
crunches or weightlifting.
A larger study was performed by an Egyptian group, to consider the effect of straining on the
perineal muscles. Here, 46 healthy volunteers with an age range of 28 to 32 years (mean 30.4
19
years) were studied and intra-abdominal pressure was measured via a rectal transducer. In this
study mean rectal pressure was found to be 7.2 cm H2O (SD 1.2) – equating to 5.3 mmHg. The
role of rectal pressure in the assessment of intra-abdominal pressure is less well-established
however, and really the only validation study for the technique comes from the same group[27].
In this study the authors compare rectal pressure to intra-abdominal pressure measured directly
by the insertion of a veress needle into the peritoneal cavity. Thirty subjects were recruited, only
11 were normal individuals, the remainder having some form of intra-abdominal pathology. The
validity of generalising from rectal pressure to intra-abdominal pressure has not been clearly
established.
A third study aspiring to address the question “What is normal intra-abdominal pressure” was
published in 2001, but this considered patients already hospitalised rather than healthy
volunteers[28]. In this study of 77 patients (mean age 67.7) mean intra-abdominal pressure was
6.5 mm Hg (range 0.2 to 16.2 mm Hg) and was found to be positively correlated to both Body
Mass Index and recent abdominal surgery. This, of course, represents a small epidemiological
study considering the incidence and associations of IAP within the general hospitalised
population rather than useful information on the normal value.
Beyond these three human studies data on normal values has been derived from animal
experiments. Perhaps the most extensive, yet historical study to address the issue of normal
intra-abdominal pressure was performed in 1911. Several species were examined with
individuals ranging from “feeble and emaciated” to “unusually muscular” cats. The author found
that the resting intra-abdominal pressure for small dogs was sub-atmospheric (-4cm H2O), cats
around 1 cm H2O and rabbits 2.5 cm H2O. The absolute values mean very little in the human
20
context but the variation between species is interesting and may represent actual
anthropomorphic differences, or perhaps just measurement artefact.
From a practical point of view, the consensus definitions produced by the World Society for the
Abdominal Compartment Syndrome suggest that “ intra-abdominal pressures greater than 12
mmHg (measured in a supine position) may exert adverse physiological sequalae[8]” and 5-7
mmHg is suggested as a normal value in critically ill adults[12].
21
Raised Intra-abdominal Pressure
The concept that pressures greater than 12 mm Hg are associated with impaired organ function
and poor outcome is based on systematic review of various reports, and the consensus opinion of
an assembled panel of experts[8]. Table 1.1. The obvious difficulty arises in that a true
randomised controlled trial based on human subjects is not possible, and so conclusions are
based on a series of observational human studies, where cause and effect is notoriously difficult
to ascribe, and animal studies which inevitably are contrived with artificially accomplished acute
rises in abdominal pressure or induced pathological states such as hypovolaemia and
septicaemia.
From a practical point of view, although artificial critical levels have been created, the problem of
elevated intra-abdominal pressure should be considered as a continuous spectrum and the
presence or absence of co-morbid conditions may well lower or raise the critical thresholds for
physiological upset in individual cases. Perhaps absolute values are of less importance
compared to firstly, a low threshold for suspicion of the condition and secondly a sensible
approach to the screening and monitoring the evolving trend of pressures in high risk patients –
with timely intervention in order to protect organ function.
22
Table 1.1. WSACS Consensus Definitions
Term Final Definition (2007) IAP The steady-state pressure concealed within the
abdominal cavity. IAP should be expressed in mmHg and measured at end expiration in the completely supine position.
Abdominal Perfusion Pressure Mean arterial pressure minus intra-abdominal pressure
Indirect IAP Measurement The reference standard for intermittent IAP measurement is via the bladder with a maximal installation volume of 25 ml of sterile saline
Normal IAP Normal IAP is approximately 5 to 7 mmHg in critically ill adults
Intra-Abdominal Hypertension IAH is defined by a sustained or repeated pathologic elevation of IAP greater than 12 mmHg
IAH Grading Grade 1: IAP 12 to 15 mmHg Grade 2: IAP 16 to 20 mmHg Grade 3: IAP 21 to 25 mmHg Grade 4: IAP greater than 25 mmHg
Abdominal Compartment Syndrome ACS is defined as a sustained IAP greater than 20 mmHg (with or without an abdominal perfusion pressure less than 60 mmHg) that is associated with new organ failure or dysfunction
Chronic IAH IAH lasting months or years (2005 definitions) Acute IAH IAH developing within hours (2005 definitions) Subacute IAH IAH developing within days (2005 definitions) Hyperacute IAH IAH that only lasts for seconds or minutes (2005
definitions) Primary ACS A condition associated with injury or disease in the
abdomino-pelvic region are frequently requires early surgical or radiological intervention
Secondary ACS ACS secondary to conditions that do not originate from the abdomino-pelvic region
Recurrent ACS ACS redeveloping following previous surgical or medical treatment of primary or secondary ACS
Indication for IAP Monitoring 1) if two or more risk factors for IAH/ACS present, baseline IAP measurement should be obtained and
2) if IAH is present, serial IAP measurements should be performed throughout the patient's critical illness
IAP Measurement Studies should adopt the standardised IAP measurement method recommended by the consensus definitions or provide sufficient detail of the technique utilised to allow accurate interpretation of the IAP data presented
Epidemiology Incidence and prevalence estimates of IAH/ACS should be based upon the consensus definitions and mean, median and maximal IAP values should be provided both on admission and during the study period
23
Medical treatment of IAH/ACS APP should be maintained above 50 to 60 mmHg in patients with IAH/ACS. As no prospective trials have yet been performed evaluating the benefits and risks of sedation and analgesia, no recommendations can be made. A brief trial of neuromuscular blockade may be considered in selected patients with mild to moderate IAH while other interventions performed to reduce IAP. The potential contribution of body position in elevating IAP should be considered in patients with moderate to severe IAH or ACS. No prospective trials have been performed to confirm the benefits of nasogastric/colonic decompression and prokinetic motility agents so no recommendations can be made at this time.
Temporary Abdominal Closure (TAC) Surgical decompression should be performed in patients with ACS that is refractory to other treatment options and presumptive decompression should be considered at the time of laparotomy in patients who demonstrate multiple risk factors for IAH/ACS. Recommendation for the type of temporary abdominal closure cannot be made at this time.
The data contained in this table is a direct summary of selected definitions presented in 2006 by the expert
working party of the World Society of the Abdominal Compartment Syndrome[12].
24
1.4 Epidemiology of Intra-Abdominal Hypertension & the Abdominal Compartment
Syndrome
Several factors have hampered the clear definition of the extent of the problems caused by raised
intra-abdominal pressure.
Firstly, as mentioned above and probably most importantly, a previous lack of a consensus
definition for the use of the terms “Intra-abdominal Hypertension” and the “Abdominal
Compartment Syndrome” has made it very difficult to compare the epidemiological data
presented in previous studies. The consensus definitions presented in 2006[12], provided they
are adhered to, will go some way to overcoming this problem in future studies.
Beyond the variable definitions and use of terminology the multitude of causes of raised IAP has
also presented difficulty, with different rates observed depending of the sub-group of patients
studied.
In general – the published literature considering the incidence and prevalence of intra-abdominal
hypertension and the abdominal compartment syndrome is challenging to interpret, as there is
great variation in the diagnostic criteria reported. This has improved somewhat subsequent to the
2006 consensus definitions[12] and only studies complying to the WSACS criteria are outlined in
detail below.
One of the earliest studies designed with the express aim of identifying the prevalence of raised
intra-abdominal pressure within a general Intensive Care Unit population was conducted in 2004
[29]. This was a multi-centre trial involving 13 ICUs across Europe, Australia, Israel and South
America. A total of 97 patients were studied and intra-abdominal pressure was measured every 6
hours for a 24 hour period using a “direct needle puncture technique[30]” (described in detail in
the next section) to assess intravesical pressure. The researchers found that the mean IAP was
25
9.8mmHg and that the overall prevalence of IAH (defined as IAP > 12mmHg) was 52%. The
prevalence of ACS (IAP > 20mmHg with organ dysfunction) was 8%. The overall figures included
both medical (59%) and surgical (41%) patients and sub-group analysis showed a higher
prevalence in the surgical group (65% vs 54.4%). This important study would therefore suggest
that around half of the patients admitted to a general ITU could be expected to have a
significantly elevated intra-abdominal pressure (IAH) and that just fewer than 1 in 10 will have the
abdominal compartment syndrome.
The same group conducted a longer-term follow-up study a year later[31] to consider the
admission characteristics of intensive care patients. This study looked at 265 consecutive ICU
admissions over a 4 week period. The mean IAP was found to be 10 mmHg (+/- 4.8) with the
prevalence on the day of admission for IAH of 32% and for ACS of 4.2%. The conclusion of the
original paper noted that the cumulative incidence of IAH was high, but the actual value was not
provided in the text of the report. A subsequent review by the same authors reported that the
cumulative incidence of IAH after 1 week was 57%[32], suggesting that around a quarter of
admissions can be expected to develop IAH subsequent to the first 24 hours of measurement.
This finding has subsequently been replicated in a single centre Argentinean study of 83 mixed
critical care patients. Of the cohort, 31% met diagnostic criteria for IAH at the time of admission
and a further 33% subsequently during their ITU stay. The cumulative incidence of ACS in this
study was 12%[33].
Further contemporary evidence of the frequency of the diagnosis is provided by a study of 100
general ITU patients revealing an incidence of IAH of 42% and ACS of 4%[34]. A more focussed
study of just medical ITU patients who were deemed at “high risk” of IAH showed an incidence of
68% for IAH, though no cases of ACS[35]. Unfortunately, this study is significantly weakened by
26
the fact that they did not expand on the baseline IAP of the majority of admissions during the
study period who were not considered “high risk” for IAH.
In addition to these studies of general ITU populations, further research to consider the incidence
within specific sub-groups of patients with specific underlying diagnoses has been undertaken.
The incidence of raised IAP varies amongst the various sub-groups, however a significant burden
of IAH has been described for virtually all diagnoses. Severe acute pancreatitis has been shown
to carry an incidence of IAH of 40 – 60% and ACS of 10 – 56%[36, 37]. Septic shock would
appear to carry a particularly high risk of 83% IAH overall (93% in surgical patients and 73% in
medical), in a study of 81 patients[38].
Although not specifically designed as epidemiological studies, a significant prevalence and
cumulative incidence has also been reported within further specific sub-groups, all of which are
known to be at particularly high risk of developing elevated IAP. These studies can be roughly
divided as considering patients following trauma, major abdominal surgery and burns - the results
are summarised below. Table 1.2. It is apparent that the lack of uniformity in defining the end-
points of IAH and ACS prevent a meaningful combination of these studies, however each may be
evaluated on it’s own merits.
27
Table 1.2. Summary of Studies Looking at the Incidence / Prevalence of IAH
Author Year Country Sub-Group n Definition Incidence (%)
Meldrum[39] 1997 USA Trauma 145 > 20 mmHg + Organ
Dysfunction
14
Ivatury[40] 1998 USA Trauma 70 > 25 mmHg 32.9 Maxwell[41] 1999 USA Trauma 1216 Laparostomy 0.5
Balogh[47] 2003 USA Trauma 156 IAH > 20 mmHg ACS > 25 mmHg + Organ Dysfunction
IAH 32 ACS 12.8
Balogh[48] 2003 USA Trauma 188 ACS > 25 mmHg + Organ Dysfunction
14
Sugrue[49] 1995 Australia Abd Surgery 88 > 20 mmHg 33 Sugrue[50] 1996 Australia Abd Surgery 73 > 20 mmHg 38.4 Sugrue[51] 1999 Australia Abd Surgery 263 > 18 mmHg 40.7
Despite a disappointing response rate in the anaesthetic arm the survey accrued a total of 354
responses, making it the largest UK survey on ACS, the third largest worldwide and the only
survey to directly compare responses from general surgeons and anaesthetists.
This survey was the first to ask directly whether respondents actually believed that ACS exists as
a diagnostic entity and it was reassuring that 90% felt that it did. This figure was broadly in
keeping with previous surveys, from the UK and elsewhere, that have asked whether
respondents had previously diagnosed ACS and for which responses ranged from 84 – 98%[145,
146, 149, 150]. Likewise, the number of cases reported as being treated within the last twelve
months was consistent from results from these other surveys, which had been published over the
last decade.
An interesting observation was that the vast majority of consultants across both specialties who
had been appointed in the last decade agreed that ACS exists and only three anaesthetists, who
did not work in ITU, felt that it did not. This may represent the more recent interest in the topic
and the fact that teaching on IAP and the ACS is gradually finding its way into many training
programmes. It was also interesting to see that overall, there appeared to be a large difference
between anaesthetists working in ITU and those who did not, where the rate for those believing in
ACS as a real clinical entity was 76 vs 99%. This may reflect the diverse range of clinical
interests amongst anaesthetic consultants and the fact that a significant proportion of those not
involved with intensive care sessions, may not come into routine contact with critically unwell
patients.
The threshold pressure for the diagnosis of ACS was highly variable in the previously reported
literature. Despite the wide dissemination of consensus definitions[152] and their subsequent
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incorporation in many of the subsequent contemporary review articles[153-158], it was surprising
that this survey again revealed a wide variation in perceived thresholds that do not seem to have
been refined by the consensus publication. It would seem therefore that whereas awareness of
ACS as a diagnosis is increasing, factual knowledge of the topic may not be. More specifically –
the finding that more than a quarter of all respondents (27% surgeons and 30% anaesthetists)
believed that an IAP in excess of 30 mmHg was required for a diagnosis of ACS is a genuine
cause for concern. The implication being that potentially lifesaving abdominal decompressions
are being delayed and intra-abdominal pressures are being allowed to rise to levels far higher
than desirable. Clearly continued and focussed education as to the internationally agreed criteria
for diagnosis needs to be pursued further and incorporation of knowledge of the ACS and its
limits for treatment should form a core part of surgical and anaesthetic training in the UK.
Perhaps also there is a need for more simple core definitions for diagnosis and guidelines for
management.
More reassuringly, it was encouraging to see what appears to be a modest improvement in the
routine measurement of IAP from 0 – 6% in previous studies[146, 148, 149] to an overall level of
9% in this survey. A further 68% of respondents reported that IAP was measured selectively in
their practice – usually on the basis of clinical suspicion of ACS or a clinical deterioration.
Patients may benefit from a more proactive approach to the measurement of IAP and practice
may well be positively influenced if a fast, economical and reliable technique for measurement
could be established and perhaps a robust protocol for screening, which could be tailored to
specific patient groups based on more detailed epidemiological data.
Where an ACS has been identified on the basis of pressure measurement within the context of
worsening organ failure, most cases will require surgical decompression by way of a
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laparostomy[152]. Whilst the reported experience of laparostomy in this series is equivalent with
previous studies, it falls far short of what could be expected from the previous finding that 8% of
all ITU patients (medical or surgical) will have an intra-abdominal pressure greater than 20 mmHg
at any point in time[159] – whether this reflects inaccuracies in measurement or a reluctance to
act on apparent results remains unclear. The anecdotally perceived battle between intensivists
and surgeons to achieve decompression is supported by the report of a “surgical reluctance” to
perform a laparostomy amongst 42% of anaesthetic respondents, although this apparent
discrepancy was not borne out by any discernable difference between surgeons and
anaesthetists in terms of actual attitudes and practice. Interestingly, the only significant
difference between intra-operative factors perceived as being important to make laparostomy
more likely, was a higher ranking of a subjectively “tight closure” amongst anaesthetists, despite
good evidence demonstrating that clinical examination is of no benefit in discerning elevated
IAP[160, 161]. There is, of course the possibility that the “perceived tight closure” by
anaesthetists is educated by an “observed and measured” increase in ventillatory pressures or
haemodynamic parameters that may not necessarily be readily accessible to the surgeon.
It was positive to see very little variation in the rankings of the various intraoperative and
postoperative factors making formation of a laparostomy more likely. Of course, all of these
factors are associated with elevated IAP and there was very little variation in the importance
afforded to each factor and also between groups of respondent. Whilst the actual rank orders for
the postoperative factors included from Mayberry’s original survey (a decade earlier) were fairly
consistent amongst our contemporary series, there was an interesting difference in ordering of
the intra-operative factors between the surgeons and anaesthetists. Anaesthetists ranked the
“surgical factors” of a planned second look, a subjectively tight closure and degree of peritoneal
contamination highest, whereas the surgeons ranked the more “critical care based” factors of
pulmonary and cardiovascular instability the highest. Table 2.8.
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The survey has undoubtedly suffered from some bias introduced by the response rate and the
failure to collect data on the type of institution worked at was a missed opportunity to determine
whether any difference in practice exists between teaching hospital and DGH practice (though
this itself may be further confounded by a possible difference in case mix between the two types
of institution). It is possible that the lower anaesthetic response rate might reflect the fact that it
was not possible to separate those anaesthetists involved in ITU work from those with no role in
postoperative care and there may have been some element of self-selection based on this
distinction in anaesthetists who did choose to respond to the survey.
2.5 Summary and Conclusions
Whilst there does seem to be some improvement in awareness of ACS, willingness to measure
IAP and knowledge of factors predisposing to elevated IAP amongst younger generations of
consultants, there is still a significant knowledge gap of the threshold levels of IAP associated
with the diagnosis of IAH and ACS.
Continued education as to these threshold values is needed - possibly with clearer guidelines and
definitions. Clinical care may be improved by the development of a fast, cheap, safe and reliable
measurement system and either routine measurement of IAP or else evidence based screening
protocols.
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Chapter 3
In-vitro and In-vivo Evaluation of the Foley Manometer Device for
the Measurement of Intra-abdominal Pressure
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3.1 Introduction – Techniques available for the Measurement of Intra-abdominal
Pressure
Studies have shown that neither clinical examination nor measurement of the abdominal
perimeter, are precise in the diagnosis of raised intra-abdominal pressure[42, 60]. Some form of
objective measurement device is clearly required, especially if effective definitions and clinical
management guidelines are to be developed and instigated. As with other systems for
measurement of physiological parameters in clinical practice, certain characteristics are highly
desirable in order to optimise uptake and ensure accurate data acquisition. Such characteristics
are outlined in Table 3.1, and will be discussed in the context of the various methods that have
been described for the measurement of intra-abdominal pressure (See Chapter 1.5) and which
are currently available for clinical use.
Table 3.1.
Ideal characteristics for a system to measure IAP
Ideal Characteristics for a System to Measure Intra-abdominal Pressure
Safe – for patient and operator
Reliable (Reproducible)
Valid (Accurate & Precise)
Simple
Fast
Cost effective
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Techniques for the Measurement of Intravesical (Urinary Bladder) Pressure
As outlined in chapter 1, the indirect measurement of IAP by via the urinary bladder remains the
commonest approach in both clinical and research settings. Various techniques exist to achieve
this measurement, all of which involve the instillation of some fluid (urine or external fluid) into the
bladder followed by electronic or mechanical measurement of pressure. This thesis deals solely
with measurement of IAP within an adult population and details of the various available
techniques are outline below. The various potential sources for error with each of the techniques,
such as volume or temperature of bladder instillate along with the effects of body positioning are
discussed in detail in chapter 4.
Direct Needle-Puncture Systems – Kron[22] & Cheatham[30]
Kron’s 1984 publication entitled “The measurement of intra-abdominal pressure as a criterion for
abdominal re-exploration” was the first to describe the popular direct needle puncture technique
for the measurement of IAP. The system was easily assembled from minor consumables that are
commonly available on the intensive care unit and has subsequently been shown in multiple trials
to be reliable and valid, probably becoming the commonest technique for the adhoc
measurement of IAP. The main drawback of the system is that it requires a separate needle
puncture of the urinary collection system for each pressure measurement, with each episode
carrying the potential for the introduction of urinary tract infection and the possibility of needle
stick injury to the operator. Although the system is simple to assemble, repeated measurements
are time consuming.
The system was modified by Cheatham in 1998[30] with replacement of the hypodermic needle
with the plastic sheath of an intravenous catheter. This sheath could be left in position, which
made subsequent pressure measurements faster to obtain, but the system still had the important
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drawbacks of the risk of needle stick injury, the fact that the sheath could easily be dislodged and
the potential for the introduction of infection. The modified technique however, remained cost
effective and safer than the original Kron technique.
Malbrain System for Continuous Monitoring[68]
To overcome these important safety issues, Malbrain in 2004, described a system whereby a
series of three-way taps was connected between the urinary catheter and collection system. This
allowed for the addition of bladder instillate via a connected syringe and the transduction of
intravesical pressure. The system was validated by Malbrain's original study, but not
subsequently. Again the components are relatively cheap and available on the majority of
intensive care units, however the set-up is slightly more complicated and requires specific
training.
Ab-Viser System
This constitutes a commercially produced system for the measurement of intravesical pressure
and is produced by Wolfe Tory (Salt Lake City, Utah, USA). The equipment is a more refined
version of Malbrain’s concept and is supplied as a relatively straightforward package which
connects between the patient’s urinary catheter and collection bag and permits the unimpeded
flow of urine between measurements, which are gathered via a standard transducer. The inter
and intra-observer variability produced by the system have been tested and found to be low with
reported Pearson’s correlation coefficients of 0.93 and 0.95 respectively [162]. The major
disadvantages being that the system is fairly elaborate and costly and, in addition to the
componentry supplied, it also requires an electronic transducer, which further adds to costs.
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Direct Urinary Manometry
Direct urine manometry carries the inherent advantage of simplicity and eliminates a potential
stage for the introduction of error, by doing away with the requirement for electronic transduction
devices. The pressure measured by such a system would be in cm of urine, however by
recalibration of the manometer tubing it is possible to convert the column of urine to mmHg
equivalent. A commercially produced system is available, which is relatively cheap and allows for
simple and rapid measurement of intra-abdominal pressure (FoleyManometer, Holtech Medical,
Denmark). The reliability and validity of this system has been tested previously in vitro, and found
to be good[163]. The only potential drawback of this system is a theoretical increase in risk of
urinary tract infection associated with the drainage of urine, trapped within the closed collection
system, back into the patient's bladder. This risk has been reported in only one clinical
paper[164] and the complication has never been described in relation to the measurement of
intra-abdominal pressure by this method. The commercially available device results in the return
of only a very small volume of urine with each pressure measurement (<10ml), which then drains
again from the bladder rapidly after measurement is complete.
This system represents our own method of choice for the measurement of intra-abdominal
pressure at the host institution, and this chapter describes a full clinical evaluation of the Holtech
system, with both in-vitro testing and in-vivo comparisons to the AbViser device and directly
transduced intraperitoneal pressure. Potential pitfalls of the device are also described.
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Techniques for the Measurement of Intra-Gastric Pressure
Gastric Balloon Tipped Catheter Systems
Air or fluid filled gastric balloon systems are commercially available for the measurement of intra-
gastric pressure. Once in position, the systems are simple and quick to use, however the
drawbacks are the expense of the consumables and also the requirement for a dedicated monitor
and software system.
Direct Gastric Manometry
Some enthusiasts have reported success with fluid manometry performed via a nasogastric
tube[69, 71], with close correlation to intravesical pressure. The key to success however, is
ensuring that the stomach is completely empty of all gas prior to the instillation of the fluid
required to make the pressure measurement. Such a requirement inevitably interferes with
nasogastric feeding regimens to a degree dependant on the frequency of pressure
measurements and may also require the placement of a second nasogastric tube, with the
accompanying risks and discomfort. Finally, the agreement between intra-gastric pressure and
intra-vesical or directly transduced intra-peritoneal pressure is yet to be categorically proven.
This manoeuvre is therefore both extremely time-consuming and difficult to verify, meaning that
the reliability of the technique outside of the two reported papers is difficult to ensure.
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Techniques for the Direct Measurement of Intra-peritoneal Pressure
Direct Intra-peritoneal Systems
A group from Israel have reported some success with the direct measurement of intraperitoneal
pressure via a PVC surgical drain. Both papers presented by the group involve the same patient
cohort and correlated the pressure transduced via a surgical drain against that measured by a
laparoscopic insufflator and by a transvesical technique respectively[165, 166]. Unfortunately the
statistical analysis of the papers is not robust, and is limited to simple correlation between the two
measurement techniques. Given that the correlation was between two different techniques for
measuring the same value (IAP), the correlation coefficient reported was excellent. This does
not, of course, provide any measure of the bias or agreement between the two measurement
methods and as such, the data presented is of very limited value.
A near identical technique for the direct transduction of intra-abdominal pressure via a surgical
drain was developed in the host institution during the work leading to this thesis, and the resulting
data is discussed in more detail elsewhere in this chapter.
A major limitation of this technique is of course, the requirement of an indwelling intra-peritoneal
drainage catheter and it is therefore limited, to all extents and purposes, to postoperative surgical
patients.
The relative merits of each of these techniques, in terms of the ideal characteristics are
summarised in Table 3.2.
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Table 3.2.
Summary of the relative merits for various techniques used for the measurement of IAP
Safe Reliable Valid Simple Fast Economical Direct Needle Puncture (After Kron[22])
No Yes Yes Yes No Yes
Modified Kron Technique (Cheatham[30])
No Yes Yes Yes Yes Yes
Malbrain System for Continuous Monitoring[68]
Yes Yes Yes No Yes Yes
Ab-Viser Device[162]
Yes Yes Yes Yes Yes No
Foley Manometer[163]
Yes Yes Yes Yes Yes Yes
Gastric Balloon Tipped Catheter Systems[66]
Yes Yes Yes Yes Yes No
NG Tube Manometry[69]
Yes No No Yes No Yes
Direct Intra-peritoneal Catheter Systems[165, 166]
Possibly Not
Yes Yes No Yes Yes
Clinical Evaluation of 3 Systems Used for the Measurement of IAP
The host institution utilised a commercially available Foley catheter manometer
(FoleyManometer) for the measurement of intra-abdominal pressure. It was felt that, in line with
the recommendations provided by the world society of the abdominal compartment syndrome[72]
and previous research in the field[52, 77], the patients of the Liver Intensive Therapy Unit were at
particularly high risk of developing raised intra-abdominal pressure. As such, the unit wished to
promote the use of a simple and safe device, which could be used to monitor the intra-abdominal
pressure of all patients admitted to the unit. The foley manometer was felt to provide such
characteristics and was therefore adopted as the instrument of choice. The only previously
published data relating to this device is an in-vitro evaluation of its reliability and validity[163]. A
full clinical evaluation to check the validity of its measurement of both intra-vesical and intra-
abdominal pressure has not yet been performed. The remainder of this chapter therefore
106
addresses this problem, in three parts. Firstly a repeated in vitro evaluation is reported in order to
determine the reliability and validity of measurements made with the device. The Foley
Manometer is then evaluated clinically by comparing its performance to directly transduced
measures of intra-peritoneal pressure and also to the other main commercially produced device
for measurement of intravesical pressure – the AbViser. Finally, potential pitfalls of the device
are described.
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3.2 In-vitro Evaluation of the Foley Manometer
Introduction
The Foley Manometer is a commercially produced water (urine) manometer which attaches
between the patient’s urinary catheter and the urine collection / measurement system. The
system permits free flow of urine to the collection bag between measurements and has a
calibrated scale to allow estimation of intravesical pressure by examination of a continuous
standing column of fluid from the bladder to the device. Figure 3.1.
Figure 3.1.
Set-up and use of the FoleyManometer system to measure IAP (reproduced with
permission of Holtech Ltd, Denmark)
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A previous in-vitro analysis, which was performed around the same time as our own experiments,
has subsequently been published and has shown the device to be reliable and accurate[163]. In
this study, 15 observers (a mixture of nurses, doctors and medical students) were asked to
measure the pressure displayed by a Foley Manometer that had been connected to a standing
column of water in a plastic 3L cylinder. The measured values were compared to those obtained
from electronically transduced air filled balloon tip catheters mounted in the same device. The
bias was found to be just 0.5mmHg, with excellent limits of agreement suggesting that the device
was as accurate as the more expensive electronic systems.
Methods
An in-vitro testing system was assembled, which comprised of a Foley Manometer device set
within a 2L plastic cylinder, on which a calibrated scale was applied to convert cmH20 to mmHg.
The cylinder was filled to a set pressure (18 mmHg) and shielded behind a screen on which the
instructions for use supplied by the device’s manufacturer were mounted. Figure 3.2. & 3.3. A
block was mounted in front of the screen corresponding to the zero-reference point for the device
and this was labelled “symphysis pubis”.
A total of 40 subjects (all qualified intensive care nurses) were asked to measure the mock intra-
abdominal pressure using the experimental apparatus. Each were given the same verbal
introduction “Please read the printed instructions for the use of this device designed for the
measurement of intra-abdominal pressure and then use the apparatus to record the simulated
pressure. This is the simulated symphysis pubis to be used.” No further assistance or
instructions were given and the first response was recorded. 20 of the subjects worked in the
liver intensive care unit and were therefore familiar with the device, which had been in standard
use in that unit for around 12 months. The other 20 subjects worked in the general intensive care
109
unit of the same hospital, where IAH was not routinely measured. None of the general ITU
nurses had any prior experience of the Foley Manometer device.
Statistical Analysis
Reported IAP was collected in an excel spreadsheet (Microsoft, Washington, USA) and analysed
using SPSS (IBM, Chicago, USA).
Means were compared by way of a t test and bias / agreement, by way of Bland and Altman
analysis in line with recommendations for analysis from WSACS[141] which were described in
detail in Chapter 1.9.
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Figure 3.2.
Manufacturers instructions supplied with the Holtech FoleyManometer (reproduced with
permission)
Figure 3.3.
Experimental apparatus constructed to simulate measurement of IAP (visual screen to
shield view of the cylinder from the subject omitted for clarity)
111
Results
All 40 subjects were able to complete the measurement successfully within 2 minutes, with only
the manufacturers instructions for guidance.
There was no difference between the mean IAP reported by either group, which was 17.9 mmHg
(p = 0.496). Table 3.3. The overall bias was 0.1 mmHg with limits of agreement of 17.5 – 18.3
mmHg. Figure 3.4. In terms of clinical significance – all reported measurements were within 0.5
mmHg of the actual simulated IAP.
Table 3.3.
Results of an in-vitro study of inter-observer variability in the use of the Holtech
FoleyManometer
n Mean Measured IAP mmHg (SD)
Absolute Bias Limits of Agreement
Liver ITU Nurse 20 17.9 (0.18)
0.1 17.5 – 18.3
General ITU Nurse
20 17.9 (0.24)
0.1 17.4 – 18.4
Overall Measurements
40 17.9 (0.21)
0.1 17.5 – 18.3
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Figure 3.4.
Measured simulated IAP using Foley Manometer (actual IAP = 18 mmHg). Bland and Altman absolute bias and limits of agreement marked by horizontal lines. (Shade of circle reflects number of responses)
Number of Responses (Shade of circle reflects multiple identical responses)
113
Conclusion
The Foley Manometer is simple to use and requires minimal instruction / training for accurate
measurements. There is excellent agreement between measurements obtained by both
experienced and novice users and the device is accurate to within <0.5 mmHg.
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3.3 Comparison of the Foley Manometer to Directly Transduced Intra-peritoneal
Pressure Recordings
Introduction
Whilst the measurement of intra-vesical pressure has been established as the “gold-standard”
technique for the assessment of IAP by an international panel of experts[12], this
recommendation is based on the previously unfounded assumption that the urinary bladder would
act as a passive diaphragm for the transmission of pressure, such that the pressure within the
bladder would correspond to that outside of the organ, within the peritoneal cavity. Subsequent
to the publication of the consensus definitions, it has been shown that there is good bias and
agreement between intra-peritoneal and intravesical pressure in a porcine model[167, 168],
however this data is not yet available in human subjects.
Given the acceptance and wide reporting of intravesical pressure in the diagnosis and
management of intra-abdominal hypertension and the abdominal compartment syndrome, its face
validity would seem to be assured. To be sure of the true content validity of using the Foley
Manometer to measure the intra-peritoneal pressure, we decided that its measurements should
be formally compared to pressures that were directly transduced from catheters lying within the
peritoneal cavity itself. We had developed a technique for this manoeuvre following on from the
care of a patient who had developed signs of an abdominal compartment syndrome following a
complex colorectal resection requiring a total cystectomy. The procedure had been complicated
by an anastamotic leak and with no urinary bladder available to measure intravesical pressure,
we transduced the IAP via a column of fluid “flushed” via the surgical tube drain. This revealed a
grossly elevated IAP and subsequent decompression resulted in a dramatic clinical improvement.
A near identical technique was subsequently described in Israel and we have further refined the
115
process such that small (3mm) “micro-drains” can be used to minimise risk to the patient, as the
smaller the drain tube the smaller the “dead space” that must be routinely flushed into the
peritoneal cavity, to facilitate IAP measurement.
Patients & Methods
Following approval of the study design by the local Research Ethics and Research &
Development Committees, a total of 20 patients undergoing orthotopic transplantation of a whole
liver for non-fulminant disease were recruited and gave their consent to be studied. All data were
collected during the subject’s stay on the Liver Intensive Care Unit, with aspects of postoperative
care, such as the administration of intra-venous fluids and the use of vaso-active agents, guided
by established unit protocol and individual clinician decisions. All subjects were nursed in a 30o
head of bed position to minimise the risk of respiratory complications, with the exception of short
periods (< 5 minutes) in order to measure supine IAP and all were calm and comfortable at the
time of measurement (Richmond Agitation and Sedation Scale – RASS of 0 or less)[142].
For each patient, intra-peritoneal IAP was recorded continuously via catheters placed in the
pelvis, at the time of operation (Minivac Drain, Unomedical, Worcestershire, UK). These
catheters were connected to a standard ICU monitor (Fakuda Denshi, Tokyo, Japan) via
electronic pressure transducers and were used solely for measurement of IAP and not for
drainage. Standard closed surgical drains were placed in the usual position to prevent
accumulation of body fluids.
The transducer was mounted to the patient by sutures at a point corresponding to the internal
position of the catheter tip on the lower abdominal wall – a position that was found to correspond
to the zero-reference point suggested by the WSACS, of the midaxillary line at the iliac crest
116
when supine. The transducers were flushed and zeroed twice daily and also following each
position change. The measured dead space of the catheter was <2ml and so a 4ml flush with
normal saline, from a sterile closed system, ensured a continuous column of fluid between the
intra-peritoneal catheter tip and the transducer which was maintained between flushes by
continuous low volume irrigation. The quality of the pressure waveform was checked hourly by
the “rapid oscillation test[68]”, whereby rapid and repeated palpation of the abdominal wall at the
level of the intra-peritoneal catheter tip was visible in real-time on the ICU monitor’s pressure
trace.
The catheters were left in place for a maximum of 72 hours, or until the point of discharge from
the Liver Intensive Care Unit, whichever came sooner.
Each patient was repositioned to lie supine at 6 hourly intervals (4 times per day) in order to
measure the supine IAP. The transducers were “re-zeroed” following each position change and
the pressure allowed to equilibrate for 5 minutes, prior to making each of these recordings. At the
same time points, the intravesical pressure was monitored by means of the Foley Manometer and
paired measurements recorded at both supine and 30o head of bed angles. All patients were
passing urine at the time of the measurements and, for the Foley Manometer device, urine was
used to measure IAP with no requirement for instillation of additional fluid.
117
Statistical Analysis
The data were recorded in a Microsoft Excel Spreadsheet (Microsoft, WA, USA) and analysed
using SPSS v15 (Chicago, IL, USA) in accordance with the recommendations for data analysis
published by the World Society for the Abdominal Compartment Syndrome[141] and described in
detail in Chapter 1.9. The normality of distribution of the pressure recordings was tested using a
Kolmogorov Smirnov test and, being parametric and normally distributed, means were compared
using a paired t-test.
The bias and agreement between the indirect and direct means of measuring pressure at the
urinary bladder were calculated using the Bland and Altman technique [169]. In accordance with
these recommendations – measurements were considered equivalent when the measure bias did
not exceed 1 mmHg, the precision 2 mmHg and the limits of agreement +/- 4 mmHg.
118
Results
A total of 169 paired pressure measurements were made at supine and 30o body positions.
Table 3.4. Figures 3.5, 3.6 & 3.7.
There was no clinically relevant difference between the mean measurements made via the pelvic
transducer and the FoleyManometer. The Bland and Altman analysis confirmed excellent
agreement between the two measures in both body positions, with a calculated bias and
precision of 0.06 mmHg and 0.6 when supine and 0.01 mmHg and 0.6 at 30o.
Table 3.4.
Results of comparison of IAP measurements made using the Holtech FoleyManometer and
via direct transduction of pelvic intra-peritoneal pressure
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169. Bland JM, Altman DG: Statistical methods for assessing agreement between two methods of clinical measurement. Lancet 1986, 1(8476):307-310.
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171. Cheatham ML, De Waele JJ, De Laet I, De Keulenaer B, Widder S, Kirkpatrick AW, Cresswell AB, Malbrain M, Bodnar Z, Mejia-Mantilla JH et al: The impact of body position on intra-abdominal pressure measurement: a multicenter analysis. Critical care medicine 2009, 37(7):2187-2190.
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172. De Waele JJ, De Laet I, De Keulenaer B, Widder S, Kirkpatrick AW, Cresswell AB, Malbrain M, Bodnar Z, Mejia-Mantilla JH, Reis R et al: The effect of different reference transducer positions on intra-abdominal pressure measurement: a multicenter analysis. Intensive care medicine 2008, 34(7):1299-1303.
173. Fusco MA, Martin RS, Chang MC: Estimation of intra-abdominal pressure by bladder pressure measurement: validity and methodology. The Journal of trauma 2001, 50(2):297-302.
174. Drakulovic MB, Torres A, Bauer TT, Nicolas JM, Nogue S, Ferrer M: Supine body position as a risk factor for nosocomial pneumonia in mechanically ventilated patients: a randomised trial. Lancet 1999, 354(9193):1851-1858.
175. Vasquez DG, Berg-Copas GM, Wetta-Hall R: Influence of semi-recumbent position on intra-abdominal pressure as measured by bladder pressure. The Journal of surgical research 2007, 139(2):280-285.
176. McBeth PB, Zygun DA, Widder S, Cheatham M, Zengerink I, Glowa J, Kirkpatrick AW: Effect of patient positioning on intra-abdominal pressure monitoring. American journal of surgery 2007, 193(5):644-647; discussion 647.
177. Malbrain ML, De Laet IE, Willems A, Van Regenmortel N, Schoonheydt K, Dits H: Localised abdominal compartment syndrome: bladder-over-gastric pressure ratio (B/G ratio) as a clue to diagnosis. Acta Clin Belg 2010, 65(2):98-106.
178. Malbrain M, De Laet I: Do we need to know body anthropomorphic data whilst measuring abdominal pressure? Intensive care medicine 2010, 36(1):180 - 182.
179. Shafik A: The anterolateral abdominal wall muscles during vesical filling and evacuation: electromyographic study. Urology 2008, 71(4):621-624.
180. Hunt L, Van Luenen H, Alexandrou E, Frost SA, Davidson PM, Hillman K, D'Amours S: A comparison of fluid instillation volumes to assess intra-abdominal pressure using Kron's methods. The journal of trauma and acute care surgery 2012.
181. Malbrain ML, Deeren DH: Effect of bladder volume on measured intravesical pressure: a prospective cohort study. Critical care (London, England) 2006, 10(4):R98.
182. Chiumello D, Tallarini F, Chierichetti M, Polli F, Li Bassi G, Motta G, Azzari S, Carsenzola C, Gattinoni L: The effect of different volumes and temperatures of saline on the bladder pressure measurement in critically ill patients. Critical care (London, England) 2007, 11(4):R82.
183. Cheatham ML, Safcsak K: Is the evolving management of intra-abdominal hypertension and abdominal compartment syndrome improving survival? Critical care medicine 2010, 38(2):402-407.
184. O'Mara MS, Slater H, Goldfarb IW, Caushaj PF: A prospective, randomized evaluation of intra-abdominal pressures with crystalloid and colloid resuscitation in burn patients. The Journal of trauma 2005, 58(5):1011-1018.
185. Matuschak GM, Pinsky MR, Rogers RM: Effects of positive end-expiratory pressure on hepatic blood flow and performance. J Appl Physiol 1987, 62(4):1377-1383.
186. Inal MT, Memis D, Sezer YA, Atalay M, Karakoc A, Sut N: Effects of intra-abdominal pressure on liver function assessed with the LiMON in critically ill patients. Canadian journal of surgery 2011, 54(3):161-166.
187. Knaus WA, Draper EA, Wagner DP, Zimmerman JE: APACHE II: a severity of disease classification system. Critical care medicine 1985, 13(10):818-829.
188. Vincent JL, Moreno R, Takala J, Willatts S, De Mendonca A, Bruining H, Reinhart CK, Suter PM, Thijs LG: The SOFA (Sepsis-related Organ Failure Assessment) score to describe organ dysfunction/failure. On behalf of the Working Group on
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Sepsis-Related Problems of the European Society of Intensive Care Medicine. Intensive care medicine 1996, 22(7):707-710.
189. Dalfino L, Tullo L, Donadio I, Malcangi V, Brienza N: Intra-abdominal hypertension and acute renal failure in critically ill patients. Intensive care medicine 2008, 34(4):707-713.
190. Cheatham ML, White MW, Sagraves SG, Johnson JL, Block EF: Abdominal perfusion pressure: a superior parameter in the assessment of intra-abdominal hypertension. The Journal of trauma 2000, 49(4):621-626; discussion 626-627.
191. D'Angelo E, Pecchiari M, Acocella F, Monaco A, Bellemare F: Effects of abdominal distension on breathing pattern and respiratory mechanics in rabbits. Respir Physiol Neurobiol 2002, 130(3):293-304.
192. Cresswell AB, Wendon JA: Hepatic function and non-invasive hepatosplanchnic monitoring in patients with abdominal hypertension. Acta clinica Belgica 2007(1):113-118.
193. McNelis J, Marini CP, Jurkiewicz A, Fields S, Caplin D, Stein D, Ritter G, Nathan I, Simms HH: Predictive factors associated with the development of abdominal compartment syndrome in the surgical intensive care unit. Arch Surg 2002, 137(2):133-136.
194. Joshi D, Saha S, Bernal W, Heaton N, Wendon J, Auzinger G: Haemodynamic response to abdominal decompression in acute Budd-Chiari syndrome. Liver Int 2011, 31(8):1171-1178.
195. Balogh Z, De Waele JJ, Kirkpatrick A, Cheatham M, D'Amours S, Malbrain M: Intra-abdominal pressure measurement and abdominal compartment syndrome: the opinion of the World Society of the Abdominal Compartment Syndrome. Critical care medicine 2007, 35(2):677-678; author reply 678-679.
196. Bongard F, Pianim N, Dubecz S, Klein SR: Adverse consequences of increased intra-abdominal pressure on bowel tissue oxygen. The Journal of trauma 1995, 39(3):519-524; discussion 524-515.
197. De laet I, Citerio G, Malbrain ML: The influence of intraabdominal hypertension on the central nervous system: current insights and clinical recommendations, is it all in the head? Acta clinica Belgica 2007(1):89-97.
198. Diebel LN, Dulchavsky SA, Wilson RF: Effect of increased intra-abdominal pressure on mesenteric arterial and intestinal mucosal blood flow. The Journal of trauma 1992, 33(1):45-48; discussion 48-49.
199. Malbrain ML, Wilmer A: The polycompartment syndrome: towards an understanding of the interactions between different compartments! Intensive care medicine 2007, 33(11):1869-1872.
200. De Keulenaer BL, De Waele JJ, Powell B, Malbrain ML: What is normal intra-abdominal pressure and how is it affected by positioning, body mass and positive end-expiratory pressure? Intensive care medicine 2009, 35(6):969-976.
201. Deeren DH, Dits H, Malbrain ML: Correlation between intra-abdominal and intracranial pressure in nontraumatic brain injury. Intensive care medicine 2005, 31(11):1577-1581.
202. Duggan JE, Drummond GB: Abdominal muscle activity and intraabdominal pressure after upper abdominal surgery. Anesth Analg 1989, 69(5):598-603.
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204. Kellerman SE, Herold J: Physician response to surveys. A review of the literature. American journal of preventive medicine 2001, 20(1):61-67.
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Appendix
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Appendix 1 - Questionnaires
i. IAP Questionnaire – Surgeons
ii. IAP Questionnaire – Anaesthetists
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Intra-abdominal Hypertension and the Abdominal Compartment Syndrome - Surgeons
Years in Consultant Practice …………… Do you participate in an emergency on-call rota? Y N Which geographical region do you work in? ………..……………… What is your main sub-speciality interest?
• Upper GI / HPB • Transplant • Coloproctology • Breast / Endocrine • Vascular • General
Is the “abdominal compartment syndrome” a real clinical entity? Y N What level (in mmHg or cm H2O) corresponds to Intra-abdominal Hypertension Abdominal Compartment Syndrome How many cases of abdominal compartment syndrome have you been involved with in the last year? What proportion of these patients were Post – op
Trauma
Medical
Is Intra-abdominal pressure measured on ITU at your institution Never
Routinely
Occasionally
If occasionally, what influences the decision to measure it? ……………………..
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How many laparostomies have you performed in the last year?
Based on IAP alone Based on operative findings Based on clinical deterioration post-op Based on other factor? (please specify) Please indicate how the following operative findings would influence your decision to leave an abdomen open 1 = Much less likely to leave abdomen open 2 = A little less likely to leave abdomen open 3 = No more or less likely to leave abdomen open 4 = A little more likely to leave abdomen open 5 = Much more likely to leave abdomen open Gross faecal soiling Massive transfusion Multi-system trauma Acidosis High Lactate Haemodynamic instability Respiratory instability Planned 2nd look Subjectively “feels tight” Measured Intra-abd pressure Please indicate how the following post-operative factors would influence your decision to perform a laparostomy 1 = Much less likely to perform a laparostomy 2 = A little less likely to perform a laparostomy 3 = No more or less likely to perform a laparostomy 4 = A little more likely to perform a laparostomy 5 = Much more likely to perform a laparostomy Worsening acidosis Worsening lactate level Worsening cardiac Index Worsening urine output Worsening LFTs Rising creatinine Rising FiO2 Rising ventilatory pressure Many thanks for taking the time to completing this questionnaire.
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Intra-abdominal Hypertension and the Abdominal Compartment Syndrome - Anaesthetists
Years in Consultant Practice …………… Do you participate in an emergency on-call rota? Y N Which geographical region do you work in? ………..……………… What is your main area of interest?
• Anaesthetics with intensive care • Anaesthetics but not intensive care • Intensive Care (Non-anaesthetist)
Is the “abdominal compartment syndrome” a real clinical entity? Y N What level (in mmHg) corresponds to Intra-abdominal Hypertension Abdominal Compartment Syndrome How many cases of abdominal compartment syndrome have you been involved with in the last year? What proportion of these patients were Post – op
Trauma
Medical
Is Intra-abdominal pressure measured on ITU at your institution Never
Routinely
Occasionally
If occasionally, what influences the decision to measure it? ……………………..
Is there a “surgical reluctance” to perform laparostomies at your institution?
Y N
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How many laparostomies have you been involved with in the past year?
Based on IAP alone Based on operative findings Based on clinical deterioration post-op Based on other factor? (please specify) Please indicate how the following operative findings should influence the decision to leave an abdomen open 1 = Much less likely to leave abdomen open 2 = A little less likely to leave abdomen open 3 = No more or less likely to leave abdomen open 4 = A little more likely to leave abdomen open 5 = Much more likely to leave abdomen open Gross faecal soiling Massive transfusion Multi-system trauma Acidosis High Lactate Haemodynamic instability Respiratory instability Planned 2nd look Subjectively “feels tight” Measured Intra-abd pressure Please indicate how the following post-operative factors would influence your decision to request a laparostomy 1 = Much less likely to request a laparostomy 2 = A little less likely to request a laparostomy 3 = No more or less likely to request a laparostomy 4 = A little more likely to request a laparostomy 5 = Much more likely to request a laparostomy Worsening acidosis Worsening lactate level Worsening cardiac Index Worsening urine output Worsening LFTs Rising creatinine Rising FiO2 Rising ventilatory pressure Many thanks for taking the time to completing this questionnaire.
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Appendix 2 – Peer-reviewed publications arising from thesis
i. Hepatic function and non-invasive hepatosplanchnic monitoring in patients with abdominal hypertension. Cresswell AB, Wendon JA. Acta Clin Belg. 2007;(1):113-8.
ii. The effect of different reference transducer positions on intra-abdominal
pressure measurement: a multicenter analysis. De Waele JJ, De Laet I, De Keulenaer B, Widder S, Kirkpatrick AW, Cresswell AB, Malbrain M, Bodnar Z, Mejia-Mantilla JH, Reis R, Parr M, Schulze R, Compano S, Cheatham M. Intensive Care Med. 2008 Jul;34(7):1299-303. Epub 2008 Apr 4.
iii. The impact of body position on intra-abdominal pressure measurement: a
multicenter analysis. Cheatham ML, De Waele JJ, De Laet I, De Keulenaer B, Widder S, Kirkpatrick AW, Cresswell AB, Malbrain M, Bodnar Z, Mejia-Mantilla JH, Reis R, Parr M, Schulze R, Puig S; World Society of the Abdominal Compartment Syndrome (WSACS) Clinical Trials Working Group. Crit Care Med. 2009 Jul;37(7):2187-90.
iv. The effect of body position on compartmental intra-abdominal pressure following
liver transplantation. Cresswell AB, Jassem W, Srinivasan P, Prachalias AA, Sizer E, Burnal W, Auzinger G, Muiesan P, Rela M, Heaton ND, Bowles MJ, Wendon JA Annals of Intensive Care. 2012 5(2):S12
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113HEPATIC FUNCTION AND NON-INVASIVE HEPATOSPLANCHNIC MONITORING IN PATIENTS WITH ABDOMINAL HYPERTENSION
Acta Clinica Belgica, 2007; 62-Supplement 1
HEPATIC FUNCTION AND NON-INVASIVE HEPATOSPLANCHNIC MONITORING IN PATIENTS WITH ABDOMINAL HYPERTENSION
–––––––––––––––Institute of Liver Studies,Division of Transplantation and Cell Based Therapy, Kings College London School of Medicine, Kings College Hospital, London, UK
Address for correspondence:Dr. J.A. WendonLiver Intensive Therapy UnitInstitute of Liver StudiesKing’s College Hospital LondonSE5 9RSUnited KingdomTel: +44 203 2999000
Original article – OA 13
ABSTRACT
A better understanding of intra-abdominal hypertension with relation to the liver is vital to the management of all forms of liver pathophysi-ology. Supporting good hepatic function within the critically ill patient is important not only in maintaining synthetic function, but also in avoiding the multi-organ complications of liver dysfunc-tion.
The resulting reduction in hepato-splanchnic blood fl ow (HSBF) observed with increasing intra-abdominal pressure has been clearly documented and seen to be exaggerated in animals with established liver disease. Unfortunately the tools required to measure this, remain diffi cult to apply routinely in the clinical setting and as such goal directed therapy to specifi cally improve the hepato-splanchnic circulation remains elusive.
Given the documented effects of IAP on HSBF and the relatively high incidence of intra-abdominal hypertension and the abdominal compartment syndrome within “liver patients” as a whole, close attention to IAP and timely correction by appropri-ate medical or surgical means would appear to be essential.
INTRODUCTION
Intra-abdominal hypertension (IAH) and the ab-dominal compartment syndrome (ACS) have clearly been shown to be important contributors to morbidity and mortality within the critical care patient population (1, 2). Despite a large volume of emerging evidence concerning cardiovascular, respiratory and renal effects of elevated intra-abdominal pressure (IAP) there is a relative paucity of data relating specifi cally to liver blood fl ow and function, with most of that which is available relating to animal studies or “healthy” subjects undergoing pneumoperitoneum for elective proce-dures.
A better understanding IAH with relation to the liver is vital to the management of all forms of liver pathophysiology. Supporting good hepatic function within the critically ill patient is important not only in maintaining synthetic function, but also in avoiding the multi-organ complications of liver dysfunction.
Specifi c medical and surgical insults upon the liver are becoming increasingly common with a rising inci-dence of both alcohol-related liver disease and non-alcoholic steato-hepatitis (NASH).
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114 HEPATIC FUNCTION AND NON-INVASIVE HEPATOSPLANCHNIC MONITORING IN PATIENTS WITH ABDOMINAL HYPERTENSION
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Surgical treatments of liver lesions, such as meta-static carcinoma and hepatocellular carcinoma, have become increasingly more aggressive with the wide-spread use of preoperative portal vein embolisation, radiofrequency ablation and staged liver resections in order to improve operability rates. In such cases pre-and perioperative optimisation of hepatic functional reserve has become vitally important and control of IAP appears to be important for hepatic regeneration (3).
The incidence of IAH following liver transplantation (4), and specifi cally its effects on renal function (5), have been previously demonstrated, and with a shrinking donor pool optimisation of support within this group is obviously as important as ever.
Signifi cant liver trauma, whether managed opera-tively or non-operatively, may be expected to lead to an elevation of IAP and for marginally ischaemic tissues, optimisation of blood fl ow is essential.
The deleterious effects of increased IAP may be considered in terms of the hepatic circulation and the biochemical function of the hepatocyte. The basic physiology and strategies for non-invasive assessment of these parameters will be discussed below with spe-cifi c reference to the effects of raised IAP.
PHYSIOLOGY OF LIVER BLOOD FLOW
The liver as an organ is unique, in that it receives its blood supply from two main sources, the hepatic artery and portal vein and, under normal conditions, will re-ceive around one quarter of the total cardiac output, accounting for approximately 20% of total body oxygen consumption. In health, the hepatic artery supplies around 30 mls/min per 100 g of liver tissue which equates to roughly 25% of the liver blood fl ow. The portal vein supplies the remaining 75% at a rate of 70 mls/min per 100g (6), and drains blood from the entire GI tract from the level of the distal oesophagus, includ-ing the spleen and pancreas (the splanchnic circulation). Portal venous blood is obviously rich in nutrients, but also by virtue of its large fl ow rate, is responsible for a signifi cant proportion of the hepatic oxygen supply. Normal portal pressure is between 5 and 8 mmHg. Hepatic vascular outfl ow is via the three hepatic veins which converge to drain into the inferior vena cava. Normal hepatic venous pressure is around 1 to 2 mmHg.
Control of liver blood fl ow is complex and occurs at the level of the splanchnic and hepatic arterioles and the portal and hepatic venules. Autoregulation is pri-
marily achieved through alterations in the hepatic arte-rial fl ow (known as the hepatic arterial buffer response (7)). In health, it is the accumulation of adenosine (8, 9) within the liver that seems to be responsible for the regulation of this buffer response.
Control of liver blood fl ow in disease states depends on the underlying pathology and cellular and biochem-ical mechanisms vary.
MEASUREMENT OF HEPATO-SPLANCHNIC BLOOD FLOW
Techniques for measuring hepatic and splanchnic blood fl ow can be broadly divided into approaches which consider fl ow in single vessels, and those providing a more global indicator of organ perfusion. By and large, most of the techniques described are employed main-ly within the research setting and routine clinical ap-plication is relatively limited.
For the invasive measurement of single vessels, dop-pler fl owmetry is commonly employed with fl ow probes surgically placed around the vessel of interest. Amongst other applications, this technique has been success-fully used to study the effects of pneumoperitoneum on the hepatic blood fl ow in anaesthetised pigs (10). More recent advances in microtechnology have allowed the development of laser doppler fl owmetry via a single fi bre microprobe. Such probes illuminate the liver tissue with a low powered laser in order to measure movement of red cells (11) and provide a regional tissue measure-ment.
In the clinical setting, non-invasive ultrasound ex-amination of the hepatic vessels has been disappointing in quantitative terms (12). The advent of colour fl ow Doppler however, has enabled the direction of fl ow within the portal vein to be ascertained (13) and micro-bubble contrast has been employed to measure he-patic vein transit times with apparent success (14).
More recently, magnetic resonance imaging has been used to estimate hepatic blood fl ow, especially with respect to the diagnosis and grading of portal hyperten-sion (15, 16).
The most commonly employed technique for the assessment of total liver blood fl ow is an indicator clearance technique, usually employing indocyanine green. This is a tri-carbocyanine dye that is actively taken up by hepatocytes and excreted exclusively into the bile. Elimination rate can be measured invasively via an hepatic vein catheter following either a continu-ous infusion (17) or bolus administration (18) of ICG or
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else non-invasively via a transcutaneous saturation probe (19). The rate of elimination, or plasma disap-pearance rate (PDR) is a composite measure of both total liver blood fl ow and hepatocyte function which correlates to hepato-splanchnic blood fl ow (20) and is sensitive in detecting subtle variations (21).
Data on ICG clearance may also be combined with hepatic vein, arterial and mixed venous oxygen tensions in order to calculate hepato-splanchnic oxygen delivery (17) .The separation of fl ow and metabolism can be obtained if hepatic venous sampling is undertaken for ICG concentration. In addition, ICG has been used as a reliable indicator of liver graft function following trans-plantation (22) and as an assessment of functional re-serve after trauma (23) and prior to hepatectomy (24).
Hepatosplanchnic function may also be assessed by use of arterial ketone body ratio, this appears to be very useful in assessing functional liver mass, but cannot unfortunately as of yet be utilized as a real time bedside parameter (25). Similarly hepatospnachnic fl ow and function can be examined utilizing galactose elimination (26); cannulation of hepatic veins and regional sampling allowing separation of fl ow and uptake. Again, this is mainly utilized in a research setting and as a technique cannot provide real time results. Metabolites of ligno-caine, (MEGX) were used in the past to obtain a com-posite assessment of fl ow and metabolic function fol-lowing a bolus dose of lignocaine (27); again lack of real time functionality seem to have resulted in decreased use and potential concerns in regard of lignocaine ac-cumulation in repeated testing, especially pertinent in the context of signifi cant liver dysfunction.
For the sake of completeness, two other invasive techniques for the measurement of global liver blood fl ow are worthy of mention, however their use is lim-ited exclusively to the experimental setting. Fluorescent microscopy involves visualising individual sinusoids within the liver substance and measuring the fl ow rate of injected contrast agent (28). Coloured microspheres have also been used to quantify global blood fl ow, however their used requires sacrifi ce of the experimen-tal subjects and digestion of the liver tissue, in order to count the individual spheres (29).
INTRA-ABDOMINAL PRESSURE AND THE HEPATO-SPLANCHNIC CIRCULATION
Elevated IAP has been associated with deterioration in renal and gut function which is likely, at least in part, to be due to reduced organ perfusion. For example an
IAP of 20 mmHg can be expected to reduce glomerular fi ltration rate by up to 25% (30), and mesenteric blood fl ow by 40 to 70% (31).
With specifi c reference to the hepatic circulation and function, clinical studies are clearly lacking. The data that is available clearly suggests that rising IAP signifi -cantly impairs hepatic blood fl ow, however a clear link between this reduction and subsequent organ dysfunc-tion has not been positively demonstrated.
In a relatively small animal study, in which IAP was raised incrementally to 10, 20, 30 and 40 mmHg in fi ve pigs, the effect on hepatic artery and portal vein blood fl ow was measured using doppler fl owmetry and the hepatic microvascular fl ow measured using laser doppler fl owmetry. At 20 mmHg arterial fl ow was found to be reduced to 45% of baseline, portal venous fl ow to 65% and microvascular fl ow to 71% (31), despite mainte-nance of the baseline mean arterial blood pressure by means of fl uid infusion.
Similar results have been found in rats, where the calculated blood fl ow for the spleen, stomach and total intestine (measured by a microsphere injection tech-nique) was reduced in a near linear fashion in the face of increasing IAP, although hepatic arterial fl ow was seen to be preserved at an IAP of 20 mmHg. An obser-vation that the authors attributed to the hepatic arte-rial buffer response (28). Similarly it was found that a pneumoperitoneum of 8 mmHg maintained for 90 minutes resulted in microcirculatory dysfunction (meas-ured by fl uorescent microscopy) and a signifi cant rise in transaminases (29).
In a further rat study, the effects of continuously raised IAP was compared in healthy rats and in those with induced cirrhosis. As before, increased IAP was found to impair liver microcirculation (assessed by laser doppler fl owmetry), however the deterioration was signifi cantly worse within the cirrhotic group. The au-thors also observed increased levels of alkaline phos-phatase, alanine aminotransferase and bilirubin concen-trations, although these changes did not reach signifi cance (11). The study does however, suggest that patients with pre-existing liver disease may be more susceptible to the effects of raised intra-abdominal pressure.
Impaired hepatic blood fl ow has been demonstrated in studies considering subjects undergoing pneumoper-itoneum for laparoscopy. In one human study of 18 patients undergoing laparoscopy for cholecystectomy or appendicectomy signifi cant impairment of blood fl ow to the stomach, jejunum, colon and liver was observed by laser doppler fl owmetry. Liver blood fl ow was reduced
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by 39% following increase of the pneumoperitoneum from 10 mmHg to 15 mmHg (32). In an equivalent study utilising a rat model, portal vein fl ow measured by dop-pler fl owmetry was similarly seemed to reduce in a linear fashion with increasing IAP (33).
Only one study has specifi cally considered the infl u-ence of IAP on hepatocyte metabolism and this consid-ered 53 rabbits at intra-abdominal pressures of 20 mmHg and 30 mmHg. Hepatic blood fl ow was measured using the ICG disappearance rate and was found to be signifi cantly impaired at both 20 and 30 mmHg. He-patic mitochondrial redox status was also evaluated and found to be unaffected at 20 mmHg. At 30 mmHg however, the mitochondrial redox status was signifi -cantly decreased with a corresponding reduction in tissue energy level. This has been the only study to consider isolated hepatocyte function in the face of raised IAP, but unfortunately the results have not since been replicated and cannot, justifi ably, be generalised to a human population.
The effect of reduced hepato-splanchnic blood fl ow on mucosal pH has been clearly demonstrated in hu-mans. One prospective study of 73 patients undergoing major abdominal surgery demonstrated a signifi cant association between raised IAP and abnormal mucosal pH, with pressures greater than 20 mmHg being associ-ated with an 11 fold increase in abnormal pHi (< 7.32) (34). Moreover an improvement in pHi has been dem-onstrated following abdominal decompression (35).
From a clinical point of view, although we can clearly demonstrate that increasing IAP does deleteri-ously effect hepato-splanchnic bloodflow and gut mucosal pH, we are not yet at a stage to say at what level either IAP or the resulting reduction in blood fl ow, will result in a signifi cant deterioration in liver func-tion.
INTRA-ABDOMINAL PRESSURE IN ACUTE LIVER FAILURE
Very little work has been published looking specifi -cally at the effects of raised IAP in acute liver failure, although the effects of IAH on the hepatic microcircu-lation have been shown to be exaggerated in cirrhotic subjects (11). A recent study, which was designed to consider the association between abdominal hyperten-sion and liver dysfunction, found a correlation between IAP and degree of hyper-bilirubinaemia but no strict association between IAP and liver dysfunction (36). This study however, set a threshold for IAH at 10 mmHg and
recruited very few patients with an IAP > 15 mmHg (the mean IAP was 10.7 mmHg.
Interim analysis of our own unpublished data, has shown that raised IAP is an extremely common fi nding in patients with acute liver failure and a better inde-pendent predictor of length of ITU stay than other contemporary scoring systems. 95% of patients were found to have IAH (> 12 mmHg) and 60% the ACS (> 20 mmHg).
In this subgroup of physiologically unstable patients, high intra-abdominal pressures can be expected to exacerbate the other specific pathophysiological changes in associated organ systems. Namely, worsen-ing the raised intracranial pressure and renal, respira-tory and cardiac dysfunction which usually accompany acute liver failure. The observed compressive effect of high IAP on the inferior vena cava (37) may lead to signifi cant problems with hepatic outfl ow resulting in further hepatic congestion.
Patients with large volume ascites are unusual in the general course of ACS, in that the relatively minor in-tervention of paracentesis can be associated with a signifi cant increase in cardiac index, stroke volume and renal function (38). In such patients, with high intra-abdominal pressures and evidence of deteriorating or-gan function, paracentesis should therefore be consid-ered early. Paradoxically, it is these patients who may tolerate high IAP the best, due to some degree of chronic IAH. Individual pressure measurements should therefore be interpreted in conjunction with the overall clinical picture.
Of particular importance in the subgroup of acute liver failure patients with decompensated cirrhosis, is the association of right atrial dysfunction. This can make the use of conventional indicators of volume loading such as central venous pressure (CVP) or pulmonary artery wedge pressure (PAWP) unreliable. In this sub-group of patients, as well as those with other causes of acute liver failure, we have found that intrathoracic blood volume index (ITBVI) provided the best correla-tion with stroke volume and cardiac index (39) and that ICG clearance may also provide a useful adjunct in the assessment of volume status.
INTRA-ABDOMINAL PRESSURE IN LIVER TRANSPLANT RECIPIENTS
Several facets of liver transplantation place recipi-ents at risk of development of high intra-abdominal pressures. Firstly it is not unusual for the transplanted
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graft to be an imperfect size match, often with a greater volume than the native liver. This is particu-larly true of the shrunken cirrhotic liver. Liver transplan-tation is, by defi nition, a major and lengthy abdominal surgery and the required disruption to mesenteric out-fl ow will inevitably produce some visceral oedema, which can be exacerbated if there is any impairment of fl ow at the portal vein anastomosis. Finally, blood loss is unavoidable and large volume transfusion is not unusual, even for elective procedures.
In the only prospective study of IAP in liver transplant recipients (beyond individual case reports) the incidence of IAH (defi ned as > 25 mmHg) was 31.5%(4). In our own unpublished data, using cut-offs of 12 and 20 mmHg for IAH and ACS, we found an incidence of 60% and 25% respectively.
In the published study a signifi cant difference in IAP was noted in individuals subsequently developing acute renal failure and IAH was associated with a relative risk for acute renal failure of 9.8 (5).
The evidence to date would suggest that liver trans-plant recipients are at signifi cant risk of developing raised abdominal pressure and that the operating sur-geon should have a low threshold for the use of pro-phylactic temporary abdominal closures. Measurement of IAP in the postoperative period should be manda-tory and in due course, strategies to predict individual risk may aid in identifi cation of particular patients re-quiring more intensive observations.
INTRA-ABDOMINAL PRESSURE AND HEPATOPANCREATOBILIARY SURGERY
There are no data relating to the incidence of raised IAP following major hepatic or pancreatic resections. Interim analysis of our own unpublished data, suggest that 72% of patients developed IAH (> 12 mmHg) and that the ACS (> 20 mmHg) can be expected in 24%. The problem is therefore signifi cant and merits further re-search, especially as raised IAP has been shown to be associated with impaired liver regeneration following animal studies of hepatectomy (3).
CONCLUSIONS
The resulting reduction in hepato-splanchnic blood fl ow (HSBF) observed with increasing IAP has been clearly documented and seen to be exaggerated in animals with established liver disease. Unfortunately
the tools required to measure this, remain diffi cult to apply routinely in the clinical setting and as such goal directed therapy to specifi cally improve the hepato-splanchnic circulation remains elusive.
Given the documented effects of IAP on HSBF and the relatively high incidence of IAH and the ACS within “liver patients” as a whole, close attention to IAP and timely correction by appropriate medical or surgical means would appear to be essential.
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8. Lautt WW, D’Almeida MS, McQuaker J, D’Aleo L. Impact of the hepatic arterial buffer response on splanchnic vascular re-sponses to intravenous adenosine, isoproterenol, and gluca-gon. Can J Physiol Pharmacol. 1988; 66: 807-13.
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11. Eleftheriadis E, Kotzampassi K. Hepatic microcirculation after continuous 7-day elevated intra- abdominal pressure in cir-rhotic rats. Hepatol Res. 2005; 32: 96-100.
12. Burns P, Taylor K, Blei AT. Doppler fl owmetry and portal hyper-tension. Gastroenterology. 1987; 92: 824-6.
13. Gorg C, Riera-Knorrenschild J, Dietrich J. Pictorial review: Colour Doppler ultrasound fl ow patterns in the portal venous system. Br J Radiol. 2002; 75: 919-29.
14. Lim AK, Taylor-Robinson SD, Patel N, et al. Hepatic vein transit times using a microbubble agent can predict disease severity non-invasively in patients with hepatitis C. Gut. 2005; 54: 128-33.
15. Annet L, Materne R, Danse E, Jamart J, Horsmans Y, Van Beers BE. Hepatic fl ow parameters measured with MR imaging and Doppler US: correlations with degree of cirrhosis and portal hypertension. Radiology. 2003; 229: 409-14.
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16. Scharf J, Zapletal C, Hess T, et al. Assessment of hepatic perfusion in pigs by pharmacokinetic analysis of dynamic MR images. J Magn Reson Imaging. 1999; 9: 568-72.
17. Matejovic M, Rokyta R, Jr., Radermacher P, Krouzecky A, Sramek V, Novak I. Effect of prone position on hepato-splanchnic he-modynamics in acute lung injury. Intensive Care Med. 2002; 28: 1750-5.
18. Grainger SL, Keeling PW, Brown IM, Marigold JH, Thompson RP. Clearance and non-invasive determination of the hepatic extrac-tion of indocyanine green in baboons and man. Clin Sci (Lond). 1983; 64: 207-12.
19. Faybik P, Krenn CG, Baker A, et al. Comparison of invasive and noninvasive measurement of plasma disappearance rate of in-docyanine green in patients undergoing liver transplantation: a prospective investigator-blinded study. Liver Transpl. 2004; 10: 1060-4.
20. Sakka SG, Reinhart K, Meier-Hellmann A. Prognostic value of the indocyanine green plasma disappearance rate in critically ill patients. Chest. 2002; 122: 1715-20.
21. Sakka SG, Reinhart K, Wegscheider K, Meier-Hellmann A. Variabil-ity of splanchnic blood fl ow in patients with sepsis. Intensive Care Med. 2001; 27: 1281-7.
22. Tsubono T, Todo S, Jabbour N, et al. Indocyanine green elimina-tion test in orthotopic liver recipients. Hepatology. 1996; 24: 1165-71.
23. Gottlieb ME, Stratton HH, Newell JC, Shah DM. Indocyanine green. Its use as an early indicator of hepatic dysfunction fol-lowing injury in man. Arch Surg. 1984; 119: 264-8.
24. Okochi O, Kaneko T, Sugimoto H, Inoue S, Takeda S, Nakao A. ICG pulse spectrophotometry for perioperative liver function in hepatectomy. J Surg Res. 2002; 103: 109-13.
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26. Gao L, Ramzan I, Baker AB. Potential use of pharmacological markers to quantitatively assess liver function during liver transplantation surgery. Anaesth Intensive Care. 2000; 28: 375-85.
27. Oellerich M, Armstrong VW. The MEGX test: a tool for the real-time assessment of hepatic function. Ther Drug Monit. 2001; 23: 81-92.
28. Yokoyama Y, Alterman DM, Sarmadi AH, et al. Hepatic vascular response to elevated intraperitoneal pressure in the rat. J Surg Res. 2002; 105: 86-94.
29. Schemmer P, Barro-Bejarano M, Mehrabi A, et al. Laparoscopic organ retrieval for living donor liver transplantation does not prevent graft injury. Transplant Proc. 2005; 37: 1625-7.
31. Diebel LN, Wilson RF, Dulchavsky SA, Saxe J. Effect of increased intra-abdominal pressure on hepatic arterial, portal venous, and hepatic microcirculatory blood fl ow. J Trauma. 1992; 33: 279-82; discussion 282-3.
32. Schilling MK, Redaelli C, Krahenbuhl L, Signer C, Buchler MW. Splanchnic microcirculatory changes during CO2 laparoscopy. J Am Coll Surg. 1997; 184: 378-82.
33. Gutt CN, Schmandra TC. Portal venous fl ow during CO(2) pneu-moperitoneum in the rat. Surg Endosc. 1999; 13: 902-5.
34. Sugrue M, Jones F, Lee A, et al. Intraabdominal pressure and gastric intramucosal pH: is there an association? World J Surg. 1996; 20: 988-91.
35. Ivatury RR, Porter JM, Simon RJ, Islam S, John R, Stahl WM. Intra-abdominal hypertension after life-threatening penetrating abdominal trauma: prophylaxis, incidence, and clinical r e l e -vance to gastric mucosal pH and abdominal compartment syndrome. J Trauma. 1998; 44: 1016-21; discussion 1021-3.
36. Dalfi no L, Malcangi V, Cinnella G, Brienza N. Abdominal hyper-tension and liver dysfunction in intensive care unit patients: an “on-off” phenomenon? Transplant Proc. 2006; 38: 838-40.
37. Wachsberg RH. Narrowing of the upper abdominal inferior vena cava in patients with elevated intraabdominal pressure: sono-graphic observations. J Ultrasound Med. 2000; 19: 217-22.
38. Savino JA, Cerabona T, Agarwal N, Byrne D. Manipulation of ascitic fl uid pressure in cirrhotics to optimize hemodynamic and renal function. Ann Surg. 1988; 208: 504-11.
39. Sutcliffe R, Meares H, Auzinger G, al. E. Preload assessment in severe liver disease associated with intra-abdominal hyperten-sion. Intensive Care Medicine. 2002; 28 (Suppl 1): S177A688.
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Intensive Care Med (2008) 34:1299–1303DOI 10.1007/s00134-008-1098-4 BRIEF REPORT
Jan J. De WaeleInneke De laetBart De KeulenaerSandy WidderAndrew W. KirkpatrickAdrian B. CresswellManu MalbrainZsolt BodnarJorge H. Mejia-MantillaRichard ReisMichael ParrRobert SchulzeSonia CompanoMichael Cheatham
The effect of different reference transducerpositions on intra-abdominal pressuremeasurement: a multicenter analysis
This study was performed on behalf of theClinical Trials Working Group of the WorldSociety for Abdominal CompartmentSyndrome. It was presented at the 2007World Congress on the AbdominalCompartment Syndrome, Antwerp,Belgium.
J. J. De Waele (�)Ghent University Hospital, SurgicalIntensive Care Unit,De Pintelaan 185, 9000 Gent, Belgiume-mail: [email protected].: +32-9-2402775Fax: +32-9-2404995
I. De laetZiekenhuis Netwerk Antwerpen, CampusStuivenberg, Intensive Care Unit,Antwerpen, Belgium
B. De KeulenaerFremantle Hospital, Intensive Care Unit,Alma Street, Fremantle, Australia
S. WidderUniversity of Calgary,Department of Surgery,Calgary, Canada
A. W. KirkpatrickFoothills Medical Centre, Departmentsof Critical Care Medicine and Surgery,Calgary, Canada
A. B. CresswellLiver Transplant Surgical Service and LiverITU Institute of Liver Studies King’sCollege Hospital,London, UK
M. MalbrainZiekenhuis Netwerk Antwerpen, CampusStuivenberg, Intensive Care Unit,Antwerpen, Belgium
Z. BodnarKenézy Teaching Hospital,Department of Surgery,Debrecen, Hungary
J. H. Mejia-MantillaUniversidad del Valle, Anesthesiaand Intensive Care,Cali, Colombia
R. ReisBratislava University,Department of Surgery,Bratislava, Slovakia
M. ParrLiverpool Hospital, Intensive Care Unit,Sydney, Australia
R. SchulzeSUNY Downstate/Kings County Hospital,Department of Surgery,Brooklyn NY, USA
S. CompanoHospital del Mar,Barcelona, Spain
M. CheathamOrlando Regional Medical Center,Department of Surgical Education,Orlando FL, USA
Abstract Objective: To investigatethe effect of different reference trans-ducer positions on intra-abdominalpressure (IAP) measurement. Threereference levels were studied: thesymphysis pubis; the phlebostaticaxis; and the midaxillary line at thelevel of the iliac crest. Design:Prospective cohort study. Setting:The intensive care units of par-ticipating hospitals Patients andparticipants: One hundred thirty-two critically ill patients at risk forintra-abdominal hypertension (IAH).Interventions: In each patient, threesets of IAP measurements were ob-tained in the supine position, usingthe different reference levels. TheIAP measurements obtained atthe different reference levels werecompared using a paired t-test andBland–Altman statistics were calcu-lated. Measurements and results:IAPphlebostatic (9.9 ± 4.67 mmHg) andIAPpubis (8.4 ± 4.60 mmHg) weresignificantly lower that IAPmidax(12.2 ± 4.66 mmHg; p < 0.0001for both comparisons). The biasbetween the IAPmidax and IAPpubiswas 3.8 mmHg (95% CI 3.5–4.1) and2.3 mmHg (95% CI 1.9–2.6) betweenthe IAPmidax and the IAPphlebostatic .The precision was 3.03 and 3.40,respectively. Conclusions: In the
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supine position, IAPmidax is higherthan both IAPphlebostatic and IAPpubis,differences found to be clinicallysignificant; therefore, the symphysispubis or phlebostatic axis reference
lines are not interchangeable with themidaxillary level.
Intra-abdominal hypertension (IAH) and abdominal com-partment syndrome (ACS) are significant causes of mor-bidity and mortality in the critically ill [1]. Several authorshave shown clinical examination to be unreliable for de-tecting the presence of elevated intra-abdominal pressure(IAP) [2, 3], and serial IAP measurements are widely ac-knowledged to be essential to both the diagnosis and treat-ment of IAH/ACS [4–6]. Current consensus recommenda-tions, published by the World Society for the AbdominalCompartment Syndrome (WSACS), suggest that IAP bemeasured using the intravesicular technique with the pa-tient in supine position and the transducer zeroed at thelevel of the midaxillary line [7].
Before this consensus was reached, the symphysis pu-bis was often used as a reference level; however, the exactlocalization of the “symphysis pubis” is subject to interpre-tation, which may lead to observer-dependent variability inIAP measurement. To overcome this problem, the WSACSconsensus definitions suggested the use of the midaxillaryline at the level of the iliac crest as a reference point, asthis bony structure is easier to palpate, even in obese pa-tients. The effect of this change in reference line on blad-der pressure measurement was never formally investigated,however, and the possible utility of other reference lines,including that standard used for all other pressure-relatedphysiologic measurements in the intensive care unit (thephlebostatic axis), has not been studied.
The aim of this analysis was thus to determine the dif-ference between transvesical IAP values when using differ-ent reference lines [symphysis pubis (IAPpubis) and phle-bostatic axis (IAPphlebostatic) compared with the midaxil-lary line at the iliac crest (IAPmidax)] with the patient inthe supine position.
Fig. 1 Localization of thedifferent reference levels used.(From the World Society for theAbdominal CompartmentSyndrome)
Patients and methods
The WSACS Clinical Trials Group initiated a prospective,multicenter trial which was approved by the institutionalreview board/ethics committee at each study site. Thestudy recruited patients between November 2005 andApril 2006. The inclusion criteria selected patients agedmore than 18 years, who were sedated and mechanicallyventilated, and demonstrated at least one risk factorfor intra-abdominal hypertension as proposed by theWSACS [7]. Patients were excluded if unable to toleratechanges in body position.
Before the first measurement, three reference levelswere identified with the patient in the supine position: thesymphysis pubis reference level at the anterior border ofthe symphysis pubis; the phlebostatic axis (or mid-chestreference level) at one half of the patient’s anteroposteriordiameter below the sternal angle; and the midaxillaryreference level at the midaxillary line (Fig. 1). Thesereference points were clearly marked to be used for allstudy measurements.
In each patient, three sets of IAP measurements wereperformed at least 4 h apart. The IAP was measured us-ing the transvesical technique after instillation of 20 ml ofsaline using an AbViser device (Wolfe-Tory Medical, SaltLake City, Utah) and expressed in milligrams of mercury(mmHg) and obtained in relaxed patients at end expira-tion. The order of measurement was also varied through-out these three sets of measurements. The transducer waszeroed prior to every single IAP measurement.
Statistical analysis was performed using Medcalc(Medcalc, Mariakerke, Belgium). The IAP measurementsobtained at the different transducer levels were comparedusing a paired t-test. Additionally, the IAP measurementsobtained at the different reference levels were compared
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using Bland–Altman statistics [8] (bias with 95% confi-dence interval, precision, i.e., the standard deviation of thebias, and the lower and upper limits of agreement), and theSpearman rank correlation coefficients were calculated.Data are reported as mean ± SD.
We considered the difference to be clinically non-significant if the bias did not exceed 1 mmHg (eitherpositive or negative) and the precision was not higher than2 mmHg, as proposed by the WSACS [9].
Results
One hundred and thirty-two (132) patients were en-rolled from 12 sites (across Europe and North America),which resulted in 396 IAP measurement sets. Forty-threepercent of the patients were admitted with a medicaldiagnosis, 39% with a surgical diagnosis, and 18% weretrauma patients. At the moment of inclusion in the study,APACHE II was 21 ± 11, SAPS II was 44 ± 18, and
Fig. 2 Bland–Altman plots of the difference between IAPmidax andIAPpubis (a) and between IAPmidax and IAPphlebostatic (b)
SOFA was 10 ± 7. The IAP ranged from 2 to 29 mmHg(mean 12.2 mmHg). In 50.8% of the measurements, IAPwas above 12 mmHg, the threshold for IAH, and in 6.4%,IAP was above 20 mmHg (which is defined as abdominalcompartment syndrome according to the WSACS con-sensus definitions, if accompanied by new or progressiveorgan dysfunction [7]) IAPphlebostatic (9.9 ± 4.67 mmHg)and IAPpubis (8.4 ± 4.60 mmHg) were significantly lowerthan IAPmidax (12.2 ± 4.66 mmHg; p < 0.0001 for bothcomparisons).
In the supine position, the bias between the IAPmidaxand IAPpubis was 3.8 mmHg (95% CI 3.5–4.1; lower andupper limits of agreement –2.16 and 9.71, respectively)and 2.3 mmHg (95% CI 1.9–2.6) between the IAPmidaxand the IAPphlebostatic (lower and upper limits of agreement–4.36 and 8.98, respectively). The precision was 3.03 and3.40, respectively. Overall, the bias was not differentacross the range of IAP values (Fig. 2).
The Spearman rank correlation coefficient betweenIAPmidax and IAPpubis and between IAPmidax andIAPphlebostatic was 0.74 and 0.70, respectively.
Discussion
In this study, IAPmidax was higher than both IAPphlebostaticand IAPpubis in the supine position; the correlation betweenIAPmidax and the IAPpubis was slightly better than betweenIAPmidax and the IAPphlebostatic . As the bias and precisionexceeded the predefined values, we considered the differ-ence to be clinically significant, and therefore, the IAPpubisand IAPphlebostatic should not be used as alternatives for theIAPmidax.
Although transvesical measurement is advocated asthe standard technique for intermittent IAP measurementby the WSACS [7], and it is the most widely usedtechnique [10], there are still some controversial issuessurrounding it, such as which reference line should be usedfor transvesical IAP measurement, or what instillationvolume should be used [11]. The WSACS consensus defi-nitions state that intra-vesical pressure should be measuredin completely supine position with the transducer zeroedat the level of the midaxillary line.
Before the 2004 consensus definition, the symphysispubis was recommended as a reference line, but in dailypractice, the exact localization of the symphysis pubis wasfound to be subject to interpretation due to differences inpatient body habitus, which leads to observer-dependentvariability in IAP measurement. The WSACS consensusdefinitions attempted to resolve this by suggesting the useof the midaxillary line as a reference level, as the midaxil-lary line is easier to identify in critically ill patients; how-ever, the effect of this change in reference level on IAPmeasurement was never formally investigated.
In addition, the possible value of other reference levels,such as the reference level used for all other pressure-
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related physiologic measurements in the intensive careunit, i.e., the level of the right atrium or phlebostaticaxis, has not been studied. Since the phlebostatic axis isdefined as a horizontal line (in supine position) halfwaybetween the anterior and posterior surface of the thoraxat the sternal angle, the phlebostatic axis level and themidaxillary level were expected to be located at approx-imately the same level in supine position. Utilization ofa single reference point for all manometric measurementsin critically ill patients would have benefits in simplifyingthe care of these patients and in the training of nursingand medical care providers. Furthermore, utilizing thephlebostatic axis offers the promise of a reference pointthat might be independent of the angle of the bed, whichis a serious concern to the adoption of continuous IAPmeasurement techniques [12].
The IAPphlebostatic was found to be considerably lowerthan IAPmidax. There are two possible explanations forthis phenomenon: either the intra-vesical pressure itselfchanged during the time between measurements; or thephlebostatic level used was localized higher (or moreanterior) than the midaxillary position in the patientsstudied. A true change in IAP is unlikely since both meas-urements were performed consecutively and in varyingorder; therefore, the second explanation is more likely.It is important to keep in mind that the phlebostatic axisrepresents the mid-chest reference point and the referencepoint for hemodynamic pressure monitoring because theleft ventricle, aorta, and pulmonary artery, as well as thetip of catheters for central venous pressure monitoring,are located at this level [13]. It is therefore not surprising,as was confirmed by the results of this study, that itcannot be used as a substitute for the midaxillary levelor the mid-abdomen level. Also, it might be difficult toidentify the mid-chest reference point reliably in criticallyill patients, since many patients are placed on specialair-cushioned mattresses and the outermost posterior edgeof the thorax is impossible to identify without changingbody position.
The IAPmidax and IAPpubis correlated slightly better,although there was a still a clinically significant differ-ence between both values. The IAPmidax was higher than
IAPpubis, which suggests that the midaxillary referencelevel was located lower (or more posterior) than the pubisreference level, which seems to be anatomically correct;however, the very large limits of agreement suggest thatthe distance between both reference levels may alsobe dependent on individual anatomical characteristicsor confusion over the theoretical localization of thesymphysis pubis point, as some clinicians use the bonysymphysis pubis and others use the overlying skin or fatpad.
From a theoretical point of view, the only correct ref-erence level to use is the mid-bladder level, i.e., the levelof the tip of the Foley catheter; however this level cannotbe identified at the bedside in clinical practice. Any sur-rogate level should ideally be easy to localize, reliably andindependently of body position. This study compared threepossible estimates of the mid-bladder level, starting fromthe midaxillary level used in the consensus definition ofthe WSACS and adding two alternatives: the phlebostaticaxis, which is already frequently used as a reference pointin ICU patients; and the symphysis pubis which was usedin the past and never formally abandoned; however, meas-urements at both levels proved to correlate poorly withmeasurement at the mid-axillary level.
Conclusion
In conclusion, there is a clinically significant differencebetween IAP measured with the reference line at differentlevels in supine position. The IAPmidax was higher thanboth IAPpubis and IAPphlebostatic . The results of this studysuggest that there may be considerable variation in de-termining the exact location of both the phlebostatic axisand the symphysis pubis, and that patient factors affectthe localization of these reference levels. As such, neitherone can satisfactorily replace the mid-axillary referencepoint advocated by the WSACS for transvesical IAPmeasurement.
Acknowledgements. This work was supported by an unrestrictedgrant from Wolfe-Tory Medical.
References
1. Malbrain ML, Chiumello D, Pelosi P,Bihari D, Innes R, Ranieri VM, delTurco M, Wilmer A, Brienza N,Malcangi V, Cohen J, Japiassu A, DeKeulenaer BL, Daelemans R, Jacquet L,Laterre PF, Frank G, de Souza P,Cesana B, Gattinoni L (2005) Incidenceand prognosis of intraabdominal hy-pertension in a mixed population ofcritically ill patients: a multiple-centerepidemiological study. Crit Care Med33:315–322
2. Kirkpatrick AW, Brenneman FD,McLean RF, Rapanos T, Boulanger BR(2000) Is clinical examination an accu-rate indicator of raised intra-abdominalpressure in critically injured patients?Can J Surg 43:207–211
3. Sugrue M, Bauman A, Jones F,Bishop G, Flabouris A, Parr M, Stew-art A, Hillman K, Deane SA (2002)Clinical examination is an inaccuratepredictor of intraabdominal pressure.World J Surg 26:1428–1431
4. De Waele JJ, De laet I, Malbrain ML(2007) Rational intraabdominal pres-sure monitoring: How to do it? ActaClin Belg Suppl 16–25
5. Kirkpatrick AW, Balogh Z, Ball CG,Ahmed N, Chun R, McBeth P, Kirby A,Zygun DA (2006) The secondaryabdominal compartment syndrome:Iatrogenic or unavoidable? J Am CollSurg 202:668–679
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6. Kirkpatrick AW, De Waele JJ, Ball CG,Ranson K, Widder S, Laupland KB(2007) The secondary and recurrentabdominal compartment syndrome.Acta Clin Belg 1(Suppl):60–65
7. Malbrain ML, Cheatham ML, Kirk-patrick A, Sugrue M, Parr M,De Waele J, Balogh Z, Leppaniemi A,Olvera C, Ivatury R, D’Amours S,Wendon J, Hillman K, Johansson K,Kolkman K, Wilmer A (2006) Resultsfrom the International Conference ofExperts on Intra-abdominal Hyper-tension and Abdominal CompartmentSyndrome. I. Definitions. IntensiveCare Med 32:1722–1732
8. Bland JM, Altman DG (1986) Statis-tical methods for assessing agreementbetween two methods of clinicalmeasurement. Lancet 1:307–310
9. Malbrain ML, De laet I, Cheatham M(2007) Consensus conference def-initions and recommendations onintra-abdominal hypertension (IAH)and the abdominal compartment syn-drome (ACS): the long road to the finalpublications, how did we get there?Acta Clin Belg 1(Suppl):44–59
10. Malbrain ML (2004) Different tech-niques to measure intra-abdominalpressure (IAP): time for a criticalre-appraisal. Intensive Care Med30:357–371
11. De Waele J, Pletinckx P, Blot S, Hoste E(2006) Saline volume in transvesicalintra-abdominal pressure measurement:enough is enough. Intensive Care Med32:455–459
12. McBeth PB, Zygun DA, Widder S,Cheatham M, Zengerink I, Glowa J,Kirkpatrick AW (2007) Effect of patientpositioning on intra-abdominal pressuremonitoring. Am J Surg 193:644–647
The impact of body position on intra-abdominal pressuremeasurement: A multicenter analysis*
Michael L. Cheatham, MD; Jan J. De Waele, MD, PhD; Inneke De Laet, MD; Bart De Keulenaer, MD;Sandy Widder, MD, FRCSC; Andrew W. Kirkpatrick, MD; Adrian B. Cresswell, MD;Manu Malbrain, MD, PhD; Zsolt Bodnar, MD; Jorge H. Mejia-Mantilla, MD; Richard Reis, MD;Michael Parr, MD; Robert Schulze, MD; Sonia Puig, MD; for the World Society of the Abdominal CompartmentSyndrome (WSACS) Clinical Trials Working Group
Elevated intra-abdominal pres-sure (IAP) is a frequent causeof morbidity and mortalityamong the critically ill (1–5).
Increased recognition of its prevalence,combined with recent advances in thediagnosis and management of intra-abdominal hypertension (IAH) and ab-
dominal compartment syndrome (ACS),has resulted in significantly improved pa-tient survival (4, 5). Serial IAP measure-ments are essential to the diagnosis andmanagement of IAH/ACS because clinicalexamination has a sensitivity of only 40%to 60% for detecting the presence of ele-vated IAP (6, 7). The World Society of the
Abdominal Compartment Syndrome(WSACS) has recently published evi-dence-based medicine consensus guide-lines for the measurement of IAP andtreatment of IAH/ACS (1, 2).
IAP has traditionally been measured us-ing the intravesicular or “bladder” tech-nique with the transducer zeroed at thesymphysis pubis (8, 9). The location of thiszero reference point, however, is subject tointerpretation, potentially leading to bothIAP measurement errors and inappropriatetherapy. A point located along the mid-axillary line at the iliac crest is more con-sistently identifiable, anatomically constantduring head of bed elevation, and physio-logically representative of the true locationof the urinary catheter tip within the blad-der (2, 9).
Head of bed elevation is widely recom-mended to reduce the incidence of venti-lator-associated pneumonia (10, 11). Tworecent clinical trials, however, have dem-onstrated that IAP measurements in-crease significantly as the patient’s headof bed is raised (12, 13). As a result, su-pine IAP measurements may underesti-
Objective: Elevated intra-abdominal pressure (IAP) is a frequentcause of morbidity and mortality among the critically ill. IAP is mostcommonly measured using the intravesicular or “bladder” technique.The impact of changes in body position on the accuracy of IAPmeasurements, such as head of bed elevation to reduce the risk ofventilator-associated pneumonia, remains unclear.
Design: Prospective, cohort study.Setting: Twelve international intensive care units.Patients: One hundred thirty-two critically ill medical and
surgical patients at risk for intra-abdominal hypertension andabdominal compartment syndrome.
Interventions: Triplicate intravesicular pressure measurementswere performed at least 4 hours apart with the patient in thesupine, 15°, and 30° head of bed elevated positions. The zeroreference point was the mid-axillary line at the iliac crest.
Measurements and Main Results: Mean IAP values at eachhead of bed position were significantly different (p < 0.0001). Thebias between IAPsupine and IAP15° was 1.5 mm Hg (1.3–1.7). Thebias between IAPsupine and IAP30° was 3.7 mm Hg (3.4–4.0).
Conclusions: Head of bed elevation results in clinically signif-icant increases in measured IAP. Consistent body positioningfrom one IAP measurement to the next is necessary to allowconsistent trending of IAP for accurate clinical decision making.Studies that involve IAP measurements should describe the pa-tient’s body position so that these values may be properly inter-preted. (Crit Care Med 2009; 37:2187–2190)
*See also p. 2310.From the Department of Surgical Education (MLC),
Orlando Regional Medical Center, Orlando, FL; SurgicalIntensive Care Unit (JJDW), Ghent University Hospital,Ghent, Belgium; Intensive Care Unit (IDL), ZiekenhuisNetwerk Antwerpen, Campus Stuivenberg, Antwerpen,Belgium; Intensive Care Unit (BDK), Fremantle Hospital,Alma Street, Fremantle, Australia; Department of Sur-gery (SW), University of Calgary, Calgary, Alberta, Can-ada; Departments of Critical Care Medicine and Sur-gery (AWK), Foothills Medical Centre, Calgary, Canada;Liver Transplant Surgical Service and Liver ITU Insti-tute of Liver Studies King’s College Hospital (ABC),London, United Kingdom; Intensive Care Unit (MM),Ziekenhuis Netwerk Antwerpen, Campus Stuivenberg,Antwerpen, Belgium; Department of Surgery (ZB), Ken-ezy Teaching Hospital, Debrecen, Hungary; Anesthesiaand Intensive Care (JHM-M), Universidad del Valle,Cali, Colombia; Department of Surgery (RR), BratislavaUniversity, Bratislava, Slovakia; Intensive Care Unit(MP), Liverpool Hospital, Sydney, Australia; Depart-
ment of Surgery (RS), SUNY Downstate/Kings CountyHospital, Brooklyn, NY; and Hospital del Mar (SP),Barcelona, Spain.
Supported, in part, by an unrestricted grant fromWolfe-Tory Medical.
Dr. Malbrain has consulted for and has stockownership with Pulsion Medical Systems. Dr. Malbrainhas received patent support from Pulsion Medical Sys-tems. He has also received royalties from HoltechMedical. The remaining authors have not disclosed anypotential conflicts of interest.
Presented, in part, at the 2007 World Congress onthe Abdominal Compartment Syndrome, Antwerp, Bel-gium.
mate true IAP if the patient’s head of bedis elevated between measurements. Thefirst of these studies, however, used asaline instillation volume of 50 mL,which exceeds the currently recom-mended volume and could potentiallyhave resulted in erroneously high IAPmeasurements (12). This study also didnot report the zero reference point used.The second study used a continuous IAPtechnique that is not widely used and forwhich the residual fluid volume withinthe bladder cannot be standardized (13).As a result of these concerns and theimportance of accurately determiningIAP, a multicenter trial was performed todetermine the clinical impact of threedifferent body positions (supine, 15°, and30° head of bed elevation) on intravesicu-lar pressure measured using a standard-ized, reproducible approach (2).
MATERIALS AND METHODS
Study Design. The WSACS Clinical TrialsWorking Group initiated a prospective, inter-ventional cohort study to test the hypothesisthat head of bed elevation significantly in-creases IAP over that measured in the supineposition. The study was designed with 80%power to detect a minimum difference be-tween IAP measurements of 2 mm Hg with atwo-tailed alpha of 0.05. A sample size of 150patients (including a 20% increase for incom-plete data, protocol violations, and patientdropout) was calculated. Study sites were re-cruited from the membership of the WSACSand provided with the study protocol. Patientscreening and enrollment were initiated afterapproval by the institutional review board orethics committee at each study site.
Patient Selection. Patients were enrolledfrom the intensive care units of each study sitebetween November 2005 and April 2006. Pa-
tients were included in the study if they wereaged �18 years, sedated (per study-site proto-col) and on mechanical ventilation, and dem-onstrated at least one risk factor for IAH orACS (Table 1). Either written informed con-sent or a waiver of informed consent, as de-termined by each study site’s institutional re-view board or ethics committee, was alsorequired. Patients were excluded if they wereunable to tolerate changes in body position(because of spinal precautions, intracranialhypertension, hemodynamic instability, etc)or intravesicular pressure measurements werecontraindicated (such as recent bladder sur-gery or injury).
Treatment Protocol. After patient enroll-ment, a point corresponding to the mid-axillary line at the level of the iliac crest wasclearly marked on the patient’s skin to serve asthe zero reference point for all the subsequentIAP measurements. To limit the occurrence ofinaccurate IAP measurements secondary toactive abdominal wall contraction and in-creased work of breathing, patients were se-dated according to the WSACS consensus rec-ommendations during measurements to aRichmond Agitation Sedation Score of �4 (2).IAP was measured using the intravesiculartechnique (AbViser, Wolfe-Tory Medical, SaltLake City, UT) with a standard instillationvolume of 20 mL per the WSACS consensusrecommendations. The intravesicular pres-sure monitoring kits were provided free ofcharge by the manufacturer to standardize theIAP measurement technique among all thestudy sites. The pressure transducer was con-nected to the electronic monitoring equip-ment available in the intensive care unit ofeach study site. Three sets of IAP measure-ments at each body position (supine, 15°, and30° head of bed elevation) were performed atleast 4 hours apart. The order of body positionduring IAP determination was varied witheach set of measurements. The pressure trans-ducer was zeroed at the marked point in themid-axillary line before each IAP measure-
ment. IAP was measured in mm Hg, at endexpiration, in the absence of active abdominalmuscle contraction, and after waiting at least30 seconds to allow for bladder detrusor mus-cle relaxation. The instilled saline was allowedto drain completely from the patient’s bladderbefore performing the next IAP measurement.
Data Collection. At the time of enrollment,information on patient demographics, includingage, sex, weight, height, admission at diagnosis/mechanism of injury, and presence of IAH riskfactors, were collected. Severity of illness duringthe 24-hour period before the first IAP measure-ment was documented through calculation ofthe Acute Physiology and Chronic Health Eval-uation score (version II), Simplified Acute Phys-iology score (version 2), and Sequential OrganFailure Assessment scores. For each set of mea-surements, IAPsupine, IAP15°, IAP30°, mean arte-rial pressure, positive end-expiratory pressure,peak inspiratory pressure, mean airway pressure,and Richmond Agitation Sedation Score wererecorded. At the conclusion of the study, thecause of IAH or ACS, if present, as well asthe occurrence of aspiration during the studyperiod was determined by the primary inves-tigator at each site. IAP, IAH, and ACS weredefined according to the WSACS consensusdefinitions statement (Table 2) (1). Patientsurvival to intensive care unit discharge wasrecorded. All study data were initially enteredonto a case report form on paper and subse-quently entered as deidentified patient datainto an online, secure (128-bit encryption)database maintained on the WSACS Web site.
Statistical Analysis. Data are reported asmean with 95% confidence interval. Repeated-measures analysis of variance was performedto determine statistical significance betweenIAP groups with paired Student’s t tests forpost hoc analysis. Bland and Altman analysiswas performed to identify the bias and limitsof agreement among the three body positions.The WSACS recommends that a bias of �1mm Hg and limits of agreement of �4 to � 4are necessary for two IAP techniques to beconsidered equivalent (14). All p values aretwo sided, with a threshold alpha of 0.05 usedto assign significance.
RESULTS
Patient enrollment occurred from Au-gust 1, 2006 to December 31, 2006. At theconclusion of the study period, 132 hadbeen enrolled from 12 international studysites. A total of 392 IAP measurements wereperformed with four patients who were un-able to tolerate the third set of measure-ments due to their critical illness. Therewere no other protocol violations or pa-tients with incomplete data. As a result, thecalculated sample size for study enrollmentwas exceeded. Patient demographics andseverity of illness are presented in Table 3.The prevalence of IAH (46%) and ACS
Table 1. Risks factors for intra-abdominal hypertension or abdominal compartment syndrome
Acidosis (pH below 7.2)Hypothermia (core temperature below 33°C)Polytransfusion (�10 units of packed red cells/24 hrs)Coagulopathy (platelet count below 55,000/mm3 or a prothrombin time below 50% or an activated
partial thromboplastin time more than two times normal or an international standardized ratio�1.5)
Sepsis (as defined by the American–European Consensus Conference definitions)BacteremiaLiver dysfunction with ascitesMechanical ventilationUse of PEEP or the presence of auto-PEEPPneumoniaAbdominal surgery, especially with tight abdominal closuresMassive fluid resuscitation (�5 L of colloid or crystalloid/24 hrs)Gastroparesis/gastric distention/ileusHemoperitoneumPneumoperitoneum
PEEP, positive end-expiratory pressure.
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(15%) are consistent with previously pub-lished trials (2, 3, 5). The risk factors forIAH that justified patient enrollment arelisted in Table 4. No patient developed as-piration as a result of being placed supineduring the study. During the study mea-surements, mean arterial pressure was 83
mm Hg (81.5–84.1), peak inspiratory pres-sure was 24 cm H2O (23.4–25.0), meanairway pressure was 13 cm H2O (12.4–13.3), and positive end-expiratory pressurewas 8 cm H2O (7.4–8.0). The mean Rich-mond Agitation Sedation Score was �3.8(�3.9 to �3.7) confirming appropriate se-dation to minimize the potential for erro-neous IAP measurements secondary to ab-dominal wall contraction. Eighty-eightpercent of patients had a closed abdomenduring their IAP measurements. Of the12% of patients with an open abdomen,56% required abdominal decompressionfor ACS, whereas the remaining 44% re-quired an open abdomen following eitherdamage control laparotomy for trauma orintestinal perforation. Twenty-four percentof the study patients died due to the follow-ing reasons: multiple system organ failure,44%; ACS, 22%; hemorrhage, 18%; andsepsis, 16%.
The triplicate IAP measurements foreach body position were compared usingrepeated-measures analysis of variance(Table 5). Both IAP15° and IAP30° weresignificantly increased compared withIAPsupine (p � 0.0001). The bias betweenIAPsupine and IAP15° was 1.5 mm Hg (1.3–1.7) with limits of agreement of �2.8 to5.8. The bias between IAPsupine and IAP30°
was 3.7 mm Hg (3.4–4.0) with limits ofagreement of �2.2 to 9.6.
When those patients with marked IAH(IAP �20 mm Hg) were considered, onlyIAP30° remained significantly increasedcompared with IAPsupine (p � 0.01) (Table5). The bias between IAPsupine and IAP15°
was �0.2 mm Hg (�1.2 to 0.8), withlimits of agreement of �5.8 to 5.4. Thebias between IAPsupine and IAP30° was 2.7mm Hg (1.3–4.2), with limits of agree-ment of �5.4 to 10.8.
DISCUSSION
The importance of serial IAP measure-ments in the assessment and resuscitationof critically ill patients has been increas-ingly recognized over the past decade (1–9).
Given the significant associated morbidityand mortality, IAP should be monitored inany patient who demonstrates risk factorsfor IAH/ACS (Table 1) (1, 2, 5). IAP is botha diagnostic measurement, given the inac-curacy of clinical examination in detectingthe presence of IAH, and a therapeuticmeasurement, because IAP-guided resusci-tation correlates with improved survival(5). As IAP measurement techniques haveevolved, several key questions have arisenincluding the optimal intravesicular salineinstillation volume, the proper zero refer-ence position for transducer placement(symphysis pubis, mid-axillary, or phlebo-static axis), and the proper body position forIAP measurements. Although previousstudies have provided answers to the firsttwo questions, this study addresses this lastand very important question (2, 9).
Head of bed elevation is commonlyused to reduce the risk of aspiration andincidence of ventilator-associated pneu-monia (10, 11). This study confirms thateven mild head of bed elevation signifi-cantly increases measured IAP above thatdetermined in the supine position. Thesepositional differences, although seem-ingly small, are both statistically andclinically significant, and could poten-tially lead to alterations in clinical ther-apy. They emphasize the importance ofconsistent body positioning from mea-surement to measurement to allow accu-rate trending of IAP for clinical decisionmaking. Furthermore, patient body posi-tion during IAP measurement should al-ways be documented both clinically andin future studies so that IAP values maybe properly interpreted and compared.
The abdominal cavity is widely consid-ered to be homogeneous and primarily flu-idic in character, behaving as a unit accord-ing to Pascal’s Law such that IAP is thesame throughout. As a result, IAP shouldremain constant regardless of changes inbody position. Three factors determine IAP:gravity, visceral shear deformation, and vis-ceral compression. In the supine position,the effects of gravity and visceral shearshould be minimal such that visceral com-pression correlates directly with intrave-sicular pressure. With head of bed eleva-tion, however, gravity and an increasedhydraulic column of fluid compressing thebladder may well play a significant role inintravesicular pressure measurements ac-cording to the formula
P2 � P1 � �� � g�h2 � h1�
where P is the hydrostatic pressure, � (rho),the density of the fluid, g, the sea level
Table 2. Definitions (1)
Parameter Definition
IAP The pressure concealed within the abdominal cavityNormal IAP is approximately 5–7 mm Hg in critically ill adults
IAH A sustained or repeated pathologic elevation of IAP �12 mm HgACS A sustained IAP �20 mm Hg (with or without an APP �60 mm Hg) that is
Patients 132Age (yrs) 59 � 18Male gender (%) 71Body mass index (kg/m2) 27 � 6Etiology of critical illness (%)
Medical 43Surgical 39Trauma 18
Severity of illness scoresAPACHE II 21 � 9SAPS 2 45 � 18SOFA 10 � 6
Intra-abdominalhypertension (%)
46
Abdominal compartmentsyndrome (%)
15
Abdominal decompression (%) 14Pulmonary aspiration (%) 0Survival to intensive care
unit discharge (%)76
APACHE II, Acute Physiology and ChronicHealth Evaluation score, version II; SAPS 2, Sim-plified Acute Physiology score, version 2; SOFA,Sequential Organ Failure Assessment score.
Table 4. Risk factors for intra-abdominal hyper-tension/abdominal compartment syndrome
Total exceeds 100% because of the presenceof multiple risk factors.
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acceleration due to Earth’s gravity, and h,the height of bed elevation for two differentbody positions (such as 30° vs. supine).
This study confirms, in a larger patientpopulation, the findings of previous studiesdemonstrating that changes in body posi-tion do alter IAP measurements and sug-gests that the abdominal cavity is hetero-geneous in nature. However, the reasonthat changes in body position significantlyalter measured IAP remains unclear. Onepossible explanation is that head of bedelevation results in visceral compression ofthe bladder, due to gravity, resulting inelevated intravesicular pressure measure-ments compared with what would be re-corded if the patients were supine. As evi-dent from this study, however, the impactof head of bed elevation appears to be lesspronounced in patients with higher gradesof IAH where the edematous viscera aremore fixed and less likely to gravitationallycompress the bladder. A more probable ex-planation is that head of bed elevation in-creases visceral compression between therigid thorax and pelvis resulting in a trueelevation in IAP. Anecdotal experiencedemonstrates a significant increase in bothintravesicular and intragastric pressurewith head of bed elevation suggesting thatgravity alone is insufficient to explain thedifferences encountered in this study (15).
The seminal studies defining the “criti-cal IAP” at which organ dysfunction andfailure begins to occur, and on which thedefinitions for IAH and ACS are based, wereall performed with patients in the supineposition. Additional research is necessary tomore fully characterize the nature of theabdominal cavity and document whetherhead of bed elevation results in uniformelevations in IAP throughout all quadrantsof the abdomen. Until studies are availabledefining new benchmarks for critical IAPvalues at various head of bed elevations, webelieve that IAP measurements should beperformed in the supine position to bothstandardize the measurement techniquefor consistent serial IAP monitoring and toremove the issue of whether IAP measure-
ments at 15° and 30° head of bed elevationare accurate or a measurement artifact. It isalso crucial for clinicians to recognize thatsupine intravesicular pressures may under-estimate the true IAP if head of bed eleva-tion is used between measurements to re-duce ventilator-associated pneumonia.
CONCLUSIONS
Head of bed elevation results in clini-cally significant increases in measured IAP.Until the implications and clinical accuracyof nonsupine IAP measurements are betterdefined, IAP measurements should be per-formed in the supine position. Future IAH/ACS research should include documenta-tion of the patient’s body position duringIAP measurement so that these values maybe properly interpreted.
ACKNOWLEDGMENTS
We like to extend our sincere apprecia-tion to the following individuals for theirassistance in this study: Karen Safcsak, RN,Orlando Regional Medical Center, Orlando,FL; Veerle Bosschem, RN, Dieter Debergh,RN, Ghent University Hospital, Ghent, Bel-gium; Ian Jenkins, FJFICM, Bruce Powell,MD, Fremantle Hospital, Fremantle, Aus-tralia; Crystal Wilson, RN, Linda Knox, RN,Foothills Medical Centre, Calgary, AB, Can-ada; Julia Wendon, FRCP, Matthew Bowles,BSc, MS, FRCS, King’s College Hospital,London, United Kingdom; Carlos Ordonez,MD, Fundacion Valle del Lili, Cali, Colom-bia; Peter Labas, MD, PhD, Anna Vdovia-kova, RN, Olina Kubisova, RN, ComeniusUniversity, Bratislava, Slovakia; Ali Ibra-him, MBChB, FRCA, Sharon Micallef, RN,Liverpool Hospital, Sydney, Australia; andAntonia Vazquez, MD, Luís Grande, MD,PhD, Hospital del Mar, Barcelona, Spain.
REFERENCES
1. Malbrain ML, Cheatham ML, Kirkpatrick A,et al: Results from the International Confer-ence of Experts on Intra-abdominal Hyper-tension and Abdominal Compartment Syn-
drome. I. Definitions. Intensive Care Med2006; 32:1722–1732
2. Cheatham ML, Malbrain ML, Kirkpatrick A,et al: Results from the International Confer-ence of Experts on Intra-abdominal Hyper-tension and Abdominal Compartment Syn-drome. II. Recommendations. Intensive CareMed 2007; 33:951–962
3. Malbrain ML, Chiumello D, Pelosi P, et al: Prev-alence of intra-abdominal hypertension in criti-cally ill patients: A multicentre epidemiologicalstudy. Intensive Care Med 2004; 30:822–829
4. Cheatham ML, Safcsak K: Is the evolvingmanagement of IAH/ACS improving sur-vival? Acta Clin Belg 2007; 62(Suppl 1):268
5. Kimball EJ, Kim W, Cheatham ML, et al:Clinical awareness of intra-abdominal hyper-tension and abdominal compartment syn-drome in 2007. Acta Clin Belg 2007;62(Suppl 1):66–73
6. Sugrue M, Bauman A, Jones F, et al: Clinicalexamination is an inaccurate predictor of in-traabdominal pressure. World J Surg 2002;26:1428–1431
7. Kirkpatrick AW, Brenneman FD, McLean RF,et al: Is clinical examination an accurate indi-cator of raised intra-abdominal pressure incritically injured patients? Can J Surg 2000;43:207–211
8. Malbrain ML, Jones F: Intra-abdominal pres-sure measurement techniques. In: Abdomi-nal Compartment Syndrome. Ivatury RR,Cheatham ML, Malbrain ML, et al (Eds). Lan-des Biomedical, Georgetown, 2006
9. De Waele JJ, Cheatham ML, De laet I, et al:The effect of different reference transducerpositions on intra-abdominal pressure mea-surement: A multicenter analysis. IntensiveCare Med 2008; 34:1299–1303
11. Drakulovic MB, Torres A, Bauer TT, et al:Supine body position as a risk factor fornosocomial pneumonia in mechanically ven-tilated patients: A randomized trial. Lancet1999; 354:1851–1858
12. Vasquez DG, Berg-Copas GM, Wetta-Hall R:Influence of semi-recumbent position on in-tra-abdominal pressure as measured by blad-der pressure. J Surg Res 2007; 139:280–285
13. McBeth PB, Zygun DA, Widder S, et al: Effect ofpatient positioning on intra-abdominal pressuremonitoring. Am J Surg 2007; 193:644–647
14. Malbrain ML, De laet I, Cheatham ML: Con-sensus conference definitions and recom-mendations on intra-abdominal hyperten-sion (IAH) and the abdominal compartmentsyndrome (ACS)—The long road to the finalpublications, how did we get there? Acta ClinBelg 2007; 62(Suppl 1); 44–59
15. Vianne D, De laet I, Vermeiren G, et al: Effectof different body positions on intra-abdomi-nal pressure estimated with 3 different meth-ods via the bladder and stomach. Acta ClinBelg 2007; 62(Suppl 1):257
Table 5. Intra-abdominal pressures by body position
All measurements IAP �20 mm Hg
Patients (n) 132 32IAPsupine 12.1 mm Hg (11.7–12.6) 22.5 mm Hg (21.6–23.4)IAP15° 13.6 mm Hg (13.2–14.1) 22.3 mm Hg (21.3–23.3)IAP30° 15.8 mm Hg (15.3–16.4) 25.2 mm Hg (23.7–26.8)
IAP, intra-abdominal pressure.
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RESEARCH Open Access
The effect of body position on compartmentalintra-abdominal pressure following livertransplantationAdrian B Cresswell, Wayel Jassem, Parthi Srinivasan, Andreas A Prachalias, Elizabeth Sizer, William Burnal,Georg Auzinger, Paolo Muiesan, Nigel D Heaton, Matthew J Bowles, Julia A Wendon*
Abstract
Background: Current assumptions rely on intra-abdominal pressure (IAP) being uniform across the abdominalcavity. The abdominal contents are, however, a heterogeneous mix of solid, liquid and gas, and pressuretransmission may not be uniform. The current study examines the upper and lower IAP following livertransplantation.
Methods: IAP was measured directly via intra-peritoneal catheters placed at the liver and outside the bladder.Compartmental pressure data were recorded at 10-min intervals for up to 72 h following surgery, and the effect ofintermittent posture change on compartmental pressures was also studied. Pelvic intra-peritoneal pressure wascompared to intra-bladder pressure measured via a FoleyManometer.
Results: A significant variation in upper and lower IAP of 18% was observed with a range of differences of 0 to 16mmHg. A sustained difference in inter-compartmental pressure of 4 mmHg or more was present for 23% of thestudy time. Head-up positioning at 30° provided a protective effect on upper intra-abdominal pressure, resulting ina significant reduction in all patients. There was excellent agreement between intra-bladder and pelvic pressure.
Conclusions: A clinically significant variation in inter-compartmental pressure exists following liver transplantation,which can be manipulated by changes to body position. The existence of regional pressure differences suggeststhat IAP monitoring at the bladder alone may under-diagnose intra-abdominal hypertension and abdominalcompartment syndrome in these patients. The upper and lower abdomen may need to be considered as separateentities in certain conditions.
IntroductionInterest in the measurement of intra-abdominal pressure(IAP) has grown steadily over the last decade and hasbeen shown to be a significant problem within the gen-eral intensive care unit (ICU) population [1,2], with thedeleterious effects of elevated IAP having been welldescribed in numerous clinical studies and reviews[3-15]. The culmination of the recent increase in inter-est in this condition has been the creation, by an inter-national panel of experts (The World Society onAbdominal Compartment Syndrome, WSACS, http://
www.wsacs.org), of a consensus document for defini-tions [16] and suggested management guidelines [17].Underpinning these recommendations, however, is a
requirement for accurate and reproducible measurementof IAP with several studies having shown that there is norole for clinical estimation of IAP, either by palpation ormeasurement of abdominal perimeter [18-20].Numerous techniques for the measurement of IAP by
both direct and indirect methods have been described,with indirect approaches utilizing measurement of thepressure concealed within a hollow intra-abdominal viscusmost usually the urinary bladder (intra-bladder pressure,IBP) [21] or stomach (intra-gastric pressure, IGP) [22].Direct methods for measuring IAP have been employedexclusively in the experimental setting whereby the IAP is
* Correspondence: [email protected] Transplant Surgical Service and Liver Intensive Care Unit, Kings CollegeLondon, Institute of Liver Studies, King’s College Hospital, Denmark Hill, SE59RS, London, UK
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transduced directly from the peritoneal cavity via a cathe-ter containing a continuous column of fluid [23], a bal-loon-tipped catheter [24] or via a laparoscopic gasinsufflation system [25]. The application of such techni-ques is clearly limited by their invasiveness, and no advan-tage over indirect measurements has been demonstratedin terms of accuracy.On the face of the available data, therefore, a non-inva-
sive technique such as the IBP or IGP method would seemmore attractive for routine clinical use. This, however,relies on two unproven assumptions regarding the trans-mission of pressure throughout the abdomen. The firstassumption is that the bladder wall will act as a passivediaphragm for the transmission of pressure, and the sec-ond is that IAP is transmitted uniformly throughout theabdominal cavity such that the measured pressure at anyone position will be reflected elsewhere in the cavity.The second assumption relies on the contents of the
intra-abdominal cavity, transmitting pressure as a singlecompartment, which, given the heterogeneous mix of con-tents, may not hold true. Such a regional variation in post-operative patients would have important implications bothfor the post-operative screening of IAP following surgeryand for the potential of a localised effect on the regionalorgan systems that may not be manifested by the measure-ment of the relatively remote IBP. This concept would besynonymous with the poly-compartment syndrome whichhas previously been suggested to affect the head, thorax,abdomen [26] and extremities.It has been shown that IAP can be influenced by body
position with an increase in bladder pressure of up to 7.5mmHg with a 45° positioning angle [27]. However, theeffect of body position on the individual intra-abdominalcompartment has not previously been described.Liver transplantation was chosen for the study as a
major intervention that has been shown to be associatedwith a significant incidence of intra-abdominal hyperten-sion (IAH) in both our own unpublished data and in stu-dies from other institutions [28]. The surgical procedureitself is relatively standardised and confined to a singleintra-abdominal compartment, which makes comparisonsbetween individual subjects easier and logically suggeststhat the chances of identifying a regional pressure phe-nomenon would be highest.The two primary aims of the current study were to
compare the IBP to that immediately outside within theintra-peritoneal pelvis and to establish whether there areany regional variations in IAP between the upper andlower abdominal compartments (upper intra-abdominalpressure, UIAP and lower intra-abdominal pressure,LIAP) following liver transplantation. A secondary end-point was to examine the effect, if any, of body positionon the compartmental pressures.
MethodsFollowing approval of the study design by the localResearch Ethics and Research & Development Commit-tees, a total of 20 patients undergoing elective orthotopictransplantation were recruited, all of whom gave informedconsent to take part in this study. All patients receivedcadaveric whole grafts and had not undergone liver trans-plantation previously. Data were collected during the sub-jects’ stay on a 15-bed dedicated Liver Intensive Care Unitwith aspects of post-operative care such as the administra-tion of intra-venous fluids and the use of vaso-activeagents, guided by established unit protocol. All subjectswere nursed in a 30° head of bed position to minimise riskof respiratory complications with the exception of shortperiods of being laid flat in order to measure supine IAP.All were calm and comfortable at the time of measure-ment (Richmond agitation-sedation scale of 0).For each patient, UIAP and LIAP were measured
directly via catheters placed under the left lobe of thetransplanted organ and in the pelvis at the time ofoperation (Minivac Drain, Unomedical, Worcestershire,UK). These catheters were connected, via a fluid columnto an electronic pressure transducer with numeric andpressure trace displayed on the ICU monitor (FukudaDenshi Co., Ltd, Tokyo, Japan). These catheters wereused solely for measurement of IAP and not for drai-nage. Standard closed surgical drains were placed in theusual position to prevent accumulation of body fluids.The electronic transducers were fixed to the patient by
sutures at a point corresponding to the internal positionof the catheter tips on the upper and lower abdominalwall. A position that was found to correspond to thezero-reference point as suggested by the WSACS, of themid-axillary line at the iliac crest when supine. Thetransducers were flushed and zeroed twice daily andafter each patient position change. The measured deadspace of the catheter was < 2 ml, and thus, a 4-ml flushwith normal saline, from a sterile closed system, ensureda continuous column of fluid between the intra-perito-neal catheter tip and the transducer which was main-tained between flushes by continuous low volumeirrigation. The quality of the pressure waveform waschecked hourly by the ‘rapid oscillation test [21]’,whereby rapid and repeated palpation of the abdominalwall at the level of the intra-peritoneal catheter tip wasvisible in real time on the ICU monitor’s pressure trace(Figure 1).Compartmental IAP was transduced continuously via
this equipment, and the monitoring system recordedpaired measurement of UIAP and LIAP at 10-min inter-val. The catheters were left in place for a maximum of72 h or until the point of discharge from the LiverIntensive Care Unit, whichever came sooner.
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Each patient was re-positioned to lie supine at 6-hourintervals (four times per day) in order to measure thesupine compartmental pressures. The transducers were‘re-zeroed’ following each position change, and the pres-sure was allowed to equilibrate for 5 min prior to mak-ing each of these recordings.In addition to the direct pressure measurements, IBP
was also recorded at 6-h intervals with the patient bothin a 30° head up and supine positions using a Foley-Manometer system (Holtech medical Company, Charlot-tenlund, Denmark), as shown in Figure 2.
Statistical analysisThe data were recorded in a Microsoft Excel Spread-sheet (Microsoft, WA, USA) and analysed using SPSSv15 (Chicago, IL, USA) in accordance with the recom-mendations for data analysis published by the WSACS[29]. Data obtained at 6-hourly intervals (IBP, LIAP andUIAP at supine and 30° head of bed angles) were com-pared by means of a Bland and Altman analysis [30].The coefficient of variance of IAP was defined as thestandard deviation of IAP divided by the mean IAP. Per-centage error of the measurement was defined as twicethe precision divided by the mean IAP. The normalityof distribution of the continuous pressure recordingswas tested using a Kolmogorov-Smirnov test, and beingparametric and normally distributed, means were com-pared using a paired t test.Following professional statistical advice and in order to
perform both within and between individual comparisonsof the difference in compartmental pressures in subjectswith differing baseline IAP, the difference between the
two compartmental recordings was converted to a per-centage of the mean of both compartments (Difference ÷(mean of UIAP + LIAP) × 100). This eliminated the effectof the underlying baseline IAP and inter-individual varia-tions. For the same reason, the trend in compartmentalpressure over time was expressed as the difference ineach subsequent pressure recording over the initial IAP.The differences in compartmental pressures over timewere normally distributed and, therefore, compared bylinear regression. For the purpose of reporting, a differ-ence of 4 mmHg or greater between the compartmentswas considered to be clinically significant.
ResultsComparison of direct and indirect measurement of lowerintra-abdominal pressureThere was no clinically relevant difference between themean measurements made via the pelvic transducer andthe foley manometer. The Bland and Altman plot(Figure 3a, b, c) confirmed excellent agreement betweenthe two measures in all body positions, with a calculatedbias and precision of -0.06 and 0.6 when supine and0.006 and 0.5 at 30°. Full details of the two measure-ments are given in Table 1.
Compartmental pressure measurementsA total of 169 synchronous measurements of IBP, LIAPand UIAP were made to obtain compartmental pressurewith subjects in a supine and 30° head of bed position at6-h intervals. In contrast to the excellent agreementbetween IBP and LIAP, comparisons of both IBP andUIAP, and LIAP and UIAP revealed very poor agreement
Figure 1 Equipment set-up to transduce LIAP and UIAP along with FoleyManometer for measurement of IBP.
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with a high measured bias, precision and percentageerror (Table 1 and Figure 4a, b). Parameters for thesecomparisons fell well outside the thresholds for agree-ment stated by the WSACS [29].The mean UIAP when supine was 11.7 mmHg, which
was reduced to 9.6 mmHg with 30° head of bed positioning(p < 0.001). Mean LIAP was 9.2 mmHg when supine andincreased to 9.6 mmHg with 30° head of bed (p < 0.001).The increase in UIAP with a move to a supine position
was observed in all patients, irrespective of which com-partment contained the higher pressure. The observedmagnitude of change in mean UIAP was not differentbetween subjects exhibiting a raised IAP (> 12 mmHg)and those with a normal IAP (2.4 and 1.8 mmHg change,respectively; p = 0.5). Similarly, although there was a sug-gestion that subjects with higher upper than lower com-partmental pressures exhibited a larger change in UIAPwhen moving to a supine position (2.4 and 1.1 mmHgchange, respectively), this difference was not statisticallysignificant (p = 0.9).
Continuous pressure measurementsA total of 5,980 automated-paired pressure measurementsof direct LIAP and UIAP were recorded with an average
of 299 per patient (range 212 to 461). Of the 20 subjects,12 revealed a higher mean pressure within the UIAP thanthe LIAP compartment, with the greatest mean pressuredifference for an individual being 5.3 mmHg.When analysed as a whole and as sub-groups with
either higher UIAP or higher LIAP, the differencebetween the compartmental pressures was highly statisti-cally significant (p < 0.001, p < 0.001 and p < 0.004,respectively). The range of differences between compart-mental pressures in the two groups also differed withthose exhibiting a higher UIAP having a broader range (0to 16 mmHg) than those with a higher LIAP (0 to 12mmHg). The mean pressures observed in each compart-ment for the subjects as a whole and for the two sub-groups are displayed in Table 2.The mean difference between the two compartments
was similar, whether it was the upper or lower compart-ment that contained the higher pressure. Expressed as apercentage of the mean of the two compartments, thisequated to a clinically significant 23.4% difference whenUIAP was highest, and 23.6% when LIAP was highest.Individual analysis of each subject’s data confirmed
the significant difference (p < 0.001) between compart-ments for all but two patients. In two individuals, the
Figure 2 Technique for using FoleyManometer for the measurement of intra-abdominal pressure. IBP marked by arrow.
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(a)
(b)
(c)
Figure 3 Bland and Altman plots comparing intra-bladder pressure (IBP) and lower intra-abdominal pressure (LIAP). (a) Bland andAltman plot to compare IBP and LIAP with a supine body position and a head of bed position of 30°. (b) Bland and Altman plot to compareIBP and LIAP with a supine body position.(c) Bland and Altman plot to compare IBP and LIAP with a head of bed position of 30°. Lower level ofagreement (LLA) and upper level of agreement (ULA) marked by dotted lines.
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compartmental pressures did not differ significantly (p =0.349 and 0.122, respectively); however, the mean IAPsfor both patients and in both compartments fell withinnormal safe limits (7.1 and 7.3 mmHg, and 11.4 and12.0 mmHg, respectively).Nine subjects displayed a continuous pressure > 12
mmHg in one or other compartment for greater than 1h. Of these, five had higher mean UIAP, and four hadhigher LIAP. There was no difference between the meandifference in compartmental pressures in subjects with asustained pressure of > 12 mmHg compared to thosewithout (2.3 and 2.1 mmHg, respectively; p = 0.772).In the higher UIAP group, a clinically significant dif-
ference of 4 mmHg or more between compartmentalpressures was observed during an average of 23% of thestudy period. This proportion was higher in the higherLIAP group at 37% of the study duration; however,these differences were not statistically significant (p =0.666). The direction of change in compartmental IAPover time correlated positively such that an overallupward trend in UIAP was accompanied by an upwardtrend in LIAP (r2 = 0.582, p < 0.001, n = 5,960).
DiscussionThe recognition and treatment of IAH and the abdom-inal compartment syndrome (ACS) are clearly reliant onan accurate and reliable system for the measurement ofIAP. The technique for IBP measurement has under-gone much refinement over the last decade [21] and hasnow been presented, by an international panel ofexperts, as the gold standard for intra-abdominal pres-sure measurement [17]. In addition to the effects ofgravity and sheer stress [31], the value of bladder pres-sure relies on two key assumptions which have beenwidely accepted without direct evidence of their validity.The first assumption is that the bladder wall will act as
a passive diaphragm to the transmission of pressure, andtherefore, the pressure measured within the urinary blad-der will accurately reflect the pressure immediately
outside within the peritoneal cavity. Several studies, inboth animal and human models, have shown good agree-ment between directly and indirectly measured intra-abdominal pressure [22,23,32,33]. All of these studies,however, have measured direct IAP at a site distant tothe urinary bladder and followed artificial elevation ofIAP by means of either saline or gas insufflation, or byinsertion of a mechanical prosthesis. Our data is the firstto directly compare the pressure measured at the intra-vesical and intra-peritoneal sides of the bladder wall andconfirms that the pressure measured within the urinarybladder demonstrates excellent agreement with the pres-sure to be measured within the pelvic peritoneal cavity.The second assumption relates to the mechanical
properties of the peritoneal contents. It has been sug-gested that the abdominal contents are primarily fluid incomposition and, therefore, that pressure transmissioncan be expected to follow Pascal’s law such that mea-surement of the IAP at any point will reflect the pres-sure contained within the entire abdominal cavity [21].In reality, however, the abdominal contents remain aheterogeneous mix of solid, liquid and gaseous compo-nents with the exact composition influenced by severaldisease processes such as paralytic ileus, visceraloedema, or the presence of ascites. Pressure transmis-sion characteristics are, therefore, likely to be rathermore complex.
Regional IAPThe implications of a regional ACS are profound withthe gold-standard technique for pressure measurementoccurring at the lowest point in the abdominal cavity,whilst the organs that have been shown to be most sus-ceptible to raised IAP all lie in the upper abdomen.Separate studies have all clearly shown the deleteriouseffects of raised IAP on the splanchnic circulation[11-13,34,35], cardiac [8,36], respiratory [9,37,38], renal[5,32,39] and neurological [40,41] functions in bothhuman and animal models.
Table 1 Comparison of IBP, LIAP and UIAP
Comparisons Number Mean IAP Range IAP COVA IAP ra p Bias Precision LLA ULA % Error
IBP vs LIAP All 338 9.43 0.0 to 19.0 43.6 0.99 < 0.001 0.03 0.59 -1.14 1.18 13
The patient positioned supine and in a 30° head of bed angle. IBP, intra-bladder pressure; LIAP, lower intra-abdominal pressure; UIAP, upper intra-abdominalpressure; HOB, head of bed, IAP, intra-abdominal pressure; COVA; coefficient of variance; LLA, Lower level of agreement; ULA, Upper level of agreement. ar =Pearson product-moment correlation coefficient.
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The possibility of a regional variation between theupper and lower IAP was identified, but not explored indetail in 1994 [22]. In this study, IGP was measured in
nine patients undergoing laparoscopic cholecystectomyat a variety of different insufflation pressures. The studywas designed to validate the measurement of IGP
(a)
(b)
Figure 4 Intra-bladder pressure (IBP) and upper intra-abdominal pressure (UIAP), and lower intra-abdominal pressure (LIAP) and UIAP.(a) Bland and Altman plot to compare IBP and UIAP with a supine body position and a head of bed position of 30°. (b) Bland and Altman plotto compare LIAP and UIAP with a supine body position and a head of bed position of 30°. LLA and ULA marked by dotted lines.
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against the pneumoperitoneum but also showed thatIGP could also be up to 4 mmHg higher or 3 mmHglower than the measured IBP. A further small study hasidentified differences in gastric and bladder pressure intwo patients within a general ICU population [42] andsuggested that such a variation could provide clues as toany underlying pathophysiological process.Our study is the largest to compare the two compart-
mental pressures within a clinical setting, without artifi-cial manipulation of IAP. In keeping with the abovestudy, we showed a significant difference between com-partmental pressures but with a much broader andmore clinically significant range of variation of up to 16mmHg and a mean difference between the compart-ments of around 20% which equates to a maximal inter-compartmental mean difference of 5.3 mmHg.Clearly, such a magnitude of variation, coupled with
the observation that compartmental pressures were seento vary by 4 mmHg or more for an average of 23% ofthe time, means that relying on the measurement of onecompartmental pressure only may lead to a significantlyelevated pressure in the other compartment beingmissed. The positive relationship that we have demon-strated between compartmental pressures should man-date separate measurement of UIAP in patients inwhom the IBP is adopting an upward trend.It was interesting to observe that the range of varia-
tion in inter-compartmental pressure was greater inthose patients concealing a higher UIAP, and this maybe related to the previous data which suggest that upperabdominal incisions result in measurable changes toabdominal wall contractile properties which may contri-bute to the generation of a locally raised IAP [43].
Body position and regional IAPPrevious clinical studies have considered the influence ofpatient positioning on IAP. In the largest [44], a multi-centre study of 132 ventilated patients, the mean differ-ence between supine and 30° IBP was 3.7 mmHg with a
range of 3.4 to 4.0 mmHg. The largest reported differ-ence in positional pressures was seen in a study of 37patients at a range of bed positions between 0 and 45°[27]. It was found that IBP increased with head-up tiltwith a mean increase of 5 mmHg at 30°, and 7.4 mmHgat 45°.Our data have also demonstrated a statistically signifi-
cant increase in the IBP with head-up positioning to30°. This was, however, a far smaller increase of just0.43 mmHg rather than the 5 mmHg seen in the abovestudy. This would lend support to the theory that LIAPwill increase as the result of a more upright posture[33]. The most likely explanation for this is that an erectposture leads to an increase in the hydrostatic weightexerted by the abdominal organs and body habituspressing downwards on the bladder much in the samemanner as increasing the height of a standing column offluid would increase the measurable pressure at the bot-tom of the column.A more interesting observation in our own data, how-
ever, is the fact that despite accurate re-zeroing of apatient mounted transducer UIAP was significantlyincreased in the supine position compared to a 30°head-up tilt. The reason for this observation remainsunclear but may be related to the re-positioning of themore mobile hollow abdominal viscera along with boththeir fluid contents and any free intra-peritoneal fluidwith a more upright posture. This observation wouldsuggest that a simple change in posture could provide aclinically significant improvement in the UIAP, which inturn, may improve hepatic, renal and splanchnic bloodflow. Such positive effects on organ perfusion wouldneed to be demonstrated by further specific studies;however, it does raise the possibility that a head-upposition may be advantageous for reasons other thansimple ventilatory mechanics. It is also particularlyencouraging to note that a larger reduction in UIAP canbe expected in those patients with a higher upper, ratherthan lower, baseline intra-abdominal pressure. The lack
Table 2 Mean continuous pressures observed in each compartment, split according to highest average compartmentpressure
Subject group Meancompartmental IAP
(mmHg, SD)
Mean difference between compartments (SD) Mean percentage difference between compartmentsa
UIAP LIAP
Higher 10.5 8.3 2.2 23.4%
UIAP (4.6) (4.5) (2.4)
Higher 8.6 10.9 2.3 23.6%
LIAP (3.8) (5.6) (3.2)
Overall 9.7 9.5 0.3 3.1%
(4.2) (4.6) (4.1)
UIAP, upper intra-abdominal pressure; LIAP, lower intra-abdominal pressure; SD, Standard Deviation. aMean percentage difference between compartments =mean difference between compartments/(mean UIAP + mean LIAP/2) × 100.
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of collection of other body anthropomorphic data tofurther examine these two groups is accepted to be anunfortunate limitation of the study.
Clinical applicationThe fact that it was impossible to predict which of thetwo compartments would conceal the higher pressuresuggests that, for this subgroup of patients, dual com-partmental pressure monitoring may be required basedupon the clinical condition of the patient. It remainsunclear, however, whether the observed variation ininter-compartmental pressure is specific to the procedureof liver transplantation, or whether the findings could begeneralised to all upper abdominal surgery, local inflam-matory conditions such as severe acute pancreatitis, orindeed the measurement of IAP in general. It is also ashortcoming that various anthropomorphic data anddetails of illness severity scores were not collected, asthese have been shown to impact on baseline IAP.Further study with a larger sample size will be
required to elucidate the relationship between the loca-tion of the higher compartmental pressure, the magni-tude of variation in compartmental pressure and theduration for which there is a significant differencebetween compartments with clinical outcome. Such astudy, with higher numbers, may be facilitated by therecent introduction of a commercially available non-invasive device for the measurement of IGP (CiMON,Pulsion Medical Systems, Munich, Germany). It wouldalso be extremely interesting to measure the retroperito-neal compartmental pressure within the upper abdomenwhich very much contains the ‘anatomical terminus’ forthe arrival and departure of the abdominal blood supply,as well as the kidneys themselves.
ConclusionIt remains to be seen and further research is certainlyrequired to discover whether the observed effects arespecific to patients undergoing liver transplantation andto define any effects on clinical outcome. The currentdata do, however, demonstrate a significant variation inregional IAP within the study group. It may be well thatwe need to consider regional IAP in more detail andconsider the different abdominal compartments, includ-ing the retroperitoneum, as more distinct entities, andpatient positioning may prove a useful utility for opti-mising compartmental pressures and perfusion.
ConsentWritten informed consent was obtained from the patientfor publication of this case report and accompanyingimages. A copy of the written consent is available forreview by the Editor-in-Chief of this journal.
AcknowledgementsThis article has been published as part of Annals of Intensive Care Volume 2Supplement 1, 2012: Diagnosis and management of intra-abdominalhypertension and abdominal compartment syndrome. The full contents ofthe supplement are available online at http://www.annalsofintensivecare.com/supplements/2/S1.Figure 2 is reproduced with the kind permission of Mr. Bo Holte, Holtech,Charlottenlund, Denmark. The authors wish to thank Pulsion MedicalSystems who have sponsored the processing fees for this article.
Authors’ contributionsABC conceived of the idea, designed the study, arranged ethical approval,conducted the study, collected the data, analysed the data and wrote themanuscript. JAW and MJB reviewed the study design, assisted with analysisand reviewed the manuscript. WJ, PS, AAP, ES, WB, GA, PM, MR and NDHassisted in the insertion and the day-to-day care of the experimentalpressure catheters.
Authors’ informationABC is now a hepatopancreatobiliary (HPB) surgeon at the BasingstokeHepatobiliary Unit, UK. WJ, PS, AAP, MR and NDH are HPB and livertransplant surgeons at King’s College Hospital, UK. JAW, ES, WB and GA areliver intensivists at King’s College Hospital, UK. MJB is an HPB surgeon atDerriford Hospital, UK but undertook this work whilst a HPB and transplantsurgeon at Kings College Hospital.
Competing interestsDr Julia Wendon is a member of the medical advisory board of PulsionMedical Systems, who have sponsored the processing fees of thissubmission. The authors declare that they have no other conflicts ofinterests.
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doi:10.1186/2110-5820-2-S1-S12Cite this article as: Cresswell et al.: The effect of body position oncompartmental intra-abdominal pressure following liver transplantation.Annals of Intensive Care 2012 2(Suppl 1):S12.
Cresswell et al. Annals of Intensive Care 2012, 2(Suppl 1):S12http://www.annalsofintensivecare.com/content/2/S1/S12
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