Vous êtes sur la page 1sur 7

Actas Urol Esp.

2013;37(5):273---279

Actas Urológicas Españolas

www.elsevier.es/actasuro

ORIGINAL ARTICLE

Renal consequences of intraabdominal hypertension in a porcine


model. Search for the choice indirect technique for
intraabdominal pressure measurement夽
L. Correa-Martín a,∗ , G. Castellanos b , M. García c , F.M. Sánchez-Margallo a

a
Unidad de Laparoscopia, Centro de Cirugía de Mínima Invasión Jesús Usón, Cáceres, Spain
b
Servicio de Cirugía General, Hospital Universitario Virgen de la Arrixaca, Murcia, Spain
c
Unidad de Anestesiología, Centro de Cirugía de Mínima Invasión Jesús Usón, Cáceres, Spain

Received 18 April 2012; accepted 30 June 2012


Available online 26 September 2013

KEYWORDS Abstract
Kidney; Objective: To study the effects on the renal system in a porcine model of intraabdominal
Intraabdominal hypertension, and to determine the indirect technique of choice for determination of the
hypertension; intraabdominal pressure.
Experimental Materials and methods: 30 pigs were used and divided into two groups according to increased
intraabdominal pressure values (20 mm Hg and 30 mm Hg). In both groups pressures were reg-
istered 8 times, summing up to 3 h, with a CO2 insufflator. Three different measures of the
intraabdominal pressure were taken: a direct transperitoneal measure, using a catheter of
Jackson-Pratt connected to a pressure transducer, and two indirect measures, a transvesical
by means of a Foley to manometer system, and a transgastric by introducing in the stomach
a catheter connected to a pressure monitor with electronic hardware. Mean arterial pressure
was calculated, along with the cardiac index, production of urine and serum creatinine.
Results: There was a greater correlation between the transvesical and the transperitoneal
intraabdominal pressures (R2 = 0.95). Average transgastric intraabdominal pressure was infe-
rior to the transperitoneal indicator in all taken measurements. The average arterial pressure
descended in both groups, with earlier significant differences observed at 30 mm Hg (p < 0.020).
Urine production was lower at 30 mm Hg compared with the 20 mm Hg group (9.63 ± 1.57 ml
versus 3.26 ± 1.73 ml). Serum creatinine increased in both groups being pathological at 30 mm
Hg after 1 h 20 min, with existing differences between early pressures (p < 0.027).
Conclusions: This study revealed marked renal affectation with higher severity at 30 mm Hg
pressures. The transvesical technique showed a greater correlation with the direct measure-
ment technique used, defining this as the method of choice for determination of intraabdominal
pressure.
© 2012 AEU. Published by Elsevier España, S.L. All rights reserved.

夽 Please cite this article as: Correa-Martín L, et al. Consecuencias renales de la hipertensión intraabdominal en modelo porcino. Búsqueda

de la técnica indirecta de elección de la medida de la presión intraabdominal. Actas Urol Esp. 2013;37:273---279.
∗ Corresponding author.

E-mail address: lcorreaccmijesususon@gmail.com (L. Correa-Martín).

2173-5786/$ – see front matter © 2012 AEU. Published by Elsevier España, S.L. All rights reserved.
274 L. Correa-Martín et al.

PALABRAS CLAVE Consecuencias renales de la hipertensión intraabdominal en modelo porcino.


Riñón; Búsqueda de la técnica indirecta de elección de la medida de la presión
Hipertensión intraabdominal
intraabdominal;
Experimental Resumen
Objetivo: Estudiar las consecuencias renales en un modelo porcino de hipertensión intraab-
dominal y determinar de la técnica indirecta de elección para la medida de la presión
intraabdominal.
Material y métodos: Se utilizaron 30 cerdos divididos en dos grupos, presión intraabdominal
incrementada en 20 mm Hg y en 30 mm Hg. En ambos, las presiones se registraron en 8 tiempos
hasta 3 horas con un insuflador de CO2 . Se realizaron tres medidas de la presión intraabdominal,
una directa trasperitoneal, empleando un catéter de Jackson-Prat conectado a un traductor de
presión, y dos indirectas, una transvesical mediante un sistema de la foley manometer y otra
transgástrica introduciendo en el estómago un catéter conectado a un monitor de presión con
hardware electrónico. Se calculó la presión arterial media, el gasto cardiaco, la producción de
orina y la creatinina sérica.
Resultados: Hubo una mayor correlación entre la presión intraabdominal transvesical y la
transperitoneal (R2 =0,95). La media de la presión intraabdominal transgástrica fue menor que
la trasperitoneal en todos los tiempos. La presión arterial media descendió en ambos grupos
observando diferencias significativas más precoces a 30 mm Hg (p<0,020). La producción de
orina fue menor a 30 mm Hg (9,63±1,57) vs (3,26ml±1,73). La creatinina aumentó en ambos
grupos siendo patológica a 30 mm Hg a partir de 1 h 20 min existiendo diferencias entre presiones
precoces (p<0,027).
Conclusiones: Hubo afectación renal más marcada a presiones de 30 mm Hg. La técnica trasvesi-
cal mostró una mayor correlación con la técnica directa empleada, por lo que consideramos
ésta como la de elección.
© 2012 AEU. Publicado por Elsevier España, S.L. Todos los derechos reservados.

Introduction abdominal distension and the presence of increased IAP. It


is therefore essential to have a reliable measurement tech-
Abdominal compartment syndrome (ACS) is a clinical entity nique of the IAP and, this way, act at the right moment.
characterized by increased intra-abdominal pressure with Consequently, the IAP measurement is essential to diagnose
marked abdominal distension and with potential to cause, the IAH and the consequent ACS, the choice of the tech-
if not diagnosed and corrected in time, multiple organ dys- nique used being critical for a proper diagnosis. This measure
function syndrome (MODS), and death of the patient.1 should be performed routinely in patients with a high prob-
The clinical manifestations of this syndrome involve ability of an IAH, with a measurement frequency of 4 h, with
mainly the cardiovascular, pulmonary, renal, and gastroin- the patient in supine and at the end of expiration.10 That is
testinal systems, although others such as the neurological why our goal has focused on comparing 2 types of indirect
one and even the abdominal wall are also included. These measures observing their correlation with transperitoneal
systems can be affected by either direct compression, as intra-abdominal pressure to determine which the technique
in the case of pulmonary dysfunction, or by a decrease in of choice in patients admitted with abdominal hypertension
perfusion of the various organs.2 is, and early identifying the renal alterations that occur with
At kidney level, there is a significant clinical associa- increased IAP.
tion between IAH and renal impairment, renal failure being
one of the main manifestations of ACS.3 Thus, renal alter-
ation and failure are a common cause of admission in ICU, Materials and methods
observing that this function is the most sensitive to the
increase of the IAH.4,5 Since 1913, it has been known that We used 30 healthy sows, weighing 20---30 kg. The study was
IAH causes a dysfunction in this system. However, it was not approved by the ethics committee of animal experimen-
until 1947 when Bradley and Bradley6 studied, for the first tation, fulfilling the European regulations on protection of
time, the effects caused by increased IAP on renal function animals used for experimental and other scientific purposes.
in humans, demonstrating the decrease in the glomeru- After the adaptation and quarantine period, the study
lar filtration rate and the renal plasma flow, decreased began. All the animals received the same anesthetic proto-
urine output being one of the first clinical manifestations col, administering intraoperative analgesia.
of IAH.7 For lifting the IAP, we used a CO2 insufflator (SCB Ther-
Currently, one of the biggest problems is to establish a moflator Karl Storz-Endoskope) using an inflow of 1---2 l/min
proper diagnosis to apply treatment as early as possible. to reach the desired pressures in each of the groups, 20 or
In relation to this, and as demonstrated by Sugrue et al.,8 30 mm Hg.
clinical examination cannot accurately assess the IAP. Simi- After reaching the desired pressure in each group, 3 types
larly, Malbrain et al.9 observed a poor correlation between of IAP measurements were conducted.
Renal consequences of intraabdominal hypertension in a porcine model 275

Transperitoneal intra-abdominal pressure 35.00

y= 0.93x + 1.05
It was calculated continuously and directly; to do so, a R2=0.95
Jackson-Prat catheter connected to a pressure transducer, 30.00
and this to a S/5TM General Electric Datex-Ohmeda compact

TV-IAP, mmHg
anesthesia monitor, was introduced laparoscopically into
the abdominal cavity over the right hypochondrium.
25.00

Transvesical intra-abdominal pressure


20.00
It was obtained intermittently and indirectly; to do so,
the animal placed in dorsal decubitus, a cystoscopy
assisted catheter was introduced, to which we connected
15.00
a Foley manometer system (Holtech Medical, Copenhagen, 15.00 20.00 25.00 30.00 35.00
Denmark® ) between the diuresis bag calibrated with marks TP-IAP, mmHg
in mm Hg from 0 to 40 mm Hg. After placing the system,
20 ml of saline solution were introduced for system purg- Figure 1 Degree of correlation and regression line between
ing. The measurement was obtained by placing the zero of the measures of the TV-IAP and TP-IAP shown throughout the
the measurement system at the level of the pubic symphysis study time. Pearson correlation coefficient.
of the hip with the rest of the system in 90◦ position rela-
tive to the horizontal one of the animal. After opening the Pearson correlation coefficient between every 2 variables.
existing forceps below the antibacterial filter, one can see The significance level in all cases was p < 0.05. To carry out
it descend, at first, the physiological saline used for purg- the statistical analysis, we used the SPSS 17.0 for Windows;
ing, and subsequently the urine contained in the system to SPP, Chicago, IL, USA.
stabilize and provide measurement of the IAP.
Results
Transgastric intra-abdominal pressure
In all the groups we were able to obtain the desired pressure.
First, the animal was placed in right lateral decubitus to The statistical analysis showed statistically significant
perform an upper digestive endoscopy to empty the stom- differences between the transperitoneal intra-abdominal
ach and thus avoid possible interferences. Once empty, a pressure (TP-IAP) and the TG-IAP, in which lower values than
catheter was inserted in the stomach to determine the trans- in the rest of the pressures were obtained. There were no
gastric intra-abdominal pressure (TG-IAP) continuously. Its statistically significant differences between the 2 pressures
proximal end was connected to a pressure monitor with measured indirectly (Table 1).
electronic hardware (Spiegelberg CD Pharma) which, after Figs. 1 and 2 show that there was a high degree of positive
filling the air balloon with a total volume of 0.05---0.1 ml correlation between the 3 IAPs measured in the study, the
and automatically adjusting the zero, measured in real-time regression coefficient (R2 ) being higher between the TP-IAP
graphically recording the TG-IAP. and the TV-IAP.
For determining the hemodynamic parameters, we used Table 2 shows the hemodynamic parameters measured in
the PICCO® system. Blood samples were removed for deter- the 2 groups; in it we can see a progressive decrease in the
mination of serum creatinine, and the production of urine
was taken into account. 35.00
The means of the monitored variables during the anes- y= 0.86x + 1.26
thetic procedure were calculated at the following times: R2=0.89
T1 after obtaining the appropriate pressure for each group;
30.00
T2 after 20 min to obtain the proper pressure (stabilization
TG-IAP, mmHg

period); T3 after 30 min of T2; T4 after 60 min of T2; T5 after


90 min of T2; T6 after 120 min of T2; T7 after 150 min of T2;
25.00
and T8 after 180 min of T2.

Statistical analysis 20.00

We obtained a descriptive statistics for each variable obtain-


ing the mean ± standard deviation. The comparison between
15.00
groups 2-2, at each of the times, was performed using 15.00 20.00 25.00 30.00 35.00
the Student’s t-test. The evolution of the parameters was TP-IAP, mmHg
analyzed using a multivariate analysis, repeated measures
ANOVA. In the case of the urine output, we took the Figure 2 Degree of correlation and regression line between
basal level as 0 and we observed its variation over time. the measures of the TG-IAP and TP-IAP shown throughout the
The degree of correlation of the variables determined the study time. Pearson correlation coefficient.
276 L. Correa-Martín et al.

Table 1 Measures of the IAP collected throughout the study in the IAP 20 and 30 mm Hg groups for 3 h.

Measures of the IAP Times TP-IAP (mm Hg) TV-IAP (mm Hg) TG-IAP (mm Hg) Sig
IAP group T1 20.83 ± 1.02a 20.40 ± 0.89ab 19.92 ± 0.87b 0.036
20 mm Hg/3 h T2 21.34 ± 1.28a 20.43 ± 0.90ab 19.91 ± 1.04b 0.003
T3 21.02 ± 1.29a 20.33 ± 0.89ab 19.85 ± 1.38b 0.037
T4 20.78 ± 1.09a 20.30 ± 1.04ab 19.48 ± 1.09b 0.007
T5 20.93 ± 1.33a 20.16 ± 0.79ab 19.64 ± 1.39b 0.019
T6 21.01 ± 1.44a 20.23 ± 0.82ab 19.55 ± 1.38b 0.010
T7 20.69 ± 1.29a 20.20 ± 0.88ab 19.40 ± 1.36b 0.017
T8 20.60 ± 1.12a 20.00 ± 1.00ab 19.36 ± 1.16b 0.014
IAP group T1 31.20 ± 1.54a 30.20 ± 1.09ab 29.72 ± 1.36b 0.011
30 mm Hg/3 h T2 31.33 ± 1.49a 30.36 ± 0.97ab 29.53 ± 1.06b 0.001
T3 31.66 ± 1.11a 30.905 ± 0.80ab 30.14 ± 0.71b 0.0001
T4 31.66 ± 1.11a 30.83 ± 0.87ab 30.02 ± 0.94b 0.0001
T5 31.46 ± 1.55a 30.43 ± 0.88ab 29.28 ± 1.43b 0.0001
T6 31.40 ± 1.63a 30.10 ± 0.96ab 29.18 ± 1.75b 0.001
T7 31.33 ± 1.44a 30.26 ± 0.84ab 29.41 ± 1.40b 0.001
T8 31.26 ± 1.79a 30.20 ± 0.79ab 29.00 ± 1.69b 0.001

Sig: significance level for the group.


Tukey test, a,b,c: different letters indicate statistically different means.

MAP in both study groups, being earlier under pressures of the start of the study, showing a lower urine output at
30 mm Hg, there being differences between pressures after pressures of 30 mm Hg.
50 min following the increase in the pressure. In the cardiac
output (CO), no significant changes were observed, we could
only observe in the T6 differences between pressures. Discussion
Table 3 reflects the values of serum creatinine through-
out the study. An increase thereof can be observed in both In the last decade, thanks to the World Society of Abdominal
study groups, there being significant differences between Compartment Syndrome, great progress has been made to
pressures from the T3. In the group of 30 mm Hg, a patho- better understand both the etiology and pathophysiology of
logical increase in creatinine can be observed from the T4. the IAH and ACS.11,12 That is why, one of the biggest prob-
Fig. 3 represents the urine output of each group at each lems we face is determining the precise point at which to
time. The differences between pressures are present from act so that the patient does not develop a MODS. This may

Table 2 Hemodynamic measures collected throughout the study in the IAP 20 and 30 mm Hg roups for 3 h.

Hemodynamic measures Times IAP group IAP group


20 mm Hg/3 h 30 mm Hg/3 h
Mean blood pressure T1 60.26 ± 4.23 59.66 ± 1.38
(mm Hg) T2 57.40 ± 3.73 55.93 ± 1.38
T3 56.66 ± 7.43 51.53 ± 3.06*,**
T4 55.80 ± 8.54 48.66 ± 3.26*,**
T5 53.40 ± 9.37 47.33 ± 3.35*,**
T6 49.33 ± 8.78* 45.86 ± 4.85*,**
T7 46.53 ± 8.65* 44.20 ± 3.74*,**
T8 44.66 ± 7.52* 42.00 ± 4.45*,**
Cardiac output T1 1.75 ± 0.37 1.81 ± 0.38
(l/min/m2 ) T2 1.30 ± 0.23 1.21 ± 0.39
T3 1.34 ± 0.25 1.37 ± 0.29
T4 1.42 ± 0.45 1.51 ± 0.47
T5 1.50 ± 0.55 1.53 ± 0.54
T6 1.52 ± 0.57 1.76 ± 0.41**
T7 1.48 ± 0.53 1.83 ± 0.30
T8 1.47 ± 0.54 1.77 ± 0.52
* p < 0.05 vs. baseline.
** p < 0.05 vs. groups with IAP.
Renal consequences of intraabdominal hypertension in a porcine model 277

Table 3 Value of serum creatinine collected throughout the study in the IAP 20 and 30 mm Hg groups for 3 h.

Renal measures Times IAP group IAP group


20 mm Hg/3 h 30 mm Hg/3 h
Creatinine T1 1.96 ± 0.57 2.34 ± 0.60
T2 2.05 ± 0.63 2.43 ± 0.62
T3 2.12 ± 0.59 2.62 ± 0.15**
T4 2.27 ± 0.50 2.81 ± 0.49**
T5 2.41 ± 0.53 2.88 ± 0.54**
T6 2.57 ± 0.56 3.10 ± 0.47*,**
T7 2.59 ± 0.58 3.17 ± 0.41*,**
T8 2.69 ± 0.54* 3.26 ± 0.44*,**
* p < 0.05 vs. baseline.
** p < 0.05 vs. IAP groups.

be related to late diagnoses,9 poor prognoses, and infec- also observed an increase in serum creatinine from 6 h. This
tious complications. Therefore, the objectives of this work circumstance is because they make the first measurement
have focused on early determining renal alterations occur- from that time without being able to determine whether
ring in the face of increased IAP and determining an indirect that increase occurred before that time. Therefore, we con-
technique of choice able to reliably measure the existing sider important to determine measurements over time of
IAP in the patient to establish an early diagnosis and proper this parameter, since it has been reported that the degree
treatment. to which serum creatinine changes with regard to a baseline
Clinically, renal involvement presents with a progres- value can reflect changes in the GFG.16
sive decrease in the diuresis as the pressure increases. This A decrease in the CO has been described as the
oliguria does not respond to fluid therapy, diuretics, or main mechanism of renal function impairment17 due to
vasoactive drugs. In general, the changes in the IAP affect a decrease of renal perfusion and an increase of the
the production of urine more than the MAP, thus, decreased renin---angiotensin---aldosterone activity. However, both
urine output being one of the first visible signs of IAH.7,13 This the compression of the vein and the renal parenchyma have
is in agreement with our results, where we observe a more also been involved as primary mediators of renal function.18
marked decrease in the urine output in the 30 mm Hg group, This is because as previous studies have shown,5,19,20 nor-
finding oliguria without actually occurring anuria at the set malization of the CO does not improve renal disorders
times of the study. This may be because a longer study time caused by increased IAP. Our results show no alteration
would be needed for anuria to occur, as demonstrated by in the CO but a renal involvement possibly attributed to
long-term studies in pigs from 24 h of study.14,15 This is con- the compression of the vessels themselves and the renal
sistent with the pathological increase in creatinine to 30 mm parenchyma as a consequence of increased pressure. Thus,
Hg that we observe in our results. Like us, Toens et al.15 we can say that there was renal involvement; however, we
consider necessary further studies that correlate the histo-
logical alterations, loss of functionality, and changes in the
12.00 renin---angiotensin---aldosterone system that occurs before
renal impairment.
10.00
It has been described that an isolated elevation of the IAP
should not be considered as a criterion for making decisions
Change in urine output (ml)

for critical patients.8,9 Because there are several studies


8.00
that show that neither the IAH nor the ACS should be diag-
nosed by means of physical examination,8,9 several methods
6.00 have been used to determine the measure of the IAP, both
directly and indirectly.
4.00
In connection with the measurement systems that have
been used directly and invasively to measure the IAP, there
are different methods, such as intraperitoneal catheters
2.00 connected to a pressure transducer, or during laparoscopic
surgery using a Veress needle.7,9,21,22 However, these direct
0.00 methods are considered too invasive and, therefore, not
1 2 3 4 5 6 7 8 suitable for critical patients due to increased risk of infec-
Times of study tion that they might involve,23 currently being used to
Groups PIA validate indirect methods.24 In our study, we used a Jackson-
20 mm Hg 30 mm Hg Prat catheter connected to a pressure transducer as a
measure of the IAP directly and continuously. This way, the
Figure 3 Changes in the urine output during all the study pressure in the abdomen could be determined, at all times,
times at the 2 pressures studied: 20 mm Hg (green) and 30 mm continuously showing a high correlation with the indirect
Hg (blue). *p < 0.05 vs. baseline; † p < 0.05 vs. groups with IAP. measured PIA methods.
278 L. Correa-Martín et al.

In relation to the 2 indirect methods used in our study, 7. Wauters J, Claus P, Brosens N, McLaughlin M, Malbrain M,
both have been validated by several authors.25---28 Although Wilmer A. Pathophysiology of renal hemodynamics and renal
the measure of the TG-IAP may have advantages over the cortical microcirculation in a porcine model of elevated intra-
TV-IAP, being a continuous method, the same as Lee et al.29 abdominal pressure. J Trauma. 2009;66:713---9.
and Malbrain et al.,26 our results show a high degree of 8. Sugrue M, Bauman A, Jones F, Bishop G, Flabouris A, Parr M,
et al. Clinical examination is an inaccurate predictor of intraab-
correlation between the two pressures, showing a higher
dominal pressure. World J Surg. 2002;26:1428---31.
correlation between the measure of the IAP directly and the 9. Malbrain ML, de laet I, van Regenmortel N, Schoonheydt K,
TV-IAP in both study groups. This shows that both pressures Dits H. Can the abdominal perimeter be used as an accu-
are closely related to each other, behaving similarly faced rate estimation of intra-abdominal pressure? Crit Care Med.
with the increase of the pressure, so we can consider the TV- 2009;37:316---9.
IAP as the technique of choice in patients admitted to the 10. Malbrain JF. Intra-abdominal pressure measurement tech-
ICU. Thus, we agree with Malbrain et al.,26,30 and De Pot- niques. In: Ivatury RR, Cheatham M, Malbrain M, Sugrue M,
ter et al.,27 on considering that it is an accurate method for editors. Abdominal compartment syndrome. Georgetown: Lan-
estimating the IAP, besides being easy and safe to perform. des Bioscience; 2006. p. 18---68.
Before the results shown, we consider that with ele- 11. Keskinen P, Leppaniemi A, Pettila V, Piilonen A, Kemppainen E,
Hynninen M. Intra-abdominal pressure in severe acute pancre-
vated IAP continuously at pressures of 30 mm Hg, there
atitis. World J Emerg Surg. 2007;2:2.
begins to be damage to the kidney, the first clinical man- 12. De Waele JJ, Hoste E, Blot SI, Decruyenaere J, Colardyn F.
ifestation being decreased urine output. With regard to the Intra-abdominal hypertension in patients with severe acute pan-
measurement methods, we consider, as the first option, creatitis. Crit Care. 2005;9:R452---7.
the manometry technique employed in this study because 13. Malbrain ML, Vidts W, Ravyts M, de Laet I, de Waele J. Acute
of the advantages that it presents, such as being easy to per- intestinal distress syndrome: the importance of intra-abdominal
form, cost-effective, rapid, and requiring minimal handling. pressure. Minerva Anestesiol. 2008;74:657---73.
14. Schachtrupp A, Toens C, Hoer J, Klosterhalfen B, Lawong AG,
Schumpelick V. A 24-h pneumoperitoneum leads to mul-
Funding tiple organ impairment in a porcine model. J Surg Res.
2002;106:37---45.
This work was supported by the Fundación Mutua Madrileña. 15. Toens C, Schachtrupp A, Hoer J, Junge K, Klosterhalfen B,
Schumpelick V. A porcine model of the abdominal compartment
syndrome. Shock. 2002;18:316---21.
Conflict of interest 16. Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P.
Acute renal failure-definition, outcome measures, animal
The authors declare that they have no conflict of interest. models, fluid therapy and information technology needs:
the Second International Consensus Conference of the Acute
Dialysis Quality Initiative (ADQI) Group. Crit Care. 2004;8:
Acknowledgement R204---12.
17. Barroso S, Hernández R, Ruiz B, Arrobas M. Deterioro de la
To the Personnel of the Surgical Area of the Minimally Inva- función renal asociado a aumento de la presión abdominal.
sive Surgery Center Jesus Usón. Nefrología. 2007;27:85---6.
18. Bloomfield GL, Blocher CR, Fakhry IF, Sica DA, Sugerman HJ. Ele-
vated intra-abdominal pressure increases plasma renin activity
References and aldosterone levels. J Trauma. 1997;42:997---1004.
19. Harman PK, Kron IL, McLachlan HD, Freedlender AE, Nolan SP.
1. Malbrain ML, Cheatham ML, Kirkpatrick A, Sugrue M, Parr M, Elevated intra-abdominal pressure and renal function. Ann Surg.
de Waele J, et al. Results from the International Conference 1982;196:594---7.
of Experts on Intra-abdominal Hypertension and Abdominal 20. Kron IL, Harman PK, Nolan SP. The measurement of intra-
Compartment Syndrome. I. Definitions. Intensive Care Med. abdominal pressure as a criterion for abdominal re-exploration.
2006;32:1722---32. Ann Surg. 1984;199:28---30.
2. Muckart D, Ivatury R, Lepäniemi R, Smith S. Definitions. In: 21. Karakoulas K, Grosomanidis V, Amaniti E, Kouvelas D, Skourtis C,
Ivatury R, Cheatham ML, Malbrain M, Sugrue M, editors. Abdom- Vasilakos D. The effect of intra-abdominal hypertension
inal compartment syndrome. Georgetown: Landes Bioscience; alone or combined intra-abdominal hypertension---endotoxemia
2006. p. 8---18. in cerebral oxygenation in a porcine model. Hippokratia.
3. Sugrue M, Hallal A, d’Amours S. Intra-abdominal hypertension 2008;12:225---9.
and the kidney. In: Ivatury R, Cheatham M, Malbrain M, Sugrue 22. Schachtrupp A, Tons C, Fackeldey V, Hoer J, Reinges M,
M, editors. Abdominal compartment syndrome. Georgetown: Schumpelick V. Evaluation of two novel methods for the direct
Landes Bioscience; 2006. p. 119---28. and continuous measurement of the intra-abdominal pressure
4. Vidal MG, Ruiz Weisser J, Gonzalez F, Toro MA, Loudet C, in a porcine model. Intensive Care Med. 2003;29:1605---8.
Balasini C, et al. Incidence and clinical effects of intra- 23. Hunter JD, Damani Z. Intra-abdominal hypertension and
abdominal hypertension in critically ill patients. Crit Care Med. the abdominal compartment syndrome. Anaesthesia.
2008;36:1823---31. 2004;59:899---907.
5. Biancofiore G, Bindi ML, Romanelli AM, Boldrini A, Consani G, 24. Al-Hwiesh AK, al-Mueilo S, Saeed I, al-Muhanna FA. Intraperi-
Bisa M, et al. Intra-abdominal pressure monitoring in liver toneal pressure and intra-abdominal pressure: are they the
transplant recipients: a prospective study. Intensive Care Med. same? Perit Dial Int. 2011;31:315---9.
2003;29:30---6. 25. Otto J, Kaemmer D, Biermann A, Jansen M, Dembinski R,
6. Bradley SE, Bradley GP. The effect of increased intra- Schumpelick V, et al. Clinical evaluation of an air-capsule tech-
abdominal pressure on renal function in man. J Clin Invest. nique for the direct measurement of intra-abdominal pressure
1947;26:1010---22. after elective abdominal surgery. BMC Surg. 2008;8:18.
Renal consequences of intraabdominal hypertension in a porcine model 279

26. Malbrain M. Validation of a novel fully automated continuous in a mixed population of critically ill patients: a multiple-center
method to measure intra-abdominal pressure. Intensive Care epidemiological study. Crit Care Med. 2005;33:315---22.
Med. 2003; Suppl. 1:S73. 29. Lee SL, Anderson JT, Kraut EJ, Wisner DH, Wolfe BM. A simplified
27. De Potter TJ, Dits H, Malbrain ML. Intra- and interobserver approach to the diagnosis of elevated intra-abdominal pressure.
variability during in vitro validation of two novel methods J Trauma. 2002;52:1169---72.
for intra-abdominal pressure monitoring. Intensive Care Med. 30. Malbrain ML, de Laet I, Viaene D, Schoonheydt K, Dits H.
2005;31:747---51. In vitro validation of a novel method for continuous intra-
28. Malbrain ML, Chiumello D, Pelosi P, Bihari D, Innes R, Ranieri VM, abdominal pressure monitoring. Intensive Care Med. 2008;34:
et al. Incidence and prognosis of intraabdominal hypertension 740---5.

Vous aimerez peut-être aussi