Hernia DOI 10.1007/s10029-014-1313-x
ORIGINAL ARTICLE
Physiologic changes with abdominal wall reconstruction in a porcine abdominal compartment syndrome model R. Mohan • H. G. Hui-Chou • H. D. Wang • A. J. Nam M. Magarakis • G. S. Mundinger • E. N. Brown • A. J. Kelamis • M. R. Christy • E. D. Rodriguez
•
Received: 6 February 2014 / Accepted: 12 September 2014 Ó Springer-Verlag France 2014
Abstract Purpose Abdominal compartment syndrome (ACS) is a severe complication of ventral hernia repair. The aims of this study were to investigate the effects of intra-abdominal pressure on the physiologic changes of abdominal wall reconstruction and component separation in a porcine model. Methods Ventral hernia repair (VHR) was simulated by abdominal fascial imbrication of a 10 9 15 cm defect in 45 Yorkshire pigs assigned to five experimental groups. ACS was simulated by a Stryker endoscopy insufflator with intra-abdominal pressure elevated to 20 mmHg in two groups. Component separation was performed in one of these groups and in one group without ACS. Physiological parameters were measured before and after the procedures
The study was presented at the American College of Surgeons 2010 Clinical Congress Surgical Forum, Washington, D.C. October 7, 2010 (Oral Presentation); at the 92nd Annual American Association of Plastic Surgeons Meeting (Poster Presentation), New Orleans, LA, April 22, 2013; and the 58th Annual Plastic Surgery Research Council (Oral Presentation), Santa Monica, CA, May 2–4, 2013.
and monitored for 4 h. The animals were euthanized for histologic analysis of organ damage. Results VHR led to an increase in intra-abdominal pressure, bladder pressure, and central venous pressure by an average of 14.89, 13.93, and 14.69 mmHg (p \ 0.001) in all animals. Component separation was performed in 25 animals and the three pressures reduced by 9.11, 8.00, 7.89 mmHg (p \ 0.001). ACS correlated with higher percentages of large and small bowel necrosis compared to groups without abdominal compartment syndrome. Conclusions The results confirm that primary repair of large abdominal wall defects leads to increased intraabdominal pressure, which can be reduced with component separation. In animals with ACS, component separation may reduce the risk of organ damage. Central venous pressure, bladder pressure, and other physiologic parameters accurately correlated with elevated intra-abdominal pressure and may have utility as markers for diagnosis of ACS. Keywords Abdominal wall reconstruction Ventral hernia repair Abdominal compartment syndrome Component separation Porcine model
R. Mohan and H. G. Hui-Chou are equally contributed authors. R. Mohan H. G. Hui-Chou H. D. Wang A. J. Nam M. Magarakis G. S. Mundinger E. N. Brown A. J. Kelamis M. R. Christy Division of Plastic, Reconstructive and Maxillofacial Surgery, R Adams Cowley Shock Trauma Center, University of Maryland Medical Center, Baltimore, MD, USA E. D. Rodriguez (&) Department of Plastic Surgery, NYU Langone Medical Center, Institute of Reconstructive Plastic Surgery, 307 E 33rd st, New York, NY 10012, USA e-mail: [email protected]
Introduction Reconstructing abdominal wall defects can be challenging in patients with complex abdominal wall hernias or open abdomen because of damage control laparotomy [1, 2]. These abdominal defects are usually a result of trauma, malignancy, or infection [3]. Many techniques have been described to reconstruct abdominal wall fascial defects, namely primary fascial repair, component separation(CS), and interpositional prosthetic meshes [4–7]. The success of
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these techniques has been described in the literature, and based on our center’s experience we devised an algorithm to approach complex abdominal wall defects with severe loss of domain [8]. However, there is a potential risk of abdominal compartment syndrome (ACS) with ventral hernia repair (VHR) and abdominal wall reconstruction which can have devastating consequences [9]. ACS is associated with massive fluid shifts into visceral organs and increased mechanical pressure, which can be exacerbated by volume resuscitation. ACS is also known to cause decreased central venous return and increased intrathoracic pressures [10]. The aims of this study were to investigate the effects of ACS, induced by sustained increases in intra-abdominal pressure (IAP), in a porcine model. Physiological parameters that can be measured in the intensive care setting were monitored. Primary VHR, CS, and simulated ACS were performed in some cohorts to assess the effect on physiological parameters and end-organ damage.
Methods After obtaining Institutional Animal Care and Use Committee’s (IACUC) approval, 45 of 3-month-old Yorkshire pigs (45 females, average weight 27.16 lbs) were purchased and housed at Thomas D. Morris, Inc. (Reisterstown, MD) during the study. The research and care facility is accredited by the American Association for the Accreditation of Laboratory Animal Care International (AAALAC-I). The animals were cared for by certified veterinarians in accordance with the principles in the Guide for Care and Use of Laboratory Animals and each received a general health evaluation by a veterinarian before inclusion in the study. The pigs were assigned to five experimental groups. (Table 1) Primary VHRs were simulated by abdominal fascial imbrication of a 10 9 15 cm defect. ACS was simulated with a Stryker endoscopy insufflator elevated to an IAP of 20 mmHg and maintained at that level for 4 h. 45 Yorkshire pigs were divided into five groups. Group 1 received VHR alone; group 2 underwent VHR and had ACS; group 3 received VHR with CS; group 4 had VHR, CS, and ACS; group 5 had VHR, CS, and a lower IAP. Physiological parameters were measured before and after the procedure. Animals were euthanized 2 weeks postoperatively for histologic analysis of organ damage. Vascular access For monitoring of animals, catheterization of the internal jugular vein, common carotid artery, and femoral vein was performed. A 2-in. vertical skin incision was made in the right neck, and the internal jugular vein and carotid artery
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Table 1 Summary of experimental groups Group
N
Imbrication
1
5
?
2
15
?
3
5
?
4
15
?
5
5
?
IAP
Component separation
Concept Primary VHR alone
??
Primary VHR with ACS ?
Primary VHR with CS
??
?
Primary VHR with CS and ACS
?
?
Primary VHR with CS and IAH
45 animals were divided into five experimental groups. Group 1 received VHR alone; group 2 underwent VHR and had ACS; group 3 received VHR and CS; group 4 had VHR, CS, and ACS; group 5 had VHR, CS, and mild ACS (IAP = 10)
were isolated. An arteriotomy was performed and a 9.5French and a 7-French catheter were inserted into these vessels, respectively. A pulmonary artery catheter (SwanGanz) was then floated into position through the internal jugular. A 2-in. skin incision was made caudal to the right inguinal line in the right groin. The right common femoral vein was catheterized with a 9.5-French catheter for monitoring central venous pressure (CVP) below the diaphragm. Foley catheter placement A 7-French urinary catheter was inserted under sterile conditions. An Ab-Viser IAP Monitoring System (Convatec, Skillman, NJ) was used to measure bladder pressures (BLP). Surgical technique: the imbrication (ventral hernia repair) model Once sedated, the animals were intubated and administered intravenous antibiotics prior to surgical incision. No muscle relaxants were administered. A skin incision was made in the midline from the xiphoid process to the level of the pubic symphysis. After reaching the abdominal fascial layer, lateral suprafascial flaps were undermined and raised bilaterally from the costal margins superiorly to the iliac crests inferiorly with the mid-axillary line serving as the lateral border. A Veress needle was placed at the midline through the linea alba to measure the IAP. A 10 cm by 15 cm ellipse was drawn at the center of the exposed fascia. Full thickness sutures using 2-0 Prolene were placed at the edges of the ellipse. (Fig. 1, top left) With the sutures tied, the fascial edges of the ellipse apposed each other and imbricated the fascia. (Fig. 1, top right) This technique was used to simulate primary VHR. The IAP was measured before and after imbrication to monitor the pressure.
Hernia Fig. 1 Intra-operative images of imbrication and component separation. Top, left Sutures were placed along the edges of the drawn ellipse to achieve imbrication. Top, right Apposition of the fascial edges of the ellipse led to a decrease in abdominal fascial girth. Bottom, left Release of external oblique fascia during component separation. Bottom, right Relaxed abdominal fascia after separation of components
Surgical technique: component separation Groups 3, 4 and 5 underwent CS after imbrication. In these animals, after lateral retraction of the suprafascial flap, the external oblique muscle and fascia were identified. An incision in the mid-axillary line through the external oblique fascia was made bilaterally with electrocautery (Fig. 1, bottom left). This maneuver relaxed the abdominal fascia (Fig. 1, bottom right). No elevation of muscle was performed. In groups 4 and 5, after component separation, the insufflator was maintained at a constant intra-abdominal pressure. Abdominal compartment syndrome model In groups 2 and 4, the intra-abdominal space was insufflated with carbon dioxide (Pneumosure Insufflator, Stryker Endoscopy, Portage, MI) until an IAP of 20 mmHg was achieved. In group 5, the IAP was only insufflated to the pressure difference measured after the CS procedure. This simulated the slight increase in pressure after a VHR with an associated CS. This average IAP, also noted as an intraabdominal hypertension state, was a mean of 10 mmHg. The animals were maintained at constant intra-abdominal pressures for 4 h of physiologic monitoring.
following parameters were measured: urine output, BLPs, heart rate, blood pressure, central venous pressure, stroke volume, cardiac output, pulmonary artery pressure, pulmonary artery wedge pressure, systemic vascular resistance, peak inspiratory pressures (PIP), tidal volume, and mean airway pressure. Additionally, arterial blood gas, complete blood count, lactate and comprehensive metabolic panel were measured pre-operatively and at 4 h postprocedure. All the catheters were removed 4 h post-operatively before the animals were extubated. The animals were followed and clinically evaluated by veterinarians. At the study end point, animals were euthanized under general anesthesia. A necropsy was performed to obtain specimens of abdominal organ samples for histological analysis. Histological analysis Abdominal organ samples obtained at necropsy were fixed in formaldehyde and embedded in paraffin. 5 lm sections were prepared and stained with hematoxylin and eosin. To assess for the presence of tissue injury or necrosis, sections were read by a board-certified pathologist who was blinded to the experimental groups. Organ damage or necrosis was defined as the presence of transmural injury in all samples for a given animal.
Post-operative monitoring and analysis Statistical analysis Animals were kept intubated and sedated for 4 h to make physiological measurements, which were taken immediately post-operatively and at every hour thereafter. The
All values are presented as mean ± standard error. The results were evaluated using GraphPad Prism 5
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software(La Jolla, CA). Comparisons between two groups were performed using Student’s t test. Comparisons of greater than two groups were performed using one-way ANOVA with Tukey’s post-test. Analysis of association of the independent variable component separation and the dependent variable organ necrosis was performed using Fisher’s exact test. Significance was set at p \ 0.05.
Results Pressure changes with imbrication and component separation Imbrication was performed on all 45 animals to study the physiological impact of VHR. Measurements of IAP, BLP, and CVP were taken before and immediately after the procedure. Imbrication led to significant immediate elevations in all three measures (Fig. 2, top). Twenty-five animals underwent component separation in addition to imbrication to examine the effects of component separation on IAP, femoral CVP, and BLP. Prior to component separation, IAP was set at 20 mmHg via insufflation. Significant, immediate reductions in IAP, BLP, and CVP were observed after CS (Fig. 2, bottom). Physiological changes with abdominal compartment syndrome To determine which physiological parameters best correlate with elevations in IAP, measurements of 14 parameters were taken. BLP, PIP, jugular CVP, femoral CVP, and systemic pulmonary artery pressure (SPAP) demonstrated correlation with increased IAP (Fig. 3). By 1 h after surgery, significant differences in these five parameters were present among the different groups (Table 2). The groups that had higher IAPs had significantly higher BLP, PIP, jugular CVP, femoral CVP, and SPAP at all four time points after surgery. No significant changes were observed with the other physiological parameters measured in the study. Laboratory changes with abdominal compartment syndrome Arterial blood gas was measured before and at 4 h after the operation to examine the effect of ACS on respiratory function. Significant changes were noted in pH, PaCO2, PaO2, and potassium (K?). Baseline pH values in the five groups were similar. Based on pH, acidemia developed 4 h after the operation (Fig. 4, top left) with the greatest amount noticed in those groups with ACS.
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Fig. 2 Changes in pressures in response to imbrication and component separation. Top Imbrication in all animals led to significant increases in intra-abdominal pressure (IAP), bladder pressure (BLP), and central venous pressure (CVP). Measurements of these parameters pre-operatively blue and after fascial plication red are shown. Bottom Animals that underwent component separation had a significant reduction in the IAP, BLP, and CVP immediately after component separation. ***p \ 0.001. Measurements of these parameters after fascial plication blue and after component separation red are shown
ACS led to significant increases in partial pressure of CO2 (Fig. 4, top right). The PaCO2 of group 2 increased from 33.48 ± 3.52 mmHg pre-operatively to 47.86 ± 5.64 mmHg at 4 h after the operation (p \ 0.001). Group 4 had a similar increase from 34.13 ± 4.78 mmHg to 48.65 ± 5.49 mmHg (p \ 0.001). No significant changes in PaCO2 occurred in the other groups. As expected, ACS led to significant decreases in PaO2 (Fig. 4, bottom left). Significant decreases in PaO2 were observed in all groups except for group 3 with the largest decreases occurring in groups 2 and 4. Based on these findings, the animals developed respiratory acidosis as a result of ACS. Complete blood count and metabolic panel were obtained before and at 4 h after the operation to assess the effect of ACS on other laboratory parameters. Significant increases in K? were observed with ACS (Fig. 4, bottom right). K? for group 2 was initially 3.73 ± 0.31 mEq/L and increased to 5.60 ± 0.60 mEq/L post-operatively (p \
Hernia Fig. 3 Changes in physiological parameters with abdominal compartment syndrome. Elevated intraabdominal pressure in groups 2 and 4 led to significant and sustained increases in bladder pressure (BLP), peak inspiratory pressure (PIP), central venous pressure (CVP), and systolic pulmonary artery pressure (SPAP). Each point represents the mean ± standard error of the mean (SEM)
0.001). In group 4, K? increased from 3.82 ± 0.14 mEq/L pre-operatively to 5.78 ± 0.47 mEq/L post-operatively (p \ 0.001). No significant trends were noted in other laboratory values. Organ injury Histological sections were prepared from abdominal organ samples obtained at the study end point to investigate the effects of ACS and CS on organ injury. Organ samples from liver, spleen, large bowel, and small bowel were examined for evidence of necrosis. Liver injury was observed in one animal in group 4, and no animals had evidence of splenic injury. Large bowel necrosis was only observed in groups with elevated IAP: 87 % in group 2, 27 % in group 4, and 20 % in group 5 (Fig. 5, top left).
Small bowel necrosis was observed in groups with elevated IAP as well: 93 % in group 2, 86 % in group 4, and 80 % in group 5 (Fig. 5, top right). Within the subset of animals with ACS, group 4 had a significantly lower percentage of large bowel necrosis compared to group 2 (p = 0.0025). Representative histologic images of large and small bowel necrosis are shown in Fig. 5 (bottom).
Discussion The results of our study confirm that primary repair of large abdominal wall defects leads to an increase in IAP, which can be reduced in the short run with CS. The explanation for this phenomenon could be that the initial repair decreases intra-abdominal volume, thereby increasing IAP.
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Hernia Table 2 Physiologic parameters
Pre-op
Post-op
1h
2h
3h
4h
BLP (mmHg) Group 1
6.60 ± 0.66
6.40 ± 1.09
6.60 ? 1.20
6.20 ± 1.10
6.00 ± 0.97
6.00 ± 0.77
Group 2
8.33 ± 2.21
12.60 ± 3.62
24.40 ± 2.81
24.47 ± 1.99
24.07 ± 1.99
24.73 ± 2.96
Group 3
5.83 ± 0.50
8.50 ± 1.08
8.00 ± 1.23
7.83 ± 1.51
7.17 ± 1.06
7.50 ± 1.53
Group 4
9.93 ± 1.04
12.47 ± 1.79
24.4 ± 1.77
24.73 ± 1.50
25.00 ± 1.81
25.36 ± 1.61
Group 5
7.00 ± 1.80
9.50 ± 1.77
14.83 ± 3.26
14.67 ± 2.98
15.5 ± 2.97
14.5 ± 2.48
p value
0.31
0.03
\0.0001
\0.0001
\0.0001
\0.0001
PIP (cm H2O) Group 1
22.00 ± 0.87
22.00 ± 0.67
22.60 ± 0.96
23.20 ± 0.57
23.60 ± 0.48
24.00 ± 0.50
Group 2
21.20 ± 2.69
23.73 ± 1.86
40.4 ± 4.04
40.47 ± 3.17
40.60 ± 2.55
41.33 ± 3.06
Group 3
19.67 ± 1.31
22.67 ± 1.31
21.67 ± 1.26
21.50 ± 2.30
21.33 ± 0.36
21.50 ± 0.62
Group 4
22.00 ± 2.89
24.2 ± 1.78
39.73 ± 2.61
40.93 ± 3.40
42.47 ± 3.21
43.13 ± 3.60
Group 5
19 ± 1.07
22.00 ± 1.73
28.67 ± 3.58
31.00 ± 4.57
30.33 ± 2.57
31.00 ± 1.61
p value
0.18
0.02
\0.0001
\0.0001
\0.0001
\0.0001
4.80 ± 0.35
5.20 ± 0.72
4.60 ± 0.48
4.60 ± 0.48
4.60 ± 0.28 11.60 ± 2.71
Jugular CVP (mmHg) Group 1 7.60 ± 0.48 Group 2
8.33 ± 0.83
7.93 ± 2.69
10.27 ± 1.95
10.67 ± 1.94
10.93 ± 1.52
Group 3
6.60 ± 0.66
5.40 ± 0.73
4.80 ± 0.47
4.20 ± 0.52
4.60 ± 0.53
4.00 ± 0.50
Group 4
7.38 ± 0.51
7.22 ± 1.44
9.02 ± 3.03
8.85 ± 1.97
9.21 ± 2.16
9.54 ± 2.42
Group 5
8.40 ± 0.81
6.80 ± 0.59
8.60 ± 0.63
8.60 ± 1.84
8.40 ± 1.55
8.80 ± 1.53
p value
0.06
0.21
0.0003
\0.0001
\0.0001
\0.0001
Femoral CVP (mmHg)
The parameters that correlated with increase in IAP are shown at various time points including pre-operatively, immediately after the operation but prior to insufflation, and hourly after the operation and insufflation were completed for 4 h. p values were obtained by comparing the five groups using one-way ANOVA
Group 1
8.40 ± 0.36
7.20 ± 0.65
7.40 ± 0.76
7.40 ± 1.06
6.60 ± 0.57
6.80 ± 0.52
Group 2
8.67 ± 0.69
10.27 ± 3.6
23.20 ± 3.43
23.73 ± 2.06
22.73 ± 1.50
23.13 ± 1.39
Group 3
8.17 ± 0.22
6.67 ± 0.92
6.00 ± 0.63
5.17 ± 0.39
5.33 ± 0.48
5.17 ± 0.41
Group 4
8.47 ± 0.80
9.67 ± 1.77
23.33 ± 1.77
24.33 ± 1.70
24.00 ± 1.36
23.47 ± 1.25
Group 5
8.50 ± 0.63
6.83 ± 1.53
10.83 ± 2.09
13.50 ± 2.04
12.17 ± 2.42
12.50 ± 2.27
p value
0.79
0.11
\0.0001
\0.0001
\0.0001
\0.0001
SPAP(mmHg) Group 1
35.20 ± 3.66
26.40 ± 0.96
24.20 ± 0.47
24.40 ± 0.91
23.80 ± 0.82
22.80 ± 0.52
Group 2 Group 3
27.00 ± 4.23 24.33 ± 1.38
26.47 ± 3.24 24.83 ± 1.08
33.73 ± 4.49 21.50 ± 1.93
33.27 ± 3.95 21.83 ± 0.92
34.87 ± 3.50 22.50 ± 1.31
36.07 ± 4.26 21.83 ± 0.75
Group 4
27.53 ± 2.52
30.33 ± 5.37
35.40 ± 3.75
37.07 ± 4.51
38.40 ± 4.13
39.20 ± 3.95
Group 5
24.50 ± 1.16
22.67 ± 1.32
25.17 ± 3.11
24.67 ± 2.89
25.50 ± 1.83
27.17 ± 1.66
p value
0.02
0.23
\0.0001
\0.0001
\0.0001
\0.0001
Increased IAPs after abdominal reconstruction increase the risk of ACS [9]. The increase in IAP can be transferred through the diaphragm to affect lung tidal volumes, ventilation, and end-organ perfusion. In our study, we noticed the development of respiratory acidosis shortly as ACS developed. After CS, intra-abdominal volume increased, resulting in a release of pressure [9]. It is surmised that the abdominal compartment is shaped like a cylinder and the outer edges relax and become more spherical after CS [11]. In patients who have undergone VHR and CS with bioprosthetic placement, some may develop an abdominal bulge or laxity associated with the lack of counterpressure or abdominal wall tension secondary to component separation and bioprosthetic placement [12]. In the cohorts in
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our study with sustained elevation of IAP, CS reduced IAP in the short run, but based on our study design, we were unable to determine if CS could prevent ACS. Based on prior studies, CS may not prevent ACS in all cases, even though it has been shown to decrease IAP because there are reports of ACS after VHR with CS [9,13]. In animals with ACS, CS may reduce the risk of organ damage since there was a significantly lower incidence of large bowel necrosis in our study. This effect could be a result of the fact that lower pressures (\ 25 mmHg) can be achieved with CS and thereby prevent end-organ damage [14]. However, the most sensitive organs such as the small bowel are susceptible to organ dysfunction in the setting of ACS, despite the method of abdominal wall reconstruction.
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Fig. 4 Changes in laboratory values with abdominal compartment syndrome. Elevated intra-abdominal pressure (IAP) is associated with significant changes in pH, PaCO2, PaO2, and K. Top, left Significant decreases in pH to below the normal range is seen in all groups with elevated IAP (groups 2, 4, and 5). Group 1 had a statistically significant change in pH, but remained within the normal range. Top, right Significant elevation in PaCO2 is observed in the groups with
IAP = 20 mmHg (groups 2 and 4) Bottom, left A corresponding large reduction in PaO2 was seen in groups 2 and 4. Groups 1 and 5 also had a significant decrease in PaO2 to a lesser extent. Bottom, right Significant increase in potassium was seen in groups 2 and 4 compared to no change in groups 3 and 5. Group 1 also had a significant increase in potassium, but to a lesser extent. ***p \ .001; **0.001 \ p \ 0.01; *0.01 \ p \ 0.05
These organs do not seem to show signs of recovery on histological analysis. In our study, femoral CVP, BLP, PIP, and SPAP best correlated with elevated IAP and should be used as surrogate markers for the diagnosis of ACS in the clinical setting. The relationship between IAP and respiratory function has been delineated in prior studies [15]. Urine output, BLP, and PIP are also frequently used in the clinical setting to monitor the development of ACS. However, in our study, these markers showed changes 2–4 h after onset of sustained elevated IAPs. This point is clinically relevant, since it points out that when urine output decreases or PIP increases in the clinical setting, ACS may have developed hours before this laboratory change had been noted. The femoral CVP was the most accurate and early measure of IAP. It was more accurate than jugular CVP. We hypothesized that the diaphragm can provide some counterforce to any increased IAP. This therefore makes the jugular CVP a less accurate measure of increased IAP. Femoral CVP is not typically used to diagnose or monitor ACS, but it is another variable worth measuring since we showed it to be an early, accurate predictor of ACS.
A prior study performed in a swine model [14] with ACS showed that each step of a procedure involving VHR and CS resulted in a significant decrease in IAP, CVP, and PIP. However, MAP had remained elevated. This study agrees with our finding that IAP, CVP, and PIP are useful markers for diagnosing ACS and that CS can help reduce these parameters that are associated with ACS. This study also showed a significant decrease in PaO2, consistent with decreased oxygenation of the lung and increased PaCO2 consistent with decreased ventilation during ACS. We conclude that close monitoring of the aforementioned physiological parameters that correlate with the development of ACS is required to arrive at an early and accurate diagnosis. Otherwise, as we have shown, acidosis and endorgan damage will ensue and in most cases are irreversible. With regard to the clinical setting, we devised an algorithm at our institution that describes how to address abdominal wall defects as described in the study of Rodriguez et al. [8]. One of the cohorts in our animal study (Group 3) mirrored our practice of performing component separation with ventral hernia repair. Compared to the older technique of primary fascial closure without CS, we showed the positive effects of CS in our study. There is a
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Fig. 5 Large and small bowel necrosis. Elevated intra-abdominal pressure is associated with a higher percentage of large and small bowel samples with necrosis on histological sections. Component separation performed in animals with elevated IAP reduced the percentage of large bowel necrosis, but had no effect on small bowel necrosis. Top, left Large bowel necrosis was present in the groups with elevated intra-abdominal pressure. Group 4 had a significantly
lower percentage of large bowel samples with necrosis compared to group 2. Top, right Small bowel necrosis was present in groups with elevated intra-abdominal pressure. There was no significant difference between groups 2 and 4. Bottom, left Representative image of large bowel necrosis on H&E section demonstrating necrosis with heavy neutrophil infiltrate. Bottom, right Small bowel necrosis with significant inflammatory infiltrate
marked decrease in the variables associated with ACS. Aside from achieving fascial closure, there is physiologic utility in performing CS. We recommend based on our study findings that careful monitoring of peak airway pressures in the operating room after VHR should be performed. If the pressures are high and it is difficult to ventilate the patient, then the tension should be relieved to reduce the pressure. The amount of fluid given intraoperatively and post-operatively should also be monitored closely, because over-resuscitation can increase postoperative edema and result in increased bladder and abdominal compartment pressures which both correlate with the development of ACS. Post-operatively, urine output and CVP should also be monitored on an hourly basis to diagnose the development of ACS. We have demonstrated the impact of reconstructing major abdominal wall defects on several hemodynamic and physiologic parameters, which revealed that BLP, femoral CVP, PIP, and SPAP were the best correlates to increased IAP. CS reduces IAP immediately following primary hernia repair, but we cannot be certain whether this technique prevents the development of ACS without
further study. The findings in this study can provide guidance for intra-operative and post-operative monitoring to allow early diagnosis of ACS. Only with early diagnosis and treatment can irreversible organ damage be avoided.
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Acknowledgments We would like to thank TDMI for their expert animal management and assistance with surgical procedures. We would also like to thank Dr. Cinthia Drachenberg for analyzing the pathological specimens from this study and Dr. Leigh Ann Price for her input on the study design. This study was funded by a Lifecell Grant ISIS.08.01.00.ER. Conflict of interest RM declares no conflict of interest. HHC declares no conflict of interest. HDW declares no conflict of interest. AJN declares no conflict of interest. JAK declares no conflict of interest. GSM declares no conflict of interest. MM declares no conflict of interest. ENB declares no conflict of interest. MRC declares no conflict of interest. EDR declares conflict of interest not directly related to the submitted work (Grant—Synthes CMF, KLS Martin; support for travel—Synthes CMF; payment for lectures—CME Outfitters). This study was funded by a grant provided by Lifecell (Grant ISIS.08.01.00.ER). Eduardo D. Rodriguez received MD DDS— Grants (Synthes CMF, KLS Martin) and payments for lectures (Synthes CMF), travel accommodations/expenses for unrelated activities (Synthes CMF).
Hernia Ethical Standards The experiments in this study comply with the current laws of the country in which they were performed.
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8. Rodriguez ED, Bluebond-Langner R, Silverman RP, Bochicchio G, Yao A et al (2007) Abdominal wall reconstruction following severe loss of domain: the R Adams Cowley Shock Trauma Center algorithm. Plast Reconstr Surg 120:669–680 9. Agnew SP, Small W Jr, Wang E, Smith LJ, Hadad I et al (2010) Prospective measurements of intra-abdominal volume and pulmonary function after repair of massive ventral hernias with the components separation technique. Ann Surg 251:981–988 10. An G, West MA (2008) Abdominal compartment syndrome: a concise clinical review. Crit Care Med 36:1304–1310 11. Buck DW 2nd, Steinberg JP, Fryer J, Dumanian GA (2010) Operative management of massive hernias with associated distended bowel. Am J Surg 200:258–264 12. Bluebond-Langner R, Keifa ES, Mithani S, Bochicchio GV, Scalea T et al (2008) Recurrent abdominal laxity following interpositional human acellular dermal matrix. Ann Plast Surg 60:76–80 13. Tobias AM, Low DW (2003) The use of a subfascial vicryl mesh buttress to aid in the closure of massive ventral hernias following damage-control laparotomy. Plast Reconstr Surg 112:766–776 14. O’Mara MS, Papasavas PK, Newton ED, Caushaj PF (2004) Modified separation of parts as an intervention for intraabdominal hypertension and the abdominal compartment syndrome in a swine model. Plast Reconstr Surg 114:1842–1845 15. De Santis L, Frigo F, Bruttocao A, Terranova O (2003) Pathophysiology of giant incisional hernias with loss of abdominal wall substance. Acta Biomed 74(Suppl 2):34–37
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ORIGINAL ARTICLE
Physiologic changes with abdominal wall reconstruction in a porcine abdominal compartment syndrome model R. Mohan • H. G. Hui-Chou • H. D. Wang • A. J. Nam M. Magarakis • G. S. Mundinger • E. N. Brown • A. J. Kelamis • M. R. Christy • E. D. Rodriguez
•
Received: 6 February 2014 / Accepted: 12 September 2014 Ó Springer-Verlag France 2014
Abstract Purpose Abdominal compartment syndrome (ACS) is a severe complication of ventral hernia repair. The aims of this study were to investigate the effects of intra-abdominal pressure on the physiologic changes of abdominal wall reconstruction and component separation in a porcine model. Methods Ventral hernia repair (VHR) was simulated by abdominal fascial imbrication of a 10 9 15 cm defect in 45 Yorkshire pigs assigned to five experimental groups. ACS was simulated by a Stryker endoscopy insufflator with intra-abdominal pressure elevated to 20 mmHg in two groups. Component separation was performed in one of these groups and in one group without ACS. Physiological parameters were measured before and after the procedures
The study was presented at the American College of Surgeons 2010 Clinical Congress Surgical Forum, Washington, D.C. October 7, 2010 (Oral Presentation); at the 92nd Annual American Association of Plastic Surgeons Meeting (Poster Presentation), New Orleans, LA, April 22, 2013; and the 58th Annual Plastic Surgery Research Council (Oral Presentation), Santa Monica, CA, May 2–4, 2013.
and monitored for 4 h. The animals were euthanized for histologic analysis of organ damage. Results VHR led to an increase in intra-abdominal pressure, bladder pressure, and central venous pressure by an average of 14.89, 13.93, and 14.69 mmHg (p \ 0.001) in all animals. Component separation was performed in 25 animals and the three pressures reduced by 9.11, 8.00, 7.89 mmHg (p \ 0.001). ACS correlated with higher percentages of large and small bowel necrosis compared to groups without abdominal compartment syndrome. Conclusions The results confirm that primary repair of large abdominal wall defects leads to increased intraabdominal pressure, which can be reduced with component separation. In animals with ACS, component separation may reduce the risk of organ damage. Central venous pressure, bladder pressure, and other physiologic parameters accurately correlated with elevated intra-abdominal pressure and may have utility as markers for diagnosis of ACS. Keywords Abdominal wall reconstruction Ventral hernia repair Abdominal compartment syndrome Component separation Porcine model
R. Mohan and H. G. Hui-Chou are equally contributed authors. R. Mohan H. G. Hui-Chou H. D. Wang A. J. Nam M. Magarakis G. S. Mundinger E. N. Brown A. J. Kelamis M. R. Christy Division of Plastic, Reconstructive and Maxillofacial Surgery, R Adams Cowley Shock Trauma Center, University of Maryland Medical Center, Baltimore, MD, USA E. D. Rodriguez (&) Department of Plastic Surgery, NYU Langone Medical Center, Institute of Reconstructive Plastic Surgery, 307 E 33rd st, New York, NY 10012, USA e-mail: [email protected]
Introduction Reconstructing abdominal wall defects can be challenging in patients with complex abdominal wall hernias or open abdomen because of damage control laparotomy [1, 2]. These abdominal defects are usually a result of trauma, malignancy, or infection [3]. Many techniques have been described to reconstruct abdominal wall fascial defects, namely primary fascial repair, component separation(CS), and interpositional prosthetic meshes [4–7]. The success of
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these techniques has been described in the literature, and based on our center’s experience we devised an algorithm to approach complex abdominal wall defects with severe loss of domain [8]. However, there is a potential risk of abdominal compartment syndrome (ACS) with ventral hernia repair (VHR) and abdominal wall reconstruction which can have devastating consequences [9]. ACS is associated with massive fluid shifts into visceral organs and increased mechanical pressure, which can be exacerbated by volume resuscitation. ACS is also known to cause decreased central venous return and increased intrathoracic pressures [10]. The aims of this study were to investigate the effects of ACS, induced by sustained increases in intra-abdominal pressure (IAP), in a porcine model. Physiological parameters that can be measured in the intensive care setting were monitored. Primary VHR, CS, and simulated ACS were performed in some cohorts to assess the effect on physiological parameters and end-organ damage.
Methods After obtaining Institutional Animal Care and Use Committee’s (IACUC) approval, 45 of 3-month-old Yorkshire pigs (45 females, average weight 27.16 lbs) were purchased and housed at Thomas D. Morris, Inc. (Reisterstown, MD) during the study. The research and care facility is accredited by the American Association for the Accreditation of Laboratory Animal Care International (AAALAC-I). The animals were cared for by certified veterinarians in accordance with the principles in the Guide for Care and Use of Laboratory Animals and each received a general health evaluation by a veterinarian before inclusion in the study. The pigs were assigned to five experimental groups. (Table 1) Primary VHRs were simulated by abdominal fascial imbrication of a 10 9 15 cm defect. ACS was simulated with a Stryker endoscopy insufflator elevated to an IAP of 20 mmHg and maintained at that level for 4 h. 45 Yorkshire pigs were divided into five groups. Group 1 received VHR alone; group 2 underwent VHR and had ACS; group 3 received VHR with CS; group 4 had VHR, CS, and ACS; group 5 had VHR, CS, and a lower IAP. Physiological parameters were measured before and after the procedure. Animals were euthanized 2 weeks postoperatively for histologic analysis of organ damage. Vascular access For monitoring of animals, catheterization of the internal jugular vein, common carotid artery, and femoral vein was performed. A 2-in. vertical skin incision was made in the right neck, and the internal jugular vein and carotid artery
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Table 1 Summary of experimental groups Group
N
Imbrication
1
5
?
2
15
?
3
5
?
4
15
?
5
5
?
IAP
Component separation
Concept Primary VHR alone
??
Primary VHR with ACS ?
Primary VHR with CS
??
?
Primary VHR with CS and ACS
?
?
Primary VHR with CS and IAH
45 animals were divided into five experimental groups. Group 1 received VHR alone; group 2 underwent VHR and had ACS; group 3 received VHR and CS; group 4 had VHR, CS, and ACS; group 5 had VHR, CS, and mild ACS (IAP = 10)
were isolated. An arteriotomy was performed and a 9.5French and a 7-French catheter were inserted into these vessels, respectively. A pulmonary artery catheter (SwanGanz) was then floated into position through the internal jugular. A 2-in. skin incision was made caudal to the right inguinal line in the right groin. The right common femoral vein was catheterized with a 9.5-French catheter for monitoring central venous pressure (CVP) below the diaphragm. Foley catheter placement A 7-French urinary catheter was inserted under sterile conditions. An Ab-Viser IAP Monitoring System (Convatec, Skillman, NJ) was used to measure bladder pressures (BLP). Surgical technique: the imbrication (ventral hernia repair) model Once sedated, the animals were intubated and administered intravenous antibiotics prior to surgical incision. No muscle relaxants were administered. A skin incision was made in the midline from the xiphoid process to the level of the pubic symphysis. After reaching the abdominal fascial layer, lateral suprafascial flaps were undermined and raised bilaterally from the costal margins superiorly to the iliac crests inferiorly with the mid-axillary line serving as the lateral border. A Veress needle was placed at the midline through the linea alba to measure the IAP. A 10 cm by 15 cm ellipse was drawn at the center of the exposed fascia. Full thickness sutures using 2-0 Prolene were placed at the edges of the ellipse. (Fig. 1, top left) With the sutures tied, the fascial edges of the ellipse apposed each other and imbricated the fascia. (Fig. 1, top right) This technique was used to simulate primary VHR. The IAP was measured before and after imbrication to monitor the pressure.
Hernia Fig. 1 Intra-operative images of imbrication and component separation. Top, left Sutures were placed along the edges of the drawn ellipse to achieve imbrication. Top, right Apposition of the fascial edges of the ellipse led to a decrease in abdominal fascial girth. Bottom, left Release of external oblique fascia during component separation. Bottom, right Relaxed abdominal fascia after separation of components
Surgical technique: component separation Groups 3, 4 and 5 underwent CS after imbrication. In these animals, after lateral retraction of the suprafascial flap, the external oblique muscle and fascia were identified. An incision in the mid-axillary line through the external oblique fascia was made bilaterally with electrocautery (Fig. 1, bottom left). This maneuver relaxed the abdominal fascia (Fig. 1, bottom right). No elevation of muscle was performed. In groups 4 and 5, after component separation, the insufflator was maintained at a constant intra-abdominal pressure. Abdominal compartment syndrome model In groups 2 and 4, the intra-abdominal space was insufflated with carbon dioxide (Pneumosure Insufflator, Stryker Endoscopy, Portage, MI) until an IAP of 20 mmHg was achieved. In group 5, the IAP was only insufflated to the pressure difference measured after the CS procedure. This simulated the slight increase in pressure after a VHR with an associated CS. This average IAP, also noted as an intraabdominal hypertension state, was a mean of 10 mmHg. The animals were maintained at constant intra-abdominal pressures for 4 h of physiologic monitoring.
following parameters were measured: urine output, BLPs, heart rate, blood pressure, central venous pressure, stroke volume, cardiac output, pulmonary artery pressure, pulmonary artery wedge pressure, systemic vascular resistance, peak inspiratory pressures (PIP), tidal volume, and mean airway pressure. Additionally, arterial blood gas, complete blood count, lactate and comprehensive metabolic panel were measured pre-operatively and at 4 h postprocedure. All the catheters were removed 4 h post-operatively before the animals were extubated. The animals were followed and clinically evaluated by veterinarians. At the study end point, animals were euthanized under general anesthesia. A necropsy was performed to obtain specimens of abdominal organ samples for histological analysis. Histological analysis Abdominal organ samples obtained at necropsy were fixed in formaldehyde and embedded in paraffin. 5 lm sections were prepared and stained with hematoxylin and eosin. To assess for the presence of tissue injury or necrosis, sections were read by a board-certified pathologist who was blinded to the experimental groups. Organ damage or necrosis was defined as the presence of transmural injury in all samples for a given animal.
Post-operative monitoring and analysis Statistical analysis Animals were kept intubated and sedated for 4 h to make physiological measurements, which were taken immediately post-operatively and at every hour thereafter. The
All values are presented as mean ± standard error. The results were evaluated using GraphPad Prism 5
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software(La Jolla, CA). Comparisons between two groups were performed using Student’s t test. Comparisons of greater than two groups were performed using one-way ANOVA with Tukey’s post-test. Analysis of association of the independent variable component separation and the dependent variable organ necrosis was performed using Fisher’s exact test. Significance was set at p \ 0.05.
Results Pressure changes with imbrication and component separation Imbrication was performed on all 45 animals to study the physiological impact of VHR. Measurements of IAP, BLP, and CVP were taken before and immediately after the procedure. Imbrication led to significant immediate elevations in all three measures (Fig. 2, top). Twenty-five animals underwent component separation in addition to imbrication to examine the effects of component separation on IAP, femoral CVP, and BLP. Prior to component separation, IAP was set at 20 mmHg via insufflation. Significant, immediate reductions in IAP, BLP, and CVP were observed after CS (Fig. 2, bottom). Physiological changes with abdominal compartment syndrome To determine which physiological parameters best correlate with elevations in IAP, measurements of 14 parameters were taken. BLP, PIP, jugular CVP, femoral CVP, and systemic pulmonary artery pressure (SPAP) demonstrated correlation with increased IAP (Fig. 3). By 1 h after surgery, significant differences in these five parameters were present among the different groups (Table 2). The groups that had higher IAPs had significantly higher BLP, PIP, jugular CVP, femoral CVP, and SPAP at all four time points after surgery. No significant changes were observed with the other physiological parameters measured in the study. Laboratory changes with abdominal compartment syndrome Arterial blood gas was measured before and at 4 h after the operation to examine the effect of ACS on respiratory function. Significant changes were noted in pH, PaCO2, PaO2, and potassium (K?). Baseline pH values in the five groups were similar. Based on pH, acidemia developed 4 h after the operation (Fig. 4, top left) with the greatest amount noticed in those groups with ACS.
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Fig. 2 Changes in pressures in response to imbrication and component separation. Top Imbrication in all animals led to significant increases in intra-abdominal pressure (IAP), bladder pressure (BLP), and central venous pressure (CVP). Measurements of these parameters pre-operatively blue and after fascial plication red are shown. Bottom Animals that underwent component separation had a significant reduction in the IAP, BLP, and CVP immediately after component separation. ***p \ 0.001. Measurements of these parameters after fascial plication blue and after component separation red are shown
ACS led to significant increases in partial pressure of CO2 (Fig. 4, top right). The PaCO2 of group 2 increased from 33.48 ± 3.52 mmHg pre-operatively to 47.86 ± 5.64 mmHg at 4 h after the operation (p \ 0.001). Group 4 had a similar increase from 34.13 ± 4.78 mmHg to 48.65 ± 5.49 mmHg (p \ 0.001). No significant changes in PaCO2 occurred in the other groups. As expected, ACS led to significant decreases in PaO2 (Fig. 4, bottom left). Significant decreases in PaO2 were observed in all groups except for group 3 with the largest decreases occurring in groups 2 and 4. Based on these findings, the animals developed respiratory acidosis as a result of ACS. Complete blood count and metabolic panel were obtained before and at 4 h after the operation to assess the effect of ACS on other laboratory parameters. Significant increases in K? were observed with ACS (Fig. 4, bottom right). K? for group 2 was initially 3.73 ± 0.31 mEq/L and increased to 5.60 ± 0.60 mEq/L post-operatively (p \
Hernia Fig. 3 Changes in physiological parameters with abdominal compartment syndrome. Elevated intraabdominal pressure in groups 2 and 4 led to significant and sustained increases in bladder pressure (BLP), peak inspiratory pressure (PIP), central venous pressure (CVP), and systolic pulmonary artery pressure (SPAP). Each point represents the mean ± standard error of the mean (SEM)
0.001). In group 4, K? increased from 3.82 ± 0.14 mEq/L pre-operatively to 5.78 ± 0.47 mEq/L post-operatively (p \ 0.001). No significant trends were noted in other laboratory values. Organ injury Histological sections were prepared from abdominal organ samples obtained at the study end point to investigate the effects of ACS and CS on organ injury. Organ samples from liver, spleen, large bowel, and small bowel were examined for evidence of necrosis. Liver injury was observed in one animal in group 4, and no animals had evidence of splenic injury. Large bowel necrosis was only observed in groups with elevated IAP: 87 % in group 2, 27 % in group 4, and 20 % in group 5 (Fig. 5, top left).
Small bowel necrosis was observed in groups with elevated IAP as well: 93 % in group 2, 86 % in group 4, and 80 % in group 5 (Fig. 5, top right). Within the subset of animals with ACS, group 4 had a significantly lower percentage of large bowel necrosis compared to group 2 (p = 0.0025). Representative histologic images of large and small bowel necrosis are shown in Fig. 5 (bottom).
Discussion The results of our study confirm that primary repair of large abdominal wall defects leads to an increase in IAP, which can be reduced in the short run with CS. The explanation for this phenomenon could be that the initial repair decreases intra-abdominal volume, thereby increasing IAP.
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Hernia Table 2 Physiologic parameters
Pre-op
Post-op
1h
2h
3h
4h
BLP (mmHg) Group 1
6.60 ± 0.66
6.40 ± 1.09
6.60 ? 1.20
6.20 ± 1.10
6.00 ± 0.97
6.00 ± 0.77
Group 2
8.33 ± 2.21
12.60 ± 3.62
24.40 ± 2.81
24.47 ± 1.99
24.07 ± 1.99
24.73 ± 2.96
Group 3
5.83 ± 0.50
8.50 ± 1.08
8.00 ± 1.23
7.83 ± 1.51
7.17 ± 1.06
7.50 ± 1.53
Group 4
9.93 ± 1.04
12.47 ± 1.79
24.4 ± 1.77
24.73 ± 1.50
25.00 ± 1.81
25.36 ± 1.61
Group 5
7.00 ± 1.80
9.50 ± 1.77
14.83 ± 3.26
14.67 ± 2.98
15.5 ± 2.97
14.5 ± 2.48
p value
0.31
0.03
\0.0001
\0.0001
\0.0001
\0.0001
PIP (cm H2O) Group 1
22.00 ± 0.87
22.00 ± 0.67
22.60 ± 0.96
23.20 ± 0.57
23.60 ± 0.48
24.00 ± 0.50
Group 2
21.20 ± 2.69
23.73 ± 1.86
40.4 ± 4.04
40.47 ± 3.17
40.60 ± 2.55
41.33 ± 3.06
Group 3
19.67 ± 1.31
22.67 ± 1.31
21.67 ± 1.26
21.50 ± 2.30
21.33 ± 0.36
21.50 ± 0.62
Group 4
22.00 ± 2.89
24.2 ± 1.78
39.73 ± 2.61
40.93 ± 3.40
42.47 ± 3.21
43.13 ± 3.60
Group 5
19 ± 1.07
22.00 ± 1.73
28.67 ± 3.58
31.00 ± 4.57
30.33 ± 2.57
31.00 ± 1.61
p value
0.18
0.02
\0.0001
\0.0001
\0.0001
\0.0001
4.80 ± 0.35
5.20 ± 0.72
4.60 ± 0.48
4.60 ± 0.48
4.60 ± 0.28 11.60 ± 2.71
Jugular CVP (mmHg) Group 1 7.60 ± 0.48 Group 2
8.33 ± 0.83
7.93 ± 2.69
10.27 ± 1.95
10.67 ± 1.94
10.93 ± 1.52
Group 3
6.60 ± 0.66
5.40 ± 0.73
4.80 ± 0.47
4.20 ± 0.52
4.60 ± 0.53
4.00 ± 0.50
Group 4
7.38 ± 0.51
7.22 ± 1.44
9.02 ± 3.03
8.85 ± 1.97
9.21 ± 2.16
9.54 ± 2.42
Group 5
8.40 ± 0.81
6.80 ± 0.59
8.60 ± 0.63
8.60 ± 1.84
8.40 ± 1.55
8.80 ± 1.53
p value
0.06
0.21
0.0003
\0.0001
\0.0001
\0.0001
Femoral CVP (mmHg)
The parameters that correlated with increase in IAP are shown at various time points including pre-operatively, immediately after the operation but prior to insufflation, and hourly after the operation and insufflation were completed for 4 h. p values were obtained by comparing the five groups using one-way ANOVA
Group 1
8.40 ± 0.36
7.20 ± 0.65
7.40 ± 0.76
7.40 ± 1.06
6.60 ± 0.57
6.80 ± 0.52
Group 2
8.67 ± 0.69
10.27 ± 3.6
23.20 ± 3.43
23.73 ± 2.06
22.73 ± 1.50
23.13 ± 1.39
Group 3
8.17 ± 0.22
6.67 ± 0.92
6.00 ± 0.63
5.17 ± 0.39
5.33 ± 0.48
5.17 ± 0.41
Group 4
8.47 ± 0.80
9.67 ± 1.77
23.33 ± 1.77
24.33 ± 1.70
24.00 ± 1.36
23.47 ± 1.25
Group 5
8.50 ± 0.63
6.83 ± 1.53
10.83 ± 2.09
13.50 ± 2.04
12.17 ± 2.42
12.50 ± 2.27
p value
0.79
0.11
\0.0001
\0.0001
\0.0001
\0.0001
SPAP(mmHg) Group 1
35.20 ± 3.66
26.40 ± 0.96
24.20 ± 0.47
24.40 ± 0.91
23.80 ± 0.82
22.80 ± 0.52
Group 2 Group 3
27.00 ± 4.23 24.33 ± 1.38
26.47 ± 3.24 24.83 ± 1.08
33.73 ± 4.49 21.50 ± 1.93
33.27 ± 3.95 21.83 ± 0.92
34.87 ± 3.50 22.50 ± 1.31
36.07 ± 4.26 21.83 ± 0.75
Group 4
27.53 ± 2.52
30.33 ± 5.37
35.40 ± 3.75
37.07 ± 4.51
38.40 ± 4.13
39.20 ± 3.95
Group 5
24.50 ± 1.16
22.67 ± 1.32
25.17 ± 3.11
24.67 ± 2.89
25.50 ± 1.83
27.17 ± 1.66
p value
0.02
0.23
\0.0001
\0.0001
\0.0001
\0.0001
Increased IAPs after abdominal reconstruction increase the risk of ACS [9]. The increase in IAP can be transferred through the diaphragm to affect lung tidal volumes, ventilation, and end-organ perfusion. In our study, we noticed the development of respiratory acidosis shortly as ACS developed. After CS, intra-abdominal volume increased, resulting in a release of pressure [9]. It is surmised that the abdominal compartment is shaped like a cylinder and the outer edges relax and become more spherical after CS [11]. In patients who have undergone VHR and CS with bioprosthetic placement, some may develop an abdominal bulge or laxity associated with the lack of counterpressure or abdominal wall tension secondary to component separation and bioprosthetic placement [12]. In the cohorts in
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our study with sustained elevation of IAP, CS reduced IAP in the short run, but based on our study design, we were unable to determine if CS could prevent ACS. Based on prior studies, CS may not prevent ACS in all cases, even though it has been shown to decrease IAP because there are reports of ACS after VHR with CS [9,13]. In animals with ACS, CS may reduce the risk of organ damage since there was a significantly lower incidence of large bowel necrosis in our study. This effect could be a result of the fact that lower pressures (\ 25 mmHg) can be achieved with CS and thereby prevent end-organ damage [14]. However, the most sensitive organs such as the small bowel are susceptible to organ dysfunction in the setting of ACS, despite the method of abdominal wall reconstruction.
Hernia
Fig. 4 Changes in laboratory values with abdominal compartment syndrome. Elevated intra-abdominal pressure (IAP) is associated with significant changes in pH, PaCO2, PaO2, and K. Top, left Significant decreases in pH to below the normal range is seen in all groups with elevated IAP (groups 2, 4, and 5). Group 1 had a statistically significant change in pH, but remained within the normal range. Top, right Significant elevation in PaCO2 is observed in the groups with
IAP = 20 mmHg (groups 2 and 4) Bottom, left A corresponding large reduction in PaO2 was seen in groups 2 and 4. Groups 1 and 5 also had a significant decrease in PaO2 to a lesser extent. Bottom, right Significant increase in potassium was seen in groups 2 and 4 compared to no change in groups 3 and 5. Group 1 also had a significant increase in potassium, but to a lesser extent. ***p \ .001; **0.001 \ p \ 0.01; *0.01 \ p \ 0.05
These organs do not seem to show signs of recovery on histological analysis. In our study, femoral CVP, BLP, PIP, and SPAP best correlated with elevated IAP and should be used as surrogate markers for the diagnosis of ACS in the clinical setting. The relationship between IAP and respiratory function has been delineated in prior studies [15]. Urine output, BLP, and PIP are also frequently used in the clinical setting to monitor the development of ACS. However, in our study, these markers showed changes 2–4 h after onset of sustained elevated IAPs. This point is clinically relevant, since it points out that when urine output decreases or PIP increases in the clinical setting, ACS may have developed hours before this laboratory change had been noted. The femoral CVP was the most accurate and early measure of IAP. It was more accurate than jugular CVP. We hypothesized that the diaphragm can provide some counterforce to any increased IAP. This therefore makes the jugular CVP a less accurate measure of increased IAP. Femoral CVP is not typically used to diagnose or monitor ACS, but it is another variable worth measuring since we showed it to be an early, accurate predictor of ACS.
A prior study performed in a swine model [14] with ACS showed that each step of a procedure involving VHR and CS resulted in a significant decrease in IAP, CVP, and PIP. However, MAP had remained elevated. This study agrees with our finding that IAP, CVP, and PIP are useful markers for diagnosing ACS and that CS can help reduce these parameters that are associated with ACS. This study also showed a significant decrease in PaO2, consistent with decreased oxygenation of the lung and increased PaCO2 consistent with decreased ventilation during ACS. We conclude that close monitoring of the aforementioned physiological parameters that correlate with the development of ACS is required to arrive at an early and accurate diagnosis. Otherwise, as we have shown, acidosis and endorgan damage will ensue and in most cases are irreversible. With regard to the clinical setting, we devised an algorithm at our institution that describes how to address abdominal wall defects as described in the study of Rodriguez et al. [8]. One of the cohorts in our animal study (Group 3) mirrored our practice of performing component separation with ventral hernia repair. Compared to the older technique of primary fascial closure without CS, we showed the positive effects of CS in our study. There is a
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Fig. 5 Large and small bowel necrosis. Elevated intra-abdominal pressure is associated with a higher percentage of large and small bowel samples with necrosis on histological sections. Component separation performed in animals with elevated IAP reduced the percentage of large bowel necrosis, but had no effect on small bowel necrosis. Top, left Large bowel necrosis was present in the groups with elevated intra-abdominal pressure. Group 4 had a significantly
lower percentage of large bowel samples with necrosis compared to group 2. Top, right Small bowel necrosis was present in groups with elevated intra-abdominal pressure. There was no significant difference between groups 2 and 4. Bottom, left Representative image of large bowel necrosis on H&E section demonstrating necrosis with heavy neutrophil infiltrate. Bottom, right Small bowel necrosis with significant inflammatory infiltrate
marked decrease in the variables associated with ACS. Aside from achieving fascial closure, there is physiologic utility in performing CS. We recommend based on our study findings that careful monitoring of peak airway pressures in the operating room after VHR should be performed. If the pressures are high and it is difficult to ventilate the patient, then the tension should be relieved to reduce the pressure. The amount of fluid given intraoperatively and post-operatively should also be monitored closely, because over-resuscitation can increase postoperative edema and result in increased bladder and abdominal compartment pressures which both correlate with the development of ACS. Post-operatively, urine output and CVP should also be monitored on an hourly basis to diagnose the development of ACS. We have demonstrated the impact of reconstructing major abdominal wall defects on several hemodynamic and physiologic parameters, which revealed that BLP, femoral CVP, PIP, and SPAP were the best correlates to increased IAP. CS reduces IAP immediately following primary hernia repair, but we cannot be certain whether this technique prevents the development of ACS without
further study. The findings in this study can provide guidance for intra-operative and post-operative monitoring to allow early diagnosis of ACS. Only with early diagnosis and treatment can irreversible organ damage be avoided.
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Acknowledgments We would like to thank TDMI for their expert animal management and assistance with surgical procedures. We would also like to thank Dr. Cinthia Drachenberg for analyzing the pathological specimens from this study and Dr. Leigh Ann Price for her input on the study design. This study was funded by a Lifecell Grant ISIS.08.01.00.ER. Conflict of interest RM declares no conflict of interest. HHC declares no conflict of interest. HDW declares no conflict of interest. AJN declares no conflict of interest. JAK declares no conflict of interest. GSM declares no conflict of interest. MM declares no conflict of interest. ENB declares no conflict of interest. MRC declares no conflict of interest. EDR declares conflict of interest not directly related to the submitted work (Grant—Synthes CMF, KLS Martin; support for travel—Synthes CMF; payment for lectures—CME Outfitters). This study was funded by a grant provided by Lifecell (Grant ISIS.08.01.00.ER). Eduardo D. Rodriguez received MD DDS— Grants (Synthes CMF, KLS Martin) and payments for lectures (Synthes CMF), travel accommodations/expenses for unrelated activities (Synthes CMF).
Hernia Ethical Standards The experiments in this study comply with the current laws of the country in which they were performed.
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