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144
Abdominal Compartment Syndrome
CHAPTER 11
Intra-Abdominal Hypertension
and the Central Nervous System
Giuseppe Citerio* and Lorenzo Berra
Abstract
n animal studies, increases in intra-abdominal pressure (IAP) raise central venous pressure
(CVP) and pleural pressure (PP) and, eventually, result in elevation of intracranial pressure
(ICP) and decrease of cerebral perfusion pressure (CPP). Clinical studies documented similar
I
correlations. Particularly, in patients with an intracranial hypertension (HICP), in which the
compensatory capacities of accepting intracranial volumes are exhausted, the effect of high IAP
may induce a further harmful increase in ICP.
In head trauma victims with associated intra-abdominal lesions accurate monitoring of IAP
is recommended, particularly if HICP is recorded. The cornerstone for treating intra-abdominal
hypertension (IAH) and abdominal compartment syndrome (ACS) is the identification of
patients at risk and the early recognition and treatment of its harmful effects. Thus, decompressive laparotomy can be a useful adjunct in the treatment of refractory HICP, after the
exclusion of other removable causes, while the use of laparoscopy should be considered an
absolute contraindication in HICP patients and should be avoided in patients with recent head
injury.
Further laboratory and clinical investigation and a strict monitoring of the IAP in HICP
patients will allow us a better understanding and treatment of this pathology to reduce the
burden of IAP on CNS.
Introduction
The effects of elevated intra-abdominal pressure (IAP) have been investigated by several
historical studies. In the 19th century, Marey and Burt described the respiratory effects of intra
abdominal hypertension (IAH). In 1911, Emerson highlighted the cardiovascular derangements in various animal models of intra-abdominal hypertension and, in 1913, Wendt described the association of IAH and renal dysfunction.
Nevertheless, only in 1994, Josephs et al
evaluated, in a porcine model, the effect of raising the IAP with a pneumoperitoneum on
intracranial pressure (ICP) and cerebral perfusion pressure (CPP). They demonstrated that
IAH causes an ICP increase; specifically, pneumoperitoneum during laparoscopy raises ICP
(Fig. 1). The authors concluded that laparoscopy should not be used in patients with severe
head injuries.
A year later, in 1995, Irgau et al
reports. Irgau reported a case of a patient with an intracranial mass lesion in which ICP aug-
*Corresponding Author: Giuseppe Citerio—UO Neuroanestesia e Neurorianimazione,
Dipartimento di Medicina Perioperatoria e Terapie Intensive, H San Gerardo, Via Donizetti,
106, 20052 Monza (Mi), Italy. Email: g.citerio@hsgerardo.org
Abdominal Compartment Syndrome, edited by Rao R. Ivatury, Michael L. Cheatham,
Manu L. N. G. Malbrain and Michael Sugrue. ©2006 Landes Bioscience.
1
at the Boston University School of Medicine
2
and Bloomfield et al3 published two interesting case
145Intra-Abdominal Hypertension and the Central Nervous System
Figure 1. Effect of 15 mm Hg pneumoperitoneum in an animal model with and without intracranial
hypertension. Modified from Josephs LG et al, J Trauma 1994; 36(6):815-819.
1
mented abruptly when the peritoneal cavity was insufflated during laparoscopic cholecystectomy. Bloomfield et al showed the successful management of a patient with severe multisystem
injury in whom abdominal decompression, indicated only by the clinical conditions, dramatically reduced high ICP, previously unresponsive to medical measures.
Since then, many laboratory and clinical investigators are tentatively trying to address the
role of the IAH and abdominal compartment syndrome (ACS) on the central nervous system
(CNS), and to answer relevant questions, as:
1. What is the physiological response of the CNS to variation of IAP?
2. How is the IAP variation transmitted to the ICP and CPP?
3. What is the role of the IAP, IAH, and ACS on CNS in presence or absence of head injury?
4. What are the maneuvers that may cause a secondary damage to the CNS in presence of
ACS?
5. How can we prevent an increase in ICP and a decrease in CPP in patients with ACS?
6. And, what should we know about the CNS approaching a patient with ACS with or without head injury?
Regardless of improvements in the understanding and treatment of ACS, many questions
remain still unanswered, especially on the effects of IAH and ACS on the CNS. At present, this
area of research is one of the most challenging and fascinating topics for many laboratory and
clinical investigators.
In the first part of the chapter we present the findings of laboratory studies and clinical
investigations reported in the literature; thereafter, we will conclude with some practical indications for a better management of this unusual relationship between two distant organ systems.
Animal Studies
Animal studies have clearly shown the effects of IAH on the ICP and CPP and illustrated
the pathophysiological pathways of these derangements.
Evidence that IAP Increments Increase the ICP
Josephs et al1 were the first group of investigators to evaluate the effect of increased IAP on
intracranial pressure dynamics, using a porcine model. Five pigs were enrolled in this animal
protocol at the Boston University Medical Center. Animals were anesthetized, tracheostomized,
ventilated and an ICP pressure transducer was inserted over the left parietal cortex. A balloon
catheter was positioned in the epidural space for reproducing high ICP. Heart rate, MAP, ICP
and arterial blood gas (ABG) measurements were recorded every 5 minutes for 30 minutes
146
Abdominal Compartment Syndrome
Table 1. Average values from the five pigs for each experimental period
Standard Standard 15 mm Hg
Basal Pneumoperitoneum High ICP + High ICP p Value
ICP
13.46 ± 0.68 18.72 ± 1.5 22.6 ± 1.75 27.4 ± 0.93 ≤ 0.0001
MAP
81.92 ± 9.81 86.78 ± 7.75 85 ± 8.26 81.64 ± 7.87 ns
PaCO
37.82 ± 2.23 40.52 ± 0.95 41.20 ± 1.43 39.00 ± 1.10 ns
2
PaO
99.2 ± 13.22 105.35 ± 8.85 108.8 ± 9.5 115 ± 9.89 ≤ 0.02
2
All values are expressed in mm Hg. Modified from Josephs LG et al; J Trauma 1994; 36(6):815-8.
15 mm Hg Pneumoperitoneum
before, during, and after establishment of 15 mm Hg CO2 pneumoperitoneum. The ICP was
then raised by inflating the epidural balloon to an ICP between 20-25 mm Hg and measurements were repeated before, during, and after pneumoperitoneum. Josephs showed that a standard pneumoperitoneum increases ICP; in particular in the uninjured model mean ICP increased from a baseline of 13.46 ± 1.01 mm Hg to 18.72 ± 1.50 mm Hg during
pneumoperitoneum (p = 0.0001). In the head injury model (epidural balloon inflated) ICP
moved from 22 ± 1.75 mm Hg to 27.40 ± 0.93 mm Hg (p = 0.0001). CPP decreased not
significantly from 62.46 to 55.02 mm Hg (Table 1).
The authors hypothesized, according to the modified Monro-Kellie doctrine, that the mechanism through which pneumoperitoneum increases ICP is simply mechanical. The Monro-Kellie
doctrine recognizes three main contents in the cranial space: vascular, cerebrospinal fluid (CSF)
and parenchyma. The doctrine states that, in adults, changes in one or more of these contents
result in reciprocal changes in the remaining compartment. The imbalance of the contents
produces, when buffers mechanisms are exhausted, an ICP increase. In other words, ICP reflects the relationship between the volume of intracranial contents (vascular, CSF, and parenchyma) and the volume of the cranial vault. In their brain injury model, Josephs et al
1
increased directly the intracranial volume by inflating the epidural balloon meanwhile, inducing
the pneumoperitoneum, they indirectly increased the vascular contents by reducing the cerebral blood outflow, due to the decreased thoracoabdominal compliance, thus producing an
ICP rise.
Evidence that IAP Increments Increase Central Venous Pressure,
Pleural Pressure, ICP and Decrease Cardiac Index and CPP
The confirmation of these aforementioned hypothesis came a few years later. Using a por-
cine model of acutely elevated IAP, Bloomfield et al
1. Clarified the mechanisms by which IAH increases ICP and decreases CPP,
2. Evaluated the effect of intravascular volume expansion upon ICP and CPP,
3. Studied the relationship between IAP, pleural pressure (PP), central venous pressure (CVP)
and ICP.
They measured the effects of elevated IAP upon ICP and CPP before and after intravascular
volume resuscitation. IAP was increased in 5 anesthetized swine by inflating an intraperitoneal
balloon to 25 mm Hg above baseline. Intravascular volume was then expanded and, finally,
abdominal decompression was performed (Fig. 2).
Changes in ICP and systemic and pulmonary hemodynamic parameters, secondary to increasing IAP, were measured. PaO
Bloomfield et al
4
showed that elevated IAP significantly increased ICP (7.6 ± 1.2 vs. 21.4 ±
and PaCO2 were maintained relatively constant.
2
1.0 mm Hg), PP and CVP whereas cardiac index (CI) and CPP (82.2 ± 6.3 vs. 62.0 ± 10.0 mm
Hg) decreased significantly. Intravascular volume expansion further significantly increased ICP
(27.8 ± 1.0 mm Hg), and increased both mean arterial pressure (MAP, 83.4 ± 14.0 versus
4
147Intra-Abdominal Hypertension and the Central Nervous System
Figure 2. Study design for elucidating effects of elevated IAP upon ICP and CPP before and after intravascular volume resuscitation. Details described in the text. Modified from Bloomfield GL et al, J Trauma 1996;
40: 936-941.
5
103.4 ± 8.9 mm Hg) and CPP (75.6 ± 9.0 mm Hg). Abdominal decompression returned ICP
toward baseline (11.2 ± 1.8 mm Hg) and further increased CPP (79.8 ± 9.7 mm Hg) (Fig. 3).
The authors concluded that elevated IAP increases CVP, PP, ICP and decreases CI, MAP
and CPP. Moreover, volume expansion, in the presence of elevated IAP, further raised the ICP
and, because of a larger increase in MAP, CPP. An interesting finding was that an IAP greater
than or equal to 25 mm Hg produces a statistically significant decrease in CPP, even in animals
without head injuries.
Figure 3. Effect of increasing intra-abdominal pressure (IAP) upon intracranial pressure (ICP), central
venous pressure (CVP) and pleural pressure before and after intravascular volume expansion (Resuscitation)
and after abdominal decompression (Release). Modified from Bloomfield GL et al. J Trauma 1996;
40(6):936-943.
5
148
Figure 4. Scheme of the Bloomfield’s study design.
Abdominal Compartment Syndrome
The results of this study confirm that the mechanism of increment of ICP is purely mechanical (at PaCO
< 45 mm Hg, and arterial pH > 7.35). According to the Monro-Kellie
2
doctrine, the authors demonstrated that cerebral venous outflow via the jugular venous system
is impeded by a significant rise in the CVP. This phenomenon was amplified by volume expansion, due to the additional rise in CVP. They suggested that the functional obstruction of the
jugular venous system and the ensuing obligatory increase in the volume of the cerebral vascular space, are the mechanisms responsible for the increased ICP caused by elevated IAP.
Evidence that Increased IAP Produces a Raise in CVP, PP, ICP
and Decreases CPP
Furthermore in 1997, Bloomfield et al5 in order to better clarify the relationship between
the PP, ICP and CPP in presence of IAH, repeated the animal-study in two groups of pigs. In
Group 1 animals had IAP increased to 25 mm Hg above baseline, then released. In Group 2, to
prevent a rise in PP, animals underwent a sternotomy and pleuropericardotomy before increasing IAP (Fig. 4).
As predicted, in the first group IAP rising to 25 mm Hg above baseline caused significant
increases in ICP, PP, PAOP, CVP and decreases in CI and CPP. Interestingly, in the second
Figure 5. Effect of increasing intra-abdominal pressure (IAP) in closed and open-chest animals on ICP
(ICP= filled boxes closed chest, open boxes animals with thoracotomy) and pleural pressure (PP= closed
circles animals without sternotomy, open triangles animals with sternotomy). Modified from Bloomfield:
Crit Care Med 1997; 25(3):496-503.
5
149Intra-Abdominal Hypertension and the Central Nervous System
group, sternotomy and pleuropericardotomy abolished all the effects of increased IAP, except
the decreased CI (Fig. 5).
In conclusion, these laboratory studies clearly showed that an IAP rise decreases the
thoracic-abdominal compliance and increases the mean intrathoracic pressures. These in turn
reduce cerebral venous outflow, causing an ICP elevation.
Clinical Studies
Despite those laboratory investigations providing evidence about the relationship between
the IAH, ICP and CPP, only recently some investigations focused on the clinical impact of
such findings.
As previously mentioned, in 1995, two case reports simultaneously confirmed the laboratory results. Yet, no clinical trial was performed in the clinical ward to asses the effect of an
increased IAP on CNS.
In 2001, the first clinical study evaluating IAP and ICP was carried out by our group
San Gerardo Hospital, Monza, Italy. We designed a prospective, sequential, nonrandomized
study to systematically measure the effects of artificially increased IAP in 15 head trauma patients and to clarify the pressure transmission modalities between different body compartments (abdomen, chest and head). IAP was increased by positioning a soft, 15-L water bag on
the patient’s abdomen. Strict inclusion criteria were implemented: intubated and mechanically
ventilated head injury adult patients were considered eligible for the study at the end of the
acute phase, after the evacuation of surgical masses and when no intracranial hypertension was
recorded (ICP < 20 mm Hg and CPP > 70 mm Hg) throughout the 24 hours preceding the
enrollment. Many parameters were monitored: IAP,
sure (IJP), jugular bulb oxygen saturation (SjO
nial compliance measured as pressurevolume index (PVI
7
MAP, CVP, ICP, CPP, jugular bulb pres-
), cerebral oxygen extraction (CEO2), intracra-
2
8
), compliance of the respiratory system divided into its pulmonary and chest wall components and gas exchange. Measurements
were carried out before and 20 minutes after the IAP rise. MAP, ICP, IAP, CVP and IJP were
6
at
We found that placing weights upon the abdomen generated a significant increase in IAP,
which rose from 4.7 ± 2.9 to 15.5 ± 4.1 mm Hg (p <.001) (Fig. 7). The rise in IAP caused
concomitant and rapid increases in CVP from 6.2 ± 2.4 to 10.4 ± 2.9 mm Hg (p <.001), IJP
from 11.9 ± 3.2 to 14.3 ± 2.4 mm Hg (p <.001), and ICP from 12.0 ± 4.2 to 15.5 ± 4.4 mm
Hg (p <.001).
All these changes required only seconds to reach a plateau and remained increased till the
IAP returned to baseline after the weight removal.
A curious result from this study was the MAP increase from 94 ± 11 to 100 ± 13 mm Hg (p
<.01), which allowed the maintenance of a stable CPP (82.4 ± 10.3 vs. 84.7 ± 11.5 mm Hg; p
= NS), despite the ICP increase. As noticed, an increase in MAP and a stable CPP do not agree
with the previous animal findings, and they speculated that the difference lies upon:
1. A different level of IAP. IAP was raised to ≥ 25 mm Hg in animals vs. 15 mm Hg in
humans;
2. Animals were heavily sedated with high dose of pentobarbital, with possible vasoplegic
effects. In the clinical setting propofol (3-6 mg/K/h) and fentanyl (1.5 γ/K/h) were used;
3. As demonstrated by physiologic studies, the rise in the intrathoracic pressure may facilitate
the systolic ejection, although decreasing the venous return.
Interestingly, we found that respiratory system compliance decreased in all patients (from
58.9 ± 9.8 to 44.9 ± 9.4 mL/cm H
O; p <.001) (Fig. 8). However, thoracic transmural pressure
2
(TTP = CVP - esophageal pressure) remained constant during the study time, while chest wall
compliance decreased significantly (from 204.7 ± 37.1 to 123.6 ± 38.0 mL/cm H
O; p <.001);
2
lung compliance did not change.
These findings let us confirm the hypothesis that HIAP displaces the diaphragm upward,
reducing the chest wall compliance, hence respiratory system compliance. The pressure in the
abdominal compartment (IAP) is directly transmitted to the thoracic compartment, raising
150
Abdominal Compartment Syndrome
Figure 6. Effect of IAP rise, obtained with a weight application (dotted line). Computerized tracing are from
top to bottom: PAM= arterial pressure; ICP= intracranial pressure; IAP= intra-abdominal pressure; IJP=
jugular pressure; PVC= central venous pressure.
intrathoracic pressures (CVP, esophageal pressure) and, thereafter, to the cerebral compartment (IJP, ICP). In other words, the ICP rise appears to be the result of an obstruction to the
cerebral venous drainage, causing elevation of pressure in the intracranial compartment.
Utilizing a simplified model of cerebral circulation, as presented by Huseby,
9
the rise in
jugular vein pressure produces the transmission of the pressure to superior sagittal sinus. This
pressure increase is transferred to the Starling’s resistor at the cortical bridging vein level. The
increase in the outflow pressure in the Starling resistor requires, for maintaining a constancy of
151Intra-Abdominal Hypertension and the Central Nervous System
Figure 7. Effect of weight application. Basal and high IAP values. All graphics white line = mean value, upper
box = 75th percentile, lower box = 25th percentile, upper error bar = highest value, lower error bar = lowest
value. * p< 0.001.
the cerebral blood downflow, a parallel rise in the cerebral venous pressure, thus a rise in ICP
(Fig. 9).
This explains also the continued effect on ICP till the increased IAP is released, thus removing the effect on the Starling’s resistor. Furthermore, all patients enrolled in the study were in a
stable condition, with a starting ICP < 20 mm Hg, and a normal intracranial compliance. This
suggests that the starting ICP of all patients was on the flat portion of the Starling pressure/
volume curve (point a in Fig. 10) and this may explain the significant but not clinically relevant
ICP increase.
Figure 8. Effect of raised IAP on PaO2, PaO2, oxygen saturation, total respiratory compliance. All graphics
white line = mean value, upper box = 75th percentile, lower box = 25th percentile, upper error bar = highest
value, lower error bar = lowest value. * p< 0.05, ** ns.
152
Figure 9. Effect of PEEP on intracranial pressure in dogs with intracranial hypertension. Modified from
Huseby, J Neurosurg 1981; 55:704-707. See text for details.
Abdominal Compartment Syndrome
We speculated that probably in the presence of an intracranial hypertension the effect of
high IAP may induce a more profound and harmful increase in ICP due to a different starting
ICP position on the Starling curve owing to the reduction/absence of the compensatory capacity.
Based on those results, our recommendations were:
1. Routine assessment of IAP could help clinicians to identify remediable causes of increased
ICP,
2. Laparoscopic techniques causing IAP rise should be used with caution in patients with
concomitant head and abdominal injury.
11
Figure 10. Pressure-volume curve of the craniospinal compartment. It illustrates the principle that in the
physiologic range, i.e., near the origin of the x-axis on the graph (point a), intracranial pressure remains
normal in spite of small additions of volume until a point of decompensation (point b), after which each
subsequent increment in total volume results in an ever larger increment in intracranial pressure (point c).
153Intra-Abdominal Hypertension and the Central Nervous System
Figure 11. Scattergram of IAP versus ICP (positive correlation). From: Deeren DH, Dits H, Malbrain ML.
Correlation between intra-abdominal and intracranial pressure in nontraumatic brain injury. Intensive Care
Med 2005; 31(11):1577-81.
These suggestions are of a great importance for patient care, because abdominal trauma is
commonly associated with head trauma. The Major Trauma Outcome Study
11
documented
that up to 40% of patients with major abdominal trauma had an associated head injury. The
Boston University Medical Center Trauma Registry described approximately 30% of the patients who are victims of blunt trauma have an intracranial injury. An Italian data collection on
head trauma victims
12
showed the presence of associated severe abdominal complications in
8% of the ICU admitted patients (90 patients out of 1086).
Recently, an interesting paper has been published by the Adams Cowley Shock Trauma
Center of University of Maryland on decompressive laparotomy to treat intractable intracranial hypertension after traumatic brain injury.
13
Seventeen head injured patients underwent
decompressive laparotomy for intractable intracranial hypertension unresponsive to maximal
therapy. Before decompression, mean ICP and mean IAP were respectively 30 ± 8.1 mm Hg
and 27.5 ± 5.2 mm Hg. After abdominal decompression ICP dropped by at least 10 mm Hg to
a mean of 17.5 ± 3.2 mm Hg. In 6 patients that died this decrease was transient. The 11
surviving had persistent decreases in ICP.
Malbrain et al
14
evaluated the effects of IAP on ICP and CPP in patients with nontraumatic
brain injury. The prevalence of intra-abdominal hypertension is high in critically ill patients.
An epidemiological survey studied patients in medical and surgical ICUs and it was found that
54.4% of medical and 65% of surgical ICU patients have an IAP of 12 mm Hg or more.
16
The
aims of this study were:
a. to confirm with a large number of measurements the positive correlation between IAP and
ICP in patients with nontraumatic brain injury, and
b. to establish the changes in ICP and CPP that accompany changes in IAP. Eleven patients
were enrolled in the study with ICP-monitoring because of ischemic (4), hemorrhagic (5)
and metabolic (2) encephalopathy. Mean ICP was 9.8 ± 3.3 mm Hg, IAP 8.1 ± 3.7 mm
Hg, CPP 82.5 ± 16.6 mm Hg. They found a tight association between increases in IAP and
increases in ICP even at only slightly elevated IAP levels, as shown in Figure 11
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