DOI:10.2214/AJR.07.2092
AJR 2007; 189:1037-1043
© American Roentgen Ray Society
Abdominal Compartment Syndrome
Aashish Patel1,
Chandana G. Lall,
S. Gregory Jennings and
Kumaresan Sandrasegaran
1 All authors: Department of Radiology, Indiana University School of Medicine,
550 N University Blvd., Suite UH 0279, Indianapolis, IN 46202.
Received February 19, 2007;
accepted after revision May 20, 2007.
Address correspondence to K. Sandrasegaran.
CME
This article is available for CME credit. See
www.arrs.org
for more information.
Abstract
OBJECTIVE. The purpose of this article is to discuss the
pathogenesis, clinical features, radiologic findings, and treatment of
abdominal compartment syndrome, which is defined as an acute elevation of the
intraabdominal pressure with organ dysfunction.
CONCLUSION. Abdominal compartment syndrome is not well reported in
the radiology literature. In this review, we discuss a range of CT signs such
as elevated diaphragm, collapsed inferior vena cava, bowel wall thickening,
bowel mucosal hyperenhancement, hemoperitoneum, and increasing abdominal
girth, which, in combination, may allow the radiologist to raise the
possibility of abdominal compartment syndrome.
Keywords: abdominal compartment syndrome • CT diagnosis • intraabdominal hypertension
Introduction
Compartment syndrome is well known in the extremities, where increased
pressure within a closed fascial space depresses capillary perfusion pressure
to a level that cannot maintain tissue viability. The effects of elevated
intraabdominal pressure are less well recognized. Normally, the abdominal
pressure is about 5 mm Hg. The intraabdominal pressure may increase with acute
and substantial accumulation of fluid within the abdomen. "Abdominal
compartment syndrome" is defined as intraabdominal pressure of at least
20 mm Hg with dysfunction of at least one thoracoabdominal organ
[1–4].
In nearly all cases, there is some amelioration of organ function after
decompressive laparotomy. Primary abdominal compartment syndrome results from
injury or disease in the abdominopelvic region, such as after liver
transplantation or pelvic fractures. Secondary abdominal compartment syndrome
occurs from disease originating from outside the abdomen, such as from major
burns or sepsis.
There are virtually no radiology reports of abdominal compartment syndrome.
One reason for this may be that CT is not ordered for the diagnosis of
abdominal compartment syndrome. The diagnosis is usually rapidly performed at
the bedside with intravesical pressure measurements. However, radiologists
should understand this entity because it is likely that many of these
patients, especially those with trauma or pancreatitis, will undergo CT
studies for determining the severity of the illness and for identifying
potential complications. In this review, we discuss the pathogenesis, clinical
features, radiologic findings, and treatment of abdominal compartment
syndrome.
Pathogenesis of Abdominal Compartment Syndrome
As intraabdominal pressure rises, progressive organ failure occurs
(Fig. 1). The kidneys and lungs
are the most affected. With abdominal pressure of 15–20 mm Hg, the
urinary output is reduced. When the pressure exceeds 30 mm Hg, anuria ensues
[3,
5]. Renal failure is caused by
external pressure on the renal vasculature and parenchyma
[6]. Ureteric obstruction is
not thought to be a cause
[5].
Mesenteric blood flow reduces to 70% of normal when intraabdominal pressure
is about 20 mm Hg and falls to 30% of normal at 40 mm Hg. Intestinal
oxygenation is impaired above a pressure of 15 mm Hg
[7]. Bowel mucosal hypoxia
results in impaired gut–mucosal barrier function, allowing bacterial
translocation and sepsis
[8].
In abdominal compartment syndrome, the diaphragm becomes elevated with
reduced excursion. The thoracic volume and compliance are reduced. The ensuing
compressive atelectasis and ventilatory perfusion mismatch lead to hypercarbia
and respiratory acidosis [9,
10]. Oxygen delivery decreases
with increasing abdominal pressure. Hypoxia is found in 20% of patients with
abdominal pressure above 15 mm Hg and in all patients when the pressure
exceeds 35 mm Hg [3].
Decompression usually results in prompt reversal of respiratory failure
[2].
Increased abdominal pressure reduces venous return from the inferior vena
cava and increases systolic arterial pressure in abdominal arteries
[10]. Increased thoracic
pressure reduces cardiac output. Elevated intracranial pressure may occur and
has been shown to decline after decompression surgery for abdominal
compartment syndrome [11].
Clinical Diagnosis
The rapid accumulation of abdominal fluid in some conditions
(Table 1) may cause organ
dysfunction. In contrast, a more gradual rise in abdominal pressure, such as
in normal pregnancy or in ascitic accumulation in liver disease or ovarian
cancer, does not normally result in abdominal compartment syndrome.
Laparoscopy with pneumoperitoneum may cause elevated intraabdominal pressure,
but the effect is transient and not to the degree required to cause abdominal
compartment syndrome [12,
13].
Findings suggestive of abdominal compartment syndrome include a tensely
distended abdomen; increased peak airway pressure; difficulty in maintaining
ventilation, with hypoxia and hypercarbia; increasing creatinine; and
oliguria. Increased gastric acidity is also a recognized finding of abdominal
compartment syndrome [14].
However, most patients with abdominal compartment syndrome are in intensive
care units, and clinical examination is usually not sensitive for diagnosing
this entity.
Diagnosis of abdominal compartment syndrome is complicated by the fact that
these patients have many other explanations for renal or pulmonary failure.
Sepsis, acute respiratory distress syndrome, hypovolemic shock, and multiorgan
failure syndrome are frequently seen in patients who are also at risk of
abdominal compartment syndrome. In some patients, these diverse and
potentially lethal conditions may coexist
[15]. Unlike in pure
hypovolemic shock, the mean arterial pressure is normal in abdominal
compartment syndrome. Central venous and pulmonary wedge pressures are poor
indicators of volume depletion in abdominal compartment syndrome because they
are artificially elevated due to the increased thoracic pressure. In contrast
to hypovolemic shock, it is unusual for renal failure to occur in patients
with abdominal compartment syndrome without concomitant respiratory failure
[16]. However, rapid IV
resuscitation of a patient in hypovolemic shock may precipitate abdominal
compartment syndrome [15].
In general, abdominal compartment syndrome should be suspected in any
patient with the appropriate clinical antecedents whose organ dysfunction
worsens or does not improve in the face of adequate supportive therapy.
Measurement of intraabdominal pressure is required in such patients and is
best assessed by a transurethral probe inserted in the urinary bladder
[17,
18]. However, intravesical
pressure measurements may not accurately reflect intraabdominal pressure if
there is a neurogenic or contracted bladder, abdominal packing, or abdominal
adhesions [12,
19].
Radiologic Findings
There is limited information, to our knowledge, regarding the radiologic
findings in abdominal compartment syndrome. The CT findings in a total of
eight adult and pediatric patients have been reported
[20–22].
We reviewed the images obtained in 21 adult patients from our institution with
clinically proven abdominal compartment syndrome on grounds of organ failure
(usually lung or kidneys) and intravesical pressure measurement of at least 20
mm Hg. The mean of the maximum recorded intravesical pressure in our series of
patients was 26.2 mm Hg (range, 20.4–34.5 mm Hg). CT was performed
between 3 days before and 26 hours after the pressure measurements. When
multiple CT scans were available, we reviewed the scans temporally closest to
the maximum measured intravesical pressure. The causes of abdominal
compartment syndrome were trauma (n =13), postoperative bleeding
(n = 4), liver transplantation (n = 1), and severe
pancreatitis (n =3).
We found several radiologic signs that may be associated with this
condition (Table 2). Because we
did not have a control group of patients with trauma or pancreatitis who did
not have abdominal compartment syndrome, we cannot comment on how specific
these findings are. An elevated diaphragm has been noted when the
intraabdominal pressure rises above 15 mm Hg
[23] (Fig.
2A,
2B,
2C,
2D,
2E,
2F). This was the single most
common finding in our group. However, quantification of the diaphragm
elevation is difficult even when comparison chest radiographs are available
because CT scanograms are performed during quiet breathing in a supine
position, whereas posteroanterior chest radiographs are not.
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TABLE 2: Preoperative CT or Sonography Findings in 21 Patients with Clinically
Proven Abdominal Compartment Syndrome
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Fig. 2A —57-year-old man with diabetes who had laparotomy for
infective aortitis. Scout CT image obtained 1 day after surgery shows normal
position of diaphragm. Reason for horizontal artifacts on this image is not
clear.
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Fig. 2B —57-year-old man with diabetes who had laparotomy for
infective aortitis. Axial CT images from same series as A show ascites,
normal position of diaphragm, and normal-sized inferior vena cava (IVC)
(arrowhead, B). Also seen are hemoperitoneum (solid white
arrow, C) and mucosal hyperenhancement of bowel (dashed
arrows, C). Postoperative free peritoneal air is present. Black
arrow in C indicates anteroposterior abdominal girth.
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Fig. 2C —57-year-old man with diabetes who had laparotomy for
infective aortitis. Axial CT images from same series as A show ascites,
normal position of diaphragm, and normal-sized inferior vena cava (IVC)
(arrowhead, B). Also seen are hemoperitoneum (solid white
arrow, C) and mucosal hyperenhancement of bowel (dashed
arrows, C). Postoperative free peritoneal air is present. Black
arrow in C indicates anteroposterior abdominal girth.
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Fig. 2E —57-year-old man with diabetes who had laparotomy for
infective aortitis. Axial CT images from same study show as D show
collapsed IVC (arrowheads) with greatly increased ascites and
evidence of layered hemoperitoneum (white arrows, F).
Anteroposterior abdominal girth (black double arrow, F)
increased from C to F. Note jejunal feeding tube (black
arrow, F) and heavily calcified iliac arteries (curved
arrow, F). Patient had intraabdominal hypertension (intravesical
pressure of 28 mm Hg). Emergency decompressive laparotomy was performed and
patient survived.
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Fig. 2F —57-year-old man with diabetes who had laparotomy for
infective aortitis. Axial CT images from same study show as D show
collapsed IVC (arrowheads) with greatly increased ascites and
evidence of layered hemoperitoneum (white arrows, F).
Anteroposterior abdominal girth (black double arrow, F)
increased from C to F. Note jejunal feeding tube (black
arrow, F) and heavily calcified iliac arteries (curved
arrow, F). Patient had intraabdominal hypertension (intravesical
pressure of 28 mm Hg). Emergency decompressive laparotomy was performed and
patient survived.
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In our experience, abdominal measurements on a single CT scan are
nonspecific, and an increased anteroposterior abdominal dimension may be seen
with chronic ascites. Hemoperitoneum may be a more sensitive indicator for
abdominal compartment syndrome than simple ascites (Figs.
3A,
3B,
3C,
4A,
4B,
4C,
5A,
5B,
6A,
6B,
6C,
6D). A previous case series of
four patients suggested that when the ratio of the maximum anteroposterior
abdominal girth to the lateral girth was higher than 0.8, abdominal
compartment syndrome was likely
[20]. In almost all of our
patients with proven abdominal compartment syndrome (20 of 21), this ratio was
lower than 0.7 (Fig. 6A,
6B,
6C,
6D). However, increasing girth
seen on serial CT scans performed at short intervals is worrisome (Fig.
2A,
2B,
2C,
2D,
2E,
2F).
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Fig. 3A —76-year-old woman after motor vehicle accident.
Contrast-enhanced CT images show spleen is nonenhancing (white arrow,
A), and grade 5 splenic injury was diagnosed. There is abdominal
distention with large hematoma (solid black arrows, A and
B), which displaces posteriorly and effaces stomach (containing
nasogastric tube [arrowheads, A and B]). Bowel wall
shows increased enhancement (arrowheads, C), and inferior vena
cava (dashed arrows, A and B) and renal veins are
flattened. These findings are also seen with severe hypotension (shock bowel),
and imaging diagnosis of abdominal compartment syndrome cannot be made with
certainty. However, at time of CT, patient was on inotropic agents and had
normal renal function and blood pressure (hence decision to use IV contrast
agent). In addition, intravesical pressure was 26 mm Hg, and patient underwent
emergency laparotomy for splenectomy and evacuation of blood clot.
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Fig. 3B —76-year-old woman after motor vehicle accident.
Contrast-enhanced CT images show spleen is nonenhancing (white arrow,
A), and grade 5 splenic injury was diagnosed. There is abdominal
distention with large hematoma (solid black arrows, A and
B), which displaces posteriorly and effaces stomach (containing
nasogastric tube [arrowheads, A and B]). Bowel wall
shows increased enhancement (arrowheads, C), and inferior vena
cava (dashed arrows, A and B) and renal veins are
flattened. These findings are also seen with severe hypotension (shock bowel),
and imaging diagnosis of abdominal compartment syndrome cannot be made with
certainty. However, at time of CT, patient was on inotropic agents and had
normal renal function and blood pressure (hence decision to use IV contrast
agent). In addition, intravesical pressure was 26 mm Hg, and patient underwent
emergency laparotomy for splenectomy and evacuation of blood clot.
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Fig. 3C —76-year-old woman after motor vehicle accident.
Contrast-enhanced CT images show spleen is nonenhancing (white arrow,
A), and grade 5 splenic injury was diagnosed. There is abdominal
distention with large hematoma (solid black arrows, A and
B), which displaces posteriorly and effaces stomach (containing
nasogastric tube [arrowheads, A and B]). Bowel wall
shows increased enhancement (arrowheads, C), and inferior vena
cava (dashed arrows, A and B) and renal veins are
flattened. These findings are also seen with severe hypotension (shock bowel),
and imaging diagnosis of abdominal compartment syndrome cannot be made with
certainty. However, at time of CT, patient was on inotropic agents and had
normal renal function and blood pressure (hence decision to use IV contrast
agent). In addition, intravesical pressure was 26 mm Hg, and patient underwent
emergency laparotomy for splenectomy and evacuation of blood clot.
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Fig. 4A —20-year-old woman who presented with traumatic placental
abruption at 26 weeks' gestation. CT was performed to exclude trauma to
abdominal organs. Contrast-enhanced CT images show high-density peritoneal
fluid (white arrows, A and B) indicating
hemoperitoneum. Bowel walls are thickened and show increased enhancement
(black arrows, A and B). Inferior vena cava is
collapsed (black arrowheads, A and B). Extravasation of
IV contrast material is seen in placenta (white arrowheads,
C). Intravesical pressure was 29 mm Hg. Patient was moribund and
underwent emergency cesarean section. She died 2 days later of multiorgan
failure.
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Fig. 4B —20-year-old woman who presented with traumatic placental
abruption at 26 weeks' gestation. CT was performed to exclude trauma to
abdominal organs. Contrast-enhanced CT images show high-density peritoneal
fluid (white arrows, A and B) indicating
hemoperitoneum. Bowel walls are thickened and show increased enhancement
(black arrows, A and B). Inferior vena cava is
collapsed (black arrowheads, A and B). Extravasation of
IV contrast material is seen in placenta (white arrowheads,
C). Intravesical pressure was 29 mm Hg. Patient was moribund and
underwent emergency cesarean section. She died 2 days later of multiorgan
failure.
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Fig. 4C —20-year-old woman who presented with traumatic placental
abruption at 26 weeks' gestation. CT was performed to exclude trauma to
abdominal organs. Contrast-enhanced CT images show high-density peritoneal
fluid (white arrows, A and B) indicating
hemoperitoneum. Bowel walls are thickened and show increased enhancement
(black arrows, A and B). Inferior vena cava is
collapsed (black arrowheads, A and B). Extravasation of
IV contrast material is seen in placenta (white arrowheads,
C). Intravesical pressure was 29 mm Hg. Patient was moribund and
underwent emergency cesarean section. She died 2 days later of multiorgan
failure.
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Fig. 5A —50-year-old man after motor vehicle accident.
Contrast-enhanced CT images show extensive hemoperitoneum in right upper
quadrant (white arrowheads). Note right rib fracture on A.
Liver dome is superiorly positioned in relation to heart in A,
indicating right hemidiaphragmatic elevation. There is inhomogeneous and
patchy hepatic enhancement. Inferior vena cava is collapsed (black
arrowhead, B). Grade 5 liver trauma was diagnosed. Intravesical
pressure was 32 mm Hg. Patient underwent emergency laparotomy but died soon
afterward.
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Fig. 5B —50-year-old man after motor vehicle accident.
Contrast-enhanced CT images show extensive hemoperitoneum in right upper
quadrant (white arrowheads). Note right rib fracture on A.
Liver dome is superiorly positioned in relation to heart in A,
indicating right hemidiaphragmatic elevation. There is inhomogeneous and
patchy hepatic enhancement. Inferior vena cava is collapsed (black
arrowhead, B). Grade 5 liver trauma was diagnosed. Intravesical
pressure was 32 mm Hg. Patient underwent emergency laparotomy but died soon
afterward.
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Fig. 6A —54-year-old man who underwent orthotopic liver
transplantation. Scout radiograph (A) and axial CT scan (B)
performed 3 days after liver transplantation show elevated left hemidiaphragm
(arrow, A) and collapsed inferior vena cava
(arrowhead, B). Note severe ascites in B. Intravesical
pressure was elevated (21 mm Hg).
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Fig. 6B —54-year-old man who underwent orthotopic liver
transplantation. Scout radiograph (A) and axial CT scan (B)
performed 3 days after liver transplantation show elevated left hemidiaphragm
(arrow, A) and collapsed inferior vena cava
(arrowhead, B). Note severe ascites in B. Intravesical
pressure was elevated (21 mm Hg).
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Fig. 6C —54-year-old man who underwent orthotopic liver
transplantation. Color Doppler sonogram shows virtually no diastolic flow in
main hepatic artery. In fact, initial reversal of diastolic flow
(arrows) is seen.
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Fig. 6D —54-year-old man who underwent orthotopic liver
transplantation. Patient underwent therapeutic paracentesis with drainage of
10.5 L of serous fluid. Postdrainage scout radiograph (same magnification as
scout image A) shows return of diaphragm to normal position and reduced
distention. Skin folds (arrowheads) were seen after acute abdominal
decompression. Decompressive surgery was not required. Abdominal compartment
syndrome is rare in patients undergoing liver transplantation at our
institution, possibly because fascia is routinely left open, and skin is
sutured. After satisfactory postoperative recovery, fascia and skin are closed
a few days later.
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Flattened inferior vena cava and increased bowel enhancement (shock bowel)
may be seen in hypovolemic shock and are not specific to abdominal compartment
syndrome (Fig. 3A,
3B,
3C). However, these findings
were seen in our patients who were not hypotensive. Therefore, we believe that
these findings can also be seen in abdominal compartment syndrome in the
absence of hypotension. In another study, two of four patients with abdominal
compartment syndrome had increased bowel enhancement and renal compression.
Flattened renal veins was a common finding on CT in our patients (n =
14). Mosaic liver perfusion was seen in some patients with trauma to the liver
(Fig. 5A,
5B).
Small-bowel dilatation was seen in only two patients. In addition, three
patients had gastric distention. The reason for gastric distention is not
clear. In the three patients with clinical suspicion of abdominal compartment
syndrome after liver transplantation, the resistive indexes of the hepatic
arteries were elevated, with virtually no diastolic flow or even reversed flow
(Fig. 7A,
7B,
7C).
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Fig. 7C —67-year-old man who presented with severe acute pancreatitis.
CT image shows severe pancreatic ascites. Ratio of maximum anteroposterior
girth to lateral abdominal girth is 0.65 (double-headed arrows).
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Acute Compartment Syndrome in Specific Situations
Trauma
Of patients with severe blunt abdominal trauma, 5–20% develop
abdominal compartment syndrome
[3,
24]. This risk is higher in
patients with grade 5 liver trauma or combined abdominopelvic injury and in
those who have undergone abdominal packing for bleeding or primary fascial
closure after laparotomy. In a series of 311 patients with abdominopelvic
trauma who subsequently developed abdominal compartment syndrome
[24], the liver was the most
frequent site of injury (Fig.
5A,
5B). Injuries to the spleen,
pancreas, and bowel have also been associated with predisposition to abdominal
compartment syndrome.
Another study of 70 patients who developed abdominal compartment syndrome
after a penetrating abdominal trauma
[14] found gastrointestinal
and vascular (arterial or venous) injury in 70% and 35% of patients,
respectively. Rarely, abdominal compartment syndrome may develop in patients
without visible organ injury
[24]. Trauma patients with
abdominal compartment syndrome show a reduction in intraabdominal pressure and
improvements in hemodynamic status and renal and pulmonary function after
decompressive laparotomy.
In our series of patients with abdominal compartment syndrome after trauma
(n = 13), the organs injured were liver (n =6), spleen
(n = 4), mesentery or small bowel (n =3), kidneys
(n = 3), pancreas (n = 2), and uterus (n = 1). Some
patients had multiple organ injuries. In all cases, the organ injury was
moderate to severe (grades 3–5), with hemoperitoneum seen on CT in 11
cases (Figs. 3A,
3B,
3C,
4A,
4B,
4C,
5A,
5B).
Liver Transplantation
Several factors associated with liver transplantation lead to elevated
intraabdominal pressure. These include bowel edema from portal vein clamping,
hepatic reperfusion edema, and donor–recipient graft-size mismatch match
[25]. The occurrence of
abdominal compartment syndrome with intraabdominal pressure of more than 25 mm
Hg after liver transplantation is thought to be 30%
[26]. After liver
transplantation, there is an increased incidence of portal vein and hepatic
artery thrombosis in patients with acute compartment syndrome compared with
those without acute compartment syndrome
[27]. In our experience,
peripheral infarction of the liver, lack of diastolic flow in the hepatic
artery branches (Fig. 6A,
6B,
6C,
6D), and to-and-fro flow in
the portal vein may be sonographic markers of rising intraabdominal
pressure.
Pancreatitis
The prevalence of intraabdominal hypertension in patients with severe acute
pancreatitis is about 40–50%
[28], and the frequency of
abdominal compartment syndrome requiring surgical decompression is about 10%
[29]. Early and aggressive
fluid resuscitation in patients with severe acute pancreatitis is likely to
result in an increased incidence of abdominal compartment syndrome. Abdominal
compartment syndrome may be confused with other metabolic syndromes that are
found in severe acute pancreatitis, including systemic inflammatory response
syndrome and multiple organ dysfunction syndrome
[30]. CT findings of
increasing peritoneal or retroperitoneal fluid collections (Fig.
7A,
7B,
7C) and bowel wall enhancement
should raise concern for abdominal compartment syndrome.
Treatment of Abdominal Compartment Syndrome
The mortality rate associated with abdominal compartment syndrome is
significant, ranging between 60% and 70%
[3,
4,
16]. The poor outcome relates
not only to abdominal compartment syndrome itself but also to concomitant
injury and hemorrhagic shock. Treatment of the shock with large-volume
resuscitation may worsen abdominal compartment syndrome by causing reperfusion
bowel edema [3].
The currently accepted treatment for abdominal compartment syndrome is
decompressive laparotomy. However, decompressive laparotomy does not prevent
death in abdominal compartment syndrome. A metaanalysis of 250 patients who
had decompressive laparotomy for abdominal compartment syndrome found a
mortality rate of 49% [31].
Other methods of reducing intraabdominal pressure include drainage of fluid
collections and muscle relaxation
[32].
Many techniques have been described for temporarily covering the abdomen
after decompression laparotomy using mesh, opened sterile saline bags,
plastic, or silicone. Others have used skin clips to achieve skin closure
while leaving the muscle and fascial layer open
[4]. The complications of
leaving the abdomen open include delayed bowel fistula and ventral hernia,
which occur in up to two thirds of patients treated with an open abdomen. A
less common but more serious complication is a potentially lethal reperfusion
syndrome with persistent hemorrhage
[33]. Nevertheless, most
surgeons would prefer to leave the abdomen open in those who are at high risk
of abdominal compartment syndrome.
Conclusions
General and trauma surgeons and intensivists are aware of abdominal
compartment syndrome and observe for clinical signs of this condition.
Radiologic input into the diagnosis of this entity has been minimal in the
past. Individual CT signs such as elevated hemidiaphragm, flattened inferior
vena cava and renal veins, and increased bowel wall enhancement are neither
sensitive nor likely specific for abdominal compartment syndrome. However,
when a combination of these findings is present in the appropriate clinical
setting or if the signs are seen to worsen on sequential imaging studies, the
radiologist should raise the possibility of abdominal compartment
syndrome.
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Abstract
Introduction
