DOI:10.2214/AJR.07.2390
AJR 2007; 189:1112-1117
© American Roentgen Ray Society
Colonoscopy Findings in End-Stage Liver Disease Patients with Incidental CT Colonic Wall Thickening
Eleanor L. Ormsby1,
Curtis Duffield1,
Farshad Ostovar-Sirjani2,
John P. McGahan1 and
Christoph Troppmann2
1 Department of Radiology, University of California, Davis Medical Center and
Lawrence J. Ellison Ambulatory Care Center, 4860 Y St., Ste. 3100, Sacramento,
CA 95817.
2 Department of Surgery, University of California, Davis Medical Center,
Sacramento, CA 95817.
Received April 10, 2007;
accepted after revision June 1, 2007.
Presented at 2006 annual meeting of the Radiological Society of North
America, Chicago, IL.
Address correspondence to J. P. McGahan
(john.mcgahan{at}ucdmc.ucdavis.edu).
Abstract
OBJECTIVE. Colonic wall thickening may occur in patients with
end-stage liver disease. This study was conducted to correlate colonoscopy
with CT-detected colonic wall thickening in this group of patients to assess
their radiologic and clinical relevance.
CONCLUSION. Our results suggest that CT findings of colonic wall
thickening in end-stage liver disease should be considered benign, and
colonoscopy is unnecessary for the evaluation of malignancy or colitis unless
it is clinically indicated.
Keywords: colonic wall thickening • colonoscopy • CT • gastrointestinal imaging • liver disease
Introduction
Many patients with end-stage liver disease are evaluated with CT for
pretransplantation workup, before transjugular intrahepatic portosystemic
shunt (TIPS) procedures, and for surveillance of hepatoma. During these CT
examinations, incidental findings of colonic wall thickening are not rare.
Several studies have evaluated the incidence of the CT colonic wall thickening
in patients with cirrhosis
[1–3].
The incidence ranges from 31% to 35%
[1–3]
and most commonly occurs in the right colon
[2,
3]. Sometimes these changes are
so dramatic they can mimic other severe processes such as ischemic colitis,
infection, hemorrhage, inflammation, or even malignancy, which poses a
particular diagnostic dilemma in patients who are undergoing a
pretransplantation workup. Although colonic thickening may be benign,
pathologic causes need to be excluded to ensure proper pretransplantation
evaluation and to facilitate timely placing of these patients on the
transplant list.
To our knowledge, no studies have been performed specifically to correlate
the CT findings of colonic wall thickening in patients with end-stage liver
disease who are undergoing transplantation evaluation with colonoscopic
findings to determine the causes of the thickening. The purpose of our study
was twofold: first, to determine the frequency and segmental distribution of
colonic wall thickening on CT examinations; and second, to correlate CT
findings with colonoscopy results in this group of patients to determine the
necessity of additional studies or investigations.
Materials and Methods
Patients
Biweekly combined conferences are held between radiology and
transplantation surgery teams to review CT images obtained at our institution
and the clinical data of patients who have been referred to our
transplantation center for liver transplantation evaluation. From the
transplantation center records, a list of our study patient population was
generated that included all patients who underwent an abdominal CT examination
at our institution and were reviewed by the combined radiology–surgery
transplantation conference from January 2002 to June 2005. The only exclusion
criterion was patient age younger than 18 years. We retrospectively reviewed
the medical records, including CT findings, radiology–surgery clinical
conference review notes, and available colonoscopy reports. Serum creatinine
and total bilirubin levels and international normalized ratios (INR) were
obtained for calculation of model of end-stage liver disease (MELD) scores. A
total of 233 patients had been referred for liver transplantation evaluation
and had undergone CT at our institution during this time period. This study
was approved by the institutional review board of the University of California
at Davis.
CT
CT was performed with a QXi LightSpeed 16-MDCT scanner (GE Healthcare).
Most (229/233) scans were obtained using four-phase liver scanning protocols
that include an unenhanced base scan with 5.0-mm reconstructions; an arterial
phase using SmartPrep (GE Healthcare) bolus tracking with 5.0-mm
reconstruction at 1.25-mm increments; a portal venous phase 65 seconds after
the injection of contrast material with 5.0-mm reconstruction at 1.25-mm
increments; and a hepatic venous phase 150 seconds after the injection with
5.0-mm reconstruction. All liver scanning protocols used 150 mL of Omnipaque
350 contrast medium (iohexol, Amersham Health [now GE Healthcare]) at an
injection rate of 4.0 mL/s. For these scans, only the abdomen was included;
scanning stopped at the iliac crest. In four patients, a three-phase abdomen
and pelvis CT protocol was performed on the same scanner using 125 mL of
Omnipaque 350 injected at 2.5 mL/s, scanned at 75 seconds (abdomen and pelvis)
and 300 seconds (abdomen only) after the injection to obtain delayed images.
The base scan of 5-mm slice thickness was used. No oral or rectal contrast
agent or air was given for either of these two protocols.
Image Analysis and Colonoscopy Correlation
We used criteria obtained from the literature
[2,
4,
5] of wall thickness 
6.0
mm to define colonic wall thickening. The width is measured as the distance
from the outer colonic wall edge, defined by identifying the mesenteric
fat–bowel wall interface, to the inner bowel wall edge. Whenever colonic
wall thickening was identified, the anatomic distribution was documented. The
location of colonic abnormalities were categorized as either isolated to the
cecum or ascending colon; isolated to the right colon and transverse colon; or
diffuse, involving almost all visualized colon. The pattern of colonic wall
thickening was categorized into two groups. The first group consisted of
patients who had preservation of the colonic wall layers with stratification
that consisted of two or three thickened layers. The term "halo
sign" has been previously used for this appearance on cross-sectional
imaging of the bowel [6]. The
second group consisted of patients with loss of the colonic wall layers with
homogeneously dense thickening in which the colon layers were not easily
discerned. Other CT features of cirrhosis and portal hypertension, including
varices, ascites, and splenomegaly, were also noted.
Patients with CT findings of colonic wall thickening were correlated with
subsequent colonoscopy examinations performed at our institution (n =
22) and at outside institutions (n = 3). All colonoscopy reports were
reviewed for findings that described changes in the colonic mucosa and for the
presence of vascular lesions or polyps. If biopsies were performed, pathology
reports were also reviewed. Colonoscopy findings were statistically compared
with the segmental distribution of CT colonic thickening.
Statistical Analysis
Statistical comparisons were made and analyzed for frequency of colonoscopy
findings to segmental distribution of the CT colonic thickening using the
Pearson chi-square test. Data are reported as the mean ± 95% CI unless
otherwise stated. Statistical significance was assumed at a level of
p < 0.05.
Results
There were 233 end-stage liver disease patients referred to our
transplantation center who underwent pretransplantation evaluation, including
CT of the abdomen, at our institution. Forty-nine of 233 (21%) patients had CT
findings of colonic wall thickening. The mean age of these 49 patients was 52
± 2.89 (SD) years. There were 28 (57%) men and 21 (43%) women. Of the
49 patients, the cause of the end-stage liver disease was as follows: 16 (33%)
with hepatitis C, 16 (33%) with combined hepatitis C and alcoholism, six (12%)
with autoimmune hepatitis, four (8%) with alcoholism, and two (4%) with
hepatitis B (4%). In addition, one patient (2%) had combined hepatitis B,
hepatitis C, and alcoholism. One patient (2%) had fulminant hepatic failure
secondary to a Tylenol (acetaminophen, McNeil) overdose. One patient (2%) had
granulomatous hepatitis. One patient (2%) had a cryptogenic or unknown cause
of the liver disease, and one (2%) had nonalcoholic steatohepatitis.
Colonic Wall Thickening Patterns and Other CT Findings
Of the 49 patients with CT colonic wall thickening, 26 (53%) had colonic
thickening, mostly at the cecum and ascending colon. Twelve patients (25%) had
colonic thickening extending from the right colon to the proximal transverse
colon. Eleven patients (22%) had diffuse thickening involving most of the
visualized colon. The colonic wall thickening ranged from 7 to 18 mm (mean,
12.5 ± 0.8 mm) for the 49 patients (see
Table 1 for the subgroup)
(Figs. 1A,
1B,
2A,
2B,
3,
4).
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TABLE 1: Characteristics of Colonic Wall Thickening in 49 Patients Who Underwent
CT and 25 Who Underwent Colonoscopy
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Fig. 1A —54-year-old man with hepatitis C end-stage liver disease. CT
scan shows diffuse colonic wall thickening extending to left colon. Masslike
thickening of ascending colon (long arrow), mildly thickened
proximal transverse colon (short arrow), and loss of bowel
wall layers are seen.
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Fig. 1B —54-year-old man with hepatitis C end-stage liver disease.
Colonoscopy shows increased vascularity, especially in cecum and right colon,
that is compatible with portal hypertensive colopathy.
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Fig. 2A —54-year-old man with end-stage liver disease from hepatitis C
and alcoholism. Contrast-enhanced CT scan of abdomen shows markedly thickened
and edematous ascending colon, preservation of bowel wall, and stratification
of layers (long arrow). Note transverse colon is not
affected. Prominent subcutaneous vessels are seen from portosystemic
collateralization (short arrow).
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Fig. 2B —54-year-old man with end-stage liver disease from hepatitis C
and alcoholism. Colonoscopy shows slightly increased chronic inflammatory
change and edema of lamina propria. Mucosa was friable and bled easily during
examination.
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Fig. 3 —67-year-old woman with hepatitis C end-stage liver disease.
Contrast-enhanced CT scan of abdomen shows stratification of bowel layer
(hyperdense inner ring with relative hypodense middle layer, long
arrows). Note shaggy mucosa of transverse colon (short
arrow). Colonoscopy (not shown) showed mild mucosa edema but was
otherwise normal.
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Fig. 4 —Contrastenhanced CT scan of abdomen in 43-year-old man with
end-stage liver disease from hepatitis C and alcoholism shows accordion sign
(arrow) and large nodular defects (arrowheads) that are
analogous to thumb-printing on radiographs. Colonoscopy (not shown) was normal
except for mucosal edema.
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All positive studies for CT colonic wall thickening showed symmetric wall
thickening. No predominant eccentric wall thickening or enhancement was seen.
Colonic wall thickening was seen in segments of colon, and no focal thickening
was noted (Figs. 1A,
1B,
2A,
2B,
3,
4). Of the 49 patients with CT
colonic wall thickening, 37 (76%) had bowel wall layer preservation with
stratification, some of which appeared as a halo on transverse images of the
bowel. Twelve patients (24%) had loss of bowel wall layers with homogeneous
attenuation along the thickened bowel wall. The two patterns were compared
among the three location groups (cecum and ascending colon vs right colon to
transverse colon vs right colon to descending colon). No statistically
significant difference was seen among the groups (p = 0.552).
Most patients with CT colonic wall thickening had ascites (39/49 patients,
80%). Thirty-seven patients (76%) had splenomegaly, and 43 (88%) had varices.
The average albumin level was 2.53 g/dL. The normal serum albumin in our
laboratory ranges from 3.8 to 4.8 g/dL. The average MELD score was 15.6.
Colonoscopy Findings
Twenty-five (51%) of the 49 patients who had CT colonic wall thickening
underwent subsequent colonoscopy examinations, most of which were performed
for screening purposes to rule out colon cancer as the cause of colonic wall
thickening. Of these patients, 13 (52%) had normal colonic mucosa except for
the presence of mild mucosa edema in a few patients (Figs.
3 and
4). No evidence of colitis was
seen. Of these 13 patients, seven had internal hemorrhoids, three had
incidental benign polyps, one had diverticulosis, and one had rectal varices.
Eleven (44%) of the 25 patients showed diffuse edematous mucosa with increased
vascularity and telangiectasia compatible with nonspecific colitis or
"portal hypertensive colopathy" according to the
gastroenterologists' reports (Figs.
1A,
1B and
2A,
2B). Of these 11 patients,
seven had internal hemorrhoids, six had incidental polyps, one had peristomal
varices with isolated arteriovenous malformation, and one had inferior rectal
varices. One patient (4%) had moderate to severe active ulcerative colitis
with discrete ulcers, diffuse edema, and multiple pseudopolyps at the hepatic
flexure. This patient had diffuse wall thickening up to 18 mm throughout the
colon (Fig. 5A,
5B,
5C).
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Fig. 5A —60-year-old man with colonic thickening, ulcerative colitis,
and primary sclerosing cholangitis. Contrast-enhanced CT scan of abdomen shows
diffuse concentric thickening of right and left colon. Minimal preservation of
mucosa (arrow) was seen. Note large ascites and portosystemic
collateral vessel (arrowhead).
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Fig. 5B —60-year-old man with colonic thickening, ulcerative colitis,
and primary sclerosing cholangitis. CT scan of pelvis shows diffuse colonic
thickening involving rectosigmoid colon (arrow), ascites, and
mesenteric stranding. Note this colonic thickening is less in this region than
in right colon as seen in A.
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Fig. 5C —60-year-old man with colonic thickening, ulcerative colitis,
and primary sclerosing cholangitis. Colonoscopy shows diffuse mucosal erythema
and superficial ulcers indicative of moderate to severe active ulcerative
colitis.
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All polyps that were removed proved to be benign according to subsequent
pathology reports. Two random biopsies of the mucosa in two patients resulted
in one normal mucosa and one mild chronic inflammatory change. No cases of
colorectal cancer were seen.
Comparing the overall frequency of the colonic findings with the segmental
distribution of colonic thickening, no statistically significant difference
(p = 0.946) was noted between the two variables, excluding the
outlier ulcerative colitis case. In addition, no statistically significant
difference was noted including the ulcerative colitis case (p =
0.552). There were more cases of CT colonic thickening isolated to the cecum
and ascending colon (54%) among the normal to mild edema group from
colonoscopy. Similarly, isolated thickening at the cecum and ascending colon
was seen in 55% of the group with colonoscopy findings of diffuse edema and
portal hypertensive colopathy (Table
2).
Transplantation Evaluation and Outcome
Fourteen patients (29%) eventually had successful liver transplantations,
whereas three patients (6%) had livers transplanted and died. Fourteen
patients (29%) were not eligible for transplantation for various reasons.
These reasons included comorbidities, a psychosocial contraindication, or a
change in medical insurance coverage. Six patients (12%) died before
transplantation and two patients (4%) voluntarily withdrew from the transplant
list. Ten patients (20%) remained eligible for transplantation at the time of
the study. In none of the patients who died was the cause of death colon
cancer.
Discussion
Colon wall thickening greater than 3–5 mm is a nonspecific CT finding
[7]. Traditionally, discovery
of thickened bowel wall on CT examinations usually mandates further
investigation such as colonoscopy
[8] because it may be
clinically significant. This colonic thickening may be secondary to underlying
colonic malignancy or other disease processes. In cirrhotic patients, CT
findings of colonic wall thickening may have different clinical significance
than in noncirrhotic patients because wall thickening is not rare in this
patient population
[1–4,
9]. However, no specific study
has been performed in the setting of end-stage liver disease to correlate the
CT finding of colonic wall thickening with colonoscopy to determine the cause
of the wall thickening. Although some prior studies have evaluated the
colonoscopy findings of cirrhotic patients compared with healthy patient
populations [10], these
findings were not directly correlated with CT findings. In these studies and
in our study, no patients had colonic distention with air or contrast
material. Therefore, the upper limits of normal in the nondistended colon may
be greater than 3- to 5-mm thickness. These studies showed that chronic
telangiectasia and edema were more likely to be seen in cirrhotic patients
than in healthy patients. However, most of these patients—unlike other
transplantation candidates—cannot afford the usual follow-up CT after a
few months because timing is crucial to be successfully listed on the
transplant list.
On the basis of our study, 44% (11/25) of our patients with CT findings of
colonic thickening who underwent colonoscopy had diffusely edematous mucosa
with increased vascularity and telangiectasia compatible with nonspecific
colitis or "portal hypertensive colopathy" (Figs.
1A,
1B and
2A,
2B). "Portal hypertensive
colopathy" is a term used by gastroenterologists regarding nonspecific
edema and chronic inflammatory changes seen on colonoscopy in patients with
portal hypertension requiring no additional workup or intervention
[11]. More than half of our
patients (13/25, 52%) had normal colonic mucosa. The one patient (1/25, 4%)
who had active ulcerative colitis had hepatic failure secondary to primary
sclerosing cholangitis that was known to be associated with ulcerative colitis
(Fig. 5A,
5B,
5C). This patient had diffuse
homogeneous colonic wall thickening involving almost all segments of the
colon. The maximum thickness of this colon was 18 mm seen on the hepatic
flexure, whereas in the descending and sigmoid colon the colonic wall
thickness was less. Perhaps the increased wall thickness in the right side of
the colon was due to the combined effect of end-stage liver disease and
ulcerative colitis. This patient had ascites, an albumin level of 2 g/dL, and
a MELD score of 21.
We found no cases of colonic neoplasm. This finding is in contradistinction
to a recently reported study by Moraitis et al.
[8] on noncirrhotic patients,
in which 14% of the patients who had incidental CT findings of thickened bowel
wall were found to have invasive adenocarcinoma of the colon on pathology
specimens from colonoscopy. In the study by Moraitis et al., the thickening
differed from our group and was not well documented as to location or extent
of the thickening. Also, in colon carcinoma the wall thickening is usually
more focal. In our study, there was no focal or eccentric bowel wall
thickening or luminal narrowing, which are more likely associated with colon
cancer [12]. Normal
colonoscopic findings (13/25, 52%) in patients with CT colonic wall thickening
may represent an early stage in the spectrum of mucosal change with edema.
Other findings of telangiectasia may reflect portal hypertension and
development of varices that could be present as telangiectasia or increased
vascularity of the colonic mucosa.
Colonic wall thickening has a variety of CT appearances, with equally
varied causes, such as inflammatory colitis, infectious colitis, neutropenic
colitis, bowel ischemia, diverticulitis, and neoplasm
[2,
13–16].
The halo sign is a nonspecific CT finding that shows stratification with a
two- or three-layered bowel wall on cross-sectional images, and it represents
bowel injury that is mostly seen in benign conditions
[6]. The inner ring may
represent inflamed mucosa and the middle ring represents edema (water) or fat
infiltration. The outer ring represents the muscularis propria
[6]. A previous study has shown
that the halo sign has a moderate sensitivity (74.5%) and high specificity
(92.5%) for benign conditions
[6]. In our series, the halo
sign had a sensitivity of 76% (37/49) for nonspecific colitis, a presumed
benign condition based on 51% (25/49) of cases with colonoscopy correlation.
For patients who do not undergo colonoscopy, CT findings of the halo sign can
be a useful tool.
The degree of colon wall thickening has been graded by Bharucha et al.
[15]as mild, moderate, and
severe, with colonic wall thickness of 3–6, 6–12, and greater than
12 mm, respectively. Our study group with colonic wall thickening ranged from
7 to 18 mm (mean, 12.5 ± 0.8 mm). Many have postulated that intestinal
wall edema and thickening in cirrhotic patients are related to hypoalbuminemia
and portal hypertension or a combination of both
[11,
17–19].
Similarly, 88% of our study patients with CT colonic wall thickening had signs
of portal hypertension and portosystemic collateral vessels. The mean albumin
level was 2.5 ± 0.19 g/dL (reference range, 3.8–4.8 g/dL). In
colonic edema caused by isolated hypoalbuminemia, bowel edema may be more
diffuse, whereas in portal hypertensive patients who are frequently also
hypoalbuminemic, colonic changes may be more isolated to the right side
because of blood flow and hydrostatic pressure
[2]. Also, differences in
venous drainage pathways and in collateral formation may explain why more
right-sided than left-sided colonic wall changes are seen. As in previous
studies that reported more involvement in the ascending colon
[1,
2,
4,
9], in our study 53% (26/49) of
patients had CT colonic wall thickening isolated to the cecum and ascending
colon.
We compared the frequency of mucosal change from colonoscopy with the
different segmental distribution of the CT colonic wall thickening. We found
no significant differences in the occurrence of mucosal change among the
ascending colon, right side extending to transverse colon, and diffuse colon
groups. Thus, although some authors have raised concern for diffuse colonic
thickening being associated with infectious or ischemic colitis
[2], it may be a nonspecific
finding.
Our study has some limitations. First, it was a retrospective review, which
may have resulted in variable consistency and sensitivity with regard to the
initial subjective findings of colonic wall thickening. Second, most of the CT
studies were performed to evaluate the liver and not the colon, and therefore
proper bowel preparation and distention were not obtained. Thus, the colon may
have not been optimally or completely scanned to evaluate colonic thickening.
Third, possible patient selection bias exists because only the patients with
advanced liver disease who were referred for liver transplantation were
included in the study. Our study population had a high incidence of hepatitis
C cirrhosis, and the clinical significance and implication of our findings may
be different in patients with other causes of cirrhosis, such as primary
sclerosing cholangitis with a history of inflammatory bowel disease.
In conclusion, CT findings of colonic wall thickening in patients with
end-stage liver disease usually resulted in a benign colonic diagnosis. The
colonoscopy changes primarily ranged from mild mucosal edema to increased
vascularity and telangiectasia, probably from hypoalbuminemia or portal
hypertension. Therefore, incidental CT findings of colonic wall thickening in
patients with end-stage liver disease, particularly in those with right-sided
wall thickening, concentric thickening with well-preserved bowel wall layers,
ascites, and a clinical history of hypoalbuminemia and portal hypertension, do
not warrant follow-up colonoscopy for the evaluation of malignancy or colitis
unless the patient has specific risk factors as published by the American
Society for Gastrointestinal Endoscopy
[20]. As a result, this
patient population may avoid colonoscopy that may expose them to unnecessary
risks (such as rupture of the colon) and delay timely transplantation
evaluation.
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Abstract
Introduction
