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Fulminant amebic colitis
ORIGINAL ARTICLE
Fulminant Amebic Colitis: Recommended Treatment to Improve
Survival
1
Hwa-Tzong Chen, Yung-Hsiang Hsu , Yao-Zen Chang
1
Department of Surgery, Pathology , Buddhist Tzu Chi General Hospital and Tzu Chi University, Hualien, Taiwan
ABSTRACT
Objective: This study was retrospectively designed to present the clinical manifestations and histopathologic features of fulminant
amebic colitis, and to evaluate the impact on the outcome of both surgical and conservative treatments. Patients and Methods: A
retrospective analysis was conducted from clinical and histopathologic data of 15 patients with fulminant amebic colitis. Nine
patients received conservative management, and 6 underwent surgery. Data were obtained from medical records from January 1994
to June 2000. Results: There were 12 men and 3 women with a median age of 51 years. The most frequent clinical manifestations
were abdominal pain, severe diarrhea, fever, unstable vital signs, and dehydration. The main histopathologic features were acute
inflammation, necrosis, the presence of trophozoites, and perforation. No significant difference was found in the clinical features
between the conservative group and surgical group, including clinical manifestations, duration before the use of metronidazole,
hemoglobin and albumin levels, white cell count, and age. The most reliable diagnostic procedure was endoscopic biopsy. All 6
patients who underwent surgery survived (6/6). Of the 9 cases that received conservative treatment, only 3 survived (mortality rate
66.7%, overall mortality rate 40%). The average age of expired and surviving patients was 55.1 and 41.7 years, respectively. The
average duration before antiamebic treatment of expired patients and surviving cases was 10 and 5 days, respectively. Older age and
longer duration before antiamebic treatment appeared to impact the mortality in our series. Conclusions: Early diagnosis, and
aggressive supportive and antiamebic treatment should be instituted once acute amebic colitis is suspected. Prompt aggressive
surgical management is recommended for the management of complicated acute fulminant amebic colitis. (Tzu Chi Med J 2004;
16:1-8)
Key words: fulminant amebic colitis, amebiasis, amebic dysentery
INTRODUCTION
Amebiasis is a parasitic infection caused by the
protozoon, Entamoeba histolytica, that infects 10% of
the world's population, resulting in 100,000 deaths per
year [1]. The colon and liver are the principal organs
affected in amebiasis. The parasite exists in 2 forms: a
motile form, called the trophozoite, and a cyst form, responsible for human transmission of the infection. The
trophozoite inhabits the colon where it produces lesions
of amebic colitis. Invasion of the colonic mucosa leads
to dissemination of the organism to extracolonic sites,
predominantly the liver. Infection by E. histolytica causes
a spectrum of intestinal illnesses as aymptomatic
infection, symptomatic noninvasive infection, acute
protocolitis (dysentery), and fulminant colitis with
perforation. For patients with amebiasis, there is a bimodal age distribution with peaks at 2-3 and > 40 years.
The gender distribution is equal in childhood, but in older
adults, males predominate [2]. The majority of E.
histolytica infections are asymptomatic. Acute amebic
colitis has a gradual onset presenting with a 1- to 2 week
history of abdominal pain, diarrhea, and tenesmus. Fe-
Received: June 20, 2003, Revised: July 15, 2003, Accepted: August 15, 2003
Address reprint requests and correspondence to: Dr. Hwa-Tzong Chen, Department of Surgery, Buddhist Tzu Chi General
Hospital, 707, Section 3, Chung Yang Road, Hualien, Taiwan
Tzu Chi Med J 2004 16 No. 1
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H. T. Chen, Y. H. Hsu, Y. Z. Chang
ver is noted in only a minority of patients. The infection
is usually self-limiting but may be recurrent especially
in endemic areas. The mortality rate is less than 0.5%
[3]. Fulminant amebic colitis, however, is a rare complication of amebic dysentery, which occurs in only 6%11% of patients with symptomatic infection [4]. It presents with rapid onset of severe bloody diarrhea, severe
abdominal pain, and high fever. The amebic invasion of
the colonic wall leads to a fierce superacute course of
massive necrosis of wide segments or of the entire colon.
The extensive necrosis usually affects all layers of the
bowel wall. Toxic megacolon and intestinal perforation
are common [5]. The perforations may be microscopic
and usually sealed off by the adjacent omentum or
bowels. They also may be macroscopic, which results
in generalized fecal peritonitis [6,7]. The mortality rate
is greater than 50% if aggressive surgical management
is not promptly initiated [8-10]. Amebic colitis has been
endemically prevalent in both Provincial Yu-Li Hospital and Yu-Li Veteran's Hospital in Yu-Li city, Taiwan
where most patients with chronic schizophrenia resides
on a long-term basis. Positive IHA serologic tests from
a survey of Provincial Yu-Li Hospital reached 46%,
and positive stool examinations were 19% according to
a CDC report [11]. Retrospectively, we encountered 15
cases of fulminant colitis referred from these 2 hospitals from 1994 to 2000. This clinical study was designed
to compare the impact of outcomes from patients receiving conservative treatment with those receiving
prompt surgical management. By examination of the
results, we attempted to offer an appropriate guide for
the management of acute fulminant amebic colitis.
PATIENTS AND METHODS
Records of 15 patients diagnosed with fulminant
Table 1.
RESULTS
All patients presented with a precedent abdominal
pain and watery or bloody diarrhea, followed by a distended abdomen, paralytic ileus, and septic shock or
hypovolemic shock. The clinical features including the
clinical manifestations, duration before use of
metronidazole, hemoglobin and albumin levels, white
cell count, and age of patients with acute fulminant amebic colitis are listed in Table 1. There were no significant differences in these clinical features between the
conservative and surgical group. The clinicopathological findings of both the surgical and conservative groups
are listed in Tables 2 and 3.
Megacolon and free air in the subphrenic space were
Clinical Features in Patients with Acute Fulminant Colitis
Clinical features
Abdominal pain
Watery or bloody diarrhea
Rebounding pain
Abdominal distension
Fever
Unstable vital sign
Duration before use of metronidazole (days)
Hemoglobin level (gm/dL)
Albumin level (gm/dL)
White count
Age (y/o)
Survival
O
amebic colitis admitted to our hospital from January 1994
to June 2000 were retrospectively reviewed. Another 4
suspicious cases were excluded as there was no positive
colon biopsy, stool, or serology to confirm the amebic
infection. These patients had all been transferred from
either Provincial Yu-li hospital or Yu-li Veteran's Hospital where amebic dysentery is endemic. Almost all
patients were first admitted to the gastrointestinal service.
The gender distribution was 12 males and 3 females.
The mean age was 51 years (range, 21 months to 82
years). Nine patients received supportive treatment and/
or metronidazole without surgery. Six patients consulted
with surgeons and underwent surgical treatment. Clinical manifestations, types of diagnosis, modalities of
treatment, morbidity, and mortality were analyzed. Risk
factors including age, duration before antiamebic
treatment, anemia, hypoalbuminemia, and leukocytosis
were investigated. The impact on the outcome from conservative and surgical management was also specifically
evaluated.
!
Conservative group
Surgical group
Significance (p score)
85.71%
100%
64.29%
100%
85.71%
71.43%
8.71±2.49
8.59±0.50
1.73±0.11
9457.14±2692.39
50.67±4.70
33.3%
100%
100%
66.67%
100%
83.33%
83.33%
9.60±3.68
8.98±0.76
2.10±0.51
9540.34±2054.17
51.67±11.5
100%
NS
NS
NS
NS
NS
NS
NS (0.839)
NS (0.660)
NS (0.354)
NS (0.982)
NS (0.928)
0.000
Tzu Chi Med J 2004 16 No. 1
Fulminant amebic colitis
Table 2.
Clinicopathologic Findings of the Surgical Group
Name
Age
Sex
Diagnosis
Perforation
Wu, JH
37
M
Colon biopsy
Microscopic
Ileostomy
Chang, HJ
2
F
Macroscopic
Chen, YL
67
M
Pathology of
resected bowel
Pathology of
resected bowel
Chan, RL
75
M
Pathology of
resected bowel
Macroscopic
Huang, ML
55
M
Macroscopic
Mon, SL
74
M
Pathology of
resected bowel
Colon biopsy and
pathology of
resected bowel
Subtotal colectomy
and ileostomy
Extended right
hemicolectomy and
ileostomy
Extended right
hemicolectomy and
ileostomy
Subtotal colectomy
and ileostomy
Left hemicolectomy
and Hartmann's
procedure
Macroscopic
Microscopic
Initial Operation
Fig. 2.
Fig. 1.
Generalized dilatation of the colon shown on a plain
abdominal X-ray.
commonly disclosed by plain abdominal X- ray or abdominal CT scan (Figs. 1- 3). In the conservative group,
3 of 9 cases fortunately survived. The other 6 cases,
however, expired. The mortality rate was 66.7% (6/9).
The overall mortality rate was 40% (6/15). Three of them
even died on day 1 or 2 after admission. All 6 patients
who died had septic and/or hypovolemic shock and
multiple organ failure. The average age of expired pa-
Tzu Chi Med J 2004 16 No. 1
Morbidity
Outcome
Colonic stricture and
intestinal intussusception
Wound sepsis
Survived
Wound sepsis, CVA
Survived
Wound sepsis
Survived
Wound sepsis
Survived
Wound sepsis
Survived
Survived
Paper-thin and diffusely dilated transverse colon
shown on abdominal CT.
tients was 55.1 years, and that of surviving patients was
41.7 years. The average duration before administration
of antiamebic drugs in the expired cases was 10 days,
and that in surviving cases was 5 days. No significant
difference was found among hemoglobin level, albumin
level, and white cell count of both expired and surviving patients in the conservative treatment group. On the
contrary, all 6 patients who underwent surgical management survived. Amebic colitis was confirmed by the
presence of amebic trophozoites in a colonoscopic biopsy in 9 cases (9/9), stool examination in 3 cases (3/
15), and tissue pathology from a resected bowel in 5
cases (5/5). Most colonoscopic findings revealed the
classic pictures of geographic transmural ulceration of
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H. T. Chen, Y. H. Hsu, Y. Z. Chang
Table 3.
Clinicopathologic Findings of the Conservative Group
Name
Chu, CF
Yang, ML
Lin, TC
Chuay, SS
Gu, LY
Lee, GL
Fu, LJ
Yang, TF
Chu, TK
Fig. 3.
Age
Sex
Diagnosis
Morbidity
Outcome
51
29
61
67
72
51
37
41
47
M
M
M
F
M
M
F
M
M
Colon biopsy
Colon biopsy, IHA
Stool
Colon biopsy, stool
Colon biopsy, IHA
Stool
Colon biopsy, stool
Colon biopsy
Colon biopsy, IHA
Multiple organ failure
Multiple organ failure
Septic shock
Septic shock
Septic shock
Septic shock
Sepsis, diarrhea
Sepsis, diarrhea, shock
Sepsis, Diarrhea
Expired on Day 1
Expired on Day 16
Expired on Day 2
Expired on Day 15
Expired on Day 13
Expired on Day 1
survived
survived
survived
Free perforation of the colon with an obvious airfluid level shown on abdominal CT.
the involved colon (Fig. 4). Some lesions mimicked ulcerative colitis and ischemic colitis. In the surgical group,
4 patients grossly presented with transmural necrosis
with macroscopic perforation, and 2 presented with toxic
megacolon with impending rupture of a paper-thin colon with adhesive wrap by the adjacent omentum or
bowels. Macroscopically, transmural ischemic necrosis
with multiple geographic flask-shaped ulcers and yellowish plaque-like lesions were shown in the resected
colon (Fig. 5). Microscopically, numerous amebic
trophozoites were present in the necrotic debris of the
colon ulcers (Fig. 6). 4 patients initially received an extensive colectomy and ileostomy, 1 underwent a left
colectomy and Hartmann's procedure, and 1 underwent
an ileostomy only. All patients experienced complication with wound sepsis after the operation. 4 patients
successfully received reconstruction of bowel continuity 3-6 months after stricture of the distal bowel was
excluded by either colonoscopy or a barium enema. One
did not have his bowel continuity further restored, as
hypoxic encephalopathy developed 2 months after
discharge. The patient who initially underwent an ileostomy experienced a complication of intestinal intussusception and severe colonic stricture, which were confirmed by both colonoscopy and a barium enema, and
an extensive colectomy was later required.
DISCUSSION
Fig. 4.
Q
Multiple geographic ulcers shown by colonoscopy.
!
Fulminant amebic colitis, in contrast to amebic
enteritis, is a disease with high mortality Uncomplicated
amebic colitis is readily treated and has a mortality rate
of less than 0.5% [3]. Complications necessitating surgical intervention develop in only 6% to 11% of patients
with symptomatic disease. However, the mortality rate
in these patients ranges from 55% to 100% and stems in
part from delays in diagnosis and treatment [8-10]. Pa-
Tzu Chi Med J 2004 16 No. 1
Fulminant amebic colitis
Fig. 5. Multiple geographic flask-shaped ulcers and multiple
yellowish plaque-like lesions shown on gross findings of the resected colon.
Fig. 6.
Microscopically, numerous amebic trophozoites
shown in the transmural colon necrotic area (H&E
stain, × 400).
tients with known amebic colitis who show signs of systemic toxicity, and localized or generalized peritonitis
are at high risk of complications; surgical consultation
should be obtained. Most patients who have fulminant
amebic colitis present the characteristic symptoms and
signs such as severe abdominal distention, sepsis, watery or bloody mucoid diarrhea, and dehydration. In endemic areas, such patients should be treated presumptively until a diagnosis of amebic colitis can be excluded.
Early diagnosis and surgical treatment significantly decrease mortality when compared with conservative treatment [9,10]
A diagnosis of amebic colitis can be difficult and
confusing [12,13]. Amebic colitis is a disease revealing
diverse clinical manifestations and gross endoscopic
Tzu Chi Med J 2004 16 No. 1
features, and is often confused with other types of colitis.
In cases of misdiagnosis as an idiopathic inflammatory
bowel disease or delayed recognition of intestinal
amebiasis, undesirable outcomes may occur resulting
from erroneous administration of steroids or delayed
antiamebic treatment. Clinical symptoms, laboratory
studies, X-ray findings, cultures, and even serological
studies may be insufficient to make an accurate
diagnosis. The gross endoscopic appearance as well as
the results of endoscopic biopsy can be extremely helpful in differentiating amebiasis from other forms of colitis
[14-16]. Large, geographic mucosal ulcers are typically
present and are accompanied by yellow-green
pseudomembranes. The muscularis externa is usually
attenuated and necrotic, imparting a "wet blotting paper" consistency. Large numbers of amebic trophozoites are present within the inflammatory exudates. The
mucosa adjacent to and undermined by the ulcers is often hemorrhagic or inflamed, resembling ischemic colitis or idiopathic inflammatory bowel disease (IBD),
respectively. Invasive amebiasis may rarely be superimposed on IBD, which further complicates the issue.
Antiamebic therapy is suggested in endemic areas in
cases of persistent IBD [17]. Radiological findings of a
barium enema include fine marginal serration, aphthoid
ulcers, minute barium flecks, marginal defects, loss of
haustration, and deformities of the bowel. Aphthoid ulcers and marginal defects are both characteristic of amebic colitis [18]. Megacolon and paper-thin colon wall
and sometimes free air may be present on plain abdominal X-rays. In addition, these findings are much more
characteristic in abdominal CT.
Perforation is not uncommon in acute fulminant
amebic colitis. In Barker's autopsy study of patients with
amebic colitis, perforations were found in 30.4% [19].
They may be localized by adhesions, or perforate into
the abdominal cavity, but they are most often retroperitoneal. Chen et al described 8 patients with free intraperitoneal perforations. In addition, they found that 75%
of patients had multiple colon perforations rather than a
single one [20]. Stein and Bank suggested that the development of abdominal tenderness in a patient with
amebic colitis indicates either actual colonic perforation or subserosal extension of the inflammatory process [21]. Abdominal CT scan is recommended in such
situations to rule out colonic perforation. Before 1970,
surgical intervention was suggested only in free perforation or abscess formation [22,23]. More recently,
authors from different countries have claimed good results from surgical treatment. Because of poor results
with nonoperative management, an international consensus indicates that early surgical treatment is the
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H. T. Chen, Y. H. Hsu, Y. Z. Chang
method of choice for acute fulminant amebic colitis [9,
24-28]. Intensive antiamebic therapy should be instituted
as soon as amebiasis is confirmed; otherwise surgical
therapy is likely to fail [3]. Chuah et al found that significant factors associated with the development of fulminant intestinal amebiasis in univariate analyses were
male gender, being age over 60 years, and having an
associated liver abscess, progressive abdominal pain, and
signs of peritonitis, leukocytosis, hyponatremia,
hypokalemia, and hypoalbuminemia [27]. Takahashi et
al also stressed that risk factors for mortality in their
series included a long duration of symptoms, lower count
of leukocytes, absence of surgery, years of operation
before 1970, a large amount of trophozoites, and depth
of invasion through the muscularis [10].
Stein and Bank listed the following indications for
surgical intervention in acute fulminant amebic colitis:
(1) no improvement with antiamebic treatment, (2) abdominal tenderness and/or increased abdominal
distention, (3) persistent severe diarrhea unremitting after antiamebic treatment for 5 days, (4) perforation with
or without abscess formation, and (5) toxic megacolon
or ulcerative colitis-type symptoms with associated hypoproteinemia and anemia [21]. Complications due to
fulminant amebiasis that require operative intervention
include stricture or fistula formation and obstruction.
What is the best surgical procedure for complicated
fulminant amebic colitis? Primary suture of the perforation and mere drainage are not recommended since high
failure rates have been encountered. A partial colectomy
with primary anastomosis is also not favored, as the extreme friability of the inflamed bowel wall will lead to
high rates of anastomotic failure. A temporary ileostomy
without colon resection is not proper as there is the possibility of developing stricture, hemorrhage and perforation of the affected colon. A staged operation is highly
recommended for complicated fulminant amebic colitis.
First, we prefer aggressive resection of the involved colon with exteriorization of the proximal and distal
transected ends,i.e., an ileostomy and mucus fistula.
Further bowel reconstruction should be deferred to 3-6
months later. We recently experienced such a case that
was complicated with colonic stricture and intestinal
intussusception (data not shown). Before bowel
reconstruction, the patency of the distal colon must be
examined by colon barium enema study and/or
colonoscopy to avoid postoperative distal obstruction
or stricture.
In our series, a definite diagnosis was obtained by
colonoscopic biopsies (100%) and all pathologies from
resected bowels (100%). But microscopic stool examination for E. histolitica is less reliable (20%). The mor-
S
!
tality rate was 66.7% in the conservative group. The risk
factors for mortality with conservative management may
mainly be related to both an older age and delayed
antiamebic treatment, but were not related to anemia or
hypoalbuminemia. It is worthwhile stressing that there
was no mortality in our surgical group. Most patients
can survive aggressive colon resection and also have a
chance to have their bowel completely restored
thereafter. There were no significant differences in the
clinical features between the conservative group and
surgical group including clinical manifestations, duration before the use of metronidazole, hemoglobin and
albumin levels, white cell count, and age.
Accordingly, we emphasize that patients from endemic areas of amebic dysentery should be promptly
treated with antiamebic drugs before a definite diagnosis is confirmed. Diagnostic procedures including stool
examination, colonoscopy, and biopsy should be
employed. If plain abdominal X-ray reveals megacolon
or if abdominal tenderness develops, an abdominal CT
scan is indicated. If the diarrhea is unremitting, anemia
and/or hypoalbuminemia persist under antiamebic
treatment, peritoneal sign becomes obvious, or perforation is highly suspected, surgical intervention should be
promptly undertaken. In conclusion, early recognition,
early antiamebic treatment, and a prompt aggressive
staged colectomy are our policy to avoid complications
and reduce mortality from fulminant amebic colitis.
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Tzu Chi Med J 2004 16 No. 1