Journal of Visceral Surgery (2015) 152, 99—105

Available online at

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www.sciencedirect.com

REVIEW

Ogilvie’s syndrome—acute colonic

pseudo-obstruction
P. Pereira a,b,∗, F. Djeudji a, P. Leduc a, F. Fanget a,
X. Barth a,b

a
Service de chirurgie digestive et de colo-proctologie, hospices civils de Lyon, hopital
Edouard-Herriot, 5, place d’Arsonval, 69437 Lyon cedex 09, France
b
Université Claude-Bernard, Lyon I, 8, avenue Rockefeller, 69374 Lyon cedex 08, France

Available online 11 March 2015

KEYWORDS Summary Ogilvie’s syndrome describes an acute colonic pseudo-obstruction (ACPO) consist-
Acute colonic ing of dilatation of part or all of the colon and rectum without intrinsic or extrinsic mechanical
pseudo-obstruction obstruction. It often occurs in debilitated patients. Its pathophysiology is still poorly under-
syndrome; stood. Since computed tomography (CT) often reveals a sharp transition or ‘‘cut-off’’ between
Ogilvie’s syndrome; dilated and non-dilated bowel, the possibility of organic colonic obstruction must be excluded.
Neostigmine; If there are no criteria of gravity, initial treatment should be conservative or pharmacologic
Colonic exsufflation; using neostigmine; decompression of colonic gas is also a favored treatment in the decision tree,
Cecostomy; especially when cecal dilatation reaches dimensions that are considered at high risk for perfo-
Cut-off ration. Recurrence is prevented by the use of a multiperforated Faucher rectal tube and oral or
colonic administration of polyethylene glycol (PEG) laxative. Alternative therapeutic methods
include: epidural anesthesia, needle decompression guided either radiologically or colonoscopi-
cally, or percutaneous cecostomy. Surgery should be considered only as a final option if medical
treatments fail or if colonic perforation is suspected; surgery may consist of cecostomy or
manually-guided transanal pan-colorectal tube decompression at open laparotomy. Surgery is
associated with high rates of morbidity and mortality.
© 2015 Elsevier Masson SAS. All rights reserved.

Introduction ischemic or cryptogenic colitis (toxic megacolon and reflux

Ogilvie’s syndrome (OS), or acute colonic pseudo-
obstruction (ACPO), consists of dilatation of part or
all of the colon and rectum without intrinsic obstruction
or extrinsic inflammatory process; this definition excludes
mechanical dilatation due to distal obstruction or due
to severe acute colitis from inflammatory bowel disease,
∗ Corresponding author at: Service de chirurgie digestive et de
colo-proctologie, hospices civils de Lyon, hopital Edouard-Herriot,
5, place d’Arsonval, 69437 Lyon cedex 09, France.
E-mail address: paulo.pereira@chu-lyon.fr (P. Pereira).
ileus in the setting of peritonitis).
The pathophysiology of OS seems to be paralysis of the
intestinal muscularis allowing passive distention without an
increase in intracolonic pressure. In 1948, Heneage Ogilvie
described two cases of patients who had neoplastic infiltra-
tion of the celiac and mesenteric autonomic plexuses and
presented with massive colonic dilatation without organic
obstruction [1]. Ten years later, HA Dudley presented thir-
teen cases of patients who underwent surgery for colonic
dilatation presumed to be due to obstruction but in whom
no evidence of obstruction was found [2]. He proposed the
first etiologic classification and coined the terminology of

http://dx.doi.org/10.1016/j.jviscsurg.2015.02.004
1878-7886/© 2015 Elsevier Masson SAS. All rights reserved.
100
acute colonic pseudo-obstruction. The acronym ACPO first
appeared in the literature in 1997 [3].
Pathophysiology
The etiologic pathogenesis of ACPO has not yet been com-
pletely elucidated, but appears to be multifactorial.
Theory of autonomic denervation
In 1948, Ogilvie posited that ACPO was due to a disturb-
ance of the autonomic innervation of the colon [1]. The role
of the autonomic nervous system in colonic motility is not
fully defined. The sympathetic innervation seems to exercise
an inhibitory effect on motility while the parasympa-
thetic innervation plays an excitatory role. The interaction
between these two systems regulates colonic motility [4].
Some investigators feel that OS is due to a decrease in
parasympathetic tone rather than to an increase in sym-
pathetic tone [5—8]. Most authors consider acute colonic
dilatation to be a consequence of decreased parasympa-
thetic activity arising from the sacral plexus (S2, S3, S4)
[8,9], resulting in distal colonic atony; this provokes a func-
tional ‘‘occlusion’’ similar to that seen in Hirschsprung’s
disease without, however, involving the myenteric plexus.
Similar phenomena have been seen with extremely painful
stimuli in the pelvis (childbirth, pelvic surgery) that may
lead to inhibition of the parasympathetic sacral plexus
resulting in distal colonic dilatation extending to the fron-
tier between vagus innervated and hypogastric innervated
colon at the level of the splenic flexure [10].
The possible role of sympathetic hypertonicity via a colo-
colic inibitory reflex has also been proposed by some authors
[11]. This seems to be confirmed by the beneficial effect of
epidural anesthesia and splanchnic nerve block.
Other studies have incriminated the interstitial cells
of Cajals (pacemaker cells) from which waves of sponta-
neous peristaltic activity originate. Histologic examination
of intestine from patients with ACPO in the series of Jain
et al. showed these cells to be absent [12].
Vascular theory
Other authors have proposed a vascular theory to account
for ACPO [13,14], based on decreased splanchnic perfusion
(hypovolemia, mesenteric vascular disease); hypoperfusion
is typically most severe at the frontier between the superior
and inferior mesenteric arterial circulation, the so-called
Zone of Griffiths, which corresponds to the typical cut-off
near the splenic flexure.
Hormonal theory
Hormonal theories have been proposed implicating
prostaglandin E [11,15], which stimulates the circular
muscle layer of the colonic wall.
Pharmacologic theory
Neurotropic medications have often been blamed because of
their anticholinergic effects [8]. In addition, opiates [16] and
other long-acting ‘‘colotoxic’’ medications (sedatives, tri-
cyclic antidepressants, clonidine, phenothiazines, calcium
channel inhibitors, anti-parkinsonian medications) may play
some role [7,10].
P. Pereira et al.
Metabolic theory
Colonic motility disturbances may also be provoked by
metabolic disorders affecting neuromuscular conduction
(hypokalemia, uremia) [17].
Infectious theory
A reactivation of herpes zoster virus (shingles) within the
enteric ganglia has also been proposed [18].
Clinical presentation
The syndrome of acute colonic pseudo-obstruction (ACPO)
resembles acute low colorectal obstruction. Clinical find-
ings are dominated by marked gaseous abdominal dilatation,
which is paradoxically well tolerated clinically without dete-
rioration of general patient condition [10,19]. The presence
of major rectal distention on digital rectal exam along with
colonic distention is evidence of megacolon. The clinical
history is important and, as Vanek has pointed out in his
literature review collecting 400 patients [10], 19% of cases
occurred following childbirth, pelvic surgery, and spinal cord
trauma. Other conditions that may be associated with the
development of ACPO include:
• orthopedic interventions (pelvic fractures) 18%;
• systemic infection (10%);
• acute cardiac events (10%);
• intensive care or volume resuscitation (9%);
• other circumstances: pharmacologic causes (opioids,
antidepressants), transplantation.
The presence of an inflammatory syndrome (fever, leuko-
cytosis, elevated CRP) or signs of peritoneal irritation should
lead to suspicion of colonic perforation. Other possibilities
in the differential diagnosis such as cecal volvulus, sigmoid
volvulus, or intrinsic or extrinsic colonic obstruction must be
systematically eliminated.
Confirmation of the diagnosis
Barium enema has been a time-honored imaging modality
to diagnose mechanical obstruction. The osmotic effect of
water-soluble contrast may sometimes lead to resolution
of an obstruction. Contrast enema is contra-indicated if
colonic perforation is suspected [20], and is less frequently
employed nowadays because of the excellent diagnostic
yield of CT.
Abdomino-pelvic CT with intravenous contrast is the
standard diagnostic test, with a sensitivity of 96% and a
specificity of 93%. It confirms the presence of proximal
colonic dilatation and excludes the presence of intrinsic or
extrinsic mechanical obstruction.
Megacolon usually begins at the level of the cecum and
right colon and extends distally up to a point of size incon-
gruence, the so-called ‘‘cut-off’’ or transition point (Fig. 1).
This image of a transition point at the splenic flexure can
also be seen in cases of acute pancreatitis with inflamma-
tion contiguous to the left phreno-colic ligament; it gives
a false impression of an obstructive point at the lieno-colic
ligament [21,22]. Inhibition of the parasympathetic nerves
arising from the sacral nerve roots results in megacolon that
ends at the frontier between the territories served by the
vagus and the hypogastric nerves. In addition, hypoperfusion
Ogilvie’s syndrome—acute colonic pseudo-obstruction
Figure 1. Transition point (‘‘cut-off’’) at the splenic flexure with
no mechanical obstruction.
due to a splanchnic low flow state will be predominant at
the watershed between the circulation of the superior and
inferior mesenteric arteries, the so-called ‘‘Griffiths Zone’’
[13,14]. When there is an appearance of ‘‘cut-off’’ at the
splenic flexure, the addition of water-soluble enteric con-
trast to the CT scan will usually help to rule out an organic
obstruction at the level of the splenic flexure.
The actual location of the transition point is vari-
able, typically occurring at the splenic flexure, but also
at the hepatic flexure, or at the recto-sigmoid junction.
Other possible variants include multiple interrupted seg-
ments of megacolon or retrograde extension along the left
colon.
Complications and maximal tolerable cecal
diameter
The major concern during conservative management is the
risk of colonic perforation, which has an incidence of 15—20%
[10,23,24], with a mortality risk of 40—50% [23]. The colon
can tolerate fairly massive dilatation and the risk of perfora-
tion is often overestimated, especially since the distention
is not associated with high intraluminal pressure. [25].
CT evidence of pneumoperitoneum, free peritoneal
fluid, or pneumatosis intestinalis involving the distended
colon should lead to strong suspicion of perforation, which
demands urgent laparotomy. While the maximal tolerable
cecal diameter is the subject of debate, all authors agree
that increasing diameter correlates with increased risk of
perforation (Fig. 2). Most series consider limits greater than
9 cm [26], whereas Vanek feels that the maximal toler-
able cecal diameter is 12 cm because more than a quarter
of patients beyond this limit will perforate [10]. Mortal-
ity risk relates more directly to underlying visceral organ
failure than to the risk of secondary colon perforation. Fac-
tors indicating poor prognosis include age, ischemia, cecal
perforation, and a delay of more than six days in colonic
decompression [10,27].
101
Figure 2. Pre-perforative cecum as judged by a diameter of
12.2 cm, requiring urgent decompression or surgery.
Treatment
Several possible therapeutic approaches can be considered:
conservative treatment, pharmacologic treatment, colono-
scopic exsufflation, and surgery. The mortality of patients
who undergo surgery varies from 30—50% versus 14—30% for
non-operated patients [8].
Conservative treatment
Conservative treatment should be instituted as soon as the
diagnosis of ACPO is considered, as long as there is no ques-
tion of perforation. Management is well codified by the
2010 guidelines of the American Society for Gastro-intestinal
Endoscopy (SAGES) [7]:
• proximal gastro-intestinal decompression (fasting, naso-
gastric suction);
• placement of a decompressive rectal tube if the disten-
tion extends as far as the sigmoid or rectum;
• intravenous fluid and electrolyte repletion (correction of
hypokalemia and hypomagnesemia).
Discontinuation of any medications that may contribute
to a pharmacologic etiology: anticholinergics, atropinics,
antihypertensives, anti-parkinsonian medications, antide-
pressants and neuroleptics, clonidine (a centrally-acting
alpha adrenergic agent), opiates (including possible opi-
ate reversal with narcotic antagonists such as nalox-
one).
Other associated measures may help to resolve the dis-
tention. Osmotic laxatives are contra-indicated since they
may promote fermentation of intestinal bacteria with a
consequent increase in gaseous distention [27]. Postural
measures may help to facilitate passage of stools and gas.
Ambulation should be encouraged as well as alternate sit-
ting in the knee-chest position or in the right or left lateral
decubitus position [7].
Conservative treatment was successful in 70% of the 1027
cases reviewed by Wegener [28], but, since the risk of per-
foration for ACPO increases beyond a delay of six days, it
102
should not be continued beyond three days [7]. Its effective-
ness can be judged by a decrease in abdominal distention,
passage of flatus and stool, and decreased cecal diameter on
abdominal plain films [7]. Several retrospective studies have
evaluated the results of conservative treatment [10,29,30]
with efficacity ranging from 35% to 96% and a risk of colonic
perforation of less than 2.5% and a mortality ranging from
0—14%.
Pharmacologic treatment
Neostigmine
Neostigmine is a reversible cholinesterase inhibitor that
reverses parasympathetic blockade and restores colonic
motility [31,32]. Three prospective randomized studies have
compared neostigmine to placebo for the treatment of ACPO
[33—35]. Neostigmine was statistically significantly more
effective than placebo in all three studies (85—91% versus
0%).
In the initial randomized prospective study by Ponec
et al., comparing neostigmine to placebo, 91% of patients
responded to a single intravenous injection of 2 mg of
neostigmine while there was no response in the placebo arm.
Plain X-rays revealed a mean decrease in cecal diameter of
5 cm in the neostigmine arm versus only 2 cm in the placebo
arm (P < 0.05) [33].
The modalities of neostigmine administration are very
much in debate at this time:
• a 2—2.5 mg IV bolus injected over 3—5 minutes results
in colonic motility within 20—30 minutes with a success
rate of 80% [27]. If success is not achieved within three
hours, a second or even a third neostigmine bolus can be
administered [36];
• slower administration with an infusion pump is also pos-
sible. Van der Spoel performed a prospective randomized
crossover study using a continuous infusion of neostigmine
at a rate of 0.4—0.8 mg/hour over 24 hours. Treatment
was successful in 19 of 24 patients [35].
Recurrence of ACPO has been reported in 17—38% of
cases after initial success with neostigmine [33,37]. The
oral administration of polyethylene glycol (PEG) has been
proposed in the literature to prevent recurrent ACPO [38].
Contra-indications to the use of neostigmine include acute
urinary retention, gastro-duodenal ulcer, acute coronary
syndrome, acidosis, asthma, bronchospasm, bradycardia,
beta blockade therapy, and renal insufficiency. Mechani-
cal bowel obstruction and colonic perforation are obviously
major contra-indications to the use of neostigmine. Undesir-
able side-effects have been noted in 10% of cases. Symptoms
may be minor (hypersalivation, abdominal cramping, nau-
sea and/or vomiting) or major (bronchospasm, bradycardia,
hemodynamic instability) [33]. Careful clinical and car-
diac monitoring is recommended during the hour following
neostigmine administration and atropine should be drawn up
in a syringe at the bedside for immediate use if necessary.
Premedication with glycopyrrolate helps to avoid hypersali-
vation.
All in all, when contra-indications are respected, neostig-
mine is effective in 64% to 91% of cases after a first dose,
with a risk of recurrent ACPO of up to 38%. It retains its
efficacity in 40% to 100% of cases when a second dose is
administered.
P. Pereira et al.
Polyethylene glycol (PEG) oral or transrectal
or via Faucher tube???
The effectiveness of PEG has been evaluated in a single con-
trolled randomized trial of 30 patients, and its adjunctive
use seems indicated to prevent recurrence of ACPO after
successful treatment with neostigmine or after colonoscopic
exsufflation [38].
Gastrografin® enema
Gastrografin® is a hyperosmotic water-soluble contrast
agent whose laxative properties have been evaluated in
one non-controlled retrospective study of 18 patients [39].
Gastrografin® , instilled per rectum under fluoroscopic con-
trol, was effective in 78% of cases, resulting in a mean
decrease of 4.6 cm in cecal diameter with no colonic per-
foration. In view of the low level of evidence, gastrografin®
cannot currently be recommended in practice.
Stimulants of intestinal motility
Erythromycin, a gastro-intestinal irritant and motility stim-
ulant, cannot be recommended in current practice, since
its reported success rate is only 40% with a recurrence rate
approaching 50% [40].
Other pharmacologic treatments
Tegaserode (a type 4 agonist for the 5-hydroxytryptamine
receptor), nicotine patches, metoclopramide, Narcan®
(naloxone-an opioid antagonist), indomethacin, and ibupro-
fen (anti-prostaglandins) have all been tested but cannot be
recommended at this time due to lack of a sufficient level
of evidence.
Epidural anesthesia
The sympathetic innervation of the colon derives from
the T11-L2 nerve roots. Sympathetic hypertonia is partly
responsible for the onset and persistence of megacolon.
Sympathetic nerve blockade creates splanchnic vasodilata-
tion and interrupts the neural flow of inhibitory pain
receptors (inhibitory colo-colic reflex). As early as 1947,
Hillemand and Viguié [41] reported that splanchnic nerve
block results in the same autonomic nervous response as
epidural anesthesia. Several protocols for splanchnic block-
ade by means of epidural anesthesia using bupivicaine or
lidocaine were proposed in papers published more than
20 years ago [8,42]. Effectiveness was demonstrated by pas-
sage of flatus and stool, a decrease in abdominal distention
and a decrease in cecal diameter; this often took effect
quite rapidly, almost simultaneously with the epidural injec-
tion.
Colonoscopic exsufflation
Colonic exsufflation via colonoscopy was first performed in
1977 by Kukora and Dent [43]. At this time, exsufflation
remains the treatment of choice if other medical treatments
have been unsuccessful, as long as there is no suspicion of
perforation. Nevertheless, the procedure is often difficult
to perform due if the intestinal lumen is filled with ster-
coral matter and the residue of water-soluble contrast; in
addition, there is a risk that insufflation required to insert
the colonoscope may result in perforation. Colonoscopy
also serves to detect colonic ischemia requiring surgical
Ogilvie’s syndrome—acute colonic pseudo-obstruction
intervention. This procedure is currently well codified by
the guidelines of SAGES:
• no colonic preparation is required;
• the patient should be sedated with benzodiazepines but
narcotics should be avoided since they inhibit colonic
motility;
• the colonoscope can be passed to the right colon in 85%
of cases, but it is not absolutely necessary to reach the
cecum. If the hepatic flexure cannot be turned, exsuf-
flation starting in the transverse colon is often sufficient
[44];
• demonstration of ischemic colonic mucosa requires that
the endoscopy be terminated and converted to surgery
[10].
The effectiveness of colonic exsufflation has been eval-
uated in several retrospective studies [44—46]. Strodel
compared the cecal diameter before and after endoscopic
decompression, noting a decrease from 12.8 cm to 8.7 cm
mean diameter; the difference was statistically significant
(P < 0.01) [44]. Successful endoscopic exsufflation has been
defined as a reduction of the cecal diameter by at least 3 cm
[10,43]. The entire procedure required 45—60 minutes and
immediate success varied from 61% to 95%, while success
after repeated procedures was 73% to 88%. The rate of recur-
rent ACPO may be as high as 40%. The rate of perforation is
2% and mortality is estimated at 1% [7,28].
Placement of a long multiperforated large-bore drainage
tube that is left to drain for 48 hours or until symptoms
resolve has been useful in preventing recurrences [38]. The
tube must be flushed every 4 to 6 hours go prevent obstruc-
tion by fecal residue. The instillation of PEG at the end of the
procedure has also been useful in preventing recurrences.
Other procedures for colonic exsufflation
Percutaneous cecostomy guided by either radiology or
colonoscopy has been reported in the literature but cannot
be recommended for general usage at this time [48]:
• percutaneous endoscopic cecostomy (PEC), a skin level
colostomy guided by colonoscopy, has a complication
rate of 40% including abdominal wall abscess, bleeding,
hematoma, perforation, and stomal retraction [49];
• CT-guided percutaneous cecostomy (CPC) [50] achieves
cecal decompression by placement of a cecostomy tube
under CT guidance.
Surgery
Surgery is the treatment of last resort, indicated only when
the above-mentioned conservative therapies have failed or
when there are clinical or radiologic indications of colonic
perforation [10]. Three types of intervention have been pro-
posed:
• colostomy;
• transanal insertion with hand-guided retrograde pas-
sage of a long multiperforated large-bore drainage tube
(Faucher tube) into the distended colon during laparo-
tomy;
• total or subtotal colectomy, usually without re-
anastomosis.
The colostomies
Tube cecostomy has been a time-honored treatment of
megacolon for many decades, despite its proper morbid-
ity and somewhat uncertain efficacity for relief of colonic
103
distention. A right transverse or left lower quadrant sig-
moid colostomy is often used. In the series of Vanek et al.,
colostomy effectively relieved colonic distention in 73% of
cases with a morbidity of 3% and a mortality of 41%. A simple
mucosa-to-skin ‘‘blow hole’’ colostomy can be performed
at one or several points around the course of the distended
colon; it might be more effective than a formal colostomy
by providing one or several pressure relief valves. Vanek
reviewed 61 cases treated by this method with a 95% imme-
diate success rate, a mortality of 21% and a morbidity of 30%
[10].
Transanal retrograde colonic with a long
multiperforated Faucher tube guided by hand
during exploratory laparotomy
Caves and Crockard first reported this technique for the
treatment of megacolon in 1970 [51]. Although rarely
reported, this technique accomplishes the surgical equa-
vlent of a decompression. It is a useful approach when
diagnostic doubt has already forced laparotomy, when acute
non-complicated megacolon is encountered during laparo-
tomy, and after failure of the above-mentioned conservative
techniques (as long as organic obstruction has been ruled
out).
A large caliber multiperforated tube (Faucher tube) is
introduced through the anus and then maneuvered around
the entire colon with the guidance of the surgeon’s hands.
Turning the angle at the splenic flexure may be difficult so
the incision must be of sufficient length and the colon may
need to be mobilized at one or both flexures in order to
safely accomplish the intubation. This strategy is similar in
technique to intra-operative colonic irrigation performed to
decompress an obstructed colon.
The intubation is accompanied by manual compressive
maneuvers to milk the colonic content toward the tube, with
proximal clamping of the terminal ileum. There is some risk
of bleeding when the tube is withdrawn. Two series have
reported a total of 13 cases treated in this way with excel-
lent results [8,10].
Colonic resections
If there is necrosis or perforation of the cecal wall, colec-
tomy is indicated; the extent of resection can vary from
right hemicolectomy to subtotal colectomy; anastomo-
sis is usually not performed in this urgent setting. This
is usually a major surgical undertaking in a debilitated
patient with a mortality estimated between 32% and 40%
[8,10].
Conclusions
The etiology and pathogenesis of ACPO is not yet entirely
clear. An imbalance between sympathetic and parasympa-
thetic tone remains the most likely etiology, and it tends to
occur in patients who are often very debilitated. Mortality is
high without treatment. Poor prognostic factors include age,
ischemia, cecal perforation, and prolonged delay in colonic
decompression. Specialty societies are working to estab-
lish a uniform management approach. If initial conservative
management is unsuccessful, further measures are defined
by a well-established decisional algorithm (Fig. 3). Pharma-
cologic treatment with neostigmine and colonic exsufflation
head the list of interventional options. The frequent recur-
rence of ACPO may be prevented by measures such as PEG
104 P. Pereira et al.

ACPO
Any suspicion of colonic perforaon

Conservave management
Delay > 48h
Pre-perforative cecum
RESOLUTION FAILURE Evidence of sepsis…

Epidural anesthesia Alternative IV NEOSTIGMINE

Connue medical treatment and
disconnue any predisposing (bupivacaine or lidocaine) (if failure, repeat dose)
medicaons or other contribung
factors

RESOLUTION FAILURE

Endoscopic colonic exsufflaon

PEG administraon to
Faucher colorectal tube
prevent recurrence

FAILURE
LAPAROTOMY:
Paent not eligible
- Transanal retrograde Paent eligible for surgery for surgery
colonic intubaon
-Colectomy

CECOSTOMY +/- under Alternave therapies:

- Percutaneous Endoscopy-guided Cecostomy (PEC)
local anesthesia
- CT-guided Percutaneous Cecostomy (CPC)
- Needle decompression

Figure 3. Decisional algorithm for management of acute colonic pseudo-obstruction (ACPO). PEG: polyethylene glycol.

administration and colonic intubation for 48 hours with a Disclosure of interest

multiperforated Faucher tube. In view of its high associ-
ated mortality, surgical intervention should only be a last The authors declare that they have no conflicts of interest
recourse after failure of endoscopic procedures or when concerning this article.
colonic perforation makes surgery unavoidable.

Key points
• Acute colonic pseudo-obstruction (ACPO) consists
of dilatation of part or all of the colon and
rectum without any intrinsic or extrinsic mechanical
obstruction.
• Its etiologic pathogenesis is not fully elucidated.
• The first therapeutic choice is conservative medical
management.
• The duration of conservative medical management
should not exceed 48—72 hours.
• Conservative management should be discontinued if
there is colonic perforation or evidence of a high-risk
pre-perforative cecum.
• Neostigmine heads the list of pharmacologic
treatment if conservative management proves
unsuccessful.
• Endoscopic colon exsufflation should be considered
if medical management fails, especially if cecal
dilatation is judged to be pre-perforative.
• The prevention of recurrent ACPO is based on
placement of a long multiperforated colonic tube for
decompression/drainage and administration of PEG.
• Surgical intervention should be a last recourse,
consisting of tube cecostomy or transanal pancolonic
intubation, hand-guided during laparotomy.
• Colonic resection should be reserved only for severe
megacolon complicated by ischemia or perforation;
it carries a very high risk of morbidity and
mortality.
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