Progressive colonic dilatation following surgery is
clinically indicative of the diagnosis of Ogilvie’s
syndrome in the absence of a mechanical obstruction.[
4]
In 1948, Sir William Heneage Ogilvie, the Chileanborn
British gastrointestinal surgeon and orthopedist,
initially described a novel clinical syndrome with a
report of two cases.[
6] This new syndrome which is
characterized by acute abdominal pain, constipation
and large bowel distention without a mechanical
obstruction was then named as Ogilvie’s syndrome. Although the exact pathophysiology of the ACPO
is still obscure, a parasympathetic deprivation is
thought to be responsible.[
7]
Ogilvie's syndrome is mostly seen in sexagenarians
and septuagenarians. Also, it is two times higher in
males than females.[4] The initial studies investigated
the etiology were concentrated on cesarean sections.
However, later studies revealed that cardiothoracic
surgery as well as lumbar spine and hip procedures
were dominantly responsible.[4,8]
Although the pathophysiological mechanism of
Ogilvie’s syndrome following cardiovascular surgery
still remains to be elucidated, it is often thought to
be neurogenic. The possible scenario explaining the
mechanism of the colonic pseudo-obstruction seems
to be the lack of parasympathetic innervation to the
colon.[4] The success of a parasympathomimetic drug
neostigmine in the treatment of the ACPO also
proves this theory of neuropraxia.[1,5] If it is a type of
a neurological dysfunction, what could be the cause
of this parasympathetic neuropraxia? Is it related to a
trauma of the parasympathetic ganglia? Alternatively,
is it solely because of excessive sympathetic discharge
due to the pain or stress during the operation?
An intraoperative trauma or direct manipulation
of the ganglia or its branches seems to be impossible
in cardiothoracic, orthopedic, and the lumbar spinal
cord operations. However, the vagus nerve, which is
the main parasympathetic trunk of the gastrointestinal
system, may be injured during CABG surgery due
to local hypothermic slush application or during
extensive lateral pericardiotomy.[9] Besides, sympathetic
discharge may occur, when the patient accidentally
awakes due to inadequate anesthesia and this excessive
sympathetic surge may easily cause relative loss of
parasympathetics.[4] Although it is still unproven,
the extracorporeal circulation during CABG surgery
may contribute to neurogenic disarrangement.[4]
An elongated extracorporeal circulation may also
lead to increased ischemia of the parasympathetic
ganglia due to hypotension, thereby, eventually cause
synaptic retardation.[10] In our case, a reasonable
cardiopulmonary bypass time was achieved comparing
to a four-vessel CABG surgery. The circulation
pressure of the heart-lung machine was around
70 mmHg during the extracorporeal circulation period
which corresponds to the normal mean value. In the
light of all these discussed hemodynamic parameters,
the possibility of a mechanical or ischemic trauma can
be excluded.
Furthermore, the diagnosis depends on the
physical examination, follow-up and imaging with
an erected abdominal roentgenogram, irrespective of
the pathophysiology. During the postoperative period,
a massive distention of the abdomen with impaired
flatus or stool outflow should always remind the
Ogilvie’s syndrome.[4]
In the treatment of Ogilvie’s syndrome, the NPO,
NG, and rectal tubes should be the first to constitute
by means of immediate colonic decompression.
The supportive intravenous medication including
fluid and electrolyte replacement should be applied
afterward. Follow-up may lead to complete resolution
of the ACPO or may show further progression. In this
presented case, as the supportive measures did not
improve the patient’s overall status, neostigmine was
initiated as an advanced treatment.[11] Neostigmine
is a parasympathomimetic which inhibits the
acetylcholinesterase enzyme, which is responsible for
the breakdown of the acetylcholine (Ach) molecule. As
it blocks the binding site of the acetylcholinesterase,
the enzyme can no longer interfere the Ach before
it interacts with the receptors of the postsynaptic
membrane.[12] It eventually helps the threshold to
be reached and the impulse can be triggered in the
next neuron. Increase in the parasympathetic activity
further initiates the intestinal motility resulting the
resolution of the abdominal distention.[13]
When any other medical treatments are useless
to resolve the state of ACPO, colonic decompression
via colonoscopy, percutaneous decompression or
laparotomy should be considered.[8,14] If left untreated,
colon perforation due to necrosis of the cecum may
cause fecal peritonitis and death, eventually.[15]
In conclusion, in case of an acute megacolon
following the CABG surgery, the diagnosis should
be considered as Ogilvie’s syndrome. Immediate
diagnosis and effective treatment are necessary to
prevent colonic necrosis and the eventual perforation.
In addition to the supportive treatment, neostigmine,
a parasympathomimetic, can be used to reconstitute
the intestinal motility. Surgical option should be
reserved as the last chance due to its high potential for
mortality.
Declaration of conflicting interests
The authors declared no conflicts of interest with
respect to the authorship and/or publication of this
article.
Funding
The authors received no financial support for the
research and/or authorship of this article.
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