This paper describes the two cases of hepatic-portal venous gas and pneumatosis intestinalis, definitively diagnosed with CT, associated with open placed jejunostomy tubes in patients who appeared clinically ill but had no evidence of bowel ischemia at surgery.
This paper describes two cases of hepatic-portal venous gas and
pneumatosis intestinalis, definitively diagnosed on CT, associated
with open placed jejunostomy tubes in patients who appeared
clinically ill but had no evidence of bowel ischemia at surgery.
The hepatic-portal venous gas and pneumatosis resolved after
surgical removal of the jejunostomy tube, decompression of the
bowel, and administration of both bowel prokinetic agents and
antibiotics.
Drs. Hofmann, Beall, Jones, and Fishman, are in the
Department of Radiology and Radiological Science, and Dr.
Heitmiller is in the Department of Surgery at The Johns Hopkins
Medical Institutions in Baltimore, MD.
Introduction
The finding of hepatic-portal venous gas (HPVG) on plain films
usually indicates a poor prognosis; it is associated with a 75%
mortality.1 Most clinicians and radiologists alike equate
hepatic-portal venous gas with bowel ischemia. Although ischemic
bowel accounts for 72%1 of cases with HPVG, there are other causes
that must be considered. HPVG is also associated with
intra-abdominal abscesses, small bowel obstruction, gastric ulcers,
ulcerative colitis usually following a double-contrast barium
enema,1 blunt abdominal trauma,2 and needle catheter jejunostomy
tubes (NCT).
A Medline review of the literature going back to 1966 found no
reported cases of HPVG and PI in association with open placed
jejunostomy tubes (OJT); there are, however, a handful of studies
describing the association of NCT and pneumatosis intestinalis
(PI).
We describe two cases of HPVG and PI associated with OJT,
definitively diagnosed on CT, in patients who appeared clinically
ill without evidence of bowel ischemia at surgery. In both cases,
the HPVG and PI resolved after surgical removal of the OJT,
decompression of the bowel, and administration of both bowel
prokinetic agents and antibiotics. These cases are illustrated to
alert radiologists and clinicians to the possibility that HPVG and
PI may be found in the clinical setting of an ill-appearing patient
without bowel necrosis.
Cases
The first patient was a 59-year-old female who underwent
proximal gastrectomy and distal esophagectomy with the placement of
a OJT for the treatment of esophageal carcinoma.3 On the eighth
postoperative day, the patient began to vomit, and her abdomen
became distended and tender. Her white blood cell count was 23,000.
Clinically, the patient appeared very ill. An abdominal CT was
requested; it demonstrated massive HPVG and PI in air-distended
small bowel loops (figure l). The patient was started on
antibiotics and rushed to surgery. In surgery, her bowel appeared
moderately distended, with normal color and good pulses in an
otherwise unremarkable abdomen. The HPVG and PI were attributed to
the combination of bowel distention and the OJT. The OJT was
removed during surgery and the OJT site in the bowel wall was
oversown. Postoperatively, the bowel was decompressed with a
nasogastric tube and prokinetic drugs. The patient had another
abdominal CT 10 days later demonstrating no evidence of HPVG or PI
(figure l). The patient recovered uneventfully from surgery, and
was subsequently discharged on the thirtieth day from
admission.
Our second patient was a 72-year-old male who underwent proximal
gastrectomy and distal esophagectomy for esophageal carcinoma with
placement of a OJT. On the seventh postoperative day, the patient
appeared ill, had a distended, tender abdomen, and had a white
blood cell count of 28,800. An abdominal CT showed massive HPVG and
PI, with air distention of the small bowel (figure 2). The patient
was started on antibiotics and taken to surgery. In surgery, the
bowel was moderately distended, but appeared normal in color,
without evidence of ischemia. Subsequently, the OJT was removed and
its site oversown. Postoperatively, the patient's bowel was
decompressed with a nasogastric tube and prokinetic drugs. He
recovered uneventfully from surgery, and was discharged on the
twenty-second day from admission.
Discussion
HPVG and PI carries a grave prognosis because it is usually
associated with an ischemic bowel. Although both of our patients
appeared ill, each had a well-perfused bowel at surgery. We are
unsure as to the exact cause of the HPVG and PI in these patients,
though we postulate that it may be due to the OJT combined with
bowel distention.
Though there are no reported cases of HPVG and PI associated
with OJT,4 there are 16 reported cases of the association between
PI and NCT, with only one of these cases also demonstrating HPVG.
Strain et al reviewed 53 patients with NCT, four patients with PI,
and one patient exhibiting both PI and HPVG, but they did not
describe the patients' clinical symptoms in their report.
Nevertheless, they did report that the patient with both HPVG and
PI went on to complete recovery with conservative treatment.5
Knechtle et al prospectively evaluated 27 consecutive patients with
PI, five of whom had a NCT.6 In four of the patients, the PI
resolved without sequelae. One patient, however, died due to bowel
infarction and subsequent septicemia. This poor outcome was
believed to be related to a prolonged episode of hypotension and
not to the NCT.
Knechtle and coworkers' article also discussed the management of
pneumatosis intestinalis. These authors advised that patients with
PI and clinical evidence of bowel obstruction or ischemia should be
managed aggressively with surgery, while asymptomatic patients
without metabolic acidosis could be managed conservatively.6 In
their investigation, Smith and Sarr described only two cases of
clinically significant PI in 217 consecutive patients with newly
placed NCT.7 Similar to our cases, both patients became febrile,
and had abdominal pain and diffuse abdominal tenderness. Smith and
Sarr's patients were managed conservatively with broad spectrum
antibiotics and cessation of enteral alimentation. Both patients
were asymptomatic within 48 hours; however, neither patient
exhibited HPVG.7 We found four other cases in the literature that
describe the association of PI and NCT.7,8 Most of these cases did
not detail clinical or laboratory findings. However, all were
treated conservatively with subsequent resolution of the PI.
For patients such as ours, who have open jejunostomy tubes, no
association with HPVG and PI has been established. An OJT uses a
larger bore catheter and is inserted into the bowel through a
tunnel created by the surgeon, using manual dissection. This
differs from the needle catheter jejunostomy tube, which uses a
needle on the tip of a small bore catheter to create its own tunnel
as it is forced through the bowel wall. The safety of OJT with
esophagectomy has been described by Gerndt and Orringer. These
authors reviewed their experience with 523 patients undergoing
esophagectomy with OJT over a 15-year period and reported a
complication rate of 2.1%, primarily either bowel obstruction or
intra-abdominal abscess. They did not report HPVG or PI in any of
their patients.4
The etiology for PI and HPVG in association with OJT or NCT has
not been clearly elucidated. Smith and Sarr proposed two separate
mechanisms for intramural air in the context of a NCT. The first
suggests that a combination of postoperative ileus, aerophagia,
and/or intraluminal bacterial fermentation of feedings from
overgrowth of the bowel flora raises the intraluminal pressure. As
a result, the air dissects into the bowel wall through the mucosal
defect created by the NCT. Their second theory proposes gas
production by gas-forming organisms that have invaded the bowel
wall via the catheter tract.7 Regardless of the mechanism of PI,
once the air is in the bowel wall, it may enter the portal venous
system.1 It also is unclear as to the relationship of HPVG and PI,
though when HPVG is present PI is almost invariably also
present.
We do not know the exact etiology of the HPVG and PI in our
cases, or why our patients appeared so sick. Both patients had an
esophagectomy and gastric pull-up, an OJT, moderate small bowel
distention, and both appeared clinically ill. We hypothesize that
increased intraluminal pressure from the ileus was sufficient to
allow air to dissect along the OJT into the bowel wall, and then
gain access into the portal venous system. Moreover, the abdominal
distention and tenderness could be attributed to the ileus.
Regardless of the etiology, the treatment for our subset of
patients has been efficacious. Considering the ill appearance of
our patients, a laparotomy was performed to rule out ischemic
bowel. At surgery, the OJT was removed. We are unsure if this was
necessary, as we do not know the exact cause of the HPVG and PI,
and studies with NCT have shown resolution of symptoms without
removal of the NCT. Postoperatively, the bowel was decompressed,
and the patients were both placed on prokinetic agents and
antibiotics.
Summary
Two patients who underwent esophagectomy and gastric pull-up
associated with the placement of a OJT are described. Both
subsequently developed massive HPVG and PI without evidence of
bowel ischemia at surgery, which resolved after removal of the OJT,
decompression of the bowel and initiation of antibiotics and
prokinetic agents. Although a few cases in the literature describe
the association of PI and NCT, none have described the association
of HPVG and PI with OJT. By extrapolating proposed mechanisms of
HPVG and PI seen with NCT, we have developed a possible theory on
the cause of HPVG and PI without bowel necrosis. AR
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