A 32-year-old man was admitted to the intensive therapy unit with multiple-system
organ failure 24 hours after the onset of severe acute biliary pancreatitis. Contrast-enhanced
abdominal computed tomography (CT) demonstrated extensive (> 50 %) pancreatic necrosis
and multiple acute fluid collections, particularly around the duodenum. His clinical
course was further complicated by infected pancreatic necrosis which required repeated
surgical debridement and drainage.
At week 6, he underwent two consecutive sessions (24 hours apart) of endoscopic hemostasis,
with local injection of epinephrine in a dilution of 1 : 10 000, at each session,
around bleeding post-bulbar kissing ulcers (Forrest grade II B) (Figure [1]). Within 48 hours a sudden decrease in hematocrit from 30 % to 23 %, occurred, along
with cholostasis, a four-fold rise of blood amylase level, and massive nasogastric
drainage. Upper gastrointestinal series and abdominal CT showed complete obstruction
of the proximal duodenum due to an extensive intramural hematoma. The poor general
condition of the patient dictated a conservative approach. At 4 weeks later, rupture
of the hematoma into the duodenal lumen relieved the obstruction and left a pseudodiverticulum
which delineated the second and third duodenal segments (Figure [2]). A contemporary CT showed an air dissection of the duodenal wall. Endoscopy demonstrated
a 5 mm tear, 2 cm below the papilla, from which bile-stained fluid issued. At 3 months
later, almost complete obliteration of the submucosal defect was documented. At 6
months the patient was discharged and was on an unrestricted diet.
Figure 1 Endoscopic image showing Forrest grade IIB post-bulbar kissing ulcers.
Figure 2 Upper gastrointestinal series showing relief of the obstruction (medium-sized arrow)
and a pseudodiverticulum of the duodenum (large arrow) after evacuation of the hematoma
into the duodenal lumen through a mucosal tear (small arrow).
Whereas in the past immediate surgical evacuation and repair were advised, current
management of intramural duodenal hematoma favours a conservative approach, including
nasogastric drainage, intravenous fluid replacement, total parenteral nutrition if
necessary, and careful observation of the emergence of complications, since obstruction
is relieved spontaneously in most cases [1].
In contrast to the subserosal location of intramural hematomas that are of traumatic
origin, blood extravasation after endoscopic hemostasis usually occurs in the submucosa.
Hence although the fate of these postendoscopic hematomas remains poorly documented
in comparison with those of traumatic origin, extraluminal rupture is rare unless
blood extravasation courses deep to the muscular layers. Spontaneous local absorption
has therefore been reported as the mechanism underlying resolution of obstructions
[2]. This report demonstrates not only that spontaneous intraluminal rupture may account
for alleviation of intestinal obstruction, but that sudden clot evacuation may leave
an intramural pouch or a false channel which communicates with the digestive lumen
through a mucosal tear, thereby mimicking arterial dissection. Clinicians should be
aware of this course, as it is conceivable that gradual fibrotic submucosal obliteration,
extraluminal rupture, compression of adjacent structures, or infection of this pseudodiverticulum
may ensue, depending upon the size and location of the mucosal draining tear.
