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| Journal of the New Zealand Medical Association,
25-July-2003, Vol 116 No 1178
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Non-surgical approach to delayed expansion of traumatic
intramural duodenal haematoma
Tanju Acar, Fahrettin Yildiz, Serdar Esgil, Basak Hosgore
and Raci Aydin
Duodenal haematoma occurs mainly in young men and children,
with 82% of the patients being younger than 30
years.1 The first known case was reported in
1838 by McLauchlan2 and to date no more than
200 cases of such injury have been reported.1
This paper reports an intramural duodenal haematoma following bicycle injury,
which caused total obstruction of the duodenum, obstructive jaundice and
pancreatitis resolving without operative management.
Case reportA 12-year-old boy fell over the
handlebars of his bicycle on the day before admission. He had mild abdominal
pain, and vomited undigested food once during the initial evaluation but had
stable vital signs and a body temperature of
36.9oC.
Abdominal examination showed a tender mass in the right
upper quadrant, extending to the midline, without peritoneal signs or
ecchymosis. Bowel sounds were hypoactive. Haemoglobin level was 135 g/l. White
blood cell count was
8.7x109/l,
total bilirubin level was 12.2 μmol/l (normal range 5.1 to 17 μmol/l
), and serum amylase level was 189 IU/L (normal range 50 to 160 IU/L). Abdominal
X-rays showed no air fluid levels and no free intraperitoneal air. An
ultrasonography showed no fluid collection or other organ injury. The CT scan
demonstrated the presence of an intramural haematoma in the second portion of
the duodenum and there was no pancreatic fracture (Figure 1).
Figure 1. CT scan showing haematoma in region of
duodenum
 The patient was observed expectantly. There were at first no
symptoms of duodenal obstruction. However, attempts at feeding were associated
with abdominal pain and vomiting. Non-surgical treatment, including bowel rest
and parenteral nutrition, was instituted because there were no associated organ
injuries requiring immediate laparotomy. The treatment was followed by gradual
improvement of symptoms.
The patient complained unexpectedly of severe pain in the
epigastrium and his serum amylase level rose to 733 IU/L by the seventh hospital
day. Haemoglobin declined to 93 g/l and 2 units of packed red-blood-cell
transfusions were given. Total bilirubin level also increased from 12.2
μmol/l to 28.7
μmol/l within 24 hours. An enhanced CT scan revealed expansion of the
duodenal haematoma (Figure 2).
Figure 2. Enhanced CT scan on the seventh hospital day
(note the enlargement of the haematoma (arrows) occupying the duodenal
lumen)
 We decided to proceed with surgery. The patient agreed to
nasogastric drainage and intravenous antibiotics with maintained parenteral
nutrition but refused laparotomy; conservative management continued. The
nasogastric drainage was initially acholic.
Both the hyperamylasaemia and jaundice improved gradually
over the next ten days. The tenderness in the abdomen subsided. The gastric
drainage decreased from an average of 850 ml to 200 ml a day and the nasogastric
drainage became bilious. Oral alimentation was begun on the 20th hospital day
and the patient was discharged five days later. A final ultrasonography after
normal diet had been resumed (five weeks after injury) showed a marked reduction
in size of the haematoma (Figure 3) and the patient was clinically normal when
discharged from follow up three months after his injury.
Figure 3. Sonography demonstrates a 1 x 2 cm mass (D)
corresponding to an intramural haematoma of duodenum located inferior to the
gall bladder (G). The mass is consistent with a five-week-old haematoma. H
indicates the lumen of the duodenum and L indicates the liver.
 DiscussionIntramural haematoma of the
alimentary tract is mainly caused by blunt abdominal injuries in
childhood.3 The duodenum is among the bowel
segments most commonly injured by blunt trauma. Duodenal haematoma occurs
frequently in the second and third segments owing to the relatively fixed
position close to the vertebral column and the rich submucosal vascular supply
of these segments.4 Shearing forces tear the
intramural vasculature and cause blood to accumulate, producing a submucosal
mass effect. The haematoma may increase in size over time because of either
continuous bleeding or the breakdown of haemoglobin, causing an increase in the
oncotic pressure in the haematoma with subsequent increase in
volume.5 This process explains the delayed
expansion of haematoma in our patient.
The typical clinical picture consists of upper abdominal
pain and bilious vomiting. Symptoms of duodenal obstruction are nearly always
present, but ampullary obstruction is uncommon. Serum amylase is elevated in 6%,
and bilirubin in 13%, of the 116 cases reviewed by Jones et
al.6
Sonography and CT have facilitated the diagnosis of duodenal
haematoma and associated lesions. The echogenicity of a haematoma on sonography
varies substantially and rapidly over time, so re-examination of the patient
within a few days may be helpful.
Both surgical and non-surgical approaches have been used to
treat duodenal haematomas. The recent consensus is that there is little reason
for emergency laparotomy during the acute phase of trauma because of the
likelihood of spontaneous resolution of the haematoma and because of the high
post-operative morbidity rate, unless associated injuries of intra-abdominal
organs requiring immediate laparotomy are
evident.4
Haematoma should be suspected in the differential diagnosis
if a mass is seen in the duodenum, especially in the setting of recent trauma
with non-specific abdominal complaints and vomiting as illustrated by this case.
There are no clear recommendations in the literature as to optimal management
and no controlled trials that address treatment of duodenal haematomas.
Conservative management seems reasonable, with operative intervention for those
with refractory obstruction.
Author information:
Tanju Acar, General Surgeon; Fahrettin Yildiz, Surgical Registrar; Serdar
Esgil, Surgical Registrar, Department of Surgery; Basak Hosgoren, Registrar of
Radiology, Department of Radiology; Raci Aydin, Professor of Surgery, Department
of Surgery, Emergency Aid and Traumatology Hospital, Balgat, Ankara,
Turkey
Acknowledgements. We
are grateful for the literature review by Mr Nuraydin Ozlem, Consultant Surgeon,
Emergency Aid and Traumatology Hospital, Balgat. The figures were prepared by Dr
Salih Tuncal at the same hospital.
Correspondence: Dr
Tanju Acar, Sogutozu sitesi, Akasya apt. No 8, Sogutozu, Ankara, Turkey. Fax:
+90 312 287 24; email: tanju_acar@yahoo.com
References:
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