Acute gastric dilation and ischemia

secondary to small bowel obstruction

Shawn Steen, MD, Jeffrey Lamont, MD, and Laura Petrey, MD
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Abstract
Acute gastric dilation leading to ischemia of the stomach is an under-diagnosed and potentially
fatal event. Multiple etiologies can lead to this condition, and all physicians should be aware of
it. Without proper and timely diagnosis and treatment, gastric perforation, hemorrhage, and other
serious complications can occur. We report a case of acute gastric dilation and ischemia
secondary to small bowel obstruction. We also review the world literature and discuss the
etiology, diagnosis, and management of this condition.
A 71-year-old man presented with a 1-day history of diffuse unrelenting abdominal pain
associated with emesis and abdominal distention. He had an episode of small bowel obstruction
5 months prior to presentation that was treated nonoperatively. His past medical history was
significant for hypertension, nephrolithiasis, and an inguinal hernia repaired when he was a child.
The initial physical examination revealed a distended abdomen tympanic to percussion in the left
upper quadrant but without peritoneal signs. An abdominal radiograph showed dilated small
bowel loops with a diffuse opacity in the left upper quadrant. On admission, his white blood cell
count was 15 10
3
/L with 10% bands and a serum lactate of 7.5 mmol/L (reference range, 0.5
2.2). An arterial blood gas analysis showed a bicarbonate level of 19 mEq/L with a base deficit
of 7. A computed tomography (CT) scan revealed complete small bowel obstruction with a
transition point in the distal ileum, associated pneumatosis intestinalis of the ileum, and
emphysematous gastritis with air at the gastroesophageal junction and in the portal vein (Figures
(Figures11 and and22).

Figure 1
CT scout image showing massive gastric dilation.

Figure 2
CT image with gastric dilation and portal venous air.
The patient was resuscitated with intravenous fluids and taken emergently to the operating room,
where a midline laparotomy was performed. The small bowel was distended but viable. A single
adhesion in the right lower quadrant causing torsion of the small bowel was released, but no
other points of obstruction were found. A nasogastric tube was placed in the emergency
department but did not function until it was repositioned in the operating room. Five liters of
brown gastric content were suctioned from the nasogastric tube in the operating room. After
decompression of the largely distended stomach, patchy areas of dark ischemic tissue along the
greater curve of the stomach were noted. No full-thickness perforation was identified. An
intraoperative esophagogastroduodenoscopy was performed that revealed severe esophagititis, as
well as patchy areas of mucosal ischemia along the entire body and greater curve of the stomach.
Good Doppler signals were found along the left and right gastric arteries and along the short
gastric vessels. It was decided to pack the abdomen and close with a wound vacuum-type
dressing and return to the operating room in 24 hours for a second look.
The patient was packed open and taken to the intensive care unit for resuscitation. His base
deficit corrected over the next few days. Two more second-look procedures were undertaken
on postoperative days 1 and 3, along with repeat esophagogastroduodenoscopies (Figure
(Figure33).

Figure 3
Esophagogastroduodenoscopy picture showing mucosal ischemia.
During subsequent operations the mucosa looked viable with some residual sloughing. No
further distension of either the small bowel or stomach was noted. No full-thickness ischemia or
perforation was identified. The fascia was closed, and a nasojejunal feeding tube was placed
during the third operation. A CT angiogram was done after the initial operation that showed a
suspected stenosis at the origin of the celiac artery with mild poststenotic dilation. The superior
and inferior mesenteric arteries were without stenosis. Vascular consultation concluded that
invasive therapy was not indicated, as the patient was recovering well and had intact collateral
flow. The patient eventually recovered and was discharged on day 21 tolerating an oral diet.
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DISCUSSION
Acute gastric dilation is described in the literature as a result of eating disorders, trauma
resuscitation, volvulus of hiatal hernias, medications, electrolyte abnormalities, psychogenic
polyphagia, superior mesenteric artery syndrome, and a myriad of other conditions (15). Acute
gastric dilation was first described by S. E. Duplay in 1833 (4). Although rare, it can have
devastating consequences. Gastric ischemia and perforation as a result of dilation has a reported
mortality rate of 80% to 100% (5).
It is rare to have ischemic events in the stomach due to its copious collateral circulation.
Ischemia in the case of gastric dilation is postulated to be due to venous insufficiency (4, 6, 7).
The pressure in the stomach lumen must be >14 mm Hg to exceed gastric venous pressure and
lead to ischemia (1, 4). As little as 3 L of fluid can distend a normal stomach to this point of
tension (6). The chronicity of stomach dilation is also a factor. Gastric volumes as high as 15 L
have been recorded in certain eating disorders such as psychogenic polyphagia and bulimia.
Gastric rupture can occur with an intragastric pressure of 120 to 150 mm Hg, which can occur
with only 4 L of fluid in a normal stomach (8). Rupture can also occur if external compression is
added, such as cardiopulmonary resuscitation (8).
Symptoms of acute gastric dilation can be initially vague. Emesis is common and occurs in
>90% of cases (1). Progressive abdominal distention and accompanying pain are common but
may initially be deceptively mild (1). Symptoms become much more marked if perforation
results (2). With perforation, peritoneal signs usually are present. Irritation of the peritoneal
cavity can lead early on to a profound vagal response resulting in neurogenic shock and later to
true septic shock (6). Cases have been reported in which blood flow from the aorta is blocked by
compression from a massively dilated stomach (9, 10). In the case of impaired blood flow to
organs and limbs, decompression of the stomach can lead to acute cardiac decompensation from
a sudden return of lactic acid and decreased afterload (10). A staged decompression to prevent
these sequela has been suggested (10). Delayed gastric hemorrhage after decompression has also
been reported (10).
Imaging is a key factor in diagnosis. Either plain radiographs or CT scans will reveal a massively
dilated stomach. CT is a more accurate method of identifying associated causes of acute gastric
dilation.
Treatment focuses on early diagnosis and decompression of the stomach, thus halting the
vascular congestion and ensuing ischemia (7). Delayed perforation or bleeding is still possible,
even after decompression. Endoscopy in the stable patient may be of useparticularly if the CT
scan suggests gastric or esophageal involvement. Most reports on acute gastric dilation note that
the majority of ischemic changes occur along the greater curve of the stomach (3). The lesser
curvature and pyloric regions of the stomach tend to be spared (1). Surgical exploration is
mandated in the presence of instability or other indications, such as associated small bowel
obstruction or ischemia of the small bowel.
The surgical approach depends on the extent of ischemia, the presence of frank necrosis, and
current or impending gastric wall perforation. Surgical resection of the gangrenous portion of the
stomach is critical. Techniques that include total gastrectomy with either esophagojejunostomy
reconstruction in a stable patient or esophagostomy in an unstable patient have been performed
(1). A feeding jejunostomy is a critical portion of the procedure (1). Other authors have
discussed successful nonoperative therapy and even partial resections or local debridement (4,
11). Many argue that if any surgical resection is needed, total gastrectomy is the safest option.
Proponents of surgical resection cite delayed ischemia and poor healing of gastric tissue left
behind. Overall, the surgical mortality rate has been described as 50% to 80% (1, 2). Without
appropriate treatment, gastric ischemia is uniformly fatal.
In our case of acute gastric dilation secondary to a small bowel adhesive obstruction, the gastric
distension of approximately 5 L of fluid seems to have led to gastric wall ischemia from venous
congestionin concurrence with reports in the literature. The arterial blood flow to the stomach
was intact based on intraoperative findings and radiographic tests. Also, as commonly reported
in the literature, the ischemia was largely located along the greater curve of the stomach. This
patient was managed without gastric tissue resection. The importance of early diagnosis and
appropriate management of acute gastric necrosis is demonstrated.
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