CASE REPORT

Acute Gastric Dilatation Causing Bacterial Cerebral
Aneurysm—Case Report
Takeshi Matsuyama, MD*
Satomin Komeda, MD
Misato Nobayashi, MD
Masami Imanishi, MD
Shoichiro Kawaguchi, MD

ABSTRACT
Objective: Acute gastric dilatation (AGD)
is a very rare entity which can sometimes
be life-threatening. We report a case of a
patient presenting with a rupture of a
BCA during the treatment of AGD.
Method: A 24-year-old woman, who
had a history of bulimia and vomiting
episodes, was transferred in shock with
marked abdominal distension. A large
nasogastric tube was inserted, and 9 liters
of viscous gastric contents were drained
out. Her circulation became stable.
Results: About 3 months after admission, she became drowsy and presented
with a right hemiparesis and aphasia.

Introduction
Bacterial cerebral aneurysm (BCA) is very rarely
seen in clinical practice. BCA occurs primarily as a
result of infectious complicating cardioaortic diseases, such as rheumatic and congenital heart diseases.1 Acute gastric dilatation (AGD), which is a
very uncommon pathology, has not been previously reported as causing BCAs. We herein report a
case of a patient presenting with a subarachnoid
hemorrhage due to the rupture of a BCA during the
treatment of AGD.

Case Report
A 24-year-old woman was transferred to our hospital in shock with marked abdominal distension.
The patient had a history of bulimia and vomiting
episodes and was routinely seen by a psychiatrist.
She was not taking any medications or toxic substances. On September 19, 2005 she was admitted
to a nearby hospital, complaining of abdominal
Accepted 14 August 2007
*Correspondence to: Takeshi Matsuyama, Department of Critical
Care and Emergency Medicine, Nara Prefectural Nara Hospital,
1-30-1 Hiramatsu-cho, Nara city 631-084, Japan.
E-mail: tmatsuya@nmu-gw.naramed-u.ac.jp
Department of Critical Care and Emergency Medicine, Nara
Prefectural Nara Hospital, Nara city, Japan
Published online 22 January 2008 in Wiley InterScience
(www.interscience.wiley.com). DOI: 10.1002/eat.20487
C 2008 Wiley Periodicals, Inc.
V

380

Computed tomography of the head
showed a diffuse thick subarachnoid
hemorrhage. Left carotid angiograms
revealed an obscurely-shaped aneurysm
in the left middle cerebral artery.
Conclusion: Trapping of the aneurysm
was performed. Thirty-four days after
admission, the patient had a residual
right hemiparesis and motor aphasia,
C 2008 by Wiley
and was discharged. V
Periodicals, Inc.
Keywords: bacterial cerebral aneurysm;
acute gastric dilatation; bulimia

(Int J Eat Disord 2008; 41:380–382)

pain that occurred after eating an enormous amount
of food. Two days after admission, she developed
shock and was transferred to our department for
treatment of her circulatory disturbance. On admission, she was a normally developed, but malnourished female with an extremely distended abdomen
(height: 160 cm; weight: 34 Kg). Her consciousness
level was normal. The patient’s blood pressure was
76/38 mm Hg, and her heart rate was 93 without arrhythmia. Heart and respiratory sounds were clear.
Her distended abdomen was tender and resistance
to palpation was noted. An abdominal X-ray
showed extreme gastric dilatation extending to the
pelvis (Fig. 1). A large nasogastric tube was inserted,
and 9 l of viscous gastric contents were drained out.
Her abdomen became flat, and the gastric dilatation was thought to regress, though the size of the
stomach did not shrink to normal. The patient’s circulation became stable. Two months after her initial admission, the patient developed a low grade
fever that continued for 5 days. At that time, laboratory tests showed acute inflammatory findings,
including elevated white blood cells, c-globulin,
and C-reactive protein. On blood cultures, a bacteremia of methicilin-resistant Staphylococcus aureus
was found. After antibiotics and c-globulin were
given, the fever subsided rapidly. The patient’s general condition started to improve and she even tried
to eat some food. However about 3 months after
her initial admission, the patient became drowsy
and presented with a right hemiparesis and aphasia. Her pupils were anisocoric (right: 1.5 mm; left:
International Journal of Eating Disorders 41:4 380–382 2008

AGD WITH BACTERIAL CEREBRAL ANEURYSM
FIGURE 1. An abdominal X-ray shows extreme gastric
dilatation extending to the pelvis.

3.0 mm). Computed tomography of the head
showed a diffuse thick subarachnoid hemorrhage
at the basal cistern and an intracerebral hemorrhage in the left temporal lobe. On laboratory testing, no abnormal findings that would have indicated infection were found. No cardiac murmurs
were audible. Cardiac ultrasound, which was frequently done to obtain information about infectious endocarditis (IE), showed no vegetations on
the valves. On the left carotid angiograms, an
obscurely shaped aneurysm involving several
branches of the sylvian portion of the left middle
cerebral artery were noted (Fig. 2). Surgical intervention was performed to prevent rebleeding from
the aneurysm and to remove the intracerebral hematoma. Trapping of the aneurysm was performed.
On visual inspection, the aneurysm was partially
thrombosed and very fragile. The specimen of the
excised aneurysm revealed that the aneurysmal
wall was infiltrated with a large amount of polynuclear neutrophils, indicating a bacterial aneurysm.
Thirty-four days after admission, the patient had a
residual right hemiparesis and motor aphasia, and
was discharged to the rehabilitation program.

Conclusion
BCA is rare, and its incidence is decreasing because
of proper use of effective antibiotics. BCA occurs in
International Journal of Eating Disorders 41:4 380–382 2008

FIGURE 2. Left carotid angiograms shows an obscurely
shaped aneurysm involving several branches of the sylvian
portion of the left middle cerebral artery, and severe narrowing, as well as obstruction of the distal arteries exiting
from the aneurysm.

0.4% of all patients with intracranial aneurysms
and in 3% of all patients with IE.1 The main etiology of BCA is IE associated with rheumatic or congenital heart diseases. The mortality rate of patients
with an unruptured BCA is 30%, but in patients
with a ruptured BCA, the mortality rate is 80%.2
The pathogenesis of BCA is caused by the lodging
of septic emboli at distal sites within the circulation. Bacterial translocation via the vasa vasorum
to the adventitia, and inflammatory necrosis
extends from the adventitia to the medial layer,
which leads to aneurysmal formation.1,2 BCA is
treated with antibiotics as well as surgical intervention. Should antibiotic therapy not control the
infection or the aneurysm enlarges, then surgical
intervention is required. Clipping is preferred, but
the involvement of the vessel wall by the infectious
process may make it difficult to do so.
AGD is a very rare entity which can sometimes
be life-threatening due to complications including
gastric necrosis, perforation, ischemic bowel injury
by compression of mesenteric vessels, and shock.3
AGD is caused by various factors, such as: excessive
eating, pylorospasm after scarring secondary to
peptic ulcer, posttrauma, pregnancy, ketoacidosis,
or postsurgery.4 The symptoms include restlessness, vomiting, dyspnea, and abdominal pain.3
Aspiration of gastric contents is a frequent and
dreaded complaint. If the syndromes are not diagnosed early and treated, then circulatory collapse
and cardiac arrest can occur.3,4 Initial therapy must
include nasogastric decompression and fluid resuscitation. Most patients respond to nasogastric tube
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MATSUYAMA ET AL.

drainage, but some require gastrectomy with esophagojejunostomy. Early recognition is essential,
since 80% mortality rate has been reported with
delayed treatment.4 Even if the patients’ stomach
shrinks and their circulation is stabilized, they will
have gastric mucosal damage.5
There has been no report of BCA following AGD.
In our case, a cardiac murmur was not heard and
on the echocardiography done before the BCA ruptured, no vegetations on the valves and no valvular
dysfunction, suggesting IE, were noted. Therefore,
the aneurysm may have been formed by bacteremia or infectious emboli originating in the necrotic
gastric mucosa, which persisted even though gastric decompression was successful. Thus, even in
stabilized patients with AGD that is well controlled
and whose infection is well controlled by proper
antibiotics, special attention must be given to gastric lesions, which could serve as infectious foci

382

and lead to systemic bacterial infections such as IE
or BCA.

References
1. Chun JY, Smith W, Halbach VV, Higashida RT, Wilson CB, Lawton
MT. Current multimodality management of infectious intracranial aneurysms. Neurosurgery 2001;48:1203–1213.
2. Pavic M, Debourdeau P, Teixeira L, Brunot J, Colle B, Flechaire
A. [Bacterial cerebral aneurysms without infectious endocarditis:
Analysis of a case and review of the literature]. Rev Med Interne
2001;22:867–871.
3. Sinicina I, Pankratz H, Buttner A, Mall G. Death due to neurogenic shock following gastric rupture in an anorexia nervosa
patient. Forensic Sci Int 2005;155:7–12.
4. Gyurkovics E, Tihanyi B, Szijarto A, Kaliszky P, Temesi V, Sas H,
et al. Fatal outcome from extreme acute gastric dilation after an
eating binge. Int J Eat Disord 2006;39:602–605.
5. Todd SR, Marshall GT, Tyroch AH. Acute gastric dilatation revisited. Am Surg 2000;66:709–710.

International Journal of Eating Disorders 41:4 380–382 2008