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Portal venous gas from ischemic bowel disease
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Sonographic Detection of Hepatic Portal Venous Gas
Originating from Ischemic Bowel Disease: A Case Report
and Literature Review
Chih-Chung Chao1, Sung-Yuan Hu2,3,4,5,6, Ying-Hock Teng1,4
Hepatic portal venous gas is a rare and ominous radiological finding and it is an important diagnostic
clue associated with patients who may be harboring an intra-abdominal catastrophe. Hepatic portal
venous gas represents a challenge for emergency physicians in terms of diagnosis and management of the
underlying cause. The most common and severest precipitating etiology is ischemic bowel disease, which
has a mortality rate of 75% to 90%. Herein, we report a case of ischemic bowel disease with rare but
typical hepatic portal venous gas by ultrasonography that led us to the identification of ischemic bowel
disease.
Key words: ischemic bowel disease, portal venous gas, ultrasonography
Introduction
An acute abdomen is a common and
emergency condition in emergency departments
(EDs). Indeed, it is necessary to investigate such
a symptom immediately and treated it without
delay. Hepatic portal venous gas (HPVG) is an
uncommon radiological sign and often portends
significant underlying intra-abdominal disease
or diseases. HPVG is most commonly caused by
mesenteric vascular accidents (61%-72%) and
has a mortality rate of 75% to 90% (1-4). HPVG
can be associated have a variety of other clinical
conditions, including inflammatory bowel disease
(8%-16%), intra-abdominal abscess and sepsis (6%11%), bowel obstruction and dilatation (9%-12%),
gastric ulcer (3%-4%), cancer (2%-3%), iatrogenic
injury and trauma (3%-4%) and being idiopathic
in nature (2%) (1-5) . Most studies found in the
medical literature mention computed tomography
(CT) as the primary imaging tool for HPVG, but
ultrasonography (US) is capable of providing
real-time imaging and this can result in clues that
allow clinicians to approach the underlying disease
earlier.
Case Report
An 88 year-old man had a history of
hypertension together with an old cerebrovascular
accident associated with right hemiplegic sequelae;
the patient was under regular medication and had
Received: December 15, 2014 Accepted for publication: December 29, 2014
From the 1Department of Emergency Medicine, Chung Shan Medical University Hospital
2
Division of Clinical Toxicology, Department of Emergency Medicine
3
Center for Translational Medicine, Department of Medical Research, Taichung Veterans General Hospital
4
School of Medicine, 5Institute of Medicine, Chung Shan Medical University
6
Department of Nursing, College of Health, National Taichung University of Science and Technology, Taichung, Taiwan, ROC
Address reprint requests and correspondence: Dr. Sung-Yuan Hu
Division of Clinical Toxicology, Department of Emergency Medicine, Taichung Veterans General Hospital
1650 Taiwan Boulevard Section 4, Taichung 40705, Taiwan (R.O.C.)
Tel: (04)23592525 ext 3670 Fax: (04)23594065
E-mail: [email protected]
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J Emerg Crit Care Med. Vol. 25, No. 1, 2014
regular follow-up. He denied any history of surgery
or trauma recently. He presented at the ED with
an intermittent fever of up to about 38oC that had
been present since the night previous to this ED
visit. In addition, he had vomited light brown
material twice and a periumbilical pain was also
noted. On arrival at the ED, his vital signs were
a body temperature of 37.9 oC, a blood pressure
of 140/98 mmHg, a heart rate of 54 beats/min
and a respiratory rate of 19 breaths/min. Physical
examination revealed tenderness over periumbilical
region without peritoneal signs. Laboratory
investigation produced a white blood cell count of
7299/μL with 68% of neutrophils and 2% of bands,
C-reaction protein level of 2.44 mg/dL, blood
urea nitrogen level of 34.45 mg/dL and creatinine
level of 1.1 mg/dL. Bedside US showed diffuse
hyperechoic branch-like, streak-like and dotlike foci within the peripheral parenchyma of the
liver, which were compatible with HPVG (Fig. 1).
Based on this clue, we arranged for an abdominal
CT in order to investigate the origin of the HPVG
under the tentative diagnosis of IBD. The CT scan
of abdomen revealed HPVG that was compatible
with the bedside US findings and with IBD of the
terminal ileum with pneumoatosis intestinalis and
poor enhancement of the bowel loops (Fig. 2-4).
The families refused surgical intervention and
aggressive treatment because of the patient’s age.
Unfortunately, the patient expired next day due
to septic shock and multiple organ failure despite
fluid replacement, treatment with a 3rd generation
cephalosporin and intensive care.
Discussion
HPVG is an ominous but rare radiological
and diagnostic sign that usually indicates the
presence of serious intra-abdominal pathology that
will require emergency surgery in the majority of
patients. HPVG was first described by Wolfe JN
in 1955 when treating six infants who died from
necrotizing enterocolitis.(6) The first adult case was
described by Susman N in 1960 in a patient with
IBD (7). The commonest cause of HPVG is IBD.
This is followed by gastrointestinal inflammation,
gastrointestinal dilatation, sepsis, peptic ulcer
disease, iatrogenic injury and trauma, cancer, other
rare causes and being idiopathic in nature (Table 1)
(1,2,4,5,8)
. An early study in 1978 indicated a high
Fig. 1 Bedside US revealed diffuse hyperechoic branch-like, streaklike and dot-like foci (white arrows) within the peripheral
parenchyma of the patient’s liver
Portal venous gas from ischemic bowel disease
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Fig. 2 An axial view of an abdominal CT showing HPVG (white
arrows) within the peripheral parenchyma of liver
Fig. 3 An axial view of an abdominal CT showing ischemic bowel
disease affecting the terminal ileum with pneumoatosis
intesnalis and poor enhancement (white arrows)
mortality rate of 75% to 90% when HPVG was
detected(1,2,9). Recent studies have reported overall
mortality rates of 29% to 39% when HPVG is
found (4,10,11) . This apparent improvement in the
survival rate can be explained by the greater use
and higher sensitivity of now available diagnostic
imaging modalities, such as US and CT scanning,
an increased in the incidence of non-fatal causes of
HPVG and the availability of adequate antibiotic
therapy when treating an intra-abdominal infection.
HPVG is typically identified using plain X-ray,
US or CT. HPVG is predominant within the portal
veins of the non-dependent left lobe and anterior
right lobe(1,2,5,12,13). The first report of HPVG was
described as a plain radiological sign in 1955(6). It
appeared as branching radiolucencies extending
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J Emerg Crit Care Med. Vol. 25, No. 1, 2014
Fig. 4 A coronary view of an abdominal CT showing HPVG (black
arrows) and ischemic bowel disease affecting the terminal
ileum with pneumoatosis intesnalis and poor enhancement
(white arrow)
Table 1 Causes of HPVG
Acute mesenteric ischemia
Gastrointestinal inflammation
Diverticulitis
Inflammatory bowel disease
Gastrointestinal dilatation
Gastric dilatation
Ileus
Mechanical obstruction
Pseudo-obstruction
Sepsis
Intra-abdominal abscess
Septic thrombophlebitis
Peptic ulcer disease
Iatrogenic injury and trauma
Intraperitoneal tumor
Idiopathic disease
Other rare causes
*Data from references 1-5
61%-72%
8%-16%
9%-12%
6%-11%
3%-4%
3%-4%
2%-3%
2%
15%
Portal venous gas from ischemic bowel disease
to the liver periphery. Sensitivity was increased in
the left lateral decubitus view, but these findings
are usually associated with a relatively late stage
of the disease and require a large volume of gas to
have accumulated(9). Thus HPVG on plain X-ray
has been considered to be a poor prognostic sign(13,13)
. On US, HPVG appears as hyperechoic dotlike, streak-like or fruit-pulp-like foci within the
portal veins or liver parenchyma(1,2,8). US is a fast,
low cost, and low radiation modality and also has
the advantage of detecting HPVG in real time
and of offering other clues as to the underlying
diagnosis. US offers comparable accuracy and
sensitivity to a CT scan (1,2,14) . US also offers
dynamic imaging of the centrifugal flow of the
portal gas to the hepatic periphery thus it can be
used to differentiate this from air in the biliary tree
(pneumobilia); furthermore, sensitivity is increased
if color Doppler flow is used(1,2,15). As a result of
the increased use and sensitivity of CT scanning,
HPVG is now diagnosed more frequently. HPVG on
a CT scan appears as branching lucencies within 2
cm of the liver capsule and these are predominantly
present in the anterior-superior aspect of the liver’s
left lobe and the hepatic periphery. HPVG must be
differentiated from pneumobilia. Pneumobilia is
typically visualized as a large confluence of air that
is located within the central portion of the liver and
this air does not extend to within 2 cm of the liver
capsule. The classic description of penumobilia
emphasizes a confluence of air within the common
hepatic duct with branching air densities at the level
of the porta hepatis with a predilection for the left
lobe of liver on the CT scan because of its more
ventral location(1-4,12).
Both US and CT are excellent tests for
detecting HPVG and CT also allows the emergency
physician to determinate the underlying cause(s).
The sensitivity of multi-detector CT (MDCT) in
this context has been markedly increasing over
time from a low of 39% to a current high of
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82%. MDCT has a highly similar sensitivity to
angiography when diagnosing IBD. Nowadays,
with the development of high-resolution advanced
imaging, it is possible to demonstrate potentially
severe pathologies at an early stage, which opens
up the possibility of prompt treatment and a
significantly reduced mortality rate (1,2) . Early
detection of HPVG and the identification of the
underlying diagnosis have facilitated timely and
targeted treatment. In addition, bedside US is able
to provide real-time imaging as well as other clues
that help the diagnosis. CT scan is able to detect
minimal HPVG and allows determination of the
precipitating etiology.
A HPVG management algorithm has been
proposed (12,14). The management of patients with
HPVG can be divided into three groups. For the
first group, urgent laparotomy is recommended
when patients have clinical or radiological signs
of bowel ischemia and the presence of HPVG has
been detected by plain abdominal radiography;
this is because previous studies have reported a
mortality rate of 75% to 90% for this group(1-4).
The second group consist of patients with
HPVG and an equivocal clinical condition with
the absence of peritonitis or bowel perforation;
this patients include those with gastrointestinal
inflammation, gastrointestinal dilatation, sepsis,
mucosal disruption and peptic ulcer disease. They
should be closely monitored with a low threshold
of surgical intervention; the risk of mortality for
these patients is 20% to 30%(4,9). They need to be
treated with a combination of intravenous fluid,
broad spectrum antibiotics, close observation and
no oral intake as well as nasogastric decompression
when required(2,12,14). The third group of patients
with HPVG are those with non-urgent conditions
or other benign causes of HPVG; these should be
managed conservatively and with watchful waiting.
The length of time to the disappearance of such
non-urgent HPVG is very variable and can be from
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J Emerg Crit Care Med. Vol. 25, No. 1, 2014
minutes to six weeks(16,17). These patients have a
negligible risk of mortality (about 0 %)(12,14).
Finally, HPVG is not a specific presentation,
but it is an important diagnostic sign and clue in
patients with an acute abdomen. In terms of realtime imaging capability, US can be a very valuable
imaging modality when evaluating HPVG and can
also provide additional clues to the emergency
physician in terms of underlying diagnosis. CT is
a diagnostic modality that is also able to disclose
the precipitating etiology. HPVG is not by itself
a surgical indication and management of HPVG
depends mainly on the underlying disease.
References
1.Abboud B, El Hachem J, Yazbeck T, Doumit
C. Hepatic portal venous gas: physiopathology,
etiology, prognosis and treatment. World J
Gastroenterol 2009;15:3585-90.
2.Hussain A, Mahmood H, El-Hasani S. Portal
vein gas in emergency surgery. World J Emerg
Surg 2008;3:21.
3.Peloponissios N, Halkic N, Pugnale M, et al.
Hepatic portal gas in adults: review of the
literature and presentation of a consecutive
series of 11 cases. Arch Surg 2003;138:136770.
4.Kinoshita H, Shinozaki M, Tanimura H, et al.
Clinical features and management of hepatic
portal venous gas: Four case reports and
cumulative review of the literature. Arch Surg
2001;136:1410-4.
5. S e b a s t i à C, Q u i r o g a S, E s p i n E, B o y é
R, A l v a r e z-C a s t e l l s A, A r m e n g o l M.
P o r t o m e s e n t e r i c v e i n g a s: p a t h o l o g i c
mechanisms, CT findings, and prognosis.
Radiographics. 2000;20:1213-24.
6.Wolfe JN, Evans WA. Gas in the portal veins
of the liver in infants; a roentgenographic
demonstration with postmortem anatomical
correlation. Am J Roentgenol Radium Ther
Nucl Med 1955;74:486-8.
7.Susman N, Senturia HR. Gas embolization of
the portal venous system. Am J Roentgenol
Radium Ther Nucl Med 1960;83:847-50.
8.Hussain A, Mahmood H, El-Hasni S. Portal
vein gas in emergency survey. World J Emerg
Surg 2008;3:21.
9.Liebman PR, Patten MT, Manny J, Benfield JR,
Hechtman HB. Hepatic–portal venous gas in
adults: Etiology, pathophysiology and clinical
significance. Ann Surg 1978;187:281-7.
10. Iannitti DA, Gregg SC, Mayo-Smith WW,
Tomolonis RJ, Cioffi WG, Pricolo VE. Portal
venous gas detected by computed tomography:
Is surgery imperative? Dig Surg 2003;20:30615.
11. Faberman RS, Mayo-Smith WW. Outcome of
17 patients with portal venous gas detected by
CT. AJR Am J Roentgenol 1997;169:1535-8.
12. Alqahtani S, Coffin CS, Burak K, Chen F,
MacGregor J, Beck P. Hepatic portal venous
gas: a report of two cases and a review of the
epidemiology, pathogenesis, diagnosis and
approach to management. Can J Gastroenterol
2007;21:309-13.
13. Schindera ST, Triller J, Vock P, Hoppe H.
Detection of hepatic portal venous gas: its
clinical impact and outcome. Emerg Radiol
2006;12:164-70.
14. Nelson AL, Millington TM, Sahani D, et
al. Hepatic portal venous gas: the ABCs of
management. Arch Surg 2009;144:575-81.
15. Yarze JC, Markowitz DM. Distinguishing
between hepatic portal vein gas and
pneumo(aero)bilia. Liver Transpl 2007;13:1476.
16.Griffiths DM, Gough MH. Gas in the hepatic
portal veins. Br J Surg 1986;73:172-6.
17.Huurman VA, Visser LG, Steens SC, Terpstra
OT, Schaapherder AF. Persistent portal venous
gas. J Gastrointest Surg 2006;10:783-5.
肝門靜脈氣體由缺血性腸病變而來
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經超音波偵測到由缺血性腸病變而來的
肝門靜脈氣體：一病例報告及文獻回顧
趙志中1　胡松原2,3,4,5,6　陳永福1,4
肝門靜脈空氣是一個罕見且預後不好的影像學發現，它對於急性腹痛的病人是一個重要的診斷線
索。肝門靜脈空氣的確切原因診斷和處置對於臨床醫師是一個挑戰。最常見及最嚴重的原因是缺血性腸
病變。在此，我們報告一例藉由超音波上罕見且典型肝門靜脈空氣影像而發現的缺血性腸病變。
關鍵詞： 缺血性腸病變，肝門靜脈氣體，超音波
收件：103年12月15日　接受刊載：103年12月29日
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4
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