Pylephlebitis: An overview of non-cirrhotic cases and factors related to outcome

Abstract

Pylephlebitis is a condition with significant morbidity and mortality. We review herein 100 relevant case reports published since 1971. Eighty-one patients were reported with acute pylephlebitis, while the remaining patients had chronic pylephlebitis. The most common predisposing infections leading to pylephlebitis were diverticulitis and appendicitis. Cultures from blood or other tissues were positive in 77%. The infection was polymicrobial in half of the patients and the most common isolates were Bacteroides spp, Escherichia coli and Streptococcus spp. Thrombosis was extended to the superior mesenteric vein (SMV), splenic vein, and intrahepatic branches of the portal vein (PV) in 42%, 12%, and 39%, respectively. Antibiotics were administered in all and anticoagulation in 35 cases. Patients who received anticoagulation had a favourable outcome compared to those who received antibiotics alone (complete recanalization 25.7% vs 14.8% (p > 0.05), no recanalization 5.7% vs 22.2% (p < 0.05), and death 5.7% vs 22.2% (p < 0.01)). Cases with complete recanalization had prompt diagnosis and management and two-thirds were recently published. Nineteen patients died; the majority of these (73.7%) died over the period 1971-1990. In conclusion, pylephlebitis remains an entity with high morbidity and mortality, but modern imaging modalities have facilitated an earlier diagnosis and have improved the prognosis. Anticoagulation has a rather beneficial effect on patients with pylephlebitis.

Full text

This article was downloaded by: [Alexandra Alexopoulou]
On: 15 August 2015, At: 09:06
Publisher: Taylor & Francis
Informa Ltd Registered in England and Wales Registered Number: 1072954 Registered office: 5 Howick Place,
London, SW1P 1WG
Scandinavian Journal of Infectious Diseases
Publication details, including instructions for authors and subscription information:
http://www.tandfonline.com/loi/infd19
Pylephlebitis: An overview of non-cirrhotic cases and
factors related to outcome
Theoni Kanellopouloua, Alexandra Alexopouloua, George Theodossiadesb, John Koskinasa &
Athanasios J. Archimandritisa
a Second Department of Medicine, Medical School, University of Athens, Hippokration
Hospital, Athens, Greece
b First Regional Transfusion and Haemophilia Centre, Hippokration Hospital, Athens, Greece
Published online: 08 Jun 2010.
To cite this article: Theoni Kanellopoulou, Alexandra Alexopoulou, George Theodossiades, John Koskinas & Athanasios J.
Archimandritis (2010) Pylephlebitis: An overview of non-cirrhotic cases and factors related to outcome, Scandinavian Journal
of Infectious Diseases, 42:11-12, 804-811
To link to this article: http://dx.doi.org/10.3109/00365548.2010.508464
PLEASE SCROLL DOWN FOR ARTICLE
Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained
in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no
representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the
Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and
are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and
should be independently verified with primary sources of information. Taylor and Francis shall not be liable for
any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever
or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of
the Content.
This article may be used for research, teaching, and private study purposes. Any substantial or systematic
reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any
form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http://
www.tandfonline.com/page/terms-and-conditions

†
Deceased.
Correspondence: A. Alexopoulou, 40 Konstantinoupoleos St, 16342 Hilioupolis, Athens, Greece. Tel: ⫹ 30 210 7774742. Fax: ⫹ 30 210 7706871.
E-mail: alexopou@ath.forthnet.gr
(Rece ived 30 Mar ch 2010; ac cepted 27 J une 2010)
Introduction
Pylephlebitis begins with thrombophlebitis of small
veins draining an area of any intra-abdominal or pel-
vic infection [1]. Thrombophlebitis may extend into
larger veins leading to septic thrombophlebitis of the
portal vein (PV) and occasionally extending further
to involve the superior mesenteric vein (SMV). The
risk of thrombosis is particularly high when patients
develop sepsis leading to disseminated intravascular
coagulation (DIC) [2]. The appropriate diagnosis and
management of pylephlebitis depends on a high
degree of clinical suspicion, the use of imaging stud-
ies, and early initiation of empiric antibacterial ther-
apy combined with anticoagulant therapy [1]. PV
thrombosis (PVT) is an increasingly recognized dis-
order, due to an increased use of and improvements
in non-invasive imaging techniques for the diagnostic
evaluation of abdominal pain [3,4].
Literature review
We identifi ed all relevant English language case
reports by a MEDLINE search for the period July
1971 to December 2009 using the terms ‘ pylephle-
bitis ’ , ‘ septic thrombosis of the PV ’ , ‘ septic throm-
bophlebitis of the PV ’ , ‘ pylethrombosis ’ , ‘ infectious
thrombosis of the PV ’ and ‘ suppurative thrombosis
of the PV ’ . We also reviewed the reference lists of
original articles. We did not include cases that had
inadequate clinical or laboratory/microbiological
information for the diagnosis and course of pyl-
ephlebitis. In addition, cases of pylephlebitis with a
cirrhotic background were excluded. We did not
include any case series of PVT of various aetiologies,
where individual data of cases with pylephlebitis
were not available. We abstracted patient demograph-
ics, predisposing factors, microbiological studies,
the method of diagnosis, treatment, and outcome.
REVIEW ARTICLE
Pylephlebitis: An overview of non-cirrhotic cases and factors
related to outcome
THEONI KANELLOPOULOU
1 , ALEXANDRA ALEXOPOULOU
1 ,
GEORGE THEODOSSIADES
2 , JOHN KOSKINAS
1 &
ATHANASIOS J. ARCHIMANDRITIS
1 †
From the
1 Second Department of Medicine, Medical School, University of Athens, Hippokration Hospital, Athens, Greece, and
2 First Regional Transfusion and Haemophilia Centre, Hippokration Hospital, Athens, Greece
Abstract
Pylephlebitis is a condition with signifi cant morbidity and mortality. We review herein 100 relevant case reports published
since 1971. Eighty-one patients were reported with acute pylephlebitis, while the remaining patients had chronic pylephle-
bitis. The most common predisposing infections leading to pylephlebitis were diverticulitis and appendicitis. Cultures from
blood or other tissues were positive in 77%. The infection was polymicrobial in half of the patients and the most common
isolates were Bacteroides spp, Escherichia coli and Streptococcus spp. Thrombosis was extended to the superior mesenteric
vein (SMV), splenic vein, and intrahepatic branches of the portal vein (PV) in 42%, 12%, and 39%, respectively. Antibiot-
ics were administered in all and anticoagulation in 35 cases. Patients who received anticoagulation had a favourable outcome
compared to those who received antibiotics alone (complete recanalization 25.7% vs 14.8% ( p ⬎ 0.05), no recanalization
5.7% vs 22.2% ( p ⬍ 0.05), and death 5.7% vs 22.2% ( p ⬍ 0.01)). Cases with complete recanalization had prompt diag-
nosis and management and two-thirds were recently published. Nineteen patients died; the majority of these (73.7%) died
over the period 1971 – 1990. In conclusion, pylephlebitis remains an entity with high morbidity and mortality, but modern
imaging modalities have facilitated an earlier diagnosis and have improved the prognosis. Anticoagulation has a rather
benefi cial effect on patients with pylephlebitis.
Scandinavian Journal of Infectious Diseases, 2010; 42: 804–811
ISSN 0 036-5548 pri nt/ ISSN 1651-1980 onli ne © 2010 Infor ma Hea lthca re
DOI : 10.3109 / 003655 48 .2010.50 84 64
Downloaded by [Alexandra Alexopoulou] at 09:06 15 August 2015

Pylephlebitis: A literature review 805
One hundred cases of pylephlebitis were found: 9
cases from 1971 to 1980, 18 cases from 1981 to
1990, 22 cases from 1991 to 2000, and 51 cases from
2001 to date. The Chi-square test was used to com-
pare categorical data.
Results
Clinical presentation
The age range was 20 days to 77 y (mean 42.3 y)
and 24% of the cases were paediatric ( ⱕ 18 y) [5 – 24].
Most of the affected individuals (68%) were males.
The condition was considered acute if symptoms
developed less than 60 days prior to hospital assess-
ment and there was no evidence of porto-systemic
collaterals and cavernomatous formation of the por-
tal vein [25]. Eighty-one patients (81%) presented
with acute pylephlebitis.
The most common presenting symptoms were
fever in 86% and abdominal pain in 82%. Symptoms
on admission are shown in Table I. Physical fi ndings
disclosed splenomegaly in 23% [5,17,20,23,26 – 34],
hepatomegaly in 42% [5,11,13,14,20,24,26,28,31,
32,34 – 42], and transient or persistent ascites in 20.5%
of instances [7,10,14,15,17,24,32,33,39,42 – 48].
Regarding laboratory tests, leukocytosis was a
common fi nding (80% of cases). Liver enzyme values
were stated in 67 cases and disclosed an elevation
of aspartate aminotransferase (AST) and/or alanine
aminotransferase (ALT) levels in 69%, an increase
of alkaline phosphatase (ALP) and/or gamma-
glutamyl transpeptidase (GGT) levels in 40%, an
increase of total bilirubin in 55%, and anaemia in
55% of cases.
Aetiology
The most common intra-abdominal infl ammatory
conditions leading to pylephlebitis were diverticulitis
(30%) [26 – 28,30,33,34,37,38,42,43,45,47 – 62] and
appendicitis (19%) [5,6,8,10,12,14 – 17,22,23,31,40,
41,46,60,63 – 65], followed by infl ammatory bowel
disease (6%) [20,21,39,44,66,67] and pancreatitis
(5%) [60,68 – 71] (Table II). Past or concomitant
medical conditions possibly related to the develop-
ment of pylephlebitis are shown in Table III. Remote
abdominal surgery (performed beyond 6 months
prior to reported admission) was reported in 18%
[11,28,30,31,35,38,42,53,66,67,69,72 – 77], whereas
a recent abdominal procedure (performed within
30 days prior to the diagnosis of pylephlebitis) was
reported in 19% of patients [22,31,33,36,41,42,
51,56,60,61,63,65,75,77 – 81]. In neonates, pyle-
phlebitis was attributed to umbilical vein cannu-
lation or umbilical sepsis in 80% of reported cases
[11,19,24].
A thrombophilic disorder was searched for in
30 patients only and was identifi ed in 11 [9,22,23,
29,34 – 36,40,54,74,80]. Malignancy possibly related
to thrombophilia was present in 6 cases [22,34 – 36,
74,80] (Table IV) and none had a medical history
of myeloproliferative disease.
A microorganism was yielded from blood culture
exclusively in 36 cases (42%) [10,11,15,16,23,26 –
29,31,35,37,40,41,43,46 – 50,52,56,58,62,64,
73 – 75,77,80 – 85], both from blood and other tissue
samples in 22 (26%) [7,30,33,34,36,38,44,48,54,
57,58,61,66,71,72,77,87 – 89], from liver abscesses or
portal vein aspiration in 13 (16%) [9,18,32,34,42,53,
59,68,69,90], and from samples other than blood in 6
patients (7%) [11,20,39,67,76,78]. No microorgan-
ism was yielded in 8 (9%) [6,9,21,24,45,63,70,91]
and there was no information about microbiological
studies for the remaining 15 subjects [5,8,12,19,22,
51,55,60,65,92,93].
Table II. Aetiology of pylephlebitis.
Local cause n (%)
Diverticulitis 30 (30%)
Appendicitis 19 (19%)
Infl ammatory bowel disease 6 (6%)
Pancreatitis 5 (5%)
Gastroenteritis 4 (4%)
Umbilical vein catheter 3 (3%)
Cholangitis 3 (3%)
Gastric/duodenal ulcer 2 (2%)
Liver abscesses 2 (2%)
Amoebiasis 2 (2%)
Evidence of intra-abdominal sepsis 3 (15%)
Aetiologies with only 1 observation
a 15 (15%)
Unrecognized cause 6 (6%)
Total 100
a Aetiologies with only 1 obser vation: umbilical sepsis; emphy-
sematous gastritis; intragastric migration of an adjustable gastric
band; percutaneous liver biopsy; acute or chronic hepatic artery
obstruction; subcapsular haematoma of the liver; toothpick
perforation and migration; necrotic segment of distal small bowel;
necrotic splenic fl exure carcinoma; incarcerated incisional
abdominal hernia; intestinal ischemia; peripancreatic ligamental
abscess; Fusobacterium necrophorum septicaemia; urinary
infection; Beh ç et ’ s disease (underlying arteritis).
Table I. Symptoms on admission.
Symptom n (%)
Fatigue/exhaustion/malaise 95 (95%)
Fever 86 (86%)
Abdominal pain 82 (82%)
Vomiting/nausea 28 (28%)
Diarrhoea 27 (27%)
Anorexia/weight loss 19 (19%)
Lethargy/confusion 8 (8%)
Apnoea/wheezing 4 (4%)
Myalgia/arthralgia 4 (4%)
Downloaded by [Alexandra Alexopoulou] at 09:06 15 August 2015

806 T. K a n ellop o u lou et al.
( n ⫽ 1) [31], and endoscopic ultrasonography
( n ⫽ 1) [45]. The mode of diagnosis was not stated
in 1 case [58].
In 56 (56%) subjects, the diagnosis of PVT was
made during the fi rst 7 days following admission,
while in the remaining subjects the diagnosis was
delayed.
Complications
Extension of thrombosis to the SMV was described
in 42% [5,7,8,10,14 – 18,20,21,23,26 – 30,33,37,39,
43,45 – 48,53,54,57,58,62 – 64,66,67,70,71,83 – 87,93]
and to the splenic vein in 12% [14,17,23,27,31,3
4,47,68,69,71,85,88]. Thrombosis of the intrahe-
patic branches of the PV was disclosed in 39% [6 – 8,
11,14 – 24, 30,33,34,36,38,42,43,45,48,52,53,55,58,59,
61,67 – 70,74,76,78,80 – 82,85,87,89] and thrombosis
of the inferior mesenteric vein in 2% [34,49]. Intra-
portal gas was visualized in 18% [35,37,43,44,48,
50,51,56 – 58,62,67 – 70,75,80,86] and there was co-
existence of liver abscesses in 37% [6,9,10,12 – 14,
20,22,24,28,30 – 32,34,41,42,45,46,48,53,54,
57,58,60,61,66,68,69,72,81,87,89] of subjects. Ten
patients had evidence of bowel ischemia on CT
scans, all of whom had thrombosis of the SMV [15,
44,51,54,60,62,65,80,85,91].
Table IV. Thrombophilic disorders possibly related to pylephlebitis.
Thrombophilic disorder n
Malignancies
a 6
Protein S defi ciency 1
Anti-thrombin III and protein C defi ciency 1
Factor XII defi ciency 1
Transient positivity of anti-cardiolipin antibodies 1
Oral contraceptives 1
No thrombotic predisposing disorder found 19
No data 70
a Colon cancer (1); acute lymphocytic leukaemia (1); adeno-
carcinoma (1), VIPoma (1); hepatocellular carcinoma (1); breast
cancer (1).
Table III. Conditions possibly related to pylephlebitis.
Medical condition n
Recent abdominal surgical procedure 19
Remote abdominal surgery 18
Immunosuppression (immunosuppressive drugs,
rheumatological conditions, other) 14
Chronic pancreatitis 5
Malignancy (solid tumours/haematological
malignancies) 6
Infl ammatory bowel disease 6
Alcoholism 8
Viral hepatitis 3
Other 3
A single microorganism was recovered in 40
(47%) [9 – 11,13,18,23,26 – 31,33,37,40,42,46,48,49,
52,53,56,64,67,68,71,73 – 77,81 – 83,85,88], 2 – 3 bac-
teria in 26 (31%) [7,15 – 17,32,34,36,38,39,43,44,
48,50,54,58,59,62,66,69,72,79,80,84,89], and more
than 3 in 11 (13%) [14,25,34,35,41,47,57,58,61,
78,86,87,90] instances. Table V shows the microor-
ganisms involved in pylephlebitis. The most common
was Bacteroides fragilis, following by Escherichia
coli and Streptococcus spp.
Diagnosis
The diagnosis of PVT was made exclusively by ultra-
sonography (US) in 12 and by computed tomogra-
phy (CT) scan in 28 cases. In 23 further cases both
methods were used for diagnosis. The diagnosis was
made by autopsy study in 16 cases (16%) [30,32,
34,42,48,59 – 61,68,75,81,90,92], 11 of which were
reported over the period 1971 – 1985 [30,32,34,42,
59 – 61,81]. The remaining were diagnosed during a
surgical procedure ( n ⫽ 8) [22,41,56,62,64,65,68,80],
by angiography ( n ⫽ 4) [33,60,71,87], magnetic
resonance imaging of the abdomen ( n ⫽ 3) [6,51,77],
positron emission tomography/CT scan ( n ⫽ 2)
[35,90], liver biopsy confi rmed later by autopsy
( n ⫽ 1) [78], Tc-99m confi rmed later by angiography
Table V. Microorganisms involved in pylephlebitis.
Type of microorganism n
Anaerobes
Bacteroides spp. 27
Clostridium spp. 11
Fusobacterium spp. 7
Peptostreptococcus spp. 5
Lactobacillus spp. 1
Propionibacterium acnes 1
Eubacterium spp. 2
Bifi dobacterium spp. 1
Aerobic bacteria
Gram-positive cocci
Streptococcus spp. 17
Staphylococcus spp. 5
Enterococcus spp. 2
Gram-negative bacilli
Escherichia coli 22
Pseudomonas aeruginosa 4
Klebsiella spp. 5
Proteus spp. 5
Eikenella corrodens 1
Acinetobacter spp. 1
Campylobacter jejuni 1
Shigella spp. 1
Corynebacterium spp. 1
Aeromonas hydrophila 1
Aerobacter aerogenes 1
Fungi
Candida spp. 7
Downloaded by [Alexandra Alexopoulou] at 09:06 15 August 2015

Pylephlebitis: A literature review 807
Outcome
The mortality rate was high since 19 patients died
(19%) [30,32,34,42,48,50,59 – 61,67,75,78,81,90,93].
Fourteen patients (73.7%) died over the period
1971 – 1990 and 5 patients (26.3%) over 1991 – 2009.
The average age was 60.1 y, and all were adults. Their
concomitant medical conditions included diabetes
mellitus [30,34,48], liver transplantation [75],
chronic renal failure [50], severe burn [91], breast
cancer [34], Crohn ’ s disease [67], alcohol abuse
[30,32,61,78], and remote abdominal operation
[30,42,67,75]. Seven patients died during the fi rst
week of hospitalization [30,32,34,48,75,92]. All the
patients who died were diagnosed to have acute
PVT. The cause of pylephlebitis was diverticulitis in
47% of cases (9 patients) [30,34,42,48,50,59 – 61].
Imaging studies and autopsy revealed SMV in
2 (10.5%) [30,67] and extension of thrombosis to
intrahepatic branches in 8 (42%) [30,34,42,59,61,
67 – 78,81] and to the splenic vein in 1 case [34].
Intraportal gas was observed in 3 (16%) [50,67,75],
liver abscesses in 8 (42%) [30,32,34,42,48,61,81],
and bowel ischemia in 2 cases (10.5%) [60,81].
Sepsis was the cause of death in most of the cases
[30,34,48,50,59,61,67,75,78], followed by peritoni-
tis [34,42,60], liver failure [32,90], bowel ischemia
[60,81], intestinal bleeding [78], and rupture of the
PV [92].
Outcome in relation to anticoagulation treatment
In the group of patients with a fatal outcome, 1
patient died at admission without any treatment [92]
and 11 were treated with antibiotics alone [30,32,
34,42,48,59,61,75,78,81,90,92], while anticoagula-
tion plus antibiotics was administered in 2 patients
[34,50]. For 5 patients who died there was no infor-
mation on whether anticoagulation was administered
or not [60,67].
Thirty-fi ve patients were treated with anticoagu-
lation and antibiotics (Table VI) [5,7,8,10,12,14 – 17,
19,20,27,28,37,38,40,43,45,47,48,50,52 – 55,58,
63,66,73,74,77,83,84]. Six (17.1%) patients had
chronic PVT at presentation [7,14,17,20,64,77]. On
admission, thrombosis of the SMV was observed in
23 (65.7%) [5,7,8,10,14 – 17,20,27,37,43,45,47,53,
54,58,63,64,66,77,83,84], and 2 of them (5.7%)
also had bowel ischemia [15,54]. Complete resolu-
tion of the thrombus was observed in 9 cases (25.7%)
[5,10,12,15,37,52,54,55,84]. No resolution was
observed in 2 patients who later died [34,50] and
improvement was observed in 23 cases (65.7%) [7,8,
14,16,17,20,27,28,38,40,43,45,47,49,53,58,
63,64,66,73,74,77,84,86]. Two patients (5.7%)
developed portal hypertension.
Treatment
During hospitalization, 47 patients underwent an
open surgical procedure due to the disease causing
pylephlebitis (appendicitis, diverticulitis, etc.). Nine-
teen were operated on prior to the diagnosis of
pylephlebitis and 28 following the diagnosis.
Antibiotics were used in all cases. Usually a com-
bination of antibiotics was used on admission as
empirical therapy, followed by a change in antibiotic
scheme targeted to the microorganism isolated from
culture. Intraportal antibiotics were administered in
2 patients [33,38]. Aspiration and drainage of pus
was performed in 6 patients [18,24,38,68,69,71],
whereas an interventional procedure (thrombectomy
in 3, aorta – superior mesenteric artery bypass in 1)
was attempted in 4 patients [10,19,87,93]. Systemic
fi brinolytic drugs were administered in 5 cases [7,18,
26,38,89] and in 1 further case intraportal fi brin-
olysis was performed [87]. Anticoagulation treat-
ment was administered after fi brinolytic treatment
in 2 patients [7,38] and aspirin in 1 [26].
Anticoagulation treatment was administered in
35 cases [5,7,8,10,12,14 – 17,19,20,27,28,34,37,38,
40,43,45,47,49,50,52 – 55,58,63,64,66,73,74,
77,83,84]. Parenteral treatment (unfractionated hep-
arin or low molecular weight heparin) was given ini-
tially to 29 patients [5,7,8,10,14,17,19,20,34,37,
38,40,43,47,49,52 – 55,63,64,66,73,74,77,82,84],
followed by oral treatment with vitamin K antago-
nists in 20 cases [5,8,10,14,17,20,34,37,47,49,52 – 54,
63,64,73,74,77,82,84], while in the remaining 6 (out
of 35) only oral anticoagulation treatment was
administered [12,15,16,45,50,86]. The course of the
disease (recanalization, improvement or no recana-
lization) was available for 89 patients who were
followed-up (Table VI).
Table VI. Outcome in patients who received anticoagulation
compared to those who did not.
Anticoagulation
Yes ( n ⫽ 35) No ( n ⫽ 54) p -Value
Acute pylephlebitis 29 (88.9%) 50 (92.5%) NS
Chronic pylephlebitis 6 (17.1%) 4 (7.4%) NS
Superior mesenteric vein
thrombosis 23 (65.7%)
a 16 (29.6%)
b p ⬍ 0.01
Complete recanalization 9 (25.7%) 8 (14.8%) NS
No recanalization 2 (5.7%) 12 (22.2%) p ⬍ 0.05
Development of portal
hypertension 2 (5.7%) 6 (11.1%)
c NS
Death 2 (5.7%) 12 (22.2%) p ⬍ 0.01
Improvement 23 (65.7%) 34 (62.9%) NS
NS, not signifi cant.
a Two patients experienced bowel ischemia.
b Five patients experienced bowel ischemia.
c Three patients already had gastric/oesophageal varices on
admission.
Downloaded by [Alexandra Alexopoulou] at 09:06 15 August 2015

808 T. K a n ellop o u l ou et al.
imaging methods demonstrating thrombus in the
PV with or without associated mesenteric vein
thrombus. Intraportal gas was not rare, occurring in
about a sixth of instances. In more than half of cases
(56%) the diagnosis was made during the fi rst week
of hospitalization. In the remaining cases, the diag-
nosis was delayed. Diagnosis was usually delayed
because pylephlebitis, as an uncommon condition,
was not considered a possible diagnosis and therefore
was not thoroughly investigated; or probably because
clinical signs and symptoms of portal vein thrombo-
sis were not specifi c and the portal vein was poorly
visualized.
Regarding aetiology, the most common inciting
infection associated with pylephlebitis was diverticu-
litis, which occurred in one third of the cases. Appen-
dicitis, cholecystitis and cholangitis, which were the
most common foci in some case series in the litera-
ture [94], were less frequent. Infl ammatory bowel
disease was revealed to be the predisposing factor in
a small proportion of cases. Bacteraemia occurred in
about 60% of cases, while cultures from blood or
other tissue samples were positive in 77%. The infec-
tion was polymicrobial in half of the instances and
the most common isolates were B. fragilis, E. coli and
Streptococcus spp. These fi ndings of the polymicro-
bial nature of infection and the isolated bacteria
Bacteroides spp. and E. coli are similar to those
reported in other series [84]. However, it is impor-
tant to note that Gram-positive bacteria, and par-
ticularly Streptococcus spp., were demonstrated to
be among the most common isolates.
There is a potential pathogenetic role of pro-
thrombotic alterations during invasive bacterial
infections [2]. A complication such as DIC has been
observed in patients with bacteraemia from Gram-
positive cocci and recent studies have indicated
platelets to play an important role in endotoxin-
induced DIC releasing antimicrobial proteins [2]. A
strong link between B. fragilis infection and PVT has
been demonstrated possibly because of the transient
development of anti-cardiolipin antibodies [54,77,95].
A more thorough study of the pathogenetic role of
bacteria in PVT is needed.
A possible underlying thrombophilic disorder
was not investigated in two thirds of case reports.
Bone marrow aspiration was not performed in most
of the patients to exclude underlying myeloprolifera-
tive disease, and the presence of the JAK2V617F
mutation was not tested. These results probably
underestimate the prevalence of an underlying
thrombophilic disorder [96].
Pylephlebitis is an entity with high morbidity
and mortality. We have shown that about one fi fth
of patients described in case reports had a fatal
outcome. The most common complications were
Fifty-four patients were treated with antibiotics
without anticoagulation. Chronic PVT at presenta-
tion occurred in 4 cases (7.4%) [9,13,31,71,87,88].
On admission, thrombosis of the SMV was observed
in 16 cases (29.6%) [18,21,26,29,30,33,39,46,48,
57,58,70,71,85,87] and bowel ischemia in 2 (9.3%)
[88]. During follow-up, complete recanalization
was reported in 8 patients (14.8%) [6,21,22,26,35,
48,77,85], whereas there was no recanalization
in 12 (22.2%) [30,32,34,42,48,59,61,75,78,80,90].
However, improvement was recognized in 34 cases
(62.9%) [9,11,13,18,29,31,33,36,41,44,46,51,56 – 58,
68 – 72,77,79,82,87 – 90]. Portal cavernoma forma-
tion was stated in 9 patients (16.7%) [11,13,18,
24,29,68,69,87] (2 had carvernoma on admission
[13,87]). Portal hypertension was stated in 6 patients
(11.1%) [9,11,24,31,71] (3 already had gastric/
oesophageal varices on admission [9,31,71]). No
patient with endoscopic fi ndings of varices had any
episode of bleeding. Comparison of the 2 groups,
with and without anticoagulation, showed a favour-
able outcome for the former (Table VI).
Analysis of the cases with complete recanalization
(18 cases) [5 – 6,10,12,15,21 – 23,26,35,37,48,52,54,
55,76,84,85] showed that all cases were reported
after 1986 and that 66.7% were from 2001 onwards
[5,6,10,12,15,26,35,37,52,54,55]. Ten patients were
adults and 8 were children [5,6,10,12,15,21 – 23].
The disease was diagnosed promptly following
admission (mean time to diagnosis 2.8 days). Seven
patients had appendicitis as the underlying focus
of infection [5,6,10,12,15,22,23], 6 diverticulitis
[26,37,48,52,54,55], 2 gastric ulcers [35,85], and
the remaining 3 various aetiologies. The disease was
rather severe, since 11 of them had thrombosis of the
SMV (61%) [5,10,15,21,23,26,37,48,54,84,85] and
7 had liver abscesses (39%) [6,10,12,22,48,54].
Discussion
Analysis of 100 case reports in the literature demon-
strated that pylephlebitis may present at any age,
from neonates to adults. The clinical manifestations
of pylephlebitis were non-specifi c and most patients
experienced abdominal pain and fever. Laboratory
tests were also non-specifi c and the most common
fi ndings were leukocytosis, anaemia and abnormal
liver function tests.
Most of the case reports described patients
diagnosed in recent years as a result of newer more
sensitive imaging techniques. It is of note that the
number of cases reported during the last decade was
equal to that reported in the previous 3 decades.
In addition, it is evident that before 1985, an impor-
tant number of cases were diagnosed by autopsy.
Ultrasound and CT were the most frequently used
Downloaded by [Alexandra Alexopoulou] at 09:06 15 August 2015

Pylephlebitis: A literature review 809
Declaration of interest: No confl ict of interest.
No fi nancial support was received.
References
Chirinos JA, Garcia J, Alcaide ML, Toledo G, Baracco GJ, [1]
Lichtstein DM. Septic thrombophlebitis: diagnosis and
management. Am J Cardiovasc Drugs 2006;6:9 – 14.
Sj ö bring U, Ringdahl U, Ruggeri ZM. Induction of platelet [2]
thrombi by bacteria and antibodies. Blood 2002;100:
4470 – 7.
Kocher G, Himmelmann A. Portal vein thrombosis (PVT): [3]
a study of 20 noncirrhotic cases. Swiss Med Wkly 2005;
135:372 – 6.
Wang JT, Zhao HY, Liu YL. Portal vein thrombosis. Hepa-[4]
tobiliary Pancreat Dis Int 2005;4:515 – 8.
Levin C, Koren A, Miron D, Lumelsky D, Nussinson E, [5]
Siplovich L, et al. Pylephlebitis due to perforated appendici-
tis in a teenager. Eur J Pediatr 2009;168:633 – 5.
Patel AJ, Ong PV, Higgins JP, Kerner JA. Liver abscesses, [6]
pylephlebitis, and appendicitis in an adolescent male. Dig
Dis Sci 2009 Jul 2. [Epub ahead of print].
Bogue CO, Leahy TR, Rea DJ, Bitnun A, Brandao LR, [7]
Kahr WH, et al. Idiopathic suppurative pylephlebitis: inter-
ventional radiological diagnosis and management. Cardio-
vasc Intervent Radiol 2009;32:1304 – 7.
Stitzenberg KB, Piehl MD, Monahan PE, Phillips JD. [8]
Interval laparoscopic appendectomy for appendicitis compli-
cated by pylephlebitis. JSLS 2006;10:108 – 13.
Muorah M, Hinds R, Verma A, Yu D, Samyn M, Mieli-[9]
Vergani G, et al. Liver abscesses in children: a single center
experience in the developed world. J Pediatr Gastroenterol
Nutr 2006;42:201 – 6.
Nishimori H, Ezoe E, Ura H, Imaizumi H, Meguro M, [10]
Furuhata T, et al. Septic thrombophlebitis of the portal and
superior mesenteric veins as a complication of appendicitis:
report of a case. Surg Today 2004;34:173 – 6.
Pacifi co L, Panero A, Colarizi P, Matrunola M, Simonetti [11]
AF, Chiesa C. Neonatal Candida albicans septic thrombosis
of the portal vein followed by cavernous transformation of
the vessel. J Clin Microbiol 2004;42:4379 – 82.
Pitcher R, McKenzie C. Simultaneous ultrasound identi-[12]
fi cation of acute appendicitis, septic thrombophlebitis of the
portal vein and pyogenic liver abscess. S Afr Med J 2003;
93:426 – 8.
Aggarwal S, Mathur NB, Garg A. Portal vein thrombosis [13]
complicating neonatal hepatic abscess. Indian Pediatr 2003;
40:997 – 1001.
Chang TN, Tang L, Keller K, Harrison MR, Farmer DL, [14]
Albanese CT. Pylephlebitis, portal-mesenteric thrombosis,
and multiple liver abscesses owing to perforated appendicitis.
J Pediatr Surg 2001;36:E19.
Vanamo K, Kiekara O. Pylephlebitis after appendicitis in a [15]
child. J Pediatr Surg 2001;36:1574 – 6.
Pohl JF, Murarka P, Farrell MK, Bezerra J. Insights. Pyle-[16]
phlebitis. J Pediatr 1999;135:529.
Kader HA, Baldassano RN, Harty MP, Nicotra JJ, von [17]
Allmen D, Finn L, et al. Ruptured retrocecal appendicitis
in an adolescent presenting as portal-mesenteric thrombo-
sis and pylephlebitis. J Pediatr Gastroenterol Nutr 1998;
27:584 – 8.
Ohtake H, Urayama H, Nozaki Z, Harada T, Kawasuji M, [18]
Wantanabe Y. Surgical drainage for idiopathic suppurative
pylephlebitis. Ann Vasc Surg 1998;12:83 – 5.
Riccabona M, Kuttnig-Haim M, Dacar D, Urlesberger B, [19]
Reiterer F, Maurer U, et al. Venous thrombosis in and after
extension of thrombosis involving the SMV, the
intrahepatic branches of the PV and the splenic
vein, and the formation of liver abscesses. The most
common causes of death were sepsis and/or perito-
nitis. The majority of patients with the worst out-
come had a severe underlying condition such as
diabetes mellitus or immunosuppression. The pre-
cipitating focus of infection did not appear to play
a role in the disease severity, since almost half of
the patients who died had diverticulitis, which was
found to be the most common aetiology in the total
cases studied. All of the patients who died were
considered to have acute pylephlebitis. However, the
outcome of this condition has improved recently
since the majority of cases (75%) died before 1990,
while only 25% died following that date [48,50,
75,90,92]. Modern imaging techniques may facili-
tate an early diagnosis and have the ability to identify
the underlying focus of infection in the abdomen or
pelvis. In addition, the wide use of broad-spectrum
antibiotics and early anticoagulant therapy may
account for the improved outcome.
The aim of anticoagulant treatment is to reverse
or prevent progression of thrombosis and treat com-
plications of established PVT. Early anticoagulation
in mesenteric and portal vein thrombosis is consid-
ered to minimize serious complications such as
bowel ischemia and infarction. A rather benefi cial
effect of anticoagulation therapy was observed in
the cases studied. Although more severe disease
with a high rate of SMV thrombosis was evident in
cases who received anticoagulation treatment, an
improved outcome was observed with a higher reca-
nalization rate, lower mortality and lower rate of
development of portal hypertension or cavernoma
formation. On the other hand, cases treated with
antibiotics alone, without coagulation, experienced
a higher rate of failure of recanalization and mortal-
ity. Finally, surgical thrombectomy was associated
with recurrence of thrombosis, surgical morbidity
and mortality and was ineffective in cases presented
in this review [10,19,87].
Aetiology and severity of the disease did not
appear to play any role in the rate of recanalization,
since recanalization occurred in cases with any kind
of local aetiology and in rather severe disease. How-
ever, the vast majority of recanalization cases were
the most recently reported and the most promptly
diagnosed and treated.
In conclusion, pylephlebitis is a serious condition
with signifi cant morbidity and mortality that can
complicate intra-abdominal sepsis of any aetiology.
Early diagnosis of pylephlebitis and management of
predisposing intra-abdominal infections followed by
combined antibiotic and anticoagulant therapy are
the most important factors for recanalization.
Downloaded by [Alexandra Alexopoulou] at 09:06 15 August 2015

810 T. Kane l l opou l o u et al.
extracorporeal membrane oxygenation: detection and follow-
up by color Doppler sonography. Eur Radiol 1997;7:1383 – 6.
Tung JY, Johnson JL, Liacouras CA. Portal-mesenteric [20]
pylephlebitis with hepatic abscesses in a patient with Crohn ’ s
disease treated successfully with anticoagulation and antibi-
otics. J Pediatr Gastroenterol Nutr 1996;23:474 – 8.
Casals S, Enriquez G, Gomez JM, Cabot A. Sonographic [21]
diagnosis of pylephlebitis in children. Pediatr Radiol 1993;
23:567 – 8.
Giuliano CT, Zerykier A, Haller JO, Wood BP. Radiological [22]
case of the month. Pylephlebitis secondary to unsuspected
appendiceal rupture. Am J Dis Child 1989;143:1099 – 100.
Shaw PJ, Saunders AJ, Drake DP. Case report: ultrasono-[23]
graphic demonstration of portal vein thrombosis in the acute
abdomen. Clin Radiol 1986;37:101 – 2.
Shah I, Bhatnagar S. Liver abscess in a newborn leading to [24]
portal vein thrombosis. Indian J Pediatr 2009;76:1268 – 9.
Webster GJ, Burroughs AK, Riordan SM. Review article: [25]
portal vein thrombosis — new insights into aetiology and
management. Aliment Pharmacol Ther 2005;21:1 – 9.
Sherigar R, Amir KA, Bobba RK, Arsura EL, Srinivas N. [26]
Abdominal pain secondary to pylephlebitis: an uncommon
disease of the portal venous system, treated with local throm-
bolytic therapy. Dig Dis Sci 2005;50:983 – 7.
Van De Wauwer C, Irvin TT. Pylephlebitis due to perforated [27]
diverticulitis. Acta Chir Belg 2005;105:229 – 30.
Etienne M, Gueit I, Abboud P, Pons JL, Jacquot S, Caron F. [28]
Fusobacterium nucleatum hepatic abscess with pylephlebitis
associated with idiopathic CD4( ⫹ ) T lymphocytopenia. Clin
Infect Dis 2001;32:326 – 8.
Sillero JM, Calvet X, Musulen E, Diaz-Ruiz MJ, Tolosa C, [29]
Pardo A, et al. Idiopathic pylephlebitis and idiopathic scle-
rosing peritonitis in a man with protein S defi ciency. J Clin
Gastroenterol 2001;32:262 – 5.
Navarro C, Clain DJ, Kondlapoodi P. Perforated diverticu-[30]
lum of the terminal ileum. A previously unreported cause of
suppurative pylephlebitis and multiple hepatic abscesses. Dig
Dis Sci 1984;29:171 – 7.
Rosenberg N, Konigsberg SF, Schwarcz SB. Case reports: [31]
Pylephlebitis and multiple liver abscesses due to Bacteroides.
Successful treatment with clindamycin. J Med Soc N J
1978;75:49 – 51.
Saltzman DA, Smithline N, Davis JR. Fulminant hepatic [32]
failure secondary to amebic abscesses. Am J Dig Dis
1978;23:561 – 7.
Juler GL, Dietrick WR, Eisenman JI. Intramesenteric perfo-[33]
ration of sigmoid diverticulitis with nonfatal venous intrava-
sation. Am J Surg 1976;132:653 – 6.
Lin CS. Suppurative pylephlebitis and liver abscess compli-[34]
cating colonic diverticulitis: report of two cases and review
of literature. Mt Sinai J Med 1973;40:48 – 55.
Mannaerts L, Bleeker-Rovers CP, Koopman M, Punt CJ, [35]
van Herpen CM. Pylephlebitis after a duodenal ulcer in a
patient with metastasised colon carcinoma treated with
chemotherapy and bevacizumab: a case report. Neth J Med
2009;67:69 – 71.
Loi TH, See JY, Diddapur RK, Issac JR. Emphysematous [36]
gastritis: a case report and a review of literature. Ann Acad
Med Singapore 2007;36:72 – 3.
Chau TN, Loke TK, Leung VK, Law ST, Lai MH, Ho YW. [37]
Hepatic portal venous gas complicating septic thrombophle-
bitis of the superior mesenteric vein. Hong Kong Med J
2007;13:69 – 72.
Takahashi H, Sakata I, Adachi Y. Treatment of portal vein [38]
septic thrombosis by infusion of antibiotics and an antifungal
agent into portal vein and superior mesenteric arter y: a case
report. Hepatogastroenterology 2003;50:1133 – 5.
Baddley JW, Singh D, Correa P, Persich NJ. Crohn ’ s disease [39]
presenting as septic thrombophlebitis of the portal vein (pyl-
ephlebitis): case report and review of the literature. Am J
Gastroenterol 1999;94:847 – 9.
Joly V, Belmatoug N, Sibert A, Carbon C, Yeni P. Septic [40]
thrombophlebitis of the portal vein. Clin Infect Dis 1996;
23:417 – 8.
Hall RI, Venables CW, Lendrum R. ERCP diagnosis of mul-[41]
tiple hepatic abscesses due to portal pylephlebitis. Br J Surg
1985;72:439.
Waxman BP, Cavanagh LL, Nayman J. Suppurative pyephle-[42]
bitis and multiple hepatic abscesses with silent colonic diver-
ticulitis. Med J Aust 1979;2:376 – 8.
Nobili C, Uggeri F, Romano F, Degrate L, Caprotti R, [43]
Perego P, et al. Pylephlebitis and mesenteric thrombophle-
bitis in sigmoid diverticulitis: medical approach, delayed
surgery. Dig Liver Dis 2007;39:1088 – 90.
Ng SS, Yiu RY, Lee JF, Li JC, Leung KL. Portal venous [44]
gas and thrombosis in a Chinese patient with fulminant
Crohn ’ s colitis: a case report with literature review. World J
Gastroenterol 2006;12:5582 – 6.
Wildi SM, Wallace MB, Hunter B, Noone TC, Hoffman BJ. [45]
EUS diagnosis of an unusual case of pylephlebitis mimick-
ing metastatic pancreatic cancer. Dig Dis Sci 2005;50:
2255 – 8.
Lim HE, Cheong HJ, Woo HJ, Kim WJ, Kim MJ, Lee CH, [46]
et al. Pylephlebitis associated with appendicitis. Korean J
Intern Med 1999;14:73 – 6.
Duffy FJ Jr, Millan MT, Schoetz DJ Jr, Larsen CR. Suppura-[47]
tive pylephlebitis and pylethrombosis: the role of anticoagu-
lation. Am Surg 1995;61:1041 – 4.
Perez-Cruet MJ, Grable E, Drapkin MS, Jablons DM, [48]
Cano G. Pylephlebitis associated with diverticulitis. South
Med J 1993;86:578 – 80.
Jaber MR, Holland C. Septic pylephlebitis mimicking biliary [49]
obstruction. Am J Gastroenterol 2008;103:807 – 8.
Mohammed AH, Mohammed AH, Khot UP, Thomas D. [50]
Portal venous gas — case report and review of the literature.
Anaesthesia 2007;62:400 – 4.
Sellner F, Sobhian B, Baur M, Sellner S, Horvath B, [51]
Mostegel M, et al. Intermittent hepatic portal vein gas com-
plicating diverticulitis — a case report and literature review.
Int J Colorectal Dis 2007;22:1395 – 9.
Dourakis SP, Tsochatzis E, Alexopoulou A, Archimandritis [52]
AJ. Pylephlebitis complicating silent diverticulitis. Lancet
2006;368:422.
El Braks R, Harnois F, Boutros N, Fallik D, Roudie J, Smadja [53]
C, et al. Mesenteric adenitis and portal vein thrombosis due
to Fusobacterium nucleatum. Eur J Gastroenterol Hepatol
2004;16:1063 – 6.
Liappis AP, Roberts AD, Schwartz AM, Simon GL. [54]
Thrombosis and infection: a case of transient anti-cardiolipin
antibody associated with pylephlebitis. Am J Med Sci 2003;
325:365 – 8.
Di Cataldo A, Lanteri R, Dell ’ Arte M, Azzarello G, Licata A. [55]
Portal vein thrombosis. A multifactorial clinical entity. Chir
Ital 2003;55:435 – 9.
Draghetti MJ, Salvo AF. Gas in the mesenteric veins as a [56]
nonfatal complication of diverticulitis: report of a case. Dis
Colon Rectum 1999;42:1497 – 8.
Saxena R, Adolph M, Ziegler JR, Murphy W, Rutecki GW. [57]
Pylephlebitis: a case report and review of outcome in the
antibiotic era. Am J Gastroenterol 1996;9:1251 – 3.
Topiel MS, Simon GL. Peptococcaceae bacteremia. Diagn [58]
Microbiol Infect Dis 1986;4:109 – 17.
Gage TP, Eagan J, Gagnier M. Diverticulitis complicated by [59]
candidal pylephlebitis. South Med J 1985;78:1265 – 6.
Downloaded by [Alexandra Alexopoulou] at 09:06 15 August 2015

Pylephlebitis: A literature review 811
Peters TG, Locke JR, Weight GR. Suppurative pylephle-[78]
bitis caused by toothpick perforation. South Med J 1988;
81:414 – 5.
Vogel RA, Hall CI, Viney RS. Septic pylephlebitis following [79]
Shigella bacteremia: case report. Tex Med 1986;82:35 – 6.
Gold RP, Seaman WB. Splenic fl exure carcinoma as a source [80]
of hepatic portal venous gas. Radiology 1977;122:329 – 30.
Palacios EJ, White HJ, Read RC. Suppurative pylephlebitis [81]
with multiple liver abscesses secondary to incarcerated
incisional abdominal hernia. Report of one case. Review of
literature. J Ark Med Soc 1971;68:73 – 4.
Tsao YT, Lin SH, Cheng CJ, Chang FY. Pylephlebitis associ-[82]
ated with acute infected choledocholithiasis. Am J Med Sci
2006;332:85 – 7.
Soo R, Gosbell I, Gallo J, Pokorny CS. Septic portal vein [83]
thrombosis due to Fusobacterium necrophorum. Aust N Z
J Med 1999;29:569 – 70.
Plemmons RM, Dooley DP, Longfi eld RN. Septic thrombophle-[84]
bitis of the portal vein (pylephlebitis): diagnosis and manage-
ment in the modern era. Clin Infect Dis 1995;21:1114 – 20.
Drabick JJ, Landry FJ. Suppurative pylephlebitis. South [85]
Med J 1991;84:1396 – 8.
Huurman VA, Visser LG, Steens SC, Terpstra OT, [86]
Schaapherder AF. Persistent portal venous gas. J Gastrointest
Surg 2006;10:783 – 5.
Gelber AC, Schachna L, Mitchell L, Schwartzman G, [87]
Hartnell G, Geschwind JF. Beh ç et ’ s disease complicated by
pylephlebitis and hepatic abscesses. Clin Exp Rheumatol
2001;19:S59 – 61.
Dean JW, Trerotola SO, Harris VJ, Snidow JJ, Hawes D. [88]
Percutaneous management of suppurative pylephlebitis.
J Vasc Interv Radiol 1995;6:585 – 8.
Arakura N, Ozaki Y, Yamazaki S, Ueda K, Maruyama M, [89]
Chou Y, et al. Abscess of the round ligament of the liver
associated with acute obstructive cholangitis and septic
thrombosis. Intern Med 2009;48:1885 – 8.
Bleeker-Rovers CP, Jager G, Tack CJ, Van Der Meer JW, [90]
Oyen WJ. F-18- fl uorodeoxyglucose positron emission tom-
ography leading to a diagnosis of septic thrombophlebitis of
the portal vein: description of a case history and review of
the literature. J Intern Med 2004;255:419 – 23.
Sakamoto H, Suga M, Ozeki I, Kobayashi T, Sugaya T, [91]
Sasaki Y, et al. Subcapsular hematoma of the liver and
pylethrombosis in the setting of cholestatic liver injury.
J Gastroenterol 1996;31:880 – 4.
Ferkolj I, Vrh-Jermancic J, Stabuc B. Fatal hemorrhage due [92]
to thrombosis and rupture of the portal vein and hepatic
artery. Wien Klin Wochenschr 2009;121:537 – 9.
Gasparri MG, Pipinos II, Bleza DA, Shepard AD. Images [93]
for surgeons. Pylephlebitis secondary to intestinal ischemia.
J Am Coll Surg 2000;190:265.
Balthazar EJ, Gollapudi P. Septic thrombophlebitis of the [94]
mesenteric and portal veins: CT imaging. J Comput Assist
Tomogr 2000;24:755 – 60.
Chawla Y, Duseja A, Dhiman RK. Review article: The [95]
modern management of portal vein thrombosis. Aliment
Pharmacol Ther 2009;30:881 – 94.
Harmanci O, Bayraktar Y. Portal hypertension due to portal [96]
venous thrombosis: etiology, clinical outcomes. World J
Gastroenterol 2007;13:2535 – 40.
Witte CL, Brewer ML, Witte MH, Pond GB. Protean [60]
manifestations of pylethrombosis. A review of thirty-four
patients. Ann Surg 1985;202:191 – 202.
Rodning CB, Williams L. Suppurative pylephlebitis due to [61]
pseudodiverticulosis coli. South Med J 1984;77:1165 – 7.
Cambria RP, Margolies MN. Hepatic portal venous gas in [62]
diverticulitis: survival in a steroid-treated patient. Arch Surg
1982;117:834 – 5.
Chang YS, Min SY, Joo SH, Lee SH. Septic thrombophlebi-[63]
tis of the portomesenteric veins as a complication of acute
appendicitis. World J Gastroenterol 2008;14:4580 – 2.
Farin P, Paajanen H, Miettinen P. Intraoperative US diagno-[64]
sis of pylephlebitis (portal vein thrombosis) as a complication
of appendicitis: a case report. Abdom Imaging 1997;22:
401 – 3.
Marshak RH, Lindner AE, Maklansky D, Goldberg MD. [65]
Mesenteric fat necrosis simulating a carcinoma of the cecum.
Am J Gastroenterol 1980;74:459 – 63.
Aguas M, Bastida G, Nos P, Beltr á n B, Grueso JL, Grueso J. [66]
Septic thrombophlebitis of the superior mesenteric vein and
multiple liver abscesses in a patient with Crohn ’ s disease at
onset. BMC Gastroenterol 2007;7:22.
Ajzen SA, Gibney RG, Cooperberg PL, Scudamore CH, [67]
Miller RR. Enterovenous fi stula: unusual complication of
Crohn disease. Radiology 1988;166:745 – 6.
Nouira K, Bedioui H, Azaiez O, Belhiba H, Messaoud MB, [68]
Ksantini R, et al. Percutaneous drainage of suppurative
pylephlebitis complicating acute pancreatitis. Cardiovasc
Intervent Radiol 2007;30:1242 – 4.
Pelsang RE, Johlin F, Dhadha R, Bogdanowicz M, [69]
Schweiger GD. Management of suppurative pylephlebitis by
percutaneous drainage: placing a drainage catheter into the
portal vein. Am J Gastroenterol 2001;96:3192 – 4.
Wakisaka M, Mori H, Kiyosue H, Kamegawa T, Uragami S. [70]
Septic thrombosis of the portal vein due to peripancreatic
ligamental abscess. Eur Radiol 1999;9:90 – 2.
Schwarz W, Honickman S, Ohki S, Buckman R, Warner E. [71]
Percutaneous diagnosis and drainage of pylephlebitis: a case
report. Surgery 1987;101:244 – 9.
De Roover A, Detry O, Coimbra C, Hamoir E, Honor é P, [72]
Meurisse M. Pylephlebitis of the portal vein complicating
intragastric migration of an adjustable gastric band. Obes
Surg 2006;16:369 – 71.
Wireko M, Berry PA, Brennan J, Aga R. Unrecognized [73]
pylephlebitis causing life threatening septic shock: a case
report. World J Gastroenterol 2005;11:614 – 5.
Tandon R, Davidoff A, Worthington MG, Ross JJ. Pylephle-[74]
bitis after CT-guided percutaneous liver biopsy. AJR Am J
Roentgenol 2005;184:S70 – 2.
Kim DY, Sedlack RE, Brandhagen DJ, Nyberg SL. Late [75]
presentation of pylephlebitis after orthotopic liver transplan-
tation. Liver Transpl 2003;9:776 – 7.
M é ndez-S á nchez N, S á nchez-G ó mez H, Rojas E, Uribe M. [76]
Pylephlebitis of portal venous system associated with urinary
infection. Dig Dis Sci 2003;48:834 – 6.
Kasper DL, Sahani D, Misdraji J. Case records of the [77]
Massachusetts General Hospital. Case 25-2005. A 40-year-
old man with prolonged fever and weight loss. N Engl J
Med 2005;353:713 – 22. Erratum: N Engl J Med 2005;
353:2827.
Downloaded by [Alexandra Alexopoulou] at 09:06 15 August 2015