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| Journal of the New Zealand Medical Association,
19-May-2006, Vol 119 No 1234
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Portal venous thrombophlebitis in a case of perforated
appendicitis: lessons from a case
Renukadas Sakalkale, Paul Reeve
Pyelephlebitis is defined as septic thrombophlebitis of the
portal vein or one of its tributaries.1 It
has been well characterised historically2
but in the modern era is rarely reported. The exact incidence of
pylephlebitis is unknown. It may not be recognised at laparotomy and may be
missed in autopsy.3 Greater use of
diagnostic radiological imaging may lead to increased recognition. We report a
patient with appendicitis who presented with atypical features of appendicitis
that was complicated by portal pyelephlebitis and a consumption
coagulopathy.
Case reportJT, a 20-year-old male cheese factory worker, presented
acutely with abdominal pain, diarrhoea, and vomiting of 72 hours duration. He
had previously been well and had no past medical history of note. On admission,
his temperature was 37.9ºC, pulse rate 108/min, and blood pressure 117/69
mmHg. His abdomen was generally tender with guarding in the lower abdomen. A
provisional diagnosis of gastroenteritis was made.
His haemoglobin was 144 g/l (normal range 130–144
g/l), white cell count 11.8 × 10[9]/l
(normal range 4–11 x 10[9]/l) and
platelets were reduced at 40,000/cu mm (normal range 150–400 x
10[9]/l). Coagulation profile revealed an
INR of 1.2 (normal range 0.8–1.2 ) and an APTT of 42 sec (normal range
25–40 sec) with increased van Clauss fibrinogen 5.6 g/l. (normal range
1.2-4 g/l).
The
X-DP (d-Dimer) was mildly elevated. His liver function tests showed raised serum
bilirubin 50 μmol/l (normal range 2–22 μmol/l) as well as
elevated alkaline phosphatase 211 U/L (normal range 40–110 U/L) and
gammaglutamaryl transferase 162 U/L (normal range 0–60 U/L).
His condition deteriorated over the first 24 hours. His
temperature spiked to 39.4ºC with rigors, and he had increasing abdominal
pain. Blood cultures grew Escherichia
coli and Streptococcus
constellatus in mixed aerobic and anaerobic bottles.
Antibiotics were then started. An abdominal ultrasound (US)
scan 18 hours after admission revealed a dilated tubular structure in the right
iliac fossa, consistent with the appendix, with two appendicoliths and
surrounding free fluid. There was oedema around the superior mesenteric vein
(SMV) and a query was raised about its patency.
A subsequent CT scan showed thrombus partially obliterating
the lumen of the SMV and proximal portal vein. (Figure) The spleen was not
enlarged.
Figure 1. CT scan with intravenous contrast in our case
showing partial occlusion of the superior mesenteric vein by a thrombus
(arrowed)
 A surgical consult was obtained and a diagnosis of
complicated appendicitis and SMV thrombophlebitis was suggested. Intravenous
fluids and broad-spectrum antibiotics were continued and he underwent open
appendicectomy after a platelet transfusion.
At operation, a perforated appendix with faecoliths was
removed. After haematological consultation, he was treated with heparin for 3
days followed by oral anticoagulation with warfarin. He was discharged after 11
days. Warfarin was stopped after 4 weeks. At 3-month clinic follow-up, he was
asymptomatic. An abdominal US revealed complete resolution of the SMV
thrombosis.
DiscussionPortal pyelephlebitis is well described as a complication of
appendicitis and other infective and inflammatory conditions affecting the
intestines, stomach, duodenum, pancreas, and biliary
tract.4 Rarer causes include urogenital
lesions, subphrenic abscesses, and malignancies. The true incidence of portal or
superior venous pyelephlebitis is unknown. It appears to be uncommon, but the
diagnosis may be obscured by the primary disease. Due to advances in management
with earlier diagnosis of its underlying cause and the use of antibiotics, it is
thought to be less common in modern era.4
Pyelephlebitis is often not recognised at laparotomy and has been missed at
autopsy.3 Both US and CT are advocated as
modalities of diagnostic imaging, but CT is less
operator-dependent.1
Plemmons et al1
reviewed 18 cases of pyelephlebitis in the literature and reported one of their
own. Bacteraemia was found in 88% of the cases. They suggested the diagnosis of
pyelephlebitis should be considered in patients with evidence of intra-abdominal
infection and high-grade bacteraemia, especially those due to
Bacteroides fragilis and/or multiple
organisms. Clinically, pyelephlebitis or at least portal bacteraemia should be
suspected in any patient with suspected appendicitis who has a
rigor.5
Pyelephlebitis secondary to infections (e.g. appendicitis)
has been distinguished from thrombosis due to other causes by its typically
non-occlusive nature, as seen in our case (Figure 1), and a lack of development
of portal hypertension.
In appendicitis, spread occurs via the ileocolic vasculature
to the superior mesentric vein and eventually to the portal
vein.6 Pyelephlebitis can also give rise
to septic emboli that lodge within liver and cause intrahepatic
abscesses.2,7 Deranged liver enzymes were
found in our case and could have been indicative of early hepatic involvement.
The suppurative focus will usually need surgical
intervention and appropriate antibiotics should also be given. The use of
heparin has been advocated,1 but a benefit
of adjunctive heparin therapy has not been clearly demonstrated. Harch et al
recommended anticoagulation on the presumption that the process might extend and
lead to enteric ischaemia.11
Proponents of anticoagulation identify several factors such
as documented progression of thrombus while on antibiotics, fever unresponsive
to treatment, and the presence of hypercoagulable state to justify
therapy.12 Anticoagulation may also reduce
septic embolisation to the liver from infected portal thrombi and prevent liver
abscesses.
The optimum duration of anticoagulation is unclear in the
literature. If thrombosis is associated with sepsis and not complicated by
infarction or embolisation and no underlying thrombophilic factors are
identified, then a short duration of therapy seems a reasonable approach,
however.
Open thrombectomy and venous
ligation13 appear to have been largely
abandoned as therapy for pyelephlebitis. Operative or radiological interventions
in the form of thrombectomy and thrombolysis with direct intravascular infusion
of thrombolytics have been advocated.8–10
for mesenteric and portal vein non-suppurative thrombosis with bowel
compromise.
Nishimori et al14
reported a 16-year-old with septic thrombophlebitis and a liver abscess, who had
appendicectomy and thrombus removal from the SMV using a Fogarty catheter. They
considered re-canalisation of the portal vein was indicated as an adjunct to
surgical removal of the appendix, which was found gangrenous.
The mortality rate reported of up to 32% in cases with SMV
thrombosis will in part be due the severity of the associated
condition15 rather than the thrombosis
itself but it has been suggested that the complications of untreated portal or
SMV thrombosis could be catastrophic.17
The high reported mortality rate without anticoagulation and
a decreased recurrence rate reported after
anticoagulation16 supports our decision to
use it in our patient.
Author information:
Renukadas P Sakalkale, Department of Paediatric Surgery; Paul Reeve, Clinical
Director, Department of General Medicine; Waikato Hospital, Hamilton
Correspondence: Dr
Paul Reeve, Clinical Director, Dept of General Medicine, Waikato Hospital,
Pembroke Street, Hamilton 2001. Fax: (07) 839 8735; email: reevepa@waikatodhb.govt.nz
References:
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