A 24-year-old man with ileocolonic Crohn disease presented with
abdominal pain and ascites. Color Doppler ultrasonography and computed
tomography revealed complete thrombosis of the portal vein, superior mesenteric
vein, and splenic vein, with newly formed collaterals and hyperemia of adjacent
intestinal structures. Esophagogastroscopy showed signs of portal hypertension
including secondary esophageal varices, fundus varices, portal hypertensive
gastropathy, and duodenopathy ([Fig. 1]).
Fig. 1 Duodenal mucosa with
signs of portal hypertension.
In addition, probe-based confocal laser endomicroscopy (pCLE)
displayed marked enhancement of the reticular pattern of duodenal microvessels
and distinctive dilatation of microvessels within the duodenal mucosa ([Fig. 2] and [Video 1])
compared with healthy controls ([Fig. 3]).
Fig. 2 a, b Probe-based
confocal laser endomicroscopic (pCLE) images showing a distinctive reticular
network of duodenal mucosal vascularization in portal vein thrombosis.
Fig. 3 Probe-based confocal
laser endomicroscopic (pCLE) image showing the pattern of reticular network of
duodenal mucosal vascularization in a healthy subject.
Qualität:
Video
1 Probe-based confocal laser
endomicroscopy (pCLE) showing the distinctive pattern of reticular network of
duodenal mucosal vascularization in a patient within portal vein
thrombosis.
Quantitative evaluation also revealed a significant increase in
vessel density (area of perfused vessels per area of duodenal villi, functional
capillary density [FCD]) within the mucosa
(FCD = 0.37) compared with healthy controls
(FCD = 0.27). The patient received intravenous heparin,
which was later substituted with warfarin.
Portal vein occlusion is a rare but serious complication of Crohn
disease, and patients with inflammatory bowel diseases have a threefold
increased risk of venous thromboembolism [1]. Multiple
aetiologic factors are thought to be responsible: thrombocytosis, decreased
levels of antithrombin III, increased levels of fibrinogen, and clotting
factors V and VIII, and postsurgical and septic complications
[2]. Due to interruption of portal blood flow, there is
vasodilatation of the hepatic arterial bed with development of collateral veins
[3]. Therapy comprises anticoagulation, although systemic
and locally applied thrombolytic agents have been successfully used
[4]. In the present patient, besides an acute flareup of
Crohn disease 2 months ago, we could not elucidate any particular risk factor
for developing portal vein thrombosis.
The recently developed technique of pCLE provides endoscopic images
at the cellular level. Intravenously administered fluorescein helps display the
intestinal mucosal vessels before diffusing into the surrounding tissue,
facilitating excellent in-vivo imaging of the capillary network. Therefore,
pCLE might become an important diagnostic tool in the in-vivo evaluation of
intestinal microvascularization in various gastrointestinal disorders, which
has not been evaluated sufficiently so far [5].
Endoscopy_UCTN_Code_CCL_1AD_2AD
