Portal
Hypertension
Portal hypertension results in
changes in various vessels along with development of multiple portosystemic
collaterals.
Along with
dilatation of portal vein, varying degrees of dilatation of splenic and superior
mesenteric veins also occur in portal hypertension. A caliber of splenic vein
over 12 mm diameter or greater should be considered a specific sign of portal
hypertension. Splenomegaly, usually associated with portal hypertension, is
also responsible for dilatation of splenic vein possibly because of increased
aplenic flow (fig. 10.1).
 |
| splenic vein with splenomegaly |
Figure 10.1: Dilated and tortuous splenic vein with
splenomegaly
Dilatation of splenic artery was also found to accompany splenomegaly
which is required to supply a more extensive capillary bed. Splenic artery
dilatation was also found to occur more frequently in cirrhosis caused by
chronic viral hepatitis than in alcohol abuse. A ratio between the diameter of
the hepatic and splenic arteries above 0.9, measured at 1.5-3 cm from their
origins, suggests an alcoholic cause for cirrhosis, whereas a lower ratio is
indicative of an infectious cause.
Another important sign of portal hypertension is the lack of variation
in caliber with respiration in the splenic and superior mesenteric veins (fig.
10.2)
 |
| Figure 10.2:Splenic venous flow pattern in a portal hypertensive |
Along with
hepatofugal portal flow, splenic vein also shows hepatofugal flow which has
proved to be closely correlated with hepatic encephalopathy.
 |
| Figure 10.3:Voluminous lienored collaterals |
At level of lower
splenic pole, lienorenal collaterals appear as tortuous vessels with a high
velocity Doppler signal and a broad spectrum of frequencies due to turbulence
(fig. 10.3). Their presence is often associated with flow reversal in the splenic
vein.
Splenic Infarction
Splenic infarcts occur in patients
with myeloproliferative syndromes, hemolytic anemias and sepsis especially in
sepsis associated with endocarditis. The striking clinical feature is sudden
onset of pain in the upper left abdomen, occasionally associated with a painful
restriction of the respiratory excursion or local pain on palpation. However,
clinical diagnosis can be difficult because pain can be associated with almost
all cases of splenomegaly and infarct may be silent.
Splenic infarcts can
be visualized at altrasound scanning and B-mode pulsed Doppler US can identify
infarct related complications.
For the imaging
diagnosis of splenic infarstion, a wide range of ultrasound appearances have
been observed. About 24 hours after therapeutic embolization of the splenic
artery for treatment of portal hypertension, splenic infarcts appear as
wedge-shaped, hypoechoic and well-demarcated lesions at sonography. This is the
typical US appearance of acute stage without complications. Scar stage of
infarction may be seen as in homogeneity of splenic texture months later.
Severe infarct
related complications might develop in the course of disease that can be
detected by follow-up US and Doppler scanning. The findings that require
surgical intervention are the following:
1. Increasing
subcapsular hemorrhage
2. Extravasation of
blood into peritoneal cavity
3. Flow phenomena in
the area of infarction as seen at B-mode pulsed Doppler
US.
In patients
demonstrating arterial signals within the infarction area, histological
examination revealed superinfection of the splenic infarcts. The presence of
arterial signals and increasing subcapsular hemorrhage were signs of occurrence
of spontaneous splenic pupture. Hence with clear sonographic signs of
life-threatening splenic rupture, splenectomy should be recommended.
Intrasplenic Pseudoaneurysm
Post-traumatic
pseudoaneurysm involving splanchnic arteries are very rare in the pediatric age
group and affect mostly the splenic artery or intrasplenic arterial branches.
Because of the potential life-threatening complications, intrasplenic
pseudoaneurysm must be diagnosed and treated immediately. Although the trend in
the management of blunt splenic injuries has been towards conservative
treatment, formation of a pseudo-aneurysm at the site of a splenic hematoma may
cause delayed splenic rupture requiring splenectomy. This has necessitated
routine follow-up of blunt splenic injuries by color Doppler sonography or CT
to detect pseudoaneurysm at an early stage when selective embolization might
prevent expansions of the hematoma and rupture of the spleen.
Intrasplenic
pseudoaneurysm are formed by active bleeding from injured intrasplenic arterial
branches. Although spontaneous thrombosis is possible, the usual evolution of
the lesions is gradual expansion of the hematoma with eventual rupture of the
splenic capsule. This unpredictable ominous complications necessitates a
meticulous search for there lesions in all cases of blunt splenic trauma.
Initial scanning in
patients who have experienced blunt splenic trauma may be performed with color
Doppler sonography or contrast-enhanced CT. Intrasplenic pseudoaneurysm apper
on gray scale sonography as nonspecific anechoic lesions. Their aneurysmal
nature can be revealed by the demonstration of arterial flow on color Doppler
sonography. Turbulent arterial flow within the lesion suggests a diagnosis of
pseudoaneurysm. Not all intrasplenic pseuoaneurysm develop at the time of initial
trauma. Somelesions develop in a delaved fashion presumably because of gradual
lysis of the clot sealing the injured arterial wall. Thus conservative
management of blunt splenic trauma should include periodic follow-up with color
Doppler sonography or CT even if admission scans are negative. Coil
embolization of splenic artery is the preferred method for hemostasis of
intrasplenic pseudoaneurysm.
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