4. Portal vein thrombosis
• Sensitivity Equal to CT – Power Doppler increase Sen.
• False positive Very low portal flow
• Partial Gray scale better than color Doppler
• Indications Before hepatic surgery
Before porto-caval shunt
Before hepatic transplantation
6. Diagnosis of malignant PV thrombosis
• Color Doppler US* PV > 23 mm in diameter
“AASLD” Arterial-like flow on Doppler
Increased serum α-FP
• FNA CT- or US-guided
• CEUS Contrast-Enhanced Ultrasound
* DeLeve L et al. AASLD practice guidelines: Vascular disorders of the liver.
Hepatology 2009 ; 49 : 1729 – 1764.
AASLD: American association of study of liver disease.
7. Portal vein thrombus in HCC
Swart J et al. Ultrasound Clin 2007 ; 2 : 355 – 375.
FNA of portal vein thrombus confirmed HCC
Gray-scale US image
Thrombus in PV & its branches
Color Doppler image
Vascularity within thrombus
Low-resistance arterial waveform
8. Malignant PV thrombosis / CEUS
38 pts (15 benigns - 23 malignants) – Conclusive (37/38)
Dănilă M et al. Medical Ultrasonography 2011 ; 13 : 102 – 107.
Gray-scale US
Malignant PVT Arterial phase
Enhancement
Portal phase
Wash-out
Late phase
Wash-out
Contrast-Enhanced US
9. Splenic vein thrombosis
Gastric cancer
Malignant thrombus tends to distend vein+ exhibit
pulsatile flow, a bland thrombus does not!
10. Superior mesenteric vein thrombosis
Pancreatic cancer
Sagittal view of pancreas & SMV
Thrombosed
SMV
Mass in
Pancreatic neck
Shunt between SMV
& systemic venous return
http://www.sonographers.ca
11. Superior mesenteric vein thrombosis
Transverse image of SMA & SMV
http://www.ultrasoundcases.info
SMA
SMV
12. Non-malignant PV thrombosis in cirrhosis
• Incidence 10 – 25%
• Pathophysiology Cirrhosis no longer hypocoagulable state
• Clinical findings Asymptomatic disease
Life-threatening condition
• Management Not addressed in any consensus publication
1st line treatment: warfarin or LMWH
2nd line treatment: thrombectomy, TIPS
Tsochatzis EA et al. Aliment Pharmacol Ther 2010; 31 : 366 – 374.
LMWH : Low molecular weight heparin, TIPS: Transjugular intrahepatic portosystemic shunts
13. Acute thrombosis of portal vein
Complete thrombosis
http://www.sites.tufts.edu
Echogenic material visualized within portal vein.
Increased diameter of portal vein.
14. Partial thrombosis of portal vein
Echogenic material occluding lumen of PV by ≈ 50%
Sacerdoti D et al. J Ultrasound 2007 ; 10 : 12 – 21.
15. Partial thrombosis of portal vein
Swart J et al. Ultrasound Clin 2007 ; 2 : 355 – 375.
Gray scale ultrasound
Partial echogenic thrombus
Color & pulsed Doppler
Complete filling of main PV
obscuring the clot
16. Portal vein pseudoclot – Augmentation
Robinson KA et al. Ultrasound Quarterly 2009 ; 25 : 3 – 13.
Color Doppler US of main portal vein
At rest
No detectable flow
Compression of lower abdomen
Augmented portal venous flow
17. Portal vein pseudoclot – Incorrect angle
Velocity: 24 cm/sec
Wall filter: medium
Angle 90°
Velocity: 7 cm/sec
Wall filter: medium
Angle < 60°
Radiol Clin N Am 2006 ; 44 : 805 – 835.
18. Chronic portal vein thrombosis
Portal cavernoma
Parikh et al. Am J Med 2010 ; 123 : 111 – 119.
Hepatopetal collaterals around thrombosed portal vein
20. Tchelepi H et al. Ultrasound Clin 2007 ; 2 : 415 – 422.
Transverse color US of stomach
Multiple dilated gastric varices
P-S collaterals / Isolated gastric varices
Collaterals via short gastric veins
Isolated gastric varices
Hepatopetal flow in LGV
Splenic vein thrombosis
21. P-S collaterals / Transcapsular collaterals
Chronic PVT due to necrotizing pancreatitis or surgery
Seeger M et al. Radiology 2010 ; 257 : 568 – 578.
Transcapuslar collateral
from SB varices to PVs
Color Doppler image
Submucosal varices
in small-bowel loop
US image
Ectopic intestinal varices
& transcapsular collaterals
Schematic diagram
SB: small bowel
22. Intestinal infarction
• Ascites
• Thinning of intestinal wall
• Lack of mucosal enhancement of thickened wall
• Development of multi-organ failure
Intestinal infarction is likely
Surgical exploration should be considered
23. Ultrasound in ischemic bowel
Thickening of small bowel wall
Loss of layering structure of wall
Chen MJ et al. J Med Ultrasound 2006 ; 14 : 79 – 85.
Thickening of small bowel wall
Bright flecks within the wall
24. Portal vein gas
Acute transmural mesenteric infarction
Tritou I et al. J Clin Ultrasound 2011 (in press).
Wiesner W et al. Radiology 2003 ; 226 : 635 – 650.
Intrahepatic PV gas in
periphery of both
lobes
CECT scan
Tiny echogenic foci
in liver parenchyma
Gray-scale US
Vertical bidirectional
spikes on PV waveform
Duplex of MPV
25. Portal cholangiopathy
• Definition Biliary & GB abnormalities in EHPVO
• Frequency 70 – 100% (symptomatic or not)
• Mechanism Mechanical extrinsic compression
Biliary ischemic injury
• Manifestation Majority asymptomatic
RUQ quadrant pain
Cholestasis & cholangitis
Secondary biliary cirrhosis
• Management Directed to symptomatic patients only
Besa C et al. Abdom Imaging 2011 .
(EHPVO: Extra hepatic portal vein obstruction)
26. Portal cholangiopathy
Biliary & GB wall abnormalities in EHPVO
Gallbladder varices
producing wall thickening
Cavernoma of portal vein
Associated with dilated bile ducts
Besa C et al. Abdom Imaging 2011.
28. Causes of Budd Chiari Syndrome
Pregnancy
Pills (birth control pills)
Platelets (thrombocytosis)
Paroxysmal nocturnal hemoglobinurea
Polycythemia rubra vera
Systemic Behcet syndrome, inflammatory bowel disease
Dahnert p 706
Thrombosis
“5Ps”
Causes Disease
Idiopathic 60%
Non
Thrombotic
Compression or invasion of IVC
Membranous obstruction/IVC diaphragm
Right atrial causes
29. Diagnosis of BCS
AASLD practice guidelines*
• Doppler US Most effective & reliable diagnostic mean
Experienced examiner aware of dg
suspicion
• MRI or CT Confirmatory study
Experienced Doppler examiner not available
• Liver biopsy Diagnosis not done by non-invasive imaging
• Venography When diagnosis remains uncertain
* DeLeve L et al. AASLD practice guidelines: Vascular disorders of the liver
Hepatology May 2009 ; 49 : 1729 – 1764.
30. Doppler US in BCS
• One/ more major hepatic veins reduced in size to <3 mm/
filled with thrombus/ not visualized
• Stenosis of hepatic veins
• Communicating intrahepatic venous collaterals
• Decreased/ absent/reversed blood flow in hepatic veins
• Flat flow/ loss of cardiac modulation in hepatic veins
• Demodulated portal venous flow = disappearance of
portal vein velocity variations with breathing
continued
31. Doppler US in BCS
• Slow flow (<11 cm/sec)/hepatofugal flow in portal vein
• portal vein congestion index >0.1
• Portal vein thrombosis (20%)
• Compression of IVC by enlarged liver/caudate lobe
• Sluggish/ reversed/ absent blood flow within IVC
• Hepatic artery resistive index >0.75
32. Doppler US in BCS
* DeLeve L et al. AASLD practice guidelines. Hepatology 2009 ; 49 : 1729 – 1764.
Obstructed HV Presence of solid endoluminal material
Hyperechoic cord replacing normal vein
Reversed flow in large hepatic vein
Dilatation of vein upstream to obstacle
HV collaterals Sipder web in vicinity of HV ostia
Subcapsular or HV to intercostal or HV veins
Caudate lobe hypertrophy with dilated veins
IVC Web – Thrombosis – Inversion of flow
33. BCS / Solid endoluminal material in HV
Solid endoluminal material in middle & left hepatic veins
Narrowing at distal end of middle hepatic vein as it joins IVC
Chaubal N et al. J Ultrasound Med 2006 ; 25 : 373 – 379.
Transverse subcostal image
34. Budd-Chiari syndrome
Hepatic veins transformed to fibrotic cords
“Hepatic vein star”
Boozari B et al. J Hepatol 2008 ; 49 : 572 – 580.
Hyperechoic cord
35. BCS / Reversed flow in large HV
Inverted flow in right hepatic vein
Normal flow in middle hepatic vein
Right intercostal view
Bargalló X et al. Am J Roentgenol 2006 ; 187 : W33 – W42.
36. BCS / Reversed flow in HV upstream to obstacle
Solid endo-luminal material in distal part of MHV
Reverse flow in proximal part of MHV
37. BCS / Sipder web in vicinity of HV ostia
Vilgrain V. Eur Radiol 2001 ; 11 : 1563 – 1577.
Segev D L. Liver Transpl 2007 ; 13 : 1285 – 1294.
Gray-scale US
Small interwoven veins near IVC
Hepatic venogram
Typical “spider web” pattern
38. BCS / Large subcapsular vein
Large tortuous subcapsular vein draining into IVC
Bargalló X et al. Am J Roentgenol 2006 ; 187 : W33 – W42.
39. BCS / HV draining into another HV
Occluded RHV draining through collateral vessel into MHV
Flow away & toward transducer in same vessel
“Bicolored hepatic vein”
Bargalló X et al. Am J Roentgenol 2006 ; 187 : W33 – W42.
40. BCS / Collateral from HV to caudate lobe vein
Brancatelli G et al. Am J Roentgenol 2007 ; 188 : W168 – W176.
Transverse Doppler US at level of caudate lobe
Lack of flow in distal portion of MHV
Collateral from MHV to caudate lobe vein
42. BCS / Caudate lobe hypertrophy
Erden A. Eur J Radiol 2007 ; 61 : 44 – 56.
Sagittal gray-scale US
Enlarged caudate lobe
Antero-posterior diameter: 7.6 cm
43. BCS / Dilated caudate lobe vein
75% of cases
Bargalló X et al. Am J Roentgenol 2003 ; 181 : 1641 – 1645.
Mildly dilated caudate vein
7 mm
Largely dilated caudate vein
21 mm
Caudate vein (≥ 3 mm) suggests diagnosis
Except for cardiac failure
44. BCS / Membranous obstruction of IVC
Kandpal H et al. RadioGraphics 2008 ; 28 : 669 – 689.
30-year-old woman, abdominal pain & distention of 3 y duration
Ostial HV narrowing
Multiple IH collaterals
Tapered IVC occlusion
at cavo-atrial junction
Reversed flow in IVC
Loss of cardiac pulsations
45. Budd-Chiari syndrome & liver hydatid disease
Retrospective study of 13 patients with HDL & BCS
Yilmaz C et al. Radiol Oncol 2009 ; 43 : 225 – 232.
Heterogeneous mass representing degenerated & collapsed membranes
Large subcapsular vein draining into suprahepatic IVC
46. BCS / IVC thrombosis
Behçet disease – Secondary BCS
Sagittal image of IVC distended with echogenic thrombus
Secondary BCS due to renal cell carcinoma
Rumack CM, Wilson SR, & Charboneau JW. Diagnostic Ultrasound.
Elsevier-Mosby, St. Louis, Missouri, USA, 3rd edition, 2005.
47. BCS / Thrombosis of PV
15% of patients – Poor prognosis
Bargalló X et al. Am J Roentgenol 2006 ; 187 : W33 – W42.
Thrombosis of portal vein
Hepatofugal flow in right portal vein
Dilated hepatic artery
48. BCS / Benign regenerative nodules
Multiple (> 10) – Small ( < 4 cm) – Hypervascular
Vilgrain V et al. Radiology 1999 ; 210 : 443 – 450.
Bargalló X et al. Am J Roentgenol 2006 ; 187 : W33 – W42.
Two iso- & hyperechoic nodules
surrounded by thin hypoechoic halo
Low resistance arterial waveform
with high velocity
49. Proposed diagnostic strategy for BCS
Valla DC. Gut 2008 ; 57 : 1469 – 1478.
DeLeve L et al. AASLD practice guidelines. Hepatology 2009 ; 49 : 1729 – 1764.
50. Doppler US in SOS
Non specific
• Main PV Decreased, to-and-fro, or reversed flow
• Hepatic artery Significant elevation of RI (> 0.80)
• Hepatic veins Normal direction – Monophasic flow
• IVC Patent with flow toward heart
McGahan J et al. Diagnostic ultrasound, Informa Healthcare, 2nd edition, 2008.
* Lassau N et al. Radiology 1997 ; 204 : 545 – 552.
• US findings Thickened GB wall – Ascites
51. Sinusoidal obstruction syndrome (SOS)
BMT for acute myelogenous leukemia
Desser TS et al. Am J Roentgenol 2003 ; 180 : 1583 – 1591.
Contrast-enhanced CT
Heterogeneous hepatic
enhancement
Color & duplex US of HV
Monophasic flow in MHV
Imaging currently not diagnostic by itself
(1) Cirrhosis+ portal hypertension (5%)
(2) Malignancy: tumor invasion by HCC, cholangiocarcinoma, pancreatic carcinoma, gastric carcinoma, metastasis I extrinsic compression by tumor
(3) Trauma: umbilical venous catheterization; surgery; Cx of splenectomy (7%, higher in patients with myeloproliferative disorders)
(4) Hypercoagulable state: blood dyscrasia; clotting disorder; estrogen therapy; severe dehydration
(5) Intraperitoneal inflammatory process (portal vein phlebitis): perinatal omphalitis; pancreatitis; appendicitis; ascending cholangitis
(6) Budd-Chiari syndrome (20%)
(7) Liver transplantation
Important unanswered questions in cirrhotic portal vein thrombosis:
Does occurrence of PVT alter the natural history of cirrhosis and therefore should asymptomatic patients be treated with
the goal of recanalization or prevention of further thrombus extension?
Should all patients with cirrhosis and PVT be aggressively anticoagulated?
Should this apply only to patients on transplantation waiting list?
If recanalization does not occur should patients be offered second-line treatment with transjugular intrahepatic portosystemic shunts?
How long should the interval be whilst being anticoagulated before considering therapy to have failed?
How should patients be monitored?
Is oral warfarin better than low-molecular weight heparin?
Schistosoma mansoni is a significant parasite of humans, a trematode that is one of the major agents of the diseaseschistosomiasis which is one type of helminthiasis, a neglected tropical disease. The schistosomiasis caused by Schistosoma mansoni is intestinal schistosomiasis.
Schistosomes are atypical trematodes in that the adult stages have two sexes (dioecious) and are located in blood vessels of the definitive host. Most other trematodes are hermaphroditic and are found in the intestinal tract or in organs, such as the liver. The lifecycle of schistosomes includes two hosts: a definitive host (i.e. human) where the parasite undergoes sexual reproduction, and a single intermediate snail host where there are a number of asexual reproductive stages. S. mansoni is named after Sir Patrick Manson, who first identified it in Formosa (now Taiwan).[1][2]
After the eggs of the human-dwelling parasite are emitted in the faeces and into the water, the ripe miracidium hatches out of the egg. The hatching happens in response to temperature, light and dilution of faeces with water. The miracidium searches for a suitable freshwater snail (Biomphalaria glabrata, Biomphalaria straminea, Biomphalaria tenagophila orBiomphalaria sudanica[10]) to act as an intermediate host and penetrates it. Following this, the parasite develops via a so-called mother-sporocyst and daughter-sporocyst generation to the cercaria. The purpose of the growth in the snail is the numerical multiplication of the parasite. From a single miracidium result a few thousand cercaria, every one of which capable of infecting a human.
Libora et al. (2010)[11] have detected in Venezuela, that a land snail Achatina fulica can also serve as a host of Schistosoma mansoni.[11]
The cercaria emerge from the snail during daylight and they propel themselves in water with the aid of their bifurcated tail, actively seeking out their final host. When they recognise human skin, they penetrate it within a very short time. This occurs in three stages, an initial attachment to the skin, followed by the creeping over the skin searching for a suitable penetration site, often a hair follicle, and finally penetration of the skin into the epidermis using cytolytic secretions from the cercarial post-acetabular, then pre-acetabularglands. On penetration, the head of the cercaria transforms into an endoparasitic larva, the schistosomule. Each schistosomule spends a few days in the skin and then enters the circulation starting at the dermal lymphatics and venules. Here, they feed on blood, regurgitating the haem as hemozoin.[12] The schistosomule migrates to the lungs (5–7 days post-penetration) and then moves via circulation through the left side of the heart to the hepatoportal circulation (>15 days) where, if it meets a partner of the opposite sex, it develops into a sexually mature adult and the pair migrate to the mesenteric veins.[13] Such pairings are monogamous.[14]
Male schistosomes undergo normal maturation and morphological development in the presence or absence of a female, although behavioural, physiological and antigenic differences between males from single-sex, as opposed to bisex, infections have been reported. On the other hand, female schistosomes do not mature without a male. Female schistosomes from single-sex infections are underdeveloped and exhibit an immature reproductive system. Although the maturation of the female worm seems to be dependent on the presence of the mature male, the stimuli for female growth and for reproductive development seem to be independent from each other.
The adult female worm resides within the adult male worm's gynaecophoric canal, which is a modification of the ventral surface of the male, forming a groove. The paired worms move against the flow of blood to their final niche in the mesenteric circulation, where they begin egg production (>32 days). The S. mansoni parasites are found predominantly in the small inferior mesenteric blood vessels surrounding the large intestine and caecal region of the host. Each female lays approximately 300 eggs a day (one egg every 4.8 minutes), which are deposited on the endothelial lining of the venous capillary walls.[15] Most of the body mass of female schistosomes is devoted to the reproductive system. The female converts the equivalent of almost her own body dry weight into eggs each day. The eggs move into the lumen of the host's intestines and are released into the environment with the faeces.
Consider only direct visualization of obstruction, and/or collaterals, of a hepatic vein or inferior vena cava, as definite evidence for the diagnosis.
One/more major hepatic veins reduced in size to <3 mm/filled with thrombus/not visualized
Stenoses of hepatic veins
Communicating intrahepatic venous collaterals
Decreased/absent/reversed blood flow in hepatic veins
Flat flow/oss of cardiac modulation in hepatic veins
Demodulated portal venous flow = disappearance of portal vein velocity variations with breathing
Slow flow (<11 cm/sec)/hepatofugal flow in portal vein
portal vein congestion index >0.1
Portal vein thrombosis (20%)
Compression of IVC by enlarged liver/caudate lobe
Sluggish/reversed I absent blood flow within IVC
Hepatic artery resistive index >0.75
Term “spiderweb” was initially used in description of angiographic findings in Budd-Chiari syndrome, and it means presence of very small interwoven veins.
Interwoven: منسوجة
Hypertrophied subcapsular veins may shunt blood from liver to systemic veins (azygos vein, intercostal veins) or directly to inferior vena cava creating new intrahepatic and extrahepatic circulation.
“Bicolored” hepatic vein
HCC appears to be a significant long-term complication (11 of 97 patients followed-up for a mean of 5 years).
αFP more specific for dg than with other liver diseases.
Risk of HCC in long-standing IVC obstruction 70-fold higher than those with pure hepatic vein involvement.
HVOD frequently develops before day 20 of bone marrow transplantation.
clinically suspected when there is jaundice, painful hepatomegaly, and fluid retention.
Intensive myeloablative chemotherapy or radiation therapy before transplantation is presumed to be the cause.
Clinical criteria for diagnosis: Seattle Criteria & Baltimore Criteria (weight gain – ascites – hepatomegaly - hyperbilirubinemia).
The diagnosis may be supported by imaging, which will demonstrate the presence of hepatomegaly and ascites and rule out biliary obstruction due to benign or malignant causes, but imaging is currently not diagnostic by itself.
The best-studied modality is gray-scale and color Doppler ultrasonography. The majority of studies suggest that no single ultrasound parameter is diagnostic for SOS.Findings that are highly suggestive of SOS are reversal of portal venous flow, attenuation of hepatic venous flow, gallbladder wall edema, and perhaps increased resistive indices to hepatic artery flow.
A composite score of gray-scale and color Doppler ultrasound criteria has been proposed, but may be too cumbersome for routine
clinical use. One study has suggested that the presence of flow in the para-umbilical vein is more common in moderate and severe SOS, but this will need to be validated by other investigators.