Doppler of the portal system 1
•Download as PPTX, PDF•
35 likes•4,358 views
This document discusses Doppler ultrasound findings related to portal vein thrombosis and Budd-Chiari syndrome. It provides details on the causes, classifications, and diagnostic criteria for each condition based on ultrasound appearance. Key findings include identifying partial or complete thrombosis, portal cavernoma formation, presence of collateral vessels, and reversed or absent flow in involved vessels. Ultrasound is established as the primary imaging method for diagnosing Budd-Chiari syndrome by detecting thrombus or narrowing of hepatic veins.
Recommended
More Related Content
What's hot
What's hot (20)
Viewers also liked
Viewers also liked (20)
Similar to Doppler of the portal system 1
Similar to Doppler of the portal system 1 (20)
More from Dr. Muhammad Bin Zulfiqar
More from Dr. Muhammad Bin Zulfiqar (20)
Recently uploaded
Recently uploaded (20)
Doppler of the portal system 1
- 1. Doppler of the portal system Pathological findings Dr. Muhammad Bin Zulfiqar PGR-II FCPS-II SIMS/SHL
- 3. Causes of Portal vein Thrombosis IDIOPATHIC : (mostly): ? neonatal sepsis SECONDARY: – (1) Cirrhosis+ portal hypertension (5%) – (2) Malignancy: – (3) Trauma: – (4) Hypercoagulable state: – (5) Intraperitoneal inflammatory process (portal vein phlebitis): – (6) Budd-Chiari syndrome (20%) – (7) Liver transplantation
- 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
- 5. Classification of portal vein thrombosis • Duration Acute Chronic • Severity Complete Partial • Causes Malignant Non-malignant
- 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
- 19. Portal cavernoma Gray-scale ultrasound Color & pulsed Doppler
- 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
- 41. BCS / Suggestive intra-hepatic collateral Erden A. Eur J Radiol 2007 ; 61 : 44 – 56. Undulated course “h-shaped” Hockey-stick Curvilinear Curved
- 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
- 52. THANK YOU
Editor's Notes
- (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.