Doppler of the portal system discusses Doppler ultrasound findings related to portal hypertension. It describes various portosystemic collaterals that can develop as compensatory pathways in portal hypertension, such as the coronary vein, umbilical vein, splenorenal collateral, and gastrorenal collateral. It also discusses Doppler ultrasound signs of portal hypertension seen in cirrhosis, including dilatation of the portal vein, decreased mean blood flow velocity, and hepatofugal or to-and-fro flow patterns. Additional findings discussed include enlargement and tortuosity of the hepatic artery and changes in hepatic vein blood flow patterns.
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Doppler of the portal system pathologies
1. Doppler of the portal system
Pathological findings
Dr. Muhammad Bin Zulfiqar
PGR-II FCPS-II SIMS/SHL
2. Doppler of the portal system
Portal hypertension
Portal vein thrombosis
3. Causes of portal hypertension
Pre-sinusoidal Congenital hepatic fibrosis
Sarcoidosis
Schistosomiasis
Lymphoma
Hyperdynamic Arterio-portal fistula or malformation
Robinson KA et al. Ultrasound Quarterly 2009 ; 25 : 3 – 13.
Intra-hepatic
Post-sinusoidal Cirrhosis
Causes Disease
Extra-hepatic Portal vein thrombosis or compression
most common cause
Supra-hepatic Budd-Chiari syndrome
Right heart insufficiency
4. Doppler US signs of PHT in cirrhosis
• P-S collaterals Highly sensitive & specific
• Portal vein Dilated PV
Decreased mean velocity (< 15 cm/sec)
To-and-fro flow /Hepatofugal flow
Increased pulsatility (VPI) >0.48+/-0.31
Arterio-portal fistula
• Hepatic vein Compression (Pseudo-portal flow)
• Hepatic artery Enlargement & tortuosity
Increased RI & PI
Harkanyi Z. Ultrasound Clin 2006 ; 1 : 443 – 455.
P-V: portovenous, VPI: Venous pulsatility index
5. Porto-systemic collaterals
High sensitivity & specificity for PHT
• Tributary collaterals
“Drain normally into PS”
Robinson KA et al. Ultrasound Quarterly 2009 ; 25 : 3 – 13.
Coronary vein (left gastric)
Short gastric veins
Branches of SMV & IMV
• Developed collaterals
“Developed or recanalized”
Recanalized umbilical vein
Spleno-renal collateral
Gastro-renal collateral
Spleno-retroperitoneal collateral
6. Common spontaneous porto-systemic collaterals
More than 20 P-S collaterals described
Patnquin1 H et al. Am J Roentgenol 1987 ; 149 : 71 – 76.
Most common: LGV – PUV – Spleno-renal – Gastro-renal
7. P-S collaterals / Coronary vein
Most prevalent (80-90%) – Most clinically important
Robinson KA et al. Ultrasound Quarterly 2009 ; 25 : 3 – 13.
Sagittal view slightly superior
Tortuosity of CV as it extends
superiorly toward GE junction
Sagittal paramedial view
Flow in CV directed superiorly
& away from splenic vein
8. P-S collaterals / Gastroesophageal collateral
Gastroesophageal collateral veins close to diaphragm
McGahan J et al. Diagnostic ultrasound, Informa Healthcare, 2nd edition, 2008.
Longitudinal view of left liver lobe
9. Normal umbilical vein anatomy
UV communicates with umbilical segment of LPV
Travels down anterior abdominal wall toward umbilicus
Eventually drains into systemic system via inferior epigastric vein
Robinson KA et al. Ultrasound Quarterly 2009 ; 25 : 3 – 13.
10. Robinson KA et al. Ultrasound Quarterly 2009 ; 25 : 3 – 13.
Hepatofugal flow within UV
Similar color Doppler viewLongitudinal US of LLL
Dilated umbilical vein (10 mm)
P-S collaterals / Recanalized umbilical vein
PUV observed only in hepatic or suprahepatic blockage
LLL: Left lobe of Liver
11. Sagittal panoramic view
PUV traveling to periumbilical region where it becomes tortuous.
UV ramifies into smaller PU collaterals when it proceeds inferiorly
P-S collaterals / Recanalized umbilical vein
Caput medusae
12. Porto-systemic collaterals
• Coronary vein & umbilical vein are the easiest
& most productive to analyze
• Other collaterals detected sonographically
albeit with more difficulty in some cases
Robinson KA et al. Ultrasound Quarterly 2009 ; 25 : 3 – 13.
13. P-S collaterals / Spleno-renal collateral
Yamada M et al. Abdom Imaging 2006 ; 31:701 – 705.
Mansour MA et al. Vascular Diagnosis. Elsevier-Saunders, Philadelphia, 1st edition, 2005.
Transverse color Doppler US
Splenic vein feeding large
splenorenal collaterals
Flow direction from SV to LRV
Reversed or to-and-fro flow in SV
Schematic drawing
14. P-S collaterals / Spleno-renal collateral
Flow inversion in splenic vein
Flow inversion in SV increases dg of spleno-renal shunt
Mansour MA et al. Vascular Diagnosis. Elsevier-Saunders, Philadelphia, 1st edition, 2005
15. P-S collaterals / Short gastric veins
Sato T et al. J Gastroenterol 2002 ; 37 : 604 – 610.
Short gastric vein as inflowing vessel to gastric varices
16. P-S collaterals / Gastro-renal collateral
Yamada M et al. Abdom Imaging 2006 ; 31 : 701 – 705.
Maruyama H et al. Acad Radiol 2008 ; 15 : 1148 – 1154.
From cranial & dorsal side to
caudal & ventral side into LRV
Long-axis view of GRS
GRS LRV
From SV at confluence
coursing backward to join LRV
Schematic drawing
17. P-S collaterals / Superior mesenteric vein
Flow toward SMV in sup branch
Flow away from SMV in inf branch
Color Doppler view
2 mesenteric branches
of superior mesenteric vein
Semicoronal view of SMV
Robinson KA et al. Ultrasound Quarterly 2009 ; 25 : 3 – 13.
18. P-S collaterals / Inferior mesenteric vein
Mansour MA et al. Vascular Diagnosis. Elsevier-Saunders, Philadelphia, 1st edition, 2005.
Hepatofugal flow in IMV originating from PV confluence
19. P-S collaterals / IMV & rectal venous drainage
Wachsberg RH. Am J Roentgenol 2005 ; 184 : 481 – 486.
Peri-rectal varices
Transverse US posterior to bladderLeft parasagittal CDUS
Hepatofugal flow in dilated IMV
20. P-S collaterals / Gallbladder varices
Harkanyi Z. Ultrasound Clin 2006 ; 1 : 443 – 455.
Serpentine area in wall of GB
Cystic vein to anterior abdominal wall or patent PV branches
Most commonly observed in PV thrombosis (30%) 80% association
(Dahnert)
21. P-S collaterals / Spleno-retroperitoneal
collateral
Prominent varices surrounding posterior aspect of spleen
Owen C et al. J Diag Med Sonography 2006 ; 22 : 317 – 328.
22. Cirrhosis & PHT / Diameter of portal vein
1 Weinreb J et al. Am J Roentgenol 1982 ; 139 : 497 – 499.
2 Goyal AK et al. J Ultrasound Med 1990 ; 9 : 45 – 48.
Robinson KA et al. Ultrasound Quarterly 2009 ; 25 : 3 – 13.
Diameter: 16.9 mm
Sign of portal hypertension
Longitudinal view of MPV
Contoversy on normal PV diameter
Up to 13 mm in one study1
Up to 16 mm in another study2
Unusual large PV: sign of PHT
Normal PV size: do not exclude PHT
23. Cirrhosis & PHT / Portal vein velocity
Low velocity: good indicator of PHT
Normal velocity: do not exclude PHT
Controversy on normal PV velocity
Difficult to rely on velocity for dg
Normal mean velocity: 15 – 18 cm/sec
Swart J et al. Ultrasound Clin 2007 ; 2 : 355 – 375.
Shrunken liver & irregular margin
Vmax: 10 cm/s
Diagnosis of PHT
Triplex image of PV
24. Portal vein pseudoclot – Incorrect velocity
Cirrhotic patient with portal hypertension
Slower flow in portal vein
demonstrated
Velocity scale: 7 cm/s
Rubens DJ et al. Ultrasound Clin 2006 ; 1 : 79 – 109.
Velocity scale: 20 cm/s
Good flow in HA anteriorly
No flow in adjacent PV
25. Cirrhosis & PHT / Portal vein flow
Normal flow
Kok Th et al. Scand J Gastroenterol 1999 ; 34 (Suppl 230) : 82 – 88.
Reversed flow
Advanced PHT
SOS
Porto-systemic shunt
To and fro flow
Advanced PHT
Heart failure
Arterio-portal fistula
SOS: Sinusoidal obstruction syndrome
26. Cirrhosis & PHT / To-and-fro flow in PV
Cardiac cycle
Hepatopetal & hepatofugal with each heart beat
Seen before frank hepatofugal flow
Wachsberg RH et al. RadioGraphics 2002 ; 22 : 123 – 140.
Duplex US of LPV during suspended respiration
27. Cirrhosis & PHT / To-and-fro flow in PV
Respiratory cycle
Robinson KA et al. Ultrasound Quarterly 2009 ; 25 : 3 – 13.
On real-time US, these alterations corresponded to respiratory cycle
Transverse color Doppler US of left portal vein
Hepatopetal flow Hepatofugal flow
28. Robinson KA et al. Ultrasound Quarterly 2009 ; 25 : 3 – 13.
Transverse CDUS of left portal vein
Hepatopetal flow Hepatofugal flow
Cirrhosis & PHT / To-and-fro flow in PV
Compression
29. Causes of to-and-fro flow
Exaggerated pulsatility
Minimum velocity below baseline
Robinson KA et al. Ultrasound Quarterly 2009 ; 25 : 3 – 13.
- Portal hypertension
- Tricuspid regurgitation
- Right heart failure
- Aerterio-portal vein fistula
30. Cirrhosis & PHT / Reversed flow of PV
Hepatopetal flow in HA & hepatofugal flow in PV
Robinson KA et al. Ultrasound Quarterly 2009 ; 25 : 3 – 13.
Not pathognomonic feature of cirrhosis
Severe PHT – Rare
31. Hepatopetal flow in HA
Hepatofugal flow in PV
Color Doppler of peripheral liver
Arterial flow above baseline
Portal venous below
baseline
Duplex Doppler of same area
Robinson KA et al. Ultrasound Quarterly 2009 ; 25 : 3 – 13.
Cirrhosis & PHT / Reversed flow in PV branches
32. Cirrhosis & PHT / Reversed flow in PV branches
Mansour MA et al. Vascular Diagnosis. Elsevier-Saunders, Philadelphia, 1st edition, 2005.
Right anterior PV branch
Hepatofugal flow
Right posterior PV branch
Hepatopetal flow
34. Hepatofugal portal / TIPS
Right portal vein to right hepatic vein
Hwang HJ et al. J Clin Ultrasound 2009 ; 37 : 511 – 524.
Reversion of hepatofugal flow
Stent devoid of color signals
Malfunction of TIPS
1 week after TIPS
Hepatofugal flow in RPV
Vigorous color flow in stent
Immediately after TIPS
35. Arterio-portal fistula / High-flow hemangioma
Hwang HJ et al. J Clin Ultrasound 2009 ; 37 : 511 – 524.
65-year-old man with high-flow hemangioma in LLL
Hypoechoic nodule with intratumoral flow
Peritumoral hepatofugal flow in segmental PV
Hepatopetal flow in proximal PV
36. Arterio-portal fistula / Post-liver biopsy
Bertolotto M et al. J Clin Ultrasound 2008 ; 36 : 527 – 538.
Vascular lesion between
HA & PV branches
Inverted flow in PV
Oblique CDUSOblique gray-scale US
Focal echogenic area
in region of biopsy
Spectral Doppler US
High-velocity flow
Low-resistance flow
Turbulent flow
38. Helical portal vein flow
Near bifurcation
• Normal subjects 2%
• Severe liver disease 20%
• TIPS
• Post-liver transplantation Donor PV > recipient PV
• Portal vein stenosis
Robinson KA et al. Ultrasound Quarterly 2009 ; 25 : 3 – 13.
39. Helical portal vein flow
If not properly recognized, it can produce
the mistaken impression of PV flow reversal
Robinson KA et al. Ultrasound Quarterly 2009 ; 25 : 3 – 13.
40. Helical portal vein flow
Mimic of hepatofugal flow
Wachsberg RH et al. RadioGraphics 2002 ; 22 : 123 – 140.
Hepatopetal flow within liver confirms that net flow is hepatopetal
41. Cirrhosis & PHT / Prominent hepatic artery
Enlarged HA with tortuous or ‘‘corkscrew’’ appearance
Increased flow in HA to compensate decreased flow in PV
Swart J et al. Ultrasound Clin 2007 ; 2 : 355 – 375.
42. Causes of enlargement of hepatic artery
• Cirrhosis
• Hepatic diseases associated with alcoholism
• Congenital hepatic fibrosis
• Vascular tumors
• Hereditary hemorrhagic telangiectasia
Buscarini E et al. Ultraschall Med 2004 ; 25 : 348 – 55.
43. Parallel channel sign
von Herbay A et al. J Clin Ultrasound 1999 ; 27 : 426 – 432.
Gray-scale US
IH parallel channel sign
Suspicious of dilated IHBD
Color & pulsed Doppler US
Flow in both intra-hepatic lumina
Portal vein & hepatic artery
Absence of dilated intra-hepatic bile duct
44. Parallel channel sign
von Herbay A et al. J Clin Ultrasound 1999 ; 27 : 426 – 432.
Gray-scale US
IH parallel channel sign
Suspicious of dilated IHBD
Color & pulsed Doppler US
Blood flow in anterior structure
No flow in posterior structure
Confirmation of dilated intra-hepatic bile duct
45. Cirrhosis & PHT / Changes of hepatic artery flow
Kok Th et al. Scand J Gastroenterol 1999 ; 34 (Suppl 230) : 82 – 88.
Decreased diastolic flow
ESLD
Reversed diastolic flow
ESLD
Normal flow
Normal in most
patients
46. Cirrhosis & PHT / Pulsatility index of HA
Cirrhotic patients vs controls – Correlation with HVPG
Schneider AW et al. J Hepatol 1999 ; 30 : 876 – 881.
PI: 0.85
20 controls
0.92 ± 0.1
PI: 1.22
50 cirrhotic patients
1.14 ± 0.18
Directly correlated with HVPG (Hepatic venous pressure gradient)
48. Damping index of HV waveform
Severe portal hypertension : HVPG > 12 mmHg
Kim MY et al. Liver International 2007 ; 27 : 1103 – 1110.
Minimum velocity of downward HV
Maximum velocity of downward HV
Damping index =
Normal value: < 0.6
Severe portal hypertension: ≥ 0.6
49. Damping index of HV waveform in cirrhosis
DI: 0.26
HVPG: 7 mmHg
DI: 0.72
HVPG: 15 mmHg
Kim MY et al. Liver International 2007 ; 27 : 1103 – 1110.
DI of 0.6: Sen 76%, Sp 82, & AUC 0.86 for severe PHT
HVPG :Hepatic venous pressure gradient
50. Doppler in cirrhosis / PHT
Prognostic implications
• Collaterals PUV High bleeding risk in surgery
Reversed LGV High bleeding risk of EV
S-R shunt Low bleeding risk of EV
• Portal vein Low flow High risk of HE
Inversed flow CI for TIPS & porto-caval
shunt
Congestion index High bleeding risk of EV
• Hepatic artery Increased PI ESLD
• Hepatic vein Monophasic ESLD
Increased DI Severe PHT (> 12 mmHg)
55. 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
56. Superior mesenteric vein thrombosis
Transverse image of SMA & SMV
http://www.ultrasoundcases.info
SMA
SMV
57. Acute thrombosis of portal vein
Complete thrombosis
http://www.sites.tufts.edu
Echogenic material visualized within portal vein.
Increased diameter of portal vein.
58. Partial thrombosis of portal vein
Echogenic material occluding lumen of PV by ≈ 50%
Sacerdoti D et al. J Ultrasound 2007 ; 10 : 12 – 21.
59. 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
60. Non-malignant PV thrombosis in cirrhosis
Systematic review – Many unresolved issue
• 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.
61. 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.
62. 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
63. 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
64. 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
65. Chronic portal vein thrombosis
Portal cavernoma
Parikh et al. Am J Med 2010 ; 123 : 111 – 119.
Hepatopetal collaterals around thrombosed portal vein
67. 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
68. 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
70. Transjugular Intrahepatic Portosystemic Shunt
TIPS
Highly effective for
– Reducing ascites
– Recurrent variceal hemorrhage
– Improving quality of life
High rate of stenosis or thrombosis
High rate of hepatic encephalopathy
72. Follow-up of TIPS by Doppler US
• 24 to 48 hours (baseline)
• 3 months
• 6 months
• 12 months
• Annually thereafter
Middleton WD et al. Ultrasound Quarterly 2003 ; 19 : 56 – 70.
Real goal of surveillance
Detect stenosis before complete thrombosis
73. TIPS / Normal
Middleton WD et al. Ultrasound Quarterly 2003 ; 19 : 56 – 70.
Stent within liver parenchyma
Hepatopetal flow in MPV
Hepatofugal flow in RPV
Color Doppler of TIPS Color & pulsed Doppler of TIPS
Monophasic pulsatile flow
Velocity: 106 cm/sec
74. TIPS / Mirror image artifact
If not recognized: migration into heart (emergency intervention)
If uncertainty persists: chest radiograph
Wachsberg RH. Ultrasound Quarterly 2003 ; 19 : 139 – 148.
Stent on either side of
diaphragm
Mirror image artifact Variant of mirror image artifact
Stent above diaphragm
True TIPS visible by rotating probe
75. TIPS / migration
Middleton WD et al. Ultrasound Quarterly 2003 ; 19 : 56 – 70.
Proximal portion migrated out of PV into parenchymal tract
This resulted in complete thrombosis of stent
Longitudinal view of TIPS
76. TIPS – Stenosis
Middleton WD et al. Ultrasound Quarterly 2003 ; 19 : 56 – 70.
Mid TIPS
Mean portal vein Right portal vein
Mid TIPS Distal TIPS
Vel 26 cm/sec
Aliasing 371 cm/sec 98 cm/sec
Hepatopetal flow
77. TIPS / occlusion
Ricci P et al. J Ultrasound 2007 ; 10 : 22 – 27.
Homogeneous hyperechoic intraluminal material
without any color flow within TIPS
78. Robinson KA et al. Ultrasound Quarterly 2009 ; 25 : 3 – 13.
Detectable flow within UV
Flow directed away from LPV
Indicating recanalization & PHT
Similar color Doppler viewLongitudinal US of LLL
UV extending from LPV
Diameter: 1.8 mm
P-S collaterals / Recanalized umbilical vein
79. Mansour MA et al. Vascular Diagnosis. Elsevier-Saunders, Philadelphia, 1st edition, 2005
P-S collaterals / Omental varices
Transverse view with linear transducer (7-MHz)
Omental varices just beneath abdominal wall
80. P-S collaterals / Lumbar & epigastric collaterals
Mansour MA et al. Vascular Diagnosis. Elsevier-Saunders, Philadelphia, 1st edition, 2005
Large collateral vein between LK & lower pole of spleen
shunting blood from splenic hilum to lumbar & epigastric veins
81.
82. Intestinal infarction
Considered from presentation until resolution of pain
• 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
83. 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
84. 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
Editor's Notes
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.
Most prevalent portal systemic collateral present in 80% to 90%of patients with portal hypertension.
Most clinically important of the portal systemic collaterals because its presence implies an increased risk for variceal hemorrhage.
Determination of flow direction in splenic vein increases the diagnostic confidence of S-R shunt.
Hepatic artery and the portal vein have blood flowing in opposite directions.
Although the role of Doppler sonography has decreased in the evaluation of the hepatic lesions with recent advances in CT and
MR imaging, it should be kept in mind that Doppler sonography has the advantage over CT and MRI of demonstrating the direction of the flow of the hepatic vasculature.
Acceleration resulting from focal compression by regenerative nodules
Portal hypertension is a clinical syndrome defined by a pathological increase in portal pressure. The development of cirrhosis of the liver is characterized by clinical manifestations related to portal hypertension like esophageal varices, ascites, bleeding, and encephalopathy. Direct measurement of portal pressure is invasive, inconvenient, and clinically impractical. Currently, the most commonly used parameter is the Hepatic Venous Pressure Gradient (HVPG), i.e., the difference between the wedged (WHVP) and the free hepatic venous pressures. HVPG represents the gradient between pressures in the portal vein and the intra-abdominal portion of inferior vena cava. When blood flow in a hepatic vein is stopped by a wedged catheter, the proximal static column of blood transmits the pressure from the preceding communicated vascular territory (hepatic sinusoids) to the catheter. Thus, WHVP reflects hepatic sinusoidal pressure and not the portal pressure itself. In the normal liver, due to pressure equilibration through interconnected sinusoids, wedged pressure is slightly lower than portal pressure, though this difference is clinically insignificant. In liver cirrhosis, the static column created by balloon inflation cannot be decompressed at the sinusoidal level due to disruption of the normal intersinusoidal communications; therefore, WHVP gives an accurate estimation of portal pressure in cirrhosis. The normal HVPG value is between 1 to 5 mmHg. Pressure higher than this defines the presence of portal hypertension, regardless of clinical evidence. HVPG >or= 10 mmHg (termed clinically significant portal hypertension) is predictive of the development of complications of cirrhosis, including death. HVPG above 12 mmHg is the threshold pressure for variceal rupture. The main advantages of HVPG are its simplicity, reproducibility, and safety. This review summarizes the technique of the HVPG measurement.
Value of 0.6 of DI showed a sensitivity of 75.9% and a specificity of 81.8% for the presence of severe portal hypertension (hepatic venous pressure gradient >12mmHg) (AUC = 0.860).
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?
Absolute contraindications to TIPS:
1- Severe hepatic encephalopathy and liver failure
2- Chronic portal vein thrombosis, especially those with narrowed and fibrotic veins or cavernous transformation
Experienced centers are often successful in placing a shunt in patients with acute or subacute thrombosis.
3- Severe right-heart failure with elevated central venous pressure
Relative contraindications to TIPS
1- Polycystic liver disease
2- Systemic hepatic infections
3- Hypervascular liver tumors
Technical success rate for placement of TIPS is greater than 90%.
The procedural complication rate ranges from 10 to 16%.
Mortality related to the TIPS procedure is usually less than 2%.
Primary patency:
1 year: 25 - 66%
2 years: 5 - 42%
3 years: 21%
4 years: 13%
5 years 13%
Radiologic revision of malfunctioning shunt usually successful, resulting in primary assisted patency rate of approximately
1 year: 85%
2 year: 61%
3 years: 46%
4 years: 42%
5 years: 36%
Early stenosis would be missed if one waited until the stent velocity dropped to 50 to 60 cm/second.