Collateral benefit : Dr N Sewgoolam · PATHOPHYSIOLOGY Cavernous transformation of the portal vein...
Transcript of Collateral benefit : Dr N Sewgoolam · PATHOPHYSIOLOGY Cavernous transformation of the portal vein...
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COLLATERAL BENEFIT
BYDR N SEWGOOLAM
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CASE PRESENTATION
29 year old maleProblems• Ascites• Hypersplenism
BMAT = hypercellular marrowno malignancy
• Jaundice
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Abdominal pain and distensionHaematemesisYellow discoloration of his eyesNo melaenaNo change in bowel habitsNo constitutional symptoms
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PAST MEDICAL HISTORY
Not a known hypertensive or diabetic
No cardiac pathology
No previous tuberculosis
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SOCIAL HISTORY
Moderate alcohol consumptionNon-smoker
No herbal medicationWater source: river
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ON EXAMINATION
Patient was comfortableJaundiced and pallorNo lymphadenopathyTemporal wastingNormotensiveApyrexial
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Abdominal examination
No prominent abdominal veinsSoft and distendedAscites 15cm firm splenomegalynon-tender and smoothDiastolic bruit to the left of the epigastriumNo hepatomegaly
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CVSCNS non-contributoryRESP
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SUMMARY
29 year old male patient problems of ascites
splenomegalyno palpable/ballotable
liverSingle episode of haematemesis
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DIFFERENTIALSPORTAL HYPERTENSION secondary
cirrhosis ? Viral ? Autoimmune Hepatitis? Alcohol related? Metabolic - Wilson’s disease
Haemochromatosis Alpha1 antitrypsin Def
Fibrosis ? Idiopathic ? schistosomiasis
Portal vein thrombosis ? 2 cirrhosis ? other
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INVESTIGATIONS
FBC: hb 8.8 wcc 1.81 plt 31PANCYTOPENIA
INR: 1.4
U&E: 138/3.9/109/21.8/4.7/73
LFT: TP 72 ALB 35 T.BIL 78ALP 85 GGT 34 ALT 21
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HEPATITIS A B negativeC
HIV negative
Cu & 24hr urine Cu NAD
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Fe studies = normal
AFP = normal range
ANF = negative
CXR Normal
Urine MCS = no evidence of parasites
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Ascitic fluid = transudateno organisms isolated
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UPPER ENDOSCOPY
Small distal varices
No signs of a recent bleed
Portal hypertensive gastropathy
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ULTRASOUND
Gross ascitesLiver = 12cm. The portal vein is thrombosed with multiple channels in the porta hepatis – cavernous transformationHepatic veins and IVC are patentSpleen – massively enlarged.
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CT abdomen
Portal vein thrombosis with portal hypertensionMassive splenomegaly with porto-systemic shunting into the left renal vein
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LIVER BIOPSYIrregular fibrosis suggesting underlying cirrhosis
No evidence of granulomatousinflammation
No schistosoma ova
No malignancy
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ASSESSMENT
29 year old male with:
1. Cirrhosis with portal hypertension2. Portal vein thrombosis3. Spontaneous spleno-renal shunt
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Portal vein thrombosis
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Recognised with increasing frequency:
Due to increasing use of ultrasonography in the evaluation of abdominal symptoms.
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Exact frequency = unknown
Approximately 5%
Occurs at any age
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definition
Restricted to thrombosis developing in the trunk of the portal veinCan extend downstream to involve the left or right branchUpstream to involve the splenicvein, superior or inferior mesenteric veins
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UPSTREAM:Little effect on the intestine as long as mesenteric venous arches remain patentIf ischemia results, infarction of the intestine may follow
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DOWNSTREAMClinical signs of liver disease are absent/transientBiochemically: albumin prothrombin ratio normalserum bilirubin
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Uncommon manifestation of portal hypertensionIn a proportion of patients etiology is unknownPathogenesis is unclear !!Pathophysiology and clinical aspectsdiffer according to the site of the thrombosis in the portal system
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PATHOPHYSIOLOGYCavernous transformation of the portal vein ie periportal collaterals occurs Development of multiple small vessels in and around the recanalising main veinLeash of fine / enlarged vessels seen in place of the PVColour/pulsed doppler: shows blood flow in these periportalcollaterals
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cavernous transformation of the PV: Appearance of a sub-hepatic sponge-like mass
Bile duct varices-pseudocholangiocarcinoma signseen on ERCP
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In portal hypertension, spontaneous spleno-renal shunting, due to the development of collaterals, may lead to clinical benefit
(ie the reduction of oesophageal varicealbleeding.)
thus representing“ COLLATERAL BENEFIT “
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15.9% of a total of 151 patients with portal hypertension,showed evidence of spontaneous spleno-renal shuntsCONCLUSION: DEVELOPMENT OF THESE SHUNTS PROVIDES PROTECTION FROM VARICEAL BLEEDING
Journal of Gastroenterology and hepatology (2002)
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causes
General thrombogenic factors (60%)
Local factors (40%)
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Inherited thrombopilias
Factor V Leiden mutation (5%)Factor II mutataion (3%)Protein C deficiency (5%)Protein S deficiency (5%)Antithrombin (1%)
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Local factors
Focal inflammatory lesionsdiverticulitisduodenal ulcerpancreatitisinflammatory bowel disease
Injury to the portal venous systemsplenectomy colectomy
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Clinical manifestations
Differ according to the stage that PVT is diagnosedEarly: abdominal pain
inflammatory statefever
Can be completely asymptomatic
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Late : thrombocytopaeniaenlarged spleens/s of portal hypertensionGIT bleeding
Compensatory mechanisms have usually developed by this time
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COLLATERAL FORMATIONGROUP 1
At the cardia of the stomach where the left gastric vein anastomoses with the intercostal , oesophageal and azygosminor veins
At the anus, involving the superior haemorrhoidal veinCan lead to rectal varices
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GROUP 2In the falciform ligament through the
para-umbilical veins
GROUP 3Where abdominal organs are in
contact with retroperitoneal tissuesThey include Lumbar veins
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GROUP 4 Portal venous blood is carried to the left renal vein usually via the splenicvein
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therapy
No controlled study of any form of RxPrompt anticoagulation is recommended as it allows recanalisation (4-6 months)Later, insertion of TIPS may be necessary to maintain portal circulation
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Recommendation is to assess patients on an individual basis and decide on optimal management accordingly
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Back to our patient….
Started on low dose duiretics, to which he responded very wellHe was also kept on PPI and a beta blocker to manage the portal gastropathyHe is currently seen in GI clinic every 6/12 with no further complications
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The end
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The end