Why does portal hypertension cause splenomegaly
Price DC Spleen: Nuclear medicine. Mosby, St Louis Google Scholar. Butterman G Radionuclide scanning in cirrhosis. Gut — Google Scholar. A receiver operator characteristic analysis of the common interpretative criteria. Radiology — Google Scholar. Burhenne R Spleen: overview. Gut — PubMed Google Scholar. Koga T Correlation between sectional area of the spleen by ultrasonic tomography and actual volume of the removed spleen.
Radiology — PubMed Google Scholar. Friedman AC Magnetic resonance imaging of the spleen. In: Radiology of the liver, biliary tract, pancreas and spleen.
Williams and Wilkins, Baltimore, pp — Google Scholar. Gut 85—90 PubMed Google Scholar. Celiac axis catheterization: uses and value in portal hypertension. In: Read AE ed The liver. Butterworth, London, pp Google Scholar. A reappraisal. Am J Gastroenterol — Google Scholar. Atkinson M, Sherlock S Intra-splenic pressure as index of portal venous pressure.
Sato S, Ohnishi K, Sugita S, Okuda K Splenic artery and superior mesenteric artery blood flow: Non-surgical Doppler ultrasound measurement in healthy subjects and patients with chronic liver disease.
Zetterstroem B Evaluation of the Xenon clearance method for measurement of blood flow in the dog spleen. Acta Chir Scand 27—33 Google Scholar.
Raven, New York, pp 95— Google Scholar. Clinical and function studies and results of operation. Sarin SK Noncirrhotic portal fibrosis. Acta Hepatospleno 28—40 Google Scholar. Surgery — PubMed Google Scholar. Sugita S, Ohnishi K, Saito M Splanchnic hemodynamics in portal hypertensive dogs with portal fibrosis produced by intraportal injection of killed non-pathogenic colon bacilli. Shaldon S, Sherlock S Portal hypertension in the myeloproliferative syndromes and the reticuloses.
Arch Surg 98— Google Scholar. Am J Med — Google Scholar. Reversal following splenectomy. A case report with a discussion of a mechanism of portal hypertension. Arch Intern Med — Google Scholar. Radiology 63—64 PubMed Google Scholar. Belli L, Puttini M, Marni A Extrahepatic portal obstruction: clinical experience and surgical treatment in patients.
J Cardiovasc Surg — Google Scholar. Novis BH, Duys P, Barbezat GO Fibreoptic endoscopy and the use of the Sengstaken tube in acute gastrointestinal hemorrhage in patients with portal hypertension and varices. Splenomegaly and hypersplenism Splenomegaly Splenomegaly is abnormal enlargement of the spleen. See also Overview of the Spleen. Splenomegaly is almost always secondary to other disorders.
Causes of splenomegaly are myriad, as are the Thrombocytopenia Overview of Platelet Disorders Platelets are cell fragments that function in the clotting system. Thrombopoietin helps control the number of circulating platelets by stimulating the bone marrow to produce megakaryocytes, Sequelae include opportunistic infections and an increased risk of Hemolysis is defined as premature destruction and hence a shortened RBC life span read more may result. Portal hypertension is often associated with a hyperdynamic circulation.
Mechanisms are complex and seem to involve altered sympathetic tone, production of nitric oxide and other endogenous vasodilators, and enhanced activity of humoral factors eg, glucagon. Portal hypertension is asymptomatic; symptoms and signs result from its complications. The most dangerous is acute variceal bleeding Varices Varices are dilated veins in the distal esophagus or proximal stomach caused by elevated pressure in the portal venous system, typically from cirrhosis. Patients typically present with sudden painless upper gastrointestinal bleeding, often massive.
Bleeding from portal hypertensive gastropathy is often subacute or chronic. Ascites Ascites Ascites is free fluid in the peritoneal cavity. The most common cause is portal hypertension. Symptoms usually result from abdominal distention. Diagnosis is based on physical examination and Portal hypertension is assumed to be present when a patient with chronic liver disease has collateral circulation, splenomegaly, ascites Ascites Ascites is free fluid in the peritoneal cavity.
Proof requires measurement of the hepatic venous pressure gradient, which approximates portal pressure, by a transjugular catheter; however, this procedure is invasive and usually not done. Imaging may help when cirrhosis is suspected. Ultrasonography or CT often reveals dilated intra-abdominal collaterals, and Doppler ultrasonography can determine portal vein patency and flow.
Esophagogastric varices and portal hypertensive gastropathy are best diagnosed by endoscopy, which may also identify predictors of esophagogastric variceal bleeding eg, red markings on a varix. Prognosis is predicted by the degree of hepatic reserve and the degree of bleeding. Ongoing endoscopic or drug therapy lowers the bleeding risk but decreases long-term mortality only marginally.
For treatment of acute bleeding, Overview of Gastrointestinal Bleeding Overview of Gastrointestinal Bleeding Gastrointestinal GI bleeding can originate anywhere from the mouth to the anus and can be overt or occult.
The manifestations depend on the location and rate of bleeding. See also Varices Nonselective beta-blockers with or without isosorbide mononitrate. In patients with esophagogastric varices that have bled, combined endoscopic and drug treatment decreases mortality and reduces risk of rebleeding better than either therapy used alone. A series of endoscopic banding sessions are done to obliterate residual varices, then periodic endoscopic surveillance is done to identify and treat recurrent varices.
Long-term drug therapy usually involves nonselective beta-blockers; these drugs lower portal pressure primarily by diminishing portal flow, although the effects vary. Agents include propranolol 40 to 80 mg orally twice a day , nadolol 40 to mg orally once a day , timolol 10 to 20 mg orally twice a day , and carvedilol 6. The abdominal ultrasound was performed using an ultrasound analyzer Acuson X , 3. For this, we used the Cairo and Niamey protocols to measure the longitudinal diameter of the spleen and classify the pattern of fibrosis as central fibrosis Pattern D , advanced fibrosis Pattern E or very advanced fibrosis Pattern F 12 Ultrasound in schistosomiasis: a practical guide to the standardized use of ultrasonography for the assessment of schistosomiasis-related morbidity: Second International Workshop.
October 22 - 26, , Niamey, Niger. Report of the second satellite symposium on ultrasound in schistosomiasis. An ultrasonographic study of liver fibrosis in patients infected with Schistosoma mansoni in north-east Brazil. Upper digestive tract endoscopy was used either to confirm or exclude the presence of esophageal varices and viral marker and liver function tests were performed to exclude viral hepatitis B and C.
Ethanol challenge in nonalcoholic patients with schistosomiasis. Stool samples were examined to detect intestinal parasites by the Lutz-Hoffman followed by Kato-Katz method. The Control Group had the same exclusion criteria as described above and were checked for possible contact with water contaminated by the cercariae of S.
The compensated hepatosplenic form corresponds to the severe form of disease and includes patients with hepatosplenomegaly and portal hypertension, but without ascites, jaundice or encephalopathy 9 9. About 15 mL of venous blood was drawn under aseptic conditions without stasis and placed in vacuum tubes Vacutainer; Becton Dickinson, UK. The first blood sample was placed in a polypropylene tube containing 0. Subsequently, the platelet free plasma was quickly distributed in 0.
A blood smear was prepared and stained for conventional microscopic analysis. The aliquots of plasma serum samples were also stored for the other tests. The study was conducted according to the norms of the Declaration of Helsinki. All subjects received an explanation about the study and signed informed consent forms. Statistical analyzes were performed using the unpaired Student t-test and Fisher's test for contingency analysis.
Furthermore, the Pearson correlation test was employed to examine the relationship between the longitudinal diameter of the spleen and platelet counts. P-values of less than 0. The Niamey classification of fibrosis showed predominance of advanced pattern E - 30 patients; Data are expressed as means. Controls vs. The D-dimer concentration was used for measure the fibrinolytic status and risk of bleeding. Upper gastrointestinal bleeding was found in 34 The mean longitudinal diameter of the spleen of the 55 patients was A total of 38 Furthermore, There was an inverse correlation between the longitudinal diameter of the spleen and the platelet count Figure 2.
It was also found that Table 2 shows the distribution of HS patients according to the type of cytopenia. Figure 3 demonstrates the massive splenomegaly of one patient with schistosomiasis.
Portal hypertension is one of the most important consequences of S. Due to the fibrotic process and venous congestion, HS patients develop hemodynamic changes associated with splenomegaly and high morbidity rates 16 Evaluation of splenomegaly in the hepatosplenic form of mansonic schistosomiasis.
Acta Trop. In a recently study in the same region, Dias et al. Associating portal congestive gastropathy and hepatic fibrosis in hepatosplenic mansoni schistosomiasis. This proves that these patients have advanced disease and that changes in liver function tests may be related to the high frequency of advanced fibrosis.
Camacho-Lobato et al. However, this study demonstrates elevated liver function tests and remarkable changes in coagulation tests. Lower values of platelet counts are seen especially in patients with HS after gastrointestinal bleeding. This was also seen in the current work with the possible cause being the increase of spleen and hypersplenism leading to frequent thrombocytopenia, leukopenia and anemia.
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