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    Portal Hypertension, A Simple Guide To The Condition, Diagnosis, Treatment And Related Conditions
    Portal Hypertension, A Simple Guide To The Condition, Diagnosis, Treatment And Related Conditions
    Portal Hypertension, A Simple Guide To The Condition, Diagnosis, Treatment And Related Conditions
    Ebook187 pages1 hour

    Portal Hypertension, A Simple Guide To The Condition, Diagnosis, Treatment And Related Conditions

    By Kenneth Kee

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    This book describes Portal Hypertension, Diagnosis and Treatment and Related Diseases
    Portal hypertension is the presence of abnormal high blood pressure in the hepatic portal vein.
    Portal hypertension is defined as a portal pressure of 12 mm Hg or more (normal 5-10 mm Hg).
    In the normal patient, free hepatic vein pressure (FHVP) is identical to inferior vena cava pressure.
    FHVP is defined as an internal zero reference point.
    Wedged hepatic venous pressure (WHVP) is the pressure gauged by inflating a balloon at the catheter tip, thus blocking a hepatic vein branch.
    Measurement of the WHVP gives a close evaluation of portal pressure.
    The hepatic venous pressure gradient (HVPG) is the difference in pressure between the portal vein and the inferior vena cava.
    The HVPG is equal to the WHVP value minus the FHVP value (i.e., HVPG = WHVP - FHVP).
    The normal HVPG is 3-6 mm Hg.
    Portal hypertension is defined as a persistent rise of portal pressure above normal.
    1. An HVPG of 8 mm Hg is believed to be the threshold above which ascites potentially can develop.
    2. An HVPG of 12 mm Hg is the threshold for the possible formation of varices.
    High portal pressures may prompt patients to a higher danger of variceal hemorrhage
    Numerous disorders are related with portal hypertension with hepatic cirrhosis being the most frequent cause of this disorder.
    The normal liver has the capability to contain large alterations in portal blood flow without large changes in portal pressure.
    Portal hypertension happens from a combination of higher portal venous inflow and higher resistance to portal blood flow.
    Patients with cirrhosis reveal higher splanchnic arterial flow and venous inflow into the liver.
    Higher splanchnic arterial flow is thought to be partly by:
    1.Reduced peripheral vascular resistance
    2.Increased cardiac output in the patient with cirrhosis.
    Nitric oxide appears to be the major driving force
    Higher resistance across the sinusoidal vascular bed of the liver is produced by fixed factors and dynamic factors
    Symptoms:
    Symptoms of Budd-Chiari syndrome are due to reduced outflow of blood from the liver, with resulting hepatic congestion and portal hypertension
    Diagnosis:
    Check the patient's blood pressure and pulse with the patient in the supine and seated positions.
    Signs of portosystemic collateral formation are:
    a.Dilated veins in the anterior abdominal wall - May indicate umbilical epigastric vein shunts
    b.Venous pattern on the flanks - May indicate portal-parietal peritoneal shunting
    c.Caput medusae (tortuous paraumbilical collateral veins)
    d.Rectal hemorrhoids
    e.Ascites
    Laboratory studies are directed towards investigating the causes of cirrhosis, which is the most frequent cause of portal hypertension.
    The rate and volume of bleeding in the patient should be evaluated.
    Measure the platelet count and prothrombin time (PT), send blood for renal and liver function tests (LFTs), and measure serum electrolyte levels.
    Ultrasound, CT Scanning and MRI may show features suggestive of hepatic cirrhosis with portal hypertension
    Upper Gastrointestinal Endoscopy is an essential diagnostic and treatment tool.
    Portal hypertension measurement will confirm portal hypertension.
    The portal hypertension itself is difficult to treat effectively, except by:
    A.Treating the underlying cause.
    B.Liver transplantation, if indicated
    Portal venous pressure can be reduced by:
    a. Beta blockers ± nitrates
    b. Shunt procedures
    Endoscopic procedures such as TIPS can decompress the portal venous system to prevent rebleeding from varices
    Surgical procedures such as portosystemic shunts prevent bleeding
    Liver transplant is required if other treatments failed.

    TABLE OF CONTENT
    Introduction
    Chapter 1 Portal Hypertension
    Chapter 2 Causes
    Chapter 3 Symptoms
    Chapter

    LanguageEnglish
    PublisherKenneth Kee
    Release dateJan 29, 2018
    ISBN9781370747481
    Portal Hypertension, A Simple Guide To The Condition, Diagnosis, Treatment And Related Conditions
    Author

    Kenneth Kee

    Medical doctor since 1972.Started Kee Clinic in 1974 at 15 Holland Dr #03-102, relocated to 36 Holland Dr #01-10 in 2009.Did my M.Sc (Health Management ) in 1991 and Ph.D (Healthcare Administration) in 1993.Dr Kenneth Kee is still working as a family doctor at the age of 74However he has reduced his consultation hours to 3 hours in the morning and 2 hours inthe afternoon.He first started writing free blogs on medical disorders seen in the clinic in 2007 on http://kennethkee.blogspot.com.His purpose in writing these simple guides was for the health education of his patients which is also his dissertation for his Ph.D (Healthcare Administration). He then wrote an autobiography account of his journey as a medical student to family doctor on his other blog http://afamilydoctorstale.blogspot.comThis autobiography account “A Family Doctor’s Tale” was combined with his early “A Simple Guide to Medical Disorders” into a new Wordpress Blog “A Family Doctor’s Tale” on http://ken-med.com.From which many free articles from the blog was taken and put together into 1000 eBooks.He apologized for typos and spelling mistakes in his earlier books.He will endeavor to improve the writing in futures.Some people have complained that the simple guides are too simple.For their information they are made simple in order to educate the patients.The later books go into more details of medical disorders.He has published 1000 eBooks on various subjects on health, 1 autobiography of his medical journey, another on the autobiography of a Cancer survivor, 2 children stories and one how to study for his nephew and grand-daughter.The purpose of these simple guides is to educate patient on health disorders and not meant as textbooks.He does not do any night duty since 2000 ever since Dr Tan had his second stroke.His clinic is now relocated to the Buona Vista Community Centre.The 2 units of his original clinic are being demolished to make way for a new Shopping Mall.He is now doing some blogging and internet surfing (bulletin boards since the 1980's) startingwith the Apple computer and going to PC.The entire PC is upgraded by himself from XT to the present Pentium duo core.The present Intel i7 CPU is out of reach at the moment because the CPU is still expensive.He is also into DIY changing his own toilet cistern and other electric appliance.His hunger for knowledge has not abated and he is a lifelong learner.The children have all grown up and there are 2 grandchildren who are even more technically advanced than the grandfather where mobile phones are concerned.This book is taken from some of the many articles in his blog (now with 740 posts) A Family Doctor’s Tale.Dr Kee is the author of:"A Family Doctor's Tale""Life Lessons Learned From The Study And Practice Of Medicine""Case Notes From A Family Doctor"

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      Book preview

      Portal Hypertension, A Simple Guide To The Condition, Diagnosis, Treatment And Related Conditions - Kenneth Kee

      Portal Hypertension,

      A

      Simple

      Guide

      To

      The Condition,

      Diagnosis,

      Treatment

      And

      Related Conditions

      By

      Dr Kenneth Kee

      M.B.,B.S. (Singapore)

      Ph.D (Healthcare Administration)

      Copyright Kenneth Kee 2018 Smashwords Edition

      Published by Kenneth Kee at Smashwords.com

      Dedication

      This book is dedicated

      To my wife Dorothy

      And my children

      Carolyn, Grace

      And Kelvin

      This book describes Portal Hypertension, Diagnosis and Treatment and Related Diseases which is seen in some of my patients in my Family Clinic.

      (What The patient Need to Treat Portal Hypertension)

      This eBook is licensed for your personal enjoyment only. This eBook may not be re-sold or given away to other people. If the patient would like to share this book with another person, please purchase an additional copy for each reader.

      If you’re reading this book and did not purchase it, or it was not purchased for your use only, then please return to Smashwords.com and purchase your own copy.

      Thank you for respecting the hard work of this author.

      Introduction

      I have been writing medical articles for my blog http://kennethkee.blogspot.com (A Simple Guide to Medical Disorder) for the benefit of my patients since 2007.

      My purpose in writing these simple guides was for the health education of my patients.

      Health Education was also my dissertation for my Ph.D (Healthcare Administration).

      I then wrote an autobiolographical account of his journey as a medical student to family doctor on his other blog http://afamilydoctorstale.blogspot.com.

      This autobiolographical account A Family Doctor’s Tale was combined with my early A Simple Guide to Medical Disorders into a new Wordpress Blog A Family Doctor’s Tale on http://kenkee481.wordpress.com.

      From which many free articles from the blog was taken and put together into 1000 eBooks.

      Some people have complained that the simple guides are too simple.

      For their information they are made simple in order to educate the patients.

      The later books go into more details of medical disorders.

      The first chapter is always from my earlier blogs which unfortunately tends to have typos and spelling mistakes.

      Since 2013, I have tried to improve my spelling and writing.

      As I tried to bring the patient the latest information about a disorder or illness by reading the latest journals both online and offline, I find that I am learning more and improving on my own medical knowledge in diagnosis and treatment for my patients.

      Just by writing all these simple guides I find that I have learned a lot from your reviews (good or bad), criticism and advice.

      I am sorry for the repetitions in these simple guides as the second chapters onwards have new information as compared to my first chapter taken from my blog.

      I also find repetition definitely help me and maybe some readers to remember the facts in the books more easily.

      I apologize if these repetitions are irritating to some readers.

      Chapter 1

      Portal hypertension

      What is Portal hypertension?

      Portal hypertension is the presence of abnormal high blood pressure in the hepatic portal vein.

      Portal hypertension is defined as a portal pressure of 12 mm Hg or more (normal 5-10 mm Hg).

      In the normal patient, free hepatic vein pressure (FHVP) is identical to inferior vena cava pressure.

      FHVP is defined as an internal zero reference point.

      Wedged hepatic venous pressure (WHVP) is the pressure gauged by inflating a balloon at the catheter tip, thus blocking a hepatic vein branch.

      Measurement of the WHVP gives a close evaluation of portal pressure.

      The hepatic venous pressure gradient (HVPG) is the difference in pressure between the portal vein and the inferior vena cava.

      The HVPG is equal to the WHVP value minus the FHVP value (i.e., HVPG = WHVP - FHVP).

      The normal HVPG is 3-6 mm Hg.

      Portal hypertension is defined as a persistent rise of portal pressure above normal.

      1. An HVPG of 8 mm Hg is believed to be the threshold above which ascites potentially can develop.

      2. An HVPG of 12 mm Hg is the threshold for the possible formation of varices.

      High portal pressures may prompt patients to a higher danger of variceal hemorrhage.

      What are the Causes of Portal Hypertension?

      Causes

      Numerous disorders are related with portal hypertension with hepatic cirrhosis being the most frequent cause of this disorder.

      The normal liver has the capability to contain large alterations in portal blood flow without large changes in portal pressure.

      Portal hypertension happens from a combination of higher portal venous inflow and higher resistance to portal blood flow.

      Patients with cirrhosis reveal higher splanchnic arterial flow and, accordingly, higher splanchnic venous inflow into the liver.

      Higher splanchnic arterial flow is thought to be partly by:

      1. Reduced peripheral vascular resistance and

      2. Increased cardiac output in the patient with cirrhosis.

      Nitric oxide appears to be the major driving force for this phenomenon.

      Also, presence for splanchnic vasodilatation is evident.

      Putative splanchnic vasodilators are:

      1. Glucagon,

      2. Vasoactive intestinal peptide,

      3. Substance P,

      4. Prostacyclin,

      5. Bile acids,

      6. Tumor necrosis factor-alpha (TNF-alpha), and

      7. Nitric oxide.

      Higher resistance across the sinusoidal vascular bed of the liver is produced by fixed factors and dynamic factors.

      66% of intra-hepatic vascular resistance can be because of fixed changes in the hepatic architecture.

      Such changes are:

      1. The development of regenerating nodules and, after the formation of collagen by activated stellate cells,

      2. Deposition of the collagen within the space of Disse.

      Dynamic factors are accountable for 33% of intra-hepatic vascular resistance.

      Stellate cells work as contractile cells for adjacent hepatic endothelial cells.

      The nitric oxide formed by the endothelial cells, in turn, controls the relative degree of vasodilatation or vasoconstriction caused by the stellate cells.

      In liver cirrhosis, the reduced local production of nitric oxide by endothelial cells lets stellate cell contraction, with outcome of vasoconstriction of the hepatic sinusoid.

      This is opposed to the peripheral circulation, where there are high circulating amounts of nitric oxide in cirrhosis.

      Higher local amounts of vasoconstriction chemicals, such as endothelin, may also add to sinusoidal vasoconstriction.

      The portal hypertension of cirrhosis is formed by the disruption of hepatic sinusoids.

      The portal hypertension may be observed in a variety of non-cirrhotic disorders.

      Pre-hepatic causes

      Pre-hepatic causes are:

      1. Splenic vein thrombosis and

      2. Portal vein thrombosis.

      These disorders often are linked with:

      1. Hyper-coagulable states and

      2. Malignancy (e.g., pancreatic cancer).

      In a retrospective study of patients with cirrhosis and portal vein thrombosis, doctors reported that warfarin anticoagulation may probably safely and effectively recover cases of more advanced portal vein thrombosis.

      They did not notice any advantage of anticoagulation on decompensation or mortality.

      Levels of albumin were significant predictors of decompensated disease at 1 year.

      Intra-hepatic causes

      Intra-hepatic causes of portal hypertension are divided into:

      1. Pre-sinusoidal,

      2. Sinusoidal, and

      3. Post-sinusoidal disorders.

      The normal sinusoidal cause of portal hypertension is cirrhosis.

      The typical form of pre-sinusoidal portal hypertension is caused by the deposition of Schistosoma oocytes in pre-sinusoidal portal venules, with the later formation of granulomata and portal fibrosis.

      Schistosomiasis is the most frequent non-cirrhotic reason of bleeding of esophageal varices worldwide.

      Schistosoma mansoni infection is found in Puerto Rico, Central and South America, the Middle East, and Africa.

      S japonicum is found in the Far East.

      S hematobium, found in the Middle East and Africa, can cause portal fibrosis but more often is linked with urinary tract deposition of eggs.

      The typical post-sinusoidal disease is a disorder known as veno-occlusive disease.

      Obliteration of the terminal hepatic venules may occur from:

      1. Ingestion of pyrrolizidine alkaloids in Comfrey tea or Jamaican bush tea or

      2. After the high-dose chemotherapy that occurs before bone marrow transplantation.

      Post-hepatic causes

      Post-hepatic causes of portal hypertension may be:

      1. Chronic right-sided heart failure and tricuspid regurgitation and

      2. Obstructing lesions of the hepatic veins and inferior vena cava.

      The latter disorders, and the symptoms they cause, are termed Budd-Chiari syndrome.

      Predisposing disorders are:

      1. Hyper-coagulable states,

      2. Tumor invasion into the hepatic vein or inferior vena cava, and

      3. Membranous blockage of the inferior vena cava.

      Inferior vena cava webs are observed most often in South and East Asia and are believed to be because of nutritional factors.

      The most frequent cause of portal hypertension is cirrhosis.

      Vascular resistance and blood flow are 2 essential factors in its formation.

      Normal portal pressure is typically considered to be between 5 and 10 mm Hg.

      Once the portal pressure rises to 12 mm Hg or greater, complications can occur such as varices and ascites.

      Esophageal varices are the main cause for the main complication of portal hypertension, massive upper gastrointestinal (GI) hemorrhage

      Pathogenesis

      The portal vein supplies about 1500 mL/min of blood from the small and large bowel, the spleen and the stomach to the liver.

      Blockage of portal venous flow, whatever the cause, leads to a rise in portal venous pressure.

      The response to higher venous pressure is the formation of

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