This document discusses portal hypertension and esophageal varices. It begins by defining portal hypertension as increased blood pressure within the portal venous system, usually caused by cirrhosis of the liver obstructing blood flow. Esophageal varices develop as collateral blood vessels when portal pressure exceeds 12 mmHg. The document then covers causes of portal hypertension, risk factors for bleeding varices, clinical presentation, investigations including endoscopy, and treatment approaches focusing on preventing or managing bleeding from varices.
Fwd: Bambury lecture on venous and lymphatic disorders of the limbJeku Jacob
---------- Forwarded message ----------
From: Henning L. Stokmo <helangen@gmail.com>
Date: 2009/2/12
Subject: Bambury lecture on venous and lymphatic disorders of the limb
To: ucdgrad09@gmail.com
ALL THE QUESTIONS ARE HAVING VERY STANDARD ANSWERS FROM THE STANDARD BOOKS)
REF : ROBBINS & COTRAN PATHOLOGIC BASIS OF DISEASE.
COMPREHENSIVE IMAGE BASED REVIEW OF PATHOLOGY BY SONI .
GARG & GUPTA PATHOLOGY REVIEW & GENETICS.
Fwd: Bambury lecture on venous and lymphatic disorders of the limbJeku Jacob
---------- Forwarded message ----------
From: Henning L. Stokmo <helangen@gmail.com>
Date: 2009/2/12
Subject: Bambury lecture on venous and lymphatic disorders of the limb
To: ucdgrad09@gmail.com
ALL THE QUESTIONS ARE HAVING VERY STANDARD ANSWERS FROM THE STANDARD BOOKS)
REF : ROBBINS & COTRAN PATHOLOGIC BASIS OF DISEASE.
COMPREHENSIVE IMAGE BASED REVIEW OF PATHOLOGY BY SONI .
GARG & GUPTA PATHOLOGY REVIEW & GENETICS.
Approach to Management of Upper Gastrointestinal (GI) BleedingArun Vasireddy
Upper gastrointestinal bleeding is gastrointestinal bleeding in the upper gastrointestinal tract, commonly defined as bleeding arising from the esophagus, stomach, or duodenum. Blood may be observed in vomit (hematemesis) or in altered form in the stool (melena). Depending on the severity of the blood loss, there may be symptoms of insufficient circulating blood volume and shock. As a result, upper gastrointestinal bleeding is considered a medical emergency and typically requires hospital care for urgent diagnosis and treatment. Upper gastrointestinal bleeding can be caused by peptic ulcers, gastric erosions, esophageal varices, and some rarer causes such as gastric cancer.
The initial assessment includes measurement of the blood pressure and heart rate, as well as blood tests to determine hemoglobin concentration. In significant bleeding, fluid replacement is often required, as well as blood transfusion, before the source of bleeding can be determined by endoscopy of the upper digestive tract with an esophagogastroduodenoscopy. Depending on the source, endoscopic therapy can be applied to reduce rebleeding risk. Specific medical treatments (such as proton pump inhibitors for peptic ulcer disease) or procedures (such as TIPS for variceal hemorrhage) may be used. Recurrent or refractory bleeding may lead to need for surgery, although this has become uncommon as a result of improved endoscopic and medical treatment.
Dr. Zahid Iqbal Mir, MBBS, MS (General Surgery), DNB (General Surgery) has done his bachelors and masters in General Surgery from the prestigious Govt Medical College Jammu and DNB in General Surgery from NBEMS New Delhi. He is a passionate surgeon, earlier practising at Government Medical College, Jammu as Registrar in Department of General Surgery. Nowadays working as Senior Resident in Department of General Surgery, Government Medical College & Hospital, Sector 32, Chandigarh and a rising name in field of surgery.
He is an enthusiastic, enigmatic and dedicated teacher as well. He is not just a resolute learner, but also an awe inspiring guiding light for his juniors, which makes him the most loveable and respected senior.
esophageal varices are the second most common cause of upper GI bleed after PUD.These are actually the dilated veins which occur secondary to increase in the pressure in the portal circulation called as Portal Hypertension..
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
1. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
SASI 2015
PORTAL HTN
PHYSIOLOGY:
Portal vein flow 900 --- 1200 ml/min.
Hepatic arterial flow 500 --- 700 ml /min.
Normal pressure 8---12 (( cmH2o))------ 5 –10 mmHg.
Pressure = flow(( rarely due to increase flow AV fistula and splenomegally x resistance(( )).
PORTAL HTN--- an increase in resting portal venous pressure > 12 mmHg.
PORTAL HTN results from:
A. Increased resistance to portal flow
B. Increased portal flow
measurement of hepatic venous pressure are useful for determining the site of resistance . The
hepatic venous pressure gradient is the difference between the wedged hepatic venous pressure and
free hepatic venous pressure.
DEFINITION:
Portal HTN is an increase in the blood pressure within the portal venous system . Normally
the veins come from the stomach ,intestine ,spleen and pancrease ,merge into the portal
veins. If the vessels in the liver are blocked ,it is hard for the blood to flow causing pressure
in the portal system.
When the pressure becomes too high ,the blood backs up and finds other ways to flow
back to the heart ,where it is pumped to the lungs ,where it gets rid of waste products and
picks up oxygen .
The blood travel to the veins in the oesophagus ,in the skin of the abdomen , and the veins
of the rectum to get around the blockages in the liver.
It is Product of portal flow volume and resistance to out flow from the portal vein.
The hydrostatic pressure is more than 5 mmHg , results initially from obstruction to portal
venous out flow.
WHAT IS THE CAUSE?
The most common symptom is cirrhosis.
PRE SINUOIDAL------ portal vein thrombosis
Portal fibrosis
Infiltrative lesions
SINUSOIDAL -------------cirrhosis
POST SINUSOIDAL ------ budd chiari syndrome
Venoocclusive lesions
In cirrhosis,
1.There is increased resistance to out flow through distorted hepatic
sinusoids
2.Enhanced portal flow due to splanchnic arteriolar dilatation
2. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
SASI 2015
CAUSES OF PORTAL HTN:
A.EXTRAHEPATIC OBSTRUCTION OF PORTAL VEIN AND ITS BRANCHES:----
1. Postal vein thrombosis
2. Splenic vein thrombosis
B. HEPATIC VENOUS OUTFLOW OBSTRUCTION:-----
1. Suprahepatic ----
i. Budd chiarri syndrome
ii. Constrictive
iii. Right heart failure
2.Smaller hepatic vein and venules---
A. Veno-occlusive disease
i. Pyrrlizidine alkaloids
ii. Radiation
iii. Anti leukemic drugs
B. Sclerosing hyaline necrosis
C. Hepatic causes:
There may be presinusoidal and sinusoidal resistance to flow
1) Presinusoidal :
1. Schistosomiasis
2. Myeloproliferative
3. Primary biliary cirrhosis
4. Sarcoid
5. Arsenic ,Vinyl chloride
6. Firopolycystic disease
7. Ideopathic P.HTN
2) Sinusoidal:
1. Cirrhosis
2. Chronic active hepatitis
3. Partial nodular transfusion
D.Increased hepatic blood flow:
Tropical splenmegally
Hematological disease with massive splenomegally
Hepatorenal A/V fistula
PORTAL VEIN THROMBOSIS:
1. Abdominal sepsis—omphalitis ,pancreatitis, umbilical sepsis ,portal sepsis
2. Collagen vascular disease, inflammatory bowel disease
3. Cirrhosis ,retroperitoneal fibrosis
4. Hepatocellular carcinoma
5. Myeloproliferative syndromes ,PNH
6. Compression or invasion of portal vein by tumor
7. Sclerotherapy
8. Hypercoagulable--Factor V leide deficiency ,protein C deficiency
9. Pregnancy
10. Trauma
Liver cirrhosis is the cause of 80% of cases.
3. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
SASI 2015
With presinusoidal P.HTN , due to blocked portal vein or narrowing of the smaller intrahepatic
portal vein branches, the WHVP is normal.
P.HTN in cirrhosis may be:
a. Sinusoidal (( high WHVP + HPVG ))
b. Pruning of portal vein branches
c. Narrowing of sinusoids due to :
Hepatocyte enlargement
Collagen deposition in the space of disse
Distortion of intrahepatic vasculature by fibrosis / nodule formation
WHAT ARE THE SYMPTOMS OF PORTAL HTN?
The onset may not always be associated with specific symptoms .the main symptoms and
complications of PORTAL HTN include:
1. GIT bleeding----black tarry stools or blood in the stools ,hematemsis
2. Ascites
3. Encephalopathy ,confusion ,forgetfulness
4. Bleeding tendency----peteichea , ecchymosis
CLINICAL SIGNS:
Signs may be related to the underlying cause or complication of P.HTN.
The spleen is usually palpable ,may be very large in young patients with :
1. Extrahepatic portal block
2. Small ,shrunken livers
Prominent abdominal wall veins are often found with P.HTN
Veins radiating away from the umbilicus are a valuable sign as they indicate that
the block is distal to the main portal vein branches. They disappears if P.V.
thrombosed.
With extrahepatic portal vein block ,there are no abdominal wall collaterals .
Collaterals may occur at the site of surgical scar and indicate only a high portal
pressure.
Prominent abdominal wall veins result on the side of an ileofemoral block ;or with
IVC obstruction " when they are bilateral and visible over the back".
Budd chiarri syndrome----Hepatomegally ,Ascitis ,Signs of IVC obstruction
The sudden development of umbilical collaterals in patients with cirrhosis suggests
an acute hepatic vein block ; inferior vena caval collaterals suggest a blocked cava.
A venous hum ;loudest during inspiration ; Heard over large upper abdominal
collaterals (( Cruveilheir --Baumarten syndrome )). There may be accompanying
thrill
HOW IS PORTAL HTN TREATED?
Most causes can't be treated. Treatment focuses on preventing or managing
complications especially bleeding from the varices.
4. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
SASI 2015
RICESVA
od to systemicolHTN portal vein and return bseen to decompress the-----VARICES
circulation.
Varices in the oesophagus tend to develop in cirrhosis when HPVG rises> 12 mmHg.
They are seen when the pressure gradient B/W portal veins and hepatic veins > 12mmHg.
5. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
SASI 2015
The portal –hepatic venous pressure gradient is obtained by hepatic venous
catheterization and with measurement of the difference between the wedged
hepatic venous pressure (( which approximates the sinusoidal and portal pressures
in cirrhosis and the free hepatic venous pressure)).
Oesophageal varices----important collateral in P. HTN
90% Oesophagus ,10% gastric area
Oesophageal varices are dilatation of normal submucosal oesophageal veins which
extend 10—15cm below gastroes-ophageal junction.
Bleeding can be slow oozing or sudden sever.
Bleeding occurs nearly always from the lower 5cm of the oesophagus.
CLINICAL PRESENTATION:
Hematemsis
Melena
Hematochezia
Upper GIT bleeding can be:
1. Bleeding varices.
2. Portal hypertensive gastropathy.
The severity depends on the amount and rapidity of blood loss.
CONSEQUENCES OF PORTAL HTN:
Increased P.V.P----distends the veins proximal to the block and spleen enlarges
Capillary pressure raises in the organs drained by the obstructed V.
6. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
SASI 2015
Fluid exudation and lymph flow both increase.
Small anastomoses connecting the portal and systemic circulation may enlarge (( often
markedly )) because of the increased portal pressure and allow portal blood to pass
directly into the systemic circulation.
Patients with cirrhosis tend to have a high cardiac output ,and increased splanchanic blood
flow may maintain an elevated portal HTN despite the development of large anastomoses.
There are three main types of anastomosis:
1. Gastro –oesophageal junction:
Veins at the oesophagogastric junction shunt blood from the left gastric and short
gastric veins into the inferior oesophageal plexus and onto the superior vena cava
via the azygous system.
Varices are dilated(( submucosal veins projecting into the lumen of oesophagus
and stomach)).
2. Venous channels from retroperitoneal visera may communicate directly with
systemic veins on the posterior abdominal wall.
3. The obliterated umbilical vein and paraumbilical veins may open up, allowing
blood to pass from the left branch of the portal vein to the umbilicus and thence
into abdominal –wall veins.
Anterior abdominal wall collaterals also occurs where adhesions exists between
abdominal viscera and parietal peritoneum or at ileostomy or colostomy site.
Localized varices in colon may be related to previous operation.
When hepatic veins are occlude "budd chiarri syndrome" ;collaterals open up
within the liver ; blood tends to be diverted through the caudate lobe whose short
hepatic veins drain directly into the inferior vena cava.
A varix explodes as a result of:
1. Increased pressure
2. Increased size
3. Thinning of its wall
Sites of bleeding:
1. Oesophageal varices
2. Gastric varices
3. Portal HTN gastropathy
4. Sclero-therapy ulcer
5. Peptic ulcer
6. Oesophageal erosions
7. Gastric erosions
May be more sever because of high IVP.
Seen in Alcoholics and NSAIDS ingestion.
8. Rectal varices
7. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
SASI 2015
IS THERE A RISK FACTORS FOR BLEEDING VARICES?
1.LOCATION OF VARICES:
Distal oesophagus ,stomach ,rectum
Gastroesophageal junction have the thinnest coat of supporting tissue.
It is most likely to rupture and bleed.
The varices in the gastric fundus bleed frequently.
Gastric varices are classified according to their location.
A. Varices in different continuity with esophagus along the lesser and greater curves of the
stomach ((gastroesophageal varices --GOV)) type 1 & 2
B. Isolated gastric varices in the fundus occur less frequently than GOV (( 10% Vx 90%))
Bleeding from isolated gastric varices in the fundus occurred much more frequently than others.
RISK FACTORS FOR RECURRENT VARICEAL BLEEDING
2.SIZE OF VARICES:
Small increase in the vessel radius result in large increase in wall tension.
F1 small straight varices
F2 enlarged tortuous varices that occupy < 1/3 of lumen
F3 large coil –shaped varices that occupy > 1/3 of lumen
Causes of hematemsis:
1. Peptic ulcer disease
2. Erosive gastritis due to hypergastrinemia , alcohol intake
Hypergastrinemia occurs due to defective metabolism by cirrhotic liver.
REBLEEDING > 6 WEEKS(LATE)REBLEEDING < 6 WEEKS(EARLY)ITEM
noyesAge >60 year
noyesSeverity if initial bleed
Anemia / blood pr low
noyesRenal failure
yesyesSeverity of hepatic failure
yesyesascites
yesnothepatoma
yesnoalcoholism
noyesActive bleeding on endoscopy
yesyesIncreased varices size
Not knownyesRed signs
Not knownyesPlatelet clot on varix
nounclearPortal pressure
8. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
SASI 2015
3.APPEARANCE OF VARICES:
Red wale marks
Cherry red spots
Hematocystic spots
Diffuse erythema
4.CLINICAL FEATURES:
Degree of liver dysfunction
H/O previous variceal bleed
5.VARICEAL PRESSURE:
By endoscopic gauge
013 mmHg≥
9%13 ----14
17%>14---- <15
50%>15----<16
72%>16
MANAGEMENT:
Investigation-----
CBP , coagulation profile , RFT ,electrolytes ,BUN ,LFT ,blood group ,Cx matching
When portal HTN is suspected ,endoscopy should be done to look for
oesophageal and gastric varices.
Increased risk of bleeding:
1) Large varices---5 mm in diameter
2) Blue varices
3) Have red wheals
P.HTN gastropathy causes chronic anemia or frank bleeding .
Red spots similar to petechiae , particularly over antrum and fundus.
Diagnostic endoscopy is mandatory as identification of the source of
bleeding and directly influence therapy.
If it is delayed for 24 hours, it may be impossible to identify the source
of bleeding.
Early endoscopy always identify source of bleeding after few hours.
Delirium tremens ----------------------------------controlled by Chloromethiazole
9. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
SASI 2015
Bleeding varices------ definitive if there is :
A. A venous { non pulsatile spurt } ; A venous ooze a varix
B. A white fibrin –platelet plug on the varix
C. Adherent blood clot ---rare
In cirrhotic patients ,there is gastric varices 10% and non variceal source 30%.
The major detrminent of subsequent mortality depends on:
A. The severity of bleeding
B. Pugh childs grading
A 10% B 25% C 50%
In patient with splenomegally or prominent abdominal wall veins ,but no varices ,P.HTN
can be confirmed by direct measurement of portal pressure by
1. Splenic puncture
2. Transhepatic cannulation of portal vein branch
Liver biopsy helpful but can be normal in:
A. Ideopathic portal HTN
B. Extrahepatic portal venous obstruction
Portography -----to detect the site of block to portal flow
Abdominal uss and CTscan
Doppler USS give information about the direction of flow.
10. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
SASI 2015
Catheterization of hepatic vein with venography.
You should asses RFT , evidence of infection –CXR ,U C/S , BLOOD CULTURE
INVESTIGATIONS:
CBC
LFT
USS ABDOMEN –asctes, splenomegally ,liver cirrhosis
Detection of oesophgeal varices:
Fibroptic endoscopy
Barium swallow
Duplex scan
Liver biopsy/ hepatitis marker
Portal venography (( prior to surgery ))
CLIP SCORING SYSTEM:
Child –Pugh stage Score
A 0
B 1
C 2
Tumor morphology :
Uninodular with extention ≤ 50% 0
Multinodular with extention ≤ 50% 1
Massive or extention > 50% 2
Alpha feto protein:
<400 0
≥400 1
Portal vein thrombosis;
NO 0
YES 1
TREATMENT :
1. Ensure clear airway
2. I.V. line ---central or peripheral (( large bore venous canula )).
3. Replacement of loss –Blood cross matching
After restoring the systolic pressure to 80—90 mmHg ;Packed cells should be given to
maintain HB 10 g/dl and the urine output 40ml/hr or more.
Monitor CVP ---I.V.ringer lactate
Fresh frozen plasma given to maintain and correct the effect of large transfusion of stored
blood .
Fresh frozen plasma If P.T. prolonged or platelet count < 50000/ml
11. PORTAL HYPERTENSION AND OESOPHAGEAL VARICES DR MAGDI AWAD
SASI 2015
Platelet transfusion if massive transfusion or thrombocytopenia
VIT K 10 mg should be given.
4. Lactulose and mg sulphate to decrease encephalopathy
5. Na containing fluid should be avoided
6. Insert Foleys catheter
7. Arrest the haemorrhage:
A. Black moor stengstaken tube---gastric and oesophageal ballon
Balloon tamponade
If the patient uncooperative or comatosed ,intubation is the solution.
Bleeding is controlled in 90% of cases.
If the bleeding is continuing ,the cause is:
a. Incorrect placement
b. Presence of coagulopathy
c. Wrong diagnosis about source of bleeding
It should not be maintained for more than 12 hours
Temporary measures is done until definitive therapy planned.
1. Linton tube(( gastric balloon ---alternative ))
Aspiration of gastric and oesophageal content
Inflation of gastric then oesophageal balloon
Not more than 24 hrs
2. VASOACTIVE DRUGS—splanchnic arteriolar vasoconstrictors
A. VASPRESSIN :
20U in 200ml fluid over 20 min---0.2 -0.4U/min for 24-48hr
C/I--- coronary artery vasospasm ,so give glyceryl nitrate" infusion or patch "
Systolic pressure should be maintained at 100mmHg or more.
Morphin is contraindicated.
Once is hemostasis stabilized ,urgent endoscopy is done with sclerotherapy
(( ethanolamine oleate)) injected into varices.
B. Glypressin 2mg/6hr/24---48hr
C. Somatostatin 250 microgm/hr for 2 ---5 days
D. Octeotide 5o microgm /hr for 2 –5 days
They don’t alter hospital mortality.
3. Operation :
Emergency operation is avoided because of higher mortality but if sclerotherapy is
failed ,there is no alternative.
Types:
Devascularization or transaction
Portosystemic shunting
4. General measures to:
A. Encephalopathy ----neomycin ,lactulose ,mg sulphate
B. Correction of clotting defect ---VIT K injection& prevention of rebleeding
C. Endoscopic therapy:
5% Ethanolamine ,1% polidocanal
Sclerotherapy is the mainstay of acute management of bleeding varices.
Oesophageal ---- inject into the varix or along side it.
Gastric -tissue adhesive(( Bucrylate)) , polymerizes in contact with bloodRepeated
sclerotherapy with regular check.
Single session of sclerotherapy 65% affective
Two session of sclerotherapy 85% affective
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No more than two sclerotherapy sessions should be used in 5 days.
This is to minimize oesophageal complications.
1. Mediastinitis
2. Deep oesophageal ulceration
3. Oesophageal stenosis
D. Devascularization and transection operation
A surgical procure that removes the bleeding varices. .This procedure done when a
TIPS or surgical shunt is no possible or is unsuccessful in controlling the bleeding.
Upper 1/3 of stomach and lower part of oesophagus are devascularized.
Gastroeosophageal junction is transected and reanastomosis by ((stapling gun)).
E. Portosystemic shunt
TIPS ---transjugular intrahepatic portosystemic stent shunt
To achive shunting with out surgery.
It is very affective.
It has higher thrombosis rate within 12 hours.
If transplantation is contemplated ,abdominal surgery should be avoided.
Portacaval ---- end to end ,side to side
Mesocaval
Proximal splenorenal
Distal splenorenal
PORTOCAVAL---portal vein is patent with good liver function.
It is very effective in lowering portal pressure.
Disadvantage ---high incidence of encephalopathy
MESOCAVAL---- used when portal vein is thrombosed.
PROXIMAL SOLENORENAL---less encephalopathy .It is less effective in preventing
further bleeding.
DISTAL SPLENORENAL ----SELECTIVE SHUNT
Right and left gastric vessels are ligated ,the distal splenic vein is jointed to renal
vein and short gastric veins are preserved.
Low incidence of encephalopathy , liver function remains normal
TRANSJUGUKAR INTRAHEPATIC PORTOSYSTEMIC SHUNT
F. Splenectomy :
It is only effective in sectorial HTN (( LT side portal HTN)) that occurs after
pancreatitis leads to splenic vein thrombosis---fundal varices
THE MAJOR COMPLICATIONS OF VARICEAL BLEEDING:
Which may lead to multiorgan failure and cause death
1. PNEUMONIA:
Especially during endoscopy or placement of balloon tamponade tube
Tracheal intubation should be used if patient comatosed.
Pulse oximetry is mandatory ,even in absence of pneumonia
As hypoxemia is common ,sepsis ,shock ,massive transfusion
2. Hepatic encephalopathy:
Lactulose
Twicw daily cleaning enema
3. Infection due to:
Enteric organism causing septicemia
Spontaneous bacterial peritonitis
Cephalosporin I.V. is the antibiotic of choice.
Nephrotoxic antibiotics should be avoided .
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As soon as infection is suspected ,it should be treated.
4. Water / electrolyte imbalance:
With ascitis and development of renal failure
Saline solutions should be avoided.
Aim ---maintain an adequate circulating volume & avoid volume overload.
Ascites should be treated.
Electrolyte abnormalities should be corrected.
5. Under nutrition:
Nutrition should be strated as soon as possible within 24 hrs wether enteral or
parenteral according to the renal function and bleeding.
REBLEEDING:
Rebleeding is the most frequent in 1st
6 weeks,accounting for 20—30% of deaths during
follow up. Patients who survived the first bleed from oesophageal varices are at significant
risk of recurrent haemorrhage: 70% of patients will experience recurrent haemorrhage and
about a third of further bleeding episodes are fatal.
Up to fifty percent of recurrent haemorrhage occurs within the first 6 weeks after the
index bleed.
The risk of re-bleeding is highest during the first five days, decreases slowly over the first 6
weeks, and becomes virtually equal to that before the index bleed after the sixth week.
Risk factors predictive of re-bleeding include the degree of hepatic decompensation, age
greater than 60, severity of initial bleed, renal insufficiency, level of portal pressure, size of
varices, active bleeding at the time of initial endoscopy and the presence of hepatoma.
All therapy decrease rebleeding and choice depends on:
1. Individual circumstances
2. Severity of liver disease
3. Feasibility of different methods of treatment
Portal systemic shunts decrease 10% + not proloning survival
Repeated sclerotherapy decrease 50% + reduce mortality
Drug therapy ----more convinent and cheaper
B—BLOCKER
Decrease cardiac output ----decrease variceal flow
Allowing unopposed α vasoconstriction of splanchanic arterioles.
Acts directly on collaterals feeding the varices.
Decrease portal pressure with increase intra hepatic resistance.
Appears that lowering the hepatic vein pressure gradient to < 80%.
Pretreatment values at 3 months reduce risk of rebleeding.
Decrease rebleeding 50% and lowers the mortality.
Portal hypotensive effect may be enhanced by isosorbide mononitrate.
affective to reduce bleeding and anemia in gastropathy.
In trials ,comparing scleropathy with B blockers ,((higher risk patients were
included)) ,there were no differences in survival /rebleeding rates.
No advantage occurred by combinig B blocker withsclerotherapy.
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CLINICAL POINTS:
HVPG—hepatic venous pressure gradient should be reduced to 12mmHg or below to eliminate the
risk of bleeding.
1ry prevention with B blocker show reduction in bleeding from varices and portal hypertensive
gastropathy and decrease in mortality.
B blocker should be given to patients with varices at risk.
1ry prevention with scleropathy /surgical shunts ,it have shown no overall benefit and increased
mortality.
Prognosis in patients with esophageal varices
Approximately 30% of patients with esophagieal varices will bleed within the first year
after diagnosis. The mortality resulting from bleeding episodes depends on the severity
of the underlying liver disease
The mortality resulting from any bleeding episode may range from < 10% in well- compensated
cirrhotic patients with Child–Pugh grade A to > 70% in those in the advanced Child–Pugh C
cirrhotic stage. The risk of re-bleeding is high, reaching 80% within 1 year
Patients with a hepatic venous pressure gradient > 20 mmHg within 24 h of variceal hemorrhage,
in comparison with those with lower pressure, are at higher risk for recurrent bleeding within the
first week of admission, or of failure to control bleeding (83% vs. 29%) and have a higher 1-year
mortality rate (64% vs. 20%)
Approximately 60% of untreated patients develop “late rebleeding '” within 1–2 years of the
index hemorrhage
TIPS:
Transjugular intrahepatic portosystemic shunt:
This procure involving placing a stent in the middle of the liver. The stent connects the hepatic
vein with the portal vein.
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DSRS---distal splenorenal shunt:
WHAT TESTS ARE REQUIRED BEFORE THE TIPS AND DSRS PROCEDURES?
Before receiving either of these procures ,the following tests may be performaed to
determine the extent and severity of the condition.
1. Evaluation of the medical history
2. Physical examination
3. Blood tests
4. Angiogram
5. Ultrasound
6. Endoscopy
7. Chest x ray
8. ECG
9. Keep plasma ready for O.T.
WHAT HAPPENS IN TIPS?
A radiologist makes a tunnel through the liver with a needle ,connecting the portal vein to
one of the hepatic veins . A metal stent often covered with a thin plastic material ,is placed
in this tunnel to keep the tunnel open.
The procedure reroutes blood flow in the liver and reduces pressure in all abnormal veins
,not only in the stomach and oesophagus ,burt also in the bowel and the liver
This not surgery , The radiologist performs the procedure within the vessels under X –ray
guidance. This process lasts one to three hours ,but you should expect to stay in the
hospital over night after the procedure.
HOW SUCCESSFUL IS THE TIPS PROCEDURE?
It controls bleeding immediately in 90% of patients.
20% of cases develop rebleeding due to narrowing of the shunt
COMPLICATIONS OF TIPS:
1. Shunt narrowing /occlusion within the 1st
year
Follow up UU examinations are performed frequently
The signs of occlusion include increased ascites and rebleeding.
Treatment ---by radiologist who re-expand the shunt with a ballon or
repeats the procedure to place a new stent
2. Encephalopathy ----can occur with sever liver disease
It can become worse when blood flow to the liver is reduced by TIPS which
may result in toxic substances reaching the brain without being metabolise
1st
by the liver.
Treated by diet ,medications ,or occluding the shunt
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WHAT HAPPENS IN THE DSRS PROCEDURE?
DSRS--- a surgical procedure during which the splenic vein is detached from
the portal vein and connected to the renal vein. .This selectively reduces
the pressure in the varices and control the bleeding. It is done only in
patients with good liver function.
HOW SUCCESSFUL IS THE DSRS SURGERY ?
It controls the bleeing in 90% of patients with the highest risk of rebleeding
occurring in the first month. It provides good long term control of bleeding.
COMPLICATIONS OF DSRS?
Ascites can occur.
FOLLOW UP:
10 days after hospital discharge , patient should follow hepatologist to
evaluate the progress .Lab work will be done at this time.
6 weeks after TIPS , 3 months ,USS should be to check the shunt.
Angiogram is done if USS indicates a problem.
6 weeks after DSRS ,3 months, USS should be done to check the shunt.
12 months after either procedures , USS to be done to check shunt.
If the shunt is working well every 6 months after the 1st
year of follow up
appointements ,have an USS ,lab work and visit the doctor