This document discusses portal hypertension and variceal bleeding. It begins by describing portal hemodynamics and defining clinically significant portal hypertension as a hepatic venous pressure gradient (HVPG) greater than 10-12 mm Hg.
The etiology of portal hypertension is categorized as prehepatic, hepatic, or posthepatic. Prehepatic causes include portal/splenic vein thrombosis. Hepatic causes include cirrhosis, which leads to fibrosis and increased production of vasoconstrictors. Posthepatic causes include Budd-Chiari syndrome.
Complications of portal hypertension include variceal bleeding, ascites, hepatic encephalopathy, and hepatorenal syndrome. Investigations for diagnosis include ultrasound Doppler,
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.
Liver transplant In India by Dr. Abhideep Chaudhary, Sir Ganga Ram Hospitaldrabhideep
This presentation is related to Liver Transplant, Liver Failure, It's causes and remedy.
Here we also talk about liver transplant scenario in india and success rate of liver transplant both cadaver or living donor.
We also give a brief about the cost of liver transplant.
Dr. Abhideep Chaudhary, is liver transplant consultant/surgeon at Sir Ganga Ram Hospital, New Delhi, India.
Email : drabhideep@yahoo.com , care@drabhideep.com
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.
Liver transplant In India by Dr. Abhideep Chaudhary, Sir Ganga Ram Hospitaldrabhideep
This presentation is related to Liver Transplant, Liver Failure, It's causes and remedy.
Here we also talk about liver transplant scenario in india and success rate of liver transplant both cadaver or living donor.
We also give a brief about the cost of liver transplant.
Dr. Abhideep Chaudhary, is liver transplant consultant/surgeon at Sir Ganga Ram Hospital, New Delhi, India.
Email : drabhideep@yahoo.com , care@drabhideep.com
Presentation by DR. MISHAL on the topic of NON CIRRHOTIC PORTAL HYPERTENSION. Its a grey area but very important topic particularly for FCPS residents .
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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
2. Hemodynamics
• Portal flow - 75% to 80% of the inflow to liver,
remainder from hepatic artery, outflow through
hepatic veins to IVC
• Normal flow is hepatopetal.
• Normal pressure
• Portal venous pressure = 5 – 10 mm of Hg
indirectly measured by HPVG
• Normal HPVG = 3- 5mm of Hg
3. •
Wedge hepatic pressure obtained by wedging the catheter into smallest branch of
hepatic vein = sinusoidal pressure
Free hepatic pressure is systemic pressure acts a zero referrence point
7. Prehepatic
1.Portal /splenic vein thrombosis - most common prehepatic cause .
- associated with umbilical vein catheterization, sepsis and dehydration in infancy.
- In adult patient associated with hypercoagulable syndromes
- Other etiologies - pancreatitis and pancreatic tumors
2 .Extrinsic compression - On the portal vein from (lymph nodes , tumors ) can occasionally
lead to portal Hypertension
3.. Arteriovenous fistula - hepatic artery to portal venous fistulas, usually secondary to
liver biopsy
8. 4. Sinistral portal hypertension - leftsided (sinistral) portal hypertension
- Isolated splenic vein thrombosis, portal vein normal and no intrahepatic block.
- Most common causes - pancreatitis and carcinoma of the body and tail of pancreas
- Large collaterals from splenic hilus to fundus of stomach
9. Extrahepatic Portal Vein Obstruction (EHPVO)
• Childhood disorder -chronic blockage of PV blood supply leading to PHT and its sequelae
with well-preserved liver function.
• As per APASL - defined as ‘‘ vascular disorder of liver, characterized by obstruction of the
extra-hepatic PV with or without involvement of intra-hepatic PV radicles or splenic or
superior mesenteric veins’’
• EHPVO is a distinct disease with well tolerated episodes of variceal bleed, splenomegaly
anemia, with accompanied growth retardation.
• Formation of portal cavernoma and development of PHT differentiates EHPVO from portal
vein thrombosis.
10. Pathogenesis
Initial acute PVT event leading to thrombus
Hepatopetal collaterals around PV in 6–20 days and cavernoma in 3 weeks
Insufficient to decompress high pressure in the splanchnic bed
Hepatofugal vessels develop at the sites of portosystemic communications
Transform into varices, lower GI bleed, splenomegaly
Cavernomatous transformation and biliopathy.
11. Diagnosis
• Doppler ultrasound (USG) - Portal cavernoma , thrombosis
• Endoscopy- Identification of gastric and esophageal varices.
• Liver Function - elevations of alkaline phosphatase and gamma-
glutamyl transpeptidase are seen with development of portal biliopathy
• CT angiography - patency of the venous and arterial systems, cavernous
transformation can be identified, planning shunt procedures
12. Hepatic - Pathophysiology
Obstruction to portal venous flow eg cirrhosis
Activated hepatic stellate cells and myofibroblasts – Fibrosis
Production of vasoconstrictors (endothelin, norepinephrine, angiotensin)
Release of splanchnic vasodilators -(NO ,VEGF) , increased splanchnic inflow.
Systemic hyperdynamic circulation
Development of Portosystemic collaterals
13. Collaterals in portal hypertension
1. Esophageal and gastric varices
2. Paraumbilical and abdominal wall.
3. Retroperitoneal collaterals
4. Mesenteric and omental varices
5. splenic collaterals
6. Rectal varices
15. Clinical manifestation
Variceal bleeding-
Incidence 8% to 11% in the cirrhotic patients
Upper gastrointestinal (GI) bleeding one of the most common and life-threatening
complication
Usually present as hematemesis and/or melena, but can also present with shock
Ascites-
Late sign of portal hypertension.
Abdominal distention, weight gain, and shortness of breath - increased fluid and
intra-abdominal pressure.
Refractory ascites - sign of decompensation of the underlying liver disease.
16. Hepatic encephalopathy
Cognitive changes, loss of coordination, and asterixis leading to coma.
Precipitated by bleeding, infection, renal failure, and other manifestations of liver
failure.
Hepatopulmonary syndrome
Triad of liver disease, arterial hypoxemia, and intrapulmonary vascular dilation .
Oxygen desaturation, shortness of breath, and dyspnea on exertion caused by
intrapulmonary shunting.
Hydrothorax (pleural effusion) - movement of fluid from the abdominal cavity into
the pleural space, usually on the right side.
Spontaneous bacterial peritonitis - fever, pain, and tenderness.
17. Non-cirrhotic portal fibrosis (NCPF)
• Known as Idiopathic PHT (IPH), hepatoportal sclerosis and obliterative venopathy-disorder of
unknown etiology
• Features of PHT, moderate to massive splenomegaly, with or without hypersplenism, preserved
liver functions, and patent hepatic and portal veins.
• More common in young males (3 to 4 decade) belonging to low socioeconomic groups.
• Infections and prothrombotic states, toxins especially arsenic and human leukocyte antigen
(HLA)-DR3.
• Absence of Cavernomatous changes and stigmata of cirrhosis
• Some Variant of NCPF develop hepatofugal flow – Hepatic enchephalopathy ( 2%)
18. APASL criteria
• Presence of moderate to massive splenomegaly
• Evidence of portal hypertension, varices, and/or collaterals
• Patent spleno-portal axis and hepatic veins on ultrasound Doppler
• Test results indicating normal or near-normal liver functions
• Normal or near-normal HVPG
• Liver histology-no evidence of cirrhosis or parenchymal injury
19. Diagnosis and evaluation
Goals of diagnostic studies
determine the presence of hepatic disease
level of obstruction to flow
presence and extent of intra-abdominal portosystemic collaterals
direction of blood flow in the portal vein (PV) (hepatopetal/hepatofugal)
Presence of thrombosis
20. Investigations
• Duplex Ultrasound- first-line examination in diagnosis and follow-up
Grayscale- evaluate overall morphology and locate focal lesion in liver
Color Doppler - Portosystemic collaterals are readily identified
• Findings -
Splenomegaly (diameter >12 cm and/or area >45 cm2 )
Dilatation of the PV (diameter >13 mm)
Reduced PV velocity
• MDCT and CT angiography-
Identify morphologic changes, regenerative and dysplastic nodules, HCC.
Portosystemic collaterals (varices) - well-defined tubular or serpentine structures.
21. Elastography
• Transient elastography performed by Fibroscan – assess liver and spleen stiffness.
(normal value - 2 and 6 kPa).
• Cirrhosis is invariably associated with liver stiffness .
• Other causes like portal vein thrombosis associated with spleen stiffness..
• Equiment uses ultrasound mounted on a vibrator-velocity of propagation of wave
directly related to tissue stiffness.
• Correlation of elastography with HPVG good till 10 mm of hg.
• Liver stiffness correlates with degree of esophageal varices
22. Endoscopy
• Esophagogastroduodenoscopy (EGD) - gold standard
– esophageal and gastric varices and hemorrhage
• Identification of risk factor, provides immediate
therapy of at-risk variceal columns( sclerotherapy,
band ligation)
• Increased variceal diameter and thin variceal wall
thickness indicated by a red color sign - predictive of
variceal bleeding
• Portal gastropathy can be identified on upper GI
endoscopy
23. Endoscopic classification
Paquet’s classification
(Esophageal varices)
•Grade I: Microcapillaries located in distal
oesophagus or oesophago-gastric junction.
•Grade II: One or two small varices located in
the distal oesophagus.
•Grade III: Medium-sized varices of any number.
•Grade IV: Large-sized varices in any part of
oesophagus.
Sarins Classification
( Gastric Varices)
•Gastro-oesophageal varices Type 1: Continuation of
oesophageal varices into lesser curvature (GOV1).
•Gastro-oesophageal varices Type 2: Oesophageal
and fundal varices are present in continuity with the
greater curvature (GOV2).
•Isolated gastric varices Type 1: Fundal varices are
present in the cardia in the absence of oesophageal
varices (IGV1).
•Isolated gastric varices Type 2: Fundal varices
present in the stomach outside of cardio-fundal
region or first part of duodenum (IGV2).
24. Other investigations
• Liver Function Test- status: bilirubin, albumin, prothrombin time, enzymes.
• Hematologic parameters - hemoglobin, platelet, white blood cell count.
• Hepatitis panel, antinuclear antibody, antimitochondrial antibody
• Metabolic disease markers - iron, copper, alpha1-antitrypsin,α-fetoprotein.
• Calculation of child pugh score – prognosis and treatment.
25. Post Hepatic – Budd Chiari syndrome
Defined as hepatic venous outflow obstruction.
- Primary – venous process ( thrombosis, phebilitis of hepatic veins)
- Secondary – compression or invasion ( malignancy)
Etiology
• Hereditary or acquired hypercoagulable state.
• Primary myeloproliferative disease
• Factor V Leiden with protein C and S defeciency
• Compression ( tumor, polycystic kidney disease)
• Abdominal trauma
26. Categorization
Acute ( fulminant)-
acute liver failure with jaundice and hepatic encephalopathy or intractable ascitis
and hepatic necrosis .
Abdominal pain( tender hepatomegaly) , distension ( ascites), variceal bleeding.
Sub acute -
Minimal ascitis with hepatic vein collaterals
Generally asymptomatic , right upper quadrant pain ( caudate lobe hypertrophy)
Chronic ( fibrosis)
Complication of cirrhosis
Portal hypertension and ascitis
27. Diagnosis
• Doppler usg – enlargment of caudate lobe, inability of visualize juction of hepatic
veins with IVC, spider we apperance nera hepatic vein ostia , flat hepatic wave form
• CT scan – delayed or absent filling of majot hepatic veins , relative clearance of
contrast from caudate lobe, intrahepatic collaterals
• Venography – if non invasive test are negative with strong clinical suspicion, gold
standard – hepativ vein venography.
• Liver fuction – elevated liver enzymes (ischemic hepatocellular damage)
28. Acute variceal bleeding
• Resuscitation – ABC protocol, iv Fluids and blood products.
• Pharmacologic intervention-somatostatin analogue and vasoconstrictive therapy
Octreotide – Initial IV bolus of 50 ug then continuous infusion 50 ug/h X 2-5 days
Terlipressin – 2 mg IV every 4 hr until bleeding control ( 48 hrs)
Maintenance – 1 mg IV every 4 hours X 2 - 5 days.
Proton pump inhibitors – continuous IV infusion
Antibiotics - Norfloxacin 400 mg X BD x 7 days or ceftriaxone (1g/day)
29. Endoscopic ligation/ sclerotherapy
Should be performed within 12 hours,
variceal ligation performed to control
bleeding
Ø EVL controls bleeding in approximately 80%
to 100% of patients better results
than sclerotherapy
Ø Multiple follow-up sessions every 1 to 2
weeks until obliteration
30. Balloon tamponade
• Sengstaken-Blakemore or Minnesota tube -
unresponsive to pharmacologic therapy and
EVL.
• Two balloons—a gastric balloon and an
esophageal balloon—to tamponade the
submucosal veins.
• Initial control of bleeding accomplished in 80%
of patients, but over 50% rebleed after the
balloons are deflated.
• Used as a temporizing measure- preparing the
patient for an emergent TIPS or surgical shunt
31.
32. Portal hypertension Emmanuel A Tsochatzis, Jaime Bosch, Andrew K Burroughs. Liver
cirrhosis. Lancet 2014; 383: 1749 36
34. Absolute contraindications
• Primary prevention of variceal bleeding
• Congestive heart failure
• Severe pulmonary hypertension
• Multiple hepatic cysts
• Active infections or sepsis
• Unrelieved biliary obstruction
Relative contraindications
• Single hepatic cyst or central hepatoma
• Hepatic vein thrombosis
• Portal vein thrombosis
• Severe coagulopathy or thrombocytopenia
• Moderate pulmonary hypertension
35. Outcome and Complications
• Clinical resolution of bleeding is achieved in 90% of cases
• Technical success of TIPS to decrease portal pressure less than 12 mm of Hg achieved in
95% of cases
Complications include-
• Rebleeding ( 9% to 40.6%)
• Intraabdominal hemorrhage
• Right heart failure
• Hepatic encephalopathy
• TIPS dysfunction(defined as ≥50% stenosis ,increase in HVPG to >12 mm Hg, or recurrence )
• Stent Thrombosis or migration.
36. Surgical management
Indications
• Symptomatic PHTN in the noncirrhotic patient with preserved liver function (eg EHPVO,
schistosomiasis)
• Budd−Chiari syndrome
• Total mesenteric venous occlusion
• Failed medical management
Divided into -
• Decompressive procedure (Selective and Non selective)
• Devascularization procedures( Modified Sugiura procedure)
37. Selective Shunts
Sarfeh mesocaval shunt
• Side-to-side shunt from SMV to IVC -
maintain forward portal flow.
• Decreases portal pressure via small, 8 mm
Dacron or PTFE grafts
• Do not expand like side-to-side portacaval
shunts to become complete shunt as it
has a prosthesis.
• No portal dissection requires and less
complicated future transplant
• lower rate of postoperative
encephalopathy, improved ascites and
variceal decompression.
38. DSRS(Distal splenorenal shunt)
• Developed by Dean Warren- selective
gastroesophageal variceal decompression and
preservation of portal flow.
• Includes
Mobilizing the SV along the inferior border of the
pancreas
Disconnecting all branches to the pancreas,
Anastomosis btw the SV and the left renal vein
Dividing other collaterals like coronary (left
gastric) vein.
39. Advantages-
Control of variceal hemorrhage( 94%)
avoidance of portal dissection
antegrade portal flow (90%)
lower incidence (15%) of hepatic
encephalopathy.
Disadvantages
Increased risk of ascites
40. Nonselective Shunts
End-to-side portacaval
Side-to-side portacaval (>10 mm)
Mesocaval shunts
Central splenorenal shunts
Disadvantages
Hepatic encephalopathy
Risk of ascites
Accelerated need for transplantation
41. Devascularization
Sugiura technique
Ligation of esophageal , short gastric, lesser and
greater curve veins.
Esophageal transection and anastomosis
splenectomy, vagotomy, and pyloroplasty
Modified Sugiura technique
Single-incision operations
Devascularization without transection.
Preservation of the vagus.