This document discusses various vascular diseases of the liver. It covers topics such as ischemic hepatitis, Budd-Chiari syndrome, congestive hepatopathy, sinusoidal obstruction syndrome, and extrahepatic portal vein obstruction. The key points are that these diseases involve primary alterations in the blood or lymphatic vessels of the liver or changes secondary to other conditions. They can result in liver ischemia, obstruction of vessels, or other vascular abnormalities. The diagnosis and treatment of each condition is also outlined.
NAFLD is a vast topic and recently gaining a lot of importance. Fatty liver, NASH, are other topics discussed here. sleissenger, sheila sherlock and Harrisons are used for reference
By Dr. Usama Ragab, Zagazig Faculty of Medicine
PSC incidence ranges from 0.5 to 1.25 cases/100 000.
The prevalence of the disease ranges between six and 20 cases/100 000.
Men are more likely to be affected (70%).
Prevalence of PSC may be increased in first degree relatives of PSC patients
Presentation by DR. MISHAL on the topic of NON CIRRHOTIC PORTAL HYPERTENSION. Its a grey area but very important topic particularly for FCPS residents .
NAFLD is a vast topic and recently gaining a lot of importance. Fatty liver, NASH, are other topics discussed here. sleissenger, sheila sherlock and Harrisons are used for reference
By Dr. Usama Ragab, Zagazig Faculty of Medicine
PSC incidence ranges from 0.5 to 1.25 cases/100 000.
The prevalence of the disease ranges between six and 20 cases/100 000.
Men are more likely to be affected (70%).
Prevalence of PSC may be increased in first degree relatives of PSC patients
Presentation by DR. MISHAL on the topic of NON CIRRHOTIC PORTAL HYPERTENSION. Its a grey area but very important topic particularly for FCPS residents .
Primary sclerosing cholangitis (PSC) is a chronic, idiopathic, cholestatic liver disease characterized histologically by peribiliary inflammation and fibrosis.
It can lead to end stage cirrhosis and is a recognized risk factor for hepatobiliary cancers
Management of Anemia in cancer patientsAjeet Gandhi
Anemia in cancer patients are important both in terms of quality of life as well as response to therapy. Cause of anemia is multi-factorial and its management is critical in optimizing best outcomes of cancer patients
Primary sclerosing cholangitis (PSC) is a chronic, idiopathic, cholestatic liver disease characterized histologically by peribiliary inflammation and fibrosis.
It can lead to end stage cirrhosis and is a recognized risk factor for hepatobiliary cancers
Management of Anemia in cancer patientsAjeet Gandhi
Anemia in cancer patients are important both in terms of quality of life as well as response to therapy. Cause of anemia is multi-factorial and its management is critical in optimizing best outcomes of cancer patients
Portal Hypertension in pediatric populationPrabinPaudyal3
PORTAL HYPERTENSION
OUTLINE:
Definition
Causes
Pathogenesis
Clinical features
Investigations
Management
Complications
Prognosis
Approach
Definition:
Defined as:
Portal Pressure > 10-12 mm Hg, with diameter >10mm Or
Hepatic Venous Pressure Gradient > 4 mm Hg
increased portal resistance or increased portal venous blood flow
major cause of morbidity and mortality in chronic liver diseases
Portal Vein:
Causes of Portal HTN:
Extrahepatic/Pre-hepatic
Hepatic
Pre-Sinusoidal
Sinusoidal
Post-Sinusoidal
Post-hepatic
A. Extra-hepatic:
Portal Vein Thrombosis- Most common
Neonates: Omphalitis, Umbilical Vein Catheterization, Dehydration, Sepsis
Older Children: Intra-abdominal infections e.g., Appendicitis, IBD, PSC
Hypercoagulable states: Deficiencies of factor V Leiden, protein C, S
Blunt Abdominal Trauma
Portal vein agenesis, atresia, stenosis
Splenic vein thrombosis
Biliary tract disease
Extrahepatic biliary atresia
Choledochal cyst
B. Intra-hepatic:
C. Post-hepatic:
Budd-Chiari Syndrome
IVC Webs
Chronic Constrictive Pericarditis
Pathogenesis And Consequence of Portal HTN
Portosystemic collaterals:
Sites:
Lower part of esophagus
Lower part of rectum
Around Umbilicus
Clinical Features:
Bleeding:
Most common presentation
risk of first bleed in cirrhosis is 22%
rises to 38% in with known varices >5-yr period
Pattern of bleeding
Hematemesis/Malena: Most common
worsened by Stress / Intercurrent illness
Size of varices → Bleeding
Splenomegaly:
2nd Most common presentation
asymptomatic or associated with cytopenia
Ascites:
Seen in 7-21% patients
Less common but important manifestations
Portal Hypertensive Biliopathy
Growth Failure
Hepatopulmonary Syndrome
Porto-pulmonary HTN
Caput Medusae:
Abnormal, dilated venous network on anterior abdominal wall, radiating from the umbilicus
Not seen in extra-hepatic portal HTN
Seen in intra-hepatic portal HTN
Continuous murmur between umbilicus and lower sternum
Cruveilhier-Baumgarten Murmur
Investigations
USG with Doppler
portal vein diameter > 10 mm
hepatic diseases, masses, presence of varices and ascites
ascertain pattern of flow
Reversal of portal blood flow (Hepatofugal flow) - Associated with bleeding varices
Cavernous transformation of the portal vein in EHPVO
Increased thickness of lesser omentum
CECT and MRA: Needed in selective cases
Selective Arteriography: When surgical decompression is being planned
GIT Endoscopy: Most reliable to detect varices
Other investigations:
CBC
LFT
Barium swallow
Portal angiogram
Percutaneous intrasplenic measurement of portal pressure
Venography
A. Emergency Management of Bleeding Varices
1st Step (Initial resuscitation):
airway protection
Obtain I/V Access
Restoration of IV volume: fluid and BT
PRBC: Target Hb: 7-9 g/dL
Correction of coagulopathy: vitamin K, FFP/PC
NG
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.
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
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
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.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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.
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!
- 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
1. VA S C U L A R D I S E A S E S O F T H E L I V E R
P r e s e n t e d b y
Dr. Nikhil Chandra Roy
2. VASCULAR DISEASES OF LIVER
• Primary alternation in the blood or lymphatic vessels
• Primary alternations consist of obstruction, fistula, aneurysms,
absence of small or large vessels (due to agenesis or
disappearance)
• Excludes the vascular changes secondary to parenchymal or
biliary disease
4. ISCHEMIC HEPATITIS
• Also called hypoxic hepatitis, ischemic hepatopathy, shock liver
• Most commonly encountered form of vascular liver disease
• Cause: Cardiovascular diseases(acute MI, arrhythmia, heart
failure),sepsis, systemic hypoxia due to respiratory failure
• Acute trauma, hemorrhage, burn and heat stroke can also cause
ischemic hepatitis, but the likelihood is substantially less in the
absence of underlying heart disease
5. • Findings of underlying precipitating medical condition
• Extreme elevations of serum aminotransferase levels (>3000 U/L)
• Profound elevation of serum LDH
• ALT/LDH ratio of less than 1.5 is more typical of ischemic hepatitis
than viral hepatitis.
• PT may be prolonged by 2 or 3 seconds
• Serum bilirubin often mildly increased
• Serum creatinine and BUN levels are often elevated due to ATN
DIAGNOSIS
6. • AST and LDH levels peak at
1 to 3 days.
• Return to normal within 7 to
10 days.
Fig: frequently observed course of serum AST and LDH levels in ischemic
hepatitis
8. TREATMENT
• Most cases are transient and self limited.
• No specific therapy.
• Rx is directed at improving cardiac output and systemic oxygenation.
• Overall prognosis depends on severity of underlying predisposing
condition, not the severity of the liver disease.
9. BUDD CHIARI SYNDROME
• Obstruction of hepatic veins or terminal inferior vena cava
• It is a rare disease, occurs in 1/100,000 in general population
10. TYPES
• Primary: arises from a venous anomaly
• Secondary: arises from initial lesion outside the veins
Tumour invasion
Extraluminal compression by cyst or focal nodular
hyperplasia
Blunt abdominal or thoracic trauma
11. AETIOLOGY
• Hypercoagulable States:
Myeloproliferative disorders,
PNH
Deficiency of protein C ,S
OCP, pregnancy
Antiphospholipid syndrome
Sickle cell disease
• Malignancy:
Carcinoma of liver, kidney ,adrenals
• Infection:
Liver abcess, hydatid cyst, schistosomiasis,
TB, filariasis
• Others:
IBD, Behcets disease, Laproscopic
cholecystectomy, sarcoidosis, polycystic liver
disease, trauma to abdomen or thorax
12. CLINICAL PRESENTATION
• Presentation may be asymptomatic, acute or chronic liver
disease
• In acute form: Rapid development of upper abdominal pain,
marked ascites with tender hepatomegaly, occasionally acute
liver failure
• In chronic form: Features of chronic liver disease and portal
hypertension
13. INVESTIGATION
• Abdominal imaging: US, CT or MRI
• Doppler US for hepatic vasculature(sensitivity>75%)
Non-visualization, thrombotic or stenotic vein with proximal dilatation
,reverse flow in one or more hepatic vein
• CT or MRI: Occlusion of hepatic veins or IVC, enlarged caudate
lobe, ascites, splenomegaly
14. CT
FIGURE . CT in a patient with Budd-Chiari syndrome. The venous phase of vascular enhancement is shown. The
liver is dysmorphic(better seen in A) and enhances in an inhomogeneous fashion. Ascites is present. The hepatic
veins are visible as slender, unenhanced structures converging toward an enhanced patent inferior vena cava
(most prominent in B) (arrow).
15. MRI
FIGURE . MRI in a patient with Budd-Chiari syndrome. Numerous regenerative macronodules less than 2 cm in
diameter are hyperintense in the T1-weighted sequence and hypointense in the T2-weighted sequence. Marked
enhancement of the nodules is seen in the arterial phase, with isointensity in the portal venous phase.
16. • Hepatic Venography:
Almost never needed for making diagnosis, but when combined with
venous pressure measurement, venography allows percutaneous therapy.
• Investigations for the underlying causes
Imaging for secondary BCS
Flow cytometry
Lupus anticoagulant etc.
17. STEPWISE THERAPEUTIC ALGORITHM FOR BCS
EASL CPG VDL. J Hepatol 2016;64:179–202
Medical treatment
Angioplasty/stenting/thromboly
sis
TIPS
Liver
transplant
18. MEDICAL TREATMENT
• Prompt anticoagulant therapy is important
• Reduce risk of clot extension
• Reduce risk of new thrombotic episodes
• Specific therapy for the underlying disease
• Medical (or endoscopic ) therapy for manifestations of
PHTN(ascites, variceal bleeding, encephalopathy)
19. ANGIOPLASTY/STENTING/THROMBOLYSIS
• Experience of correcting hepatic venous outflow obstruction with
thrombolysis is limited
• Angioplasty/stenting is the definitive treatment for less than 10% of
western BCS patients
• Consider angioplasty/stenting as the first-line decompressive procedure
in patients with short hepatic vein stenosis or IVC stenosis
20. TIPS
• Surgical shunts have not demonstrated a survival advantage in patients
with BCS
• However, TIPS has a lower morbidity and mortality rate than surgery
and is feasible in most patients with IVC obstruction and in those with
severe IVC stenosis
21. LIVER TRANSPLANTATION
• Liver transplantation is the last therapeutic step
BCS may recur after LTx
Incidence of recurrent BCS after LTx is markedly reduced by early
anticoagulation treatment and lifelong maintenance
22. BUDD–CHIARI SYNDROME AND PREGNANCY
EASL CPG VDL. J Hepatol 2016;64:179–202
• Excellent maternal outcome provided disease is well controlled
• Fetal outcome is less favourable
Pregnancies reaching week 20 of gestation have acceptable prognosis
• Vitamin K antagonists associated with high risk of miscarriage and
congenital malformation
Perform pregnancy test as soon as possible
If positive, switch to LMWH
• Periodic monitoring of anti-Xa activity
23. CONGESTIVE HEPATOPATHY
• Right sided heart failure results in centrilobular congestion and
sinusoidal edema that further decrease oxygen delivery
• Superimposed ischemic hepatitis are common in these patients
• Very rarely, long standing cardiac failure and hepatic congestion
give rise to cardiac cirrhosis.
24. CONGESTIVE HEPATOPATHY
• Right sided heart failure results in centrilobular congestion and
sinusoidal edema that further decrease oxygen delivery
• Superimposed ischemic hepatitis are common in these patients
• Very rarely, long standing cardiac failure and hepatic congestion
give rise to cardiac cirrhosis.
25. DIAGNOSIS
• Symptoms and signs of heart failure are predominant features
• Right quadrant discomfort, Tender hepatomegaly, ascites. Spider telangiectasia
and varices are usually not present, jaundice in <10% patient with severe or
acute heart failure
• Mild elevation of serum bilirubin(<3mg/dl)
• Prothrombin time is prolonged in more than 75%of cases
• Other liver biochemical tests are often normal or mildly elevated
• SAAG - High
26. TREATMENT
• Treatment of underlying heart disease
• Supportive treatment for liver component
• Mortality rate is determined by the severity of underlying cardiac
disease
27. SINUSOIDAL OBSTRUCTION SYNDROME
• Previously called hepatic veno-occlusive disease
• Destruction of sinusoidal endothelial cells predominantly in the central
part of hepatic lobule with focal obstruction of sinusoidal lumen
• Nonthrombotic occlusion of central hepatic vein may also be present
28. PATHOGENESIS
Massive centrilobular & midlobular
congestion, obliteration of terminal hepatic
vein
Toxic agent > damage sinusoidal endothelial cells >
sloughing of sinusoidal endothelial cells > obstruction
around central veins
29. AETIOLOGY
• Conditioning for HSCT
• Chemotherapy with oxaliplatin for metastatic HCC
• Hepatic chemoradiation for abdominal organ malignancy
• Immunosuppressive agents
• Pyrrolizidine alkaloid used to make tea.
30. DIAGNOSIS
• Lack of specific clinical signs or serological diagnostic tools makes
recognition of SOS challenging
• Consider a diagnosis of SOS whenever liver disease occurs in patients
with HSCT, cancer chemotherapy, immunosuppression in solid organ
transplantation or IBD
• Consider SOS in patients with weight gain, associated with or without
ascites, tender hepatomegaly and jaundice. Exclude other common
causes of these symptoms
• In patients who do not meet clinical criteria of SOS or when other
diagnoses have to be excluded, use transjugular liver biopsy
31. SOS: PROPHYLAXIS AND TREATMENT
• Recognition of risk factors is helpful to prevent SOS
• Pre-existing liver disease
• Previous SOS
• High intensity regimen
• Abnormal pre-operative GGT, age, female sex, cycles of chemotherapy, and a short interval
between the end of chemotherapy and surgical liver resection
• Routinely control risk factors for SOS
• Use defibrotide to prevent SOS in patients undergoing HSCT
• Supportive measures for the treatment of complications of established SOS
• Bevacizumab have been reported to protect against oxaliplatin related SOS
33. EXTRAHEPATIC PORTAL VEIN OBSTRUCTION
• EHPVO may or may not extend into the intrahepatic portal veins
• Primary EHPVO: acute PVT and portal cavernoma
• Secondary EHPVO: malignant invasion, compression
• EHPVO is second most important cause of portal HTN and most
important cause of non-cirrhotic portal HTN in third world countries
• In children , the causes are umbilical sepsis, umbilical catheterization,
developmental anomalies, dehydration, multiple exchange transfusion
35. ACUTE PVT
• Characterized by presence of thrombus in the lumen of portal vein on
imaging
• The recent onset of symptoms should be added to these criteria has
been debated
36. DIAGNOSIS
• Severe abdominal pain
• Fever
• Features of intestinal ischemia(per rectal bleeding, ascites) due
to mesenteric vein thrombosis-may be present
• Physical examination is unremarkable
37. • Blood count may reflect SIRS or underlying blood disease
• Liver biochemical test : no alternations or minor transient
changes
• US: solid material filling the lumen of portal vein
• Doppler US: absence of flow in portal vein – is preferred to US
alone
• Contrast enhanced CT is more accurate for showing filling defect
in portal vein lumen.
38. FIGURE . CT in a patient with acute portal vein thrombosis. The portal venous phase is shown and demonstrates
vascular enhancement. The portal and mesenteric veins are enlarged and lack enhancement(arrowhead).
Dilated veins are seen in the porta hepatis, particularly in the gallbladder wall (arrow).
39. TREATMENT
• Anticoagulation: complete recanalization(40%), partial
recanalization(15%)
• Thrombolysis: Recanalization rates similar to those for
anticoagulation, usually not given
• Surgery
40. ACUTE PORTAL VEIN THROMBOSIS: AIMS OF THERAPY
EASL CPG VDL. J Hepatol 2016;64:179–202
• Prevent extension of thrombosis to mesenteric veins
• Leading to mesenteric venous infarction
• Achieve portal vein recanalization
Abdominal pain and systemic inflammation
and/or thrombophilic factor
Confirm acute PVT on unenhanced
and contrast CT scan
Screen for general
and local cause
Discuss urgent laparotomy with
expert surgeon
1. Close monitoring
2. 6 months anticoagulation with coumarin
Inform radiologist of
PVT suspicion
Start LMWH
• Persisting abdominal pain despite
adequate anticoagulation?
• Organ failure?
• Rectal bleeding?
YES NO
Add antibiotics if
septic thrombophlebitis
Treat cause when accurate
41. ACUTE PORTAL VEIN THROMBOSIS: PROGNOSIS
EASL CPG VDL. J Hepatol 2016;64:179–202
• Recanalization of the portal vein can occur up to 6 months
following treatment
• Recanalization of mesenteric and splenic veins increases steadily
up to 12 months
• Over half (55%) of the patients not achieving recanalization will
develop gastroesophageal varices
42. PORTAL CAVERNOMA
• Following acute thrombosis in the absence of recanalization
• Portal venous lumen obliterates
• Porto-portal collaterals develop
• Portoportal collaterals arise from preexisting veins in porta
hepatis and pancreas.
• This lead to development of portal cavernoma
43.
44. DIAGNOSIS
• GI bleeding related to portal HTN
• Splenomegaly
• Liver biochemical test are normal or near normal
• Thrombocytopenia due to hypersplenism.
• US: numerous tortuous vessel occupying the portal vein bed
• Multiphase CT: numerous vascular structures in the region of
portal vein, which enhance during portal venous phase , not
during arterial phase.
45. Normal portal vein is not seen. Serpiginous
anechoic structure in porta hepatis
Serpiginous structure fills with color indicating
vascular structure
47. TREATMENT
• Patient without esophageal varices and strong risk factor for
thrombosis may benefit from anticoagulation therapy
• Recurrent variceal bleeding – EVL, non selective beta blockers
• Surgical portocaval shunt or TIPS – limited role
48. NONCIRRHOTIC PORTAL HYPERTENSION
• Heterogenous group of disorders of vascular origin, leading to
portal hypertension in absence of cirrhosis
• Often asymptomatic until complications develop
50. POSTHEPATIC: Inferior Vena caval web, Constrictive
pericarditis, Severe right sided heart failure, Restrictive
cardiomyopathy
51. IDIOPATHIC NONCIRRHOTIC PORTAL HYPERTENSION
• Portal HTN in presence of patent hepatic vein and extrahepatic
portal vein
• Absence of identifiable cause of intrahepatic noncirrhotic portal
HTN(Schistosomiasis, Congenital Hepatic Fibrosis, SOS)
• Absence of Cirrhosis and of a cause of Cirrhosis
52. AETIOLOGY
• Unknown
• Conditions associated with INCPH
(1) prolonged exposure to certain drugs and toxins (e.g.,
azathioprine, arsenic ,oxaliplatin)
(2) immune disorders(e.g., connective tissue diseases,Crohns
disease, HIV infection;
(3) prothrombotic conditions(e.g.,myeloproliferative disorders,
antiphospholipid syndrome, protein C and protein S deficiency)
(4) genetic anomalies(e.g.,Turner syndrome)
53. DIAGNOSTIC CRITERIA OF INCPH
*Splenomegaly must be accompanied by additional signs of portal hypertension in order to fulfil this criterion;
†Chronic liver disease must be excluded since severe fibrosis might be understaged on liver biopsy
EASL CPG VDL. J Hepatol 2016;64:179–202
• All 5 criteria must be fulfilled
2. Exclusion of cirrhosis on liver biopsy
5. Patent portal and hepatic veins
1. 1 clinical sign of portal hypertension
• Splenomegaly*/hypersplenism
• Oesophageal varices
• Ascites (non-malignant)
• Portovenous collaterals
3. Exclusion of CLD causing cirrhosis
or non-cirrhotic portal hypertension†
• Chronic HCV or HBV
• NASH/ASH
• Autoimmune hepatitis
• Hereditary haemochromatosis
• Wilson disease
• Primary biliary cirrhosis
4. Exclusion of conditions causing
non-cirrhotic portal hypertension
• Congenital liver fibrosis
• Sarcoidosis
• Schistosomiasis
54. INCPH: TREATMENT
• Treatment and prophylaxis of variceal GI bleeding
-Endoscopic therapy controls acute variceal bleeding in 95% of patients
and reduces risk of rebleeds
• Despite lack of data, endoscopic band ligation is preferable
-TIPS should be considered in case of uncontrolled bleeding
• Anticoagulation cannot be generally recommended
• Can be considered in patients with clear underlying prothrombotic
conditions or in those who develop PVT
• EASL CPG VDL. J Hepatol 2016;64:179–202
Recommendations
Manage portal hypertension according to the guidelines for cirrhosis B 1
Screen, at least every 6 months, for the occurrence of PVT B 1
Consider liver transplantation in INCPH patients who develop liver failure
or unmanageable portal hypertension-related complications
B 1