2. The hepatic portal
circulation carries blood
from GI tract (i.e. from the
distil esophagus to
anorectal junction) to the
liver.
Porto–systemic
anastomosis occurs in
junctional areas of venous
drainage.
Portal venous blood drain
into venous sinusoids of
liver and hence in to the
hepatic veins.
3. NORMAL PORTAL HYPERTENSION
Pressure = Flow X
Resistance
Portal pressure : 5-10
mm Hg
Normal elevation:
Eating
Exercise
Valsalva
10 mmHg (prolonged) →
Shunting
Lt Gastric → esophageal
Short Gastric → Gastric
Submucosal
Lt portal → epigastric
Retroperetoneal and
anorectal collateral
12 mm Hg → Bleeding
4. Portal hypertension develop
when there is elevation of
portal pressure is greater
than 12 mmHg, while normal
portal pressure is 5 –
10mmHg.
As portal hypertension
produce no symptoms it is
usually diagnosed following
presentation with
decompensated chronic liver
disease encephalopathy,
ascites or variceal bleeding.
7. Cirrhosis results in scarring (perisinusoidal
deposition of collagen)
Scarring narrows and compresses hepatic
sinusoids (fibrosis)
Progressive increase in resistance to portal
venous blood flow results in PH
Portal vein thrombosis, or hepatic venous
obstruction also cause PH by increasing the
resistance to portal blood flow
As pressure increases, blood flow decreases
and the pressure in the portal system is
transmitted to its branches
Results in dilation of venous tributaries
Increased blood flow through collaterals and
subsequently increased venous return cause an
increase in cardiac output and total blood
volume and a decrease in systemic vascular
resistance
With progression of disease, blood pressure
usually falls
8. Oesophageal and gastric varices(lt
gastric vein+short gastric vein(P)-
intercostal,diaphragmatic,esophageal
,azygos vein(VC) )
Haemorrhoids (superior hemohhoidal
vein(P)-middle and inferior
hemorrhoidal veins(VC) )
Caput medusae (remnant of umbilical
circulation-large paraumbilical vein-
epigastric venous system around the
umbilicus )
Retroperitoneal veins-
gastrointestinal veins through the
bare areas of the liver
Omental and lumbar veins
11. Specific treatment in some pre cirrhotic lesions:
Wilson disease—D penicillamine,
Hemochromatosis---phlebotomy,
Antiviral drugs for chronic viral hepatitis
In established cirrhosis-treatment of complications
Screening for hepatocellular carcinoma
Liver transplantation
Maintenance of nutrition
12. Caused by hepatic venous obstruction at the level of the inferior
vena cava, the hepatic veins, or the central veins within the liver itself
Result of congenital webs (in Africa and Asia), acute or chronic
thrombosis (in the West), and malignancy
Acute symptoms include hepatomegaly, RUQ abdominal pain,
nausea, vomiting, ascites
Chronic form present with the sequelae of cirrhosis and portal
hypertension, including variceal bleeding, ascites, spontaneous
bacterial peritonitis, fatigue, and encephalopathy
Diagnosis is most often made by US evaluation of the liver and its
vasculature. Cross-sectional imaging using contrast-enhanced CT or
MRI . Gold standard for the diagnosis has been angiography
Management has traditionally been surgical intervention (surgical
decompression with a side-to-side portosystemic shunt)
Minimally invasive treatment using TIPS may be first-line therapy now
Response rates to medical therapy are poor
13. Most common cause in children (fewer than 10% of adult pts.)
Normal liver function and not as susceptible to the development of
complications, such as encephalopathy
Diagnosis by sonography, CT and MRI
Often, the initial manifestation of portal vein thrombosis is variceal
bleeding in a noncirrhotic patient with normal liver function
Causes:
Umbilical vein infection (the most common cause in children)
Coagulopathies (protein C and antithrombin III deficiency),
Hepatic malignancy, myeloproliferative disorders
Inflammatory bowel disease
pancreatitis
trauma
Most cases in adults are idiopathic
Therapeutic options are esophageal variceal ligation and sclerotherapy
Distal splenorenal shunt
Rex shunt in patients whose intrahepatic portal vein is patent (most
commonly children)
14. Most often caused by disorders of the
pancreas (acute and chronic pancreatitis,
trauma, pancreatic malignancy, and pseudocysts)
Related to the location of the splenic vein
Gastric varices are present in 80% of patients
Occurs in the setting of normal liver function
Readily cured with splenectomy (variceal
hemorrhage), although observation for
asymptomatic patients is acceptable.
15. Decrease or reverse portal blood flow to the liver
promote the development of the portosystemic
anastomosis between the portal system and
systemic circulation-dilated veins around umbilicus.
Liver cell dysfunction/liver failure occurs in
hepatic and post – hepatic causes
Ascites
Splenomegaly (hypersplenism may be result)
The CHILD – PUGH classification is used to asses the
severity.
Jaundice
Anemia
Signs of encephalopathy-asterexsis
16. Conditions 1 2 3
Bilirubin (md/dl) <2 2-3 >3
Albumin (g/L) >3.5 2.8 – 3.4 <2.8
Prothrombin
index(%)
>70 40-70 <40
Ascites None Slight-
Moderate
Moderate –
severe
Encephalopathy None Slight-
Moderate
Moderate –
severe
5-7 =A
7-10 =B
>10 =C
Child A – mild
B → non-
transplant
surgery
Child C –
advanced B →
transplant
17. GI bleeding due to gastric and esophageal varices
Ascites
Hepatic encephalopathy
portal hypertensive gastropathy and colopathy.
congestive splenomegaly,hypersplenism
Hepatorenal syndrome
Hepato pulmonary syndrome
18. 1- FBC, Urea & electrolytes ,LFT and clotting fn.tests
2- Screening tests for the causes of the cirrhosis
3- CT & ultrasound scan to assess liver morphology,
diagnose portal hypertension and assess cause.
4- Transabdominal Doppler ultrasound to assess blood
flow in the portal vein and hepatic artery.
5-Gastroscopy in acute variceal bleeding
6-portal venogram
7-measurement of portal venous pressure through
transjugular cannulation of hepatic veins(high in
sinusoidal and postsinusoidal PH)
19. General resuscitation
Anti – coagulation for Budd – Chiari syndrome
Treatment of hepatic cause
Treatment Of Chronic Complication such as Esophageal gastric
varices:
1- Beta – blocker (propranolol or nadolol), reduce portal venous
pressure due to vasodilatory effects on both splanchnic arterial bed and
portal venous system and reduced cardiac output.
2- Repeated injection sclerotherapy or variceal ligation
3- Elective porto – systemic shunt (spleno – renal anastomosis)
4- Liver transplant may be considered for treatment if associated with
severe liver diseases.
Rectal Varices: Injection sclerotherapy
Symptomatic splenomegaly: laparoscopic or open splenectomy.
Ascites: Oral spironolactone, in cases of ascites, paracentesis may be
required with IV albumin replacement.
20. Hemorrhage from the varices is acute complication of the portal
hypertension.
Mortality rate of first variceal bleed established portal hypertension is
30%.
Bleeding arises from oesophageal varices mostly or from gastric varices
Causes & Features:
Typical variceal bleeding is rapid in onset, copious dark blood with little
mixing with food.
Feature of established portal hypertension e.g. capute medusae
Feature of developing hepatic encephalopathy
Factors like NSAIDS intake,high portal pressure,large varices,endoscopic
variceal stigma(red spots,red stripes),tense ascites precipitate bleeding
Symptoms and signs of shock(tachycardia,systolic Bp <90mmHg,urine
output <30ml/hr)
21. Established large caliber IV access, give crystalloid fluid up to 1000
mL, if tachycardic or hypotensive.
Only use O - ve blood if the patient is in extreme shock, otherwise
wait for cross – match blood.
Catheterize and place on fluid balance chart if hypotensive.
Send blood for FBC, HB conc. WCC, U&E, Na, K, LFT, albumin and
clotting.
Monitor pulse rate, BP and urinary output.
Insertion Of Sengstaken Blackemore gastro-esophageal tube may
be a life saving. To be deflated after 24 hrs.If bleeding stops remove
in another 24 hrs.
22. Decreases the rate of bleeding
Enhances the endoscopic ability to visualize the site of bleeding
1.Vasopressin - potent splanchnic vasoconstrictor; decreases portal
venous blood flow and pressure.0.1-0.5 units/min for 4-12 hrs then
reduce dose upto 48 hrs. Terlipressin is better in hepatorenal syndrome
Somatostatin: direct splanchnic vasoconstrictor.250 microgm bolus
followed by 250 microgm/hr infusion
Octreotide:Synthetic somatostatin analogue.50 microgm bolus IV foll by
50 microgm/hr
Short acting nitrates(NTG)-lower portal pressure by direct vasodilation of
porto systemic collaterals
23. Endoscopic Sclerotherapy with sodum morrhuate,absolute
alcohol,ethanolamine oleate: complications occur in 10-30%
and include retrosternal chest pain, perforation,ARDS,sepsis
Endoscopic band variceal ligation: becoming the initial
intervention of choice; success rates range from 80-100%
Surgery
Porto systemic shunt-selective,nonselective
Totally diverting (end-side portacaval)
Partially diverting (side-side portacaval)
Selective (distal splenorenal shunt)
Splenectomy –splenic vein thrombosis
Liver transplantation
24. Primary prophylaxis: prevent 1st episode of bleeding
Secondary prophylaxis: prevent recurrent episodes of
bleeding
Include control of underlying cause of cirrhosis and
pharmacological, surgical interventions to lower portal
pressure
Beta blockade: Beta blockade (Nadolol, Propranolol)
Sclerotherapy
Endoscopy band variceal ligation
TIPSS
Portosystemic Shunt Surgery
Prevent encephalopathy by giving lactulose
25. Neuropsychiatric complication of cirrhosis
Results from spontaneous or surgical / radiological
portal-systemic shunt + chronic liver failure
Failure to metabolize neurotoxic substances
Alterations of astrocyte morphology and function
(Alzheimer type II astrocytosis)
Types:
1.acute or subacute-reversible
2.chronic-progressive leading to coma and death
26.
27. Increased nitrogen load(GI
Bleed,uremia,constipation,in
creased protein intake)
Electrolyte
imbalance(hypokalemia,hyp
ovolemia,hypoxia,alkalosis)
Drugs(narcotics,diuretics,se
datives)
Large binge of alcohol
Large volume paracentesis
TIPSS
Infection,surgery ,acute liver
disease
28. Identify and treat
precipitating factor
Infection
GI hemorrhage
Prerenal azotemia
Sedatives
Constipation
Lactulose (adjust to 2-3
bowel movements/day)
Protein restriction, short-
term (if at all)
29.
30. Hepatorenal Syndrome Hepatopulmonary syndrome
6 criterias
1.Cirrhosis with ascites
2.Creatinine>1.5 mg%
3.Absence of other cause of renal
failure
4.No treatment with nephrotoxic
drugs
5.Absence of shock
6.Kidney is anatomically, histologically
functionally normal
Type 1:acute,rapid,poor prognosis
Type 2:chronic,stable,better prognosis
Decreased blood volume and
increased sympathetic tone
Treat precipitating factors,
saline/albumin,midodrine,octreotide
Liver transplant
4 criterias
1.Advanced chronic liver disease
2.Arterial hypoxemia
3.Intra pulmonary vasodilation
(defective clearance of vasodilatory
substance by liver)
4.No primary cardiopulmonary disorder
Clinical
Platypnoea(dyspnoea in upright)
Orthodeoxia(desaturation in upright)
Inv
Contrast enhanced ECHO
Technetium-99m macroaggregated
albumin lung perfusion scan
Treat
Oxygen,drugs like almitrine,methylene
blue, garlic-increase pulmonary vasc
resistance+pulm art pressure
TIPS,liver transplant
31. CAUSES
Prehepatic, hepatic ,posthepatic
COMPLICATIONS
GI bleeding due to gastric and esophageal varices
Ascites
Hepatic encephalopathy
portal hypertensive gastropathy and colopathy.
congestive splenomegaly
Hepato renal,hepato pulmonary syndrome
TREATMENT
Treat the cause, reduce portal pressure, liver
transplant