1. Portal hypertension
DR/ Walid Elshazly

2. Portal hypertension
Portal hypertension is an increase in the blood pressure within a system of veins called the portal venous system
Normal portal pressure is generally defined between 5 and 10 mm Hg.

3. Portal hypertension
The portal vein drains blood from the small and large intestines, stomach, spleen, pancreas, and gallbladder.

4. Portal Vein Anatomy

6. Portal hypertension
The superior mesenteric vein and the splenic vein unite behind the neck of the pancreas to form the portal vein.

8. Etiology Functional Organic Pre-sinusoidal extra-hepatic
Pre-sinusoidal intra-hepatic ( Fibrosis)
Post-sinusoidal intra-hepatic ( Cirrhosis)
Post-sinusoidal extra-hepatic

9. Etiology Presinusoidal Extrahepatic Intrahepatic
Cavernomatous malformation
Malignant portal & splenic vein obstruction
Intrahepatic
Schistosomiasis
Congenital hepatic Fibrosis
Sarcoidosis

10. Etiology Post sinusoidal Intrahepatic Extra hepatic Cirrhosis
Venoocclusive disease
Extra hepatic
Hepatic vein obstruction
Budd Chiari syndrome
Constrictive pericadritis

11. Pathogenesis Backward resistance theory (to initiate)
It denotes increase resistance in the liver bed through a
constant component (liver fibrosis and regenerating nodules)
variable component through the action of humoral substances (endothelin, prostaglandins, adrenergic sububstances, and serotonin)

12. Pathogenesis Forward flow theory (to maintain)
It denotes increase in inflow to the liver through the action of humoral substances that cause
hyperdynamic and
hypervolemic circulation (nitric oxide, glucagon and, prostacylin)

13. Mechanism of portal hypertension In Shistosomiasis
Peri-portal fibrosis
Portal hyper-volaemia
Release of vaso-spastic substances
Angiomatous mass
Endo- arterial obstruction

14. Complication of portal hypertension
Spleno-megally
GIT congestion
Ascites
Opening of porto-systemic collaterals
Hepatocelluar failure
Portosystemic encephalopathy

15. Splenomegally Mechanisms RES hyper-plasia Opening of A/V shunts
Venous congestion
hypersplenism

16. Splenomegally Clinical picture Pressure manifestations Splenic pain
Hypersplenism
Psychic trauma

17. GIT congestion Gastric dyspepsia related to type of food
Haematemesis dt gastropathy which cause sever form of bleeding

18. Ascites etiology of ascites
Hormonal factors lead to salt and water retention
Hypo-proteinaemia
Portal hypertension
Lymphorrhoea
Disturbed renal function

20. Ascites ( treatment) Bed rest Diet Albumin infusion
Fresh frozen plasma
Diuretics
Refractory ascites require
Therapeutic para-centesis
Recirculation therapy
Peritoneo-venous shunt
Sapheno-peritoneal shunt

21. Porto-systemic Collaterals
Cephalic
Lower end of esophagus
Bare area of liver
Caudal
Around umbilicus
Rectal
Retro-peritoneal

22. Portal Vein Collaterals
Five Principle Routes
Esophageal Varices
Umbilical Vein
Hemorrhoids
Veins of Retzius
Adhesions
Five principle routes for portosystemic collaterals
Listed here in increasing order of surgical importance

23. 1 4 2 3

24. Lower end of esophagus
There is four rather than three plexuses of veins (intraepithelial, superficial, sub mucus and periesophageal) with the intraepithelial plexus in excess

25. Lower end of esophagus
In the palisade zone the veins are oriented in a special way, different from the gastric, perforator or truncal zones

26. Lower end of esophagus
The veins are condensed in the superficial plexus, rather than in the submucosal plexus opposite to the distribution in other zones

27. Endoscopic Views

28. Classification System
Cirrhosis
Endoscopy
No Varices
Varices
q 2 years
1st Variceal Bleed
b-blocker
Evaluation
Banding
Rebleeding
Childs C / Liver Failure
Childs A or B
Surgical Shunt /
TIPS
Transplant
Medical Tx
Childs-Pugh
Classification System
Parameter 1 Point 2 Points 3 Points
Bilirubin < >3
Albumin > <2.8
D PTT >6
Ascites None Slight Moderate
Encepha- None
lopathy
5 – 6 Class A
7 – 9 Class B
> 10 Class C

29. Hepato-cellular failure ( etiology)
Infection
Bleeding
Drugs
Anesthesia
surgery

30. Hepato-cellular failure (C/P)
Weakness
Jaundice
Fetor hepaticus
Palmer erytems
Spider angioma
Gynaecomastia
Loss of axially and pubic hair
Testicular atrophy
Acute liver failure

31. Gynecomastia

33. Hepato-cellular failure (R)
Treat precipitating factors
Diet
Drugs
Renal failure
Correct clotting abnormalites
If no response
Exchange transfusion
Cross circulation between donor and patient
Extra-corporeal perfusion through pigs liver

34. Porto-systemic encephalopathy
Due to materials that by pass the liver with its toxic effect over the brain (GABA, ammonia, methionine & short chain FA )
Clinically
Personality changes
Disorientation
Slurring speech
Flappy tremors
Cogwheel rigidity
Ankle clonus
coma

35. Porto-systemic encephalopathy
Treatment
Chemical
Intestinal antiseptic
Lactulose
Mechnical
Liver support
Nerve cell support glutamic acid

36. Investigations Laboratory Stool Urine CBC Kidney function
Liver function
Synthesis (proteins, prothrombin)
Excretory ( bilirubin, dye excretion)
Cell insult (SGOT, SGPT, alk phospatase, LDH)

37. Investigations Radiological Instrumental U/S Doppler B swallow B enema
Portography
CT scan
MRI
Radio-isotope
Instrumental
Upper endoscopy
Laparscopy
Laparscopic U/S

38. Child-Pugh Classification
Points 1 2 3
Bilirubin (mg/dL)
< 2
2 – 3
> 3
Albumin (g/dL)
> 3.5
2.8 – 3.5
< 2.8
Prothrombin time (seconds ↑)
1 – 3
4 – 6
> 6
Ascites
None
Slight
Moderate
Encephalopathy
Minimal
Advanced
Grade A, 5-6 points; Grade B, 7-9 points; Grade C, points

39. Angio-graphy Indirect trans-femoral porto-grapgy Direct portigraphy
Per-cutaneous trans-splenic
Per-cutaneous trans-hepatic
Umbilical catherization
Direct operative
Wedged hepatic venograpgy

40. Treatment (Bleeder) Active bleeder Resusitation Specific measures
Non-operative
Naso-gastric
Tr-iluminal tube
Edo-scopic injection
Operative
Measures to prevent encephalopathy
Cold case
Child C
injection sclerotherapy
liver transplantation
Child A&B
Non shunt
Hassab
Sugura
Tanner
Shunt
Non selective
selective

41. Treatment (Non-Bleeder)
Small spleen
No varices
conserve
Varices
Sclerotherapy
Decongestion prophylactic ??
Huge splenomegally or hyper-splenism
Decongestion

42. Treatment (Bleeder) Active bleeder Resusitation Specific measures
Non-operative
Naso-gastric
Tr-iluminal tube
Edo-scopic injection
Operative
Measures to prevent encephalopathy

43. Active bleeder Resusitation
On patient admission and after clinical evaluation three lines are installed
I.V. line for blood sample, blood and fluid replacement
Urinary catheter for monitoring tissue perfusion together with pulse and BP
Nasogastric tube or Sangestaken Blackmore tube for monitoring the bleeding, and doing gastric lavage to prepare for endoscopy

44. Active bleeder Resusitation
Resuscitation with transfusion of
Colloids (blood) and
Crystalloids (Ringer, or lactated Ringer or saline solutions) at the same time with monitoring the blood pressure, pulse and urinary output.

45. Active bleeder Resusitation
Sandostatin infusion (0.25 microg in 500 ml glucose over 4 to 8 hours, with or without an intramuscularly administered shot)
Sangestaken tube to arrest the bleeding
Sclerotherapy
can be done immediately, however,
it is better to be postponed until the hemodynamics of the patient are corrected and the stomach is washed from the retained blood which obscure the procedure and make it very difficult

48. Endoscopic Banding

50. Endoscopic Sclerotherapy
Intravariceal
Paravariceal

51. Surgical treatment Shunt Direct Non-selective Varix ligation
Non shunt
Direct
Varix ligation
Stappler trans-section& reanstmosis
Indirect
Hassab
Tanner
Sugura
Shunt
Non-selective
Porto-caval
Mesocaval
proximal- lieno-renal
Selective
Warren’s
Modified warrien’s
Coronary caval
Sarfeh

52. Transjugular Intrahepatic PC Shunt

53. TIPS Transjugular Intrahepatic Portocaval Shunt

54. TIPS

55. TIPS

56. The spleen is excised
decrease the amount of portal blood flow
help diaphragmatic excursions, and thus increase chest negativity.
It also relieves the mechanical compression of the stomach that can cause dyspepsia.
The left gastric is ligated and cut thus causing portoazugus disconnection
The lower esophagus and the upper stomach are devascularized thus disconnecting the main stream from the esophageal varices area

57. These are devascularisaion operations aiming at portazygus disconnection by interrupting the intrinsic submucosal plexus continuity (Tanner operation)

58. The spleen is also excised decreasing portal blood flow
The esophagus in the thorax as well as in the abdomen is devascularized with the upper half of the stomach (can be done at two stages)
The left gastric is not cut or ligated and left going up to the chest for azygus connection, only perforators are cut (paraesopahgeal devascularization rather than esophageal devascularization)
The esophagus or the cardia is transected to interrupt the submucosal blood flow from below to feed the variceal area, in this step the vagus is cut, and pyloromyotomy should be added.

59. Splenorenal or Warren Shunt
Connect the splenic v. to the renal v.
Ligate and divide:
Coronary v.
R-gastroepiploic v.
Inf. mesenteric v.
Only the splenic, right gastric, and esophageal veins are shunted.
Mesenteric flow still goes to the liver

60. Distal Splenorenal Shunt

71. Surgical Shunts – Pros and Cons
Long term reduction in portal pressures
Reduces ascites
Reduces risk of bleeding
Cons –
Massively invasive procedure
Can cause encephalopathy
If total shunt, abolishes portal flow
Can cause liver failure
Patients are no longer candidates for transplant

72. Total Shunts End to Side Portocaval Side to Side Portocaval
Interposition Shunts
Central Splenorenal

73. Total Shunt Results Prevent rebleed > 90% Thrombosis with graft
Encephalopathy rate 40%

74. Thank you