Definition, pathophysiology and surgical aspects in management of portal hypertension

1. Portal Hypertension
&
Management
Presented by : Dr. Krishnaprasad Bashyal
Resident – Department of General Surgery

2. INTRODUCTION
 Management of Portal Hypertension has changed dramatically over
past two decades.
 Wide spectrum, of etiologies mandates need for MDT approach.
 Role of surgeon is changed with now mainly being in transplant &
shunt surgery reserved for 15 – 20 % of patients.

3. HISTORY
 Ascites was first chief complication to be recognised in 19th century.
 Next 100 yrs many theories like foreward (Banti) & backward (Mc Indoe)
for Portal Hypertension reigned.
 Later, era of decompressive surgeries to manage the hypertension
syndrome.
 Portacaval shunts was initially performed in dogs by Nicolai Eck in
St. Petersburg in 1890, but it was Pavlov who documented risks as
progressive hepatic failure, encephalopathy.

4.  Whipple & colleagues significantly advanced the field.
 Selective shunts were pioneered by Warren & Inokuchi who showed
that variceal decompression could be achieved by maintaining
perfusion to the cirrhotic liver.
 Sclerotherapy had become the realm of Gastroenterologists but it was
a surgeon introduced variceal banding.
 TIPS was pioneered by Rosche & widely used in 1990s
 Liver Transplantation was introduced by Starzl & Calne in 1970s.

5. ANATOMY

6. Major changes of clinical
significance is around the
GEJ.
Radiologic studies using
morphometry &
corrosion casting have
clarified venous
pathologic changes at
this location.

7.  Gastric Zone : 2-3 cms below GEJ. Veins
run longitudinally in submucosa & lamina
propria to short gastric & left gastric veins.
 Palisade Zone : multiple communication
between the veins in LP but no
perforating ein
 Perforating Zone : Vessels perforate
through the esophageal wall linking the
internal & external veins.
 Truncal Zone : 8-10 cms up the
esophagus, irregular perforating veins
from submucosa to external esophageal
plexus.

8. PATHOPHYSIOLOGY
 Normal Portal Venous pressure is 5 – 8 mmHg with normal Portal
flow in 1 – 1.5 L/min range.
 PV is a passive conduit from gut that carries blood back to liver.
 Total liver blood flow is regulated by intrinsic & extrinsic
mechanisms with alteration in Portal venous flow having direct
reciprocal increase/decrease in hepatic arterial flow.

9.  Theres increased passive resistance to Portal flow secondary to
fibrosis & regenerative nodules.
 Increased hapatic vascular resistance due to active vasoconstriction by
norepinephrine, endothelin , angiotensin & other humoral
vasoconstrictors.
 Increased Portal venous inflow secondary to splanchnic vasodilation
contributes to portal hypertensive syndrome.

10.  Posrtosystemic collaterals develop at not just at GEJ also in
abdominal wall & retroperitoneum.
 A systemic hyperdynamic circulation develops with increased cardiac
output, low total systemic vascular resistance, and further aggravation
of the splanchnic hyperemia and overall hyperdynamic state.

12. IMAGING & MEASUREMENT OF PORTAL
VEIN
 Simplest initial investigation is abdominal USG.
 Large PV suggests Portal HTN but not diagnostic.
 Doppler ultrasound is capable of outlining anatomy, r/o thrombus,
direction of portal flow. Evaluating surgical shunt & TIPSS flow.
 CT & MR angiography reveal PV anatomy as well as patency.

13.  Visceral angiography & PV venography reserved for cases not
satisfactorily evaluated by non invasisve methods & require further
clarification.
 Hepatic venography most accurate method to determine Portal
HTN.
 FHVP & WHVP
 Hepatic venous pressure gradient ; HVPG = WHVP – FHVP

15.  DEFINITION :
 WHVP or direct PV pressure that’s 5mmHg more than IVC
 Splenic pressure of more than 15mmHg
 Portal venous pressure measured directly in surgery >30 cm of saline.

16. ETIOLOGY

17. CLINICAL PRESENTATION
 Variceal bleed is one of the most lethal complications of Portal HTN.
 30% of patients with cirrhosis develop varices
 30% with varices bleed from them
 Patients with large varices are more at risk from bleeding than with
smaller varices.

18.  Patients with varices & preserved liver function have more options
for therapy.
 UGIE in cirrhotic patients required for
 Prophylactic therapy
 Management of acute bleeding episode.
 Therapy to prevent recurrent variceal bleed.

19.  Ascites sign of decompensation
 Liver failure, encephalopathy.
 Portopulmonary syndromes have been recently recognised as
important componenet of clinical presentation of Portal HTN.

20. EVALUATION

22. MANAGEMENT OF VARICEAL BLEEDING

26. TIPS
Indications :
 Variceal Bleed
 Gastric varices & Gastropathy
 Ectopic Varices
 Ascites
 Hepatic hydrothorax (5-10% cirrhotic patients).
 Budd Chiari syndrome (failing anticoagulation therapy)
 Pre operative decompression

27. Contraindications (relative) :
 Right heart failure
 Cavernomatous transformation of the Portal Vein
 Polycystic liver disease.
 SBP

29. SURGICAL SHUNTS IN AGE OF TIPS
 Most common cause of TIPS failure are shunt thrombosis & stenosis leading
to variceal rehaemorrhage.
 Survival data after TIPS are not comparable to surgical shunts, most notably
small diameter prosthetic HGPCs shunt.
 In 2005 a RCT of 132 patients undergoing TIPS v HGPCS was reported.
 Showed that stenosis/thrombosis occurred significantly in more patients than
HGPCS

30.  In 32 of them 66 interventions &/or revisions required in 1yr f/u to
maintain shunt patency, only 7 required interventions in HGPCS for
patency.
 5 had irreversible TIPS occlusion.
 Irreversible shunt occlusion presented as major variceal hemorrhage.
 Of the 32, 20 of them had major variceal bleed in 30 days, 2
rehemorrhaged after 30 days whereas none had stenosed or occluded
shunts in HGPCS grp.

31.  Median time of death after TIPS was 29 mths, 56 mths after HGPCS.
 For all patients of CTP classes, TIPS had a median time to failure of
14 mths compared with median time failure of 43 mths in HGPCS
patients.
 TIPS has proven to be more expensive than pharmacologic,
endoscopic or surgical shunt owing to repeated interventions to
maintain patency

32. SURGICAL SHUNTS
 Portosystemic shunts are very effective in preventing recurrent
variceal haemorrhage in Portal HTN.
 They decompress the Portal Venous system to varying degrees by
shunting the portal flow in the low pressure systemic blood flow.
 This blood also carries hepatotropic hormones, nutrients & toxins
which is responsible for consequences as portosystemic
encephalopathy & accelerated liver failure.

33.  Depending on wether they completely decompress, compartmentalize
or partially decompress shunts are classified as nonselective, selective
or partial.
 In addition to variceal decompression, selective/partial shunts also
aim to preserve hepatic portal perfusion hence minimising adverse
effects.

34. NON SELECTIVE SHUNTS :
 End to side Porta Caval shunt (Eck fistula)
 Side to side Porta Caval shunt
 Large diameter interpositional shunts
 Conventional Splenorenal shunt (proximal)
SELECTIVE SHUNTS :
 Distal Splenorenal shunt (Warren)
 Left gastric venacaval shunt (Inokuchi)

35. PARTIAL SHUNTS :
 Small diameter interposition Porta caval shunt (PTFE).
 Mesocaval shunt.

36. NON SELECTIVE SHUNTS
 Eck fistula is of historical importance.
 Portacaval shunts ideally should not be done in patients who are
candidates for liver transplant.
 Current recommendations include emergency surgery for variceal
haemorrhage, elective procedure in significant ascites unresponsive to
non surgical procedures in patients who are not to transplant surgery,
treatment of Budd Chiari syndrome.

41.  No survival benefit could be shown for shunt patients although they
had a crossover bias for medical management as they failed medical
managemenet were crossed over to surgery grp.
 Bleeding effectively stopped in shunt patients, 70% medically treated
patients bled.
 Encephalopathy occurred in 20-40% of shunted patients.

42.  End to side portacaval shunt compared with side to side shunt in a
controlled trial showed no significant clinical differences.
 The interposition mesocaval shunt was studied in a randomized trial
comparing with side to side portacaval shunt & no clinical or
hemodynamic differences were evident.
 Nevertheless it avoids dissection in porta hepatis which is
advantageous for future liver transplant candidates.

43. SELECTIVE SHUNTS
 The DISTAL SPLENO RENAL SHUNT was developed by Warren &
colleagues in 1967 to achieve selective variceal decompression preventing
recurrent bleed.
 Prior experiences of Warren & Zeppa led to evolution of this technique.
 Warren observed total shunts control bleeding but at the cost of liver
failure, whereas Zeppa had seen devascularization procedures maintain
Portal perfusion but at cost of significant risk of rebleeding.
 Over the four decades DSRS became the most widely used surgery to
control variceal bleeding.

44. INDICATIONS :
 Patients with variceal bleed refractory to pharmacologic & endoscopic therapy with
preserved & stable LFT.
 Patients with Portal HTN & normal livers, such as with Portal vein thrombosis
with refractory bleeding & patent spleenic vein.
 Geographical location due to which theres single chance to control bleeding &
patients cannot return for multiple visits required for management with endoscopy
or TIPS.
 CTP class A or B (7 or 8 points), usually without ascites, stable liver function & not
candidates for transplant for next 5 yrs.

45. CONTRAINDICATIONS:
 Medically intractable ascites.
 Prior splenectomy
 Splenic vein diameter <7mm (relative)

46.  Imaging of PV anatomy done as part of evaluation.
 Doppler used to visualise superior mesenteric, splenic, PV as well as
the hepatic veins for outflow.
 CT or MR angiography.
 Arteriography may sometimes be required for final definition of veins
before surgery.

47.  Evaluation includes
 HVPG
 Lt. Renal vein anatomy & drainage (abnormal in 20% of population)
 Sup. Mesenteric, PV, splenic vein patency flow direction & anatomy in venous
phase of arterial study.

48.  DSRS consists of anastomosis of distal end of splenic vein to left renal
vain & interruption of all collateral vessels (eg. Coronary & gastroepiploic
veins) which connect the superior mesenteric vein gastrosplenic
components of the splanchnic venous circulation.
 It results in separation of portal venous circulation into a decompressed
gastrosplenic venous circuit & high pressure superior mesenteric venous
system that continues to perfuse the liver.
 Even when all major collaterals are interrupted, portal flow may gradually
be diverted through pancreatic collateral network (pancreatic siphon)

49.  To prevent this pathway, full length of splenic vein from pancreas,
splenopancreatic disconnection, which results in better preservation
of hepatic portal perfusion.

51. RESULTS :
 Bleeding control is equal to greater than 90% (Henderson et al,
Elwood et al 2006)
 Highest risk of rebleeding is in the first month.
 Technical failure rate should be less than 5% & it should be defined
before hospital discharge by shunt catherization.

52.  In a randomized trial of DSRS v TIPS in CTP class A & B patients
rebleeding rates were 6% & 11%, but 83% TIPS patients required re
intervention & dilatation to achieve this.
 Zeppa & colleagues documented poorer survival in alcoholic
patients.

53.  LEFT GASTRIC VENA CAVAL SHUNT consists of interposition
of a vein graft between the left gastric (coronary) & IVC.
 Therefore it directly & selectively decompresses the esophagogastric
varices.
 But only a minority of patients have appropriate anatomy for this &
experiences are limited to Japan& no controlled trials have been
performed.

54. PARTIAL SHUNTS
 H – Graft Portacaval Shunt (HGPCS), uses a small diameter
interpositional shunt (<10mm, usually 8mm) of PTFE graft with
ligation of coronary vein & collaterals.
 Objective of partial shunt is similar to selective shunt :
 Effective decompression of varices
 Preservation of hepatic perfusion
 Maintain residual Portal HTN

55.  When the prosthetic graft is 10mm or less in diameter , hepatic portal
perfusion is preserved in most patients, atleast during early postoperative
period.
 Near 20mmHg PV – IVC gradient is observed prior to shunting, with about
30mmHg in PV & 10mmHg in IVC.
 Pressure are again measured after shunting & the gradient falls to less than
10 mmHg usually to 6-7mmHg.
 New onset encephalopathy or ascites should raise suspicion for graft
stenosis or PV thrombosis.

56.  Early experience with these shunts is that fewer than 15% shunts
have thrombosed & most opened by successful radiologic
intervention.
 A prospective RCT of partial (8mm) v non selective (16mm)
portacaval shunt has shown lower frequency of encephalopathy in
partial shunt with similar survival rates.
 In another controlled trial, HGPCS showed a lower overall failure
rate of compared to TIPS.

60. DEVASCULARIZATION
 These procedure have been more extensively used in Japan & Egypt
than USA.
 Non shunting procedures include devascularization, splenectomy &
esophageal transection.
 It is disconnection of esophagogastric veins from hypertensive portal
tributaries.

61.  Spence & colleagues showed that large vessels in lamina propria
communicate directly with dilated intraepithelial blood channels.
 These intraepithelial channels seen histoligically represent the cherry
red spots viewed endoscopically.
 Ideal technique to control bleeding varices would be obliteration of
varices in lower periesophageal vessels & intraepithelial dilated
vessels.

62.  HASSAB (1967) proposed a method for Gastroesophageal
decongestion & splenectomy (GEDS) for management of bleeding
varices.
 It includes
 Splenectomy.
 Perihiatal devascularization of the lower lower 3-4 inches of esophagus.
 Ligation of left gastric artery branches to stomach
 Devascularization of proximal half of stomach & to re peritonealize it.

64.  SUGIURA procedure is a nonshunting technique of extensive
paraesophagogastric devascularization with esophageal transection &
splenectomy through 2 incisions – thoracic & abdominal (later)
 Modified approach is completion of surgery through single abdominal
incision.
 Modified- esophageal transection done with circular EEA stapler through a
small gastrotomy.
 Devascularization facilitated by division of anterior vagus nerve for which
pyloroplasty is needed.

66.  Complication of Hassab procedure GOO d/t vagus trunk
transection w/o pyloroplasty.
 Specific complication of Sugiura is esophageal leak & stenosis from
transection.

67. Despite advances in endoscopic therapy,
interventional techniques & liver transplant,
surgical shunts are important tools in select
patients.

68. THANK YOU