Portal hypertension, cirrhosis Udon thani hospital

1. ATopic review
By
Tansakul M. ,Yutchawit P.
Under supervision of …
Wiwatthanachang O.
Department of Medicine, UdonThani Hospital

2. Normal portal pressure
gradient 1-5 mmHg
Portal hypertension =
portal pressure gradient >5
mmHg
Clinically significant
portal hypertension
>= 10 mmHg.

3. Increase resistance in
hepatic circulation Increase portal
bloodflow

5. Medications associated with idiopathic
noncirrhotic portal hypertension
• Azathiopine
• Cyclophosphamide
• Doxurubicin
• Bleomycin

6. Complication of portal hypertension
• Variceal hemorrhage
• Portal hypertensive gastropathy
• Ascites
• Spontaneous bacterial peritonitis
• Hepatorenal syndrome
• Hepatic hydrothorax
• Hepatopulmonary syndrome
• Portopulmonary hypertension
• Cirrhotic cardiomyopathy

7. Variceal hemorrhage : prophylaxis
• Primary prophylaxis
• Secondary prophylaxis

8. Variceal hemorrhage : Primary
prophylaxis
• Endoscopy of all patient with cirrhosis if normal follow up q 2-3
years
• Non selective Beta blocker (propranolol, carvedilol)
• Esophageal variceal band ligation
• Transjugular intrahepatic portosystemic shunt

9. Drug : variceal bleeding
• Splanchnic vasoconstriction
• Somatostatin 250 mcg iv bolus, then drip 250 mcg/hr
• Octreotide 50 mcg iv bolus, then drip 50 mcg/hr
• Terlipressin0.5-2 mg iv q 4 hr in 48 hr then 1 mg iv in q 4 hr (Caution in
CAD,PVD)
• Antibiotic prophylaxis
• Norfloxacin400 mg bid x 7 days (ciprofloxacin)
• IV ceftriaxone1 g/dayx 7 days ( in childB-C, NPO)
3-5 days

10. Secondary prevention

11. Conciseand practicalpoint

12. Definition of ‘Ascites’
•Accumulation of fluid within peritoneal cavity.
•Most common cause = portal HT
•Other cause = malignant , infection
Cirrhosis - 81%
Cancer - 10%
Heart Failure - 3%
Tuberculosis - 2%
Dialysis - 1%
Pancreatic Disease - 1%
Other - 2%

13. Pathogenesis
Figure 41-2
Harrison’s
Gastroenterology
And hepatology
17th Edition

14. Clinical presentation
•Abdominalgirth
•Peripheral edema
•Compromised respiratory function
•Hepatic hydrothorax
•Other unspecific symptom and fatigue / malnourished

15. Diagnosis
•Physicalexamination
•Abdominalimaging ; U/S or CT abdomen
•Abdominal paracentesis
… for total protein, albumin, cell diff and count,
G/S, C/S (in some setting –amylase, cytology)

16. SAAG ;
Serum ascites-to-albumin gradient
•Cut point is 1.1
•Transudate vs exudate
Portal cause
Non-Portalcause

17. Ascites Profile
•SAAG
•Very low ascites protein
>> increased risk of developing SBP
•High level of RBC
>>Trauma ?, HCC ?, rupture omental varix?
•PMN count > 250 cell/mm3
>> Infection ?

18. Treatment of ascites
•Salt restriction !! ( < 2 g /day or 88 mmol/day)
+ water restriction (1-1.5l/day)
•Weight measurement ***
•Diuretics (Na excretion > 78 mmol/day)
• Spironolactone 100-200 mg (max 400 mg/day)
• Combination with furosemide 20-40 mg (max 160mg/day)
•Avoid NSAID and steroid use
•Refractory ascites may need Large volume paracentesis
/TIPS / liver transplantation to correct.

19. SBP; A complication of ascites
•Spontaneous vs secondary bacterial peritonitis
•Bacterial overgrowth and translocation
•Presentation : abdominal pain, fever,
accelerated ascites or hepatic encephalopathy
•Exclude secondary bacterial peritonitis first.
•PMN > 250 cell/mm3 +- C/S +ve
•Organism : E. coli, K. pneumoniae and
sometimes G+ve
•ATB : Ceftriaxone , Cefotaxime

20. AmericanAssociationforthe Study of Liver Diseases(AASLD) 2012

21. Albumin therapy in SBP !?
This graphicshows that the additionof albuminto cefotaximeclearlyprevented
renal impairmentand improved mortalitywhen comparedwith cefotaximealone.
p values: renal impairmentp=0.002, in-hospitalmortalityp=0.01, 3 month
mortalityp=0.03
Sort P, Navasa M, Arroyo V, et al. N Engl J Med. 1999;341:403-9

22. AmericanAssociationforthe Study of Liver Diseases(AASLD) 2012

23. ** SBP prophylaxis ;Why ?
•Cirrhotic patient with ascites or previous SBP
have high recurrent rate. (70%)
•High mortality rate of SBP
(9 mo of mean survival time)
•Selective intestinal decontamination
•Increased risk of drug resistant ?

24. ** SBP prophylaxis ;When ?
•Primary prophylaxis
•Cirrhotic ascites with GI hemorrhage
•Cirrhotic ascites with LOW protein in ascites
(<1.5g/dl) + Cr > 1.2 mg/dl or BUN > 25 mg/dl
or serum Na <130 mEQ/l
•Cirrhosis with Child Pugh score > 9 (Child C) +
serum TB > 3 mg/dl
•Secondary prophylaxis
•Hx of previous SBP
AmericanAssociationforthe Study of Liver Diseases(AASLD) 2014

25. ** SBP prophylaxis ; How ?
•Ciprofloxacin or other fluoroquinoloneor
Bactrim
Ciprofloxacindose = 500 mg / day
•NPO ? >>Ceftriaxone 1 g iv OD
•Duration ? >> life long or out of cirrhosis
forGIB case… 7 days
AmericanAssociationforthe Study of Liver Diseases(AASLD) 2014

26. A brief review of

27. Definition
•A serious complication of chronic liver disease ,
defined as an alteration in mental status and
cognitive function occurring in liver failure.
•Ammonia level
•A.K.A. Portosystemic encephalopathy
•Types : A-B-C
Testing for Asterixis (Flap Test)
To test for asterixis, the arms are extended
and the wrists dorsiflexed.

28. InternationalSocietyfor Hepatic EncephalopathyandNitrogen Metabolism(ISHEN)

30. Common precipitating factors
‘BIGSCALP’
B = Blood transfusion
I = Infection
G = GI bleed
S = sedative drug and tranquilizer
C = constipation
A = alkalosis
L = low k
P = high protein diet, Portosystemic shunt

31. Lactulose
•Synthetic disaccharide >>>
Monosaccharide +VFA + hydrogen
ion + methane
•VFA >> bacterial growth
•H+ ion >> decreased pH
•Acidic pH helps..
•Leeching NPH3
•Decreased harmful bacteria proliferation ;
decreased NH3 production
•Decreased NH3 >> NH4 conversion.

32. Summary points for HE
• Overt hepatic encephalopathy consists of neurological and psychiatric
abnormalities that can be detected by bedside clinical tests, whereas
minimal hepatic encephalopathy can only be distinguished by specific
psychometric tests.
• There are many grading scales available for hepatic encephalopathy,
including the long standing West Haven Criteria, which is the most
commonly used system.
• Diagnosis of overt hepatic encephalopathy requires the exclusion of
alternate causes of altered mental status. Serum ammonia levels
should not be used as a diagnostic tool or as a means of monitoring
response to treatment.
• Treatment of acute overt hepatic encephalopathy should include: (1)
supportive care, (2) identifying and treating any precipitating factors,
(3) reduction of nitrogenous load in the gut, and (4) assessment of need
for long-term therapy and liver transplant evaluation.

33. Summary points for HE
• Lactulose can be used as initial drug therapy for the treatment of acute
hepatic encephalopathy. Rifaximin should be added for those patients
who do not have an adequate response to lactulose. Subsequently, the
addition of oral branched-chain amino acids or intravenous L-ornithine-
L-aspartate can be considered in patients who do not respond to the
combination of lactulose and rifaximin.
• Prevention of recurrent hepatic encephalopathy or treatment of persistent
hepatic encephalopathy includes drug therapy as well as prevention or
avoidance of precipitating factors.
• Protein restriction should be avoided as a general rule, as it can actually
lead to worsening of hepatic encephalopathy. Cirrhotic patients are
advised to consume 1.25 to 1.5 g/kg protein daily.
• Liver transplant evaluation should be considered in appropriate
candidates once a diagnosis of overt hepatic encephalopathy is made.
Liver transplantation is indicated in patients who have liver failure and
recurrent intractable overt hepatic encephalopathy.

34. Reference