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Q.What are the proposed measures for the improvement of Sarcopenia and

Frailty in cirrhosis?

The principal approaches toward the improvement of sarcopenia in cirrhosis for

optimization prior to transplant include:

• Nutrition: High-protein/high-calorie diet, late evening snacks, BCAA

supplementation.

• Exercise: 30- to 60-min sessions of combined aerobic and resistance training

with the goal to achieve 150+ min/week of moderate intensity exercise. The min-

imum duration of any exercise intervention program has been shown to be at

least 3 months (Chodzko-Zajko WJet al. Medicine and science in sports and

exercise 2009).

• Testosterone supplementation.

• -ornithine -aspartate and rifaximin.

Further Reading

Carey EJ, etal. A North American expert opinion statement on sarcopenia in liver transplantation.

Hepatology. 2019;70(5):1816–29.

Buchard B, et al. Assessment of malnutrition, sarcopenia and frailty in patients with cirrhosis:

which tools should we use in clinical practice? Nutrients. 2020;12(1):186.

Sinclair M, etal. Sarcopenia in cirrhosis–aetiology, implications and potential therapeutic inter-

ventions. Aliment Pharmacol Ther. 2016;43(7):765–77.

17 Sarcopenia andFrailty inLiver Disease

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Ltd. 2022

V. Singh, A. Roy (eds.), Clinical Rounds in Hepatology,

https://doi.org/10.1007/978-981-16-8448-7_18

Y. Kumar · A. Roy · V. Singh (*)

Department of Hepatology, Post Graduate Institute of Medical Education and Research,

Chandigarh, Punjab, India

Miscellaneous Topics inLiver Disease

YogendraKumar, AkashRoy, andVirendraSingh

Q.How do you assess surgical risk in cirrhosis?

The consensus on 30-day mortality after surgery in cirrhosis based upon Child

Turcotte Pugh score is as follows:

• CTP-A 10%

• CTP-B 30%

• CTP-C of 76–82%

Factors affecting adverse outcomes after surgery include:

• Liver injury due to anesthetic or hypotension during surgery.

• Shifts in uid balance.

• Delayed wound healing.

• Bleeding tendency.

Role of MELD: MELD has been shown to be a good predictor of 30-day mortality

after surgery. It shows a linear relationship with mortality, with mortality rising by 1%

for each MELD point below 20 and by 2% for higher MELD scores. In 2007, the larg-

est study to predict mortality in cirrhotics undergoing surgery using the MELD scores

was conducted. The median survival based on MELD score is shown in table. This

study’s results were used to formulate the Mayo Clinic Model, which gives the Mayo

Risk Score (MRS), which comprises Age, ASA class, bilirubin, INR, creatinine,

and etiology of cirrhosis. The study was based upon a review of case records of 700

patients undergoing cardiac, orthopedic, or gastrointestinal surgeries (except

Cholecystectomy) from 1980 to 2004. It showed increased mortality at 90 days

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postoperatively compared with ambulatory patients. However, the study is limited by

the fact that the majority of patients had low baseline MELD score (Median MELD-8)

with platelet count >60000/μl and INR<1.5 (Teh SH et al. Gastroenterology, 2007).

Other factors that may affect outcomes after surgery include:

• Hyponatremia

• Low serum albumin

• Older age

• Serum creatinine

• Emergency versus elective surgery

• Type of surgery—abdominal/GI surgery possibly has the worst outcomes

Q.What Is the VOCAL-Penn Risk Assessment Score?

Recently researchers from the University of Pennsylvania have devised a new score

new score called the VOCAL-penn (Veteran’s Outcome and Cost Associated with

Liver Disease), which incorporates the following parameters:

• Age

• Albumin

• Bilirubin

• Platelet count

• Presence or absence of NAFLD (non alcoholic fatty liver disease)

• BMI>30

• ASA score

• Type of surgery

• Emergency of surgery

The performance of the score was found to be superior to MELD, MELD-Na,

CTP, and Mayo Risk Score at predicting 0, 90, and 180-day postoperative mortality.

Q.How to manage pruritus in Cholestatic Liver Disease?

Ans: Stepwise approach for the treatment of pruritus in liver diseases:

Approach

Drug Dose

Interactions/precautions

1st line Cholestyramine 4–16 g/day Interference with intestinal absorption and

hence 4-h interval with administration of

concomitant medications like

ursodeoxycholic acid

2nd line Rifampicin 150–600 mg/day Enzyme induction leading to altered drug

metabolism and potential risk of

hepatotoxicity

3rd line Bezabrate

200–400 mg/day Nephrotoxicity

Myopathy and rhabdomyolysis

4th line Naltrexone 25–50 mg/day To be started at lower doses and careful

titration

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Approach

Drug Dose

Interactions/precautions

5th line Sertraline 75–100 mg/day QTc prolongation and potential for

malignant neuroleptic syndrome

6th line Experimental

approaches

Gabapentin

Phenobarbital

UVB light

Albumin dialysis

Nasobiliary

drainage

Administration recommended only in

specialized centers

FITCH Trial: Bezabrate in cholestatic liver disease and sclerosing cholangitis with moderate to

severe pruritus. A total of 45% of the patients experienced a 50% or higher reduction in itch inten-

sity within 3 weeks of treatment (de Vries etal., Hepatology, 2019)

Q.What is portal cavernoma cholangiopathy (PCC)?

PCC is dened as abnormalities in the extrahepatic biliary system, including the

cystic duct and gallbladder with or without abnormalities in the 1st- and 2nd-

generation biliary ducts in a patient with portal cavernoma.

All of the following criteria should be satised for making the diagnosis:

• Presence of a portal cavernoma

• Typical cholangiographic changes on ERCP or MRCP

• Absence of other causes of these biliary changes

Q.What are the cholangiographic abnormalities seen in PCC?

The characteristic cholangiographic abnormalities include:

• Extrinsic impressions/indentations

• Shallow impressions/indentations

• Irregular ductal contour

• Stricture

• Filling defects

• Bile duct angulation

• Upstream dilatation

• Ectasia

Q.What are the venous plexuses around the biliary tract?

Two venous plexuses drain the biliary tract, which includes a ne reticular epicho-

ledochal venous plexus of Saint on the wall of the bile duct, which drains into the

paracholedochal venous plexus of Petren (also called marginal veins or parabiliary

venous system), which in turn is connected to the posterior superior pancreatico-

duodenal vein, gastrocolic trunk, right gastric vein, and superior mesenteric vein

inferiorly as well as intrahepatic portal vein branches superiorly.

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Q.What is the pathophysiology of biliary changes in PCC?

The development of biliary changes in PCC is due to two components :

(a) Reversible component (55%): These occur due to compression of the bile ducts

by engorged collaterals and tend to reverse after shunt surgery.

(b) Fixed component (45%): Likely due to ischemic changes in the bile duct.

Q.What is the natural history of PCC?

Usually, a diagnosis of EHPVO when associated with PCC usually antedates symp-

tomatic PCC by 8–10 years. The natural history of PCC can be divided into

four stages:

1. Preclinical: Presence of portal cavernoma but no PCC with normal liver bio-

chemistry and no symptoms of PCC.

2. Asymptomatic: Early changes on cholangiography with normal or abnormal

liver biochemistry but no symptoms.

3. Symptomatic: Advanced changes on cholangiography with abnormal liver bio-

chemistry and presence of symptoms without complications.

4. Complicated: Presence of liver dysfunction or brosis, extensive biliary changes

like multifocal strictures or calculi above strictures.

Q.What are the diagnostic modalities used in PCC?

1. USG with color doppler is the initial imaging modality for suspected cases of PCC.

2. MRCP with MR portovenography:

(a) Serves as a comprehensive noninvasive technique.

(b) As accurate as ERCP in delineating biliary changes.

(d) Presence of shuntable vein can be ascertained.

(e) Helps to distinguish between bile duct varices and common bile duct stones.

3. EUS is helpful in delineating the type of choledochal collaterals:

(a) Paracholedochal: Varices at a distance from the bromuscular layer.

(b) Pericholedochal: Large varices (>1mm) which lie outside and adjacent to

the bromuscular layer.

the bro-muscular layer.

(d) Intracholedochal:

(i) Varices at <1mm distance from stent or stone.

(ii) Varices with CBD wall on both sides.

4. ERCP

Traditionally been the gold standard for diagnosis of PCC.

Due to its invasive nature, risk of complications, and need for sequential

imaging, it has now been replaced by noninvasive radiological modalities for

diagnosis. Classication systems include:

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Chandra classication:

Type I: Involvement of extrahepatic ducts only.

Type II: Involvement of intrahepatic bile ducts only.

Type IIIa: Extrahepatic bile duct with unilateral intrahepatic bile duct

involvement.

Type IIIb: Extrahepatic bile duct with bilateral intrahepatic bile duct

involvement.

Llop classication:

Grade I: Irregularities or angulations of the biliary tree.

Grade II: Indentations or strictures without upstream biliary dilation.

Grade III: Strictures with upstream biliary dilation.

*Dilatation is dened as ductal diameter of >7mm for extrahepatic duct

and/or >4mm for intrahepatic ducts.

5. IDUS and cholangioscopy

Q.What are the management strategies in PCC?

Asymptomatic patient: No treatment is advocated. Patients with PCC and other

associated abnormalities like deranged LFT without symptoms should be regarded

as having asymptomatic PCC, and are not candidates for endoscopic therapy.

Approach to symptomatic PCC:

Phased manner of symptomatic PCC management:

First phase:

Sphincterotomy and biliary drainage, with CBD stone removal if present.

Further management:

• Repeated plastic stent exchange or placement of removable covered metal stents.

• Repeated stent exchanges over short periods of time (3–5 years) may occasion-

ally result in the resolution of stenosis.

• Concomitant use of ursodeoxycholic acid (UDCA) may be benecial.

Portal decompression surgery:

• Can be used as rst phase of therapy in patients in whom endoscopic intervention

is not required (e.g., patient with isolated stenosis of CBD and with a shunt-

able vein).

• Usually used as second phase of therapy in symptomatic PCC.

• Involves portal decompression surgery by proximal splenorenal shunt or TIPSS.

• Shunt procedures result in regression of changes of cholangiopathy in 62–88%

of patients.

• 25–30% of patients will require further intervention for PCC after a successful

shunt procedure.

• Nonsurgical candidates: Absent shuntable vein (5–30%) or advanced liver

dysfunction.

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Third phase of therapy: Patients who remain symptomatic despite shunt proce-

dure either due to blockage of shunt or due to persistent obstruction despite patent

shunt may be candidates for second-stage biliary drainage surgery like hepaticoje-

junostomy or choledochoduodenostomy.

Liver transplantation: Secondary biliary cirrhosis is the only accepted indica-

tion for liver transplantation in patients with complicated PCC.

Q.Describe in brief AIDS cholangiopathy

• Stricture formation of the biliary tract due to opportunistic infections leading to

biliary obstruction and cholestatic liver damage.

• Prevalence—Variably reported (26–46% in Pre-HAART era).

• Risk factors

– CD4<100.

• Etiology

– Cryptosporidium parvum is the commonest pathogen associated with AIDS

cholangiopathy—(20–57%).

– Cytomegalovirus: Up to 20% of cases are due to vascular injury.

– Microsporidia: 10%

• Symptoms—Variable presentations ranging from asymptomatic to severe right

upper quadrant pain associated gastrointestinal symptoms:

– Fever and jaundice are less commonly seen

– Substantial weight loss is commonly seen

– Pruritus is remarkably uncommon

• Diagnosis—MRCP and ERCP have the same sensitivity for diagnosis of AIDS

cholangiopathy:

– Papillary stenosis (PS) is the commonest reported nding.

– In 2/3rd papillary stenosis (PS) is present either alone or in combination with

intrahepatic ductal dilatation and multifocal intrahepatic biliary strictures

with alternating normal segments or saccular dilatations.

– 20% of cases may have a characteristic beaded appearance.

– 6–15% have 1–3cm segmental extrahepatic biliary stricture with or without

intrahepatic involvement.

• Management

– Symptomatic treatment: Opioids and neural plexus blocks for abdominal pain.

– Treatment of opportunistic infection is usually ineffective.

– Use of UDCA has been shown to improve abdominal pain and normalization

of liver function abnormalities after sphincterotomy for papillary stenosis.

– The best treatment is the restoration of immune function using HAART or

switching to second-line HAART if there is resistance.

– Endoscopic sphincterotomy.

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Q.What are the diagnostic criteria for Ig-G4 cholangiopathy?

Diagnostic items

1. Biliary tract imaging reveals diffuse or segmental narrowing of the intrahepatic

and/or extra-hepatic bile duct associated with the thickening of the bile duct wall.

2. Hematological examination shows elevated serum IgG4 concentrations

(≥135mg/dl).

3. Associated disease: Coexistence of autoimmune pancreatitis, IgG4-related dac-

ryoadenitis/sialadenitis, or IgG4-related retroperitoneal brosis.

4. Histopathological examination shows:

(a) Marked lymphocytic and plasmacyte inltration and brosis.

(b) Inltration of IgG4-positive plasma cells: >10 IgG4-positive plasma

cells/HPF.

(d) Obliterative phlebitis.

Optional: Effectiveness of steroid therapy

Denite diagnosis: (1) + (3) or (1) + (2) + (4) a, b or (4) a, b, c or (4) a, b, d

Probable diagnosis: (1) + (2) + Optional criteria

Possible diagnosis: (1) + (2)

It is necessary to exclude PSC, malignant diseases such as pancreatic or biliary

cancers, and secondary sclerosing cholangitis. When it is difcult to differentiate

from malignant conditions, a patient must not be treated with empirical steroid ther-

apy but should be referred to a specialized medical facility.

Q.How do you distinguish between IgG4-SC and Primary Sclerosing

Cholangitis (PSC)?