TRIPASS XR تري باس

 

85

The AASLD guidelines mention that as the level of experience as well as

technology with TIPS improves, the outcomes associated with TIPS in future trials

may also improve.

38 Currently, the AASLD treatment guidelines continue to

recommend TIPS for the treatment of refractory ascites in patients for whom

paracentesis is contraindicated, ineffective as determined by the frequency of

repeated paracentesis (more than 3 times per month), or intolerant of repeated largevolume paracentesis.

86

p. 545

p. 546

PERITONEOVENOUS SHUNT

A peritoneovenous shunt consists of a surgically implanted valve in the abdominal

wall, an intra-abdominal cannula, and an outflow tube tunneled subcutaneously from

the valve to a vein that empties directly into the superior vena cava. In this manner,

ascitic fluid can be withdrawn from the abdominal cavity and be returned to the

vascular space. Multiple contraindications exist to surgical shunts and significant

surgical risks increase in likelihood with worsening hepatic function.

87 The lack of

survival benefit, surgical complications, including fibrous adhesions complicating

future liver transplantation, and the high risk of shunt occlusion have led to the

reserving of peritoneovenous shunt procedures for patients with refractory ascites

that are not candidates for paracentesis, liver transplantation, or TIPS.

38

CLONIDINE

It has been shown that the activation of the sympathetic nervous system leads to renal

hypoperfusion and sodium retention. The activated sympathetic nervous system

stimulates renal α1

-adrenoreceptors and causes decreases in renal blood flow and

glomerular filtration rate. Additionally, norepinephrine increases proximal tubular

reabsorption of sodium and enhances renin, aldosterone, and vasopressin

secretions.

88–90 Preliminary evidence suggests that clonidine may be of benefit in

refractory ascites and an activated sympathetic nervous system. Lenaerts et al.

91

conducted a very small study in patients randomly assigned to receive repeated

large-volume paracentesis (4–5 L every 48 hours) plus IV albumin (7 g/L ascites)

until ascites disappeared, or a combination of clonidine 0.075 mg BID for 8 days and

then clonidine 0.075 mg BID with spironolactone 200 to 400 mg daily for 10 days.

Both groups were discharged with spironolactone adjusted according to individual

response. During the first hospitalization, the mean weight loss in the paracentesis

group was higher than in the clonidine group, but the mean hospital stay was shorter

in the clonidine group (p ≤ 0.01). Clonidine decreased sympathetic activity and

increased glomerular filtration rate. During the follow-up, the number of rehospitalizations for ascites was higher and the mean time to the first readmission was

shorter in the paracentesis group than in the clonidine group (p ≤ 0.01).

91

In another

trial, Lenaerts et al.

90

found that the time to first readmission for tense ascites was

shorter in the placebo group than in the clonidine group. Both groups received

spironolactone and furosemide.

90 The addition of clonidine to diuretic therapy may

be an effective therapeutic modality; however, a large randomized trial is needed to

establish the role of clonidine in the treatment of ascites. Currently, the use of

clonidine is considered experimental by the AASLD guidelines.

38

In consideration of R.W.’s increasing serum creatinine concentration, rising BUN,

and the grave prognosis of hepatorenal syndrome, TIPS is a reasonable therapeutic

alternative if R.W. cannot tolerate or requires frequent large-volume paracentesis.

Patients with a history of spontaneous bacterial peritonitis (SBP) and ascites with

advanced liver failure or renal impairment appear to benefit from SBP prophylaxis.

R.W. would benefit from the addition of SBP prophylaxis because of his history of

SBP (see Chapter 70, Intra-Abdominal Infections).

ESOPHAGEAL VARICES

Treatment

CASE 25-2

QUESTION 1: C.V., a 55-year-old, pale-looking woman with alcohol-induced cirrhosis, was admitted for a

chief complaint of hematemesis. C.V. has a history of recurrent upper GI bleeding and documented esophageal

varices. She has no other significant medical history. She is not taking any medications and has no known drug

allergies. On examination, her blood pressure (BP) was 78/40 mm Hg, pulse rate was 110 beats/minute, and

respiratory rate was 22 breaths/minute. Her skin was cold; chest and cardiac examinations were within normal

limits and abdominal examination revealed ascites and a palpable spleen. Bowel sounds were normal.

Laboratory values included the following:

Hgb, 7 g/dL

Hct, 22%

Albumin, 3.0 g/dL

AST, 160 IU

ALT, 250 IU

Alkaline phosphatase, 40 IU

Creatinine, 2.0 mg/dL

PT, 18 seconds (INR, 1.5)

Serum electrolytes, all within normal limits

An electrocardiogram revealed sinus tachycardia. What are the immediate goals of therapy and treatment

measures of the highest priority in managing C.V.’s hematemesis?

GOALS OF THERAPY

Most patients with cirrhosis develop portal hypertension, which in turn can progress

to bleeding varices (dilated veins in the upper GI tract that protrude into the

esophageal or gastric lumens). Of patients with Child–Turcotte–Pugh class A

cirrhosis, 40% develop esophageal varices, as compared with 85% of those with

Child–Turcotte–Pugh class C.

24,92 Unless varices bleed, they do not cause significant

complications or symptoms.

The progression and severity of varices is directly related to the severity of portal

hypertension. The major site of concern in portal hypertension is the coronary vein,

draining the bottom of the esophagus and upper stomach. The scarring and fibrosis

associated with cirrhosis initially leads to an increase in portal vein pressure (PVP),

which may eventually rise, causing backflow of blood supply and subsequent

increased pressure in the veins coming off the portal vein. Hyperkinetic circulation in

the branches of the portal vein raises the esophageal trans-mural pressure and

increases the risk of upper GI bleeding. Because the veins are designed for lowpressure circulation (5–8 mm Hg) and generally cannot tolerate a sustained

hyperdynamic circulation, the shunting of high portal pressure blood results in gastric

and esophageal varices. When PVP exceeds 12 mm Hg, patients are at increased risk

of variceal hemorrhage.