Wednesday May 27th Management of liver cirrhosis

On Wednesday, we talked about some management of ascities in the setting of cirrhosis.

Management of the underlying cause of cirrhosis (hepatitis hemochromatosis, etc), and approach to a patient with new onset ascites is a whole other topic on its own.

In general, all patients with new onset ascites should have a diagnostic paracentesis. When deciding on what to send this fluid for, consider the C’s as with taking fluid from anywhere else.

1.     CBC with diff (specically focussing on >500 WBC or 250 PMN for spontaneous bacterial peritonitis. A high amount of Red blood cells possibly suggestive of bleed/malignancy.

2.     Culture and gram stain: for SBP, E.coli, Kelbsiella, and Strep pneumo being the most common agents. If we see a polymicrobial culture one should consider secondary peritonitis (perforation in colon).

3.     Chemistry: Total protein and albumin, which is useful when we compare this to that in the serum. When commenting on a exudative fluid in ascetic fluid, it is actually more proper to refer to the SAAG, the serum ascities albumin gradient. A value >11 would imply a chronic process associated with increase portal pressures – a transudative process such as cirrhosis, heart failure, budd chiari, portal vein thrombosis. A SAAG < 11 would imply an acute inflammatory process and not typically associated with increased portal pressures: autoimmune disorders, nephrotic syndrome, TB, pancreatitis.

4.     Cytology: can be sent in new onset asicites especially when malignancy is being considered, yield is higher with sending three samples, however in a patient with chronic ascities due to liver disease, going in for a routine tap, this would be a waste of resources to send.

5.      

Of note choosing wisely Canada and American guidelines bring up that is not necessary to give FFP (for high INR) or platelets to these individuals as paracentesis carries a low risk of bleed and bleeding risk is more operator dependant rather than based on INR and platelets.

*note, this is different from high INR on warfarin

The pathophysiology of ascites is still somewhat controversial. Portal hypertension appears to be more a result of cirrhosis, and associated with ascities but actually not the cause. It is clear that there is splanchnic vasodilation, possible from an increase in nitric oxide in response to portal hypertension that may make liver capillaries more leaky. Also with lower splanchnic BP this likely causes kidnesy to reabsorb more sodium/water.

In morning report we talked about more chronic management of these patients as opposed to some of the acute complications (which I will briefly touch on at the end of this post).

1.     Screening for varices: It is recommended that patients with a new diagnosis of cirrhosis undergo EGD to screen for esophageal varices since these bleeds have a high mortality. With large varices, these can be banded to prevent future bleeds and a follow up EGD is usually done ~2 weeks after. Patients with low risk decompensated cirrhosis (liver function is ok, no ascities), might not need to be screened unless new symptoms/anemia develop. Beta blockers can be given for varices however some patients may not tolerate them as their baseline BP is low.

2.     Fluid balance: Lasix 40 spironolactone 100 is the classic ratio of diuretics, as that’s what’s been studied. Specifically the spironolactone can help with increasing potassium (which may be lowered by Lasix). Sodium of less than 2 grams of salt per day. Patients should get used to weighing themselves daily and be cognizant of increasing weight with abdo distension. Often patients should be educated how to increase their diuretics, to loose up to 1 kg/day if they have peripheral edema (500g without). Patients who are refractory to diuretics (after checking for adherence) may undergo large volume paracentesis ~2-4 weeks. Drains are not ideal as they can get infected. TIPS procedure done by interventional radiology is a way of bypassing the liver and may help refractory ascities, but can cause hepatic encephalopathy ~30%. Asking patients to stay on a restricted fluid diet is generally more realistic when they are hyponatremic from their liver disease  (sodium <130). This should be a conversation with the patient, if they can’t adhere to this, probably best to just increase their diuretics.

3.     Hepatic encephalopathy: There are different stages of this, coma being stage 4, that’s just no fun for anyone, patient’s that are confused can be checked for asterixis.. The mechanism behind this is also of debate, uptodate has like 6. Lactulose works, potentially by acidifying the intestines for ammonia to get turned into ammonium and can get excreted. So what do you do for these comatose patients? An NG tube can be put in, or a lactulose enema.  PEG can also be used as a relatively recent trial, the HELP trial http://archinte.jamanetwork.com/article.aspx?articleid=1907002

Showed that PEG actually helped resolved HE more quickly than lactulose. Patient’s who get HE without clear precipitants should be on this regularly, but choosing wisely guidelines in the states say this can be stopped if they were encephalopathy from a clear event. So… they may not have to be on this for life which is great for them because it tastes disgusting.

Other complications to pay attention to:

Patient with ascities that comes in with increased creatinine and sig. edema. DO NOT give them their diuretics, in the biggest concerns is hepatorenal syndrome, you need to check their urine (to make sure there is no ATN, GN,) and give them a fluid challenge! If there have tense ascities, may take off 4 liters, no more.

Patient with cirrhosis comes in with fever, abdo pain: rule out SBP! Will likely be on lifelone antibiotics after.

Patient with cirrhosis comes in with anemia, melena. Rule out upper GI bleed, triple therapy with octreotide (bolus 50 then 50 mcg/hr until scope) and PPI 80 mg bolus then 8 mg/hr until scope. And ceftriaxone 1 g daily to prevent SBP  - the only thing that has been shown to have mortality benefit in this situation.

Other pearl: It is generally recommended that you may remove 5 L via paracentsis without replacing albumin, after that we generally replace 6 g/kg of weight.  Our albumin comes in 100 mL 25% (25 g) bottles.

Baclofen can be used to reduce alcohol cravings in cirrhotics who continue to drink

Below is the choosing wisely recommendations from AASLD (American Association for the Study of LIver disease)

Below is updated 2012 recommendations form AASLD

http://aasld.org/practiceguidelines/Pages/guidelinelisting.aspx