Module 7: Complication of Cirrhosis Flashcards
Dr. Covert EXAM VI
Which factors are used to classify the stage of liver disease when using Child-Pugh?
-determines the severity of liver disease
-used for considerations in drug dosing
-Tbili, PT (prothrombin time), Albumin, Ascites, Encephalopathy
A: 5-6 points
B: 7-9 points
C: 10-15 points (severe)
Model of End-stage Liver disease (MELD)
-assess the 1-year mortality and
-assess the position on the transplant list
score
10-19: 6% mortality
20-29: 19.6%
30-39: 52.6%
>40: 71:3%
Maddrey Discriminate Function
(just know what it is for)
-help to decide if steroids are needed in EtOH-related liver disease
asses PT and Tbili
-if >32 -> poor prognosis, use steroids
-Prednisolone 40 mg PO daily x 4 weeks, then 2-week taper
What causes fluid accumulation in the peritoneal cavity?
-activated RAAS system:
sodium and fluid retention (in the blood vessels)
-reduction in albumin
decreased oncotic pressure in the blood vessel -> fluid shifts to tissues
What is a Paracentesis?
-catheter instilled into the abdomen and the fluid is drained off
-some patients may have it acutely or chronically (depending on how quickly the fluid backs up)
In patients who undergo Paracentesis, what should be administered to them?
if a large volume of removal (>5L paracentesis)
6-8g of 25% (25g/100ml) albumin /L removed
if more than 10L paracentesis ->
60-80g of 25% albumin / L removed
-there are also 5% (5g/100ml) products -> but 25% is better bc we want more albumin to restore the oncotic pressure and 5% would need more volume which they have more than enough!
Which diuretics are used in Ascites management?
-Spironoalctone and furosemide
(ratio of 100 mg spironolactone: 40 mg furosemide)
-goal is to facilitate Na excretion, and maintain eukalemia
Explain the ratio between Spironolactone and furosemide
in ascites: spironolactone is ued as the diurtetic
whereas in HF patients it is used to mitigate the RAAS system
is furosemide not the stronger diuretic???
in patients with hyperkalemia use a higher dose of furosemide than spironolactone (since K sparing)
Which electrolytes should be restricted to cirrhosis patients with Ascites?
-Sodium (Na+) restricted: <2g/day
-fluid restricted: <1L/day, only if severe hyponatremia (<125 mmol/L)
Vaptans (tolvaptan, conivaptan) improve Na but not outcomes
ADR: hepatotoxicity -> so not often used
short-term (<30 day) use only
Why are Vaptans often not used in patients with Ascites?
-they are often hypotonic hypervolemic hyponatremia -> sodium and fluid restriction works best
-Vaptans provide aquaresis -> excretion of water without electrolytes
What causes Encephalopathy in patients with cirrhosis?
-accumulation of nitrogenous substances
-Hyperammonemia (bc the liver can’t eliminate it)
-cause CNS toxicity (altered mental status)
-treat only symptomatic patients
Who should be treated with Hepatic Encephalopathy prophylaxis?
-high-risk patients
-patients with a history of encephalopathy
How is hepatic Encephalopathy treated?
-Lactulose:
*MOA: traps ammonia from the blood to the gut (converts it to ammonium, charged), kills bacteria, and osmotically removes ammonia from the body with the stool
*titrate to 2-3 loose bowel movements per day, not to a dose
-Rifaximin
*adjunctive to Lactulose, avoid monotherapy
it has only 1 MOA, whereas Lactulose has 3
Esophageal varices
-varices are small blood vessels around the esophagus (where it connects to the stomach)
-they develop to to reduce pressure in severe portal hypertension -> blood flows through this vessels to relieve pressure
-these vessels are fragile and may burst (upper GI bleeding)
Who is indicated to receive therapy for Esophageal varices?
-varices > 5 mm - need endoscopy to assess
treat with medication or endoscopic variceal ligation (EVL)
-varices < 5mm + increased risk of bleeding
Child pugh B or C
-acute hemorrhage (variceal bleed)
patients vomit blood, hemodynamically unstable, anemic
What are Primary prevention therapy options in Esophageal varices?
Non-selective BB: Propanolol, Nadolol, Carvedilol
-if they can’t tolerate BB or other reasons to not start BB (severe COPD?) -> endoscopic variceal ligation (EVL) every 2-8 weeks
-> esophagogastroduodenoscopy (EDG) 3-6 months after EVL, then every 6-12 months
What is the goal BP when treating patients with BB in esophageal varices?
SBP >90 mmHg
HR: 55-60 bpm
Endoscopic Variceal Ligation (EVL) vs Sclerotherapy
-EVL: putting a band over the varices
-Sclerotherapy: injecting a sclerosing agent into variceal lumen
Treatment options in variceal hemorrhage?
variceal is bleeding (different from varices that are identified but do not bleed)
-Blood transfusion/ volume resuscitation
-Control acute bleeding and prevent re-bleed (drugs or endoscopy)
-Prophylaxis for spontaneous bacterial peritonitis (SBP)
Drugs used to stop variceal bleeding
-after volume resuscitation and giving blood
-prevent worsening of the bleed
-Octreotide: selective vasoconstriction of varices
50 mcg IV bolus
50 mcg/h continuous infusion for 2-5 days
also Vasopressin, Somatostatin, Terlipressin
Other treatment options in variceal bleeds
-Transjugular Intrahepatic Portosystemic Shunt
(TIPS)
*a placed stent between portal and hepatic vein, no pharmacologic need for secondary treatment
-Balloon Occluded Retrograde Transvenous Obliteration (BRTO)
balloon applies pressure to the bleeding varices
What are the treatment options for secondary prevention?
for life-time
-Propanolol: twice a day
20-40 mg PO BID
max (no ascites): 320 mg PO daily
max (w/ ascites): 160 mg PO daily
-Nadolol
20-40 mg PO daily
max (no ascites): 160 mg PO daily
max (ascites): 60 mg PO daily
-EVL: every 1-4 weeks until variceal eradication
-Prophylaxis for spontaneous bacterial peritonitis (SBP) X 7 days
Which organism may cause Spontaneous bacterial peritonitis (SBP)
-Infection of ascitic fluid:
Klebsiella pneumonia, E. coli, S. pneumo
-develops in 10-20% of patients with ascites
How is SBP diagnosed?
-assess polymorphonuclear leukocytes (PMNs, immature white blood cells) after Paracentesis in ascitic fluid -> treat if > 250
-treat when SBP s/sx are seen: fever, abdominal pain, high WBC, AKI, acidosis, encephalopathy
When to use SBP prophylaxis (prevention)?
-prophylaxis (prevention), not treatment
-in patients with Variceal bleed
Ceftriaxone 1g IV daily X 7 days
Ciprofloxacin 750 mg PO daily or 400 mg IV BID X 7 days
-in survivors of SBP (life-long prophylaxis, high risk of reinfection)
Ciprofloxacin 500 mg PO daily
Bactrim 1 DS tab PO daily
Treatment of SBP
cover Klebsiella pneumo, E. coli, Strep pneumo
-Cefotaxime (or Ceftriaxone) 2 g IV Q 8h, Ceftriaxone 2 g IV daily X 7 days
-consider covering MRSA and Pseudomonas if the patient with healthcare-associated SBP
-25% albumin: greater benefit in patients with AKI and jaundice
1.5g/kg on day 1
1g/kg on day 3
When does albumin have a great benefit when treating SBP?
patients with AKI and jaundice
Pathophysiology of Hepatorenal Syndrome
-Portal HTN -> splanchnic (organs of the abdomen) vasodilation -> lowering circulation volume, causing hypotension
-due to hypotension -> activation of the RAAS system
RAAS causes sodium retention (Ascites)
RAAS causes vasoconstriction (Hepatorenal syndrome)
How is Hepatorenal Syndrome diagnosed?
-Cirrhosis + ascites
-increase in SCr >/= 0.3 from baseline with 48h or more than 50% increase in 7 days
-no response after 2 days of diuretics (due to ascites) being stopped and albumin (1g/kg) infusion
-no shock
-no nephrotoxic meds
-no structural kidney disease
Hepatorenal Syndrome Treatment
EXAM
-ultimately liver transplant (mortality w/o a transplant is 50-70%)
- Albumin + diuretic withdrawal
-Albumin 25%: 1 g/kg/day (max of 100 g/ day) on day 1, then 40-50 g/day while on vasoconstrictor
if no response add Vasoconstrictor
-Vasoconstrictors: treats splanchnic vasodilation -> increase circulating volume -> (-) RAAS
Terlipressin (Newly FDA-approved)
Norepinephrine
Octreotide + Midodrine (less effective)
If no response after 7 days, may discontinue therapy
If response, continue for up to 14 days
