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830 > Cirrhosis > Flashcards

Cirrhosis Flashcards

1
Q

Cirrhosis Complications

A
  1. Ascites
  2. Hepatic Encephalopathy
  3. Variceal Bleeds
  4. Infection
  5. SBP
  6. Renal Effects
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2
Q

Ascites

A
  • Most frequent cirrhosis complication
  • Rationale for treatment: most people who develop ascites die within 2 years, leads to other complications when left uncontrolled
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3
Q

Ascites Goals for Treatment

A
  • Minimize fluid overload to minimize risk of infection and other complications
  • Improve QoL since overload can be uncomfortable and limit lifestyle
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4
Q

Ascite Treatment Options

A
  • Salt Restriction
  • Diuretics
  • Paracentesis
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5
Q

Salt Restriction

A
  • Recommended forall cirrhotics with ascites
  • Max of 2g/day
  • Less salt, less fluid retention, less overload
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6
Q

Diuretics

A
  • Spironolactone: 50-100 mg daily, max 400 mg/day
  • Blocks RAAS and can be used for MILD fluid overload
  • Spironolactone 100 mg + Furosemide 40 mg: Furosemide should be started at 20-40 mg and can be titrated up to 160 mg
  • AVOID furosemide alone - can cause salt reabsorption and is less effective than spironolactone monotherapy
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7
Q

Overdiuresis

A
  • Overdiuresis with diuretics can potentiate renal failure
  • Monitor aggressive diuresis
  • Spironolactone monotherapy may be preferred for the reduced risk for overdiuresis
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8
Q

Diuretic SE

A
  • Renal impairment from volume depletion: hold diuretics if SCr changes by >50% from baseline
  • Hyponatremia
  • Hepatic encephalopathy
  • Spironolactone can cause painful gynecomastia, hyperkalemia
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9
Q

Parencentesis

A
  • Good for patients with refractory ascites, not responding to diuretics, severe SE
  • Large (>5 L of ascite fluid) and small volumes (assess fluid for things like infection)
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10
Q

Large Volume Parencentesis

A
  • Can be done outpatient
  • SE relief only
  • Recurrent paracentesis also has infection risk and impairs endogenous albumin production (continue ascite pattern)
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11
Q

Parecentesis Complication

A
  • PICD (Paracentesis induced circulatory dysfunction)
  • Increase in plasma renin activity because of decreased arterial blood volume
  • Causes re-accumulation of ascites, shorter survival time, reduced renal function
  • Prevent with albumin 6-10 g per liter of fluid removed when they have large volume removal
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12
Q

Hepatic Encephalopathy

A
  • Confusion/disorientation due to toxin build up
  • Exact cause/mechanism is unknown
  • Mainstay: Lactulose
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13
Q

Hepatic Enceph. Treatment Options

A
  • Lactulose
  • Rifaximin
  • Systemic Antibiotics
  • Flumazenil
  • Protein Restrictions: encourage patients to obtain protein from dairy/vegetables instead of meat
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14
Q

Lactulose

A
  • Non absorbable disaccharide broken down by bacteria in colon to acidify colon and prevent ammonia absorption and slow GI motility
  • Dosed: 45 mL every 1-2 hours until loose bowel movement
  • Titrate to have 2-3 loose movements per day
  • Use chronically
  • Taste and SE not well liked, makes adherence difficult
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15
Q

Lactulose SE

A
  • Diarrhea
  • Flatulence
  • Abdominal cramping
  • Aspiration for patients with nasogastric tube
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16
Q

Rifaximin

A
  • Semi-synthetic, non-systemic abtibiotic for prophylaxis
  • Causes fewer/shorter hospitalizations, and thus reduced hospital costs
  • Better tolerated and faster onset than lactulose
  • Dose: 550mg BID
  • EXPENSIVE
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17
Q

Systemic Antibiotics

A
  • Reduce urease producing bacteria in GI tract have been used
  • Fallen out of favor due to SE
  • Neomycin: accumulation can cause nephrotoxicity and ototoxicity
  • Metronidazole: risk of peripheral neuropathy for long term use
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18
Q

Flumazenil

A
  • Benzo antagonist used for refractory cases

- Also used for suspected benzo overdoses (rare)

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19
Q

Variceal Bleeds

A
  • Medical emergency requires endoscopic evaluation (EGD)

- Goal: stop bleed and prevent rebleeding

20
Q

Acute Bleed Treatment

A
  • Octreotide 25-50 mcg IV bolus, then 25-50 mcg/hr continuous infusion for 3-5 days until EGD (rubber bands) performed
  • Octreotide: synthetic analog of somatostatin normally found throughout GI tract and acts to decrease BP
  • Temporary way to reduce bleed until endoscopy
21
Q

Bleed Infection Prophylaxis

A
  • Quinolones
  • 3rd Generation Cephalosporins
  • Rationale: concern for bacterial translocation with resulting infection, reduces mortality for prophylaxis
22
Q

Quinolones for Bleed Prophylaxis

A
  • Norfloxacin 400 mg BID x 3-7 days (not common)
  • Cipro 400 mg IV BID x 3-7 days
  • Cipro 500 mg PO BID x 3-7 days
23
Q

3rd Generation Cephalosporins for Bleed Prophylaxis

A
  • Ceftriaxone 1g IV QD x 3-7 das
  • Ceftriaxone 2g IV q8h x 3-7 days
  • *CHOICE FOR PATIENTS WITH ASCITES, MALNUTRITION, ENCEPHALOPATHY, BILIRUBIN > 3, OR FLUOROQUINOLONE RESISTANCE**
24
Q

Other Bleed Goals/Interventions

A
  • Volume resuscitation
  • Loss of volume can lead to other complications
  • Normal saline is first choice, but blood/blood products are given if hemoglobin < 8
25
Q

Bleed Prevention

A
  • Medium to large varices => reduce portal tributary blood flow and reduce intrahepatic resistance to reduce pressure
  • Treatment: NON-selective beta blocker like Propranolol 20 mg PO BID or Nadolol 40 PO QD
  • Titrate up as tolerated to 25% reduction of HR
  • SE: lightheaded, fatigue, SOB (nadolol better tolerated)
26
Q

BB Efficacy/Controversy

A
  • Reduce risk of first bleed with medium/large varices
  • Patients with ascites may have increased mortality on BB from altered CO and circulatory abnormalities
  • Cost effective
  • DON’T USE SELECTIVE BETA BLOCKER
27
Q

Infection Risk

A
  • Liver is important for innate immunity (biosynthesis of proteins)
  • Cirrhotic changes affect immune function: altered structure allows for increased permeability and translocation of bacteria
28
Q

Cirrhosis + Spleen Function

A
  • Largest lymphoid organ, produces opsonizing antibody critical for clearance of encapsulated bacteria
  • Lack of spleen/hypofunction associated with overwhelming sepsis
  • Portal hypertension causes splenomegaly which impairs function
29
Q

SBP

A
  • Spontaneous Bacterial Peritonitis

- Infection of ascitic fluid without evidence of abdominal source(50% associated with bacteremia)

30
Q

SBP Risk Factor

A
  • Prior Episode
  • Variceal Bleed
  • Ascitic Fluid protein < 1g/dL
  • Serum total bilirubin >2.5 mg/dL
  • Use of PPIs
  • *20% mortality rate and 70% recurrence rates**
31
Q

Diagnosing SBP

A
  • Clinical signs of fever
  • Abdominal pain
  • Unexplained encephalopathy
  • Ascitic fluid culture: PMN > 250 highly suspecious of SBP (TREAT!)
  • *60% with PMN count and symptoms don’t have SBP**
32
Q

Causers/Treating SBP

A
  • Causation: gut bacteria, enterobacteriaceae
  • Treatment: empiric therapy targets gram negative pathogens
  • Options: Cefotaxime 2g IV q8h x 5-10 days or Ceftriaxone 1g IV q24h x 5-10 days
  • Alternatives: fluoroquinolones, amoxicillin-clavulanic acid
33
Q

SBP Prophylaxis

A
  • Goal: decontaminate GI tract to minimize risk of infection
  • Primary: managing acute bleeds
  • Secondary: antibiotic options for SBP survivors to prevent recurrence
34
Q

SBP Secondary Prophylaxis

A
  • Bactrim DS 1 PO daily or 5x/week
  • Cipro 250-500 mg PO daily
  • Cipro 750 mg PO q week (resistance concerns)
  • Levo 250 mg PO daily or Norfloxacin 400 mg PO daily (latter isn’t available in US)
35
Q

Other Spontaneous Infections

A
  • Similar pathogenic mechanisms and management with no obvious bacterial source
  • Risk increases with progressive liver disease
36
Q

Renal Effects of Cirrhosis

A
  • Portal hypertension causes systemic vasodilation to compensate which leads to hypoperfusion in the kidneys
  • RAAS/sympathetic NS is then activated in response causing salt/water retention
  • Decline in GFR can be acute/chronic, monitor SCr changes
37
Q

Renal Failure in Cirrhotics

A
  • SCr increases by more than 50% of baseline and is over 1.5 mg/dL
  • Greatest loss of GFR when SCR increases from 1-2 mg/dL
38
Q

AKI

A
  • Likely occurs much earlier and is evidence with increase in SCr by 0.3 mg/dL within 48 hours
  • AVOID all nephrotoxic agents to prevent renal damage
39
Q

AKI Causers

A
  • Renal hypoperfusion: most common. Includes hemorrhage, vomiting/diarrhea, sepsis. Medication: NSAIDs, ACE-I, diuretics
  • Acute tubular necrosis: direct insult to kidneys. Medications: NSAIDs, aminoglycoside therapy
40
Q

Hepatorenal Syndrome

A
  • Cirrhosis/severe liver disease patients having both the liver and kidney fail
  • If both fail, only option is dual organ transplant which is very limited
  • Type I: rapidly progressive with SCr doubling or a 50% drop in CrCl to < 20 mL/min in LESS THAN TWO WEEKS
  • Type II: Slowly progressive due to systemic effects of cirrhosis, goal: minimize renal insult by avoiding nephrotoxic agents and preventing renal injury
41
Q

Type I Hepatorenal Syndrome Risk

A
  • SBP/other infections are risks for renal failure due to exacerbation of hypoperfusion
  • Patients with confirmed SBP are at high risk of developing renal dysfunction if bilirubin >4, BUN 30, and/or SCr > 1
42
Q

Hepatorenal Treatment

A
  • Albumin + Vasopressor
  • Albumin increases volume to help GFR
  • Vasopressors indirectly help with renal perfusion
43
Q

Vasopressor Examples

A
  • Midrodrine/Octreotide: not approved and small studies
  • NE: small studies, improves BP and is often used for ICU care
  • Terlipressin: not approved in US guidelines, studies ongoing
44
Q

Overall Hepatorenal Management

A
  • Maintain volume (albumin, fluid, packed blood)
  • Stopping diuretic use if possible
  • Preventing/treating sepsis
  • Any major changes in volume or infections are risks for renal injury and therefore hepatorenal syndrome
45
Q

Albumin Use in Cirrhosis

A
  • Albumin is not used in all cirrhotic patients routinely because there are concerns of harm
  • ay increase risk of mortality in critically ill patients with hypovolemia due to burns or hypoalbuminemia
  • After infusion of albumin, there is increased degradation and decreased endogenous production of albumin
46
Q

Bleeding Risk

A
  • Cirrhosis affected clotting factors and changes in coagulation, results in elevated INR
  • Fresh frozen plasma (FFP): acute bleed management
  • Vitamin K: not likely the cause of elevated INR in cirrhosis patients, but can trial it for 3 days to make sure and stop if no change in INR is seen
47
Q

Pain + Liver Disease

A
  • Tylenol: Acute, short term use (<14 days) of <2g/day appears to be safe (don’t use with alcohol, caution with combo products)
  • NSAIDs/Aspirin: should be avoided due to increases bleeding risk, blunt diuretic response, and impaired GFR
  • COX-2I: little data, not recommended
  • Opioids: require understanding of kinetics and clinical judgement (can precipitate encephalopathy due to decreased GI motility)
  • Avoid nephrotoxic agents
  • Avoid meds that cause electrolyte abnormalities, renal insufficiency, or pose a bleeding risk (biggest problems with cirrhosis patients)

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