Cirrhosis Flashcards
1
Q
Cirrhosis Complications
A
- Ascites
- Hepatic Encephalopathy
- Variceal Bleeds
- Infection
- SBP
- Renal Effects
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
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
4
Q
Ascite Treatment Options
A
- Salt Restriction
- Diuretics
- Paracentesis
5
Q
Salt Restriction
A
- Recommended forall cirrhotics with ascites
- Max of 2g/day
- Less salt, less fluid retention, less overload
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
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
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
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)
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)
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
12
Q
Hepatic Encephalopathy
A
- Confusion/disorientation due to toxin build up
- Exact cause/mechanism is unknown
- Mainstay: Lactulose
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
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
15
Q
Lactulose SE
A
- Diarrhea
- Flatulence
- Abdominal cramping
- Aspiration for patients with nasogastric tube
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
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
18
Q
Flumazenil
A
- Benzo antagonist used for refractory cases
- Also used for suspected benzo overdoses (rare)
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)
